http://www.virtualmedicalcentre.com/drugs/ Virtual Medical Centre - Medical Drug List en-us Copyright 2013 Virtual Medical Centre. All Rights Reserved. 6/20/2013 720 http://www.virtualmedicalcentre.com/drugs/alu-tab/3 Antacid. Neutralises gastric acid, also has mild astringent and absorbent properties. Phosphate excretion. Forms nonabsorbable phosphate salts in the bowel and therefore increases phosphate excretion. http://www.virtualmedicalcentre.com/drugs/amfamox/4 Competitive inhibitor of histamine H2-receptors. The primary clinically important pharmacological activity of Amfamox is inhibition of gastric juice secretion. Amfamox reduces the acid and pepsin content, as well as the volume of basal, nocturnal and stimulated gastric secretion. Pharmacology Gastrointestinal effects: Amfamox is a competitive inhibitor of histamine H2-receptors. The primary clinically important pharmacological activity of Amfamox is inhibition of gastric secretion. Both the acid concentration and volume of gastric secretion are suppressed by Amfamox, while changes in p http://www.virtualmedicalcentre.com/drugs/andrews-tums-antacid/5 Calcium carbonate neutralises excess acid produced by the stomach, thereby reducing the burning symptoms associated with indigestion. Sustained calcium levels in the blood also help to prevent excess bone resorption associated with osteoporosis. http://www.virtualmedicalcentre.com/drugs/ausran/6 Ranitidine acts by competitively blocking H2 receptors on gastric parietal cells thereby reducing gastric acid secretion. http://www.virtualmedicalcentre.com/drugs/carafate/7 Carafate is not an antacid, but rather a cytoprotectant substance, which works by creating a barrier at the ulcer site and protecting it from the harmful action of the stomachs natural acid. It also protects against the digestive substances pepsin and bile. In addition to providing a protective layer, sucralfate also forms a complex with pepsin and bile as a further method of protecting the ulcer from their corrosive properties. http://www.virtualmedicalcentre.com/drugs/chem-mart-ranitidine/9 Ranitidine is a histamine H2-receptor antagonist with no action at H1-receptors and works to prevent gastric acid secretion in the stomach. Acid secretion in response to basal stimulation, histamine, food and other stimulatory factors is prevented equally. A plasma Ranitidine concentration of 50ng/ml will reduce gastric acid secretion by 50%. Gastric acid secretion stimulated by pentagastrin is inhibited according to Ranitidine dose. Secretion of gastric mucus and pancreatic enzymes is not affected by Ranitidine, and bacterial growth is not affected by the decreased acid levels in the stom http://www.virtualmedicalcentre.com/drugs/cytotec/12 Misoprostol is a prostaglandin E1 analogue. It protects the gastrointestinal mucosa by increasing the secretion of mucus in the stomach and by stimulating bicarbonate secretion in the duodenum. Misoprostol also has a direct action on gastric parietal cells to inhibit acid secretion. http://www.virtualmedicalcentre.com/drugs/gastrogel/19 The ingredients in Gastrogel have antacid activity, meaning they can neutralise existing acid in the stomach. This increased stomach pH provides relief from hyperacidity symptoms. They have no activity in preventing more acid production. Antacids that contain aluminium, as Gastrogel does, also have a cytoprotective effect on the gastric mucosa, and the combination with magnesium salts helps balance the constipating effects that aluminium can have. The role of simethicone is to reduce the surface tension of gastric contents thereby reducing flatulence. http://www.virtualmedicalcentre.com/drugs/gaviscon/20 The main ingredient in Gaviscon, alginic acid, works as an anti-reflux agent. It reacts with gastric acid to produce a frothy layer over the stomach contents, which immediately prevents reflux. The sensitive mucosa of the oesophagus is no longer exposed to gastric acid and the pain associated with these conditions is relieved. Continued use of Gaviscon and ongoing prevention of reflux allows the damaged tissues to be repaired. Gaviscon ceases activity on leaving the stomach, the alginic acid being neutralised by the alkalinity of the duodenum. It is not absorbed from the gastrointestinal syste http://www.virtualmedicalcentre.com/drugs/gaviscon-double-strength/21 The main ingredient in Gaviscon Double Strength, sodium alginate, works as an anti-reflux agent. It reacts with gastric acid to produce a frothy layer over the stomach contents, which immediately prevents reflux. The sensitive mucosa of the oesophagus is no longer exposed to gastric acid and the pain associated with these conditions is relieved. Continued use of Gaviscon Double Strength and ongoing prevention of reflux allows the damaged tissues to be repaired. Gaviscon Double Strength ceases activity on leaving the stomach, the alginic acid being neutralised by the alkalinity of the duodenum. http://www.virtualmedicalcentre.com/drugs/genrx-cimetidine/23 Cimetidine acts by competitively blocking H2 receptors on gastric parietal cells thereby reducing gastric acid secretion. http://www.virtualmedicalcentre.com/drugs/genrx-ranitidine/24 Ranitidine acts by competitively blocking H2 receptors on gastric parietal cells thereby reducing gastric acid secretion. http://www.virtualmedicalcentre.com/drugs/healthsense-ranitidine/25 Ranitidine is a histamine H2-receptor antagonist with no action at H1-receptors and works to prevent gastric acid secretion in the stomach. Acid secretion in response to basal stimulation, histamine, food and other stimulatory factors is prevented equally. A plasma Ranitidine concentration of 50ng/ml will reduce gastric acid secretion by 50%. Gastric acid secretion stimulated by pentagastrin is inhibited according to Ranitidine dose. Secretion of gastric mucus and pancreatic enzymes is not affected by Ranitidine, and bacterial growth is not affected by the decreased acid levels in the stom http://www.virtualmedicalcentre.com/drugs/hexal-ranitic/26 Ranitidine acts by competitively blocking H2 receptors on gastric parietal cells thereby reducing gastric acid secretion. http://www.virtualmedicalcentre.com/drugs/infant-gaviscon/28 The alginate salts in Infant Gaviscon work as anti-reflux agents. They react with gastric acid to produce a frothy layer over the stomach contents, which immediately prevents reflux. The sensitive mucosa of the oesophagus is no longer exposed to gastric acid and the pain associated with these conditions is relieved. Continued use of Infant Gaviscon and ongoing prevention of reflux allows the damaged tissues to be repaired. Infant Gaviscon ceases activity on leaving the stomach, the alginate salts being neutralised by the alkalinity of the duodenum. It is not absorbed from the gastrointestinal http://www.virtualmedicalcentre.com/drugs/klacid-hp-7/29 Omeprazole: a protein-pump inhibitor that reduces gastric acid production in the stomach. It has also been shown to have a small amount of antimicrobial activity against H. pylori, but this effect is suppressive rather than eradicative. Amoxycillin: an antibiotic that is bactericidal through inhibition of synthesis of cell wall mucopeptide. Clarithromycin: an antibiotic that works by inhibiting bacterial protein synthesis Klacid HP 7: the combination of the above three drugs has been shown to eradicate H. pylori much more effectively than the two antibiotics alone. The mechanism of this sy http://www.virtualmedicalcentre.com/drugs/losec-hp-7/30 Omeprazole: a protein-pump inhibitor that reduces gastric acid production in the stomach. It has also been shown to have a small amount of antimicrobial activity against H. pylori, but this effect is suppressive rather than eradicative. Amoxycillin: an antibiotic that is bactericidal through inhibition of synthesis of cell wall mucopeptide. Clarithromycin: an antibiotic that works by inhibiting bacterial protein synthesis Losec HP 7: the combination of the above three drugs has been shown to eradicate H. pylori much more effectively than the two antibiotics alone. The mechanism of this syn http://www.virtualmedicalcentre.com/drugs/losec-intravenous/31 Omeprazole inhibits the proton pump in the wall of the parietal cells of the antrum of the stomach. This works to reversibly reduce the amount of gastric acid produced in response to all stimuli. The action of Omeprazole is dose dependant and specific, with no effect on histamine or acetylcholine receptors. Inhibition of acid production begins approximately one hour after dose and is maximal at 2 hours. The maximum effect of treatment is usually reached within 4 days. A 10mg dose of Losec intravenous is equivalent to a 20mg dose of Losec tablets (orally). http://www.virtualmedicalcentre.com/drugs/losec-tablets/32 Omeprazole magnesium inhibits the proton pump in the wall of the parietal cells of the antrum of the stomach. This works to reversibly reduce the amount of gastric acid produced in response to all stimuli. The action of Omeprazole is dose dependant and specific, with no effect on histamine or acetylcholine receptors. Inhibition of acid production begins approximately one hour after dose and is maximal at 2 hours. The maximum effect of treatment is usually reached within 4 days. Omeprazole magnesium has also been found to have some antibacterial action and is useful in combination with http://www.virtualmedicalcentre.com/drugs/magicul/33 Cimetidine is a histamine receptor antagonist, and blocks the H2-receptors by competitive inhibition. This blockade of the histamine receptors causes a decreased amount of acid to be produced by the parietal cells of the stomach. Cimetidine blocks acid production in response to all stimuli such as basal regulation, food, histamine, pentagastrin and caffeine. http://www.virtualmedicalcentre.com/drugs/maxor/34 Omeprazole is a proton pump inhibitor. It suppresses gastric acid secretion by irreversibly inactivating the hydrogen/potassium ATPase enzyme system (proton pump). When Omeprazole is ceased the synthesis of new hydrogen/potassium ATPase restores acid secretion. http://www.virtualmedicalcentre.com/drugs/mucaine-2-in-1/37 Mucaine 2 in 1 works as both an antacid and to disperse built-up gas in the stomach. The Aluminium and Magnesium hydroxide components react with the acidic contents of the stomach and neutralise them. As they are antacids only, they have no effect on acid production by the stomach. Simethicone acts to reduce the surface tension of gas bubbles and this disperses any gas that may form due to the reaction of the antacid with the gastric acid. http://www.virtualmedicalcentre.com/drugs/mucaine-suspension/38 Mucaine suspension combines an antacid effect (Aluminium hydroxide and Magnesium hydroxide) with a topical local anaesthetic (Oxethazaine), which helps relieve the pain associated with hyperacidic conditions. Aluminium and Magnesium hydroxide react with stomach acid to neutralise it, but as they are antacids only, they have no effect on acid production by the stomach. The Aluminium hydroxide also lines inflamed gastric mucosa, and this lining helps hold the Oxethazaine in place. Oxethazaine is a stronger local anaesthetic than both cocaine hydrochloride and lignocaine hydrochloride. It has a http://www.virtualmedicalcentre.com/drugs/mylanta-double-strength/39 Mylanta acts by neutralising the hydrochloric acid secreted by gastric parietal cells. http://www.virtualmedicalcentre.com/drugs/mylanta-heartburn-relief/40 The alginic acid component of Mylanta Heartburn Relief forms a colloidal gel by reacting with the gastric acid. This gel floats on the surface of the gastric contents and prevents the reflux of gastric acid into the oesophagus. The gel slowly releases antacid into the gastric contents neutralising gastric acid and inactivating pepsin. http://www.virtualmedicalcentre.com/drugs/mylanta-original/41 Mylanta acts by neutralising the hydrochloric acid secreted by gastric parietal cells. http://www.virtualmedicalcentre.com/drugs/mylanta-rolltabs/42 Calcium carbonate neutralises excess acid produced by the stomach, thereby reducing the burning symptoms associated with indigestion. Sustained calcium levels in the blood also help to prevent excess bone resorption associated with osteoporosis. http://www.virtualmedicalcentre.com/drugs/nexium/44 Esomeprazole is a proton pump inhibitor.1-3 It suppresses acid secretion (both basal and stimulated) by irreversibly binding tonbsp;the hydrogen/potassium ATPase enzyme system in parietal cells.1-3 http://www.virtualmedicalcentre.com/drugs/pepcid/47 Famotidine is a histamine (H2) receptor antagonist that competitively inhibits these receptors to reduce gastric acid secretion. Acid secretion in response to basal stimulation, histamine, food and other stimulatory factors is prevented equally. By reducing the amount of time the oesophagus and stomach lining are exposed to acid, Famotidine helps heal conditions such as reflux oesophagitis and peptic ulcer disease. http://www.virtualmedicalcentre.com/drugs/pepcidine/48 Famotidine is a histamine (H2) receptor antagonist that competitively inhibits these receptors to reduce gastric acid secretion. Acid secretion in response to basal stimulation, histamine, food and other stimulatory factors is prevented equally. By reducing the amount of time the oesophagus and stomach lining are exposed to acid, Famotidine helps heal conditions such as reflux oesophagitis and peptic ulcer disease. http://www.virtualmedicalcentre.com/drugs/probitor/50 Omeprazole inhibits the proton pump in the wall of the parietal cells of the antrum of the stomach. This works to reversibly reduce the amount of gastric acid produced in response to all stimuli. The action of Omeprazole is dose dependant and specific, with no effect on histamine or acetylcholine receptors.Inhibition of acid production begins approximately one hour after dose and is maximal at 2 hours. The maximum effect of treatment is usually reached within 4 days.Omeprazole has also been found to have some antibacterial action and is useful in combination with antibiotics in triple therapy http://www.virtualmedicalcentre.com/drugs/rani-2/52 Ranitidine acts by competitively blocking H2 receptors on gastric parietal cells thereby reducing gastric acid secretion. http://www.virtualmedicalcentre.com/drugs/ranihexal/53 Ranitidine acts by competitively blocking H2 receptors on gastric parietal cells thereby reducing gastric acid secretion. http://www.virtualmedicalcentre.com/drugs/ranihexal-injection/54 Ranitidine acts by competitively blocking H2 receptors on gastric parietal cells thereby reducing gastric acid secretion. http://www.virtualmedicalcentre.com/drugs/ranitidine-bc/55 Ranitidine acts by competitively blocking H2 receptors on gastric parietal cells thereby reducing gastric acid secretion. http://www.virtualmedicalcentre.com/drugs/ranoxyl/56 Ranitidine acts by competitively blocking H2 receptors on gastric parietal cells thereby reducing gastric acid secretion. http://www.virtualmedicalcentre.com/drugs/rennie-spearmint-flavour/57 Calcium carbonate neutralises excess acid produced by the stomach, thereby reducing the burning symptoms associated with indigestion. Sustained calcium levels in the blood also help to prevent excess bone resorption associated with osteoporosis. http://www.virtualmedicalcentre.com/drugs/sigma-liquid-antacid/59 Aluminium hydroxide and Magnesium hydroxide are antacids, they work to neutralise the gastric acid produced by the stomach. They have no effect on the amount of acid produced by parietal cells. Simethicone acts to reduce the surface tension of gas bubbles and this disperses any gas that may form due to the reaction of the antacid with the gastric acid. The combination of these two mechanisms of action relieves symptoms such as heartburn and indigestion as well as flatulence and belching. http://www.virtualmedicalcentre.com/drugs/somac-tablets-20mg-or-40mg-on-prescription/61 The active ingredient in Somac is pantoprazole, a proton pump inhibitornbsp;(PPI). PPIs inhibit the enzyme (H+/K+-ATPase) responsible for the secretion of gastric acid, a process which occurs in the parietal cells of the stomach. Pantoprazole enters and accumulates in the parietal cells in its inactive form as a substituted benzimidazole. It is converted to an active from (sulphenamide) in the acidic environment of the parietal cells and binds to H+/K+-ATPase. This results in proton pump inhibition and long-lasting suppression of gastric acid secretion, regardless of whether acid secretion is http://www.virtualmedicalcentre.com/drugs/somac-injection/62 The active ingredient in Somac is pantoprazole, a proton pump inhibitornbsp;(PPI). PPIs inhibit the enzyme (H+/K+-ATPase) responsible for the secretion of gastric acid, a process which occurs in the parietal cells of the stomach. Pantoprazole enters and accumulates in the parietal cells in its inactive form as a substituted benzimidazole. It is converted to an active from (sulphenamide) in the acidic environment of the parietal cells and binds to H+/K+-ATPase. This results in proton pump inhibition and long-lasting suppression of gastric acid secretion, regardless of whether acid secretion is http://www.virtualmedicalcentre.com/drugs/tagamet/63 Cimetidine acts by competitively blocking H2 receptors on gastric parietal cells thereby reducing gastric acid secretion. http://www.virtualmedicalcentre.com/drugs/tazac/64 Nizatidine is a histamine H2-receptor antagonist with no action at H1-receptors and works to prevent gastric acid secretion in the stomach. Acid secretion in response to basal stimulation, histamine, food and other stimulatory factors is prevented equally. Gastric acid secretion stimulated by pentagastrin is inhibited according to Nizatidine dose. Secretion of gastric mucus and pancreatic enzymes is not affected by Nizatidine, and bacterial growth is not affected by the decreased acid levels in the stomach. http://www.virtualmedicalcentre.com/drugs/ranitidine-terry-white-chemists/65 Ranitidine is a histamine H2-receptor antagonist with no action at H1-receptors and works to prevent gastric acid secretion in the stomach. Acid secretion in response to basal stimulation, histamine, food and other stimulatory factors is prevented equally. A plasma Ranitidine concentration of 50ng/ml will reduce gastric acid secretion by 50%. Gastric acid secretion stimulated by pentagastrin is inhibited according to Ranitidine dose. Secretion of gastric mucus and pancreatic enzymes is not affected by Ranitidine, and bacterial growth is not affected by the decreased acid levels in the stomach. http://www.virtualmedicalcentre.com/drugs/titralac/66 The calcium carbonate component of Titralac acts by neutralising the hydrochloric acid secreted by gastric parietal cells. http://www.virtualmedicalcentre.com/drugs/ulcyte/68 Ulcyte is not an antacid, but rather a cytoprotective substance, which works by creating a barrier at the ulcer site and protecting it from the harmful action of the stomachs natural acid. It also protects against the digestive substances pepsin and bile. In addition to providing a protective layer, Sucralfate also forms a complex with pepsin and bile as a further method of protecting the ulcer from their corrosive properties. http://www.virtualmedicalcentre.com/drugs/zantac/69 Ranitidine acts by competitively blocking H2 receptors on gastric parietal cells thereby reducing gastric acid secretion. http://www.virtualmedicalcentre.com/drugs/zantac-relief/70 Ranitidine is a histamine H2-receptor antagonist with no action at H1-receptors and works to prevent gastric acid secretion in the stomach. Acid secretion in response to basal stimulation, histamine, food and other stimulatory factors is prevented equally. A plasma Ranitidine concentration of 50ng/ml will reduce gastric acid secretion by 50%. Gastric acid secretion stimulated by pentagastrin is inhibited according to Ranitidine dose. Secretion of gastric mucus and pancreatic enzymes is not affected by Ranitidine, and bacterial growth is not affected by the decreased acid levels in the stomach. http://www.virtualmedicalcentre.com/drugs/zoton/71 Lansoprazole inhibits the proton pump in the wall of the parietal cells of the antrum of the stomach. This works to reversibly reduce the amount of gastric acid produced in response to all stimuli. The action of Lansoprazole is dose dependant and specific, with no effect on histamine or acetylcholine receptors. Lansoprazole has also been found to have some antibacterial action and is useful in combination with antibiotics in triple therapy for H. pylori eradication. The mechanism of this synergy is not understood. http://www.virtualmedicalcentre.com/drugs/atrobel-atrobel-forte/73 The active ingredients in Atrobel and Atrobel Forte exert their anticholinergic effects by blocking the response to stimulation of postganglionic cholinergic nerves, particularly those innervating smooth muscle and exocrine glands. http://www.virtualmedicalcentre.com/drugs/pro-banthine/82 Propantheline bromide is an anticholinergic agent. It inhibits the neural impulses of the parasympathetic nervous system and the ganglia of the sympathetic nervous system. It does not cross the blood-brain barrier hence only peripheral effects are seen. It works in the gastrointestinal system to reduce gastric acid secretion and inhibit gastrointestinal motility. It also has anti-spasmodic action. Propantheline bromide also reduces other secretions such as pancreatic juices, sweat and saliva. http://www.virtualmedicalcentre.com/drugs/actilax/85 Portal systemic encephalopathy: PSE is caused by exposure of the brain to nitrogenous substances (especially ammonia) produced by the gut. Bacteria in the colon degrade Actilax, producing acetic and lactic acids, and this raises the colonic pH. This raised pH results in ammonia being retained in its ionised form and hence trapped in the colon. It is therefore no longer absorbed into the blood, and in fact moves into the colon from the blood. Actilax also suppresses urease-producing organisms in the colon such as E.coli. The laxative action of Actilax also removes the trapped ammonia f http://www.virtualmedicalcentre.com/drugs/benefiber/87 Benefiber consists of modified guar gum, a source of pure fibre. It provides a supplement for people who do not have enough fibre in their diet, or who find they suffer from constipation even when trying to eat a high fibre diet. It is also useful in making up a balanced diet in those consuming a pureed diet or being tube-fed. http://www.virtualmedicalcentre.com/drugs/bisacodyl-suppositories/88 Bisacodyl acts by directly stimulating the nerve endings in the mucosa of the colon, increasing intestinal motility. http://www.virtualmedicalcentre.com/drugs/bisalax/89 Bisacodyl acts by directly stimulating the nerve endings in the mucosa of the colon, increasing intestinal motility. http://www.virtualmedicalcentre.com/drugs/coloxyl-tablets/94 Docusate is a laxative that works by softening the stool. It stimulates intestinal secretions promoting water movement into the faeces, which softens it. http://www.virtualmedicalcentre.com/drugs/coloxyl-with-senna/95 Docusate is a laxative that works by softening the stool. It stimulates intestinal secretions promoting water movement into the faeces, which softens it. Sennosides pass into the colon without being digested or absorbed, where they are thought to act directly on intestinal smooth muscle, stimulating peristalsis http://www.virtualmedicalcentre.com/drugs/duphalac/96 Portal systemic encephalopathy: PSE is caused by exposure of the brain to nitrogenous substances (especially ammonia) produced by the gut. Bacteria in the colon degrade Actilax, producing acetic and lactic acids, and this raises the colonic pH. This raised pH results in ammonia being retained in its ionised form and hence trapped in the colon. It is therefore no longer absorbed into the blood, and in fact moves into the colon from the blood. Actilax also suppresses urease-producing organisms in the colon such as E.coli. The laxative action of Actilax also removes the trapped ammonia from the http://www.virtualmedicalcentre.com/drugs/durolax/97 Bisacodyl acts by directly stimulating the nerve endings in the mucosa of the colon, increasing intestinal motility. http://www.virtualmedicalcentre.com/drugs/fleet-laxative-preparations/99 Bisacodyl acts by directly stimulating the nerve endings in the mucosa of the colon, increasing intestinal motility. http://www.virtualmedicalcentre.com/drugs/genlac/104 Portal systemic encephalopathy: PSE is caused by exposure of the brain to nitrogenous substances (especially ammonia) produced by the gut. Bacteria in the colon degrade Actilax, producing acetic and lactic acids, and this raises the colonic pH. This raised pH results in ammonia being retained in its ionised form and hence trapped in the colon. It is therefore no longer absorbed into the blood, and in fact moves into the colon from the blood. Actilax also suppresses urease-producing organisms in the colon such as E.coli. The laxative action of Actilax also removes the trapped ammonia from the http://www.virtualmedicalcentre.com/drugs/glycerin-suppositories/105 Glycerin suppositories allow direct application of Glycerol to the bowel contents. Glycerol acts to make the stool softer and easier to pass out of the colon. http://www.virtualmedicalcentre.com/drugs/lac-dol/112 Portal systemic encephalopathy: PSE is caused by exposure of the brain to nitrogenous substances (especially ammonia) produced by the gut. Bacteria in the colon degrade Actilax, producing acetic and lactic acids, and this raises the colonic pH. This raised pH results in ammonia being retained in its ionised form and hence trapped in the colon. It is therefore no longer absorbed into the blood, and in fact moves into the colon from the blood. Actilax also suppresses urease-producing organisms in the colon such as E.coli. The laxative action of Actilax also removes the trapped ammonia from the http://www.virtualmedicalcentre.com/drugs/normacol-plus/117 Sterculia is a vegetable gum that is able to absorb vast quantities of water, up to 60 times its own volume. It passes through the gastrointestinal system without being absorbed, and on reaching the colon causes movement of water into the stool. This acts to soften the stool and make it easier to pass. Frangula bark is a peristaltic stimulant, and stimulates contraction of the intestinal muscles to aid in evacuation of the stool. http://www.virtualmedicalcentre.com/drugs/sorbilax/126 Sorbitol is an alcohol compound that is poorly absorbed when taken orally. It travels all the way to the colon where it acts as an osmotic laxative, drawing water into the stool and causing stool softening. http://www.virtualmedicalcentre.com/drugs/bis-pectin/128 Aluminium hydroxide is an antacid agent. It works to neutralise the hydrochloric acid produced by parietal cells. Codeine phosphate is an analgesic agent. It is a weak opioid agent, which works by binding opioid receptors in the central nervous system. It also works on the peripheral nervous system, where one of its side effects (used as a therapeutic effect in Bis Pectin) is constipation. Kaolin and Pectin are adsorbent antidiarrhoeal agents. They supposedly bind toxins and bacteria and form a protective intestinal lining. The effectiveness of Kaolin and Pectin as antidiarrhoeal agents ha http://www.virtualmedicalcentre.com/drugs/dipentum/130 Olsalazine has a local anti-inflammatory action on the bowel wall, however, its exact mechanism of action is unknown. http://www.virtualmedicalcentre.com/drugs/entocort/132 Corticosteroids act by binding to intracellular cytoplasmic receptors and regulating the expression of corticosteroid-responsive genes. By regulating these genes corticosteroids suppress the normal physiological inflammation and immune responses. Budesonide is in a formulation that enables it to be delivered predominantly to the ileum and ascending colon having mainly local effects in these regions. There is high first-pass metabolism so systemic absorption is reduced however some systemic effects still occur. http://www.virtualmedicalcentre.com/drugs/mesasal/139 Mesalazine has a local anti-inflammatory action on the bowel wall, however, its exact mechanism of action is unknown. http://www.virtualmedicalcentre.com/drugs/pyralin-en/140 The exact mechanism of action is unknown, however, sulfasalazine is known to have anti-inflammatory and immunosuppressive actions. http://www.virtualmedicalcentre.com/drugs/salazopyrin-salazopyrin-en-tabs/141 Sulfasalazine has been found to have immunosuppressive activity as well as a wide range of activities in a number of different body tissues. However, its mode of action in the treatment of ulcerative colitis and rheumatoid arthritis is not known. In ulcerative colitis it is thought that the salicylate component has an anti-inflammatory effect, whilst a metabolite of the drug inhibits an antigen-antibody complex that may have a role in the pathophysiology of the bowel disease. Sulfasalazine also appears to have a slight antibacterial effect. http://www.virtualmedicalcentre.com/drugs/salofalk-enemas/142 Mesalazine has been identified as the active component of sulfasalazine in the treatment of inflammatory bowel disease. The mechanism of action is not yet fully known. However, it is thought to act in multiple ways against several inflammatory mediators. For example, the effects of mesalazine on prostaglandin concentration in the intestinal mucosa has been demonstrated. Also it has been found to have influence in leukotriene production. From investigations, mesalazine has a role in lipoxygenase inhibition. It may also function as a radical scavenger of reactive oxygen compounds. http://www.virtualmedicalcentre.com/drugs/salofalk-tablets/143 Mesalazine has been identified as the active component of sulfasalazine in the treatment of inflammatory bowel disease. The mechanism of action is not yet fully known. However, it is thought to act in multiple ways against several inflammatory mediators. For example, the effects of mesalazine on prostaglandin concentration in the intestinal mucosa has been demonstrated. Also it has been found to have influence in leukotriene production. From investigations, mesalazine has a role in lipoxygenase inhibition. It may also function as a radical scavenger of reactive oxygen compounds. http://www.virtualmedicalcentre.com/drugs/creon-500010000-and-forte/146 Pancreatic enzymes are important in the digestion of proteins, carbohydrates and fats. Creon 5000, Creon 10000 and Creon Forte contain active pancreatic extract that is contained in minimicrospheres with a pH sensitive coating to prevent it being broken down in gastric acid. This coating is then quickly dissolved by the alkalinity of the duodenum where pancreatic secretions would usually be released. The enzymes contained in the minimicrospheres then digest food as normal. http://www.virtualmedicalcentre.com/drugs/pancrease/156 Pancreatic enzymes are important in the digestion of proteins, carbohydrates and fats. Pancrease contains active pancreatic extract that is contained in microspheres with a pH sensitive coating to prevent it being broken down in gastric acid. This coating is then quickly dissolved by the alkalinity of the duodenum where pancreatic secretions would usually be released. The enzymes contained in the microspheres then digest food as normal. http://www.virtualmedicalcentre.com/drugs/panzytrat-25000/157 Pancreatic enzymes are important in the digestion of proteins, carbohydrates and fats. Pancrease contains active pancreatic extract that is contained in microtablets with a pH sensitive coating to prevent it being broken down in gastric acid. This coating is then quickly dissolved by the alkalinity of the duodenum where pancreatic secretions would usually be released. The enzymes contained in the microtablets then digest food as normal. http://www.virtualmedicalcentre.com/drugs/ursofalk/160 Ursofalk is used in the treatment of chronic cholestatic liver disease, although its mechanism of action is not fully understood.1,2 Ursodeoxycholic acid is a bile acid. It alters the composition of bile, decreasing the concentration of potentially toxic bile acids, such as cholic and chenodeoxycholic acids. It also increases bile acid secretion and stimulates the flow of bile.1-3 Ursodeoxycholic acid may have an additional immunological effect, decreasing expression of abnormal HLA class 1 molecules on hepatocytes and suppressing immunoglobulins and cytokines.1,2 http://www.virtualmedicalcentre.com/drugs/predsol-retention-enema-suppositories/166 The active ingredient in Predsol Enema and Suppositories is Prednisolone, a synthetic corticosteroid with glucocorticoid and anti-inflammatory effects. It is thought to act on protein synthesis, influencing the biochemical behaviour of cells and thereby exerting its therapeutic effect. The topical application of Prednisolone via the Enema or Suppository places the drug directly at the desired site of action where it relieves the pain and inflammation associated with inflammatory bowel disease and proctitis. It is simply for symptom relief, corticosteroids are never curative. More than http://www.virtualmedicalcentre.com/drugs/fefol/362 Iron is an essential trace element that is required for the formation of haemoglobin and myoglobin. Fefol tablets also contain a sufficient amount of folic acid to prevent the development of folate deficiency during pregnancy. http://www.virtualmedicalcentre.com/drugs/fergon/363 Iron supplement. Fergon provides a source of elemental iron that will correct iron deficiency and iron deficiency anaemias. http://www.virtualmedicalcentre.com/drugs/ferrograd-c/364 Iron is an essential trace element that is required for the formation of haemoglobin and myoglobin. Ferrograd C also contains a high dose of vitamin C, which enhances the absorption of iron. http://www.virtualmedicalcentre.com/drugs/ferro-gradumet/365 Ferro-gradumet provides the iron needed to produce haemoglobin and iron-containing enzymes, and resaturates iron storage organs. Controlled release of the majority of the iron content in the small intestine reduces gastric irritation. http://www.virtualmedicalcentre.com/drugs/fgf/366 Iron is an essential trace element that is required for the formation of haemoglobin and myoglobin. FGF tablets also contain a sufficient amount of folic acid to prevent the development of folate deficiency during pregnancy. http://www.virtualmedicalcentre.com/drugs/zovirax-ophthalmic-ointment/417 Aciclovir is a synthetic purine nucleoside analogue. It is an antiviral agent, active against the herpes simplex virus (HSV) types 1 amp; 2, and the varicella zoster virus (VSV). Development of resistance by HSV to aciclovir has been documented. Aciclovir is phosphorylated to the active antiviral compont aciclovir triphosphate in cells infected with HSV or VZV. Aciclovir triphosphate inhibits further DNA viral synthesis. Oral: Aciclovir is variably and only partially absorbed from the gut. Following oral administration, the mean half life ranges from 2.5-3.3 hours and is approximately 2.0 hou http://www.virtualmedicalcentre.com/drugs/maxidex/422 Corticosteroids pass through the cell membrane and bind to cytoplasmic receptors in the nucleus. This modifies the expression of corticosteroid responsive genes, leading to suppression of immune or inflammatory responses. http://www.virtualmedicalcentre.com/drugs/alphagan-eye-drops/427 Brimonidine is a selective alpha;2receptor agonist.1-3 It reduces intraocular pressure by:1-3nbsp; Inhibiting the formation of aqueous humourIncreasing the uveoscleral outflow of aqueous humour http://www.virtualmedicalcentre.com/drugs/genrx-salbutamol/428 Salbutamol is a beta-agonist selective for beta2-receptors. When inhaled, it acts on the autonomic nerves of the bronchial smooth muscle and causes muscle relaxation and vasodilation. Salbutamol also increases the clearance of mucous from the airways and reduces the effect of respiratory allergens by decreasing mucosal inflammation. Salbutamol has its effect immediately, so is known as a ¡°reliever¡± medication for asthma. http://www.virtualmedicalcentre.com/drugs/healthsense-ipratropium/429 Ipratropium is an anticholinergic bronchodilator. It blocks vagal reflexes and inhibits cholinergic bronchomotor tone. It protects against acetylcholine bronchospasm as well as partially protecting against histamine and allergen induced bronchospasm. http://www.virtualmedicalcentre.com/drugs/healthsense-salbutamol/430 Salbutamol is a relative selective agonist for beta 2 adrenoreceptors, hence stimulating bronchodilation. Side effects due to salbutamol are a result of peripheral stimulation of beta 2 receptors as well as stimulation of beta 1 receptors as selectivity is not absolute. http://www.virtualmedicalcentre.com/drugs/ipratrin-uni-dose/431 Promote bronchodilation by inhibiting cholinergic bronchomotor tone Ipratropium is as effective as inhaled beta 2 agonists in maintenance treatment of COPD. It is also indicated for severe acute asthma in addition to short-acting beta 2 agonists Duration of action of Ipratropium is approximately 6 hours, thus it can be used to augment the duration of bronchodilatation achieved with beta 2 agonist therapy. Ipratropium has shorter duration of action than the other anticholinergic bronchodilator, Tiotropium. Anticholinergic effects such as dry mouth occur less often with Ipratropium than Tiot http://www.virtualmedicalcentre.com/drugs/ipravent/432 Promote bronchodilation by inhibiting cholinergic bronchomotor tone Ipratropium is as effective as inhaled beta 2 agonists in maintenance treatment of COPD. It is also indicated for severe acute asthma in addition to short-acting beta 2 agonists Duration of action of Ipratropium is approximately 6 hours, thus it can be used to augment the duration of bronchodilatation achieved with beta 2 agonist therapy. Ipratropium has shorter duration of action than the other anticholinergic bronchodilator, Tiotropium. Anticholinergic effects such as dry mouth occur less often with Ipratropium than Tiot http://www.virtualmedicalcentre.com/drugs/oxis-turbuhaler/433 Relax bronchial smooth muscle by stimulating beta 2 adrenoreceptors Long duration of action (12hours) Eformeterol has quicker onset of action than the other long acting beta 2 agonist, Salmeterol. (Eformoterol has an onset of action of 1 to 3 minutes and Salmeterol 10 to 20 minutes) Eformeterol and Salmeterol have similar efficacy http://www.virtualmedicalcentre.com/drugs/salbutamol-inhalation-solution/434 Salbutamol is a relative selective agonist for beta 2 adrenoreceptors, hence stimulating bronchodilation. Side effects due to salbutamol are a result of peripheral stimulation of beta 2 receptors as well as stimulation of beta 1 receptors as selectivity is not absolute. http://www.virtualmedicalcentre.com/drugs/serevent-inhaler-and-accuhaler/435 - Relax bronchial smooth muscle by stimulating beta 2 adrenoreceptors - Long duration of action (12hours) - Salmeterol slower onset of action than the other long acting beta 2 agonist, Eformeterol. (Salmeterol has an onset of action of 10 to 20 minutes and Eformoterol 1 to 3 minutes) - Salmeterol and eformeterol have similar efficacy http://www.virtualmedicalcentre.com/drugs/ipratropium-terry-white-chemists/436 Ipratropium is an anticholinergic bronchodilator. It blocks vagal reflexes and inhibits cholinergic bronchomotor tone. It protects against acetylcholine bronchospasm as well as partially protecting against histamine and allergen induced bronchospasm. http://www.virtualmedicalcentre.com/drugs/salbutamol-terry-white-chemists/437 Salbutamol is a relative selective agonist for beta 2 adrenoreceptors, hence stimulating bronchodilation. Side effects due to salbutamol are a result of peripheral stimulation of beta 2 receptors as well as stimulation of beta 1 receptors as selectivity is not absolute. http://www.virtualmedicalcentre.com/drugs/herceptin/438 Trastuzumab is a recombinant monoclonal antibody that targets the human epidermal growth factor 2 (HER2) protein. HER2 is a proto-oncogene that is over-expressed in 25-30% of primary breast cancers. Breast cancers that express HER2 have been found to be particularly aggressive and associated with a poor prognosis. Inhibition of HER2 by Trastuzumab slows the proliferation of these tumour cells and increases antibody dependent cell mediated cytotoxicity. http://www.virtualmedicalcentre.com/drugs/hexalen/439 Altretamine is a synthetic cytotoxic antineoplastic agent. Although similar in structure to alkylating agents, Altretamine has not been shown to have alkylating activity, and it is active against tumours that have developed resistance to other alkylating agents. The exact method by which Altretamine exerts its cytotoxic effect is therefore not fully understood. What is known is that Altretamine requires metabolism before it becomes cytotoxic. Its metabolites form bonds with DNA molecules, but the importance of this in antitumour activity is unknown. http://www.virtualmedicalcentre.com/drugs/mabthera/440 Mabtheranbsp;belongs to a group of medicines known as monoclonal antibodies. It binds to antigen CD20 which is located on pre-B and mature B lymphocytes.1,2 Antigen CD20 is expressed largely (more than 95%) of all the B cell non-Hodgkinrsquo;s lymphomas (NHL).2 Whennbsp;Mabthera binds to CD20, it starts an immune response where the normal and malignant B cells will be destroyed. At the same time, there is also induction of apoptosis.1 http://www.virtualmedicalcentre.com/drugs/natulan/441 Procarbazine is a cytostatic agent. It interferes with cells at a number of sites to prevent DNA and protein synthesis and mitosis. http://www.virtualmedicalcentre.com/drugs/anzemet/445 Dolasetron mesylate is a selective 5HT3-antagonist used in the prevention of nausea and vomiting associated with chemotherapy. 5HT3-receptors are found on preganglionic and postganglionic neurones and neurones of the sensory and enteric nervous systems. Importantly, they are also found in the area postrema, a chemoreceptor trigger zone in the fourth ventricle associated with vomiting. The mechanism by which post-operative nausea and vomiting are caused is not completely understood but may share common pathways with chemotherapy agents. Chemotherapy agents cause vomiting by releasing serotonin http://www.virtualmedicalcentre.com/drugs/ethyol/447 Ethyol contains the active drug amifostine which selectively guards normal tissues (but not tumors) from the cytotoxic effects of ionizing radiation and DNA binding chemotherapeutic agents like cyclophosphamide, mitomycin C and platinum-containing drugs.1,2 http://www.virtualmedicalcentre.com/drugs/resonium-a/463 Resonium A is a cation exchange resin, which lowers the serum potassium by exchanging potassium for sodium in the wall of the intestine, increasing the amount of potassium that is excreted in the faeces. Resonium A exerts its greatest effect in the large intestine, where more excretion of potassium takes place. http://www.virtualmedicalcentre.com/drugs/antabuse/467 Deters alcohol use. Disulfiram prevents the usual metabolism of alcohol (irreversibly inhibits aldehyde dehydrogenase) blocking acetaldehyde breakdown which causes unpleasant potentially serious effects if alcohol is consumed. e.g. flushing, sweating, nausea and vomiting, palpitations, headache, dyspnoea, chest pain, hypotension, cardiovascular collapse, convulsions, arrhythmias. http://www.virtualmedicalcentre.com/drugs/biodone-forte/468 Methadone is an opioid analgesic. Opioids mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems to produce analgesia. Opioids prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioids also produce respiratory depression and constipation. http://www.virtualmedicalcentre.com/drugs/campral/469 Chemical structure is similar to that of gamma amino butyric acid (GABA) and taurine. Mechanism of action is unclear- possibly involves restoration of normal activity in glutamate and GABA-ergic systems. http://www.virtualmedicalcentre.com/drugs/methadone-syrup/470 Methadone is an opioid receptor agonist. Reduces withdrawal symptoms and craving for opioids in opioid dependence http://www.virtualmedicalcentre.com/drugs/nicabatecq-and-nicobatecq-clear/471 Nicotine replacement reduces the severity of tobacco withdrawal symptoms and increases the likelihood of smoking cessation.2 http://www.virtualmedicalcentre.com/drugs/nicabate-cq-lozenges/473 Nicotine replacement reduces the severity of tobacco withdrawal symptoms and increases the likelihood of smoking cessation.2 http://www.virtualmedicalcentre.com/drugs/revia/479 Opioid antagonist. In alcohol dependence it reduces craving for alcohol and possibly reduces some of the pleasurable effects, by blocking the effects of endogenous opioids. In maintenance of opioid abstinence, reversibly blocks opioid receptors for (24-72hours) preventing opioid effects e.g. euphoria http://www.virtualmedicalcentre.com/drugs/subutex/480 Buprenorphine is a partial opioid receptor agonist. Reduces withdrawal symptoms and craving for opioids in opioid dependence http://www.virtualmedicalcentre.com/drugs/zyban-sr/481 Zyban is a selective catecholamine reuptake inhibitor. It selectively inhibits the reuptake of noradrenaline and dopamine from the synapses, with little or no effect on serotonin and monoamine oxidase. However, it is still largely unknown how this aids patients to abstain from smoking.1 http://www.virtualmedicalcentre.com/drugs/folic-acid-injection/636 Folic acid is a B group vitamin that is required for DNA synthesis, amino acid metabolism and erythropoiesis. Folic acid is involved in the maturation of all rapidly proliferating tissues. It is particularly important during embryonic organogenesis especially in neural tube closure. http://www.virtualmedicalcentre.com/drugs/calcium-gluconate-injection-10andpermil/652 Calcium Gluconate Injection 10% works to replace the body¡¯s calcium when it is deficient. Calcium is required for enzymatic reactions, nerve impulses, muscle contractions, renal function, respiration and blood coagulation. Plasma calcium is usually controlled by exchange with bone calcium, and in deficient states this may lead to bone weakness. Calcium as a gluconate salt is the preferred way to replace calcium, the calcium saccharate (0.5%) acts as a stabiliser. http://www.virtualmedicalcentre.com/drugs/calcium-gluconate-injection-bp-dbl/653 Calcium Gluconate Injection 10% works to replace the body¡¯s calcium when it is deficient. Calcium is required for enzymatic reactions, nerve impulses, muscle contractions, renal function, respiration and blood coagulation. Plasma calcium is usually controlled by exchange with bone calcium, and in deficient states this may lead to bone weakness. Calcium as a gluconate salt is the preferred way to replace calcium, the calcium saccharate (0.5%) acts as a stabiliser. http://www.virtualmedicalcentre.com/drugs/gastrolyte/657 http://www.virtualmedicalcentre.com/drugs/sodium-bicarbonate-injection/674 Bicarbonate in the body acts as a buffer. Excess hydrogen ions react with bicarbonate resulting in the formation of carbon dioxide and water. The former is excreted from the lungs and the latter from the kidneys. Sodium bicarbonate therapy buffers excess hydrogen ion concentration, raises blood pH, and reverses clinical manifestations of metabolic acidosis, by increasing plasma bicarbonate. It is excreted mainly in the urine, therefore making it alkaline. http://www.virtualmedicalcentre.com/drugs/sodium-bicarbonate-injection-84andpermil-wv-bp/675 Bicarbonate in the body acts as a buffer. Excess hydrogen ions react with bicarbonate resulting in the formation of carbon dioxide and water. The former is excreted from the lungs and the latter from the kidneys. Sodium bicarbonate therapy buffers excess hydrogen ion concentration, raises blood pH, and reverses clinical manifestations of metabolic acidosis, by increasing plasma bicarbonate. It is excreted mainly in the urine, therefore making it alkaline. http://www.virtualmedicalcentre.com/drugs/sodium-bicarbonate-intravenous-infusion-bp-84andpermil/676 Bicarbonate in the body acts as a buffer. Excess hydrogen ions react with bicarbonate resulting in the formation of carbon dioxide and water. The former is excreted from the lungs and the latter from the kidneys. Sodium bicarbonate therapy buffers excess hydrogen ion concentration, raises blood pH, and reverses clinical manifestations of metabolic acidosis, by increasing plasma bicarbonate. It is excreted mainly in the urine, therefore making it alkaline. http://www.virtualmedicalcentre.com/drugs/duromine/686 Phentermine is a sympathomimetic amine.1-3 It works by stimulating the central nervous system, increasing the use of energy.1,2 It stimulates the release of catecholamines such as dopamine and noradrenaline which then causes suppression of appetite and increase use of the bodys energy.1-3 http://www.virtualmedicalcentre.com/drugs/xenical/689 Xenical contains thenbsp;active ingredient orlistat, a gastrointestinal lipase inhibitor that prevents the breakdown of dietary triglycerides and, in doing so, prevents the absorption of up to 20% of dietary fat. Dietary triglycerides are digested with the aid of gastric and pancreatic lipases. These lipases enzymatically break triglycerides down into free fatty acids, which can then be absorbed in the small intestine. Pancreatic and gastric lipase inhibitors form covalent bonds with the active serine site of gastric and pancreatic lipases in the lumen of the stomach and small intestine, rend http://www.virtualmedicalcentre.com/drugs/loette/692 Loette is a standard monophasic combined oral contraceptive. That is, each active tablet contains the same strength of levonorgestrel and ethinyloestradiol. Levonorgestrel is a synthetic progesterone derived from 19-nortestosterone. It has androgenic activity as well as mineralocorticoid activity.3 The contraceptive action of Loette, like all combined oral contraceptives, is a result of the combination of several effects it has on the body. The significant effects are:Inhibition of ovulationChanges to the endometrial lining to discourage implantationnbsp;Thickening of cervical mucous secretio http://www.virtualmedicalcentre.com/drugs/yasmin/701 Yasmin is a standard monophasic combined oral contraceptive. That is, each active tablet contains the same strength of drospirenone and ethinyloestradiol. Drospirenone is a steroidal progestin that closely mimics naturally produced progesterone. It is a spironolactone derivative that exhibits mineralocorticoid antagonistic properties, few androgenic properties, and offsets oestrogens stimulation of the renin-angiotensin system.3 The contraceptive action of Yasmin, like all combined oral contraceptives, is a result of the combination of several effects it has on the body. The significant effec http://www.virtualmedicalcentre.com/drugs/locilan-28-day/703 Locilan 28 Day is a progestogen only contraceptive.nbsp;Its actual mechanism of action remains unknown. However, it is suggested thatnbsp;Locilan 28 Day worksnbsp;by increasing viscosity of the cervical mucus, changing the endometrial lining which makes it unsuitable for implantation andnbsp;inhibiting of the secretion of pituitary gonadotrophins.2 http://www.virtualmedicalcentre.com/drugs/mirena/706 Levonorgestrel is a potent progestin of the 19-nortestosterone class. It has mainly local progestrogenic effects in the uterine cavity. Thickening of the cervical mucus inhibits sperm motility which prevents passage of sperm through the cervical canal. Ovulation is also inhibited in some women.1,2 Following insertion of Mirena IUD, the initial release of levonorgestrel into the uterine cavity is 20mcg every 24 hours. This provides a stable plasma levonorgestrel concentration, which after the first weeks following insertion, levels off at 0.4 and 0.6 nmol/L in women at child bearing age and http://www.virtualmedicalcentre.com/drugs/postinor-2/708 The exact mode of action of Postinor-2 is not known. The active ingredient of Postinor-2 is levonorgestrel.nbsp;Levonorgestrel isnbsp;a progestogen. Progestogens thickens cervical mucous, impeding the passage of sperm. It is thought to suppress the release of pituitary luteinising hormone, thus inhibiting ovulation.nbsp;It may also change the endometrium, discouraging implantation.1,2 http://www.virtualmedicalcentre.com/drugs/bupivacaine-injection-bp/847 Bupivacaine is an amide local anaesthetic agent. On injection, it stabilises the neuronal membranes and prevents the initiation and transmission of nerve impulses. Bupivacaine has a rapid onset of action and a duration of action four times that of lignocaine. http://www.virtualmedicalcentre.com/drugs/emla/854 Lignocaine and prilocaine are amide local anaesthetics that stabilize the neuronal membranes inhibiting the initiation and conduction of nerve impulses. This effectively causes local anaesthesia. http://www.virtualmedicalcentre.com/drugs/lignocaine-2andpermil-gel/860 Lignocaine is a local anaesthetic of the amide type. It produces a reversible loss of sensation by preventing or diminishing the conduction of peripheral sensory nerve impulses near the site of application. It is readily absorbed from mucous membranes and damaged skin producing rapid, local anaesthesia in these areas1,2. http://www.virtualmedicalcentre.com/drugs/lignocaine-2andpermil-gel-with-chlorhexidine-005andpermil/861 Lignocaine is a local anaesthetic of the amide type. It produces a reversible loss of sensation by preventing or diminishing the conduction of peripheral sensory nerve impulses near the site of application. It is readily absorbed from mucous membranes and damaged skin producing rapid, local anaesthesia in these areas. Chlorhexidine is an antiseptic effective against a wide range of Gram-positive and Gram-negative organisms, some viruses and some fungi. It is ineffective against bacterial spores at room temperature and acid-fast bacteria are inhibited but not killed. 1,2 http://www.virtualmedicalcentre.com/drugs/marcain-05andpermil-marcain-spinal-05andpermil-heavy/866 Bupivacaine is a neuronal membrane stabiliser. It prevents initiation and transmission of nerve impulses. It has a rapid onset and long duration of action. http://www.virtualmedicalcentre.com/drugs/penthrox-inhalation/872 The active ingredient in Penthrox, methoxyflurane, is believed to inhibit neurological ion channel activity and excitement. In doing so, the drug causes hypnosis and amnesia. Methoxyflurane also immobilises the spinal cord and inhibits its response to pain stimuli.3 http://www.virtualmedicalcentre.com/drugs/xylocaine-viscous/889 Xylocaine viscous stabilizes the neuronal membrane and prevents the initiation and conduction of nerve impulses, thereby exerting a local anaesthetic action. http://www.virtualmedicalcentre.com/drugs/atropine-injection-bp/905 Atropine is an anticholinergic agent that acts both centrally and peripherally, by competitively inhibiting the muscarinic actions of acetylcholine (on muscarinic receptors). Atropine activity is on structures innervated by postganglionic cholinergic nerves and on smooth muscle. 1 http://www.virtualmedicalcentre.com/drugs/atropine-sulfate-injection-bp/906 Atropine is an anticholinergic agent that acts both centrally and peripherally, by competitively inhibits the muscarinic actions of acetylcholine (on muscarinic receptors). Atropine activity is on structures innervated by postganglionic cholinergic nerves and on smooth muscle1. http://www.virtualmedicalcentre.com/drugs/atropine-sulfate-injection-bp/907 Atropine is an anticholinergic agent that acts centrally and peripherally. It competitively inhibits the muscarinic actions of acetylcholine (on muscarinic receptors). Atropine activity is on structures innervated by postganglionic cholinergic nerves and on smooth muscle. http://www.virtualmedicalcentre.com/drugs/accure/1049 Isotretinoin is a retinoid which inhibits sebaceous gland function and keratinisation. Pharmacology. The exact mechanism of action of Accure is unknown. Cystic acne. Clinical improvement in cystic acne patients occurs in association with a reduction in sebum secretion. The decrease in sebum secretion is reversible and the extent is related to the dose and duration of treatment with Accure and reflects a reduction in sebaceous gland size and an inhibition of sebaceous gland differentiation. Pharmacokinetics. There is considerable interindividual variation in the bioavailability of oral isotreti http://www.virtualmedicalcentre.com/drugs/lamisil-cream/1116 Lamisil (Terbinafine) Cream is a topical antifungal. Terbinafine is an allylamine that mainly fights against dermatophytes. Terbinafine works to specifically inhibit fungal ergosterol synthesis at an earlier step compared to azole antifungals, leading to a deficiency in ergosterol and an intracellular accumulation of squalene, resulting in membrane disruption and cell death. Terbinafine also acts by inhibition of squalene epoxidase in the fungal cell membrane. Lamisil cream, with the concentration in the cream formulation is also effective against Candida.1,2 http://www.virtualmedicalcentre.com/drugs/lamisil-dermgel/1117 Lamisil (Terbinafine) DermGel is a topical antifungal. Terbinafine is an allylamine that mainly fights against dermatophytes. Terbinafine works to specifically inhibit fungal ergosterol synthesis at an earlier step compared to azole antifungals, leading to a deficiency in ergosterol and an intracellular accumulation of squalene, resulting in membrane disruption and cell death. Terbinafine also acts by inhibition of squalene epoxidase in the fungal cell membrane.1,2 http://www.virtualmedicalcentre.com/drugs/acihexal-cream/1142 Acyclovir is an antiviral agent which is active against types 1 and 2 of herpes simplex virus types 1 and 2 and varicella zoster virus. Varicella zoster virus is far less sensitive to Acyclovir than Herpes simplex virus is. Acyclovir is phosphorylated within the cell to form acyclovir triphosphate which is active against the virus. In normal cells there is very limited conversion of acyclovir to acyclovir triphosphate and the cellular DNA polymerase is not very sensitive to the active compound. In cells infected with HSV or VZV, HSV or VZV coded thymidine kinase allows the acyclovir t http://www.virtualmedicalcentre.com/drugs/zolaten-cold-sore-cream/1156 Aciclovir is a synthetic purine nucleoside analogue. It is an antiviral agent, active against the herpes simplex virus (HSV) types 1 amp; 2, and the varicella zoster virus (VSV). Development of resistance by HSV to aciclovir has been documented. Aciclovir is phosphorylated to the active antiviral compont aciclovir triphosphate in cells infected with HSV or VZV. Aciclovir triphosphate inhibits further DNA viral synthesis. Oral: Aciclovir is variably and only partially absorbed from the gut. Following oral administration, the mean half life ranges from 2.5-3.3 hours and is approximately 2.0 hou http://www.virtualmedicalcentre.com/drugs/propecia/1173 Propecia is a competitive and specific inhibitor of type II 5-alpha-reductase.nbsp;Inhibition of this enzyme blocks the peripheral conversion of testosterone to the androgen dihydrotestosterone (DHT).nbsp;Hair follicles contain type II 5alpha-reductase. In men with male pattern hair loss, the balding scalp contains miniaturised hair follicles and increased amounts of DHT. Administration ofnbsp;Propecia decreases scalp and serum DHT concentrations in these men.2 http://www.virtualmedicalcentre.com/drugs/ciloxan/1186 Fluoroquinolone is an antibacterial active against a broad spectrum of Gram positive and Gram negative ocular pathogens. It interruptsnbsp;the synthesis of bacterial DNA via interference with the enzyme DNA gyrase.Gram positive organisms susceptible to floroquinolonenbsp;includenbsp;Staphylococcus aureus (including methicillin susceptible and methicillin resistant strains), Staphylococcus. epidermidis, Streptococcus pneumoniae, viridans group of Streptococcus. Susceptible gram negative organisms include Pseudomonas aeruginosa, Serratia marcescens, Haemophilus influenzae. Most strains of Pse http://www.virtualmedicalcentre.com/drugs/genoptic/1187 Genoptic is an aminoglycoside antibiotic which is effective against a wide variety of pathogenic Gram negative and Gram positive bacteria. It exerts its bactericidal activity via inhibition of bacterial protein systhesis.2 http://www.virtualmedicalcentre.com/drugs/azopt-eye-drops-10andpermil/1197 Azopt eye drops reduces intraocular pressure by decrease the amount of aqueous humour formed by inhibition of the enzyme, carbonic anhydrase II, in the eye.3 http://www.virtualmedicalcentre.com/drugs/cosopt-eye-drops/1201 Cosopt is comprised of two components: dorzolamide hydrochloride, a topical carbonic anhydrasenbsp;and timolol maleate, a topical beta-adrenergic receptor blocking agent. Both ingredientsnbsp;help to decrease elevated intraocular pressure (IOP) by reducing aqueous humour secretion via two different mechanisms.nbsp;Dorzolamide hydrochloride decreases aqueous humour secretion, presumably by slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport. The actual mechanism of action of timolol maleate remains unclear. However, it is related to reduced aqueo http://www.virtualmedicalcentre.com/drugs/diamox/1202 Acetazolamide is a non-competitive and reversible inhibitor of carbonic anhydrase subtype II. Carbonic anhydrase is the enzyme that catalyses the conversion of CO2 and OH- to HCO3- (bicarbonate).nbsp;It is abundantly present in the proximal tubular epithelial cells. The enzyme is also present in extra-renal tissues, such as the eye, gastric mucosa, pancreas, central nervous system and erythrocytes.3 Inhibition of carbonic anhydrase in the ciliary processes of the eye prevents formation of bicarbonate, a major component of the aqueous humor. Consequently, the secretion of aqueous humor into th http://www.virtualmedicalcentre.com/drugs/trusopt/1220 The active ingredient of Trusopt is dorzolamide hydrochloride.Dorzolamide hydrochloride isnbsp;a carbonic anhydrase inhibitor which works to inhibit carbonic anhydrase II, a predominant subtype of the carbonic anhydrase enzyme found in the ciliary processes of the eye. This results in a reduction of aqueous humour formation, by decreasing the formation of bicarbonate ions, subsequently reducing sodium and fluid transport.1,2 http://www.virtualmedicalcentre.com/drugs/atropt/1223 Atropine is a belladonna alkaloid which acts in the eye to block the action of acetylcholine, relaxing the cholinergically innervated sphincter muscle of the iris. This results in dilation of the pupil (mydriasis). The cholinergic stimulation of the accommodative ciliary muscle of the lens is also blocked. This results in paralysis of accommodation. (cycloplegia).1,2 http://www.virtualmedicalcentre.com/drugs/genteal-lubricant-eye-drops/1259 Hypromellose and Carbomer 980 are lubricants that relieve irritation of ocular tissue.1,2 Genteal contains a preservative system of sodium perborate which reacts with water to form the preservative hydrogen peroxide.2 When the eye drop is placed on the eye, the ocular enzymes break down the preservative into oxygen and water.2 This reduces the problem of a preservative causing irritation to the eye.2 In Genteal Gel, once the drop is placed into the eye, it forms a clear, long lasting protective film on the surface of the eye without causing blurry vision.2 http://www.virtualmedicalcentre.com/drugs/refresh/1274 Refresh is a synthetic polymer in aqueous solution. Refresh acts to it lubricate the eye by increasing the volume of tears and by stabilising the precorneal tear film. It also assists to increase the retention of drugs given as eye drops and relieves the symptoms of dry eyes. http://www.virtualmedicalcentre.com/drugs/refresh-liquigel/1275 Refresh Liquigel is a synthetic polymer in aqueous solution. Refresh Liquigel acts to it lubricate the eye by increasing the volume of tears and by stabilising the precorneal tear film. It also assists to increase the retention of drugs given as eye drops and relieves the symptoms of dry eyes. http://www.virtualmedicalcentre.com/drugs/patanol/1304 Olopatadine is a selective histamine H1-antagonist that inhibits type I immediate hypersensitivity reactions. It has been shown to inhibit the release of proinflammatory mediators from human conjunctival mast and epithelial cells.1 http://www.virtualmedicalcentre.com/drugs/visudyne/1309 Verteporfin is used in Photodynamic Therapy (PDT).1-3 Once verteporfin is taken up by choroidal neovasculature in the eye, it produces highly active oxygen radicals in the presence of oxygen and laser light. These radicals cause cytotoxic damage to the neovascular epithelium. This leads to the temporary closing off of the blood vessel through vasoconstriction, platelet aggregation and clot formation due to the release of procoagulant and vasoactive factors from the damaged epithelium.1,2 http://www.virtualmedicalcentre.com/drugs/voltaren-ophta/1310 The active ingredient of Voltaren Ophta is diclofenac sodium.nbsp;Diclofenac sodiumnbsp;inhibits the synthesis ofnbsp;prostaglandins, which are responsible for inflammation and pain. It has been found to inhibit miosis during cataract surgery and to reduce inflammation following surgical interventions.1,2 http://www.virtualmedicalcentre.com/drugs/aquaear/1311 The acetic acid in Aquaear decreases the pH of the ear canal environment, hence reducing the growth of micro-organisms. The isopropyl alcohol has a drying effect and reduces moisture and may have some antibacterial effect.1,2 http://www.virtualmedicalcentre.com/drugs/ciproxin-hc-ear-drops/1315 The Ciprofloxacin component of Ciproxin HC Ear Drops has activity towards a broad range of gram positive and gram negative organisms. It exerts itrsquo;s bactericidal action by disrupting the synthesis of bacterial DNA by interfering enzyme DNA gyrase.1 The Hydrocortisone is a corticosteroid which has anti-inflammatory effect.1nbsp; http://www.virtualmedicalcentre.com/drugs/aldecin-aqueous-nasal-spray/1328 Produce local anti-inflammatory effects, decrease capillary permeability and mucous production, and produce vasoconstriction in the nasal mucosa Onset of action within 3-7 hours; effective on an as-needed basis; optimum effect after several days of regular use http://www.virtualmedicalcentre.com/drugs/aldecin-hayfever-aqueous-nasal-spray/1329 Produce local anti-inflammatory effects, decrease capillary permeability and mucous production, and produce vasoconstriction in the nasal mucosa Onset of action within 3-7 hours; effective on an as-needed basis; optimum effect after several days of regular use http://www.virtualmedicalcentre.com/drugs/allermax-aqueous-nasal-spray/1330 Produce local anti-inflammatory effects, decrease capillary permeability and mucous production, and produce vasoconstriction in the nasal mucosa Onset of action within 3-7 hours; effective on an as-needed basis; optimum effect after several days of regular use http://www.virtualmedicalcentre.com/drugs/atrovent-nasalatrovent-nasal-forte/1331 Promote drying of nasal secretions by cholinergic inhibition. http://www.virtualmedicalcentre.com/drugs/azep-nasal-spray/1332 Antagonise the action of histamine at H1 receptors, reducing histamine-related vasodilation and increased capillary permeability http://www.virtualmedicalcentre.com/drugs/beconase-allergy-24-hr-fluticasone-aqueous-nasal-spray/1334 Produce local anti-inflammatory effects, decrease capillary permeability and mucous production, and produce vasoconstriction in the nasal mucosa. Onset of action within 3-7 hours; effective on an as-needed basis; optimum effect after several days of regular use. http://www.virtualmedicalcentre.com/drugs/beconase-hayfever/1336 Produce local anti-inflammatory effects, decrease capillary permeability and mucous production, and produce vasoconstriction in the nasal mucosa. Onset of action within 3-7 hours; effective on an as-needed basis; optimum effect after several days of regular use. http://www.virtualmedicalcentre.com/drugs/budamax-aqueous-nasal-spray-64-mcg/1337 Budenoside is a topical glucocorticoid which reduces inflammation. http://www.virtualmedicalcentre.com/drugs/drixine-nasalpaediatric/1339 Produce vasoconstriction in nasal mucosa; decrease nasal blood flow and congestion Maximal effect lasts for 6 hours http://www.virtualmedicalcentre.com/drugs/livostin-nasal-spray/1341 Antagonise the action of histamine at H1 receptors, reducing histamine-related vasodilation and increased capillary permeability http://www.virtualmedicalcentre.com/drugs/logicin-rapid-relief-nasal-spray/1342 Produce vasoconstriction in nasal mucosa; decrease nasal blood flow and congestion Maximal effect lasts for 6 hours http://www.virtualmedicalcentre.com/drugs/nasex-nasal-decongestant/1345 The active ingredient oxymetazoline causes stimulation of alpha-adrenergic receptors in the vascular network within the nasal mucosa causing vasoconstriction. This reduces nasal blood flow and congestion. http://www.virtualmedicalcentre.com/drugs/nasonex-aqueous-nasal-spray/1346 Mometasone in Nasonex Aqueous Nasal Spray produces local anti-inflammatory effects, decreases capillary permeability and mucous production, and produces vasoconstriction in the nasal mucosa.1 Its action onset is within 3-7 hours and is effective on an as-needed basis. Optimum effect may be achieved after several days of regular use1. Systemic effects of mometasone were not detected in adults, adolescents or children following the administration. Mometasone furoate suspension is very poorly absorbed from the gastrointestinal tract, and the small amount that may be swallowed and absorbed http://www.virtualmedicalcentre.com/drugs/otrivin-nasal-drops-junioradult/1347 Produce vasoconstriction in nasal mucosa; decrease nasal blood flow and congestion Maximal effect lasts for 6 hours http://www.virtualmedicalcentre.com/drugs/rhinocort-aqueous-nasal-spray/1348 Produce local anti-inflammatory effects, decrease capillary permeability and mucous production, and produce vasoconstriction in the nasal mucosa. Onset of action within 3-7 hours; effective on an as-needed basis; optimum effect after several days of regular use. http://www.virtualmedicalcentre.com/drugs/rhinocort-hayfever/1349 Produce local anti-inflammatory effects, decrease capillary permeability and mucous production, and produce vasoconstriction in the nasal mucosa. Onset of action within 3-7 hours; effective on an as-needed basis; optimum effect after several days of regular use. http://www.virtualmedicalcentre.com/drugs/rynacrom-metered-dose-nasal-spray/1350 Act by inhibiting release of inflammatory mediators from mast cells http://www.virtualmedicalcentre.com/drugs/rynacrom-4andpermil/1351 Act by inhibiting release of inflammatory mediators from mast cells http://www.virtualmedicalcentre.com/drugs/spray-tish/1352 Produce vasoconstriction in nasal mucosa; decrease nasal blood flow and congestion Maximal effect lasts for 6 hours http://www.virtualmedicalcentre.com/drugs/vicks-sinex/1354 Produce vasoconstriction in nasal mucosa; decrease nasal blood flow and congestion Maximal effect lasts for 6 hours http://www.virtualmedicalcentre.com/drugs/betadine-sore-throat-gargle/1358 Povidone-iodine is a topical microbicidal antiseptic which kills bacteria, viruses, fungi, protozoa, yeasts and spores. http://www.virtualmedicalcentre.com/drugs/difflam-solution/1368 Benzydamine is an anti-inflammatory agent that chemically differs from other non-steroidal anti-inflammatory drugs (NSAIDs). Like all NSAIDs, benzydamine possesses analgesic, antipyretic and anti-inflammatory activity. Although the exact mechanism of benzydamine is yet to be elucidated, its pharmacological properties are likely related to the inhibition of prostaglandin biosynthesis. In addition, benzydamine possesses local anaesthetic activity at concentrations used for topical administration.1,2 http://www.virtualmedicalcentre.com/drugs/difflam-sugar-free-lozenges/1369 Difflam Sugar-Free Lozenges contain two active ingredients Benzydamine Hydrocloride and Cetylpyridinium Chloride which are contributing to the anti-inflammatory and antibacterial effects.Benzydamine exerts an anti-inflammatory and analgesics effect which are structurally different to steroid group, it is also different to non-steroidal anti-inflammatory drugs (NSAID) which it is a base, unlike NSAID which is an acid.1,2In animal studies, when used topically Benzydamine also exerts local anesthetic effect.1,2Cetylpyridinium Chloride is a cationic surfactant and has bactericidal and antifungal p http://www.virtualmedicalcentre.com/drugs/minidine-sore-throat-gargle/1374 Ingredients: Povidone-iodine. Minidine is rapidly effective against bacteria, viruses and spores http://www.virtualmedicalcentre.com/drugs/periactin/1402 Periactin (cyproheptadine hydrochloride) is a serotonin and histamine antagonist. It competes at the H1 receptors to antagonize the action of histamine at H1 receptors, resulting in decreased histamine related vasodilation and inceased capillary permeability. They also have anticholinergic activity and sedative effects.nbsp; http://www.virtualmedicalcentre.com/drugs/phenergan/1403 Promethazine is a phenothiazine derivative, and is a long-acting antihistamine with mild atropine-like anticholinergic effects and some antiserotonin effects. http://www.virtualmedicalcentre.com/drugs/phenergan-injection/1404 Promethazine is a phenothiazine derivative, and is a long-acting antihistamine with mild atropine-like anticholinergic effects and some antiserotonin effects. http://www.virtualmedicalcentre.com/drugs/actacode/1417 http://www.virtualmedicalcentre.com/drugs/actifed/1418 Antihistamine and decongestant. Pseudoephedrine has direct and indirect sympathomimetic activity, and is an effective upper respiratory tract decongestant http://www.virtualmedicalcentre.com/drugs/actifed-cc-dry-cough/1419 Opioid derivative- suppresses the medullary cough centre http://www.virtualmedicalcentre.com/drugs/actifed-chesty-cough-and-nasal-congestion-liquid-filled-capsules/1420 -Pseudoephedrine ndash; nasal decongestant via indirect and direct sympathomimetic action Guaifenesin ndash; expectorant via increasing viscosity of sputum by increasing water content. http://www.virtualmedicalcentre.com/drugs/actifed-dry-cough-and-nasal-congestion-liquid-filled-capsules/1421 -Pseudoephedrine ndash; nasal decongestant via indirect and direct sympathomimetic action -Dextromethorphan- antitussive via suppression of medullary cough centre http://www.virtualmedicalcentre.com/drugs/action-cold-and-flu-effervescent/1422 Chlorpheniramine maleate ndash;antihistamine and anticholinergic.Phenylephrine tartrate-nasal decongestant by stimulation of alpha adrenergic receptorsAsprin- analgesic, antipyretic and anti inflammatoryAscorbic acid ndash; replacement therapy as ascorbic acid is reduced within leucocytes and plasma during infection. http://www.virtualmedicalcentre.com/drugs/actuss/1423 -Opioid derivative- suppresses the medullary cough centre http://www.virtualmedicalcentre.com/drugs/avil-decongestant/1424 Pheniramine is a H1-receptor antagonists. It inhibits the effect of histamine on capillary permeability and smooth muscle. It depresses the CNS at therapeutic doses. It also acts as an anticholinergic and local anaesthetic. http://www.virtualmedicalcentre.com/drugs/benadryl-family-chesty-cough-and-nasal-congestion/1425 Pseudoephedrine – nasal decongestant via indirect and direct sympathomimetic action Guaifenesin – expectorant, increases viscosity of sputum by increasing water content. http://www.virtualmedicalcentre.com/drugs/benadryl-family-chesty-forte/1426 -Guaifenesin – expectorant, increases viscosity of sputum by increasing water content. -Bromhexine - a mucolytic, breaks down fibres within thick secretions making them more viscous http://www.virtualmedicalcentre.com/drugs/benadryl-family-dry/1427 Diphenhydramine -H1-receptor antagonist. Relieves hypersensitivity reactions, nausea, vomiting and sedation. It also acts as an antitussive and is anticholinergic at muscarinic receptors. -Pseudoephedrine –nasal decongestant via indirect and direct sympathomimetic action -Dextromethorphan- antitussive via suppression of medullary cough centre http://www.virtualmedicalcentre.com/drugs/benadryl-family-dry-forte/1428 Opioid derivative- suppresses the medullary cough centre http://www.virtualmedicalcentre.com/drugs/benadryl-family-original/1429 Diphenhydramine -H1-receptor antagonist. Relieves hypersensitivity reactions, nausea, vomiting and sedation. It also acts as an antitussive and is anticholinergic at muscarinic receptors. Ammonium chloride is an expectorant. http://www.virtualmedicalcentre.com/drugs/bisolvon-drybisolvon-dry-junior/1433 Opioid derivative- suppresses the medullary cough centre http://www.virtualmedicalcentre.com/drugs/demazin-sinussinus-12-hour-controlled-release/1451 Act on alpha adrenoreceptors on vascular smooth muscle in the respiratory tract, producing vasoconstriction of dilated nasal vessels, reducing tissue swelling and nasal congestion http://www.virtualmedicalcentre.com/drugs/dexi-tuss-liquid/1452 Opioid derivative- suppresses the medullary cough centre http://www.virtualmedicalcentre.com/drugs/dimetapp-cold-and-flu-liquid-capsules/1454 Dimetapp Cold amp; Flu Liquid Caps contain several active ingredients which work together to alleviate symptoms associated with the common cold. The different ingredients act as follows:Dextromethorphan:The antitussive effect of dextromethorphan elevates thenbsp;cough by depressing the medullary cough centre, it provides symptomaticnbsp;relief of non productive cough. Pseudoephedrine: Pseudoephedrine exerts its decongestant effect through vasoconstriction of dilated blood vessels thus relieving nasal congestion and reducing tissue swelling. It acts on alpha adrenoreceptors of the vascular s http://www.virtualmedicalcentre.com/drugs/dimetapp-sinus-liquid-caps/1465 Act on alpha adrenoreceptors on vascular smooth muscle in the respiratory tract, producing vasoconstriction of dilated nasal vessels, reducing tissue swelling and nasal congestion http://www.virtualmedicalcentre.com/drugs/durotuss-expectorant/1469 Pholcodine is a drug chemically related to morphine, which possesses cough suppressant activity but no analgesic action. Pholcodine acts directly on the cough centre in the medulla of the CNS, suppressing the cough reflex. Pholcodine is as effective as codeine in its antitussive actions, and has a long half-life. Unlike codeine, pholcodine acts selectively on the cough centre without causing respiratory depression, constipation, euphoria and dependence.1,3 Bromhexine is a mucolytic agent that reduces mucous viscosity by fragmenting acid mucopolysaccharide fibres that are found in mucoid sputum http://www.virtualmedicalcentre.com/drugs/linctus-tussinol/1480 Opioid derivative- suppresses the medullary cough centre http://www.virtualmedicalcentre.com/drugs/logicin-cough-suppressant/1484 Opioid derivative- suppresses the medullary cough centre http://www.virtualmedicalcentre.com/drugs/logicin-sinus-tablet/1491 Act on alpha adrenoreceptors on vascular smooth muscle in the respiratory tract, producing vasoconstriction of dilated nasal vessels, reducing tissue swelling and nasal congestion http://www.virtualmedicalcentre.com/drugs/nucosef-dm-oral-liquid/1493 Opioid derivative- suppresses the medullary cough centre http://www.virtualmedicalcentre.com/drugs/panadol-sinus/1501 Parecetamol is a para-aminophenol derivate. It has analgesic and antipyretic activity but not anti-inflammatory activity.Pseudoephedrine is a nasal decongestant via indirect and direct sympathomimetic action. http://www.virtualmedicalcentre.com/drugs/panadol-sinus-day-night/1502 Panadol Sinus Day/Night contains three different active ingredients, Paracetamol, Pseudoephedrine and Chlorpheniramine. Paracetamol is a para-aminophenol derivative with antipyretic and analgesic activity. It treats mild to moderate pain and fever by reducing the activity of prostaglandins. Pseudoephedrine is a sympathomimetic agent that acts both directly and indirectly. It stimulates adrenergic receptors, causing vasoconstriction of the small blood vessels in the nose, thereby relieving nasal congestion. Chlorpheniramine is an antihistamine that can be used to relieve hypersensitivity rea http://www.virtualmedicalcentre.com/drugs/parke-davis-day-and-night-cold-and-flu-capsules/1504 Parke-Davis Day Night Cold Flu Capsules contain four different active ingredients, Paracetamol, Pseudoephedrine, Dextromethorphan and Chlorpheniramine. Paracetamol is a para-aminophenol derivative with antipyretic and analgesic activity. It treats mild to moderate pain and fever by reducing the activity of prostaglandins. Pseudoephedrine is a sympathomimetic agent that acts both directly and indirectly. It stimulates adrenergic receptors, causing vasoconstriction of the small blood vessels in the nose, thereby relieving nasal congestion. Dextromethorphan is an antitussive agent. It work http://www.virtualmedicalcentre.com/drugs/rikodeine-oral-liquid/1507 Opioid derivative- suppresses the medullary cough centre http://www.virtualmedicalcentre.com/drugs/robitussin-dx-extra-strength-cough-control/1510 Opioid derivative- suppresses the medullary cough centre http://www.virtualmedicalcentre.com/drugs/robitussin-honey-cough-syrup/1513 Opioid derivative- suppresses the medullary cough centre http://www.virtualmedicalcentre.com/drugs/strepsils-cough-relief/1518 Opioid derivative- suppresses the medullary cough centre http://www.virtualmedicalcentre.com/drugs/sudafed-congestion-and-sinus-pain-relief/1519 Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Ibuprofen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/sudafed-daytimenightime-relief-tablets/1520 Sudafed Daytime/Nightime Relief Tablets contain three different active ingredients, Paracetamol, Pseudoephedrine and Triprolidine. Paracetamol is a para-aminophenol derivative with antipyretic and analgesic activity. It treats mild to moderate pain and fever by reducing the activity of prostaglandins. Pseudoephedrine is a sympathomimetic agent that acts both directly and indirectly. It stimulates adrenergic receptors, causing vasoconstriction of the small blood vessels in the nose, thereby relieving nasal congestion. Triprolidine is an antihistamine agent that can be used Nightime preparati http://www.virtualmedicalcentre.com/drugs/sudafed-sinus-and-nasal-decongestant/1521 Act on alpha adrenoreceptors on vascular smooth muscle in the respiratory tract, producing vasoconstriction of dilated nasal vessels, reducing tissue swelling and nasal congestion http://www.virtualmedicalcentre.com/drugs/sudafed-sinus-pain-and-allergy-relief/1522 Parecetamol is a para-aminophenol derivate. It has analgesic and antipyretic activity but not anti-inflammatory activity. Pseudoephedrine is a nasal decongestant via indirect and direct sympathomimetic action. Triprolidine is an antihistamine http://www.virtualmedicalcentre.com/drugs/sudafed-sinus-pain-relief/1523 Sudafed Sinus Pain Relief contains two active ingredients, Paracetamol and Pseudoephedrine. Paracetamol is a para-aminophenol derivative with antipyretic and analgesic activity. It treats mild to moderate pain and fever by reducing the activity of prostaglandins. Pseudoephedrine is a sympathomimetic agent that acts both directly and indirectly. It stimulates adrenergic receptors, causing vasoconstriction of the small blood vessels in the nose, thereby relieving nasal congestion. http://www.virtualmedicalcentre.com/drugs/tussinol-for-dry-coughs/1528 Opioid derivative- suppresses the medullary cough centre http://www.virtualmedicalcentre.com/drugs/aminophylline-inject-bp-dbl/1535 Not entirely understood Possible effects include bronchial smooth muscle relaxation; anti-inflammatory effects; increase in diaphragm contractility and CNS stimulation http://www.virtualmedicalcentre.com/drugs/bricanyl/1536 The active component terbutaline, relaxes bronchial smooth muscle by stimulating beta 2 adrenoreceptors.1 It tends to be selective for these receptors. Bricanyl has a rapid onset of action to relieve bronchoconstriction. Its maximum effect occurs about 30 minutes after subcutaneous injection, one hour after aerosol, and two to three hours after oral administration.4 The duration of action is between four and five hours. http://www.virtualmedicalcentre.com/drugs/brondecon-expectorant/1538 Not entirely understoodPossible effects include bronchial smooth muscle relaxation; anti-inflammatory effects; increase in diaphragm contractility and CNS stimulation. http://www.virtualmedicalcentre.com/drugs/nuelin-sr/1540 Not entirely understood Possible effects include bronchial smooth muscle relaxation; anti-inflammatory effects; increase in diaphragm contractility and CNS stimulation http://www.virtualmedicalcentre.com/drugs/nuelin-syrup/1541 Not entirely understood Possible effects include bronchial smooth muscle relaxation; anti-inflammatory effects; increase in diaphragm contractility and CNS stimulation http://www.virtualmedicalcentre.com/drugs/airomir-mdiaccuhaler/1543 - Relax bronchial smooth muscle by stimulating beta 2 adrenoreceptors - Onset of action (5-15 minutes) - Short duration of action (3-6 hours) - Of the short acting beta 2 agonists, salbutamol, terbutaline and fenoterol all have similar efficacy. Orciprenaline is rarely used because it is less selective than other beta 2 agonists and more likely to cause adverse cardiovascular effects http://www.virtualmedicalcentre.com/drugs/alupent/1544 Relax bronchial smooth muscle by stimulating beta 2 adrenoreceptors Onset of action (5-15 minutes) Short duration of action (3-6 hours) Orciprenaline is rarely used because it is less selective than other beta 2 agonists and more likely to cause adverse cardiovascular effects. http://www.virtualmedicalcentre.com/drugs/apoven/1545 Promote bronchodilation by inhibiting cholinergic bronchomotor tone Ipratropium is as effective as inhaled beta 2 agonists in maintenance treatment of COPD. It is also indicated for severe acute asthma in addition to short-acting beta 2 agonists Duration of action of Ipratropium is approximately 6 hours, thus it can be used to augment the duration of bronchodilatation achieved with beta 2 agonist therapy. Ipratropium has shorter duration of action than the other anticholinergic bronchodilator, Tiotropium. Anticholinergic effects such as dry mouth occur less often with Ipratropium than Tiot http://www.virtualmedicalcentre.com/drugs/asmol-cfc-free-inhaler/1546 - Relax bronchial smooth muscle by stimulating beta 2 adrenoreceptors - Onset of action (5-15 minutes) - Short duration of action (3-6 hours) - Of the short acting beta 2 agonists, salbutamol, terbutaline and fenoterol all have similar efficacy. Orciprenaline is rarely used because it is less selective than other beta 2 agonists and more likely to cause adverse cardiovascular effects http://www.virtualmedicalcentre.com/drugs/asmol-uni-dose/1547 - Relax bronchial smooth muscle by stimulating beta 2 adrenoreceptors - Onset of action (5-15 minutes) - Short duration of action (3-6 hours) - Of the short acting beta 2 agonists, salbutamol, terbutaline and fenoterol all have similar efficacy. Orciprenaline is rarely used because it is less selective than other beta 2 agonists and more likely to cause adverse cardiovascular effects http://www.virtualmedicalcentre.com/drugs/atrovent-nebulising-solution/1548 Promote bronchodilation by inhibiting cholinergic bronchomotor tone Ipratropium is as effective as inhaled beta 2 agonists in maintenance treatment of COPD. It is also indicated for severe acute asthma in addition to short-acting beta 2 agonists Duration of action of Ipratropium is approximately 6 hours, thus it can be used to augment the duration of bronchodilatation achieved with beta 2 agonist therapy. Ipratropium has shorter duration of action than the other anticholinergic bronchodilator, Tiotropium. Anticholinergic effects such as dry mouth occur less often with Ipratropium than Tiot http://www.virtualmedicalcentre.com/drugs/atrovent-mdi/1549 Promote bronchodilation by inhibiting cholinergic bronchomotor tone Ipratropium is as effective as inhaled beta 2 agonists in maintenance treatment of COPD. It is also indicated for severe acute asthma in addition to short-acting beta 2 agonists Duration of action of Ipratropium is approximately 6 hours, thus it can be used to augment the duration of bronchodilatation achieved with beta 2 agonist therapy. Ipratropium has shorter duration of action than the other anticholinergic bronchodilator, Tiotropium. Anticholinergic effects such as dry mouth occur less often with Ipratropium than Tiot http://www.virtualmedicalcentre.com/drugs/berotec-mdi/1550 Relax bronchial smooth muscle by stimulating beta 2 adrenoreceptors Onset of action (5-15 minutes) Short duration of action (3-6 hours) Of the short acting beta 2 agonists, fenoterol, salbutamol, and terbutaline all have similar efficacy. Orciprenaline is rarely used because it is less selective than other beta 2 agonists and more likely to cause adverse cardiovascular effects. http://www.virtualmedicalcentre.com/drugs/chem-mart-ipratropium/1551 Ipratropium bromide is an anticholinergic bronchodilator. Anticholinergic agents inhibit the action of acetylcholine in the bronchi and cause relaxation of the respiratory smooth muscle. This results in a dilatory effect of airways, relieving the symptoms of asthma. Ipratropium begins to have an effect in 3-5 minutes, having its peak of activity at 1.5-2 hours and lasting up to six hours. http://www.virtualmedicalcentre.com/drugs/chem-mart-salbutamol/1552 Salbutamol is a relative selective agonist for beta 2 adrenoreceptors, hence stimulating bronchodilation. Side effects due to salbutamol are a result of peripheral stimulation of beta 2 receptors as well as stimulation of beta 1 receptors as selectivity is not absolute. http://www.virtualmedicalcentre.com/drugs/combivent-metered-dose-aerosol/1553 Salbutamol component: Relax bronchial smooth muscle by stimulating beta 2 adrenoreceptors Onset of action (5-15 minutes) Short duration of action (3-6 hours) Ipratropium component: Promote bronchodilation by inhibiting cholinergic bronchomotor tone Duration of action of Ipratropium is approximately 6 hours, thus it can be used to augment the duration of bronchodilatation achieved with beta 2 agonist therapy. http://www.virtualmedicalcentre.com/drugs/dbl-ipratropium/1554 Ipratropium is an anticholinergic bronchodilator. It blocks vagal reflexes and inhibits cholinergic bronchomotor tone. It protects against acetylcholine bronchospasm as well as partially protecting against histamine and allergen induced bronchospasm. http://www.virtualmedicalcentre.com/drugs/epaq-inhaler/1555 Salbutamol is a relative selective agonist for beta 2 adrenoreceptors, hence stimulating bronchodilation. Side effects due to salbutamol are a result of peripheral stimulation of beta 2 receptors as well as stimulation of beta 1 receptors as selectivity is not absolute. http://www.virtualmedicalcentre.com/drugs/foradile/1556 Foradilenbsp;is a potent, long acting, selective beta2-adrenoreceptor agonists. It exerts a bronchodilator effect in patients with reversible airways obstruction.1,2 http://www.virtualmedicalcentre.com/drugs/genrx-ipratropium/1557 Ipratropium is an anticholinergic bronchodilator. It blocks vagal reflexes and inhibits cholinergic bronchomotor tone. It protects against acetylcholine bronchospasm as well as partially protecting against histamine and allergen induced bronchospasm. http://www.virtualmedicalcentre.com/drugs/ventolin-cfc-free-inhaler/1558 Salbutamol is a relative selective agonist for beta 2 adrenoreceptors, hence stimulating bronchodilation. Side effects due to salbutamol are a result of peripheral stimulation of beta 2 receptors as well as stimulation of beta 1 receptors as selectivity is not absolute. http://www.virtualmedicalcentre.com/drugs/ventolin-disks/1559 Salbutamol is a relative selective agonist for beta 2 adrenoreceptors, hence stimulating bronchodilation. Side effects due to salbutamol are a result of peripheral stimulation of beta 2 receptors as well as stimulation of beta 1 receptors as selectivity is not absolute. http://www.virtualmedicalcentre.com/drugs/ventolin-respirator-solution-and-nebules/1560 Salbutamol is a relative selective agonist for beta 2 adrenoreceptors, hence stimulating bronchodilation. Side effects due to salbutamol are a result of peripheral stimulation of beta 2 receptors as well as stimulation of beta 1 receptors as selectivity is not absolute. http://www.virtualmedicalcentre.com/drugs/ventolin-rotacaps/1561 Salbutamol is a relative selective agonist for beta 2 adrenoreceptors, hence stimulating bronchodilation. Side effects due to salbutamol are a result of peripheral stimulation of beta 2 receptors as well as stimulation of beta 1 receptors as selectivity is not absolute. http://www.virtualmedicalcentre.com/drugs/chromese-sternebs/1564 Act by inhibiting release of inflammatory mediators from mast cells http://www.virtualmedicalcentre.com/drugs/flixotide-mdiaccuhaler/1565 Fluticasone propionate given by inhalation has potent glucocorticoid activity in the airways, reducing bronchial inflammation and hypersensitivity. This in turn reduces the symptoms of asthma, decreases the use of bronchodilator medications and may improve lung function over time.4 As it is inhlaed topically, there is less side effects than with systemic corticosteroid treatment. http://www.virtualmedicalcentre.com/drugs/flixotide-nebules/1566 Fluticasone propionate when inhaled into the lungs has potent glucocorticoid activity in the airways, reducing bronchial inflammation and hypersensitivity. This in turn reduces the symptoms of asthma, decreases the use of bronchodilator medications and may improve lung function over time.3 As it is inhlaed topically, there is less side effects than with systemic corticosteroid treatment. http://www.virtualmedicalcentre.com/drugs/intal/1567 Act by inhibiting release of inflammatory mediators from mast cells http://www.virtualmedicalcentre.com/drugs/intal-cfc-free-formulations/1568 Act by inhibiting release of inflammatory mediators from mast cells http://www.virtualmedicalcentre.com/drugs/pulmicort-turbuhalerrepsules/1569 Reduce bronchial mucosal inflammation and bronchial hyper-reactivity. http://www.virtualmedicalcentre.com/drugs/qvar-mdiautohaler-cfc-free/1570 Not entirely understood Possible effects include bronchial smooth muscle relaxation; anti-inflammatory effects; increase in diaphragm contractility and CNS stimulation http://www.virtualmedicalcentre.com/drugs/seretide-accuhaler-dpi/1572 Salmeterol component2,3 Stimulates beta;2-adrenoreceptors, causing relaxation of bronchial smooth muscleLong duration of action (gt;12 hours)Onset of action: 10-30 minutesFluticasone component1,3 Glucocorticoid activity in the airways, reducing bronchial mucosal inflammation and hyper-reactivityImproves symptoms, allows reduction of other drugs (eg. rescue bronchodilators) and may limit the risk of decline in lung function over time http://www.virtualmedicalcentre.com/drugs/tilade-cfc-free/1573 Act by inhibiting release of inflammatory mediators from mast cells http://www.virtualmedicalcentre.com/drugs/accolate/1574 -Inhibit cysteinyl leukotriene receptor; antagonize airway smooth muscle contraction and inflammation caused by leukotrienes http://www.virtualmedicalcentre.com/drugs/singulair/1578 Montelukast is a selective and orally active leukotriene receptor antagonist that specifically inhibits the cysteinyl leukotriene CysLT1-receptor. The cysteinyl leukotrienes (LTC4, LTD4, LTE4) are potent inflammatory eicosanoids released from various cells. These important pro-asthmatic mediators bind to cysteinyl leukotriene receptors (CysLT) found in the airways and cause bronchoconstriction, secretion of mucous, vascular permeability and eosinophil recruitment.1,4 Montelukast is an orally active compound which has been shown in asthmatic patients to reduce peripheral blood eosinophil http://www.virtualmedicalcentre.com/drugs/fluvax/1591 Fluvax contains inactivated particles of the influenza virus which induce an immune response when injected. The antibody response provides protection against influenza virus within 2ndash;3 weeks of vaccination, for up to 6ndash;12 months.1 http://www.virtualmedicalcentre.com/drugs/havrix-1440-havrix-junior/1593 Pharmacology. Havrix contains inactivated HAV units, and induces anti-HAV antibodies in normal, healthy individuals, thus inducing immunity. Havrix produces a titre of anti-HAV antibodies greater than that produced following passive immunisation with specific HAV immune serum globulins. Long term antibody persistence is under evaluation, though early data from 5 year follow up shows persistence consistent with a projected 20 year persistence (based on mathematical calculations). Studies suggest specific anti-HAV antibodies are elicited in 88% of adult vacinees 93% of child vacinees a http://www.virtualmedicalcentre.com/drugs/h-b-vax-ii/1594 H-B-Vax II is an inactivated vaccine against the Hepatitis B virus (HBV). Each dose contains 10ƒİg (paediatric: 5ƒİg, dialysis: 40ƒİg) of HBV surface antigen, which, once in the body, stimulates the immune system to produce protective levels of antibodies against it. In the event of future infection with the virus, the body is able to mount a rapid immune response and the person does not develop the disease. Vaccines cannot be 100% protective, but H-B-Vax II gives 10-year effective protection against the development of Hepatitis B in 95% of people, the rate being higher in young people and sl http://www.virtualmedicalcentre.com/drugs/infanrix/1596 Infanrix contains Diphtheria toxoid, tetanus toxoid, purified B.pertussis antigens, it induces antibodies against all vaccine components. Vaccinees generally produce adequate serum antibody levels to the vaccine components after about a month. http://www.virtualmedicalcentre.com/drugs/infanrix-hepb/1597 Infanrix Hep B is a combined vaccine against diphtheria, tetanus, pertussis and hepatitis B. As with all vaccines, the components, once in the body, stimulate the immune system to produce antibodies against them. In the event of future infection with the microorganisms, the body is able to mount a rapid immune response and the person does not develop the diseases. The diphtheria toxoid is isolated from Corynebacterium diphtheriae and detoxified and purified. The same is done to the tetanus toxoid, which is isolated from Clostridium tetani. Three antigens of Bordetella pertussis are extracted http://www.virtualmedicalcentre.com/drugs/m-m-r-ii/1607 Pharmacology. The MMR-II vaccine induces antibody formation in 95-99% of cases and is well tolerated in most patients. MMR-II vaccine induced antibody levels persist for at least 2 two years without substantial decline. http://www.virtualmedicalcentre.com/drugs/pneumovax-23/1611 Polysaccharide vaccine which promotes immune response and protection against Streptococcus Pneumoniae http://www.virtualmedicalcentre.com/drugs/vaqta-hepatitis-a-vaccine-inactivated/1623 VAQTA Hepatitis A Vaccine is an inactivated whole virus vaccine. On entering the body, the antigens present on the proteins of the inactivated virus stimulate the immune system to produce protective levels of antibodies against it. In the event of future infection with the virus, the body is able to mount a rapid immune response and the person does not develop the disease. VAQTA Hepatitis A Vaccine is a very effective vaccine, with 99% of patients showing full seroconversion (ie: protection from infection) 4 weeks after vaccination. Protection has been shown to last at least six years in pre http://www.virtualmedicalcentre.com/drugs/varilrix-powder-for-injection/1624 Varilrix causes attenuated, subclinical infection with varicella and an antibody response. Varicella-specific antibodies are produced by the vaccinated individual.1 http://www.virtualmedicalcentre.com/drugs/varivax-refrigerated-powder-for-injection/1625 Varivax is a lyophilised preparation of the Oka/Merck strain of live, attenuated varicella virus. Varivax causes attenuated, subclinical infection with varicella and an antibody response. Varicella-specific antibodies are produced by the vaccinated individual.1 http://www.virtualmedicalcentre.com/drugs/intragam-p/1631 Intragram P consists of normal human immunoglobulin, which is used to replace immunoglobulin in deficient states. Immunoglobulins are specific proteins produced by plasma cells to aid in fighting infection. They take part in various immune responses to bacteria or foreign material, including modulation of complement activation, suppression of various inflammatory mediators, suppression of idiotypic antibodies and many other effects. Because of its wide range of effects, normal immunoglobulin is used for a variety of indications, including treatment of infection in immunodeficiency states and i http://www.virtualmedicalcentre.com/drugs/intraglobin-f/1632 Intraglobin F contains mainly IgG with a broad spectrum of other antibodies present in a normal population. Intraglobin F usually contains antibodies pooled from one thousand donors. Known mechanisms of action are replacement therapy and immunomodulatory effects. http://www.virtualmedicalcentre.com/drugs/normal-immunoglobulin-viral-inactivated/1633 Normal Immunoglobulin contains mainly IgG with a broad range of other antibodies against various infections that are common in the general population (through infection or vaccination), such as Hepatitis A, poliomyelitis and measles. http://www.virtualmedicalcentre.com/drugs/zoster-immunoglobulin-vf-solution-for-injection/1638 Zoster Immunoglobulin-VF is human plasma containing at least 200 IU/vial of varicella zoster antibody. It is obtained from the blood of voluntary donors who have recently experienced chicken pox or shingles, because this blood naturally contains high levels of varicella antibodies. The antibodies are passed on to the immunoglobulin recipient and provide immunity against varicella infection.1 http://www.virtualmedicalcentre.com/drugs/aldara/1639 Imiquimod stimulates immune system cells, interferon and cytokines, which in turn cause an enhanced immune response against viral infections and tumour cells.1-3 http://www.virtualmedicalcentre.com/drugs/arava/1640 Leflunomide acts by inhibiting activity of dihydro-orotate dehydrogenase and subsequently inhibiting pyrimidine synthesis in leucocytes and other rapidly dividing cells. Leflunomide is an immunosuppressant and also has an immunomodulatory action, anti-proliferative properties and uricosuric effects. http://www.virtualmedicalcentre.com/drugs/avonex/1642 The active component of Avonex is Interferon beta-1a which is a recombinant form of a naturally occurring interferon within the human body.2 Interferons are cytokines that modulate the immune systems response to viruses and other noxious stimuli. Interferon beta is usually produced by a number of different cells in the body such as fibroblasts and macrophages. It exerts its immunomodulatory effects by binding to specific cellular receptors which subsequently initiate a cascade of events leading to expression of certain gene products.3 The exact mechanism of Avonex in the treatment of mult http://www.virtualmedicalcentre.com/drugs/azahexal/1643 Azathioprine is metabolised to form mercaptopurine which through altering purine synthesis impairs cellular immunity, depresses cell proliferation and inhibits cellular inflammatory responses. http://www.virtualmedicalcentre.com/drugs/azamun/1644 Azathioprine is metabolised to form mercaptopurine which through altering purine synthesis impairs cellular immunity, depresses cell proliferation and inhibits cellular inflammatory responses. http://www.virtualmedicalcentre.com/drugs/betaferon/1645 The active component of Betaferon is interferon beta-1b a modified form of a naturally occurring interferon within the human body.4 Interferons are cytokines that modulate the immune systems response to viruses and other noxious stimuli. Interferon beta is usually produced by a number of different cells in the body such as fibroblasts and macrophages. It exerts its immunomodulatory effects by binding to specific cellular receptors which subsequently initiate a cascade of events leading to expression of certain gene products.3 The exact mechanism of Betaferon in the treatment of multiple http://www.virtualmedicalcentre.com/drugs/cellcept/1646 Mycophenolate mofetil contains mycophenolic acid, which selectively inhibits inosine monophosphate dehydrogenase and enzyme necessary for the de novo pathway of guanosine nucleotide synthesis. In order to proliferate T and B-lymphocytes are dependent on de novo synthesis of purines, and are unable to use salvage pathways unlike other cell types and by inhibiting the de novo pathway of guanosine nucleotide synthesis mycophenolic acid inhibits the proliferation of lymphocytes. In experimental animal models mycophenolate mofetil has been shown to prolong the survival of allogeneic transplants and http://www.virtualmedicalcentre.com/drugs/copaxone/1647 Copaxone contains the active component glatiramer acetate which is a synthetic polypeptide of four naturally occurring amino acids.1,5 The precise mechanism of this drug in treatment of MS is not entirely understood. It is thought that Copaxone may have immune modifying effects such as blocking the presentation of myelin antigens to T lymphocytes which is a factor involved in the pathogenesis of the disease.1 Two placebo controlled trials have supported that Copaxone reduces the frequency of relapses in patients with relapsing-remitting multiple sclerosis (RRMS).5 http://www.virtualmedicalcentre.com/drugs/cysporin/1648 Cyclosporin is an immunosuppressive agent that has been shown in animal studies to inhibit the development of cell mediated reactions, lymphokine production and lymphokine release. Cyclosporin is thought to act specifically on resting lymphocytes blocking them in the G0 or G1 phase of the cell cycle, and inhibits the antigen triggered release of lymphokines such as interleukin 2 and T cell growth factor by activated T cells. http://www.virtualmedicalcentre.com/drugs/enbrel/1649 Etanercept acts by binding to tumour necrosis factor and blocking its activity. Tumour necrosis factor is an endogenous cytokine that is involved in normal inflammatory and immune responses. In patients with rheumatoid arthritis, tumour necrosis factor is found in increased concentrations in the synovial tissues. http://www.virtualmedicalcentre.com/drugs/genrx-azathioprine/1650 Azathioprine is metabolised to form mercaptopurine which through altering purine synthesis, impairs cellular immunity, depresses cell proliferation and inhibits cellular inflammatory responses. http://www.virtualmedicalcentre.com/drugs/imuran/1652 Azathioprine is metabolised to form mercaptopurine which through altering purine synthesis impairs cellular immunity, depresses cell proliferation and inhibits cellular inflammatory responses. http://www.virtualmedicalcentre.com/drugs/intron-a/1653 Interferons are naturally occurring substances in the body that are involved in the immune response to various viruses and other chemical and biological inducers. They act by binding to cell surfaces and initiating a complex series of intracellular events including enzyme induction. These events are thought to enable the cells to inhibit viral replication, suppress cell replication and enhance activity of other immune cells such as macrophages and lymphocytes. Intron A provides the body with an extra dose of a specific interferon, Interferon alfa-2b, which has specific effects making it usef http://www.virtualmedicalcentre.com/drugs/intron-a-redipen/1654 Interferons are naturally occurring substances in the body that are involved in the immune response to various viruses and other chemical and biological inducers. They act by binding to cell surfaces and initiating a complex series of intracellular events including enzyme induction. These events are thought to enable the cells to inhibit viral replication, suppress cell replication and enhance activity of other immune cells such as macrophages and lymphocytes. Intron A Redipen provides the body with an extra dose of a specific interferon, Interferon alfa-2b, which has specific effects making http://www.virtualmedicalcentre.com/drugs/prograf-oral-capsules/1658 Tacrolimus is a macrolide lactone (found initially in fungus, but made by a Streptomyces species) immunosuppressive. Tacrolimus appears to inhibit the formation of cytotoxic lymphocytes, preventing a cell mediated response to allograft. Tacrolimus: suppresses T-cell activation;suppresses T-helper-cell-dependent B-cell proliferation;suppresses production of cytokines including Il-2, Il-3 and y-interferon; anddownregulates Il-2 receptor.Intracellularly, the effects of tacrolimus appear to be mediated by binding to FKBP (FK-506 Binding Protein; FK-506 is a formerly used name of tacrolimus). A com http://www.virtualmedicalcentre.com/drugs/rebetron-combination-therapy/1661 Rebetron Combination Therapy is made up of therapy with Interferon alfa-2b and Ribavirin. Interferon alfa-2b Interferons are naturally occurring substances in the body that are involved in the immune response to various viruses and other chemical and biological inducers. Intron A Redipen provides the body with an extra dose of a specific interferon, Interferon alfa-2b, which acts by binding to cell surfaces and initiating a complex series of intracellular events including enzyme induction. These events are thought to enable the cells to inhibit viral replication, suppress cell replication an http://www.virtualmedicalcentre.com/drugs/rebif/1662 The active component of Rebif is Interferon beta-1a which is a recombinant human Interferon beta produced in Chinese hamster ovary cells.4 Interferons are cytokines that modulate the immune systems response to viruses and other noxious stimuli. The exact mechanism of Rebif in the treatment of multiple sclerosis is not known but it is thought to have immuno-regulatory actions such as inhibiting gamma interferon, reducing cytokine release and amplifying suppressor T-cell function.1 Rebif mediates this action by binding to specific cellular receptors which subsequently initiate a cascade of even http://www.virtualmedicalcentre.com/drugs/remicade/1663 Humanised murine monoclonal antibody against tumour necrosis factor alfa (TNF-a), which prevents inflammatory cell responses in chronic inflammatory conditions. http://www.virtualmedicalcentre.com/drugs/roferon-a/1664 Interferons are naturally occurring substances in the body that are involved in the immune response to various viruses and other chemical and biological inducers. They act by binding to cell surfaces and initiating a complex series of intracellular events including enzyme induction. These events are thought to enable the cells to inhibit viral replication, suppress cell replication and enhance activity of other immune cells such as macrophages and lymphocytes. Roferon-A provides the body with an extra dose of a specific interferon, Interferon alfa-2b, which has specific effects making it u http://www.virtualmedicalcentre.com/drugs/sandimmun/1665 Cyclosporine is a calcineurin inhibitor and acts by blocking the action of calcineurin in activated T cells. This prevents the increase in cytokine production, which is normally responsible for the stimulation of B and T cell proliferation and differentiation. http://www.virtualmedicalcentre.com/drugs/synagis/1667 The drug Synagis (Palivizumab) is an IgG1 monoclonal antibody that is directed against a fusion protein on the surface of respiratory syncytial virus.3 This results in the drug inhibiting the replication of the RSV virus.3 http://www.virtualmedicalcentre.com/drugs/thioprine/1668 Azathioprine is used for the suppression of the immune response.Pharmacology. Azathioprine is rapidly broken down in vivo into 6-MP and a methylnitroimidazole moiety. The 6-MP readily crosses cell membranes and is converted intracellularly into a number of purine thioanalogues, which include the main active nucleotide, thioinosinic acid. The rate of conversion varies from one person to another. Nucleotides do not traverse cell membranes and therefore do not circulate in body fluids. Irrespective of whether it is given directly or is derived in vivo from azathioprine, 6-MP is eliminated main http://www.virtualmedicalcentre.com/drugs/alkeran/1683 Melphalan is an alkylating agent that interferes with cellular replication by forming cross-linkages between DNA strands. http://www.virtualmedicalcentre.com/drugs/alkeran-injection/1684 Melphalan is an alkylating agent that interferes with cellular replication by forming cross-linkages between DNA strands. http://www.virtualmedicalcentre.com/drugs/bicnu/1685 Carmustine is an alkylating agent. Alkylating agents work on DNA in three different ways to disrupt its function and result in cell death. Firstly, they add alkyl groups to the bases making up the DNA. As normal repair enzymes try to replace the alkylated bases, the DNA is fragmented. Secondly, alkylating agents form cross-links between DNA strands, which prevents the strands from separating and undergoing replication. The final mechanism by which alkylating agents disrupt DNA is by causing mismatching of DNA bases. The alkylated bases are different from the original bases, and may pair incorr http://www.virtualmedicalcentre.com/drugs/ceenu/1686 - CeeNU is a antitumour agent, a cancer chemotherapeutic agent, a cytotoxic agent and an alkylating agent. - It is not well known on the exact mode of action by which it works but CeeNU efficacy may be related to the alkylation of nucleic acids, carbamoylation of proteins, or interference with enzymatic actions. - CeeNUs efficacy is also largely due to its highly reactive intermediate molecules which are responsible for reducing tumour activity, however, the exact details are poorly understood. Overall DNA and RNA synthesis is inhibited. http://www.virtualmedicalcentre.com/drugs/cycloblastin/1687 Cyclophosphamide is a nitrogen mustard bis-alkylating agent. Cyclophosphamide is a prodrug (which permits oral administration), and requires bioactivation in the liver by CYP2B to become pharmacologically active.3 Bioactivation of cyclophosphamide also produces the highly toxic metabolite acrolein, which can result in haemorrhagic cystitis on accumulation in the bladder.4 This side effect can be prevented by coadministration with mesna (sodium 2-mercaptoethanesulfonate), a sulfhydryl compound that inactivates acrolein.2 Cyclophosphamide possesses two alkylating groups, and once bioactivated to http://www.virtualmedicalcentre.com/drugs/endoxan/1688 Cyclophosphamide is a nitrogen mustard bis-alkylating agent. Cyclophosphamide is a prodrug (which permits oral administration), and requires bioactivation in the liver by CYP2B to become pharmacologically active.3 Bioactivation of cyclophosphamide also produces the highly toxic metabolite acrolein, which can result in haemorrhagic cystitis on accumulation in the bladder.4 This side effect can be prevented by coadministration with mesna (sodium 2-mercaptoethanesulfonate), a sulfhydryl compound that inactivates acrolein.2 Cyclophosphamide possesses two alkylating groups, and once bioactivated to http://www.virtualmedicalcentre.com/drugs/holoxan/1689 Ifosfamide is an antineoplastic known as an alkylating agent. Ifosfamide itself is not active, but when it is converted by liver enzymes its metabolites are biologically active. Alkylating agents work on DNA in three different ways to disrupt its function and result in cell death. Firstly, they add alkyl groups to the bases making up the DNA. As normal repair enzymes try to replace the alkylated bases, the DNA is fragmented. Secondly, alkylating agents form cross-links between DNA strands, which prevents the strands from separating and undergoing replication. The final mechanism by which al http://www.virtualmedicalcentre.com/drugs/leukeran/1690 Chlorambucil is an alkylating agent that interferes with cellular replication by forming cross-linkages between DNA strands. http://www.virtualmedicalcentre.com/drugs/temodal/1693 Temozolamide is an antineoplastic agent known as an alkylating agent. Alkylating agents work on DNA in three different ways to disrupt its function and result in cell death. Firstly, they add alkyl groups to the bases making up the DNA. As normal repair enzymes try to replace the alkylated bases, the DNA is fragmented. Secondly, they form cross-links between DNA strands, which prevents the strands from separating and undergoing replication. Finally, they disrupt DNA is by causing mismatching of DNA bases. The alkylated bases are different from the original bases, and may pair incorrect http://www.virtualmedicalcentre.com/drugs/thiotepa/1694 Thiotepa is a polyfunctional alkylating agent. This means that it has more than one alkyl group that can react with DNA. Alkylating agents work on DNA in three different ways to disrupt its function and result in cell death. Firstly, they add alkyl groups to the bases making up the DNA. As normal repair enzymes try to replace the alkylated bases, the DNA is fragmented. Secondly, alkylating agents form cross-links between DNA strands, which prevents the strands from separating and undergoing replication. The final mechanism by which alkylating agents disrupt DNA is by mismatching of DNA bases. http://www.virtualmedicalcentre.com/drugs/cytarabine-dbl/1696 Cytarabine is an antineoplastic agent, bone marrow suppressant and immunosuppressant that is converted to cytarabine triphosphate intracellularly, which is believed to inhibit DNA polymerase, thereby inhibiting DNA synthesis. Cytarabines actions are cell-cycle specific. http://www.virtualmedicalcentre.com/drugs/cytarabine-injection/1697 Cytarabine is an antineoplastic agent, bone marrow suppressant and immunosuppressant that is converted to cytarabine triphosphate intracellularly, which is believed to inhibit DNA polymerase, thereby inhibiting DNA synthesis. Cytarabines actions are cell-cycle specific. http://www.virtualmedicalcentre.com/drugs/efudix/1698 Fluorouracil is a uracil analogue and an antimetabolite. Following conversion to its active metabolite, it interferes with the replication of rapidly dividing cells (including cancer cells) by preventing the conversion of folic acid to folinic acid, a building block for new DNA. Fluorouracil aims to reduce tumour size and prolong life for cancer sufferers. http://www.virtualmedicalcentre.com/drugs/fluorouracil-injection-bp/1699 Fluorouracil is a uracil analogue and an antimetabolite. Following conversion to its active metabolite, it interferes with the replication of rapidly dividing cells (including cancer cells) by preventing the conversion of folic acid to folinic acid, a building block for new DNA. Fluorouracil aims to reduce tumour size and prolong life for cancer sufferers. http://www.virtualmedicalcentre.com/drugs/fluorouracil-injection-bp-dbl/1700 Fluorouracil is a uracil analogue and an antimetabolite. Following conversion to its active metabolite, it interferes with the replication of rapidly dividing cells (including cancer cells) by preventing the conversion of folic acid to folinic acid, a building block for new DNA. Fluorouracil aims to reduce tumour size and prolong life for cancer sufferers. http://www.virtualmedicalcentre.com/drugs/gemzar/1701 Gemcitabine is a pyrimidine analogue. Its cytotoxic action against tumor cells and mediated by inhibiting ribonucleotide reductase and competing with nucleosides to be included within DNA. Cells are killed in the S phase or DNA synthesis phase of the cell cycle. http://www.virtualmedicalcentre.com/drugs/hydrea/1703 Hydroxyurea inhibits DNA synthesis by interfering with the conversion of ribonucleotides to deoxyribonucleotides. http://www.virtualmedicalcentre.com/drugs/ledertrexate/1705 Methotrexate is an anti-folate antimetabolite agent. It interferes with the replication of rapidly dividing cells (including cancer cells) by preventing the conversion of folic acid to folinic acid, a building block for new DNA. Methotrexate aims to reduce tumour size and prolong life for cancer sufferers. Its mechanism of action in rheumatoid arthritis is unknown. http://www.virtualmedicalcentre.com/drugs/leustatin/1707 Cladribine acts by inhibiting the synthesis and the repair of DNA in lymphocytes and monocytes. http://www.virtualmedicalcentre.com/drugs/methoblastin/1708 Methotrexate is an anti-folate antimetabolite agent. It interferes with the replication of rapidly dividing cells (including cancer cells) by preventing the conversion of folic acid to folinic acid, a building block for new DNA. Methotrexate aims to reduce tumour size and prolong life for cancer sufferers. Its mechanism of action in rheumatoid arthritis is unknown. http://www.virtualmedicalcentre.com/drugs/methotrexate-injection-and-tablets-dbl/1709 Methotrexate has cytotoxic, immunosuppressive, and anti-inflammatory actions. It inhibits DNA synthesis and cell replication by competitively inhibiting the conversion of folic acid to folinic acid. http://www.virtualmedicalcentre.com/drugs/methotrexate-injection-bp/1710 Methotrexate has cytotoxic, immunosuppressive, and anti-inflammatory actions. It inhibits DNA synthesis and cell replication by competitively inhibiting the conversion of folic acid to folinic acid. http://www.virtualmedicalcentre.com/drugs/taxotere/1713 Docetaxel is an antimetabolite antineoplastic agent known as a taxane. Taxanes are cytotoxic agents that work on the cytoplasmic protein tubulin, an important building block of microtubules. Microtubules are vital in forming spindle fibres, which are required for separation of chromosomes and cell division. Taxanes cause tubulin to be assembled into stable non-functional microtubules, which cells then cant disassemble. The non-functional microtubules strand the cell in the late G2 and M phases of cell division. http://www.virtualmedicalcentre.com/drugs/tomudex/1714 Raltitrexed is an antimetabolite. It directly and specifically inhibiting the enzyme thymidylate synthetase, which is vital in the production of thymidine triphosphate, a nucleotide required for DNA synthesis. Failure of production of thymidine triphosphate leads to DNA fragmentation and cell death. http://www.virtualmedicalcentre.com/drugs/xeloda/1715 Capecitabine is an oral antineoplastic agent. It is a pyrimidine analogue that is metabolised to its active form, 5-fluorouracil (5-FU), by thymidine phosphorylase, an enzyme found mainly in tumours. 5-FU is metabolised to eventually form 5-fluoro-2 deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP). FdUMP prevents cell proliferation by interfering with DNA synthesis. FUTP is incorporated into RNA, which causes incorrect processing of ribosomal and messenger RNA. This effect is most marked in tumour cells, as they metabolise 5-FU at a higher rate than other cells. F http://www.virtualmedicalcentre.com/drugs/navelbine/1717 Vinorelbine tartrate is a vinca alkaloid. It is a cell cycle specific agent that works by arresting mitosis in metaphase. Vinorelbine binds tubulin monomers and inhibits the production of microtubules. Microtubules are vital in forming spindle fibres, which are required for separation of chromosomes and cell division. Without these spindle fibres, cell division cannot occur and the cell dies http://www.virtualmedicalcentre.com/drugs/oncovin/1718 The action of Oncovin is not yet fully understood. It causes mitotic arrest in in vitro neoplastic cells. The antineoplastic effects of Oncovin are related to interference with intracellular tubulin function. Clinical evidence shows that Oncovin does not penetrate well into the cerebrospinal fluid. http://www.virtualmedicalcentre.com/drugs/velbe/1719 Vinblastine is a vinca alkaloid. It is a cell cycle specific agent that works by arresting mitosis in metaphase. Vinblastine binds tubulin monomers and inhibits the production of microtubules. Microtubules are vital in forming spindle fibres, which are required for separation of chromosomes and cell division. Without these spindle fibres, cell division cannot occur and the cell dies. http://www.virtualmedicalcentre.com/drugs/vinblastine-sulfate-injection-dbl/1720 Vinblastine is a vinca alkaloid. It is a cell cycle specific agent that works by arresting mitosis in metaphase. Vinblastine binds tubulin monomers and inhibits the production of microtubules. Microtubules are vital in forming spindle fibres, which are required for separation of chromosomes and cell division. Without these spindle fibres, cell division cannot occur and the cell dies. http://www.virtualmedicalcentre.com/drugs/vincristine-sulfate-injection/1721 It is thought that Vincristine arrests cell mitosis by binding tubulin subunits and hence preventing microtubule polymerization during metaphase. Cells affected in such a way cannot form a mitotic spindle and tend to undergo apoptosis.1-3 http://www.virtualmedicalcentre.com/drugs/vincristine-sulfate-injection-dbl/1722 Vincristine is a vinca alkaloid antineoplastic drug. It acts by specifically arresting cells in the metaphase and subsequently blocking mitosis. http://www.virtualmedicalcentre.com/drugs/adriamycin-solution/1723 Doxorubicin is from the family of chemotherapy drugs known as anthracyclines. Anthracyclines act directly on DNA as intercalating agents, which means they wedge themselves between base pairs in DNA and block DNA synthesis. They also inhibit the enzyme responsible for repairing breaks in the DNA (topoisomerase II). Anthracyclines are non-cell-cycle specific drugs, meaning cells do not have to be actively dividing to be affected. Doxorubicin also has immunosuppressive activity. http://www.virtualmedicalcentre.com/drugs/blenamax/1724 Bleomycin is an antineoplastic antibiotic. It has no antimicrobial activity. The exact mechanism by which Bleomycin works is not fully known, but it is thought to create single and double strand breaks in DNA, which inhibits DNA synthesis and cell division. Due to its specificity for dividing cells, Bleomycin is known as a cell cycle specific chemotherapeutic agent. Bleomycin is also useful in the treatment of malignant pleural effusion, probably by creating a local inflammatory effect, the healing of which is followed by a fibrous adhesion. However, a cytotoxic effect cannot be ruled out i http://www.virtualmedicalcentre.com/drugs/blenoxane/1725 Bleomycin is an antineoplastic antibiotic. It has no antimicrobial activity. The exact mechanism by which Bleomycin works is not fully known, but it is thought to create single and double strand breaks in DNA, which inhibits DNA synthesis and cell division. Due to its specificity for dividing cells, Bleomycin is known as a cell cycle specific chemotherapeutic agent. Bleomycin is also useful in the treatment of malignant pleural effusion, probably by creating a local inflammatory effect, the healing of which is followed by a fibrous adhesion. However, a cytotoxic effect cannot be ruled out in http://www.virtualmedicalcentre.com/drugs/bleomycin-sulfate-for-injection-dbl/1726 Bleomycin is an antineoplastic antibiotic. It has no antimicrobial activity. The exact mechanism by which Bleomycin works is not fully known, but it is thought to create single and double strand breaks in DNA, which inhibits DNA synthesis and cell division. Due to its specificity for dividing cells, Bleomycin is known as a cell cycle specific chemotherapeutic agent. Bleomycin is also useful in the treatment of malignant pleural effusion, probably by creating a local inflammatory effect, the healing of which is followed by a fibrous adhesion. However, a cytotoxic effect cannot be ruled out in http://www.virtualmedicalcentre.com/drugs/daunorubicin-injection/1729 Daunorubicin has several mechanisms of action. It inhibits DNA and DNA-dependent RNA synthesis by intercalating base pairs with uncoiling of the helix, it interferes with topoisomerase II function, preventing re-ligation of DNA strand breaks and it also is produces peroxide and free radicals. As well as antineoplastic activity, daunorubicin also has immunosuppressive activity. http://www.virtualmedicalcentre.com/drugs/doxorubicin-hydrochloride-injection-dbl/1731 Doxorubicin is from the family of chemotherapy drugs known as anthracyclines. Anthracyclines act directly on DNA as intercalating agents, which means they wedge themselves between base pairs in DNA and block DNA synthesis. They also inhibit the enzyme responsible for repairing breaks in the DNA (topoisomerase II). Anthracyclines are non-cell-cycle specific drugs, meaning cells do not have to be actively dividing to be affected. Doxorubicin also has immunosuppressive activity. http://www.virtualmedicalcentre.com/drugs/doxorubicin-hydrochloride-injection-usp/1732 Doxorubicin is from the family of chemotherapy drugs known as anthracyclines. Anthracyclines act directly on DNA as intercalating agents, which means they wedge themselves between base pairs in DNA and block DNA synthesis. They also inhibit the enzyme responsible for repairing breaks in the DNA (topoisomerase II). Anthracyclines are non-cell-cycle specific drugs, meaning cells do not have to be actively dividing to be affected. Doxorubicin also has immunosuppressive activity. http://www.virtualmedicalcentre.com/drugs/fludara/1733 Fludarabine phosphate is an antineoplastic agent that is dephosphorylated to fludarabine, taken up by cells, and then phosphorylated intracellularly to the active form, fludarabine triphosphate. This metabolite inhibits DNA synthesis and partially inhibits RNA and protein synthesis, thereby contributing to inhibition of cell growth. The effect is thought to be mainly from inhibiting DNA synthesis, which is achieved by inhibiting DNA polymerase, ribunucleotide reductase and DNA primase. Apoptosis has also been observed to occur. http://www.virtualmedicalcentre.com/drugs/mitomycin-c-kyowa/1734 Mitomycin inhibits the synthesis of deoxyribonucleic acid (DNA), and at high concentrations suppresses the synthesis of cellular RNA and proteins. http://www.virtualmedicalcentre.com/drugs/mitozantrone-injection/1735 Mitozantrone is a potent anti-neoplastic belonging to the anthracycline class.3 Its precise mechanism of action is not fully-understood but it is thought to act by intercalating itself into deoxyribonucleic acid (DNA) causing strand breaks and inhibiting DNA synthesis.4 In addition it is thought to interfere with RNA synthesis and topoisomerase function (an important agent in uncoiling DNA for repair). Mitozantrone is described as cell cycle non-specific as it has cytotoxic effects on both proliferating and non-proliferating cells.1,3 Like other anthracyclines, Mitozantrone also has immuno http://www.virtualmedicalcentre.com/drugs/novantrone/1736 Mitozantrone is an antineoplastic agent known as an anthracycline. It is a non-cell cycle specific cytotoxic agent. The mechanism of action of Mitozantrone is not fully understood, but it has similar activity to other anthracyclines. Anthracyclines act directly on DNA as intercalating agents, which means they wedge themselves between base pairs in DNA and block DNA synthesis. They also inhibit the enzyme responsible for repairing breaks in the DNA (topoisomerase II). Mitozantrone may have slightly less cardiotoxic activity than other anthracyclines. http://www.virtualmedicalcentre.com/drugs/onkotrone/1737 Mitozantrone is an antineoplastic agent known as an anthracycline. It is a non-cell cycle specific cytotoxic agent. The mechanism of action of Mitozantrone is not fully understood, but it has similar activity to other anthracyclines. Anthracyclines act directly on DNA as intercalating agents, which means they wedge themselves between base pairs in DNA and block DNA synthesis. They also inhibit the enzyme responsible for repairing breaks in the DNA (topoisomerase II). Mitozantrone may have slightly less cardiotoxic activity than other anthracyclines. http://www.virtualmedicalcentre.com/drugs/zavedos/1739 Idarubicin is from the family of chemotherapy drugs known as anthracyclines. Anthracyclines act directly on DNA as intercalating agents, which means they wedge themselves between base pairs in DNA and block DNA synthesis. They also inhibit the enzyme responsible for repairing breaks in the DNA (topoisomerase II). Anthracyclines are non-cell-cycle specific drugs, meaning cells do not have to be actively dividing to be affected. http://www.virtualmedicalcentre.com/drugs/androcur-100/1741 Cyproterone acetate competitively inhibits endogenous and exogenous androgens at the target organs, thus reducing the stimulating effects of androgens. http://www.virtualmedicalcentre.com/drugs/arimidex/1742 Anastrazole is a potent, highly selective aromatase inhibitor. The aromatase enzyme complex is important in the conversion of androstenedione to oestrone (which is subsequently converted to oestradiol). Many breast cancers have oestrogen receptors, and by reducing the amount of circulating oestrogen, Anastrazole can stop the growth of these tumours. Due to its selectivity, Anastrazole does not affect other steroid hormones and side effects are reduced1. http://www.virtualmedicalcentre.com/drugs/aromasin/1743 Exemestane is an irreversible steroidal aromatase inactivator. It acts on the active site of the enzyme aromatase which inhibits the conversion of androgen into oestrogen in peripheral tissues. Oestrogen deprivation through aromatase inhibition is an effective and selective treatment for hormone dependent breast cancer in postmenopausal women. http://www.virtualmedicalcentre.com/drugs/chem-mart-tamoxifen/1744 Tamoxifen is a non-steroidal anti-oestrogen. It probably works by binding to oestrogen receptors, and this inhibits the effects of endogenous oestrogen. Many breast cancers have oestrogen receptors and therefore have their growth stimulated by the presence of oestrogen. By inhibiting oestrogen, Tamoxifen inhibits tumour growth. http://www.virtualmedicalcentre.com/drugs/cosudex/1745 Bicalutamide is an antiandrogen agent. It binds to androgen receptors and prevents gene expression, therefore inhibiting the androgen stimulus. Inhibition of androgen receptors in prostate cancer stops the growth and promotes apoptosis of cancer cells. 2 http://www.virtualmedicalcentre.com/drugs/eulexin/1748 Nonsteroidal, orally active antiandrogen.Flutamide demonstrates potent antiandrogenic effects by inhibiting androgen uptake and/or by inhibiting nuclear binding of androgen in target tissues.Pharmacology. Flutamide exhibits specific antiandrogenic effects, largely directed to the prostate as target organ. Flutamide, administered orally to intact immature male rats at doses ranging from 1 to 25 mg/kg, significantly reduced prostate and seminal vesicle weights. Other endocrine structures were not altered. In studies of dogs with benign prostatic hypertrophy, daily oral administration of flutamid http://www.virtualmedicalcentre.com/drugs/femara/1750 The active ingredient of Femara is letrozole, a nonsteroidal aromatase inhibitor. Letrozole inhibits aromatase enzymes which convert androstenedione and testosterone to oestrone (which is subsequently converted to oestradiol).1-3 Many breast cancers have oestrogen receptors, and by reducing the amount of circulating oestrogen, letrozole can stop the growth of these tumours. Due to its selectivity, letrozole does not affect other steroid hormones sonbsp;there are fewer side effects.1-3 http://www.virtualmedicalcentre.com/drugs/flutamin/1751 Nonsteroidal, orally active antiandrogen.Pharmacology. Flutamide demonstrates potent antiandrogenic effects by inhibiting androgen uptake and/or by inhibiting nuclear binding of androgen in target tissues.Flutamide exhibits specific antiandrogenic effects, largely directed to the prostate as target organ. When administered orally to intact immature male rats at doses ranging from 1 to 25 mg/kg, flutamide significantly reduced prostate and seminal vesicle weights, without altering other endocrine structures. In studies of dogs with benign prostatic hypertrophy, daily oral administration of flut http://www.virtualmedicalcentre.com/drugs/genox/1753 Tamoxifen is a non-steroidal anti-oestrogen. It probably works by binding to oestrogen receptors, and this inhibits the effects of endogenous oestrogen. Many breast cancers have oestrogen receptors and therefore have their growth stimulated by the presence of oestrogen. By inhibiting oestrogen, Tamoxifen inhibits tumour growth. http://www.virtualmedicalcentre.com/drugs/genrx-tamoxifen/1754 Tamoxifen is a non-steroidal anti-oestrogen. It probably works by binding to oestrogen receptors, and this inhibits the effects of endogenous oestrogen. Many breast cancers have oestrogen receptors and therefore have their growth stimulated by the presence of oestrogen. By inhibiting oestrogen, Tamoxifen inhibits tumour growth. http://www.virtualmedicalcentre.com/drugs/healthsense-tamoxifen/1755 Tamoxifen is a non-steroidal anti-oestrogen. It probably works by binding to oestrogen receptors, and this inhibits the effects of endogenous oestrogen. Many breast cancers have oestrogen receptors and therefore have their growth stimulated by the presence of oestrogen. By inhibiting oestrogen, Tamoxifen inhibits tumour growth. http://www.virtualmedicalcentre.com/drugs/lucrin/1757 Lucrin (Leuprorelin) is a synthetic analogue of gonadotrophin releasing hormone (GnRH). 2 When administered over long periods of time, through a negative feedback effect, it has been found that Lucrin is a potent inhibitor of steroid production in both the ovaries and the testes. 2 Through this inhibition it acts to inhibit tumour growth and also causes atrophy of the gonads. 2 http://www.virtualmedicalcentre.com/drugs/lucrin-depot/1758 Leuprorelin acetate is a synthetic GnRH (LHRH) analogue. When administered chronically, it inhibits pituitary release of gonadotrophin and therefore suppresses testicular steroidogenesis. This inhibition results in circulating hormone levels similar to those seen in a surgically castrated man. Decreasing hormone levels helps inhibit the growth of testosterone dependent prostate cancer. The testicular inhibiting effects of Lucrin Depot are reversible on discontinuation of therapy. http://www.virtualmedicalcentre.com/drugs/megace/1759 Synthetic progestogen (progestational agent).The antitumour action of megestrol acetate on carcinoma of the breast is unclear. However, it is known to compete for progesterone, androgen and glucocorticoid receptors and affect pituitary functions.Pharmacology. Megestrol acetate is chemically related to progesterone. It differs by the addition of a 17-acetoxy group, a double bond at position 6 and the presence of a methyl group. It exhibits classical progestational activity. Megestrol acetate possesses little or no oestrogenic, androgenic or adrenocorticoid action.Pharmacokinetics. Peak plasma c http://www.virtualmedicalcentre.com/drugs/nolvadex-nolvadex-d/1760 Tamoxifen is a non-steroidal anti-oestrogen. It probably works by binding to oestrogen receptors, and this inhibits the effects of endogenous oestrogen. Many breast cancers have oestrogen receptors and therefore have their growth stimulated by the presence of oestrogen. By inhibiting oestrogen, Tamoxifen inhibits tumour growth. http://www.virtualmedicalcentre.com/drugs/tamosin/1761 Tamoxifen is a non-steroidal anti-oestrogen. It probably works by binding to oestrogen receptors, and this inhibits the effects of endogenous oestrogen. Many breast cancers have oestrogen receptors and therefore have their growth stimulated by the presence of oestrogen. By inhibiting oestrogen, Tamoxifen inhibits tumour growth. http://www.virtualmedicalcentre.com/drugs/tamoxen/1762 Tamoxifen is a non-steroidal anti-oestrogen. It probably works by binding to oestrogen receptors, and this inhibits the effects of endogenous oestrogen. Many breast cancers have oestrogen receptors and therefore have their growth stimulated by the presence of oestrogen. By inhibiting oestrogen, Tamoxifen inhibits tumour growth. http://www.virtualmedicalcentre.com/drugs/tamoxifen-hexal/1763 Tamoxifen is a non-steroidal anti-oestrogen. It probably works by binding to oestrogen receptors, and this inhibits the effects of endogenous oestrogen. Many breast cancers have oestrogen receptors and therefore have their growth stimulated by the presence of oestrogen. By inhibiting oestrogen, Tamoxifen inhibits tumour growth. http://www.virtualmedicalcentre.com/drugs/tamoxifen-bc/1764 Tamoxifen is a non-steroidal anti-oestrogen. It probably works by binding to oestrogen receptors, and this inhibits the effects of endogenous oestrogen. Many breast cancers have oestrogen receptors and therefore have their growth stimulated by the presence of oestrogen. By inhibiting oestrogen, Tamoxifen inhibits tumour growth. http://www.virtualmedicalcentre.com/drugs/tamoxifen-terry-white-chemists/1765 Tamoxifen is a non-steroidal anti-oestrogen. It probably works by binding to oestrogen receptors, and this inhibits the effects of endogenous oestrogen. Many breast cancers have oestrogen receptors and therefore have their growth stimulated by the presence of oestrogen. By inhibiting oestrogen, Tamoxifen inhibits tumour growth. http://www.virtualmedicalcentre.com/drugs/zoladex-36mg-and-108-mg-implant/1767 Goserelin acetate is a potent synthetic luteneising hormone releasing hormone (LHRH) agonist. In the short term, it causes the release of luteinizing hormone (LH) from the anterior pituitary. Given in chronic use, Goserelin also inhibits gonadotrophin production, which results in gonadal suppression and sex organ regression. This can also result in a serum testosterone level equivalent to that seen in surgically castrated men. 1 http://www.virtualmedicalcentre.com/drugs/agrylin/1768 The mechanism through which anagrelide reduces blood platelet levels is not known. In vitro studies have demonstrated that anagrelide selectively and reversibly inhibits the maturation of megakaryocytes in the post-mitotic fphase, resulting in a reduced platelet count.1,2 http://www.virtualmedicalcentre.com/drugs/camptosar/1770 Irinotecan hydrochloride is an antineoplastic of the topoisomerase I inhibitor class. The enzyme topoisomerase I is responsible for relieving torsional strain on DNA by inducing reversible single strand breaks. Irinotecans inhibition of topoisomerase I means that these strand breaks cannot be repaired. When DNA synthesis then occurs for cell division, double strand DNA damage arises and the cell cannot divide and dies. Irinotecan is converted to SN-38, which is a much more powerful inhibitor of topoisomerase I, but the exact role of SN-38 in the activity of Camptosar is unknown. Irinote http://www.virtualmedicalcentre.com/drugs/carboplatin-injection/1771 Carboplatin is an analogue of cisplatin and contains platinum. It binds and crosslinks DNA which inhibits its synthesis and hence replication. http://www.virtualmedicalcentre.com/drugs/carboplatin-injection-dbl/1772 Carboplatin is an analogue of cisplatin and contains platinum. It binds and crosslinks DNA which inhibits its synthesis and hence replication. http://www.virtualmedicalcentre.com/drugs/cisplatin-injection/1773 Cisplatin is a platinum compound that works as an antineoplastic agent. It produces cross links within and between strands of DNA, modifying DNA structure and inhibiting DNA synthesis. Protein and RNA synthesis are also inhibited to a lesser extent. Inhibition of production of these components leads to prevention of cell division and eventual cell death. Cisplatin is a non cell-cycle specific antineoplastic agent. http://www.virtualmedicalcentre.com/drugs/cisplatin-injection-dbl/1774 Cisplatin is a platinum compound that works as an antineoplastic agent. It produces cross links within and between strands of DNA, modifying DNA structure and inhibiting DNA synthesis. Protein and RNA synthesis are also inhibited to a lesser extent. Inhibition of production of these components leads to prevention of cell division and eventual cell death. Cisplatin is a non cell-cycle specific antineoplastic agent. http://www.virtualmedicalcentre.com/drugs/dacarbazine-for-injection-dbl/1775 Following activation in the liver, Dacarbazine functions as an alkylating agent interfering with cellular replication by forming cross-linkages between DNA strands. http://www.virtualmedicalcentre.com/drugs/dtic/1776 Following activation in the liver, Dacarbazine functions as an alkylating agent interfering with cellular replication by forming cross-linkages between DNA strands. http://www.virtualmedicalcentre.com/drugs/eloxatin/1777 Oxaliplatin is a platinum based antineoplastic agent.1,2 Its structure is slightly different from cisplatin, another platinum-based chemotherapeutic agent, which makes it useful in the treatment of cancers that are cisplatin-resistant.2 Biotransformation of oxaliplatin releases metabolites, which are thought to interact with DNA.2 They form intra- and inter-strand cross links, which results in disruption of DNA synthesis and eventual cell death.1,2 http://www.virtualmedicalcentre.com/drugs/etopophos/1778 Etopophos is converted to etoposide in vivo. Etoposide is a podophyllotoxin derivative. It damages DNA thereby inhibiting DNA synthesis. It preferentially kills cells in the G2 and S phases of the cell cycle. http://www.virtualmedicalcentre.com/drugs/etoposide-injection/1779 Etoposide is a podophyllotoxin derivative that inhibits topoisomerase II, subsequently producing single strand breaks in DNA and affecting the S and G2 phases of the cell cycle. http://www.virtualmedicalcentre.com/drugs/etoposide-injection-dbl/1780 Etoposide is a podophyllotoxin derivative that inhibits topoisomerase II subsequently producing single strand breaks in DNA and affecting the S and G2 phases of the cell cycle. http://www.virtualmedicalcentre.com/drugs/glivec/1781 Imatinib mesylate is a tyrosine kinase inhibitor which blocks proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukaemic cells from CML patients. Imatinib mesylate also targets a tumour protein that is the suspected cause of gastrointestinal stromal tumours by inhibiting the growth of cancerous cells.1,2 http://www.virtualmedicalcentre.com/drugs/leucovorin-calcium-injection-usp/1783 Leucovorin Calcium, otherwise known as folinic acid, is a derivative of the active form of folic acid, and is an important component of DNA synthesis. Folic acid antagonists, such as methotrexate, bind the enzyme dihydrofolate reductase, effectively blocking the conversion of folic acid to folinic acid. Leucovorin is used as an antidote for these folic acid antagonists. By ensuring there is adequate folinic acid for DNA synthesis in healthy cells, use of Leucovorin following treatment with methotrexate reduces the haemopoietic and reticuloendothelial toxicity of the folic acid antagonist. Leuc http://www.virtualmedicalcentre.com/drugs/leucovorin-calcium-injection-usp-and-tablets-dbl/1784 Leucovorin Calcium, otherwise known as folinic acid, is a derivative of the active form of folic acid, and is an important component of DNA synthesis. Folic acid antagonists, such as methotrexate, bind the enzyme dihydrofolate reductase, effectively blocking the conversion of folic acid to folinic acid. Leucovorin is used as an antidote for these folic acid antagonists. By ensuring there is adequate folinic acid for DNA synthesis in healthy cells, use of Leucovorin following treatment with methotrexate reduces the haemopoietic and reticuloendothelial toxicity of the folic acid antagonist. Leuc http://www.virtualmedicalcentre.com/drugs/metoclopramide-injection/1786 Metoclopramide is an antiemetic agent. It stimulates the motility of the upper gastrointestinal tract without increasing secretions of the stomach, gallbladder or pancreas. Although its mechanism of action is not fully understood, Metoclopramide appears to sensitise tissues to the actions of acetylcholine. This increases the tone and amplitude of gastric contractions and increases peristalsis of the duodenum and jejunum, facilitating gastric emptying. It also increases the resting tone of the oesophageal sphincter, preventing upward movement of stomach contents. Metoclopramide is unlikely to c http://www.virtualmedicalcentre.com/drugs/navoban/1787 Tropisetron is a selective 5HT3-antagonist used in the prevention of nausea and vomiting associated with chemotherapy.1,2 5HT3-receptors are found on preganglionic and postganglionic neurones and neurones of the sensory and enteric nervous systems.1,2 They are also found in the area postrema, a chemoreceptor trigger zone in the fourth ventricle associated with vomiting.1,2 Chemotherapy agents cause vomiting by releasing serotonin from enterochromaffin cells of the small intestine, which is detected by vagal afferents. Tropisetrons antagonism of 5HT3-receptors at vagal and central sites http://www.virtualmedicalcentre.com/drugs/quadramet/1790 Quadramet contains radioactive Samarium that has been complexed with ethylenediaminetetra methylenephosphonic acid monohydrate (EDTMP) for intravenous injection. Samarium has an affinity for bone and quickly localises in areas of growing bone matrix. Once concentrated in areas of bone metastases, Quadramet helps relieve the pain they cause. The mechanism by which it achieves this is unknown. http://www.virtualmedicalcentre.com/drugs/sodium-iodide-solution-bp-therapy/1791 After oral administration, sodium iodide is rapidly absorbed and distributed in the extracellular fluid. A proportion is taken up by the functioning thyroid tissue, where it disrupts the functioning of the cells, thereby decreasing thyroid hormone production and eliminating symptoms of hyperthyroidism. http://www.virtualmedicalcentre.com/drugs/uromitexan-injection/1793 Pharmacology. Uromitexan is a detoxifying agent used to reduce and prevent the urothelial toxicity (haemorrhagic cystitis) induced by oxazaphosphorine alkylating agents, e.g. ifosfamide or cyclophosphamide.Analogous to the physiological cysteine-cystine system, following intravenous administration, mesna is rapidly and easily converted by auto-oxidation to its only metabolite, disodium 2,2-dithio-bisethane sulfonate (mesna disulfide, dimesna) forming a disulfide link. Following intravenous injection, only a small portion of the administered dose is detected in the blood as a reduced thiol com http://www.virtualmedicalcentre.com/drugs/uromitexan-tablets/1794 Pharmacology. Uromitexan is a detoxifying agent used to reduce and prevent the urothelial toxicity (haemorrhagic cystitis) induced by oxazaphosphorine alkylating agents, e.g. ifosfamide or cyclophosphamide.Analogous to the physiological cysteine-cystine system, mesna is rapidly and easily converted by auto-oxidation to its only metabolite, disodium 2,2-dithio-bisethane sulfonate (mesna disulfide, dimesna) forming a disulfide link. Following intravenous injection, only a small portion of the administered dose is detected in the blood as a reduced thiol compound (mesna). Mesna disulfide remains http://www.virtualmedicalcentre.com/drugs/zofran/1795 Ondansetron is a potent, selective 5HT3-antagonist used in the prevention of nausea and vomiting associated with chemotherapy. 5HT3-receptors are found on preganglionic and postganglionic neurones and neurones of the sensory and enteric nervous systems. They are also found in the area postrema, a chemoreceptor trigger zone in the fourth ventricle associated with vomiting. Chemotherapy agents cause vomiting by releasing serotonin from enterochromaffin cells of the small intestine, which is detected by vagal afferents. Ondansetrons antagonism of 5HT3-receptors at vagal and central sites helps p http://www.virtualmedicalcentre.com/drugs/abbocillin-vk/1796 Phenoxymethylpenicillin is a penicillin antibiotic that has bactericidal activity against penicillin sensitive organisms. It is not active against penicillinase producing organisms. Bacteria that are susceptible to Phenoxymethylpenicillin potassium include: - Streptococci, including sensitive strains of Streptococcus pyogenes - Clostridium tetani - C. perfringens - Corynebacterium diphtheriae - Bacillus anthracis Of the gram negative bacteria, Neisseria meningitidis and N. gonorrhoeae are sensitive to some extent. Haemophilus influenzae is moderately resistant, and all other gram negative baci http://www.virtualmedicalcentre.com/drugs/amohexal/1799 Amoxycilllin inhibits of biosynthesis of cell wall mucopeptide in susceptible Gram positive and Gram negative organisms. http://www.virtualmedicalcentre.com/drugs/amoxil-oralduo/1800 Amoxil belongs to the penicillin group of antibiotics, and has a similar gram positive and gram negative spectrum to ampicillin. Its action is bactericidal against sensitive strains, and is thought to act by inhibiting the synthesis of cell wall mucopeptide. http://www.virtualmedicalcentre.com/drugs/amoxil-parenteral/1801 Amoxil belongs to the penicillin group of antibiotics, and has a similar gram positive and gram negative spectrum to ampicillin. Its action is bactericidal against sensitive strains and is thought to act by inhibiting the synthesis of cell wall mucopeptide. http://www.virtualmedicalcentre.com/drugs/ampicyn/1802 Ampicillin has similar bactericidal action against sensitive organisms as benzylpenicillin. It inhibits cell wall mucopeptide biosynthesis during the active stage of multiplication. Ampicillin differs from benzylpenicillin in its activity against gram negative pathogens, and is generally less effective against gram positive bacteria than benzylpenicillin. Susceptible organisms might include: Gram positives: S.pyogenes; S.pneumoniae; S.viridans; S. faecalis; non-penicillinase producing Staphylococci, L.monocytogenes, Gram negatives: H.influenzae; E.coli; P.mirabilis; N.meningitidis; S http://www.virtualmedicalcentre.com/drugs/augmentin/1803 Bactericidal; penicillins interfere with bacterial cell wall peptidoglycan synthesis. Moderate spectrum penicillins like amoxicillin are active primarily against gram positive organisms. The addition of clavulanic acid to amoxicillin extends spectrum of activity to cover many beta-lactamse producing gram positive (S. aureus) and gram negative organisms (Moraxella Catarrhalis, H. Influenzae, Proteus spp., E. coli, Klebsiella spp.), including gram negative anaerobes. http://www.virtualmedicalcentre.com/drugs/augmentin-duo-forte/1805 Bactericidal; penicillins interfere with bacterial cell wall peptidoglycan synthesis Moderate spectrum penicillins like amoxicillin are active primarily against gram positive organisms The addition of clavulanic acid to amoxicillin extends spectrum of activity to cover many beta-lactamse producing gram positive (S. aureus) and gram negative organisms (Moraxella Catarrhalis, H. Influenzae, Proteus spp., E. coli, Klebsiella spp.), including gram negative anaerobes http://www.virtualmedicalcentre.com/drugs/austrapen/1809 Ampicillin has similar bactericidal action against sensitive organisms as benzylpenicillin. It inhibits cell wall mucopeptide biosynthesis during the active stage of multiplication. Ampicillin differs from benzylpenicillin in its activity against gram negative pathogens, and is generally less effective against gram positive bacteria than benzylpenicillin. Susceptible organisms might include: Gram positives: S.pyogenes; S.pneumoniae; S.viridans; S. faecalis; non-penicillinase producing Staphylococci, L.monocytogenes, Gram negatives: H.influenzae; E.coli; P.mirabilis; N.meningitidis; S http://www.virtualmedicalcentre.com/drugs/benpen/1810 Microbiology: Benzylpenicillin exerts bactericidal activity against many Gram positive organisms. Including: most Gram positive bacilli and spirochaetes (e.g. T.pallidum), many strains of S.pneumoniae, S.viridans S.pyogenes, most non-beta-lactamase producing Staphylococci, some Gram negative cocci (e.g. gonococci, meningococci). Benzylpenicillin is inactivated by bacterial beta-lactamases. Pharmacokinetics: Effective concentrations last for 4-6 hours. In the presence of normal renal function, 70% of the dose is excreted within 6 hours. 30% is inactivated by the liver and 4.5% is ex http://www.virtualmedicalcentre.com/drugs/chem-mart-amoxycillin/1814 Amoxicillin is a broad spectrum antibiotic with similar bactericidal activity to ampicillin. It acts by inhibiting cell wall mucopeptide biosynthesis. It is active against both Gram positive and negative pathogens, including P.mirabilis, H.influenzae, alpha beta haemolytic Streptococci, S.pneumoniae, S.faecalis, non-penicilliase producing Staphylococci, N.gonorrhoea, N.meningitidis. However, some organisms are only susceptible to amoxicillin at concentrations achieved in the urine, and gonococci strains relatively resistant to benzylpenicillin are likely to be resistant to amoxicillin. http://www.virtualmedicalcentre.com/drugs/cilicaine-vk/1817 Phenoxymethylpenicillin is a penicillin antibiotic that has bactericidal activity against penicillin sensitive organisms. It is not active against penicillinase producing organisms. Bacteria that are susceptible to Phenoxymethylpenicillin potassium include: - Streptococci, including sensitive strains of Streptococcus pyogenes - Clostridium tetani - C. perfringens - Corynebacterium diphtheriae - Bacillus anthracis Of the gram negative bacteria, Neisseria meningitidis and N. gonorrhoeae are sensitive to some extent. Haemophilus influenzae is moderately resistant, and all other gram negativ http://www.virtualmedicalcentre.com/drugs/cilopen-vk/1818 Phenoxymethylpenicillin is a penicillin antibiotic that has bactericidal activity against penicillin sensitive organisms. It is not active against penicillinase producing organisms. Bacteria that are susceptible to Phenoxymethylpenicillin potassium include: - Streptococci, including sensitive strains of Streptococcus pyogenes - Clostridium tetani - C. perfringens - Corynebacterium diphtheriae - Bacillus anthracis Of the gram negative bacteria, Neisseria meningitidis and N. gonorrhoeae are sensitive to some extent. Haemophilus influenzae is moderately resistant, and all other gram negativ http://www.virtualmedicalcentre.com/drugs/flucil/1824 Flucloxacillin is a penicillin antibiotic with a narrow spectrum of activity. It is bacteriostatic by inhibition of bacterial cell wall peptidoglycan synthesis. Aspen Flucil is active against the following gram positive bacteria: - Staphylococcus aureus (including beta-lactamase producing strains) - Streptococcus pyogenes - S. pneumoniae Flucloxacillin is less active than benzylpenicillin against organisms that are susceptible to benzylpenicillin. It has no activity against gram negative bacilli, MRSA or Streptococcus faecalis. http://www.virtualmedicalcentre.com/drugs/flucloxacillin-sodium-for-injection-dbl/1825 Flucloxacillin is a narrow spectrum antibiotic with considerable activity against the following Gram-positive organisms: beta-lactamase producing Staphylococcus aureus penicillin sensitive Staphylococcus aureus beta-haemolytic Streptococci such as Streptococcus pyogenes Streptococcus pneumoniae Flucloxacillun does not have activity against gram-negative bacilli, methicillin resistant Staphylococcus aureus or Streptococcus faecalis. http://www.virtualmedicalcentre.com/drugs/genrx-amoxycillin/1826 Amoxicillin is a broad spectrum antibiotic with similar bactericidal activity to ampicillin. It acts by inhibiting cell wall mucopeptide biosynthesis. It is active against both Gram positive and negative pathogens, including P.mirabilis, H.influenzae, alpha beta haemolytic Streptococci, S.pneumoniae, S.faecalis, non-penicilliase producing Staphylococci, N.gonorrhoea, N.meningitidis. However, some organisms are only susceptible to amoxicillin at concentrations achieved in the urine, and gonococci strains relatively resistant to benzylpenicillin are likely to be resistant to amoxicillin. A http://www.virtualmedicalcentre.com/drugs/healthsense-amoxycillin/1827 Amoxicillin is a broad spectrum antibiotic with similar bactericidal activity to ampicillin. It acts by inhibiting cell wall mucopeptide biosynthesis. It is active against both Gram positive and negative pathogens, including P.mirabilis, H.influenzae, alpha beta haemolytic Streptococci, S.pneumoniae, S.faecalis, non-penicilliase producing Staphylococci, N.gonorrhoea, N.meningitidis. However, some organisms are only susceptible to amoxicillin at concentrations achieved in the urine, and gonococci strains relatively resistant to benzylpenicillin are likely to be resistant to amoxicillin. A http://www.virtualmedicalcentre.com/drugs/lpv/1828 Phenoxymethylpenicillin is a penicillin antibiotic that has bactericidal activity against penicillin sensitive organisms. It is not active against penicillinase producing organisms. Bacteria that are susceptible to Phenoxymethylpenicillin potassium include: - Streptococci, including sensitive strains of Streptococcus pyogenes - Clostridium tetani - C. perfringens - Corynebacterium diphtheriae - Bacillus anthracis Of the gram negative bacteria, Neisseria meningitidis and N. gonorrhoeae are sensitive to some extent. Haemophilus influenzae is moderately resistant, and all other gram negativ http://www.virtualmedicalcentre.com/drugs/moxacin-injection/1830 Amoxil belongs to the penicillin group of antibiotics, and has a similar gram positive and gram negative spectrum to ampicillin. Its action is bactericidal against sensitive strains, and is thought to act by inhibiting the synthesis of cell wall mucopeptide. http://www.virtualmedicalcentre.com/drugs/penhexal-vk/1832 Phenoxymethylpenicillin is a penicillin antibiotic that has bactericidal activity against penicillin sensitive organisms. It is not active against penicillinase producing organisms. Bacteria that are susceptible to Penhexal VK include:Streptococci, including sensitive strains of Streptococcus pyogenesClostridium tetaniC. perfringensCorynebacterium diphtheriaeBacillus anthracis Of the gram negative bacteria, Neisseria meningitidis and N. gonorrhoeae are sensitive to some extent. Haemophilus influenzae is moderately resistant, and all other gram negative bacilli are resistant. Treponema pallidum http://www.virtualmedicalcentre.com/drugs/tazocin/1836 Piperacillin is a broad spectrum, semisynthetic penicillin with bactericidal activity (cell wall synthesis inhibitor) against many Gram positive, Gram negative and anaerobic bacteria. Tazobactam is a potent beta lactamase inhibitor, and extends the antibacterial spectrum of piperacillin to include many beta lactamase producing bacteria usually resistant to it. Antimicrobial activity against: Gram negative bacteria: E.coli; Citrobacter sp.; Klebsiella sp.; Enterobacter sp.; Proteus mirabilis and vulgaris; Serrattia sp.; Pseudomonas sp. (including P.aeruginosa); N.gonorrhoea and meningitidi http://www.virtualmedicalcentre.com/drugs/amoxycillin-terry-white-chemists/1837 Amoxicillin is a broad spectrum antibiotic with similar bactericidal activity to ampicillin. It acts by inhibiting cell wall mucopeptide biosynthesis. It is active against both Gram positive and negative pathogens, including P.mirabilis, H.influenzae, alpha beta haemolytic Streptococci, S.pneumoniae, S.faecalis, non-penicilliase producing Staphylococci, N.gonorrhoea, N.meningitidis. However, some organisms are only susceptible to amoxicillin at concentrations achieved in the urine, and gonococci strains relatively resistant to benzylpenicillin are likely to be resistant to amoxicillin. A http://www.virtualmedicalcentre.com/drugs/timentin/1838 Ticarcillin has a bactericidal effect during active multiplication. The addition of clavulanic acid offers beta lactamase inhibition to extend the antibacterial spectrum Susceptible organisms include: Gram Negative bacteria: P.aeruginosa, E.coli, P.mirabilis, P.vulgaris, Providencia rettgeri, Morganella morganii, Enterobacter sp, H.influenzae, N.meningitidis, Salmonella sp, K.pneumoniae, and some strains of Mima, Herellea, Citrobacter and Serratia. Gram Positive bacteria: S.aureus, S.epidermidis, S.pneumoniae, S.faecalis, S.pyogenes Anaerobic bacteria: Bacteroides sp, Clostridium sp, Eubacteri http://www.virtualmedicalcentre.com/drugs/cefalexin-bc/1843 Cephalexin is a semisynthetic first generation cephalosporin antibiotic. It is bactericidal due to inhibition of bacterial cell wall synthesis. It is active against the following bacteria: - beta-haemolytic Streptococci - Staphylococci – including coagulase positive, coagulase negative and penicillinase-producing strains - Streptococcus pneumoniae - Escherichia coli - Proteus mirabilis - Klebsiella spp. Most strains of Enterococcus faecalis are resistant, as are some strains of Staphylococci. Cephalexin does not have activity against: - most strains of Enterobacter - Morganella morga http://www.virtualmedicalcentre.com/drugs/cefazolin-bc/1844 Cephazolin is a semisynthetic cephalosporin antibiotic. It is bactericidal by inhibition of bacterial cell wall synthesis. Cephazolin is active against the following bacteria: - Staphylococcus aureus (including penicillin resistant) - Streptococci, including group A beta-haemolytic Streptococci and Streptococcus pneumoniae - Escherichia coli - Proteus mirabilis - Klebsiella spp. - Enterobacter aerogenes - Haemophilus influenzae Notable exceptions to the spectrum of Cephazolin include: - most strains of Enterobacter cloacae - indole positive Proteus spp. (P. vulgaris, P. rettgeri) - http://www.virtualmedicalcentre.com/drugs/cefkor-cd/1846 Microbiology. Cefaclor is a cephalosporin antibiotic with bactericidal activity. It is stable in the presence of bacterial beta-lactamases, and therefore may be active against beta-lactamase producing bacteria resistant to penicillins and some cephalosporins. The following bacteria may be susceptible: Gram positive organisms: Staph.aureus (not including methicillin resistant Staphylococci), Staph.saprophyticus, Strep.pneumoniae, Strep.pyogenes. Gram negative organisms: H.influenzae, M.catarrhalis, E.coli, K.pneumoniae, P.mirabilis The following bacteria are resistant to cefaclor: Pseu http://www.virtualmedicalcentre.com/drugs/cefotaxime-sodium-for-injection-dbl/1847 Microbiology. Cefotaxime is a semisynthetic broad spectrum cephalosporin with bactericidal action. Cefotaxime is usually active against the following microorganisms: Gram positive: Staphylococci (including penicillinase producing 85% of methicillin susceptible S.aureus), S.pyogenes, S.pneumoniae Gram negative: Klebsiella sp, Enterobacter sp, Serratia sp, H.influenzae, Neisseria sp, Proteus sp, E.coli (including many gentamicin and cephalothin resistant strains). The following bacteria commonly show resistance to cefotaxime. Gram positive: methicillin resistant Staphylococci, C.pe http://www.virtualmedicalcentre.com/drugs/cefotaxime-bc/1848 Microbiology. Cefotaxime is a semisynthetic broad spectrum cephalosporin with bactericidal action. Cefotaxime is usually active against the following microorganisms: Gram positive: Staphylococci (including penicillinase producing 85% of methicillin susceptible S.aureus), S.pyogenes, S.pneumoniae Gram negative: Klebsiella sp, Enterobacter sp, Serratia sp, H.influenzae, Neisseria sp, Proteus sp, E.coli (including many gentamicin and cephalothin resistant strains). The following bacteria commonly show resistance to cefotaxime. Gram positive: methicillin resistant Staphylococci, C.pe http://www.virtualmedicalcentre.com/drugs/cefoxitin-sodium-for-injection-dbl/1849 Cefoxitin is a second generation cephalosporin antibiotic, also known as a cephamycin antibiotic. It is bactericidal by inhibition of bacterial cell wall peptidoglycan synthesis. Cefoxitin sodium for injection is active against the following bacteria: - Staphylococci (including penicillinase-producing strains) - group A and B beta-haemolytic Streptococci - Streptococcus pneumoniae - Neisseria gonorrhoea (including penicillinase-producing strains) - Neisseria meningitidis - Escherichia coli - Klebsiella pneumoniae - Proteus mirabilis - indole positive Proteus spp. - Morganella morgani http://www.virtualmedicalcentre.com/drugs/ceftriaxone-bc/1851 Microbiology: Ceftriaxone is a semisynthetic broad spectrum cephalosporin antibiotic with bactericidal activity against Gram negative and Gram positive bacteria (including those with beta-lactamases) Ceftriaxone is usually active against the following pathogens: Gram negative anaerobes: E.aerogenes, E.cloacae, E.coli, H.influenzae (including ampicillin resistant strains), Klebsiella sp., N.gonorrhoea (including penicillinase non penicillinase producing strains), N.meningitidis, P.mirabilis, P.vulgaris, M.morganii, S.marcescens, P.aeruginosa (other Pseduomonas sp are usually resistan http://www.virtualmedicalcentre.com/drugs/cephazolin-sodium-for-injection-dbl/1853 Cephazolin is a semisynthetic cephalosporin antibiotic. It is bactericidal by inhibition of bacterial cell wall synthesis. Cephazolin is active against the following bacteria: - Staphylococcus aureus (including penicillin resistant) - Streptococci, including group A beta-haemolytic Streptococci and Streptococcus pneumoniae - Escherichia coli - Proteus mirabilis - Klebsiella spp. - Enterobacter aerogenes - Haemophilus influenzae Notable exceptions to the spectrum of Cephazolin include: - most strains of Enterobacter cloacae - indole positive Proteus spp. (P. vulgaris, P. rettgeri) - http://www.virtualmedicalcentre.com/drugs/chem-mart-cephalexin/1856 Cephalexin is a semisynthetic first generation cephalosporin antibiotic. It is bactericidal due to inhibition of bacterial cell wall synthesis. It is active against the following bacteria: - beta-haemolytic Streptococci - Staphylococci – including coagulase positive, coagulase negative and penicillinase-producing strains - Streptococcus pneumoniae - Escherichia coli - Proteus mirabilis - Klebsiella spp. Most strains of Enterococcus faecalis are resistant, as are some strains of Staphylococci. Cephalexin does not have activity against: - most strains of Enterobacter - Morganella morga http://www.virtualmedicalcentre.com/drugs/cilex/1857 Cefalexin-BC is available in capsules (Cephalexin 250mg and 500mg) and powder for suspension (Cephalexin 125mg/5ml and 250mg/5ml). Both should be stored below 25¢ªC, except when the powder has been reconstituted, in which case it should be stored at 2-8¢ªC for no longer than 14 days. Contraindications: - known hypersensitivity to the cephalosporin family of antibiotics - previous major allergic reaction to penicillin antibiotics - bacterial infections of the brain and spinal cord Specific considerations: Hypersensitivity - patients should be closely observed following the first administ http://www.virtualmedicalcentre.com/drugs/fortum/1860 Microbiology. Ceftazidime is bactericidal, and stable in the presence of most beta lactamases, making it active against many ampicillin and cephalothin resistant strains (but not methicillin resistant strains). It has activity against the following organisms: Gram negative: Pseudomonas sp (including P.aeruginosa), K.pneumoniae, P.mirabilis, P.vulgaris, M.morganii, P.rettgeri, Providencia sp., E.coli, Enterobacter sp., Citrobacter sp., Serratia sp., Acinetobacter sp., N.gonorrhoea, N.meningitidis, H.influenzae (including ampicillin resistant strains). Gram positive: S.aureus (methic http://www.virtualmedicalcentre.com/drugs/genrx-cephalexin/1863 Cephalexin is a semisynthetic first generation cephalosporin antibiotic. It is bactericidal due to inhibition of bacterial cell wall synthesis. It is active against the following bacteria: - beta-haemolytic Streptococci - Staphylococci – including coagulase positive, coagulase negative and penicillinase-producing strains - Streptococcus pneumoniae - Escherichia coli - Proteus mirabilis - Klebsiella spp. Most strains of Enterococcus faecalis are resistant, as are some strains of Staphylococci. Cephalexin does not have activity against: - most strains of Enterobacter - Morganella morga http://www.virtualmedicalcentre.com/drugs/healthsense-cephalexin/1866 Cephalexin is a semisynthetic first generation cephalosporin antibiotic. It is bactericidal due to inhibition of bacterial cell wall synthesis. It is active against the following bacteria: - beta-haemolytic Streptococci - Staphylococci – including coagulase positive, coagulase negative and penicillinase-producing strains - Streptococcus pneumoniae - Escherichia coli - Proteus mirabilis - Klebsiella spp. Most strains of Enterococcus faecalis are resistant, as are some strains of Staphylococci. Cephalexin does not have activity against: - most strains of Enterobacter - Morganella morga http://www.virtualmedicalcentre.com/drugs/ibilex/1867 Cephalexin is a semisynthetic first generation cephalosporin antibiotic. It is bactericidal due to inhibition of bacterial cell wall synthesis. It is active against the following bacteria: - beta-haemolytic Streptococci - Staphylococci – including coagulase positive, coagulase negative and penicillinase-producing strains - Streptococcus pneumoniae - Escherichia coli - Proteus mirabilis - Klebsiella spp. Most strains of Enterococcus faecalis are resistant, as are some strains of Staphylococci. Cephalexin does not have activity against: - most strains of Enterobacter - Morganella morga http://www.virtualmedicalcentre.com/drugs/keflex/1868 Cephalexin is a semisynthetic first generation cephalosporin antibiotic. It is bactericidal due to inhibition of bacterial cell wall synthesis. It is active against the following bacteria: - beta-haemolytic Streptococci - Staphylococci – including coagulase positive, coagulase negative and penicillinase-producing strains - Streptococcus pneumoniae - Escherichia coli - Proteus mirabilis - Klebsiella spp. Most strains of Enterococcus faecalis are resistant, as are some strains of Staphylococci. Cephalexin does not have activity against: - most strains of Enterobacter - Morganella morga http://www.virtualmedicalcentre.com/drugs/kefzol/1872 Cephazolin is a semisynthetic cephalosporin antibiotic. It is bactericidal by inhibition of bacterial cell wall synthesis. Cephazolin is active against the following bacteria: - Staphylococcus aureus (including penicillin resistant) - Streptococci, including group A beta-haemolytic Streptococci and Streptococcus pneumoniae - Escherichia coli - Proteus mirabilis - Klebsiella spp. - Enterobacter aerogenes - Haemophilus influenzae Notable exceptions to the spectrum of Cephazolin include: - most strains of Enterobacter cloacae - indole positive Proteus spp. (P. vulgaris, P. rettgeri) - http://www.virtualmedicalcentre.com/drugs/mefoxin/1875 Cefoxitin is a second generation cephalosporin antibiotic, also known as a cephamycin antibiotic. It is bactericidal by inhibition of bacterial cell wall peptidoglycan synthesis. Cefoxitin sodium for injection is active against the following bacteria: - Staphylococci (including penicillinase-producing strains) - group A and B beta-haemolytic Streptococci - Streptococcus pneumoniae - Neisseria gonorrhoea (including penicillinase-producing strains) - Neisseria meningitidis - Escherichia coli - Klebsiella pneumoniae - Proteus mirabilis - indole positive Proteus spp. - Morganella morgani http://www.virtualmedicalcentre.com/drugs/rocephin/1876 Ceftriaxone is a semisynthetic broad spectrum antibiotic of the cephalosporin family. Its bactericidal effect is due to inhibition of bacterial cell wall synthesis. Ceftriaxone is a third generation cephalosporin, therefore has a high degree of stability against beta-lactamase (type I, II and III) producing organisms. It has activity against the following microorganisms: - Enterobacter aerogenes - Enterobacter cloacae - Escherichia coli - Haemophilus influenzae - Klebsiella spp. (including K. pneumoniae) - Neisseria gonorrhoeae - N. meningitidis - Proteus mirabilis - P. vulgaris - Mo http://www.virtualmedicalcentre.com/drugs/sporahexal/1877 Cephalexin is a semisynthetic first generation cephalosporin antibiotic. It is bactericidal due to inhibition of bacterial cell wall synthesis. It is active against the following bacteria: - beta-haemolytic Streptococci - Staphylococci – including coagulase positive, coagulase negative and penicillinase-producing strains - Streptococcus pneumoniae - Escherichia coli - Proteus mirabilis - Klebsiella spp. Most strains of Enterococcus faecalis are resistant, as are some strains of Staphylococci. Cephalexin does not have activity against: - most strains of Enterobacter - Morganella morga http://www.virtualmedicalcentre.com/drugs/cephalexin-terry-white-chemists/1880 Cephalexin is a semisynthetic first generation cephalosporin antibiotic. It is bactericidal due to inhibition of bacterial cell wall synthesis. It is active against the following bacteria: - beta-haemolytic Streptococci - Staphylococci – including coagulase positive, coagulase negative and penicillinase-producing strains - Streptococcus pneumoniae - Escherichia coli - Proteus mirabilis - Klebsiella spp. Most strains of Enterococcus faecalis are resistant, as are some strains of Staphylococci. Cephalexin does not have activity against: - most strains of Enterobacter - Morganella morga http://www.virtualmedicalcentre.com/drugs/achromycin/1882 Tetracylcine is bacteriostatic. It is thought to exert its effect through protein synthesis inhibition.A variety of gram positive and negative bacteria are susceptible to tetracyclines. The drugs in the tetracycline class have similar antimicrobial spectra, and resistance to one tetracycline is likely to extend to other drugs in the class. Tetracycline is rapidly though incompletely absorbed from the gut. Food, milk, antacids and cations (divalent amp; trivalent) impair absorption. Most of the absorbed dose is eliminated unchanged in urine and bile, any additional absorbed drug is metabolised http://www.virtualmedicalcentre.com/drugs/chem-mart-doxycycline-capsules/1884 Doxycycline is from the tetracycline family and is a broad spectrum antibiotic. It is bacteriostatic by inhibition of protein synthesis and has activity against a wide variety of gram positive and gram negative organisms including: - Mycoplasma pneumoniae - Rickettsiae - Chlamydia psittaci - Calymmatobacterium granulomatis - Borreliae - Chlamydia trachomatis - Vibrio cholerae - Brucella spp. - Yersinia pestis - Fracisella tularensis - Bartonella bacilliformis - Bacteroides spp. - Treponema pallidum - Neisseria gonorrhoeae - Propionibacterium acnes Doxycycline is also active ag http://www.virtualmedicalcentre.com/drugs/chem-mart-doxycycline-tablets/1885 Doxycycline is from the tetracycline family and is a broad spectrum antibiotic. It is bacteriostatic by inhibition of protein synthesis and has activity against a wide variety of gram positive and gram negative organisms including: - Mycoplasma pneumoniae - Rickettsiae - Chlamydia psittaci - Calymmatobacterium granulomatis - Borreliae - Chlamydia trachomatis - Vibrio cholerae - Brucella spp. - Yersinia pestis - Fracisella tularensis - Bartonella bacilliformis - Bacteroides spp. - Treponema pallidum - Neisseria gonorrhoeae - Propionibacterium acnes Doxycycline is also active ag http://www.virtualmedicalcentre.com/drugs/doryx/1886 Microbiology. Doxycycline has a primarily bacteriostatic action against a variety of organisms, including: M.pneumoniae, Rickettsiae, C.psittaci, C.trachomatis, Borreliae, Calymmatobacterium, (Donovania) granulomatis Gram negative organisms: Vibrio sp, Brucella sp, Y.pestis, Francisella tularenis, Bartonella bacilliformis, Bacteroides sp, T.pallidum, T.perenue, N.gonorrhoea. Protozoa: P.falciparum, P.vivax (Doxycline should be used routinely with other antimalarial agents (e.g. chloroquine) Doxycycline is not the drug of choice against staphylococcal sp, streptococaal sp, H.influenzae http://www.virtualmedicalcentre.com/drugs/doxsig/1887 Microbiology. Doxycycline has a primarily bacteriostatic action against a variety of organisms, including: M.pneumoniae, Rickettsiae, C.psittaci, C.trachomatis, Borreliae, Calymmatobacterium, (Donovania) granulomatis Gram negative organisms: Vibrio sp, Brucella sp, Y.pestis, Francisella tularenis, Bartonella bacilliformis, Bacteroides sp, T.pallidum, T.perenue, N.gonorrhoea. Protozoa: P.falciparum, P.vivax (Doxycline should be used routinely with other antimalarial agents (e.g. chloroquine) Doxycycline is not the drug of choice against staphylococcal sp, streptococaal sp, H.influenzae http://www.virtualmedicalcentre.com/drugs/doxy-tablets/1888 Microbiology. Doxycycline has a primarily bacteriostatic action against a variety of organisms, including: M.pneumoniae, Rickettsiae, C.psittaci, C.trachomatis, Borreliae, Calymmatobacterium, (Donovania) granulomatis Gram negative organisms: Vibrio sp, Brucella sp, Y.pestis, Francisella tularenis, Bartonella bacilliformis, Bacteroides sp, T.pallidum, T.perenue, N.gonorrhoea. Protozoa: P.falciparum, P.vivax (Doxycline should be used routinely with other antimalarial agents (e.g. chloroquine) Doxycycline is not the drug of choice against staphylococcal sp, streptococaal sp, H.influenzae http://www.virtualmedicalcentre.com/drugs/doxycycline-bc/1890 Doxycycline has a primarily bacteriostatic action against a variety of organisms, including: M.pneumoniae, Rickettsiae, C.psittaci, C.trachomatis, Borreliae, Calymmatobacterium, (Donovania) granulomatis Gram negative organisms: Vibrio sp, Brucella sp, Y.pestis, Francisella tularenis, Bartonella bacilliformis, Bacteroides sp, T.pallidum, T.perenue, N.gonorrhoea. Protozoa: P.falciparum, P.vivax (Doxycline should be used routinely with other antimalarial agents (e.g. chloroquine) Doxycycline is not the drug of choice against staphylococcal sp, streptococaal sp, H.influenzae Pharmacokinet http://www.virtualmedicalcentre.com/drugs/doxyhexal-tablets/1891 Doxycycline inhibits bacteria synthesising protein by reversibly binding to a sub-unit of the ribosome. http://www.virtualmedicalcentre.com/drugs/doxylin/1892 Doxycycline inhibits bacteria synthesising protein by reversibly binding to a sub-unit of the ribosome. http://www.virtualmedicalcentre.com/drugs/genrx-doxycycline-capsules/1893 Doxycycline is from the tetracycline family and is a broad spectrum antibiotic. It is bacteriostatic by inhibition of protein synthesis and has activity against a wide variety of gram positive and gram negative organisms including: - Mycoplasma pneumoniae - Rickettsiae - Chlamydia psittaci - Calymmatobacterium granulomatis - Borreliae - Chlamydia trachomatis - Vibrio cholerae - Brucella spp. - Yersinia pestis - Fracisella tularensis - Bartonella bacilliformis - Bacteroides spp. - Treponema pallidum - Neisseria gonorrhoeae - Propionibacterium acnes Doxycycline is also active ag http://www.virtualmedicalcentre.com/drugs/healthsense-doxycycline-capsules/1895 Doxycycline is from the tetracycline family and is a broad spectrum antibiotic. It is bacteriostatic by inhibition of protein synthesis and has activity against a wide variety of gram positive and gram negative organisms including: - Mycoplasma pneumoniae - Rickettsiae - Chlamydia psittaci - Calymmatobacterium granulomatis - Borreliae - Chlamydia trachomatis - Vibrio cholerae - Brucella spp. - Yersinia pestis - Fracisella tularensis - Bartonella bacilliformis - Bacteroides spp. - Treponema pallidum - Neisseria gonorrhoeae - Propionibacterium acnes Doxycycline is also active ag http://www.virtualmedicalcentre.com/drugs/healthsense-doxycycline-tablets/1896 Doxycycline is from the tetracycline family and is a broad spectrum antibiotic. It is bacteriostatic by inhibition of protein synthesis and has activity against a wide variety of gram positive and gram negative organisms including: - Mycoplasma pneumoniae - Rickettsiae - Chlamydia psittaci - Calymmatobacterium granulomatis - Borreliae - Chlamydia trachomatis - Vibrio cholerae - Brucella spp. - Yersinia pestis - Fracisella tularensis - Bartonella bacilliformis - Bacteroides spp. - Treponema pallidum - Neisseria gonorrhoeae - Propionibacterium acnes Doxycycline is also active ag http://www.virtualmedicalcentre.com/drugs/minomycin/1898 Microbiology. Minocycline is a tetracycline antibiotic, with bacteriostatic activity against a variety of Gram negative and Gram positive bacteria. Culture and sensitivity tests are recommended as many strains of susceptible Gram negative and Gram positive bacteria are resistant. Pharmacokinetics. Peak plasma levels are achieved within 2-4 hours after oral administration. These levels are slightly decreased and delayed when administered with food. Plasma half life approaches 13 hours. Minocycline distributes widely to most body tissues and is highly plasma protein bound. An unknow http://www.virtualmedicalcentre.com/drugs/doxycycline-capsules-terry-white-chemists/1899 Doxycycline is from the tetracycline family and is a broad spectrum antibiotic. It is bacteriostatic by inhibition of protein synthesis and has activity against a wide variety of gram positive and gram negative organisms including: - Mycoplasma pneumoniae - Rickettsiae - Chlamydia psittaci - Calymmatobacterium granulomatis - Borreliae - Chlamydia trachomatis - Vibrio cholerae - Brucella spp. - Yersinia pestis - Fracisella tularensis - Bartonella bacilliformis - Bacteroides spp. - Treponema pallidum - Neisseria gonorrhoeae - Propionibacterium acnes Doxycycline is also active ag http://www.virtualmedicalcentre.com/drugs/doxycycline-tablets-terry-white-chemists/1900 Doxycycline is from the tetracycline family and is a broad spectrum antibiotic. It is bacteriostatic by inhibition of protein synthesis and has activity against a wide variety of gram positive and gram negative organisms including: - Mycoplasma pneumoniae - Rickettsiae - Chlamydia psittaci - Calymmatobacterium granulomatis - Borreliae - Chlamydia trachomatis - Vibrio cholerae - Brucella spp. - Yersinia pestis - Fracisella tularensis - Bartonella bacilliformis - Bacteroides spp. - Treponema pallidum - Neisseria gonorrhoeae - Propionibacterium acnes Doxycycline is also active ag http://www.virtualmedicalcentre.com/drugs/tetrex/1901 Tetrex has a bacteriostatic action on sensitive micro-organisms. It inhibits protein synthesis by binding reversibly to the 30S unit on the ribosome. http://www.virtualmedicalcentre.com/drugs/vibramycin-vibra-tabs-50/1902 Doxycycline is from the tetracycline family and is a broad spectrum antibiotic. It is bacteriostatic by inhibition of protein synthesis and has activity against a wide variety of gram positive and gram negative organisms including: - Mycoplasma pneumoniae - Rickettsiae - Chlamydia psittaci - Calymmatobacterium granulomatis - Borreliae - Chlamydia trachomatis - Vibrio cholerae - Brucella spp. - Yersinia pestis - Fracisella tularensis - Bartonella bacilliformis - Bacteroides spp. - Treponema pallidum - Neisseria gonorrhoeae - Propionibacterium acnes Doxycycline is also active ag http://www.virtualmedicalcentre.com/drugs/biaxsig/1903 Roxithromycin is a semisynthetic antibiotic, it belongs to the macrolide group. Roxithromycin is bacteriostatic at low concentrations and bactericidal at high concentrations, it also has a prolonged post-antibiotic effect. Therapeutic doses of roxithromycin have clinical activity against the following microorganisms: S.pneumoniae, S.pyogenes, M.pneumoniae, H.influenzae, M.catarrhalis, U.urealyticum, non-methicillin resistant S.aureus and Chlamydia sp. Roxithromycin is not active against: multi-resistant S.aureus, Enterobacteriacae, Pseudomonas sp. and Acinebacter sp. Roxithromycin h http://www.virtualmedicalcentre.com/drugs/dbl-erythromycin/1904 Erythromycin is a macrolide antibiotic derived from the bacteria Streptomyces erythraeus. It is bacteriostatic at low concentrations and bactericidal at high concentrations. The mechanism of action of Erythromycin is well understood. It binds to the 50S ribosomal subunit of susceptible bacteria and inhibits protein synthesis whilst having no action on nucleic acid synthesis. It is usually active against the following bacteria: - Streptococcus pyogenes - alpha-haemolytic Streptococci - S. pneumoniae - Staphylococcus aureus - Corynebacterium diphtheriae - Corynebacterium minutissimum - Pr http://www.virtualmedicalcentre.com/drugs/ees/1905 Erythromycin is a macrolide antibiotic derived from the bacteria Streptomyces erythraeus. It is bacteriostatic at low concentrations and bactericidal at high concentrations. The mechanism of action of Erythromycin is well understood. It binds to the 50S ribosomal subunit of susceptible bacteria and inhibits protein synthesis whilst having no action on nucleic acid synthesis. It is usually active against the following bacteria: - Streptococcus pyogenes - alpha-haemolytic Streptococci - S. pneumoniae - Staphylococcus aureus - Corynebacterium diphtheriae - Corynebacterium minutissimum - Pr http://www.virtualmedicalcentre.com/drugs/e-mycin/1906 Erythromycin is a macrolide antibiotic derived from the bacteria Streptomyces erythraeus. It is bacteriostatic at low concentrations and bactericidal at high concentrations. The mechanism of action of Erythromycin is well understood. It binds to the 50S ribosomal subunit of susceptible bacteria and inhibits protein synthesis whilst having no action on nucleic acid synthesis. It is usually active against the following bacteria: - Streptococcus pyogenes - alpha-haemolytic Streptococci - S. pneumoniae - Staphylococcus aureus - Corynebacterium diphtheriae - Corynebacterium minutissimum - Pr http://www.virtualmedicalcentre.com/drugs/eryc/1907 Erythromycin is a macrolide antibiotic derived from the bacteria Streptomyces erythraeus. It is bacteriostatic at low concentrations and bactericidal at high concentrations. The mechanism of action of Erythromycin is well understood. It binds to the 50S ribosomal subunit of susceptible bacteria and inhibits protein synthesis whilst having no action on nucleic acid synthesis. It is usually active against the following bacteria: - Streptococcus pyogenes - alpha-haemolytic Streptococci - S. pneumoniae - Staphylococcus aureus - Corynebacterium diphtheriae - Corynebacterium minutissimum - Pr http://www.virtualmedicalcentre.com/drugs/erythrocin-iv/1909 Erythromycin is produced by a strain of Streptomyces erythreus, belongs to the macrolide antibiotic group, and inhibits bacterial protein synthesis. It is bacteriostatic at low concentrations and bactericidal at high concentrations. It is especially active against Gram positive cocci and bacilli. Erythromycin is usually active against the following microorganisms although not all strains are sensitive: S.pyogenes, alpha haemolytic Streptococci (viridans group), S.pneumoniae, S. aureus, M.pneumoniae, H.influenzae, L.pneumophilia, T.pallidum, N.gonorrhoeae, C.diphtheriae, C.minitissiumum, L.m http://www.virtualmedicalcentre.com/drugs/erythromycin-lactobionate-for-intravenous-infusion-dbl/1911 Erythromycin is produced by a strain of Streptomyces erythreus, belongs to the macrolide antibiotic group, and inhibits bacterial protein synthesis. It is bacteriostatic at low concentrations and bactericidal at high concentrations. It is especially active against Gram positive cocci and bacilli. Erythromycin is usually active against the following microorganisms although not all strains are sensitive: S.pyogenes, alpha haemolytic Streptococci (viridans group), S.pneumoniae, S. aureus, M.pneumoniae, H.influenzae, L.pneumophilia, T.pallidum, N.gonorrhoeae, C.diphtheriae, C.minitissiumum, L.m http://www.virtualmedicalcentre.com/drugs/klacid/1912 Microbiology. Clarithromycin is a semi-synthetic macrolide antibiotic. It is active against the following bacteria: C.pneumoniae, H.influenzae, H.parainfluenzae, H.pylori, L.pneumophilia, M.catarrhalis, Mycobacterium avium, M.chelonae, M.intracellulare, Mycoplasma.pneumoniae, S.aureus, S.pneumoniae, S.pyogenes, S.viridans. Non-sensitive bacteria include Enterobacteriaceae, Pseudomonas sp, M.tuberculosis and most strains of methicillin or oxacillin resistant Staphylococci. Clarithromycin is 2-10 times more active than erythromycin. Pharmacokinetics. Clarithromycins’s absolute bio http://www.virtualmedicalcentre.com/drugs/rulide/1913 Roxithromycin is a semisynthetic antibiotic, it belongs to the macrolide group. Roxithromycin is bacteriostatic at low concentrations and bactericidal at high concentrations, it also has a prolonged post-antibiotic effect. Therapeutic doses of roxithromycin have clinical activity against the following microorganisms: S.pneumoniae, S.pyogenes, M.pneumoniae, H.influenzae, M.catarrhalis, U.urealyticum, non-methicillin resistant S.aureus and Chlamydia sp. Roxithromycin is not active against: multi-resistant S.aureus, Enterobacteriacae, Pseudomonas sp. and Acinebacter sp. Roxithromycin h http://www.virtualmedicalcentre.com/drugs/zithromax/1914 Zithromax has a bacteriostatic action on sensitive micro-organisms. It inhibits protein synthesis by binding reversibly to the 50S unit on the ribosome. It has a broad spectrum action against gram-positive bacteria and some gram-negative bacteria. It is also effective against:Mycoplasma Treponema pallidum BordetellaChlamydiaLegionella. http://www.virtualmedicalcentre.com/drugs/avelox/1915 Moxifloxacin in a synthetic, broad spectrum quinolone antibiotic with bactericidal action. The bactericidal activity results from an inhibition of bacterial DNA repair, transcription, repair and recombination, and is concentration dependent. The action of quinolones is different to that of macrolides, betalactams, aminoglycosides and tetracyclines, as such moxifloxacin may exert activity against pathogens resistant to other classes of antibiotics. Cross-resistance has been observed between moxifloxacin and other fluoroquinolones against Gram negative bacteria, however against Gram positive http://www.virtualmedicalcentre.com/drugs/c-flox/1916 C-Flox has a broad spectrum of antibiotic activity. It is bactericidal by a mechanism of interfering with DNA gyrase of a number of bacteria, more Gram-negative than Gram-positive. Gram-negative organisms that are usually susceptible include: - Escherichia coli - Klebsiella spp. - Enterobacter spp. - Citrobacter spp. - Salmonella spp. - Shigella spp. - Proteus mirabilis, vulgaris - Providencia stuartii, rettgeri - Morganella morganii - Serratia spp. - Campylobacter spp. - Haemophilus influenzae - Neisseria gonorrhoeae - Moraxella catarrhalis Susceptible Gram-positive organisms http://www.virtualmedicalcentre.com/drugs/chem-mart-norfloxacin/1917 Microbiology. Norfloxacin is a broad spectrum, synthetic fluoroquinolone antibiotic. It is bacteriostatic and bactericidal. Norfloxacin shows in vitro activity against the following organisms: Urinary tract infection pathogens: Aerobic bacteria. Gram positive bacteria including S.faecalis, S.aureus, S.epidermidis, S.saprophyticus. Gram negative bacteria including E.coli, E.cloacae, K.oxytoca, K.pneumoniae, P.mirabilis, P.aeruginosa, C.diversus, C.freundii. Gastrointestinal tract infection pathogens: Shigella, E.coli, S.typhi. Others: N.gonorrhoea. The development of resistance duri http://www.virtualmedicalcentre.com/drugs/ciproxin/1918 Ciproxin has a broad spectrum of antibiotic activity. It is bactericidal by a mechanism of interfering with DNA gyrase of a number of bacteria, more Gram-negative than Gram-positive. Gram-negative organisms that are usually susceptible include: - Escherichia coli - Klebsiella spp. - Enterobacter spp. - Citrobacter spp. - Salmonella spp. - Shigella spp. - Proteus mirabilis, vulgaris - Providencia stuartii, rettgeri - Morganella morganii - Serratia spp. - Campylobacter spp. - Haemophilus influenzae - Neisseria gonorrhoeae - Moraxella catarrhalis Susceptible Gram-positive organism http://www.virtualmedicalcentre.com/drugs/ciproxin-iv/1919 Ciproxin IV has a broad spectrum of antibiotic activity. It is bactericidal by a mechanism of interfering with DNA gyrase of a number of bacteria, more Gram negative than Gram positive. Gram negative organisms that are usually susceptible include: - Escherichia coli - Klebsiella spp. - Enterobacter spp. - Citrobacter spp. - Salmonellaspp. - Shigella spp. - Proteus mirabilis, vulgaris - Providencia stuartii, rettgeri - Morganella morganii - Serratia spp. - Campylobacter spp. - Haemophilus influenzae - Neisseria gonorrhoeae - Moraxella catarrhalis Susceptible Gram positive organi http://www.virtualmedicalcentre.com/drugs/genrx-norfloxacin/1920 Microbiology. Norfloxacin is a broad spectrum, synthetic fluoroquinolone antibiotic. It is bacteriostatic and bactericidal. Norfloxacin shows in vitro activity against the following organisms: Urinary tract infection pathogens: Aerobic bacteria. Gram positive bacteria including S.faecalis, S.aureus, S.epidermidis, S.saprophyticus. Gram negative bacteria including E.coli, E.cloacae, K.oxytoca, K.pneumoniae, P.mirabilis, P.aeruginosa, C.diversus, C.freundii. Gastrointestinal tract infection pathogens: Shigella, E.coli, S.typhi. Others: N.gonorrhoea. The development of resistance duri http://www.virtualmedicalcentre.com/drugs/healthsense-norfloxacin/1921 Microbiology. Norfloxacin is a broad spectrum, synthetic fluoroquinolone antibiotic. It is bacteriostatic and bactericidal. Norfloxacin shows in vitro activity against the following organisms: Urinary tract infection pathogens: Aerobic bacteria. Gram positive bacteria including S.faecalis, S.aureus, S.epidermidis, S.saprophyticus. Gram negative bacteria including E.coli, E.cloacae, K.oxytoca, K.pneumoniae, P.mirabilis, P.aeruginosa, C.diversus, C.freundii. Gastrointestinal tract infection pathogens: Shigella, E.coli, S.typhi. Others: N.gonorrhoea. The development of resistance duri http://www.virtualmedicalcentre.com/drugs/insensye/1922 Microbiology. Norfloxacin is a broad spectrum, synthetic fluoroquinolone antibiotic. It is bacteriostatic and bactericidal. Norfloxacin shows in vitro activity against the following organisms: Urinary tract infection pathogens: Aerobic bacteria. Gram positive bacteria including S.faecalis, S.aureus, S.epidermidis, S.saprophyticus. Gram negative bacteria including E.coli, E.cloacae, K.oxytoca, K.pneumoniae, P.mirabilis, P.aeruginosa, C.diversus, C.freundii. Gastrointestinal tract infection pathogens: Shigella, E.coli, S.typhi. Others: N.gonorrhoea. The development of resistance duri http://www.virtualmedicalcentre.com/drugs/norflohexal/1923 Microbiology. Norfloxacin is a broad spectrum, synthetic fluoroquinolone antibiotic. It is bacteriostatic and bactericidal. Norfloxacin shows in vitro activity against the following organisms: Urinary tract infection pathogens: Aerobic bacteria. Gram positive bacteria including S.faecalis, S.aureus, S.epidermidis, S.saprophyticus. Gram negative bacteria including E.coli, E.cloacae, K.oxytoca, K.pneumoniae, P.mirabilis, P.aeruginosa, C.diversus, C.freundii. Gastrointestinal tract infection pathogens: Shigella, E.coli, S.typhi. Others: N.gonorrhoea. The development of resistance duri http://www.virtualmedicalcentre.com/drugs/norfloxacin/1924 Microbiology. Norfloxacin is a broad spectrum, synthetic fluoroquinolone antibiotic. It is bacteriostatic and bactericidal. Norfloxacin shows in vitro activity against the following organisms: Urinary tract infection pathogens: Aerobic bacteria. Gram positive bacteria including S.faecalis, S.aureus, S.epidermidis, S.saprophyticus. Gram negative bacteria including E.coli, E.cloacae, K.oxytoca, K.pneumoniae, P.mirabilis, P.aeruginosa, C.diversus, C.freundii. Gastrointestinal tract infection pathogens: Shigella, E.coli, S.typhi. Others: N.gonorrhoea. The development of resistance duri http://www.virtualmedicalcentre.com/drugs/noroxin/1925 Noroxin belongs to a group of antibacterials called quinolones. It is bactericidal. It acts by inhibiting bacterial DNA synthesis by blocking DNA gyrase and topoisomerase IV.1 http://www.virtualmedicalcentre.com/drugs/roxin/1926 Microbiology. Norfloxacin is a broad spectrum, synthetic fluoroquinolone antibiotic. It is bacteriostatic and bactericidal. Norfloxacin shows in vitro activity against the following organisms: Urinary tract infection pathogens: Aerobic bacteria. Gram positive bacteria including S.faecalis, S.aureus, S.epidermidis, S.saprophyticus. Gram negative bacteria including E.coli, E.cloacae, K.oxytoca, K.pneumoniae, P.mirabilis, P.aeruginosa, C.diversus, C.freundii. Gastrointestinal tract infection pathogens: Shigella, E.coli, S.typhi. Others: N.gonorrhoea. The development of resistance duri http://www.virtualmedicalcentre.com/drugs/tequin/1927 Tequin is a synthetic broad spectrum quinolone antibiotic that acts intracellularly by inhibiting DNA gyrase. It has been shown to be effective against a wide variety of gram positive and gram negative aerobes, anaerobes, and atypical bacteria such as Chlamydia and Legionella. Gatifloxacin is well absorbed from the gastrointestinal tract after oral administration and can be given without regard to food. The absolute bioavailability of gatifloxacin is 96%. Peak plasma concentrations of gatifloxacin occur 1-2 hours after oral dosing. Tequin is primarily excreted through the kidneys - less th http://www.virtualmedicalcentre.com/drugs/norfloxacin-terry-white-chemists/1928 Microbiology. Norfloxacin is a broad spectrum, synthetic fluoroquinolone antibiotic. It is bacteriostatic and bactericidal. Norfloxacin shows in vitro activity against the following organisms: Urinary tract infection pathogens: Aerobic bacteria. Gram positive bacteria including S.faecalis, S.aureus, S.epidermidis, S.saprophyticus. Gram negative bacteria including E.coli, E.cloacae, K.oxytoca, K.pneumoniae, P.mirabilis, P.aeruginosa, C.diversus, C.freundii. Gastrointestinal tract infection pathogens: Shigella, E.coli, S.typhi. Others: N.gonorrhoea. The development of resistance duri http://www.virtualmedicalcentre.com/drugs/amikacin-injection-dbl/1929 Microbiology. Amikacin is a semisynthetic aminoglycoside antibiotic, and has a concentration dependent bactericidal effect. It is active against a variety of pathogens. Including: Gram negative: Pseudomonas sp.; Proteus sp.; K.pneumoniae; E.cloacae; Serratia sp.; Providencia stuartii; Citrobacter freundii; E.coli. Gram positive: Staphylococcus sp. (penicillinase and non-penicillinase producing, including methicillin resistant). It is resistant to most of the bacterial enzyme inactivation responsible for poor sensitivity other aminoglycosides. Pharmacology. Following intramusc http://www.virtualmedicalcentre.com/drugs/amikin/1930 Microbiology. Amikacin is a semisynthetic aminoglycoside antibiotic, and has a concentration dependent bactericidal effect. It is active against a variety of pathogens. Including: Gram negative: Pseudomonas sp.; Proteus sp.; K.pneumoniae; E.cloacae; Serratia sp.; Providencia stuartii; Citrobacter freundii; E.coli. Gram positive: Staphylococcus sp. (penicillinase and non-penicillinase producing, including methicillin resistant). It is resistant to most of the bacterial enzyme inactivation responsible for poor sensitivity other aminoglycosides. Pharmacology. Following intramusc http://www.virtualmedicalcentre.com/drugs/gentamicin-injection-bp/1931 Gentamicin is a bactericidal antibiotic, which acts by inhibiting protein synthesis, a vital process for bacterial survival. It is active against a wide range of Gram-negative bacteria including: Escherichia coli. Pseudomonas aeruginosa. Proteus spp. Klebsiella spp. Enterobacter spp. Serratia spp. Gentamicin also has activity against Salmonella and Shigella species. Of the Gram-positives, Gentamicin is active against Staphylococcus species, including MRSA. Some resistance to aminoglycoside antibiotics has been seen amongst Streptococcus pneumoniae and anaerobic bacteria such as http://www.virtualmedicalcentre.com/drugs/gentamicin-injection-bp-dbl/1932 Gentamicin is a bactericidal antibiotic, which acts by inhibiting protein synthesis, a vital process for bacterial survival. It is active against a wide range of Gram-negative bacteria including: - Escherichia coli - Pseudomonas aeruginosa - Proteus spp. - Klebsiella spp. - Enterobacter spp. - Serratia spp. Gentamicin also has activity against Salmonella and Shigella species. Of the Gram-positives, Gentamicin is active against Staphylococcus species, including MRSA. Some resistance to aminoglycoside antibiotics has been seen amongst Streptococcus pneumoniae and anaerobic bacteria such http://www.virtualmedicalcentre.com/drugs/nebcin/1933 Nebcinnbsp;is bactericidal. Itnbsp;acts by inhibiting the synthesis of protein in bacterial cells.1 http://www.virtualmedicalcentre.com/drugs/septopal/1936 Septopal beads contain an aminoglycoside antibiotic called gentamicin. It has a broad spectrum of antibacterial activity against both Gram negative and Gram positive microorganisms, including E. coli, Klebsiella, Enterobacter, Pseudomonas and Proteus. It exerts its activity via inhibition of bacterial protein synthesis. The beads release gentamicin over a prolonged period of time.1 http://www.virtualmedicalcentre.com/drugs/tobramycin-injection-bp/1937 Tobramycin sulfate and other aminoglycoside antibiotics have a concentration-dependent bactericidal effect on sensitive bacteria. Mechanism of action is by irreversibly binding to the 30S ribosomal unit. This results in inhibition of protein synthesis. http://www.virtualmedicalcentre.com/drugs/tobramycin-injection-bp-dbl/1938 Tobramycin sulfate and other aminoglycoside antibiotics have a concentration-dependent bactericidal effect on sensitive bacteria. Mechanism of action is by irreversibly binding to the 30S ribosomal unit. This results in inhibition of protein synthesis. http://www.virtualmedicalcentre.com/drugs/alprim/1939 Microbiology. Trimethoprim inhibits bacterial nucleic acid and protein biosynthesis. It is active against the pathogens commonly responsible for urinary tract infections (e.g. E.coli, P.mirabilis, K.pneumoniae). Trimethoprim is found in vaginal secretions and faeces, and can suppress normal vaginal and bowel flora. It is not active against Pseudomonas sp. Developing resistance is more likely to occur in hospital than in domiciliary use. Pharmacokinetics. Trimethoprim is rapidly absorbed from the gut, with a half life of 8-12 hours (in patients with normal renal function). Excreti http://www.virtualmedicalcentre.com/drugs/bactrim/1941 Microbiology. Cotrimoxazole is a synthetic antibacterial combination that inhibits bacterial biosynthesis at two consecutive steps. It is active against a variety of Gram negative and Gram positive pathogens. Including: E.coli, Neisseria, Salmonella, Klebsiella-Enterobacter, Shigella, H.influenzae, Proteus, V.cholerae, B.pertussis, Streptococcus (including pneumococcus), Staphylococcus. It effective against the protozoan Pneumocystic carinii to. Cotrimoxazole is not effective against M.tuberculosis or T.pallidum and P.aeruginosa is often resistant. Pharmacokinetics. Cotrimoxazole is rapidly ab http://www.virtualmedicalcentre.com/drugs/chem-mart-trimethoprim-with-sulfamethoxazole-ds/1942 Trimethoprim and sulfonamides both have a bacteriostatic action by interfering with folate production which is essential for bacterial growth. Sulfamethoxazole competitively inhibits bacterial synthesis of folate in the form of dihydrofolic acid by competing with para-aminobenzoic acid. Trimethoprim blocks the conversion of tetrahydrofolic acid from dihydrofolic acid by binding to and reversibly inhibiting dihydrofolate reductase http://www.virtualmedicalcentre.com/drugs/chloromycetin-succinate/1943 Chloramphenicol sodium succinate inhibits protein synthesis in intact bacterial cells. Its effect is mainly bacteriostatic against several Gram negative and Gram positive bacteria as well as rickettsial organisms, the lymphogranuloma-psittacosis group, Vibrio cholerae, Salmonella typhi and Haemophilus influenzae. http://www.virtualmedicalcentre.com/drugs/flagyl/1950 Microbiology: Metronidazole has bactericidal activity against important species of obligate anaerobic bacteria and other micro-organisms. The mechanism by which it reduces papules and pustules in rosacea is unknown. Including: Bacteroides sp.; Fusobacteri sp.; Eubacteria sp.; Clostridia sp.; and anaerobic Streptococci; Trichonomads, E.histiolytica, G.Lamblia, B.coli. Pharmacokinetics: Maximum concentrations occur within 1-2 hours after oral administration, and at the end of an intravenous infusion, with biological half lives of 6 and 7.3 hours respectively. The suppository form is http://www.virtualmedicalcentre.com/drugs/genrx-trimethoprim-with-sulfamethoxazole-ds/1954 Trimethoprim and sulfonamides both have a bacteriostatic action by interfering with folate production which is essential for bacterial growth. Sulfamethoxazole competitively inhibits bacterial synthesis of folate in the form of dihydrofolic acid by competing with para-aminobenzoic acid. Trimethoprim blocks the conversion of tetrahydrofolic acid from dihydrofolic acid by binding to and reversibly inhibiting dihydrofolate reductase. http://www.virtualmedicalcentre.com/drugs/healthsense-trimethoprim-with-sulfamethoxazole-ds/1955 Trimethoprim and sulfonamides both have a bacteriostatic action by interfering with folate production which is essential for bacterial growth. Sulfamethoxazole competitively inhibits bacterial synthesis of folate in the form of dihydrofolic acid by competing with para-aminobenzoic acid. Trimethoprim blocks the conversion of tetrahydrofolic acid from dihydrofolic acid by binding to and reversibly inhibiting dihydrofolate reductase. http://www.virtualmedicalcentre.com/drugs/merrem-iv/1959 Microbiology. Meropenem is a carbapenem antibiotic with bactericidal action. It acts synergistically with various antibiotics, and has a post-antibiotic effect. Meropenem is usually active against the following antibiotics: Gram positive aerobes: E.faecalis, S.aureus (penicillinase negative positive), coagulase negative Staphylococci, Streptococci sp. Gram negative aerobes: E.coli, H.influenzae (including beta lactamase positive strains), M.catarrhalis, N.gonorrhoeam N.meningitidis, Klebsiella sp, M.morganii, P.mirabilis, Serratia sp, Acinetobacter anitratus, Citrobacter sp, Ente http://www.virtualmedicalcentre.com/drugs/metrogyl/1960 Metronidazole is metabolised to active metabolites that are thought to act be interfering with DNA synthesis. http://www.virtualmedicalcentre.com/drugs/metronidazole-intravenous-infusion-baxter/1961 Metronidazole is an antibiotic agent with activity against anaerobic bacteria and protozoa. Against anaerobic bacteria it is bactericidal, by a mechanism thought to be interfering with DNA synthesis. Anaerobic bacteria susceptible to Metronidazole include: - Bacteroides fragilis - other Bacteroids spp. - Fusobacterium - Eubacterium - Clostridium - anaerobic Streptococci Pathogenic protozoa that are killed by Metronidazole include: - Trichomonas vaginalis - other trichomonads - Entamoeba histolytica - Giardia Lamblia - Balantidium coli - causative organisms of active ulcerative gin http://www.virtualmedicalcentre.com/drugs/metronidazole-intravenous-infusion-pharmacia/1962 Metronidazole is an antibiotic agent with activity against anaerobic bacteria and protozoa. Against anaerobic bacteria it is bactericidal, by a mechanism thought to be interfering with DNA synthesis. Anaerobic bacteria susceptible to Metronidazole include: - Bacteroides fragilis - other Bacteroids spp. - Fusobacterium - Eubacterium - Clostridium - anaerobic Streptococci Pathogenic protozoa that are killed by Metronidazole include: - Trichomonas vaginalis - other trichomonads - Entamoeba histolytica - Giardia Lamblia - Balantidium coli - causative organisms of active ulcerative gin http://www.virtualmedicalcentre.com/drugs/metronide/1963 Metronidazole is an antibiotic agent with activity against anaerobic bacteria and protozoa. Against anaerobic bacteria it is bactericidal, by a mechanism thought to be interfering with DNA synthesis. Anaerobic bacteria susceptible to Metronidazole include: - Bacteroides fragilis. - Other Bacteroids. - Fusobacterium. - Eubacterium. - Clostridium. - Anaerobic Streptococci. Pathogenic protozoa that are killed by Metronidazole include: - Trichomonas vaginalis. - Other trichomonads. - Entamoeba histolytica. - Giardia Lamblia. - Balantidium coli. - Causative organisms of active ul http://www.virtualmedicalcentre.com/drugs/ralodantin/1966 Microbiology. Nitrofurantoin is a synthetic, nitrofuran derivative antibiotic. It is bacteriostatic at low concentrations and bactericidal at higher concentrations. Nitrofurantoin has activity against common Gram negative and Gram positive urinary tract pathogens, including E.coli. However some strains of Pseudomonas, Proteus and Klebsiella are insensitive. Bacteriological culture and susceptibility testing is recommended. Developed resistance by bacteria to furan derivatives is limited. Pharmacokinetics. Nitrofurantoin is well absorbed from the gut, peak plasma levels are achieve http://www.virtualmedicalcentre.com/drugs/trimethoprim-with-sulfamethoxazole-ds-terry-white-chemists/1973 Trimethoprim and sulfonamides both have a bacteriostatic action by interfering with folate production which is essential for bacterial growth. Sulfamethoxazole competitively inhibits bacterial synthesis of folate in the form of dihydrofolic acid by competing with para-aminobenzoic acid. Trimethoprim blocks the conversion of tetrahydrofolic acid from dihydrofolic acid by binding to and reversibly inhibiting dihydrofolate reductase. http://www.virtualmedicalcentre.com/drugs/trimoxazole-bc/1974 Trimethoprim and sulfonamides both have a bacteriostatic action by interfering with folate production which is essential for bacterial growth. Sulfamethoxazole competitively inhibits bacterial synthesis of folate in the form of dihydrofolic acid by competing with para-aminobenzoic acid. Trimethoprim blocks the conversion of tetrahydrofolic acid from dihydrofolic acid by binding to and reversibly inhibiting dihydrofolate reductase. http://www.virtualmedicalcentre.com/drugs/vancocin-cp/1977 Microbiology. Vancomycin is bactericidal. It is active against: C.difficile; Staphylococci (counting S.aureus and epidermidis and including heterogenous methicillin resistant strains), Streptococci, Enterococci, diphtheroids, L.monocytogenes, Lactobacillus sp., Actinomyces sp. Clostridium sp., and Bacillus sp. Vancomycin acts synergistically with aminoglycosides against most strains of S.aureus, Streptococci (including nonenterococcal group D) and Enterococci. Vancomycin acts synergistically with cephalosporins against some strains of S.epidermidis. Vancomycin acts in partial synergy wi http://www.virtualmedicalcentre.com/drugs/vancocin/1978 Microbiology. Vancomycin is bactericidal. It is active against: C.difficile; Staphylococci (counting S.aureus and epidermidis and including heterogenous methicillin resistant strains), Streptococci, Enterococci, diphtheroids, L.monocytogenes, Lactobacillus sp., Actinomyces sp. Clostridium sp., and Bacillus sp. Vancomycin acts synergistically with aminoglycosides against most strains of S.aureus, Streptococci (including nonenterococcal group D) and Enterococci. Vancomycin acts synergistically with cephalosporins against some strains of S.epidermidis. Vancomycin acts in partial synergy wi http://www.virtualmedicalcentre.com/drugs/vancomycin-hydrochloride-for-intravenous-infusion/1979 Vancomycin is a glycopeptide antibiotic. It is active against Gram-positive bacteria only, with no activity against Gram-negative bacteria, mycobacteria or fungi. It appears to act by inhibiting the production of bacterial cell wall mucopeptide, a component vital for the survival of the bacteria. This is a similar action to penicillins, but Vancomycin acts at a different site and is therefore active against several bacteria showing resistance to penicillin (eg: S. pneumoniae). The inhibition of cell wall production results in secondary disruption of the bacterial cytoplasm, an effect that cont http://www.virtualmedicalcentre.com/drugs/vancomycin-hydrochloride-for-intravenous-infusion-dbl/1980 Vancomycin is a glycopeptide antibiotic. It is active against Gram-positive bacteria only, with no activity against Gram-negative bacteria, mycobacteria or fungi. It appears to act by inhibiting the production of bacterial cell wall mucopeptide, a component vital for the survival of the bacteria. This is a similar action to penicillins, but Vancomycin acts at a different site and is therefore active against several bacteria showing resistance to penicillin (eg: S. pneumoniae). The inhibition of cell wall production results in secondary disruption of the bacterial cytoplasm, an effect that cont http://www.virtualmedicalcentre.com/drugs/amphocil/1985 Microbiology. Amphocil is a stable complex of Amphotericin B and sodium cholesterol sulfate, and is slightly less effective than conventional Amphotericin B at equivalent doses, though at higher tolerated doses it is equivalent to of more effective than Amphotericin B. Amphotericin is a macrocyclic antibiotic derived from Streptomyces nodosus with fungicidal activity against a variety of fungal species, including: Aspergillus sp., Candida sp., Coccidiodes immitis, Cryptococcus.neoformans, Blastmomycoses dermatityidu, Histoplasma capsulatum, Sporothrix schenkii. Amphocin has little to no acti http://www.virtualmedicalcentre.com/drugs/cancidas/1987 Cancidas inhibits the synthesis of the integral component of the fungal cell wall, and hence alters cell membrane permeability.1,2 http://www.virtualmedicalcentre.com/drugs/diflucan/1988 Diflucannbsp;belongs to the class of medications called azoles.1 It has fungistatic activity.1nbsp; Fluconazole impair the synthesis of ergosterol which is essential building block in fungal cell membrane.1 This impairment leads to fungal cell leakage and death due to the lytic activity of the host defense mechanism.1 http://www.virtualmedicalcentre.com/drugs/fungilin/1989 Microbiology. Amphocil is a stable complex of Amphotericin B and sodium cholesterol sulfate, and is slightly less effective than conventional Amphotericin B at equivalent doses, though at higher tolerated doses it is equivalent to of more effective than Amphotericin B. Amphotericin is a macrocyclic antibiotic derived from Streptomyces nodosus with fungicidal activity against a variety of fungal species, including: Aspergillus sp., Candida sp., Coccidiodes immitis, Cryptococcus.neoformans, Blastmomycoses dermatityidu, Histoplasma capsulatum, Sporothrix schenkii. Amphocin has little to no acti http://www.virtualmedicalcentre.com/drugs/lamisil-tablets/1993 Lamisil (Terbinafine) is an allylamine which is an antifungal agent that mainly fights against dermatophytes. Terbinafine works to specifically inhibit fungal ergosterol synthesis at an earlier step compared to azole antifungals, leading to a deficiency in ergosterol and an intracellular accumulation of squalene, resulting in membrane disruption and cell death. Terbinafine also acts by inhibition of squalene epoxidase in the fungal cell membrane. When taken orally, Terbinafine concentrates in skin and nails at levels associated with antifungal effects.1,2 http://www.virtualmedicalcentre.com/drugs/nizoral/1995 Nizoral inhibits ergosterol biosynthesis in Candida albicans, which leads to alterations in the composition and properties of the cell membrane. These alterations are probably the origin of increased susceptibility of the invasive yeast cell to lytic activity of the host defence system.2 http://www.virtualmedicalcentre.com/drugs/aciclovir/1998 Acyclovir is an antiviral agent which is active against types 1 and 2 of herpes simplex virus types 1 and 2 and varicella zoster virus. Varicella zoster virus is far less sensitive to Acyclovir than Herpes simplex virus is. Acyclovir is phosphorylated within the cell to form acyclovir triphosphate which is active against the virus. In normal cells there is very limited conversion of acyclovir to acyclovir triphosphate and the cellular DNA polymerase is not very sensitive to the active compound. In cells infected with HSV or VZV, HSV or VZV coded thymidine kinase allows the acyclovir to be conv http://www.virtualmedicalcentre.com/drugs/aciclovir-intravenous-infusion-dbl/1999 - Aciclovir is active in vitro against Herpes simplex virus, types I and II and Varicella zoster virus, however its clinical response in therapy has not been fully established - It is a synthetic acyclic purine nucleoside analogue - It becomes phosphorylated to its active compound, aciclovir triphosphate which acts as an inhibitor of, and substrate for the specific DNA polymerase for the Herpes virus, which prevents further viral DNA production http://www.virtualmedicalcentre.com/drugs/aciclovir-bc-infusion/2000 Aciclovir is a synthetic purine nucleoside analogue. It is an antiviral agent, active against the herpes simplex virus (HSV) types 1 amp; 2, and the varicella zoster virus (VSV). Development of resistance by HSV to aciclovir has been documented. Aciclovir is phosphorylated to the active antiviral compont aciclovir triphosphate in cells infected with HSV or VZV. Aciclovir triphosphate inhibits further DNA viral synthesis. Oral: Aciclovir is variably and only partially absorbed from the gut. Following oral administration, the mean half life ranges from 2.5-3.3 hours and is approximately 2.0 hou http://www.virtualmedicalcentre.com/drugs/aciclovir-bc-tablets/2001 Aciclovir is a synthetic purine nucleoside analogue. It is an antiviral agent, active against the herpes simplex virus (HSV) types 1 amp; 2, and the varicella zoster virus (VSV). Development of resistance by HSV to aciclovir has been documented. Aciclovir is phosphorylated to the active antiviral compont aciclovir triphosphate in cells infected with HSV or VZV. Aciclovir triphosphate inhibits further DNA viral synthesis. Oral: Aciclovir is variably and only partially absorbed from the gut. Following oral administration, the mean half life ranges from 2.5-3.3 hours and is approximately 2.0 hou http://www.virtualmedicalcentre.com/drugs/acihexal/2002 Acyclovir is an antiviral agent which is active against types 1 and 2 of herpes simplex virus and varicella zoster virus. Varicella zoster virus is far less sensitive to Acyclovir than Herpes simplex virus is. Acyclovir is phosphorylated within the cell to form acyclovir triphosphate which is active against the virus. In normal cells there is very limited conversion of acyclovir to acyclovir triphosphate and the cellular DNA polymerase is not very sensitive to the active compound. In cells infected with HSV or VZV, HSV or VZV coded thymidine kinase allows the acyclovir to be converted to acycl http://www.virtualmedicalcentre.com/drugs/acihexal-intravenous-infusion/2003 Acyclovir is an antiviral agent which is active against types 1 and 2 of herpes simplex virus types 1 and 2 and varicella zoster virus. Varicella zoster virus is far less sensitive to Acyclovir than Herpes simplex virus is. Acyclovir is phosphorylated within the cell to form acyclovir triphosphate which is active against the virus. In normal cells there is very limited conversion of acyclovir to acyclovir triphosphate and the cellular DNA polymerase is not very sensitive to the active compound. In cells infected with HSV or VZV, HSV or VZV coded thymidine kinase allows the acyclovir to be conv http://www.virtualmedicalcentre.com/drugs/acyclo-v/2004 Acyclovir is an antiviral agent which is active against types 1 and 2 of herpes simplex and varicella zoster virus. Varicella zoster virus is far less sensitive to Acyclovir than Herpes simplex virus is. Acyclovir is phosphorylated within the cell to form acyclovir triphosphate which is active against the virus. In normal cells there is very limited conversion of acyclovir to acyclovir triphosphate and the cellular DNA polymerase is not very sensitive to the active compound. In cells infected with HSV or VZV, HSV or VZV coded thymidine kinase allows the acyclovir to be converted to acyclovir m http://www.virtualmedicalcentre.com/drugs/combivir/2007 Virology. Zidovudine inhibits some retroviral replications, including HIV Lamivudine selectively and potently inhibits HIV-1 and HIV-2 replication. The two usually act synergistically at inhibiting HIV. Pharmacokinetics. Both lamivudine and zidovudine are well absorbed after oral administration, with mean peak concentrations reached within 0.5 and 0.75 hours respectively. The presence of food reduces the rate of absorption, however the clinical significance of this is not known. The relationship between drug clearance and renal function is linear. Elimination is predominantly ren http://www.virtualmedicalcentre.com/drugs/crixivan/2008 Microbiology. Indivir is a specific protease inhibitor against HIV-1. (There is a tenfold selectivity for HIV-1 over HIV-2) Indivir has synergistic antiretroviral activity with zidovudine, didanosine or a non-nucleoside reverse transcriptase inhibitor. Drug resistance has occurred in some patients. Cross resistance has been noted between indivir and ritonavir Pharmacokinetics. Indivir is rapidly absorbed from the gut, peak plasma concentrations are achieved after 0.8 hours, although the administration with high calorie/fat/protein meals greatly reduce absorption and peak levels, a http://www.virtualmedicalcentre.com/drugs/famvir/2010 Famciclovir is rapidly converted to penciclovir in vivo. Penciclovir is then phosphorylated to penciclovir triphosphate in virus infected cells by viral and cellular enzymes. The triphosphate inhibits viral DNA polymerase, preventing DNA synthesis.1-3 http://www.virtualmedicalcentre.com/drugs/fortovase/2011 Virology. Saquinavir is a highly selective HIV protease inhibitor, with only a weak affinity for human proteases. Saquinavir exerts synergistic effects against HIV in double and triple combination regimens with reverse transcriptase inhibitors (e.g. zidovudine, zalcitabine, didanosime, lamivudine, stavudine, nevipramine) in the absence of increased toxicity. Cross resistance between saquinavir and reverse transcriptase inhibitors is unlikely due to their different enzyme targets. HIV strains with reduced susceptibility to saquinavir have been isolated in vitro. Pharmacokinetics. Saqu http://www.virtualmedicalcentre.com/drugs/foscavir/2012 Microbiology. Foscarnet is a broad spectrum antiviral agent that inhibits viral specific DNA polymerase and reverse transcriptase. It is active against human herpes viruses (including HSV type I, HSV type 2, HHV 6), varicella zoster virus, Epstein Barr virus, CMV, and some retroviruses including HIV. Viral polymerase is about 100 times more sensitive to Foscarnet than human polymerase. Pharmacokinetics. The terminal half-life of Foscarnet is approximately 1-8 days. Plasma clearance after intravenous administration varies from 130-160 mL/minute. Foscarnet does not undergo metabolic co http://www.virtualmedicalcentre.com/drugs/genrx-aciclovir/2013 Aciclovir is a synthetic purine nucleoside analogue. It is an antiviral agent, active against the herpes simplex virus (HSV) types 1 2, and the varicella zoster virus (VSV). Development of resistance by HSV to aciclovir has been documented. Aciclovir is phosphorylated to the active antiviral compont aciclovir triphosphate in cells infected with HSV or VZV. Aciclovir triphosphate inhibits further DNA viral synthesis. Oral: Aciclovir is variably and only partially absorbed from the gut. Following oral administration, the mean half life ranges from 2.5-3.3 hours and is approximately 2.0 hou http://www.virtualmedicalcentre.com/drugs/healthsense-aciclovir/2014 Acyclovir is an antiviral agent which is active against types 1 and 2 of herpes simplex virus types 1 and 2 and varicella zoster virus. Varicella zoster virus is far less sensitive to Acyclovir than Herpes simplex virus is. Acyclovir is phosphorylated within the cell to form acyclovir triphosphate which is active against the virus. In normal cells there is very limited conversion of acyclovir to acyclovir triphosphate and the cellular DNA polymerase is not very sensitive to the active compound. In cells infected with HSV or VZV, HSV or VZV coded thymidine kinase allows the acyclovir t http://www.virtualmedicalcentre.com/drugs/hivid/2015 Zalcitabine is a synthetic pyrimidine nucleoside analogue active against HIV by inhibiting the viral DNA synthesis. http://www.virtualmedicalcentre.com/drugs/invirase/2016 Virology. Saquinavir is a highly selective HIV protease inhibitor, with only a weak affinity for human proteases. Saquinavir exerts synergistic effects against HIV in double and triple combination regimens with reverse transcriptase inhibitors (e.g. zidovudine, zalcitabine, didanosime, lamivudine, stavudine, nevipramine) in the absence of increased toxicity. Cross resistance between saquinavir and reverse transcriptase inhibitors is unlikely due to their different enzyme targets. HIV strains with reduced susceptibility to saquinavir have been isolated in vitro. Pharmacokinetics. Saqu http://www.virtualmedicalcentre.com/drugs/lovir/2018 Acyclovir is an antiviral agent which is active against types 1 and 2 of herpes simplex virus types 1 and 2 and varicella zoster virus. Varicella zoster virus is far less sensitive to Acyclovir than Herpes simplex virus is. Acyclovir is phosphorylated within the cell to form acyclovir triphosphate which is active against the virus. In normal cells there is very limited conversion of acyclovir to acyclovir triphosphate and the cellular DNA polymerase is not very sensitive to the active compound. In cells infected with HSV or VZV, HSV or VZV coded thymidine kinase allows the acyclovir t http://www.virtualmedicalcentre.com/drugs/relenza/2020 The active ingredient in Relenza is zanamivir,nbsp;a potent neuraminidase inhibitor.1 Neuraminidase is a surface enzyme of the influenza virus that facilitates the transfer of newly formed virus particles from infected cellsnbsp;to healthy cells. Influenza virus replication takes place in the epithelium of the respiratory tract.1 Relenza is orally inhaled so that the medication enters the respiratory tract, where itnbsp;inhibits the release of new virus particles from infected cells andnbsp;effectively blocks the virus replication process.1 http://www.virtualmedicalcentre.com/drugs/rescriptor/2021 Rescriptor is a non-nucleoside reverse transcriptase inhibitor. It binds directly to HIV-1 reverse transcriptase to inhibit viral DNA and RNA activity. It is metabolised primarily by cytochrome P450 3A (CYP3A) and has been shown to inhibit the activity of CYP3A – leading to many potential interactions with a variety of medications. http://www.virtualmedicalcentre.com/drugs/retrovir-capsules-and-syrup/2022 Retrovir is a nucleoside analogue reverse transcriptase inhibitors active against HIV virus by inhibiting viral reverse transcriptase and DNA synthesis.1,2 http://www.virtualmedicalcentre.com/drugs/stocrin/2023 Stocrin non-competitively inhibits HIV-1 reverse transcriptase with respect to primer, template or nucleoside triphosphates. http://www.virtualmedicalcentre.com/drugs/tamiflu/2024 Oseltamivir carboxylate, the active metabolite of the prodrug oseltamivir phosphate, acts as a selective neuraminidase inhibitor.2 Neuraminidase is a viral particle envelope glycoprotein, which acts as an enzyme to cleave the link between host cells and progeny virions (produced through viral replication), thus liberating them. Neuraminidase also act to counteract entrapment of the virions in respiratory secretions due to self aggregation.7 Through inhibition of neuraminidase, Tamiflu reduces influenza virus replication and release from cells.1 It may also suppress virus entry into the epithel http://www.virtualmedicalcentre.com/drugs/aciclovir-terry-white-chemists/2025 Aciclovir is a synthetic purine nucleoside analogue. It is an antiviral agent, active against the herpes simplex virus (HSV) types 1 amp; 2, and the varicella zoster virus (VSV). Development of resistance by HSV to aciclovir has been documented. Aciclovir is phosphorylated to the active antiviral compont aciclovir triphosphate in cells infected with HSV or VZV. Aciclovir triphosphate inhibits further DNA viral synthesis. Oral: Aciclovir is variably and only partially absorbed from the gut. Following oral administration, the mean half life ranges from 2.5-3.3 hours and is approximately 2.0 hou http://www.virtualmedicalcentre.com/drugs/3tc/2026 Lamivudine is a nucleoside reverse transcriptase inhibitor. Once it is converted by cellular enzymes to an active phosphorylated metabolite, it inhibits the reproduction of human immunodeficiency virus (HIV) by inhibiting viral reverse transcriptase and in turn viral DNA synthesis.1-3 http://www.virtualmedicalcentre.com/drugs/trizivir/2027 Nucleoside reverse transcriptase inhibitors are converted to metabolites that inhibit viral DNA synthesis, thus preventing HIV replication. http://www.virtualmedicalcentre.com/drugs/zeffix/2036 Lamivudine is a nucleoside reverse transcriptase inhibitor. Nucleoside reverse transcriptase inhibitors are converted by cellular enzymes to active phosphorylated metabolites. The phosphorylated metabolites inhibit viral reverse transcriptase and viral DNA synthesis, preventing human immunodeficiency virus (HIV) from replicating. http://www.virtualmedicalcentre.com/drugs/zerit/2037 Zerit is a synthetic thymidine analogue active against HIV virus by inhibiting viral reverse transcriptase and DNA synthesis.1,2 http://www.virtualmedicalcentre.com/drugs/zovirax-intravenous-infusion/2039 Acyclovir is an antiviral agent which is active against types 1 and 2 of herpes simplex virus types 1 and 2 and varicella zoster virus. Varicella zoster virus is far less sensitive to Acyclovir than Herpes simplex virus is. Acyclovir is phosphorylated within the cell to form acyclovir triphosphate which is active against the virus. In normal cells there is very limited conversion of acyclovir to acyclovir triphosphate and the cellular DNA polymerase is not very sensitive to the active compound. In cells infected with HSV or VZV, HSV or VZV coded thymidine kinase allows the acyclovir to be conv http://www.virtualmedicalcentre.com/drugs/zovirax-tablets/2040 Acyclovir is an antiviral agent which is active against types 1 and 2 of herpes simplex virus types 1 and 2 and varicella zoster virus. Varicella zoster virus is far less sensitive to Acyclovir than Herpes simplex virus is. Acyclovir is phosphorylated within the cell to form acyclovir triphosphate which is active against the virus. In normal cells there is very limited conversion of acyclovir to acyclovir triphosphate and the cellular DNA polymerase is not very sensitive to the active compound. In cells infected with HSV or VZV, HSV or VZV coded thymidine kinase allows the acyclovir to be conv http://www.virtualmedicalcentre.com/drugs/zyclir-tablets/2041 Acyclovir is an antiviral agent which is active against types 1 and 2 of herpes simplex virus types 1 and 2 and varicella zoster virus. Varicella zoster virus is far less sensitive to Acyclovir than Herpes simplex virus is. Acyclovir is phosphorylated within the cell to form acyclovir triphosphate which is active against the virus.In normal cells there is very limited conversion of acyclovir to acyclovir triphosphate and the cellular DNA polymerase is not very sensitive to the active compound. In cells infected with HSV or VZV, HSV or VZV coded thymidine kinase allows the acyclovir to be conve http://www.virtualmedicalcentre.com/drugs/capastat/2042 Capastat is a polypeptide antibiotic derived from the bacteria Streptomyces capreolus. It is active against the strains of Mycobacterium tuberculosis that are found in humans. There are varying amounts of cross-resistance seen with Capastat and other anti-tuberculosis agents. Cross-resistance occurs frequently with viomycin, occasionally with kanamycin and neomycin and it has not been observed with isoniazid, aminosalicylic acid, cycloserine, streptomycin ethioamide or ethambutol. http://www.virtualmedicalcentre.com/drugs/cycloserine/2043 Microbiology. Cycloserine inhibits cell wall synthesis in susceptible strains of Gram positive and Gram negative bacteria, and in M.tuberculosis. Pharmacology. Cycloserine has a low therapeutic index. Toxicity is usually associated with blood levels 30 mg/L. Administration should be discontinued or the dosage reduced if the patient shows signs or symptoms of allergic dermatitis, or CNS toxicity. http://www.virtualmedicalcentre.com/drugs/isoniazid/2044 Isoniazid is an antibacterial agent active only against Mycobacteria. Its mechanism of action is unclear, but it may act by inhibiting synthesis of mycolic acids (components of the mycobacterial cell wall). Resistance to Isoniazid alone develops quickly in individual patients, so it should always be given in combination with other anti-tuberculosis agents. http://www.virtualmedicalcentre.com/drugs/myambutol/2046 Microbiology. Ethambutol is an oral anti-tuberculosis agent. It diffuses into actively growing mycobacterium cells, inhibiting metabolite synthesis and causing cell death. Cross-resistance between ethambutol and other anti-tuberculosis agents has not been demonstrated. Pharmacokinetics. Peak plasma levels are achieved within 2-4 hours after oral administration, with the drug being undetectable in the serum by 24 hours after the last dose in patients with normal renal function. Ethambutol is partially metabolised in the liver, with 50% of the dose is excreted in the urine unchanged, http://www.virtualmedicalcentre.com/drugs/mycobutin/2047 Microbiology Rifabutin is a wide spectrum, semi-synthetic ansamycin antibiotic. It is active against acid-fast bacilli, including atypical and multi-drug resistant mycobacteria. Pharmacokinetics. Following oral administration, rifabutin has a bioavailability of 85% in healthy adults, with peak plasma levels achieved within 2-4 hours. High fat meals do not affect the extent of absorption, despite slowing the rate of absorption. Rifabutin is highly lipophilic and distributes preferentially to intracellular compartments in various organs with the exception of the brain. For example lung tis http://www.virtualmedicalcentre.com/drugs/rifadin/2048 Rifampicin is an antibiotic with activity against a number of extracellular and intracellular organisms. Its most important activity is its bactericidal effect against Mycobacterium tuberculosis, a slow and intermittently growing intracellular organism. Rifampicin interacts with and inhibits bacterial RNA polymerase, but does not affect the mammalian enzyme, thereby not affecting human cells. http://www.virtualmedicalcentre.com/drugs/rimycin/2049 Rifampicin is an antibiotic with activity against a number of extracellular and intracellular organisms. Its most important activity is its bactericidal effect against Mycobacterium tuberculosis, a slow and intermittently growing intracellular organism. Rifampicin interacts with and inhibits bacterial RNA polymerase, but does not affect the mammalian enzyme, thereby not affecting human cells. http://www.virtualmedicalcentre.com/drugs/chlorquin/2051 Chloroquine has antimalarial, amoebicidal and anti-inflammatory activity http://www.virtualmedicalcentre.com/drugs/daraprim/2052 Pharmacology. Pyrimethamine inhibits the enzyme dihydrofolate reducatase (DHFR) and therefore blocks protein synthesis and nuclear division. This interference has a much greater affinity for protozoal DHFR than mammalian DHFR. Pyrimethamine has synergism with sulfonamides. Pharmacokinetics. Peak plasma levels are achieved 2-4 hours after oral administration. Half life is approximately 90 hours. http://www.virtualmedicalcentre.com/drugs/fansidar/2053 Microbiology. Fansidar is an antimalarial agent that attacks the different stages of parasite’s development. Trophozoites and schizonts are rapidly eliminated from the blood, pre-erythrocytic stages are disrupted, and the gametocytes are rendered non-infective the mosquito. This mechanism of action reduces the risk of resistance developing. It is usually effective against chloroquine resistant strains of Plasmodium falciparum Pharmacology. Little is known about the absorption, distribution and metabolism of Fansidar. Pyrimethamine: peak plasma levels in about 2 hours; half live appro http://www.virtualmedicalcentre.com/drugs/lariam/2054 Pharmacology. Mefloquine is an antimalarial agent, structurally related to quinine. It acts by destroying the asexual erythrocytic forms of the malarial pathogens. It is active against P.falciparum infections resistant to other antimalarials, though resistance has been seen in a few clinical isolates, and cross resistance has been shown between mefloquine and quinine (especially in isolates from parts of South-East Asia). Pharmacokinetics. Peak plasma levels are achieved about 14 days after oral dosing. Mefloquine is metabolised to several compounds, the major one being the microbiol http://www.virtualmedicalcentre.com/drugs/paludrine/2056 Microbiology. Proguanil’s metabolite cycloguanil is active against the tissue forms of some strains of P.falciparum, prevent schizogony and development of primary tissue schizonts. Pharmacokinetics. Proguanil is well absorbed from the gut, with peak plasma levels achieved approximately 4 hours after dosing. The peak plasma level of the active metabolite cycloguanil occurs 1 hour later. Elimination half lives are approximately 12-16 hours. With repeated dosing there is a small degree of drug accumulation. Approximately 3% of Caucasians lack the appropriate enzyme to convert proguan http://www.virtualmedicalcentre.com/drugs/primacin/2057 Primaquine phosphate is an aminoquinolone antimalarial agent. It is active against malarial agents once they have entered the body, and is thought to prevent them entering blood and other body cells. It is active against the exoerythrocytic stages of Plasmodium vivax and P. ovale, and the primary exoerythrocytic stage of P. falciparum. It also has activity against the gametocytes of plasmodia, including P. falciparum. Primaquine is more active against these tissue and gamete forms of plasmodia than asexual blood forms. http://www.virtualmedicalcentre.com/drugs/quinine-dihydrochloride-6andpermil/2058 Quinine has a number of actions. - Antimalarial: the exact mechanism of action is uncertain, but it is thought that quinine acts on plasmodial DNA to prevent protein synthesis. - Antimyotonic: increases the refractory period of skeletal muscle, thus diminishing the response to stimulation. It also decreases the excitability of the motor end-plate region, reducing the responses to repetitive nerve stimulation and to acetylcholine. This reduces muscle spasms and cramps. http://www.virtualmedicalcentre.com/drugs/stromectol/2068 Stromectol activates the release of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter, which prevents signals from transmitting from the ventral cord interneurons to the excitatory motor neurons in the nematodes. Stromectol does NOT readily enter the central nervous system of mammals and hence does not interfere with GABA neurotransmission in humans. http://www.virtualmedicalcentre.com/drugs/ditropan/2078 The active component of Ditropan, oxybutynin chloride, has direct antispasmodic effects on smooth muscles and inhibits the muscarinic action of acetylcholine on smooth muscles. Ditropan therefore relaxes the bladder detrusor muscle in patients with involuntary bladder contractions. This subsequently increases bladder capacity and reduces the urge to urinate.3,4 http://www.virtualmedicalcentre.com/drugs/proscar/2082 Proscar inhibits 5-alpha-reductase conversion of testosterone to dihydrotestosterone (DHT). In benign prostatic hyperplasia (BPH), enlargement of the prostate gland is dependent upon the conversion of testosterone to DHT within the prostate. Proscar is highly effective in reducing circulating and intraprostatic DHT. It reduces prostate size, decreases urinarynbsp;outflow resistance and reduces symptoms.1,2nbsp;nbsp;nbsp; http://www.virtualmedicalcentre.com/drugs/canesten-clotrimazole/2092 Clotrimazole is an imidazole derivative with a broad spectrum antimycotic activity. 2 It impairs biosynthesis of ergosterol for cytoplasmic membrane, hence inhibiting fungal growth. 1 http://www.virtualmedicalcentre.com/drugs/canesten-clotrimazole-thrush-treatment-once-pessary-cream/2093 Clotrimazole is an imidazole derivative with a broad spectrum antimycotic activity. 2 It impairs biosynthesis of ergosterol for cytoplasmic membrane, hence inhibiting fungal growth. 1 http://www.virtualmedicalcentre.com/drugs/vagifem-pessaries/2106 A decrease in endogenous hormone levels in postmenopausal women often leads to symptoms such as atrophic vaginitis. Vagifem is an intravaginal hormone replacement therapy (HRT) preparation containing oestradiol, which is the active form of human oestrogen. Vagifem therefore acts to replace the endogenous oestradiol levels in postmenopausal women and relieve the associated urogenital symptoms.1,2nbsp; It has been observed that plasma oestradiol and conjugated oestrogens marginally increase after treatment. The absorption of oestradiol has been indicated by the observation of a suppression of p http://www.virtualmedicalcentre.com/drugs/viagra/2110 Viagra is a PDE-5 inhibitor. It increases erectile function, causing more blood to flow to the penis when a man becomes sexually excited.1 It exerts its effects by enhancing the nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) pathway. This pathway is activated in response to sexual stimulation, so in the absence of sexual stimulation, Viagra has no pharmacological effect.1 When the NO/cGMP pathway is activated, nitric oxide is released into the corpus cavernosa. This activates guanylate cyclase which increases levels of cGMP, causing relaxation of smooth muscles in the corpus caverno http://www.virtualmedicalcentre.com/drugs/celestone-chronodose/2111 Betamethasone sodium phosphate and betamethasone acetate are both ester prodrugs, which are converted in vivo to active form by esterase enzymes. Betamethasone sodium phosphate is a water-soluble salt. Itnbsp;is rapidly delivered to the blood stream following IM injection, where it is converted to betamethasone to exert its pharmacological effects. Betamethasone acetate is a lipophillic ester prodrug suspended in aqueous solution which is designed to release the prodrug over a prolonged period, hence producing a depot effect.2 Betamethasone binds to and activates the cytosolic glucocorticoid http://www.virtualmedicalcentre.com/drugs/cortate/2112 Corticosteroids act by binding to intracellular cytoplasmic receptors and regulating the expression of corticosteroid-responsive genes. By regulating these genes corticosteroids suppress the normal physiological inflammation and immune responses. Hydrocortisone has a combination of glucocorticoid and mineralocorticoid effects. Glucocorticoid effects include gluconeogenesis, proteolysis and lipolysis while mineralocorticoid effects include hypertension, sodium and water retention and potassium loss. http://www.virtualmedicalcentre.com/drugs/depo-medrol/2113 Corticosteroids act by binding to intracellular cytoplasmic receptors and regulating the expression of corticosteroid-responsive genes. By regulating these genes corticosteroids suppress the normal physiological inflammation and immune responses. http://www.virtualmedicalcentre.com/drugs/depo-nisolone/2114 Naturally occurring glucocorticoids (hydrocortisone), which also have salt retaining properties, are used in replacement therapy in adrenocortical deficiency states. Their synthetic analogues are used primarily for their potent anti-inflammatory effects in disorders of many organ systems. Glucocorticoids cause profound and varied metabolic effects. In addition, they modify the bodys immune response to diverse stimuli. http://www.virtualmedicalcentre.com/drugs/dexamethasone-sodium-phosphate-injection-usp-dbl/2115 Dexamethasone is a synthetic adrenocorticosteroid with glucocorticoid activity about 25-30 times that of hydrocortisone. Dexamethasone has no mineralocorticoid activity. Except in the treatment of adrenal insufficiency, Dexamethasone does not cure disease but rather suppresses the symptoms associated with disease. It is useful in treating inflammatory disorders and preventing hypersensitivity responses following antigen-antibody reactions. Dexamethasone also has the following metabolic actions: gluconeogenesis glycogen deposition protein and calcium metabolism mobilisation, oxidation, s http://www.virtualmedicalcentre.com/drugs/dexmethsone/2116 Corticosteroids pass through the cell membrane and bind to cytoplasmic receptors in the nucleus. This modifies the expression of corticosteroid responsive genes, leading to suppression of immune or inflammatory responses. http://www.virtualmedicalcentre.com/drugs/florinef/2117 Fludrocortisone acetate is a synthetic adrenocortical steroid possessing very potent mineralocorticoid properties and high glucocorticoid activity. The physiological action is similar to that of hydrocortisone. However, the effects of fludrocortisone acetate, particularly on electrolyte balance, but also on carbohydrate metabolism, are considerably heightened and prolonged. In small oral doses, it produces marked sodium retention and increased urinary potassium excretion. It also causes a rise in blood pressure, apparently because of these effects on electrolyte levels. http://www.virtualmedicalcentre.com/drugs/hysone/2118 Corticosteroids act by binding to intracellular cytoplasmic receptors and regulating the expression of corticosteroid-responsive genes. By regulating these genes corticosteroids suppress the normal physiological inflammation and immune responses. Hydrocortisone has a combination of glucocorticoid and mineralocorticoid effects. Glucocorticoid effects include gluconeogenesis, proteolysis and lipolysis while mineralocorticoid effects include hypertension, sodium and water retention and potassium loss. http://www.virtualmedicalcentre.com/drugs/kenacort-a/2119 Corticosteroids act by binding to intracellular cytoplasmic receptors and regulating the expression of corticosteroid-responsive genes. By regulating these genes corticosteroids suppress the normal physiological inflammation and immune responses. http://www.virtualmedicalcentre.com/drugs/methylprednisolone-sodium-succinate-for-injection-usp-dbl/2120 Methylprednisolone is a corticosteroid medication with potent glucocorticoid effects. It also has mild mineralocorticoid effects causing some retention of sodium and water.4 Methylprednisolone acts on specific receptors that alter gene expression of various agents involved in inflammatory and immune responses. Thus it influences carbohydrate, protein, fat and purine metabolism, electrolyte and water balance and impacts on various organs and tissues within the body.3,4 The overall effect however is to suppress excessive inflammatory and immune responses.1 http://www.virtualmedicalcentre.com/drugs/panafcortelone/2121 Corticosteroids act by binding to intracellular cytoplasmic receptors, regulating the expression of corticosteroid-responsive genes. By regulating these genes corticosteroids suppress the normal physiological inflammation and immune responses. Prednisolone has predominantly glucocorticoid activity with minimal mineralocorticoid activity. http://www.virtualmedicalcentre.com/drugs/predmix-oral-liquid/2122 Corticosteroids act by binding to intracellular cytoplasmic receptors, regulating the expression of corticosteroid-responsive genes. By regulating these genes corticosteroids suppress the normal physiological inflammation and immune responses. Prednisolone has predominantly glucocorticoid activity with minimal mineralocorticoid activity. http://www.virtualmedicalcentre.com/drugs/redipred-oral-liquid/2123 Corticosteroids act by binding to intracellular cytoplasmic receptors, regulating the expression of corticosteroid-responsive genes. By regulating these genes corticosteroids suppress the normal physiological inflammation and immune responses. Prednisolone has predominantly glucocorticoid activity with minimal mineralocorticoid activity. http://www.virtualmedicalcentre.com/drugs/solone/2124 Solone is a synthetic corticosteroid with glucocorticoid activity and anti-inflammatory effects.2 It is three times more potent compared to the parent compound (hydrocortisone) in terms of its glucocorticoid activity and anti-inflammatory effects, but it is less effective in the mineralocorticoid activity.2It influence and modify the biochemical behavior of most tissues in the body by controlling the protein synthesis.2 It forms steroid-receptor complexes with protein receptors in the cytoplasm of sensitive cells in many tissues.2 http://www.virtualmedicalcentre.com/drugs/solucortef/2125 Hydrocortisone sodium succinate is an anti-inflammatory adrenocortical steroid. It has the same metabolic and anti-inflammatory mechanisms as hydrocortisone. http://www.virtualmedicalcentre.com/drugs/solumedrol/2126 Methylprednisolone sodium succinate is a potent anti-inflammatory adrenocortical steroid. It has the same metabolic and anti-inflammatory mechanisms as methylprednisolone. Methylprednisolone has greater anti-inflammatory potency than prednisolone and fewer tendencies than prednisolone to induce sodium and water retention. http://www.virtualmedicalcentre.com/drugs/sone/2127 Corticosteroids act by binding to intracellular cytoplasmic receptors, regulating the expression of corticosteroid-responsive genes. By regulating these genes corticosteroids suppress the normal physiological inflammation and immune responses. Prednisone has predominantly glucocorticoid activity with minimal mineralocorticoid activity. http://www.virtualmedicalcentre.com/drugs/androcur/2129 Cyproterone acetate is an antiandrogenic hormone preparation that prevents the effect of endogenous and exogenous androgens on target organs by means of competitive inhibition. http://www.virtualmedicalcentre.com/drugs/androderm/2130 Androderm provides and replace the physiological level of testosterone which follows after the normal circadian rhythm of normal young men.2It is used in place to replace the low level of testosterone which results in male hypogonadism.2 Testosterone is important for the healthy growth and maintenance of male sex organs as well as secondary sex characteristics.2 Deficiency of testosterone which result in male hypogonadism can present with a range of symptoms which includes impotence, reduced sexual desire, tired, lack of energy, regression of secondary sexual characteristics and depression.2 http://www.virtualmedicalcentre.com/drugs/climara/2136 Climara (oestradiol) is identical to endogenous human oestradiol. Climara therefore suppresses FSH and LH secretion, and thus may be used to alleviate symptoms caused by oestrogen deficiency. Climara also has favourable effects on bone mineral density and on urogenital oestrogen deficiency syndrome in menopausal women. The transdermal adminstration of Climaranbsp;causesnbsp;a lower first-pass effect when compared with oral administration of oestradiol. Transdermal delivery also more closely resembles the natural plasma level of oestradiol. This means that the ratio of oestradiol to oestrone http://www.virtualmedicalcentre.com/drugs/depo-provera/2142 Medroxyprogesterone acetate is a progestational agent. It transforms proliferative into secretory endometrium, maintains pregnancy, delays parturition and suppresses ovulation. Depo-Provera is thermogenic, and at high doses can be used to treat certain cancers, where it has corticoid-like activity. http://www.virtualmedicalcentre.com/drugs/depo-ralovera/2143 Medroxyprogesterone acetate is a progestational agent. It transforms proliferative into secretory endometrium, maintains pregnancy, delays parturition and suppresses ovulation. Depo-Ralovera is thermogenic, and at high doses can be used to treat certain cancers, where it has corticoid-like activity. http://www.virtualmedicalcentre.com/drugs/estraderm/2151 Oestradiol (an oestrogen) is a steroid hormone that freely diffuses across the plasma membrane into the cytosol of cells. Once inside the cell, oestradiol binds to the intracellular oestrogen receptor to form a hormone-receptor complex, which subsequently dimerizes (ie. two oestradiol-receptor complexes bind to form a dimer). This dimer complex migrates to the cell nucleus where it interacts with oestrogen response elements present in DNA and promotes or inhibits the transcription of specific genes. These actions form the basis of the physiological effects of oestradiol.3 Oestradiol receptors http://www.virtualmedicalcentre.com/drugs/estrofem/2153 Estrofem (oestradiol) is identical to endogenous human oestradiol. Estrofem therefore suppresses FSH and LH secretion, and thus may be used to alleviate symptoms caused by oestrogen deficiency. Estrofem has favorable effects on the LDL to HDL ratio and on urogenital oestrogen deficiency syndrome.1-3 http://www.virtualmedicalcentre.com/drugs/femoston/2154 The oestradiol component of Femoston, exerts similar pharmacological actions as endogenous oestradiol hormone. It alleviates the vasomotor symptomsnbsp;that results fromnbsp;a reduction in oestrogen production associated with natural or artificial menopause. Replacement therapy with oestrogen has also been shown to impede or cease postmenopausal bone mass density loss i.e. osteoporosis.Oestrogen treatment alone has been demonstrated to increase endometrial carcinoma risk. In a uterus that has been primed by oestrogen, a secretory endometrium can be induced by including dydrogesterone into th http://www.virtualmedicalcentre.com/drugs/genoral/2156 Genoral contains oestrone, a substancenbsp;similar tonbsp;oestrogen. Oestrogen binds to certain receptors in oestrogen-specific tissues that promote oestrogenic effects.1 http://www.virtualmedicalcentre.com/drugs/kliogest/2158 Oestradiol helps to relieve the symptoms of postmenopause, whilenbsp;norethisterone prevents overgrowth of the endometrium in those patients who have an intact uterus.1,2 http://www.virtualmedicalcentre.com/drugs/kliovance/2159 Kliovance is used as replacement therapy for oestrogen. Oestradiol is the major type of oestrogen secreted by the ovaries. During and after menopause, womennbsp;the secretion of oestrogen is decreased. This can lead to the symptoms often associated with menopause, such as atrophic vaginitis and poor thermoregulation. This decreased secretion can also be linked with osteoporosis, as oestrogen plays a role in skeletal development. Therefore, by acting as an oestrogen replacement, Kliovance acts to reduce the effects of decreased oestrogen levels.1,2 The norethisterone acetate in Kliovance is a http://www.virtualmedicalcentre.com/drugs/medroxyhexal/2161 Medroxyprogesterone acetate is a progestational agent. It transforms proliferative into secretory endometrium, maintains pregnancy, delays parturition and suppresses ovulation. Medroxyhexal is thermogenic, and at high doses can be used to treat certain cancers, where it has corticoid-like activity. http://www.virtualmedicalcentre.com/drugs/menorest/2164 Menorest is used as replacement therapy for oestrogen .Oestradiol is the major oestrogen secreted by the ovaries. During and after menopause women encounter a decrease in the secretion of oestrogen. This decrease can lead to the symptoms often associated with menopause such as; atrophic vaginitis and poor thermoregulation. The loss of oestrogen secretion can also be linked with osteoporosis as oestrogen plays a role in skeletal development. Therefore by replacing the oestrogen via oestradiol patch. Menorest acts to reduces the effects of decreased oestrogen levels.1,2 http://www.virtualmedicalcentre.com/drugs/premia/2171 Premia 2.5 Continuous and Premia 5 Continuous combination tablets are hormone replacement therapy packs. Premia 5 and Premia 10 are composite hormone replacement therapy packs.Pharmacology. Oestrogen production occurs primarily in the ovarian follicles in women from the menarche to the menopause and is important in the development and maintenance of the female urogenital system and secondary sex characteristics.During the menopause the ovarian oestrogen production decreases and in postmenopausal women, when the ovaries have ceased to function, only a small amount of oestrogen is still produced http://www.virtualmedicalcentre.com/drugs/provelle-28/2179 Combination (oestrogen and progestagen) hormone replacement therapy.Pharmacology. Oestrogen production occurs primarily in the ovarian follicles in women from the menarche to the menopause and is important in the development and maintenance of the female urogenital system and secondary sex characteristics.During the menopause the ovarian oestrogen production decreases and in postmenopausal women, when the ovaries have ceased to function, only a small amount of oestrogen is still produced.This decrease and eventual cessation of oestrogen production in perimenopausal and postmenopausal women, re http://www.virtualmedicalcentre.com/drugs/provera/2180 Pharmacology. Animal. Medroxyprogesterone acetate induces responses in laboratory animals comparable to those caused by progesterone. It is more potent than progesterone. Medroxyprogesterone acetate induces glandular maturation in the endometrium, maintains pregnancy, delays parturition, inhibits ovulation and suppresses oestrous cycles. It is devoid of androgenic and oestrogenic activity. In selected animal tests it has some adrenal corticoid-like activity and in dogs increases serum growth hormone levels.Human. Provera is a progestational agent. When administered in recommended doses to wome http://www.virtualmedicalcentre.com/drugs/ralovera/2182 Medroxyprogesterone acetate is a progestational agent. It transforms proliferative into secretory endometrium, maintains pregnancy, delays parturition and suppresses ovulation. Ralovera is thermogenic, and at high doses can be used to treat certain cancers, where it has corticoid-like activity. http://www.virtualmedicalcentre.com/drugs/sandrena/2183 Pharmacology. Sandrena is an alcohol based, percutaneously applied gel for hormone replacement therapy with oestradiol as its active ingredient. The pharmacodynamics of Sandrena are similar to those of oral oestrogens but the major difference to oral administration lies in the pharmacokinetic profile. The clinical efficacy of Sandrena in the treatment of menopausal symptoms is comparable to that of peroral oestrogen. Combined with medroxyprogesterone acetate, percutaneous oestradiol treatment lowers total cholesterol without reducing the HDL cholesterol level. Clinical trials. Preclinical safe http://www.virtualmedicalcentre.com/drugs/testosterone-implants/2186 Testosterone is a naturally occurring hormone made by the Leydig cells in the testes under the control of the anterior pituitary gland, which controls the development and maintenance of the male sex organs and the male secondary sex characteristics. http://www.virtualmedicalcentre.com/drugs/bromocriptine-bc/2189 Bromocriptine-BC contains the active component bromocriptine that belongs to a class of drugs called the ergot alkaloids. Its primary action involves stimulation of dopamine receptors principally within the central nervous system. Bromocriptine does not cause uterine contraction or vasoconstriction like other drugs within its class.3 Bromocriptines action causes inhibition of prolactin secretion from lactotrophs within the anterior pituitary without altering release of other compounds (if given at recommended doses). Bromocriptine has been shown to arrest the growth or to reduce the size of p http://www.virtualmedicalcentre.com/drugs/bromolactin/2191 Bromocriptine has a pharmacological spectrum unlike that of most classical ergot compounds, having no uterotonic and little vasoconstrictor activity. Its principal effects derive from dopaminergic receptor stimulant activity. It inhibits prolactin secretion and the effect can be demonstrated after single or repeated oral administration of the drug. Moreover, the effect is relatively specific in that doses necessary to produce inhibition of prolactin secretion do not interfere with release of gonadotrophins or thyrotrophin. However, bromocriptine elevates growth hormone for a few hours after ea http://www.virtualmedicalcentre.com/drugs/humatrope/2199 Somatropin is a synthetic human growth hormone. It promotes the growth of skeletal and muscle tissues, stimulates protein breakdown and also has effects on fat and mineral metabolism. http://www.virtualmedicalcentre.com/drugs/kripton/2201 Bromocriptine has a pharmacological spectrum unlike that of most classical ergot compounds, having no uterotonic and little vasoconstrictor activity. Its principal effects derive from dopaminergic receptor stimulant activity. It inhibits prolactin secretion and the effect can be demonstrated after single or repeated oral administration of the drug. Moreover, the effect is relatively specific in that doses necessary to produce inhibition of prolactin secretion do not interfere with release of gonadotrophins or thyrotrophin. However, bromocriptine elevates growth hormone for a few hours after ea http://www.virtualmedicalcentre.com/drugs/parlodel/2207 Bromocriptine has a pharmacological spectrum unlike that of most classical ergot compounds, having no uterotonic and little vasoconstrictor activity. Its principal effects derive from dopaminergic receptor stimulant activity. It inhibits prolactin secretion and the effect can be demonstrated after single or repeated oral administration of the drug. Moreover, the effect is relatively specific in that doses necessary to produce inhibition of prolactin secretion do not interfere with release of gonadotrophins or thyrotrophin. However, bromocriptine elevates growth hormone for a few hours after ea http://www.virtualmedicalcentre.com/drugs/pitressin/2208 Pitressin exerts its antidiuretic effect by increasing the resorption of water by the renal tubules. Pitressin also acts as a vasoconstrictor, and causes contraction of the smooth muscle of the gastrointestinal tract and all parts of the vascular bed, especially the capillaries, arterioles and venules, thereby reducing blood flow to a particular area of the body. http://www.virtualmedicalcentre.com/drugs/sandostatin/2214 Octreotide is a synthetic analogue of naturally occurring somatostatin, that has similar effects but a longer duration of action. It inhibits the secretion of growth hormone, and of serotonin and the gastroenteropancreatic peptides such as gastrin, VIP, glucagon, insulin, secretin, motilin and pancreatic polypeptide. http://www.virtualmedicalcentre.com/drugs/sandostatin-lar/2215 Octreotide is a synthetic analogue of naturally occurring somatostatin, that has similar effects but a longer duration of action. It inhibits the secretion of growth hormone, and of serotonin and the gastroenteropancreatic peptides such as gastrin, VIP, glucagon, insulin, secretin, motilin and pancreatic polypeptide. http://www.virtualmedicalcentre.com/drugs/somatuline-la/2218 Somatuline LA consists of an active ingredient known as lanreotide, which acts as an inhibitory peptide (somastostain analogue) suppressing the secretion of a number of endocrines, neuroendocrine, exocrine and paracrine hormones (1,2,3). It has a marked affinity and selectivity for the peripheral somatostatin receptor and long duration of action than that of the natural somastostain (1,2,3). The pharmacological features of this drug make it a suitable candidate for treatment of acromegaly. http://www.virtualmedicalcentre.com/drugs/actos/2227 Actos is a thiazolidinedione antidiabetic agent that depends on the presence of insulin for its mechanism of action. Actos decreases insulin resistance in the periphery and in the liver resulting in increased insulin dependent glucose disposal and decreased hepatic glucose output. Unlike sulfonylureas, pioglitazone is not an insulin secretagogue.Pioglitazone is a potent and highly selective agonist for peroxisome proliferator activated receptor gamma (PPARgamma). PPAR receptors are found in tissues important for insulin action such as adipose tissue, skeletal muscle and liver. Activation of PP http://www.virtualmedicalcentre.com/drugs/amaryl/2228 Glimepiride is a sulfonylurea antidiabetic agent which decreases blood glucose concentrations. The primary mechanism of action of glimepiride appears to be dependent on stimulating the release of insulin from functioning pancreatic beta cells. Glimepiride acts in concert with glucose by improving the sensitivity of beta cells to physiological glucose stimulus, resulting in insulin secretion in the rhythm of meals. http://www.virtualmedicalcentre.com/drugs/avandia/2229 The active ingredient in Avandia is rosiglitazone.nbsp;Rosiglitazone isnbsp;a selective and potent agonist ofnbsp;PPARgamma (peroxisome proliferator-activated gamma) nuclear receptors, whichnbsp;have a rolenbsp;in the regulation of genes involved in lipid and glucose metabolism control.2Rosiglitazone improves insulin sensitivity in adipose tissue, skeletal muscle and the liver.1Rosiglitazonenbsp;helps improve glucose metabolism by decreasing hepatic glucose output, andnbsp;lowering circulating insulin and free fatty acids.1,2 http://www.virtualmedicalcentre.com/drugs/chem-mart-metformin/2230 Biguanides are orally active hypoglycaemic agents that do not require functioning B cells. Their action is complex and incompletely understood. Metformin works by increasing the biological efficacy of insulin, thereby increasing peripheral uptake of glucose. Metformin does not stimulate insulin release but does require the presence of insulin to exert its antihyperglycaemic effect. Its possible mechanisms of action include inhibition of gluconeogenesis in the liver, delay in glucose absorption from the gastrointestinal tract and an increase in peripheral uptake of glucose. Metformin also has http://www.virtualmedicalcentre.com/drugs/daonil/2231 Daonil lowers the blood glucose levelnbsp;by stimulating the release of insulin from the pancreas. Itnbsp;improves sensitivity of beta cells to physiological glucose stimulus and leads to an insulin secretion in the rhythm of meals.2 http://www.virtualmedicalcentre.com/drugs/diabex/2232 Metformin is an oral biguanide antihyperglycaemic agent which increases sensitivity of the available exogenous and endogenous insulin.1 It increases the peripheral uptake of glucose and reduces hepatic glucose production. It does not stimulate insulin release but does require presence of insulin to exert its blood glucose lowering effect.2 http://www.virtualmedicalcentre.com/drugs/diaformin/2233 Biguanides are orally active hypoglycaemic agents that do not require functioning B cells. Their action is complex and incompletely understood. Metformin works by increasing the biological efficacy of insulin, thereby increasing peripheral uptake of glucose. Metformin does not stimulate insulin release but does require the presence of insulin to exert its antihyperglycaemic effect. Its possible mechanisms of action include inhibition of gluconeogenesis in the liver, delay in glucose absorption from the gastrointestinal tract and an increase in peripheral uptake of glucose. Metformin also ha http://www.virtualmedicalcentre.com/drugs/diamicron/2234 Gliclazide is a hypoglycaemic agent from the sulfonylurea class. It requires some residual islet cell function to have its effect. It stimulates insulin secretion from pancreatic islet cells and also increases the sensitivity of these islet cells to a glucose stimulus. Gliclazide restores the first-phase insulin secretion that has become diminished in non-insulin dependent diabetic (NIDDM) patients. Gliclazide has also been shown to have extrapancreatic effects, including improvement in insulin-mediated glucose utilisation and potentiation of postreceptor insulin sensitive pathways. It is http://www.virtualmedicalcentre.com/drugs/diamicron-mr/2235 Gliclazide is a hypoglycaemic agent from the sulfonylurea class. It requires some residual islet cell function to have its effect. It stimulates insulin secretion from pancreatic islet cells and also increases the sensitivity of these islet cells to a glucose stimulus. Gliclazide restores the first-phase insulin secretion that has become diminished in non-insulin dependent diabetic (NIDDM) patients. Gliclazide has also been shown to have extrapancreatic effects, including improvement in insulin-mediated glucose utilisation and potentiation of postreceptor insulin sensitive pathways. It is http://www.virtualmedicalcentre.com/drugs/genrx-metformin/2236 Biguanides are orally active hypoglycaemic agents that do not require functioning B cells. Their action is complex and incompletely understood. Metformin works by increasing the biological efficacy of insulin, thereby increasing peripheral uptake of glucose. Metformin does not stimulate insulin release but does require the presence of insulin to exert its antihyperglycaemic effect. Its possible mechanisms of action include inhibition of gluconeogenesis in the liver, delay in glucose absorption from the gastrointestinal tract and an increase in peripheral uptake of glucose. Metformin also has http://www.virtualmedicalcentre.com/drugs/glimel/2237 Glibenclamide is an orally active hypoglycaemic agent. It acts to lower the blood glucose in both healthy individuals and type 2 diabetic patients by stimulating the release of insulin from the pancreas. Subsequently, the pancreatic beta-cells must be functional for the drug to be effective. Glibenclamide acts together with glucose (improved sensitivity of beta-cells to physiological glucose stimulus), leading to the rhythmic secretion of insulin. The hypoglycaemic action associated with short-term therapy may also include a reduction in basal hepatic glucose production and enhancement of peri http://www.virtualmedicalcentre.com/drugs/glucobay/2238 Acarbose works via the gastrointestinal tract. It inhibits the intestinal enzymes (alpha-glucosidases) involved in the degradation of ingested disaccharides, oligosaccharides, polysaccharides, but not monosaccharides. This therefore leads to a delayed digestion of these carbohydrates. As a result, absorbable monosaccharides (such as dextrose) originating from these carbohydrates are released more slowly and therefore are taken up into the blood more slowly. However, the absorption of monosaccharides is not affected. By this, acarbose reduces the post-prandial increase in blood glucose levels, http://www.virtualmedicalcentre.com/drugs/glucohexal/2239 Biguanides are orally active hypoglycaemic agents that do not require functioning B cells. Their action is complex and incompletely understood. Metformin works by increasing the biological efficacy of insulin, thereby increasing peripheral uptake of glucose. Metformin does not stimulate insulin release but does require the presence of insulin to exert its antihyperglycaemic effect. Its possible mechanisms of action include inhibition of gluconeogenesis in the liver, delay in glucose absorption from the gastrointestinal tract and an increase in peripheral uptake of glucose. Metformin also has http://www.virtualmedicalcentre.com/drugs/glucomet/2240 Biguanides are orally active hypoglycaemic agents that do not require functioning B cells. Their action is complex and incompletely understood. Metformin works by increasing the biological efficacy of insulin, thereby increasing peripheral uptake of glucose. Metformin does not stimulate insulin release but does require the presence of insulin to exert its antihyperglycaemic effect. Its possible mechanisms of action include inhibition of gluconeogenesis in the liver, delay in glucose absorption from the gastrointestinal tract and an increase in peripheral uptake of glucose. Metformin also has http://www.virtualmedicalcentre.com/drugs/glucophage/2241 Biguanides are orally active hypoglycaemic agents that do not require functioning B cells. Their action is complex and incompletely understood. Metformin works by increasing the biological efficacy of insulin, thereby increasing peripheral uptake of glucose. Metformin does not stimulate insulin release but does require the presence of insulin to exert its antihyperglycaemic effect. Its possible mechanisms of action include inhibition of gluconeogenesis in the liver, delay in glucose absorption from the gastrointestinal tract and an increase in peripheral uptake of glucose. Metformin also has http://www.virtualmedicalcentre.com/drugs/glyade/2242 Gliclazide is a hypoglycaemic agent from the sulfonylurea class. It requires some residual islet cell function to have its effect. It stimulates insulin secretion from pancreatic islet cells and also increases the sensitivity of these islet cells to a glucose stimulus. Gliclazide restores the first-phase insulin secretion that has become diminished in non-insulin dependent diabetic (NIDDM) patients. Gliclazide has also been shown to have extrapancreatic effects, including improvement in insulin-mediated glucose utilisation and potentiation of postreceptor insulin sensitive pathways. It is th http://www.virtualmedicalcentre.com/drugs/healthsense-metformin/2243 Biguanides are orally active hypoglycaemic agents that do not require functioning B cells. Their action is complex and incompletely understood. Metformin works by increasing the biological efficacy of insulin, thereby increasing peripheral uptake of glucose. Metformin does not stimulate insulin release but does require the presence of insulin to exert its antihyperglycaemic effect. Its possible mechanisms of action include inhibition of gluconeogenesis in the liver, delay in glucose absorption from the gastrointestinal tract and an increase in peripheral uptake of glucose. Metformin also has http://www.virtualmedicalcentre.com/drugs/metformin-bc/2245 Biguanides are orally active hypoglycaemic agents that do not require functioning B cells. Their action is complex and incompletely understood. Metformin works by increasing the biological efficacy of insulin, thereby increasing peripheral uptake of glucose. Metformin does not stimulate insulin release but does require the presence of insulin to exert its antihyperglycaemic effect. Its possible mechanisms of action include inhibition of gluconeogenesis in the liver, delay in glucose absorption from the gastrointestinal tract and an increase in peripheral uptake of glucose. Metformin also ha http://www.virtualmedicalcentre.com/drugs/nidem/2247 Gliclazide is a hypoglycaemic agent from the sulfonylurea class. It requires some residual islet cell function to have its effect. It stimulates insulin secretion from pancreatic islet cells and also increases the sensitivity of these islet cells to a glucose stimulus. Gliclazide restores the first-phase insulin secretion that has become diminished in non-insulin dependent diabetic (NIDDM) patients. Gliclazide has also been shown to have extrapancreatic effects, including improvement in insulin-mediated glucose utilisation and potentiation of postreceptor insulin sensitive pathways. It is th http://www.virtualmedicalcentre.com/drugs/eutroxsig/2249 The active ingredient in Eutroxsig is thyroxine sodium, a monosodium salt derived from thyroxine, the principal hormone secreted by the thyroid gland. Thyroxine sodium acts like endogenous thyroid hormones to increase metabolic rate and regulate cell growth and differentiation. It also regulates thyroid function.1 http://www.virtualmedicalcentre.com/drugs/neo-mercazole/2250 Carbimazole exerts its antithyroid effect by blocking the binding of iodine through inhibition of the iodination of tyrosine. It also has some effect on peroxidase, which is a catalyst in the synthesis of thyroxine by the thyroid gland. http://www.virtualmedicalcentre.com/drugs/oroxine/2251 Thyroxine sodium, also known as levothyroxine sodium, is a monosodium salt of the levo isomer of thyroxine, the principal secretion of the thyroid gland. Eutroxsig is used as thyroid replacement therapy for the treatment of hypothyroidism. The principal pharmacological effect of thyroid hormones is to increase the metabolic rate of body tissues. Thyroid hormones are also involved in the regulation of cell growth and differentiation. Thyroxine is the major component of normal secretions of the thyroid gland; therefore it is the essential determinant of normal thyroid function. http://www.virtualmedicalcentre.com/drugs/propylthiouracil/2252 Propylthiouracil blocks the peripheral conversion of thyroxine (T4) to triiodithyronine (T3) by inhibiting the incorporation of iodide into tyrosine. http://www.virtualmedicalcentre.com/drugs/sodium-iodide-capsules-therapy/2253 After oral administration, sodium iodide is rapidly absorbed and distributed in the extracellular fluid. A proportion is taken up by the functioning thyroid tissue, where it disrupts the functioning of the cells, thereby decreasing thyroid hormone production and eliminating symptoms of hyperthyroidism. http://www.virtualmedicalcentre.com/drugs/tertroxin/2254 Lithyronine sodium is a naturally occurring thyroid hormone. Its biological action is similar to thyroxine, however its effects develop in a few hours and disappear within 24 to 48hours of stopping treatment. Thyroxine is a hormone produced by the thyroid gland that has several actions such as a) oxygen use and basal metabolic rate, b) cellular metabolism, and c) growth and development. http://www.virtualmedicalcentre.com/drugs/actonel/2255 Risedronate inhibits bone resorption by inhibiting the activity of osteoclasts. http://www.virtualmedicalcentre.com/drugs/aredia/2256 Disodium pamidronate is an inhibitor of osteoclastic bone resorption. Osteoclast precursors migrate to bone, where they eventually mature into resorbing osteoclasts. Mature osteoclasts are responsible for the resorption of bone and resulting calcium release into the bloodstream. This occurs at a certain rate normally, but may increase out of control in certain diseases. Disodium pamidronate suppresses the initial migration of osteoclast precursors into bone, thereby preventing bone resorption and associated hypercalcaemia.1,2 http://www.virtualmedicalcentre.com/drugs/bonefos/2257 Clodronate is a bisphosphonate that works by reducing the activity of osteoclasts in the bone which in turn reduces bone breakdown.1-3 It has a strong affinity for calcium phosphate is therefore is distributed mainly in the skeleton.2 In bone metastases or bone lesions, clodronate works by:2 Inhibiting the progression of present lesions and formation of new ones and: reducing pain by preventing abnormal tumor induced osteolysis. Reduces the risk of fractures. In Hypercalcaemia, clodronate works by:2 Reducing high levels of serum calcium. http://www.virtualmedicalcentre.com/drugs/calcijex/2258 Calcitriol is involved in the regulation of calcium homeostasis. It increases intestinal absorption and renal reabsorption of both calcium and phosphate. The resulting increase in calcium levels promotes bone mineralisation. http://www.virtualmedicalcentre.com/drugs/citrihexal/2259 Calcitriol is involved in the regulation of calcium homeostasis. It increases intestinal absorption and renal reabsorption of both calcium and phosphate. The resulting increase in calcium levels promotes bone mineralisation. http://www.virtualmedicalcentre.com/drugs/didrocal/2260 Calcium carbonate neutralises excess acid produced by the stomach, thereby reducing the burning symptoms associated with indigestion. Sustained calcium levels in the blood also help to prevent excess bone resorption associated with osteoporosis. http://www.virtualmedicalcentre.com/drugs/disodium-pamidronate-concentrated-injection-dbl/2262 Pamidronate inhibits bone resorption by inhibiting the activity of osteoclasts. http://www.virtualmedicalcentre.com/drugs/evista/2263 Raloxifene is a selective oestrogen receptor modulator (SERM). It has oestrogen agonistic effects on bone mass and lipid increasing bone density and lowering lipid levels. It also has oestrogen antagonistic effects at other oestrogen-receptive tissues such as the breast and uterus. http://www.virtualmedicalcentre.com/drugs/fosamax/2264 Fosamax contains alendronate sodium, which is a bisphosphonate that preferentially distributes to sites of bone resorption to hinder osteoclastic bone resorption.1 http://www.virtualmedicalcentre.com/drugs/kosteo/2265 Calcitriol is involved in the regulation of calcium homeostasis. It increases intestinal absorption and renal reabsorption of both calcium and phosphate. The resulting increase in calcium levels promotes bone mineralisation. http://www.virtualmedicalcentre.com/drugs/pamisol/2267 Pamidronate is a bisphosphonate that works by reducing the activity of osteoclasts in the bone, which in turn reduces bone breakdown.1-3 In hypercalcaemia, pamidronate works by reducing levels of serum calcium.2 http://www.virtualmedicalcentre.com/drugs/phosphate-sandoz/2268 Oral administration of phosphate produces a fall in serum calcium in patients with hypercalcaemia. This is because phosphate binds calcium ions in the gut, thereby preventing its absorption into the blood. The tablets also contain sodium ions which aid the correction of dehydration and sodium depletion that is seen in hypercalcaemia. http://www.virtualmedicalcentre.com/drugs/rocaltrol/2269 Calcitriol is involved in the regulation of calcium homeostasis. It increases intestinal absorption and renal reabsorption of both calcium and phosphate. The resulting increase in calcium levels promotes bone mineralisation. http://www.virtualmedicalcentre.com/drugs/sitriol/2270 Calcitriol is involved in the regulation of calcium homeostasis. It increases intestinal absorption and renal reabsorption of both calcium and phosphate. The resulting increase in calcium levels promotes bone mineralisation. http://www.virtualmedicalcentre.com/drugs/zometa/2272 Zoledronic acid is a bisphosphonate that inhibits osteoclastic bone resorption. Bisphosphonates have a high affinity for mineralised bone. The exact mechanism of inhibition of osteoclastic activity remains unclear. In long-term animal studies, Zoledronic acid has been shown to inhibit bone resorption and increase bone mineralisation without adversely affecting bone formation or mechanics. Clinical studies in tumour-induced hypercalcaemia demonstrated that Zoledronic acid decreases both the serum calcium and the urinary calcium excretion.1,3 Preclinical studies demonstrated that, in addition t http://www.virtualmedicalcentre.com/drugs/aranesp/2275 Darbepoetin Alfa is a recombinant glycoprotein, which binds to erythropoietin receptors on erythroid progenitor cells which are stimulated to proliferate and mature to increase erythropoiesis which also increases reticulocyte count, hematocrit, and haemoglobin concentration. 1,2,3 http://www.virtualmedicalcentre.com/drugs/eprex/2276 Eprex is a recombinant glycoprotein which mimics the endogenous erythropoietin in the stimulation of red blood cell production. Eprex binds to erythropoietin receptors on erythroid progenitor cells in the kidney. Eprex acts by stimulating erythropoesis, increasing reticulocyte count, haematocrit and haemoglobin concentration.1,2 Its clinical effect is not observed for at least up to 2 weeks after the commencement of therapy as erythroid progenitors need several days to mature and be released into the circulation.2 http://www.virtualmedicalcentre.com/drugs/ferrum-h/2277 Iron is an element used for the conctruction of haemoglobin and myoglobin.1-3 Iron polymaltose, when injected caused a local inflammatory reaction and undergoes active reabsorption where it is transfer to local lymph nodes without being broken down.2 The complex then enters the bloodstream and is taken up by cells of reticuloendothelial system where it slowly gets ionised to Fe3+ and polymaltose. Most of Fe3+ gets bound to transferring which then supplied to the bone marrow where it is integrated into haemoglobin. The remainder is kept in ferritin or myoglobin or haem containing enzymes http://www.virtualmedicalcentre.com/drugs/aclin/2278 Sulindac is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. After it is absorbed Sulindac is metabolised to form sulphide metabolite and an inactive sulfone metabolite. The sulphide metabolite is the one that actively inhibits prostaglandin synthesis. By inhibiting prostaglandin synthesis Sulindac has anti-inflammatory, analgesic and antipyretic properties an http://www.virtualmedicalcentre.com/drugs/actiprofen/2280 Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Ibuprofen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/aleve/2281 Naproxen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Naproxen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/anaprox/2282 Naproxen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Naproxen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/arthrexin/2283 Indomethacin is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Indomethacin has anti-inflammatory, analgesic, and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/brufen/2285 Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Ibuprofen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/bugesic/2286 Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Ibuprofen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/celebrex/2288 Celecoxib is a COX-2 selective nonsteroidal anti-inflammatory drug (NSAID). NSAIDs have analgesic, antipyretic and anti-inflammatory actions through the blockade prostaglandin synthesis by inhibiting cyclo-oxygenase (COX). COX has 2 forms COX-1 and COX-2. Celecoxib selectively inhibits COX-2 which results in its anti-inflammatory and analgesic actions. In theory the lack of inhibition of COX-1 means than celecoxib should be less likely to produce gastrointestinal and antiplatelet side effects.1, 3 http://www.virtualmedicalcentre.com/drugs/clinoril/2292 Sulindac is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. After it is absorbed Sulindac is metabolised to form sulphide metabolite and an inactive sulfone metabolite. The sulphide metabolite is the one that actively inhibits prostaglandin synthesis. By inhibiting prostaglandin synthesis Sulindac has anti-inflammatory, analgesic and antipyretic prop http://www.virtualmedicalcentre.com/drugs/crysanal/2293 Naproxen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Naproxen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/diclofenac-bc/2294 Diclofenac is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain, inflammation and fever by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase (COX) an enzyme involved in the pathway of prostaglandin synthesis. There are two form of COX - COX1 and COX2. Diclofenac inhibits both of these COX enzymes. By inhibiting prostaglandin synthesis Diclofenac has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and pro http://www.virtualmedicalcentre.com/drugs/diclohexal/2295 Diclofenac is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain, inflammation and fever by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase (COX) an enzyme involved in the pathway of prostaglandin synthesis. There are two form of COX – COX1 and COX2. Diclofenac inhibits both of these COX enzymes By inhibiting prostaglandin synthesis Diclofenac has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and prom http://www.virtualmedicalcentre.com/drugs/dynastat/2298 In the body Dynastat (parecoxib) is bioconverted into the drug valdecoxib. Valdecoxib is the drug moiety responsible for the effects seen when parecoxib is administered. As a selective inhibitor of the COX-2 (cyclooxygenase-2) isozyme, valdecoxib prevents formation of prostanoid inflammatory mediators. As a result, Dynastat has analgesic, anti-inflammatory and antipyretic actions. Dynastat does not inhibit the COX-1 isozyme, andnbsp;therefore it is thought thatnbsp;it may decrease the risk of gastrointestinal adverse events in comparison to non-selective NSAIDs.1,2 http://www.virtualmedicalcentre.com/drugs/feldene/2299 The mode of action of Piroxicam has not been fully established however it is known that piroxicam acts in several ways to diminish immune and inflammation responses. Piroxicam is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit Cyclo-oxygenase (COX), an enzyme involved in the pathway of prostaglandin synthesis. There are two forms of Cyclo-oxygenase, COX-1 and COX-2. Piroxicam inhibits both forms. - Piroxicam inhibits neutro http://www.virtualmedicalcentre.com/drugs/fenac-fenac-25/2300 Diclofenac is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain, inflammation and fever by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase (COX) an enzyme involved in the pathway of prostaglandin synthesis. There are two form of COX – COX1 and COX2. Diclofenac inhibits both of these COX enzymes By inhibiting prostaglandin synthesis Diclofenac has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and prom http://www.virtualmedicalcentre.com/drugs/genrx-diclofenac/2302 Diclofenac is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain, inflammation and fever by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase (COX) an enzyme involved in the pathway of prostaglandin synthesis. There are two form of COX - COX1 and COX2. Diclofenac inhibits both of these COX enzymes By inhibiting prostaglandin synthesis Diclofenac has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and prom http://www.virtualmedicalcentre.com/drugs/genrx-piroxicam-capsules/2303 The mode of action of Piroxicam has not been fully established however it is known that piroxicam acts in several ways to diminish immune and inflammation responses. Piroxicam is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit Cyclo-oxygenase (COX), an enzyme involved in the pathway of prostaglandin synthesis. There are two forms of Cyclo-oxygenase, COX-1 and COX-2. Piroxicam inhibits both forms. Piroxicam inhibits: Neutrop http://www.virtualmedicalcentre.com/drugs/genrx-piroxicam-dispersible-tablets/2304 The mode of action of Piroxicam has not been fully established however it is known that piroxicam acts in several ways to diminish immune and inflammation responses. Piroxicam is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit Cyclo-oxygenase (COX), an enzyme involved in the pathway of prostaglandin synthesis. There are two forms of Cyclo-oxygenase, COX-1 and COX-2. Piroxicam inhibits both forms. Piroxicam inhibits: Neutrop http://www.virtualmedicalcentre.com/drugs/healthsense-diclofenac/2305 Diclofenac is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain, inflammation and fever by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase (COX) an enzyme involved in the pathway of prostaglandin synthesis. There are two form of COX - COX1 and COX2. Diclofenac inhibits both of these COX enzymes By inhibiting prostaglandin synthesis Diclofenac has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and prom http://www.virtualmedicalcentre.com/drugs/healthsense-piroxicam-capsules/2306 The mode of action of Piroxicam has not been fully established however it is known that piroxicam acts in several ways to diminish immune and inflammation responses. Piroxicam is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit Cyclo-oxygenase (COX), an enzyme involved in the pathway of prostaglandin synthesis. There are two forms of Cyclo-oxygenase, COX-1 and COX-2. Piroxicam inhibits both forms. Piroxicam inhibits: Neutrop http://www.virtualmedicalcentre.com/drugs/healthsense-piroxicam-dispersible-tablets/2307 The mode of action of Piroxicam has not been fully established however it is known that piroxicam acts in several ways to diminish immune and inflammation responses. Piroxicam is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit Cyclo-oxygenase (COX), an enzyme involved in the pathway of prostaglandin synthesis. There are two forms of Cyclo-oxygenase, COX-1 and COX-2. Piroxicam inhibits both forms. Piroxicam inhibits: neutrop http://www.virtualmedicalcentre.com/drugs/hexal-diclac-anti-inflammatory-tablets/2308 Diclofenac is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain, inflammation and fever by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase (COX) an enzyme involved in the pathway of prostaglandin synthesis. There are two form of COX - COX1 and COX2. Diclofenac inhibits both of these COX enzymes By inhibiting prostaglandin synthesis Diclofenac has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and prom http://www.virtualmedicalcentre.com/drugs/indocid/2309 Indomethacin inhibits the synthesis of prostaglandins by inhibiting cyclooxygenase, the enzyme that converts arachidonic acid to Prostaglandin G2. There are two known forms of cyclooxygenase - COX-1 COX-2. Prostaglandins are involved in the mediation of pain and have been shown to sensitise afferent nerves and potentiate the action of bradykinin in inducing pain in animal models. Prostaglandins are also mediators of inflammation and fever. By inhibiting prostaglandin synthesis indomethacin is effective in relieving pain, swelling and other symptoms and signs of inflammation. Although http://www.virtualmedicalcentre.com/drugs/inza/2310 The exact mechanism of Naprosyn’s anti-inflammatory action is unknown. Naproxen has anti-inflammatory, anti-pyretic and analgesic properties. It blocks cyclo-oxygenase and therefore inhibits prostaglandin synthetase. http://www.virtualmedicalcentre.com/drugs/mobic/2312 Meloxicam is a selective COX-2 NSAID.1-3 The inhibition of cyclo-oxygenase-1 (COX-1) results in the anti-platelet effects associated with nonselective NSAIDs.1-3 The inhibition of COX-2 is associated with anti-inflammatory and analgesic properties, and selective COX-2 NSAIDs may cause less gastro toxicity thannbsp;is seen with nonselective NSAIDs.1-3 http://www.virtualmedicalcentre.com/drugs/mobilis/2313 The mode of action of Piroxicam has not been fully established however it is known that piroxicam acts in several ways to diminish immune and inflammation responses. Piroxicam is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit Cyclo-oxygenase (COX), an enzyme involved in the pathway of prostaglandin synthesis. There are two forms of Cyclo-oxygenase, COX-1 and COX-2. Piroxicam inhibits both forms Piroxicam inhibits neutroph http://www.virtualmedicalcentre.com/drugs/naprogesic/2314 Naproxen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Naproxen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/naprosyn/2315 The exact mechanism of Naprosyns anti-inflammatory action is unknown. Naproxen has anti-inflammatory, anti-pyretic and analgesic properties. It blocks cyclo-oxygenase and therefore inhibits prostaglandin synthetase. http://www.virtualmedicalcentre.com/drugs/naprosyn-sr/2316 Naproxen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Naproxen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/nurofen/2317 Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Ibuprofen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/nurolasts/2320 Naproxen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Naproxen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/orudis/2321 Ketoprofen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Ketoprofen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/oruvail-sr/2323 Nonsteroidal anti-inflammatory drug.Pharmacology. Animal pharmacological studies have shown that ketoprofen has anti-inflammatory, analgesic and antipyretic properties. It also inhibits prostaglandin synthetase. Ketoprofen has been shown to possess antibradykinin activity in guinea pigs and mice. Inhibition of platelet aggregation has been demonstrated in rabbits.Ketoprofen reduces joint pain and inflammation and facilitates increase in mobility and functional independence. As with other NSAIDs, it does not cure the underlying disease.Pharmacokinetics. Absorption. The sustained release form of http://www.virtualmedicalcentre.com/drugs/pirohexal-d/2324 The mode of action of Piroxicam has not been fully established however it is known that piroxicam acts in several ways to diminish immune and inflammation responses. Piroxicam is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit Cyclo-oxygenase (COX), an enzyme involved in the pathway of prostaglandin synthesis. There are two forms of Cyclo-oxygenase, COX-1 and COX-2. Piroxicam inhibits both forms Piroxicam inhibits neutroph http://www.virtualmedicalcentre.com/drugs/proxen-sr/2326 Naproxen has anti-inflammatory, antipyretic and analgesic effects. The exact mechanism of action is not fully understood, although it is known that the anti-inflammatory effect of Naproxen is independent of the pituitary axis. Like other NSAIDs, it inhibits prostaglandin synthetase, an important enzyme in the production of prostaglandins. http://www.virtualmedicalcentre.com/drugs/rafen/2327 Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Ibuprofen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/piroxicam-capsules-terry-white-chemists/2330 The mode of action of Piroxicam has not been fully established however it is known that piroxicam acts in several ways to diminish immune and inflammation responses. Piroxicam is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit Cyclo-oxygenase (COX), an enzyme involved in the pathway of prostaglandin synthesis. There are two forms of Cyclo-oxygenase, COX-1 and COX-2. Piroxicam inhibits both forms. Piroxicam inhibits: Neutrop http://www.virtualmedicalcentre.com/drugs/piroxicam-dispersible-tablets-terry-white-chemists/2331 The mode of action of Piroxicam has not been fully established however it is known that piroxicam acts in several ways to diminish immune and inflammation responses. Piroxicam is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit Cyclo-oxygenase (COX), an enzyme involved in the pathway of prostaglandin synthesis. There are two forms of Cyclo-oxygenase, COX-1 and COX-2. Piroxicam inhibits both forms. Piroxicam inhibits: Neutrop http://www.virtualmedicalcentre.com/drugs/tri-profen/2334 Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Ibuprofen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/vioxx-no-longer-available/2335 http://www.virtualmedicalcentre.com/drugs/voltaren-rapid-125-25-50/2336 The active ingredient of Voltaren Rapidnbsp;is diclofenac,nbsp;anbsp;nonsteroidal anti inflammatory drug (NSAID). Diclofenacnbsp;has antipyretic, anti-inflammatory and analgesic actions. Diclofenacnbsp;works by inhibiting cyclooxygenase (COX), which has two forms (i.e. COX-1 and COX-2).nbsp;Thisnbsp;results in the inhibitionnbsp;of prostaglandin synthesis. Diclofenac is non-selective, and inhibits both COX-1 and COX-2. The inhibition of COX-1 results in anti-platelet effects and the inhibition of gastric cytoprotection. On the other hand, the inhibition of COX-2 results in anti-inflamm http://www.virtualmedicalcentre.com/drugs/plaquenil/2340 Plaquenil is an antimalarial agent that has a beneficial effect in mild discoid and systemic lupus erythematosus and in patients with rheumatoid arthritis. Its mechanism of action is not entirely understood. Plaquenil is highly active against the erythrocytic forms of Plasmodium vivax and P. malariae and most strains of P. falciparum. http://www.virtualmedicalcentre.com/drugs/baclo/2342 Baclo is an antispastic agent that acts on the spinal cord as well as centrally to cause central nervous system depression. It has a unique mechanism of action compared to other antispasmodic agents and works by stimulating GABAB receptors (as it is a gamma-aminobutyric acid (GABA ) analogue).1,3 This subsequently inhibits release of excitatory amino acids (glutamate and aspartate) and reduces muscle spasm. In the aforementioned conditions Baclo relieves painful spasm which can improve mobility and patient independence.3 Baclofen also provides pain relief but the mechanism and clinical signifi http://www.virtualmedicalcentre.com/drugs/baclohexal/2343 Baclohexal (baclofen) is an antispastic agent that acts on the spinal cord as well as centrally to cause central nervous system depression. It has a unique mechanism of action compared to other antispasmodic agents and works by stimulating GABAB receptors (as it is a gamma-aminobutyric acid (GABA ) analogue).1,2 This subsequently inhibits release of excitatory amino acids (glutamate and aspartate) and reduces muscle spasm. In the aforementioned conditions Baclohexal relieves painful spasm which can improve mobility and patient independence.3 Baclofen also provides pain relief but the mechanism http://www.virtualmedicalcentre.com/drugs/chem-mart-baclofen/2345 - Baclo is an antispastic agent that acts on the spinal cord - It also acts as a central nervous system depressant - It depresses monosynaptic and polysynaptic reflex transmission, most likely due to the stimulation on GABAB receptors which inturn inhibit the release of excitatory amino acids (e.g. glutamate and aspartate) - hence lessening nerve impulses to muscles in spasm. - Baclo also has an antinociceptive effect (pain relief) however the mechanism by which this occurs is not yet known http://www.virtualmedicalcentre.com/drugs/clofen/2346 - Baclo is an antispastic agent that acts on the spinal cord - It also acts as a central nervous system depressant - It depresses monosynaptic and polysynaptic reflex transmission, most likely due to the stimulation on GABAB receptors which inturn inhibit the release of excitatory amino acids (e.g. glutamate and aspartate) - hence lessening nerve impulses to muscles in spasm. - Baclo also has an antinociceptive effect (pain relief) however the mechanism by which this occurs is not yet known http://www.virtualmedicalcentre.com/drugs/dantrium-capsules/2347 Dantrium contains the active component Dantrolene which is a direct muscle relaxant.1 Following oral administration, Dantrium is slowly absorbed into the bloodstream where it reaches the muscle tissue itself to exert its effects. Studies have demonstrated that Dantrium works by uncoupling excitation and contraction of muscle fibres by inhibiting calcium release from the sarcoplasmic reticulum.1,3 This causes relaxation of the contractile state of skeletal muscles.3 Dantrium preferentially inhibits fast muscle fibres although all muscle fibres tend to be affected. In addition, Dantrium may have http://www.virtualmedicalcentre.com/drugs/dantrium-powder-for-injection/2348 Dantrium contains the active component Dantrolene sodium which is a direct muscle relaxant.2,4 Studies have demonstrated that Dantrolene works by uncoupling excitation and contraction of muscle fibres by inhibiting calcium release from the sarcoplasmic reticulum.4 In the acute anaesthetic setting this action is thought to inhibit the acute catabolism in skeletal muscle cells.4 This subsequently reverses the physiological, metabolic and biochemical changes associated with malignant hyperthermia. Dantrium tends to act specifically on skeletal muscle with little effect on cardiovascular and respi http://www.virtualmedicalcentre.com/drugs/genrx-baclofen/2350 - Baclo is an antispastic agent that acts on the spinal cord - It also acts as a central nervous system depressant - It depresses monosynaptic and polysynaptic reflex transmission, most likely due to the stimulation on GABAB receptors which inturn inhibit the release of excitatory amino acids (e.g. glutamate and aspartate) - hence lessening nerve impulses to muscles in spasm. - Baclo also has an antinociceptive effect (pain relief) however the mechanism by which this occurs is not yet known http://www.virtualmedicalcentre.com/drugs/healthsense-baclofen/2351 - Baclo is an antispastic agent that acts on the spinal cord - It also acts as a central nervous system depressant - It depresses monosynaptic and polysynaptic reflex transmission, most likely due to the stimulation on GABAB receptors which inturn inhibit the release of excitatory amino acids (e.g. glutamate and aspartate) - hence lessening nerve impulses to muscles in spasm. - Baclo also has an antinociceptive effect (pain relief) however the mechanism by which this occurs is not yet known http://www.virtualmedicalcentre.com/drugs/lioresal/2352 - Baclo is an antispastic agent that acts on the spinal cord - It also acts as a central nervous system depressant - It depresses monosynaptic and polysynaptic reflex transmission, most likely due to the stimulation on GABAB receptors which inturn inhibit the release of excitatory amino acids (e.g. glutamate and aspartate) - hence lessening nerve impulses to muscles in spasm. - Baclo also has an antinociceptive effect (pain relief) however the mechanism by which this occurs is not yet known http://www.virtualmedicalcentre.com/drugs/norflex/2355 Norflex is a skeletal muscle relaxant that acts on the central nervous system (CNS). The exact mechanism of action has not been determined, but it may be related to a CNS depressant effect. Norflex also has analgesic activity and mild anticholinergic actions. http://www.virtualmedicalcentre.com/drugs/baclofen-terry-white-chemists/2362 Baclo is an antispastic agent that acts on the spinal cord. It also acts as a central nervous system depressant. It depresses monosynaptic and polysynaptic reflex transmission, most likely due to the stimulation on GABAB receptors which inturn inhibit the release of excitatory amino acids (e.g. glutamate and aspartate) - hence lessening nerve impulses to muscles in spasm. Baclo also has an antinociceptive effect (pain relief) however the mechanism by which this occurs is not yet known. http://www.virtualmedicalcentre.com/drugs/hexal-diclac-anti-inflammatory-gel/2377 Diclofenac is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain, inflammation and fever by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase (COX) an enzyme involved in the pathway of prostaglandin synthesis. There are two form of COX – COX1 and COX2. Diclofenac inhibits both of these COX enzymes By inhibiting prostaglandin synthesis Diclofenac has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and prom http://www.virtualmedicalcentre.com/drugs/voltaren-emulgel/2388 The active ingredient of Voltaren Emulgel is diclofenac, a non-steroidal anti-inflammatory drug (NSAID).1 The anti-inflammatory effect of NSAIDsnbsp;is thought to be achieved by inhibiting cyclooxygenase. Cyclooxygenase is important for the synthesis of prostaglandin, which has a role in causing inflammation.1,2 The aqueous alcoholic base of Voltaren Emulgel (including diethylamine, isopropyl alcohol and propylene glycol) has a soothing and cooling effect upon topical application to the skin.1 http://www.virtualmedicalcentre.com/drugs/allohexal/2391 Allopurinol inhibits xanthine oxidase the enzyme responsible for uric acid production. Allopurinol is metabolised to oxypurinol, which also inhibits xanthine oxidase. By reducing uric acid production allopurinol and oxypurinol lower the plasma and urinary urate concentrations http://www.virtualmedicalcentre.com/drugs/allopurinol-bc/2392 Allopurinol inhibits xanthine oxidase, the enzyme responsible for uric acid production. Allopurinol is metabolised to oxypurinol, which also inhibits xanthine oxidase. By reducing uric acid production allopurinol and oxypurinol lower the plasma and urinary urate concentrations. http://www.virtualmedicalcentre.com/drugs/capurate/2394 Allopurinol inhibits xanthine oxidase the enzyme responsible for uric acid production. Allopurinol is metabolised to oxypurinol, which also inhibits xanthine oxidase. By reducing uric acid production allopurinol and oxypurinol lower the plasma and urinary urate concentrations http://www.virtualmedicalcentre.com/drugs/colgout/2395 Colchicine reduces the inflammatory reaction to urate crystals by inhibiting neutrophil migration, chemotaxis, adhesion and phagocytosis. Colchicine has no effect on uric acid production or excretion. http://www.virtualmedicalcentre.com/drugs/pro-cid/2396 Probenecid increases the renal excretion of uric acid by preventing its reabsorption in the renal tubules. It also reduces the renal tubular excretion of acidic drugs such as penicillins and some cephalosporins and subsequently increases the plasma concentration and the duration of action of these drugs. http://www.virtualmedicalcentre.com/drugs/progout/2397 Allopurinol inhibits xanthine oxidase the enzyme responsible for uric acid production. Allopurinol is metabolised to oxypurinol, which also inhibits xanthine oxidase. By reducing uric acid production allopurinol and oxypurinol lower the plasma and urinary urate concentrations. http://www.virtualmedicalcentre.com/drugs/zyloprim/2398 Allopurinol inhibits xanthine oxidase, the enzyme responsible for uric acid production. Allopurinol is metabolised to oxypurinol, which also inhibits xanthine oxidase. By reducing uric acid production allopurinol and oxypurinol lower the plasma and urinary urate concentrations. http://www.virtualmedicalcentre.com/drugs/botox/2399 Botox is a neuromuscular blocking agent that binds to presynaptic cholinergic nerve terminal receptors and blocks neuromuscular conduction by inhibiting the release of the neurotransmitter acetylcholine.1 Chronic migraine The action by which Botox works to prevent chronic migraine is not well understood, though evidence currently suggests it does so by reducing sensitisation processes.1nbsp;nbsp; Blepharospasm Botox causes localised paralysis of the target muscles which induces muscle relaxation and reduces the abnormal and excessive muscle contractions characterising blepharospasm. Dist http://www.virtualmedicalcentre.com/drugs/mestinon/2401 - Mestinon competitively inhibits a cholinesterase enzyme (used for breaking down the neurotransmitter acetylcholine) that normally hydrolyses acetylcholine at synapses and neuronal junctions - The result is a cholinergic effect which leads to increased skeletal tone and increased intestinal movement as well as other effects including pupil contraction, uterine and bronchial muscle activity, and increased secretions - Mestinon also acts directly on skeletal muscle in a way similar to acetylcholine to increase muscle tone http://www.virtualmedicalcentre.com/drugs/anamorph/2403 Morphine is an opioid analgesic. Opioid medications mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems. Here, they prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioid analgesics also cause respiratory depression via direct activity on brainstem respiratory centres, and have many direct gastrointestinal effects due to action on organs containing smooth muscle. http://www.virtualmedicalcentre.com/drugs/codeine-phosphate/2406 Codeine phosphate is an opioid analgesic that binds with stereospecific receptors at many sites within the CNS to alter processes affecting both the perceptions of pain and the emotional response to pain. There are multiple subtypes of opioid receptor, each mediating various therapeutic and/or side effects of drugs. Its analgesic effect is thought to be due to its partial metabolic conversion to morphine. Codeine has about one-sixth the analgesic activity of morphine.Pharmacokinetics. Absorption. Codeine is well absorbed after administration by mouth or injection. Codeine is absorbed from the http://www.virtualmedicalcentre.com/drugs/dilaudid/2410 Hydromorphone is a hydrogenated ketone of morphine and is an opioid analgesic thought to be eight times as strong as morphine. Opioid analgesics act primarily through the central nervous system, where they act on opiate receptors via a mechanism that is not fully understood. By interacting with these receptors, Hydromorphone can cause analgesia without causing loss of consciousness, although sedation commonly occurs. Opioid analgesics also cause respiratory depression via direct activity on brainstem respiratory centres, and have many direct gastrointestinal effects due to action on org http://www.virtualmedicalcentre.com/drugs/durogesic/2412 Durogesic is the trade name for fentanyl, an opioid analgesic agent that acts predominantly on the mu-opioid receptor. Fentanyl binds these receptors within the central nervous system to cause analgesia and sedation. Secondary and unwanted effects include alterations in mood (such as euphoria or dysphoria), respiratory depression, pupil constriction and nausea and vomiting.4 http://www.virtualmedicalcentre.com/drugs/endone/2414 Endone is an opioid analgesic containing the active ingredient oxycodone hydrochloride. Like other opioids, oxycodone mimics the action of endogenous opioids. It activates opioid receptors in the central and peripheral nervous systems, producing an analgesic response by reducing the transmission of pain signals through the synaptic connections of the spinal cord. Pathways through which pain is processed by the brain are also inhibited. The central nervous system effects can also induce respiratory depression, cough suppression, sedation and constipation.2 http://www.virtualmedicalcentre.com/drugs/fentanyl/2415 Fentanyl is an opioid analgesic. Opioids mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems to produce analgesia. Opioids prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioids also produce respiratory depression and constipation. http://www.virtualmedicalcentre.com/drugs/fentanylfentanyl-injection-dbl/2416 Fentanyl is an opioid analgesic. Opioids mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems to produce analgesia. Opioids prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioids also produce respiratory depression and constipation. http://www.virtualmedicalcentre.com/drugs/fortral/2417 Pentazocine is an opioid analgesic. Opioids mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems to produce analgesia. Opioids prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioids also produce respiratory depression and constipation. Pentazocine is an opioid agonist–antagonist that has a non-maximum ceiling response. Above this dose increases in dose will not http://www.virtualmedicalcentre.com/drugs/kapanol/2418 Morphine is an opioid analgesic. Opioids mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems to produce analgesia. Opioids prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioids also produce respiratory depression and constipation. http://www.virtualmedicalcentre.com/drugs/morphine-sulfate-injection/2421 Morphine is an opioid analgesic. Opioids mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems to produce analgesia. Opioids prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioids also produce respiratory depression and constipation. http://www.virtualmedicalcentre.com/drugs/morphine-sulfate-injection-bp-dbl/2422 Morphine is an opioid analgesic. Opioids mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems to produce analgesia. Opioids prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioids also produce respiratory depression and constipation. http://www.virtualmedicalcentre.com/drugs/morphine-tartrate-injection-dbl/2423 Morphine is an opioid analgesic. Opioid analgesics work by mimicking the body¡¦s natural opioids. They bind to receptors in the brain, spinal cord and other tissues (including intestinal smooth muscle) and stimulate these to produce their pharmacological effects of: - analgesia - decreased gastrointestinal motility - respiratory depression - cough suppression - drowsiness - miosis - mood changes - reduction in body temperature - alterations in endocrine and autonomic nervous systems The pain impulse is inhibited by morphine reducing the release of neurotransmitters and the activity o http://www.virtualmedicalcentre.com/drugs/ms-contin/2424 Morphine is an opioid analgesic. Opioids mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems to produce analgesia. Opioids prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioids also produce respiratory depression and constipation. http://www.virtualmedicalcentre.com/drugs/ms-mono/2425 Morphine is an opioid analgesic. Opioids mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems to produce analgesia. Opioids prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioids also produce respiratory depression and constipation. http://www.virtualmedicalcentre.com/drugs/nurofen-plus/2427 Ibuprofen inhibits prostaglandin synthetase, resulting in antiinflammatory, analgesic and antipyretic effects. Codeine phosphate acts on opioid receptors to produce a narcotic analgesic effect. It undergoes biotransformation to morphine in vivo. http://www.virtualmedicalcentre.com/drugs/ordine/2428 Morphine is an opioid analgesic. Opioids mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems to produce analgesia. Opioids prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioids also produce respiratory depression and constipation. http://www.virtualmedicalcentre.com/drugs/oxycontin/2429 Oxycontin is an opioid analgesic. Opioids mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems to produce analgesia. Opioids prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioids also produce respiratory depression and constipation. http://www.virtualmedicalcentre.com/drugs/oxynorm/2430 Oxynorm is an opioid analgesic. Opioids mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems to produce analgesia. Opioids prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioids also produce respiratory depression and constipation. http://www.virtualmedicalcentre.com/drugs/pethidine-hydrochloride/2434 Pethidine hydrochloride is a synthetic opioid with analgesic and sedative properties.1-3 Pethidine exerts its analgesic effects in the same manner as morphine, by acting as an agonist and activating the opioid receptors in both the central and peripheral nervous systems.3 In addition, pethidine acts pre-synaptically and post-synaptically in the spinal cord and modulates the descending inhibitory pathways from the brain, which enables it to inhibit the transmission of pain impulses.3 In doing so, the pain threshold is elevated and the brains awareness of pain is decreased. http://www.virtualmedicalcentre.com/drugs/pethidine-injection-bp-dbl/2436 Pethidine hydrochloride is a synthetic opioid with analgesic and sedative properties.1-3 Pethidine exerts its analgesic effects in the same manner as morphine, by acting as an agonist and activating the opioid receptors in both the central and peripheral nervous systems.3 In addition, pethidine acts pre-synaptically and post-synaptically in the spinal cord and modulates the descending inhibitory pathways from the brain, which enables it to inhibit the transmission of pain impulses.3 In doing so, the pain threshold is elevated and the brains awareness of pain is decreased. http://www.virtualmedicalcentre.com/drugs/physeptone/2437 Methadone is an opioid analgesic similar to morphine. Opioid medications mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems. Here, they prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioid analgesics also cause respiratory depression via direct activity on brainstem respiratory centres, and have many direct gastrointestinal effects due to action on organs containing sm http://www.virtualmedicalcentre.com/drugs/sublimaze/2441 Opioid action http://www.virtualmedicalcentre.com/drugs/tramal-sustained-release-tablets-50-mg-100-mg-150-mg-200-mg/2443 The active ingredient in Tramal is tramadol hydrochloride, a synthetic analgesic from the aminocyclohexanol group. This group of medications act on the central nervous system and relieve pain in a similar manner to opioid analgesics. However, tramadol hydrochloride is not chemically related to opioids and is produced from synthetic materials.1 The exact action of Tramal is not fully understood, though at least two pain-relieving mechanisms have been identified. The mechanisms are similar to those of opioid analgesics. Tramadol hydrochloride binds with low affinity to micro;-opioid receptors, http://www.virtualmedicalcentre.com/drugs/alka-seltzer/2445 Alka-Seltzer contains sodium citrate and aspirin. Sodium citrate is an antacid which acts immediately to neutralise gastric acid and maintains an elevated pH in the stomach. At the raised pH aspirin is predominantly in an ionised state and thus is unable to be absorbed through the lipid barrier of the gastric mucosa. This avoids irritation of the gastric mucosa by aspirin. Aspirin is then absorbed in the small intestine to provide analgesia by inhibiting prostaglandin synthesis. Alka-Seltzer also promotes accelerated gastric emptying because of the elevated gastric pH and increased so http://www.virtualmedicalcentre.com/drugs/bayer-aspirin/2447 Aspirin is a nonsteroidal anti-inflammatory drug (NSAID) that has analgesic and antipyretic actions. Aspirin block prostaglandin synthesis by inhibiting cyclo-oxygenase (COX). COX has 2 forms COX-1 and COX-2 and aspirin inhibits both these forms. http://www.virtualmedicalcentre.com/drugs/disprin/2450 Aspirin is a nonsteroidal anti-inflammatory drug (NSAID) that has analgesic and antipyretic actions. Aspirin block prostaglandin synthesis by inhibiting cyclo-oxygenase (COX). COX has 2 forms COX-1 and COX-2 and aspirin inhibits both these forms. http://www.virtualmedicalcentre.com/drugs/ecotrin/2452 Aspirin is a nonsteroidal anti-inflammatory drug (NSAID) that has analgesic and antipyretic actions. Aspirin block prostaglandin synthesis by inhibiting cyclo-oxygenase (COX). COX has 2 forms COX-1 and COX-2 and aspirin inhibits both these forms. http://www.virtualmedicalcentre.com/drugs/febridol/2453 Paracetamol has analgesic and antipyretic effects but no anti-inflammatory effects Paracetamol reduces central and peripheral prostaglandin synthesis but has no significant action on COX-1 or COX-2 which explains its lack of anti-inflammatory action. The mechanism of action of paracetamol is not entirely understood but there are a few theories around which have yet to be confirmed by further studies. Possible mechanisms of action include Paracetamol selectively inhibits COX-3 (a previously unknown cyclooxygenase enzyme distinct from COX-1 and COX-2) that is found only in the brain and sp http://www.virtualmedicalcentre.com/drugs/herron-aspirin/2455 Aspirin is a nonsteroidal anti-inflammatory drug (NSAID) that has analgesic and antipyretic actions. Aspirin block prostaglandin synthesis by inhibiting cyclo-oxygenase (COX). COX has 2 forms COX-1 and COX-2 and aspirin inhibits both these forms. http://www.virtualmedicalcentre.com/drugs/herron-paracetamol/2456 Parecetamol is a para-aminophenol derivate. It has analgesic and antipyretic activity but not anti-inflammatory activity. http://www.virtualmedicalcentre.com/drugs/panadol/2457 Panadol is a p-aminophenol derivative that exerts analgesic and antipyretic activity, but does not possess anti-inflammatory activity. http://www.virtualmedicalcentre.com/drugs/panadol-children/2458 Parecetamol is a para-aminophenol derivate. It has analgesic and antipyretic activity but not anti-inflammatory activity. http://www.virtualmedicalcentre.com/drugs/panadol-extend/2460 Parecetamol is a para-aminophenol derivate. It has analgesic and antipyretic activity but not anti-inflammatory activity. http://www.virtualmedicalcentre.com/drugs/panamax/2461 Parecetamol is a para-aminophenol derivate. It has analgesic and antipyretic activity but not anti-inflammatory activity. http://www.virtualmedicalcentre.com/drugs/paracetamol/2463 Paracetamol has analgesic and antipyretic effects but no anti-inflammatory effects. Paracetamol reduces central and peripheral prostaglandin synthesis but has no significant action on COX-1 or COX-2 which explains its lack of anti-inflammatory action. The mechanism of action of paracetamol is not entirely understood but there are a few theories around which have yet to be confirmed by further studies. Possible mechanisms of action include: Paracetamol selectively inhibits COX-3 (a previously unknown cyclooxygenase enzyme distinct from COX-1 and COX-2) that is found only in the br http://www.virtualmedicalcentre.com/drugs/parahexal/2464 Paracetamol has analgesic and antipyretic effects but no anti-inflammatory effects Paracetamol reduces central and peripheral prostaglandin synthesis but has no significant action on COX-1 or COX-2 which explains its lack of anti-inflammatory action. The mechanism of action of paracetamol is not entirely understood but there are a few theories around which have yet to be confirmed by further studies. Possible mechanisms of action include Paracetamol selectively inhibits COX-3 (a previously unknown cyclooxygenase enzyme distinct from COX-1 and COX-2) that is found only in the brain and http://www.virtualmedicalcentre.com/drugs/paralgin/2465 Paracetamol has analgesic and antipyretic effects but no anti-inflammatory effects Paracetamol reduces central and peripheral prostaglandin synthesis but has no significant action on COX-1 or COX-2 which explains its lack of anti-inflammatory action. The mechanism of action of paracetamol is not entirely understood but there are a few theories around which have yet to be confirmed by further studies. Possible mechanisms of action include • Paracetamol selectively inhibits COX-3 (a previously unknown cyclooxygenase enzyme distinct from COX-1 and COX-2) that is found only in the brain and http://www.virtualmedicalcentre.com/drugs/solprin/2467 Aspirin is a nonsteroidal anti-inflammatory drug (NSAID) that has analgesic and antipyretic actions. Aspirin block prostaglandin synthesis by inhibiting cyclo-oxygenase (COX). COX has 2 forms COX-1 and COX-2 and aspirin inhibits both these forms. http://www.virtualmedicalcentre.com/drugs/spren/2468 Aspirin is a nonsteroidal anti-inflammatory drug (NSAID) that has analgesic and antipyretic actions. Aspirin block prostaglandin synthesis by inhibiting cyclo-oxygenase (COX). COX has 2 forms COX-1 and COX-2 and aspirin inhibits both these forms. http://www.virtualmedicalcentre.com/drugs/tylenol/2469 Paracetamol has analgesic and antipyretic effects but no anti-inflammatory effects. Paracetamol reduces central and peripheral prostaglandin synthesis but has no significant action on COX-1 or COX-2 which explains its lack of anti-inflammatory action. The mechanism of action of paracetamol is not entirely understood but there are a few theories around which have yet to be confirmed by further studies. Possible mechanisms of action include: Paracetamol selectively inhibits COX-3 (a previously unknown cyclooxygenase enzyme distinct from COX-1 and COX-2) that is found only in the br http://www.virtualmedicalcentre.com/drugs/vincents-powders/2470 Aspirin is a nonsteroidal anti-inflammatory drug (NSAID) that has analgesic and antipyretic actions. Aspirin block prostaglandin synthesis by inhibiting cyclo-oxygenase (COX). COX has 2 forms COX-1 and COX-2 and aspirin inhibits both these forms. http://www.virtualmedicalcentre.com/drugs/aspalgin/2472 Aspirin irreversibly inhibits the enzyme cyclooxygenase 1, thereby preventing the production of thromboxane A2. Thromboxane A2 is a promoter of platelet aggregation and hence thrombus formation. By inhibiting the production of thromboxane A2, aspirin inhibits haemostasis and thrombosis and therefore increases bleeding time and decreases the risk of thrombus formation. Aspirin also inhibits prostaglandin synthesis, hence its antiinflammatory and antipyretic effects. The analgesic properties of aspirin have been attributed to its ability to block peripheral pain impulse generation and al http://www.virtualmedicalcentre.com/drugs/panadeine/2489 Paracetamol has analgesic as well as antipyretic effects due to inhibition of prostaglandin synthesis. It has minimal anti-inflammatory effects. Codeine is an opioid analgesic and works by activating opioid receptors in the central and peripheral nervous systems to produce analgesic effects (as well as respiratory depression and confusion). It also acts at the level of the spinal cord to prevent the transmission of pain impulses. http://www.virtualmedicalcentre.com/drugs/panamax-co/2492 Paracetamol has analgesic as well as antipyretic effects due to inhibition of prostaglandin synthesis. It has minimal anti-inflammatory effects. Codeine is an opioid analgesic and works by activating opioid receptors in the central and peripheral nervous systems to produce analgesic effects (as well as respiratory depression and constipation). It also acts at the level of the spinal cord to prevent the transmission of pain impulses. http://www.virtualmedicalcentre.com/drugs/paracetamolcodeine/2493 Paracetamol has analgesic as well as antipyretic effects due to inhibition of prostaglandin synthesis. It has minimal anti-inflammatory effects. Codeine is an opioid analgesic and works by activating opioid receptors in the central and peripheral nervous systems to produce analgesic effects (as well as respiratory depression and constipation). It also acts at the level of the spinal cord to prevent the transmission of pain impulses. http://www.virtualmedicalcentre.com/drugs/alodorm/2495 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/euhypnos/2496 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects). http://www.virtualmedicalcentre.com/drugs/halcion/2497 Halcion is a potent short acting hypnotic agent.nbsp;Itnbsp;reduced sleep latency, increased duration of sleep and decreased the number of nocturnal awakenings compared to baseline.1,2 http://www.virtualmedicalcentre.com/drugs/hypnodorm/2499 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/hypnovel/2500 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA) throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/imovane/2501 Zolpiclone, the active ingredient of Imovane, is a short acting hypnotic agent. Zopiclone has similar profile to those of benzodiazepines despite structurally unrelated to existing hypnotics. Zopiclone potentiates inhibitory effects of gamma-aminobutyric acid (GABA). Hence, reduces the time taken to fall asleep, increasing the duration of sleep and decreasing the number of awakenings.1,2nbsp; http://www.virtualmedicalcentre.com/drugs/midazolam-injection/2502 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA) throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/midazolam-injection-bp-dbl/2503 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA) throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/mogadon/2504 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/nocturne/2506 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/normison/2507 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/stilnox/2510 Potentiation of inhibitory affects of gamma amino butyric acid (GABA) http://www.virtualmedicalcentre.com/drugs/temaze/2511 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects. http://www.virtualmedicalcentre.com/drugs/unisom-sleepgels/2513 Antagonises the effects of histamine at H1 receptors, causing a reduction of histamine related vasodilation. Also has anticholinergic effects. http://www.virtualmedicalcentre.com/drugs/alepam/2514 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/antenex/2518 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects. http://www.virtualmedicalcentre.com/drugs/ativan/2519 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects). http://www.virtualmedicalcentre.com/drugs/buspar/2520 Partial agonist at serotonin 5HT1A receptors http://www.virtualmedicalcentre.com/drugs/diazepam-injection-dbl/2522 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects). http://www.virtualmedicalcentre.com/drugs/ducene/2523 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/frisium/2524 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/kalma/2526 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/lexotan/2527 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/serepax/2529 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/valium/2531 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA) throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects. http://www.virtualmedicalcentre.com/drugs/valpam/2532 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/xanax/2533 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects). http://www.virtualmedicalcentre.com/drugs/aldazine/2534 Antipsychotic actions are thought to be mediated (at least in part) by blockade of dopaminergic transmission in various parts of the brain (in particular, the limbic system). Although all antipsychotics block D2 receptors, there is some evidence to suggest that blockade of other dopamine receptors (e.g. D1) may influence therapeutic and adverse effects. http://www.virtualmedicalcentre.com/drugs/clopine/2536 D2/D3 antagonist predominantly in the limbic area of the brain. Low affinity for serotonin, adrenergic, histaminergic and muscarinic receptors http://www.virtualmedicalcentre.com/drugs/clopixol/2537 Antipsychotic actions are thought to be mediated (at least in part) by blockade of dopaminergic transmission in various parts of the brain (in particular, the limbic system). Although all antipsychotics block D2 receptors, there is some evidence to suggest that blockade of other dopamine receptors (e.g. D1) may influence therapeutic and adverse effects. http://www.virtualmedicalcentre.com/drugs/clozaril/2538 D2/D3 antagonist predominantly in the limbic area of the brain. Low affinity for serotonin, adrenergic, histaminergic and muscarinic receptors. http://www.virtualmedicalcentre.com/drugs/droleptan/2539 Pharmacology1 Droleptan produces general sedation and a reduced responsiveness to environmental stimuli. Animals There is little or no effect on respiration or myocardial contractile force, heart rate and cardiac output in dogs. The blood pressure is lowered, in part as a direct vasodilator effect and in part because of adrenergic blockade. Droleptan markedly reduces the ability of apomorphine to produce emesis in dogs. Human Pharmacology Droleptan produces marked tranquillization and sedation. It also produces an antiemetic effect as evidenced by the antagonism of the emetic effect of a http://www.virtualmedicalcentre.com/drugs/fluanxol/2540 Fluanxol is a potent, relatively nonsedating neuroleptic drug of the thioxanthene class.2 http://www.virtualmedicalcentre.com/drugs/fluphenazine-decanoate-oily-injection-bp-dbl/2541 Fluphenazine is a dopamine receptor antagonist of the phenothiazine class. It has an affinity for D and D2 receptors and its therapeutic action is thought to be due to its dopamine receptor blockade in the mesolimbic pathways. http://www.virtualmedicalcentre.com/drugs/haldol-decanoate/2542 Haldol decanoate is a butyrophenone antipsychotic. It acts by blocking a variety of receptors in the brain, but particularly dopamine receptors. Haloperidol also increases the turnover rate of dopamine. Haldol decanoate is administered as an IM depot injection in sesame oil, so esterases in the blood and tissues hydrolyse the drug to produce a slow release of the depot into the systemic circulation. http://www.virtualmedicalcentre.com/drugs/lithicarb/2544 Unknown; actions include inhibition of dopamine release, enhancement of serotonin release and decrease formation of intracellular second messengers. Lithium has little or no psychotropic effect in normal individuals. http://www.virtualmedicalcentre.com/drugs/melleril/2545 Antipsychotic actions are thought to be mediated (at least in part) by blockade of dopaminergic transmission in various parts of the brain (in particular, the limbic system). Although all antipsychotics block D2 receptors, there is some evidence to suggest that blockade of other dopamine receptors (e.g. D1) may influence therapeutic and adverse effects. http://www.virtualmedicalcentre.com/drugs/modecate/2546 Fluphenazine is a dopamine receptor antagonist of the phenothiazine class. It has an affinity for D and D2 receptors and its therapeutic action is thought to be due to its dopamine receptor blockade in the mesolimbic pathways. http://www.virtualmedicalcentre.com/drugs/navane/2547 Antipsychotic actions are thought to be mediated (at least in part) by blockade of dopaminergic transmission in various parts of the brain (in particular, the limbic system). Although all antipsychotics block D2 receptors, there is some evidence to suggest that blockade of other dopamine receptors (e.g. D1) may influence therapeutic and adverse effects. http://www.virtualmedicalcentre.com/drugs/orap/2549 Antipsychotic actions are thought to be mediated at least in part by blockade of dopaminergic transmission in various parts of the brain (in particular, the limbic system). Although all antipsychotics block D2 receptors, there is some evidence to suggest that blockade of other dopamine receptors (e.g. D1) may influence therapeutic and adverse effects. http://www.virtualmedicalcentre.com/drugs/quilonum-sr/2550 Unknown; actions include inhibition of dopamine release, enhancement of serotonin release and decrease formation of intracellular second messengers. Lithium has little or no psychotropic effect in normal individuals. http://www.virtualmedicalcentre.com/drugs/serenace/2552 Haloperidol is a psychotropic drug. Its precise mechanism of action is unknown, but it acts on dopamine in the brain. It competitively blocks postsynaptic (D2) dopamine receptors, which renders it selective to the central nervous system, and causes an increased turnover of dopamine in the brain. This causes the tranquillising effect. With medium-term use, release of dopamine decreases and this, combined with the D2 blockade, leads to the antipsychotic effect of Haloperidol. Haloperidol also blocks dopamine receptors in the substantia nigra, resulting in extrapyramidal side effects. Some hor http://www.virtualmedicalcentre.com/drugs/seroquel/2553 Quetiapine is an atypical antipsychotic drug. It antagonises 5-HT2 and dopamine receptors in the brain, resulting in anti-psychotic effects, including relief from symptoms such as hallucinations, delusions or abnormal behaviour/thought.1-3 http://www.virtualmedicalcentre.com/drugs/solian/2554 D2/D3 antagonist predominantly in the limbic area of the brain. Low affinity for serotonin, adrenergic, histaminergic and muscarinic receptors. http://www.virtualmedicalcentre.com/drugs/stelazine/2555 Antipsychotic actions are thought to be mediated (at least in part) by blockade of dopaminergic transmission in various parts of the brain (in particular, the limbic system). Although all antipsychotics block D2 receptors, there is some evidence to suggest that blockade of other dopamine receptors (e.g. D1) may influence therapeutic and adverse effects. http://www.virtualmedicalcentre.com/drugs/zyprexa/2556 Zyprexanbsp;is an atypical antipsychotic, antimanic and mood stabilizing agent that has a broad pharmalogical actions across a number of receptor systems. Its antipsychotic actions are thought to be mediated by blockade of dopamidergic transmission in various parts of the brain, especially the limbic system.1,2 http://www.virtualmedicalcentre.com/drugs/allegron/2557 Nortriptyline is a tricyclic antidepressant (TCA). The mechanism of mood elevation by TCAs is currently not well understood.3 TCAs are thought to inhibit pre-synaptic reuptake of serotonin and noradrenaline in the CNS.2 They may also have additional receptor effects, including inhibition of cholinergic, histaminergic, alpha-1-adrenergic and serotonergic receptors.1, 2 There are marked inter-individual variations in steady-state plasma concentrations at the same dosage, and plasma concentration measurements may be of value in some circumstances. Individual dosage adjustment is required to ac http://www.virtualmedicalcentre.com/drugs/anafranil/2558 Tricylcic antidepressants (TCA’s) inhibit reuptake of noradrenaline and serotonin into presynaptic terminals. Although unrelated to therapeutic effects of TCAs, they also block cholinergic, histaminergic, alpha 1 adrenergic and serotonergic receptors TCA’s are absorbed rapidly after oral administration and are metabolized by the liver Long half life and can therefore be given once daily, usually at night There are marked inter-individual variations in steady-state plasma concentrations at the same dosage and plasma concentration measurements may be of value in some circumstances Individual http://www.virtualmedicalcentre.com/drugs/arima/2559 Competitive and reversible inhibition of monoamine oxidase (MAO). It is relatively selective for type A (MAO-A). Synaptic concentrations of serotonin, noradrenaline, and dopamine are increased. Full activity of the MAO-A enzyme is restored within 24-48 hours of stopping the drug When used at higher than recommended doses, moclobemide will also inhibit MAO-B (dietary restrictions would then be warranted) http://www.virtualmedicalcentre.com/drugs/aropax/2560 Antidepressant action by selective inhibition of pre-synaptic uptake of serotonin (5- hydroxytryptamine, 5-HT). Paroxtine has the shortest half life of the SSRIs and has no active metabolite. http://www.virtualmedicalcentre.com/drugs/aurorix/2561 Aurorixnbsp;is an antidepressant which affects the monoaminergic cerebral neurotransmitter system by means of a reversible inhibition of monoamine oxidase. It is relatvelynbsp;selective for type A monoamine oxidase (MAO-A). The metabolism of dopamine, noradrenaline and serotonin is decreased by this effect, and this leads to increased synaptic concentrations of these neuronal transmitters. As a result of its elevating effect on mood and psychomotor activity, Aurorix relieves symptoms such as dysphoria, exhaustion, lack of drive and poor ability to concentrate.1,2 http://www.virtualmedicalcentre.com/drugs/auscap/2562 SSRIs work by selective inhibition of pre-synaptic uptake of serotonin (5- hydroxytryptamine, 5-HT) Fluoxetine has an active metabolite norfluoxetine, that contributes significantly to its effects and has a long half life (up to 16 days). Fluoxetine inhibits CYP2D6 and its active metabolite, norfluoxetine, inhibits CYP3A4. This contributes to specific drug interactions http://www.virtualmedicalcentre.com/drugs/avanza/2563 Post-synaptic blockade of serotonin 5HT2 and 5HT3 receptors, presynaptic blockade of alpha-2-adrenergic inhibitory autoreceptors. http://www.virtualmedicalcentre.com/drugs/chem-mart-clomipramine/2564 Clomipramine inhibits the neuronal reuptake of noradrenaline and serotonin released in the synaptic cleft. It is inhibition of serotonin uptake that exerts the dominant antidepressant effect. http://www.virtualmedicalcentre.com/drugs/chem-mart-fluoxetine/2565 Fluoxetine exerts its antidepressant and antiobsessional effects by inhibiting the CNS neuronal uptake of serotonin. http://www.virtualmedicalcentre.com/drugs/chem-mart-moclobemide/2566 Moclobemide is an antidepressant that affects the monoaminergic cerebral neurotransmitter system by reversibly inhibiting monoamine oxidase. There are two types of monamine oxidases, A and B, and moclobemide is selective for type A. http://www.virtualmedicalcentre.com/drugs/cipramil/2567 Selective inhibition of pre-synaptic uptake of serotonin (5- hydroxytryptamine, 5-HT). SSRIs inhibit Cytochrome P450 enzymes, thus potentially interacting with those drugs by decreasing their metabolism. http://www.virtualmedicalcentre.com/drugs/clobemix/2568 Competitive and reversible inhibition of monoamine oxidase (MAO). It is relatively selective for type A (MAO-A). Synaptic concentrations of serotonin, noradrenaline, and dopamine are increased. Full activity of the MAO-A enzyme is restored within 24-48 hours of stopping the drug When used at higher than recommended doses, moclobemide will also inhibit MAO-B (dietary restrictions would then be warranted) http://www.virtualmedicalcentre.com/drugs/clomipramine-bc/2569 Clomipramine inhibits the neuronal reuptake of noradrenaline and serotonin released in the synaptic cleft. It is inhibition of serotonin uptake that exerts the dominant antidepressant effect. http://www.virtualmedicalcentre.com/drugs/clopram/2570 Tricylcic antidepressants (TCAs) inhibit reuptake of noradrenaline and serotonin into presynaptic terminals. Although unrelated to therapeutic effects of TCAs, they also block cholinergic, histaminergic, alpha 1 adrenergic and serotonergic receptors. TCAs are absorbed rapidly after oral administration and are metabolized by the liver. Long half life and can therefore be given once daily, usually at night. There are marked inter-individual variations in steady-state plasma concentrations at the same dosage and plasma concentration measurements may be of value in some circumstances. http://www.virtualmedicalcentre.com/drugs/deptran/2571 Tricylcic antidepressants (TCAs) inhibit reuptake of noradrenaline and serotonin into presynaptic terminals. Although unrelated to therapeutic effects of TCAs, they also block cholinergic, histaminergic, alpha 1 adrenergic and serotonergic receptors. TCAs are absorbed rapidly after oral administration and are metabolized by the liver. Long half life and can therefore be given once daily, usually at night. There are marked inter-individual variations in steady-state plasma concentrations at the same dosage and plasma concentration measurements may be of value in some circumstances. http://www.virtualmedicalcentre.com/drugs/dothep/2572 Tricylcic antidepressants (TCAs) inhibit reuptake of noradrenaline and serotonin into presynaptic terminals. Although unrelated to therapeutic effects of TCAs, they also block cholinergic, histaminergic, alpha 1 adrenergic and serotonergic receptors. TCAs are absorbed rapidly after oral administration and are metabolized by the liver. They have a long half life and can therefore be given once daily, usually at night. There are marked inter-individual variations in steady-state plasma concentrations at the same dosage and plasma concentration measurements may be of value in some cir http://www.virtualmedicalcentre.com/drugs/edronax/2573 1, 2Edronax is highly selective for and potently inhibits noradrenaline reuptake. Edronax also weakly inhibits reuptake of serotonin and has no effect on dopamine reuptake. Consequently, the levels of noradrenaline in the synaptic cleft increases, which leads to its antidepressant effect. http://www.virtualmedicalcentre.com/drugs/efexor/2574 Venlafaxine is an antidepressant unrelated to any other class. It is believed to exert its antidepressant effect by potentiating neurotransmitter activity in the brain. It has been shown to be a potent inhibitor of serotonin and noradrenaline reuptake and a weak inhibitor of dopamine reuptake. Venlafaxine does not have activity at muscarinic, H1-histaminic or alpha1-adrenergic receptors, meaning it is free of the sedative, cardiovascular and anticholinergic effects seen with other antidepressants. http://www.virtualmedicalcentre.com/drugs/efexor-xr/2575 Venlafaxine is an antidepressant unrelated to any other class. It is believed to exert its antidepressant effect by potentiating neurotransmitter activity in the brain. It has been shown to be a potent inhibitor of serotonin and noradrenaline reuptake and a weak inhibitor of dopamine reuptake. Venlafaxine does not have activity at muscarinic, H1-histaminic or alpha1-adrenergic receptors, meaning it is free of the sedative, cardiovascular and anticholinergic effects seen with other antidepressants. http://www.virtualmedicalcentre.com/drugs/endep/2576 Tricylcic antidepressants (TCAs) inhibit reuptake of noradrenaline and serotonin into presynaptic terminals. Although unrelated to therapeutic effects of TCAs, they also block cholinergic, histaminergic, alpha 1 adrenergic and serotonergic receptors. TCAs are absorbed rapidly after oral administration and are metabolized by the liver. They have a long half life and can therefore be given once daily, usually at night. There are marked inter-individual variations in steady-state plasma concentrations at the same dosage and plasma concentration. Measurements may be of value in som http://www.virtualmedicalcentre.com/drugs/faverin/2577 Antidepressant action by selective inhibition of pre-synaptic uptake of serotonin (5- hydroxytryptamine, 5-HT) Fluvoxamine inhibits the cytochrome P450 isoforms, CYP1A2 and CYP3A4, creating interaction potential with a wide range of drugs http://www.virtualmedicalcentre.com/drugs/fluohexal/2578 SSRIs work by selective inhibition of pre-synaptic uptake of serotonin (5- hydroxytryptamine, 5-HT). Fluoxetine has an active metabolite norfluoxetine, that contributes significantly to its effects and has a long half life (up to 16 days). Fluoxetine inhibits CYP2D6 and its active metabolite, norfluoxetine, inhibits CYP3A4. This contributes to specific drug interactions. http://www.virtualmedicalcentre.com/drugs/fluoxetine-bc/2579 Fluoxetine exerts its antidepressant and antiobsessional effects by inhibiting the CNS neuronal uptake of serotonin. http://www.virtualmedicalcentre.com/drugs/genrx-clomipramine/2580 Clomipramine inhibits the neuronal reuptake of noradrenaline and serotonin released in the synaptic cleft. It is inhibition of serotonin uptake that exerts the dominant antidepressant effect. http://www.virtualmedicalcentre.com/drugs/genrx-fluoxetine/2581 Fluoxetine exerts its antidepressant and antiobsessional effects by inhibiting the CNS neuronal uptake of serotonin. http://www.virtualmedicalcentre.com/drugs/genrx-moclobemide/2582 Moclobemide is an antidepressant that affects the monoaminergic cerebral neurotransmitter system by reversibly inhibiting monoamine oxidase. There are two types of monamine oxidases, A and B, and moclobemide is selective for type A. http://www.virtualmedicalcentre.com/drugs/healthsense-clomipramine/2583 Clomipramine inhibits the neuronal reuptake of noradrenaline and serotonin released in the synaptic cleft. It is inhibition of serotonin uptake that exerts the dominant antidepressant effect. http://www.virtualmedicalcentre.com/drugs/healthsense-fluoxetine/2584 Fluoxetine exerts its antidepressant and antiobsessional effects by inhibiting the CNS neuronal uptake of serotonin. http://www.virtualmedicalcentre.com/drugs/lovan/2586 SSRIs work by selective inhibition of pre-synaptic uptake of serotonin (5- hydroxytryptamine, 5-HT). Fluoxetine has an active metabolite norfluoxetine, that contributes significantly to its effects and has a long half life (up to 16 days). Fluoxetine inhibits CYP2D6 and its active metabolite, norfluoxetine, inhibits CYP3A4. This contributes to specific drug interactions. http://www.virtualmedicalcentre.com/drugs/lumin/2587 Mianserin is an atypical antidepressant that differs chemically from the tricyclic antidepressants (TCAs).2, 3 Mianserin possesses a2-adrenergic autoreceptor blocking activity, thus reducing the presynaptic inhibition of neurotransmitter synthesis and exocytosis.2, 4 The net effect is enhanced postsynaptic receptor activity, leading to a therapeutic response. In addition, mianserin inhibits the reuptake of noradrenaline by blocking the noradrenaline reuptake transporter, further increasing neurotransmitter levels in the synaptic cleft and promoting downstream signaling.4Mianserin has also been http://www.virtualmedicalcentre.com/drugs/luvox/2588 Antidepressant action by selective inhibition of pre-synaptic uptake of serotonin (5- hydroxytryptamine, 5-HT) Fluvoxamine inhibits the cytochrome P450 isoforms, CYP1A2 and CYP3A4, creating interaction potential with a wide range of drugs http://www.virtualmedicalcentre.com/drugs/maosig/2589 Competitive and reversible inhibition of monoamine oxidase (MAO). It is relatively selective for type A (MAO-A). Synaptic concentrations of serotonin, noradrenaline, and dopamine are increased. Full activity of the MAO-A enzyme is restored within 24-48 hours of stopping the drug When used at higher than recommended doses, moclobemide will also inhibit MAO-B (dietary restrictions would then be warranted) http://www.virtualmedicalcentre.com/drugs/melipramine/2590 Tricylcic antidepressants (TCA’s) inhibit reuptake of noradrenaline and serotonin into presynaptic terminals. Although unrelated to therapeutic effects of TCAs, they also block cholinergic, histaminergic, alpha 1 adrenergic and serotonergic receptors TCA’s are absorbed rapidly after oral administration and are metabolized by the liver Long half life and can therefore be given once daily, usually at night There are marked inter-individual variations in steady-state plasma concentrations at the same dosage and plasma concentration measurements may be of value in some circumstances Individual http://www.virtualmedicalcentre.com/drugs/mirtazon/2591 Post-synaptic blockade of serotonin 5HT2 and 5HT3 receptors, presynaptic blockade of alpha-2-adrenergic inhibitory autoreceptors. http://www.virtualmedicalcentre.com/drugs/moclobemide-bc/2592 Moclobemide is an antidepressant that affects the monoaminergic cerebral neurotransmitter system by reversibly inhibiting monoamine oxidase. There are two types of monamine oxidases, A and B, and moclobemide is selective for type A. http://www.virtualmedicalcentre.com/drugs/mohexal/2593 Competitive and reversible inhibition of monoamine oxidase (MAO). It is relatively selective for type A (MAO-A). Synaptic concentrations of serotonin, noradrenaline, and dopamine are increased. Full activity of the MAO-A enzyme is restored within 24-48 hours of stopping the drug When used at higher than recommended doses, moclobemide will also inhibit MAO-B (dietary restrictions would then be warranted) http://www.virtualmedicalcentre.com/drugs/nardil/2594 Irreversible, non-selective inhibition of the enzymes, monoamine oxidase-A and monoamine oxidase-B. This action leads to elevation of synaptic concentrations of adrenaline, noradrenaline, dopamine and serotonin in the brain and other tissues. The duration of action is 2-3 weeks while new enzymes form. http://www.virtualmedicalcentre.com/drugs/oxetine/2595 Antidepressant action by selective inhibition of pre-synaptic uptake of serotonin (5- hydroxytryptamine, 5-HT). Paroxtine has the shortest half life of the SSRIs and has no active metabolite. http://www.virtualmedicalcentre.com/drugs/parnate/2596 Irreversible, non-selective inhibition of the enzymes, monoamine oxidase-A and monoamine oxidase-B. This action leads to elevation of synaptic concentrations of adrenaline, noradrenaline, dopamine and serotonin in the brain and other tissues. The duration of action is 2-3 weeks while new enzymes form http://www.virtualmedicalcentre.com/drugs/paxtine/2597 Antidepressant action by selective inhibition of pre-synaptic uptake of serotonin (5- hydroxytryptamine, 5-HT) Paroxtine has the shortest half life of the SSRIs and has no active metabolite http://www.virtualmedicalcentre.com/drugs/placil/2598 Tricylcic antidepressants (TCA’s) inhibit reuptake of noradrenaline and serotonin into presynaptic terminals. Although unrelated to therapeutic effects of TCAs, they also block cholinergic, histaminergic, alpha 1 adrenergic and serotonergic receptors TCA’s are absorbed rapidly after oral administration and are metabolized by the liver Long half life and can therefore be given once daily, usually at night There are marked inter-individual variations in steady-state plasma concentrations at the same dosage and plasma concentration measurements may be of value in some circumstances Individual http://www.virtualmedicalcentre.com/drugs/prothiaden/2599 Tricylcic antidepressants (TCA’s) inhibit reuptake of noradrenaline and serotonin into presynaptic terminals. Although unrelated to therapeutic effects of TCAs, they also block cholinergic, histaminergic, alpha 1 adrenergic and serotonergic receptors TCA’s are absorbed rapidly after oral administration and are metabolized by the liver Long half life and can therefore be given once daily, usually at night There are marked inter-individual variations in steady-state plasma concentrations at the same dosage and plasma concentration measurements may be of value in some circumstances Individual http://www.virtualmedicalcentre.com/drugs/prozac/2600 SSRIs work by selective inhibition of pre-synaptic uptake of serotonin (5- hydroxytryptamine, 5-HT). Fluoxetine has an active metabolite norfluoxetine, that contributes significantly to its effects and has a long half life (up to 16 days). Fluoxetine inhibits CYP2D6 and its active metabolite, norfluoxetine, inhibits CYP3A4. This contributes to specific drug interactions. http://www.virtualmedicalcentre.com/drugs/remeron/2601 1, 2Remeron is classed as a tetracyclic piperazinoazepine analogue of mianserin and is used to treat episodes of major depression. It works by blocking postsynaptic serotonin 5HT2 and 5HT3 receptors as wells as blocking pre-synaptic central alpha2- auto receptors. The result is an increase in both serotonin and noradrenaline release. http://www.virtualmedicalcentre.com/drugs/sinequan/2603 Tricylcic antidepressants (TCA’s) inhibit reuptake of noradrenaline and serotonin into presynaptic terminals. Although unrelated to therapeutic effects of TCAs, they also block cholinergic, histaminergic, alpha 1 adrenergic and serotonergic receptors TCA’s are absorbed rapidly after oral administration and are metabolized by the liver Long half life and can therefore be given once daily, usually at night There are marked inter-individual variations in steady-state plasma concentrations at the same dosage and plasma concentration measurements may be of value in some circumstances Individual http://www.virtualmedicalcentre.com/drugs/surmontil/2604 Tricylcic antidepressants (TCA’s) inhibit reuptake of noradrenaline and serotonin into presynaptic terminals. Although unrelated to therapeutic effects of TCAs, they also block cholinergic, histaminergic, alpha 1 adrenergic and serotonergic receptors TCA’s are absorbed rapidly after oral administration and are metabolized by the liver Long half life and can therefore be given once daily, usually at night There are marked inter-individual variations in steady-state plasma concentrations at the same dosage and plasma concentration measurements may be of value in some circumstances Individual http://www.virtualmedicalcentre.com/drugs/talohexal/2605 Selective inhibition of pre-synaptic uptake of serotonin (5- hydroxytryptamine, 5-HT) SSRIs inhibit Cytochrome P450 enzymes, thus potentially interacting with those drugs by decreasing their metabolism http://www.virtualmedicalcentre.com/drugs/clomipramine-terry-white-chemists/2606 Clomipramine inhibits the neuronal reuptake of noradrenaline and serotonin released in the synaptic cleft. It is inhibition of serotonin uptake that exerts the dominant antidepressant effect. http://www.virtualmedicalcentre.com/drugs/fluoxetine-terry-white-chemists/2607 Fluoxetine exerts its antidepressant and antiobsessional effects by inhibiting the CNS neuronal uptake of serotonin. http://www.virtualmedicalcentre.com/drugs/moclobemide-terry-white-chemists/2608 Moclobemide is an antidepressant that affects the monoaminergic cerebral neurotransmitter system by reversibly inhibiting monoamine oxidase. There are two types of monamine oxidases, A and B, and moclobemide is selective for type A. http://www.virtualmedicalcentre.com/drugs/tofranil/2609 Tricylcic antidepressants (TCAs) inhibit reuptake of noradrenaline and serotonin into presynaptic terminals. Although unrelated to therapeutic effects of TCAs, they also block cholinergic, histaminergic, alpha 1 adrenergic and serotonergic receptors. TCAs are absorbed rapidly after oral administration and are metabolized by the liver. Long half life and can therefore be given once daily, usually at night There are marked inter-individual variations in steady-state plasma. concentrations at the same dosage and plasma concentration measurements may be of value in some circumstances Indiv http://www.virtualmedicalcentre.com/drugs/tolvon/2610 Mianserin is an atypical antidepressant that differs chemically from the tricyclic antidepressants (TCAs).2, 3 Mianserin possesses a2-adrenergic autoreceptor blocking activity, thus reducing the presynaptic inhibition of neurotransmitter synthesis and exocytosis.2, 4 The net effect is enhanced postsynaptic receptor activity, leading to a therapeutic response. In addition, mianserin inhibits the reuptake of noradrenaline by blocking the noradrenaline reuptake transporter, further increasing neurotransmitter levels in the synaptic cleft and promoting downstream signaling.4Mianserin has also been http://www.virtualmedicalcentre.com/drugs/tryptanol/2611 Tricylcic antidepressants (TCA’s) inhibit reuptake of noradrenaline and serotonin into presynaptic terminals. Although unrelated to therapeutic effects of TCAs, they also block cholinergic, histaminergic, alpha 1 adrenergic and serotonergic receptors TCA’s are absorbed rapidly after oral administration and are metabolized by the liver Long half life and can therefore be given once daily, usually at night There are marked inter-individual variations in steady-state plasma concentrations at the same dosage and plasma concentration measurements may be of value in some circumstances Individual http://www.virtualmedicalcentre.com/drugs/zactin/2612 SSRIs work by selective inhibition of pre-synaptic uptake of serotonin (5- hydroxytryptamine, 5-HT). Fluoxetine has an active metabolite norfluoxetine, that contributes significantly to its effects and has a long half life (up to 16 days). Fluoxetine inhibits CYP2D6 and its active metabolite, norfluoxetine, inhibits CYP3A4. This contributes to specific drug interactions. http://www.virtualmedicalcentre.com/drugs/zoloft/2613 Zoloft is a potent and selective serotonin reuptake inhibitor. Its efficacy in depression, OCD, PMDD, panic disorders and social phobias is presumed to be associated with its inhibition of neuronal reuptake of serotonin in the central nervous system.1, 2 http://www.virtualmedicalcentre.com/drugs/aricept/2614 Aricept selectively inhibits acetylcholinesterase within the central nervous system. It therefore improves cholinergic neurotransmission in cortical regions with decreased cholinergic activity. A decrease in cholinergic neurotransmission is a feature of Alzheimers disease which has been linked to impaired cognitive ability.2 http://www.virtualmedicalcentre.com/drugs/attenta/2615 Proposed mode of action of psychostimulants in ADHD is enhancement of dopaminergic and noradrenergic neurotransmission. http://www.virtualmedicalcentre.com/drugs/dexamphetamine-tablets/2617 Proposed mode of action of psychostimulants in ADHD is enhancement of dopaminergic and noradrenergic neurotransmission. http://www.virtualmedicalcentre.com/drugs/exelon/2618 Exelon consists of an active ingredient known as rivastigmine hydrogen tartrate, which is a brain selective, pseudo-irreversible inhibitor of acetyl and butyryl-cholinesterase enzymes.1,2 One of the apparent pathological features of Alzheimers disease is the deficiency in cholinergic neurotransmitter activity in the brain. Exelon can decrease the breakdown of acetylcholine released from functionally intact cholinergic neurons, thus facilitating the cholinergic neurotransmission in the brain.1,2 Another pathological features of Alzheimers disease is formation of amyloidogenic beta-amy http://www.virtualmedicalcentre.com/drugs/reminyl/2620 Galantamine is a cholinomimetic with a dual mechanism of action. It is a reversible inhibitor of the enzyme acetylcholinesterase, and it also enhances the intrinsic action of acetylcholine on nicotinic receptors.2,4 http://www.virtualmedicalcentre.com/drugs/ritalin-10/2621 Proposed mode of action of psychostimulants in ADHD is enhancement of dopaminergic and noradrenergic neurotransmission. http://www.virtualmedicalcentre.com/drugs/cabaser/2625 Cabaser contains cabergoline which is a potent and long-acting dopamine receptor agonist. Cabaser thus binds to dopamine receptors within the central nervous system to enhance dopaminergic activity. Interaction with dopamine receptors on pituitary lactotrophic cells causes a reduction in prolactin in a dose dependent fashion.3 Other cabergoline medications have been used to inhibit prolactin secretion to reduce the size of prolactinomas and in the prevention of lactation in the puerperium for clearly defined medical reasons.1 However, Cabaser has not been marketed for these indications. An http://www.virtualmedicalcentre.com/drugs/sinemet/2633 Sinemet contains levodopa (the metabolic precursor of dopamine) and carbidopa (a peripheral dopa-decarboxylase inhibitor). Levodopa is converted to dopamine in the brain to replenish the deficiency that causes symptoms of Parkinsons disease. The addition of a dopa decarboxylase inhibitor (carbidopa or benserazide) prevents levodopa being decarboxylated to dopamine in peripheral tissues.1 This allows a greater amount of unchanged levodopa to reach the central nervous system thus reducing the frequency and amount of dosage needed to achieve therapeutic levels within the brain.4 In addition, thi http://www.virtualmedicalcentre.com/drugs/sinemet-cr/2634 Parkinsons disease is a degenerative neurological disorder characterised by the progressive loss of dopaminergic nigrostriatal neurons.3 Sinemet CR contains levodopa (the metabolic precursor of dopamine) and carbidopa (a peripheral dopa-decarboxylase inhibitor). Levodopa is converted to dopamine in the brain to replenish the deficiency that causes symptoms of Parkinsons disease. The addition of a dopa decarboxylase inhibitor (carbidopa) prevents levodopa being decarboxylated to dopamine in peripheral tissues (particularly intestinal mucosa).1 This allows a greater amount of unchanged levodop http://www.virtualmedicalcentre.com/drugs/symmetrel/2635 The precise mechanism of action of Symmetrel (amantadine) in Parkinsons disease is not entirely understood. However it is thought to increase dopamine release from central neurons and inhibit reuptake into synaptic vesicles (dopamine agonist activity) and exert anticholinergic activity by blocking receptors.1,2 This restores the abnormal chemical balance present in Parkinsons disease, thus improving signs and symptoms and improving functional ability.2 These effects are usually seen within one to two days of starting the drug. To offer prophylaxis against influenza, Symmetrel prevents v http://www.virtualmedicalcentre.com/drugs/carbamazepine-bc/2638 The mechanisms of action of Carbamazepine are only partially understood. Carbamazepine blocks voltage-dependent and use-dependent sodium channels and by doing this stabilises hyperexcited nerve membranes, prevents repetitive neuronal discharges and reduces synaptic propagation of excitatory impulses. Carbamazepine reduces glutamate release and stabilises neuronal membranes, which is thought to be the basis of its antiepileptic effects. The antimanic effects of carbamazepine are thought to be due to reduction of dopamine and noradrenaline turnover. Carbamazepine also has anticholinerg http://www.virtualmedicalcentre.com/drugs/dbl-gabapentin-capsules/2639 - The way in which gabapentin exerts its anticonvulsant effect is unknown - The drug is structurally related to the neurotransmitter GABA (gamma-aminobutyric acid) but its mechanism of action differs to other drugs that interact with GABA synapses - The binding site of gabapentin is yet to be established - It also does not affect sodium channels, a means by which other anticonvulsants may work http://www.virtualmedicalcentre.com/drugs/dilantin/2640 - Dilantin acts upon the motor cortex in the brain to inhibit the spread of seizure activity. - Dilantin encourages sodium efflux from neurons, thus stabilising over excitability caused by the seizure trigger. - Overall this drug reduces the maximum activity of brain centres associated with the tonic phase of grand mal seizures. http://www.virtualmedicalcentre.com/drugs/epilim/2642 Mode of action is not fully understood. The anticonvulsant effect can be attributed to the blockage of voltage dependent Na+ channels, and increased levels of the inhibitory synaptic transmitter, gamma-aminobutyric acid (GABA). Epilim increases GABA via inhibiting GABA degradative enzymes, for example, GABA transaminase and/or succinic semialdehyde dehydrogenase and/or by inhibiting the reuptake of GABA by neuronal cells. It is thought that the increased GABA levels also account for the drugs antimanic properties. http://www.virtualmedicalcentre.com/drugs/gantin/2644 The way in which gabapentin exerts its anticonvulsant effect is unknown. The drug is structurally related to the neurotransmitter GABA (gamma-aminobutyric acid) but its mechanism of action differs to other drugs that interact with GABA synapses. The binding site of gabapentin is yet to be established. It also does not affect sodium channels, a means by which other anticonvulsants may work. http://www.virtualmedicalcentre.com/drugs/genrx-gabapentin/2645 - The way in which gabapentin exerts its anticonvulsant effect is unknown - The drug is structurally related to the neurotransmitter GABA (gamma-aminobutyric acid) but its mechanism of action differs to other drugs that interact with GABA synapses - The binding site of gabapentin is yet to be established - It also does not affect sodium channels, a means by which other anticonvulsants may work http://www.virtualmedicalcentre.com/drugs/neurontin/2648 Gapapentin is structurally related to the neurotransmitter gamma-aminobutyric acid (GABA) however, the mechanism of action of Gapapentin is unknown. http://www.virtualmedicalcentre.com/drugs/paxam/2650 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/pendine/2651 Gapapentin is structurally related to the neurotransmitter gamma-aminobutyric acid (GABA) however the mechanism of action of Gapapentin is unknown. http://www.virtualmedicalcentre.com/drugs/phenobarbitone/2652 - Phenobarbitone is a central nervous system (CNS) depressant that it mainly used for the management of seizures - The complete mechanism by which this drug exerts its action is not known however, it may act by enhancing or mimicking the synaptic action of the neurotransmitter gamma aminobutyric acid (GABA) - Seizure control is thought to occur due to the reduction of synaptic transmission and the increase in threshold for electrical stimulation to the motor cortex (responsible for producing gross movement) of the brain http://www.virtualmedicalcentre.com/drugs/phenobarbitone-injection-dbl/2653 - Phenobarbitone is a central nervous system (CNS) depressant that it mainly used for the management of seizures - The complete mechanism by which this drug exerts its action is not known however, it may act by enhancing or mimicking the synaptic action of the neurotransmitter gamma aminobutyric acid (GABA) - Seizure control is thought to occur due to the reduction of synaptic transmission and the increase in threshold for electrical stimulation to the motor cortex (responsible for producing gross movement) of the brain http://www.virtualmedicalcentre.com/drugs/phenytoin-injection-bp-dbl/2654 Phenytoin reduces neuronal excitability and the spread of electrical activity that characteristically occurs in epileptic seizures. Phenytoin blocks sodium channels and may also stimulate the sodium pump to reduce sodium influx thereby suppressing sodium action potentials. Other mechanisms of action of phenytoin include inhibition of neuronal calcium influx, enhancement of GABA neurotransmission and block of inotropic receptors for glutamate which may also contribute to its anti-epileptic activity. Phenytoins antiarrhythmic action is due to the reduction of sodium and calcium influx into http://www.virtualmedicalcentre.com/drugs/rivotril/2657 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/tegretol/2659 Carbamazepine obstructs voltage dependant and use dependant sodium channels and therefore prevents repetitive neuronal discharge in the brain.1-3 However, carbamazepine also has anticholinergic and antidiuretic activity and possibly suppresses ventricular automaticity, all these account for some of its side effects.1-3 http://www.virtualmedicalcentre.com/drugs/teril/2660 The mechanisms of action of Carbamazepine are only partially understood Carbamazepine blocks voltage-dependent and use-dependent sodium channels and by doing this stabilises hyperexcited nerve membranes, prevents repetitive neuronal discharges and reduces synaptic propagation of excitatory impulses Carbamazepine reduces glutamate release and stabilises neuronal membranes, which is thought to be the basis of its antiepileptic effects. The antimanic effects of carbamazepine are thought to be due to reduction of dopamine and noradrenaline turnover. Carbamazepine also has anticholinergic and a http://www.virtualmedicalcentre.com/drugs/valpro/2663 Mode of action is not fully understood. The anticonvulsant effect can be attributed to the blockage of voltage dependent Na+ channels, and increased levels of the inhibitory synaptic transmitter, gamma-aminobutyric acid (GABA). Sodium valproate increases GABA via inhibiting GABA degradative enzymes, for example, GABA transaminase and/or succinic semialdehyde dehydrogenase and/or by inhibiting the reuptake of GABA by neuronal cells. It is thought that the increased GABA levels also account for the drugs antimanic properties1. http://www.virtualmedicalcentre.com/drugs/avomine/2665 Promethazine is an antihistamine agent. It blocks H1 histamine receptors which helps prevent nausea and vomiting due to a number of causes. The sedative and anticholinergic effects may also contribute to the antiemetic effect. http://www.virtualmedicalcentre.com/drugs/dramamine/2666 Dramamine blocks histamine H1 receptors. It alsonbsp;displays additional anticholinergic and sedative properties which enhance antiemetic activity and directly acts on the vestibular system.1nbsp;The site of action of Dramamine remainsnbsp;unclear. However, it is thought thatnbsp;Dramamine acts either on the overstimulated labyrinth, depresses transmission of nerve stimuli centrallynbsp;or at the chemoreceptor trigger zone.2 http://www.virtualmedicalcentre.com/drugs/maxolon-solution-for-injection/2669 Maxolon is a centrally-acting dopamine antagonist with sedative effects. Its exact mechanism of action remains unclear.1 Maxolon is known to increase motility of the upper gastrointestinal tract and appears to sensitise tissues to acetylcholine. It does not stimulate biliary, gastric or pancreatic secretions and is not dependent on intact vagal innervation.1 Maxolon increases gastric contractions, particularly antral contractions. It is also relaxes the pyloric sphincter and stimulates peristalsis of the duodenum and jejunum, resulting in faster gastric emptying with little apparent effect o http://www.virtualmedicalcentre.com/drugs/motilium/2670 Motilium works by antagonizing dopamine receptors. Because motilium does not readily penetrate the blood-brain barrier, it rarely causes extrapyramidal side effects. Motilium also has anti-emetic properties which may be due to its peripheral gastrokinetic effects as well as its antagonistic effect on central dopamine receptors. http://www.virtualmedicalcentre.com/drugs/pramin/2671 Pharmacology. Metoclopramide (2-methoxy-5-chloro-procainamide) resulted from efforts to alter the procaine molecule so that its antiemetic properties would equal those of the phenothiazines. Like the phenothiazines, metoclopramide acts on the brain by blocking dopamine receptors; it induces extrapyramidal symptoms and stimulates prolactin secretion but has weak antipsychotic properties. In contrast to procainamide, metoclopramide has negligible cardiac effects and poor local anaesthetic activity.Since metoclopramide and its congeners sulpiride, sultopride and tiapride differ in some clinical a http://www.virtualmedicalcentre.com/drugs/stemetil/2672 Prochlorperazine is a phenothiazine drug that has both strong antiemetic and antipsychotic activity. Prochlorperazine has several mechanisms of action. It has an anti-dopamine action, anti-alpha-adrenoreceptor action and potentiates the action of noradrenaline by blocking its reuptake into nerve terminals. It also has weak anti-acetylcholine, anti-histamine and anti-serotonin actions. http://www.virtualmedicalcentre.com/drugs/travacalm-original/2674 Dimenhydrinate, one of the active ingredients of Travacalm Original,nbsp;is an antihistamine with central anticholinergic effects and is highly effective in the prevention of motion sickness.1,2 Hyoscine hydrobromide is a belladonna alkaloid possessing antimuscarinic properties whichnbsp;has strong CNS anticholinergic effects.2Caffeine is used for its stimulating effect tonbsp;offset the sedative side effects of the other two ingredients, dimenhydrinate and hyoscine hydrobromide.2 http://www.virtualmedicalcentre.com/drugs/travacalm-ho/2675 Hyoscine hydrobromide is a belladonna alkaloid possessing antimuscarinic properties whichnbsp;has strong CNS anticholinergic effects.2 http://www.virtualmedicalcentre.com/drugs/accupril/2676 Accupril is an angiotensin converting enzyme (ACE) inhibitor. ACE-inhibitors block the conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. Angiotensin II induces vasoconstriction, and aldosterone release from the adrenal cortex resulting in renal sodium and fluid reabsorption. By reducing the formation of Angiotensin II, ACE-inhibitors produce vasodilatation and increased sodium and fluid loss from the kidneys resulting in a subsequent drop in blood pressure. The decrease in blood pressure produced by ACE-inhibitors has a minimal effect on heart rate, re http://www.virtualmedicalcentre.com/drugs/acenorm/2678 Captopril is an angiotensin converting enzyme (ACE) inhibitor. ACE-inhibitors block the conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. Angiotensin II induces vasoconstriction, and aldosterone release from the adrenal cortex resulting in renal sodium and fluid reabsorption. By reducing the formation of Angiotensin II, ACE-inhibitors produce vasodilatation and increased sodium and fluid loss from the kidneys resulting in a subsequent drop in blood pressure. The decrease in blood pressure produced by ACE-inhibitors has a minimal effect on heart rate, r http://www.virtualmedicalcentre.com/drugs/adalat-10-adalat-20/2679 Adalat contains nifedipine, one of the dyhydrpyridines which selectively block calcium channels within the vascular system. Cardiac muscle and the smooth muscle of the blood vessels are dependent on calcium ions to contract. Nifedipine inhibits calcium ions from entering these cells causing the muscle cells to relax. Nifedipine is a peripherally acting calcium channel blocker that has minimal effect on myocardial cells at therapeutic doses.2 By relaxing arterial smooth muscle Nifedipine causes dilatation of the coronary arteries and arterioles and inhibits of coronary artery spasm. This increa http://www.virtualmedicalcentre.com/drugs/adalat-oros/2680 Adalat Oros contains nifedipine, one of the dyhydropyridines which selectively block calcium channels within the vascular system. Thus it is a peripherally acting agent that has minimal effect on myocardial cells at therapeutic doses.2 Nefedipine acts by inhibiting the transmembrane influx of calcium ions into vascular smooth muscle cells which subsequently inhibits contractile processes within these cells. The exact mechanisms by which nifedipine relieves angina and reduces blood pressure are not fully understood but it is thought to be related to its vasodilatory action. This produces a redu http://www.virtualmedicalcentre.com/drugs/agon-sr/2681 Calcium channel blockers block the inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L-type calcium channels. Felodipine, a dihydropyridine-type calcium channel blocker acts mainly on vascular smooth muscle to reduce peripheral vascular resistance, and have minimal effect on normal myocardial cells at therapeutic doses. http://www.virtualmedicalcentre.com/drugs/aldomet/2682 Aldomet (Methyldopa) is a centrally acting alpha 2 adrenoceptor agonist that acts as an antihypertensive agent, by reducing sympathetic tone. Aldomet is effective in reducing both supine and standing blood pressure. Although Aldomet is an effective antihypertensive agent, it is not the first line agent as it is less well tolerated as compared to other antihypertensives and there is no evidence about their benefits on cardiovascular risk.1,2 http://www.virtualmedicalcentre.com/drugs/alphapress/2683 Hydralazine lowers blood pressure by causing peripheral vasodilation. It does this by direct relaxation of vascular smooth muscle in resistance vessels, primarily arterioles. The exact cellular mechanism by which this relaxation occurs is not fully understood. Peripheral vasodilation results in a significant decrease in arterial blood pressure, diastolic decreasing more than systolic. The body compensates for this rapid drop in blood pressure by increasing heart rate, cardiac output and stroke volume. Due to these compensatory mechanisms, much of the therapeutic action of Hydralazine may be http://www.virtualmedicalcentre.com/drugs/alphapril/2684 Enalapril maleate is a prodrug which when administered orally is hydrolysed to release the active converting enzyme inhibitor enalaprilat. The liver appears to be the main site for this conversion. Administration of enalapril to patients with hypertension results in a reduction of both supine and standing blood pressure without a significant increase in heart rate. http://www.virtualmedicalcentre.com/drugs/amprace/2685 The active ingredient of Amprace is enalapril maleate. The mechanism of action of Amprace is not fully understood. The most favoured mechanism is the inhibition of the angiotensin converting enzyme (ACE) that catalyses the conversion of angiotensin I tonbsp;angiotensin II.nbsp;Inhibition of ACE results in decreased plasma angiotensin II, which leads to increased plasma renin activitynbsp;and decreased aldosterone secretion. The suppression of the renin-angiotensin-aldosterone system leads to lowered blood pressure.nbsp;Amprace may also block the degradation of bradykinin, a potent vasodepr http://www.virtualmedicalcentre.com/drugs/anpec/2686 Calcium channel blockers block the inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L-type calcium channels. Verapamil acts mainly on the heart to reduce contractility, slow the heart rate and slow conduction but has less effect on vascular smooth muscle. http://www.virtualmedicalcentre.com/drugs/anpec-sr/2687 Calcium channel blockers block the inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L-type calcium channels. Verapamil acts mainly on the heart to reduce contractility, slow the heart rate and slow conduction but has less effect on vascular smooth muscle. http://www.virtualmedicalcentre.com/drugs/apresoline/2688 Hydralazine lowers blood pressure by causing peripheral vasodilation. It does this by direct relaxation of vascular smooth muscle in resistance vessels, primarily arterioles. The exact cellular mechanism by which this relaxation occurs is not fully understood. Peripheral vasodilation results in a significant decrease in arterial blood pressure, diastolic decreasing more than systolic. The body compensates for this rapid drop in blood pressure by increasing heart rate, cardiac output and stroke volume. Due to these compensatory mechanisms, much of the therapeutic action of Hydralazine may be http://www.virtualmedicalcentre.com/drugs/atacand/2690 Candesartan competitively antagonises the action of angiotensin II, specifically at type 1 angiotensin (AT1) receptors.1-3 This complex results in reduced sodium reabsorption, aldosterone release and the vasoconstrictive properties of angiotensin.1-3 Because angiotensin-converting enzyme is not inhibited, bradykinin is broken down and bradykinin-mediated adverse effectsnbsp;are reduced.1-3 http://www.virtualmedicalcentre.com/drugs/atacand-plus-16125/2691 Atacand is a prodrug that is suitable for oral administration. It is converted to candesartan (an angiotensin II receptor antagonist) by ester hydrolysis during gastrointestinal absorption. Angiotensin II is a major cause of hypertension, other cardiovascular disorders and end organ hypertrophy and damage. Angiotensin II is responsible for mediating vasoconstriction, stimulating aldosterone production, regulating of salt and water homeostasis and stimulating cell growth. These effects all occur via the type 1 (AT1) receptor, for which Atacand is selective, but has no agonis http://www.virtualmedicalcentre.com/drugs/auspril/2692 Enalapril maleate is a prodrug which when administered orally is hydrolysed to release the active converting enzyme inhibitor enalaprilat. The liver appears to be the main site for this conversion. Administration of enalapril to patients with hypertension results in a reduction of both supine and standing blood pressure without a significant increase in heart rate. http://www.virtualmedicalcentre.com/drugs/avapro/2693 Irbesartan is a specific antagonist of angiotensin II receptors (AT1 subtype).1,2,3 It competitively and selectively blocks the potent vasoconstrictor, sodium reabsorption and aldosterone secreting effects of angiotensin II on the receptors of vascular smooth muscle cells and adrenal cortex.1,2 http://www.virtualmedicalcentre.com/drugs/avapro-hct/2694 Avapro HCT an oral antihypertensive agent that consists of two active ingredients, irbesartan and hydrochlorothiazide. Irbesartan is a specific antagonist of angiotensin II receptors (AT1 subtype).1-3 It competitively and selectively blocks the potent vasoconstrictor, sodium reabsorption and aldosterone secreting effects of angiotensin II on the receptors of vascular smooth muscle cells and adrenal cortex.1,2 Hydrochlorothiazide is a thiazide diuretic with natriuretic and anti-hypertensive effects.1,2 The exact anti-hypertensive mechanism of thiazide diuretics is not fully known. Howe http://www.virtualmedicalcentre.com/drugs/capoten/2695 Captopril is an angiotensin converting enzyme (ACE) inhibitor. ACE-inhibitors block the conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. Angiotensin II induces vasoconstriction, and aldosterone release from the adrenal cortex resulting in renal sodium and fluid reabsorption. By reducing the formation of Angiotensin II, ACE-inhibitors produce vasodilatation and increased sodium and fluid loss from the kidneys resulting in a subsequent drop in blood pressure. The decrease in blood pressure produced by ACE-inhibitors has a minimal effect on heart http://www.virtualmedicalcentre.com/drugs/captohexal/2696 Captopril is an angiotensin converting enzyme (ACE) inhibitor. ACE-inhibitors block the conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. Angiotensin II induces vasoconstriction, and aldosterone release from the adrenal cortex resulting in renal sodium and fluid reabsorption. By reducing the formation of Angiotensin II, ACE-inhibitors produce vasodilatation and increased sodium and fluid loss from the kidneys resulting in a subsequent drop in blood pressure. The decrease in blood pressure produced by ACE-inhibitors has a minimal effect on heart rate, r http://www.virtualmedicalcentre.com/drugs/captopril/2697 Captopril is an angiotensin converting enzyme (ACE) inhibitor. ACE-inhibitors block the conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. Angiotensin II induces vasoconstriction, and aldosterone release from the adrenal cortex resulting in renal sodium and fluid reabsorption. By reducing the formation of Angiotensin II, ACE-inhibitors produce vasodilatation and increased sodium and fluid loss from the kidneys resulting in a subsequent drop in blood pressure. The decrease in blood pressure produced by ACE-inhibitors has a minimal effect on heart http://www.virtualmedicalcentre.com/drugs/captopril-bc/2698 Captopril is an angiotensin converting enzyme (ACE) inhibitor. ACE-inhibitors block the conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. Angiotensin II induces vasoconstriction, and aldosterone release from the adrenal cortex resulting in renal sodium and fluid reabsorption. By reducing the formation of Angiotensin II, ACE-inhibitors produce vasodilatation and increased sodium and fluid loss from the kidneys resulting in a subsequent drop in blood pressure. The decrease in blood pressure produced by ACE-inhibitors has a minimal effect on heart http://www.virtualmedicalcentre.com/drugs/cardizem-cd/2699 -Diltiazem is a slow calcium channel blocker. -It inhibits the influx of calcium ions during membrane depolarisation of cardiac and vascular smooth muscle. -Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/chem-mart-captopril/2701 Captopril is an angiotensin converting enzyme (ACE) inhibitor. ACE-inhibitors block the conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. Angiotensin II induces vasoconstriction, and aldosterone release from the adrenal cortex resulting in renal sodium and fluid reabsorption. By reducing the formation of Angiotensin II, ACE-inhibitors produce vasodilatation and increased sodium and fluid loss from the kidneys resulting in a subsequent drop in blood pressure. The decrease in blood pressure produced by ACE-inhibitors has a minimal effect on heart http://www.virtualmedicalcentre.com/drugs/chem-mart-enalapril/2702 Enalapril maleate is a prodrug which when administered orally is hydrolysed to release the active converting enzyme inhibitor enalaprilat. The liver appears to be the main site for this conversion. Administration of enalapril to patients with hypertension results in a reduction of both supine and standing blood pressure without a significant increase in heart rate. http://www.virtualmedicalcentre.com/drugs/chem-mart-lisinopril/2704 Lisinopril is a long acting angiotensin converting enzyme inhibitor. It is a peptidyl dipeptidase inhibitor, which inhibits the angiotensin converting enzyme (ACE) that catalyses the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased concentrations of plasma angiotensin II which results in decreased vasopressor activity and decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium. http://www.virtualmedicalcentre.com/drugs/chem-mart-nifedipine/2705 Nifedipine is a calcium channel blocker Cardiac muscle and the smooth muscle of the blood vessels are dependent on calcium ions to contract. Nifedipine inhibits calcium ions from entering these cells causing the muscle cells to relax. By relaxing arterial smooth muscle Nifedipine causes dilatation of the coronary arteries and arterioles and inhibits of coronary artery spasm. This increases the supply of oxygen to the myocardium and reduces the occurrence of angina attacks By dilating peripheral blood vessels Nifedipine reduces afterload and decreases the work of the heart reducing its http://www.virtualmedicalcentre.com/drugs/chem-mart-prazosin/2706 Prazosin is an alpha-adrenergic antagonist. Blockade of arteriolar alpha-adrenergic receptors results in vasodilation and an overall decrease in total peripheral resistance. Selectivity of Prazosin for alpha1 receptors means there is no reflex tachycardia, increase in cardiac output or increase in renal blood flow. The resulting decrease in blood pressure affects diastolic blood pressure more than systolic, and affects both supine and standing blood pressure. The activity of Prazosin on the alpha-adrenergic receptors of the prostate allows it to be used in the treatment of benign prostatic hyp http://www.virtualmedicalcentre.com/drugs/coversyl/2708 Perindopril is a prodrug, and following hydrolysis to perindoprilat, inhibits angiotensin converting enzyme (ACE). It is thought that ACE inhibitors reduce blood pressure by inhibiting the enzyme which catalyses the conversion of angiotensin I to angiotensin II. Decreased plasma angiotensin II leads to increased plasma renin activity and a decrease in aldosterone. In addition to its effects on circulating ACE, Coversyl binds to and inhibits tissue converting enzyme, predominantly in the kidney and vascular wall. http://www.virtualmedicalcentre.com/drugs/coversyl-plus/2709 Coversyl Plus is a combination of perindopril, an angiotensin converting enzyme (ACE) inhibitor and indapamide, a diuretic.Perindopril inhibits the conversion of angiotensin I to angiotensin II. Angiotensin II induces vasoconstriction, and aldosterone release from the adrenal cortex resulting in renal sodium and fluid reabsorption. By reducing the formation of Angiotensin II, perindopril produces vasodilatation and increased sodium and fluid loss from the kidneys resulting in a subsequent drop in blood pressure. Indapamide acts on the proximal segment of the distal tubule in the kidney and h http://www.virtualmedicalcentre.com/drugs/cozaar/2710 Losartan is an angiotensin II receptor antagonist. Angiotensin II binds to the AT1 receptor found in many tissues such as vascular smooth muscle, adrenal gland, kidneys and the heart. The actions of angiotensin II include vasoconstriction and the release of aldosterone from the adrenal cortex resulting in renal sodium and fluid reabsorption. By blocking the Angiotensin II receptor, Losartan produces vasodilatation and increased sodium and fluid loss from the kidneys resulting in a subsequent drop in blood pressure. Unlike ACE inhibitors Losartan does not affect angiotensin-converting en http://www.virtualmedicalcentre.com/drugs/enahexal/2713 Enalapril maleate is a prodrug which when administered orally is hydrolysed to release the active converting enzyme inhibitor enalaprilat. The liver appears to be the main site for this conversion. Administration of enalapril to patients with hypertension results in a reduction of both supine and standing blood pressure without a significant increase in heart rate. http://www.virtualmedicalcentre.com/drugs/enalapril-bc/2714 Enalapril is a prodrug which is converted in the liver to form the active converting enzyme inhibitor Enalaprilat. The mechanism by which enalapril lowers blood pressure is not entirely clear however it is thought that it inhibits angiotensin converting enzyme, an enzyme responsible for catalysing the conversion of angiotensin I to angiotensin II. Angiotensin II induces vasoconstriction, and aldosterone release from the adrenal cortex resulting in renal sodium and fluid reabsorption. By reducing the formation of Angiotensin II, Enalaprilat produces vasodilatation and increased sodium http://www.virtualmedicalcentre.com/drugs/felodur-er/2715 Calcium channel blockers block the inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L-type calcium channels. Felodipine, a dihydropyridine-type calcium channel blocker acts mainly on vascular smooth muscle to reduce peripheral vascular resistance, and have minimal effect on normal myocardial cells at therapeutic doses. http://www.virtualmedicalcentre.com/drugs/fibsol/2716 Lisinopril is a long acting angiotensin converting enzyme inhibitor. It is a peptidyl dipeptidase inhibitor, which inhibits the angiotensin converting enzyme (ACE) that catalyses the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased concentrations of plasma angiotensin II which results in decreased vasopressor activity and decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium. http://www.virtualmedicalcentre.com/drugs/genrx-captopril/2717 Captopril is an angiotensin converting enzyme (ACE) inhibitor. ACE-inhibitors block the conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. Angiotensin II induces vasoconstriction, and aldosterone release from the adrenal cortex resulting in renal sodium and fluid reabsorption. By reducing the formation of Angiotensin II, ACE-inhibitors produce vasodilatation and increased sodium and fluid loss from the kidneys resulting in a subsequent drop in blood pressure. The decrease in blood pressure produced by ACE-inhibitors has a minimal effect on heart http://www.virtualmedicalcentre.com/drugs/genrx-enalapril/2718 Enalapril maleate is a prodrug which when administered orally is hydrolysed to release the active converting enzyme inhibitor enalaprilat. The liver appears to be the main site for this conversion. Administration of enalapril to patients with hypertension results in a reduction of both supine and standing blood pressure without a significant increase in heart rate. http://www.virtualmedicalcentre.com/drugs/genrx-lisinopril/2720 Lisinopril is a long acting angiotensin converting enzyme inhibitor. It is a peptidyl dipeptidase inhibitor, which inhibits the angiotensin converting enzyme (ACE) that catalyses the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased concentrations of plasma angiotensin II which results in decreased vasopressor activity and decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium. http://www.virtualmedicalcentre.com/drugs/genrx-nifedipine/2721 Nifedipine is a calcium channel blocker Cardiac muscle and the smooth muscle of the blood vessels are dependent on calcium ions to contract. Nifedipine inhibits calcium ions from entering these cells causing the muscle cells to relax. By relaxing arterial smooth muscle Nifedipine causes dilatation of the coronary arteries and arterioles and inhibits of coronary artery spasm. This increases the supply of oxygen to the myocardium and reduces the occurrence of angina attacks By dilating peripheral blood vessels Nifedipine reduces afterload and decreases the work of the heart reducing its http://www.virtualmedicalcentre.com/drugs/genrx-prazosin/2722 Prazosin is an alpha-adrenergic antagonist. Blockade of arteriolar alpha-adrenergic receptors results in vasodilation and an overall decrease in total peripheral resistance. Selectivity of Prazosin for alpha1 receptors means there is no reflex tachycardia, increase in cardiac output or increase in renal blood flow. The resulting decrease in blood pressure affects diastolic blood pressure more than systolic, and affects both supine and standing blood pressure. The activity of Prazosin on the alpha-adrenergic receptors of the prostate allows it to be used in the treatment of benign prostatic hyp http://www.virtualmedicalcentre.com/drugs/healthsense-captopril/2724 Captopril is an angiotensin converting enzyme (ACE) inhibitor. ACE-inhibitors block the conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. Angiotensin II induces vasoconstriction, and aldosterone release from the adrenal cortex resulting in renal sodium and fluid reabsorption. By reducing the formation of Angiotensin II, ACE-inhibitors produce vasodilatation and increased sodium and fluid loss from the kidneys resulting in a subsequent drop in blood pressure. The decrease in blood pressure produced by ACE-inhibitors has a minimal effect on heart http://www.virtualmedicalcentre.com/drugs/healthsense-enalapril/2725 Enalapril maleate is a prodrug which when administered orally is hydrolysed to release the active converting enzyme inhibitor enalaprilat. The liver appears to be the main site for this conversion. Administration of enalapril to patients with hypertension results in a reduction of both supine and standing blood pressure without a significant increase in heart rate. http://www.virtualmedicalcentre.com/drugs/healthsense-lisinopril/2727 Lisinopril is a long acting angiotensin converting enzyme inhibitor. It is a peptidyl dipeptidase inhibitor, which inhibits the angiotensin converting enzyme (ACE) that catalyses the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased concentrations of plasma angiotensin II which results in decreased vasopressor activity and decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium. http://www.virtualmedicalcentre.com/drugs/healthsense-nifedipine/2728 -Nifedipine is a calcium channel blocker. It inhibits the slow inward calcium ion channels -It is a relaxant of vascular smooth muscle and an inhibitor of coronary artery spasm thus improving myocardial oxygen supply. -It inhibits the influx of calcium ions causing relaxation and peripheral vasodilatation, which in turn reduces the afterload against which the heart works. -It directly decreases myocardial oxygen consumption. -Reduction in blood pressure is mediated by relaxation of vascular -Nifedipine is a calcium channel blocker. It inhibits the slow inward calcium ion channels -It is http://www.virtualmedicalcentre.com/drugs/healthsense-prazosin/2729 Prazosin is an alpha-adrenergic antagonist. Blockade of arteriolar alpha-adrenergic receptors results in vasodilation and an overall decrease in total peripheral resistance. Selectivity of Prazosin for alpha1 receptors means there is no reflex tachycardia, increase in cardiac output or increase in renal blood flow. The resulting decrease in blood pressure affects diastolic blood pressure more than systolic, and affects both supine and standing blood pressure. The activity of Prazosin on the alpha-adrenergic receptors of the prostate allows it to be used in the treatment of benign prostatic hyp http://www.virtualmedicalcentre.com/drugs/isoptin-isoptin-sr/2733 Calcium channel blockers block the inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L-type calcium channels. Verapamil acts mainly on the heart to reduce contractility, slow the heart rate and slow conduction but has less effect on vascular smooth muscle. http://www.virtualmedicalcentre.com/drugs/karvea/2734 Irbesartan blocks the potent vasoconstrictor and aldosterone secreting effects of angiotensin II by selective antagonism of the angiotensin II (AT1 subtype receptors) localised on vascular smooth muscle cells and in adrenal cortex. Angiotensin II is an important component of the renin angiotensin system. Renin is an enzyme synthesised by the kidneys which acts on a globulin substrate to produce angiotensin I. Angiotensin I, an inactive decapeptide is converted by angiotensin converting enzyme (ACE) to octapeptide angiotensin II, a potent endogenous vasoconstrictor. Angiotensin II stimulates al http://www.virtualmedicalcentre.com/drugs/karvezide/2735 Karvezide is a mixture combining an angiotensin II receptor antagonist, irbesartan, and a thiazide diuretic, hydrochlorothiazide. Irbesartan competitively antagonises the action of angiotensin II specifically at type 1 angiotensin (AT1) receptors.1-3 This complex results in reduced sodium reabsorption, aldosterone release and vasoconstrictive properties of angiotensin.1-3 Hydrochlorothiazide is a benzothiadiazine (thiazide) diuretic inhibiting the reabsorption of sodum and chloride in the proximal part of the distal convulated tubule.1-3 The result of the combination is a decrease in blood http://www.virtualmedicalcentre.com/drugs/lisinopril-bc/2736 Lisinopril is a long acting angiotensin converting enzyme inhibitor. It is a peptidyl dipeptidase inhibitor, which inhibits the angiotensin converting enzyme (ACE) that catalyses the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased concentrations of plasma angiotensin II which results in decreased vasopressor activity and decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium. http://www.virtualmedicalcentre.com/drugs/lisodur/2737 Lisinopril is a long acting angiotensin converting enzyme inhibitor. It is a peptidyl dipeptidase inhibitor, which inhibits the angiotensin converting enzyme (ACE) that catalyses the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased concentrations of plasma angiotensin II which results in decreased vasopressor activity and decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium. http://www.virtualmedicalcentre.com/drugs/trental-400/2739 Pharmacology: -Oxpentifylline and it’s metabolites reduce blood viscosity, thus improving blood flow in the microcirculation and increasing tissue oxygenation. -Reduced blood viscosity may be due to improved red blood cell flexibility, decreased plasma fibrinogen and improved platelet deaggregation. However the precise mode of action are yet to be clearly defined. -Apparent half-lifes: oxpentifylline 0.4-0.8 hours, it’s metabolites : 1-1.6 hours. http://www.virtualmedicalcentre.com/drugs/micardis/2740 Telmisartan is a specific angiotensin II (type AT1) receptor antagonist. It displaces angiotensin II with very high affinity from its binding site at the AT1 receptor subtype, which is responsible for the known actions of angiotensin II. It therefore blocks the vasoconstricting (hence reducing systemic vascular resistance) and aldosterone-secreting effects mediated by angiotensin II. As there is no inhibition on angiotensin converting enzyme which also degrades bradykinin, potentiation of bradykinin-mediated adverse effects or oedema is not expected. Antihypertensive activity occurs gradually http://www.virtualmedicalcentre.com/drugs/minipress/2741 Prazosin is an alpha-adrenergic antagonist. Blockade of arteriolar alpha-adrenergic receptors results in vasodilation and an overall decrease in total peripheral resistance. Selectivity of Prazosin for alpha1 receptors means there is no reflex tachycardia, increase in cardiac output or increase in renal blood flow. The resulting decrease in blood pressure affects diastolic blood pressure more than systolic, and affects both supine and standing blood pressure. The activity of Prazosin on the alpha-adrenergic receptors of the prostate allows it to be used in the treatment of benign prostatic hyp http://www.virtualmedicalcentre.com/drugs/monoplus/2742 Fosinopril is an angiotensin-converting enzyme (ACE) inhibitor. ACE converts angiotensin I to angiotensin II, a powerful vasoconstrictor. Angiotensin II also stimulates aldosterone secretion, which contributes to sodium and water retention. Inhibition of ACE prevents the formation of angiotensin II, and thereby reduces two significant contributors to increased blood pressure, vasoconstriction and fluid overload. These effects have been shown to reduce both supine and standing blood pressure, without orthostatic effects. ACE inhibitors are effective alone or in combination with other antihypert http://www.virtualmedicalcentre.com/drugs/monopril/2743 Fosinopril is an angiotensin-converting enzyme (ACE) inhibitor. ACE converts angiotensin I to angiotensin II, a powerful vasoconstrictor. Angiotensin II also stimulates aldosterone secretion, which contributes to sodium and water retention. Inhibition of ACE prevents the formation of angiotensin II, and thereby reduces two significant contributors to increased blood pressure, vasoconstriction and fluid overload. These effects have been shown to reduce both supine and standing blood pressure, without orthostatic effects. ACE inhibitors are effective alone or in combination with other antihypert http://www.virtualmedicalcentre.com/drugs/nifecard/2747 Nifedipine is a calcium channel blocker. It inhibits the slow inward calcium ion channels. It is a relaxant of vascular smooth muscle and an inhibitor of coronary artery spasm thus improving myocardial oxygen supply. It inhibits the influx of calcium ions causing relaxation and peripheral vasodilatation, which in turn reduces the afterload against which the heart works. It directly decreases myocardial oxygen consumption. Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/nifedipine-bc/2748 Nifedipine is a calcium channel blocker. It inhibits the slow inward calcium ion channels. It is a relaxant of vascular smooth muscle and an inhibitor of coronary artery spasm thus improving myocardial oxygen supply. It inhibits the influx of calcium ions causing relaxation and peripheral vasodilatation, which in turn reduces the afterload against which the heart works. It directly decreases myocardial oxygen consumption. Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/nifehexal/2749 Nifedipine is a calcium channel blocker. It inhibits the slow inward calcium ion channels It is a relaxant of vascular smooth muscle and an inhibitor of coronary artery spasm thus improving myocardial oxygen supply. It inhibits the influx of calcium ions causing relaxation and peripheral vasodilatation, which in turn reduces the afterload against which the heart works. It directly decreases myocardial oxygen consumption. Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/norvasc/2750 Amlodipine inhibits the influx of calcium ions a) through slow calcium channels and b) across the membranes of cardiac and vascular smooth muscle cells. Amlodipine is selective for vascular smooth muscle cells as opposed to cardiac muscle cells. Amlodipine causes peripheral arterial vasodilatation and a reduction in peripheral vascular resistance and blood pressure. Amlodipine is useful in the treatment of angina because it reduces the total ischaemic burden by: 1) Dilating peripheral arterioles and reducing the total peripheral resistance (afterload), therefore reducing myocardial http://www.virtualmedicalcentre.com/drugs/nyefax/2751 -Nifedipine is a calcium channel blocker. It inhibits the slow inward calcium ion channels -It is a relaxant of vascular smooth muscle and an inhibitor of coronary artery spasm thus improving myocardial oxygen supply. -It inhibits the influx of calcium ions causing relaxation and peripheral vasodilatation, which in turn reduces the afterload against which the heart works. -It directly decreases myocardial oxygen consumption. -Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/plendil-er/2753 Calcium channel blockers block the inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L-typecalcium channels. Felodipine, a dihydropyridine-type calcium channel blocker acts mainly on vascular smooth muscle to reduce peripheral vascular resistance, and have minimal effect on normal myocardial cells at therapeutic doses. http://www.virtualmedicalcentre.com/drugs/prazosin-bc/2757 Prazosin is an alpha-adrenergic antagonist. Blockade of arteriolar alpha-adrenergic receptors results in vasodilation and an overall decrease in total peripheral resistance. Selectivity of Prazosin for alpha1 receptors means there is no reflex tachycardia, increase in cardiac output or increase in renal blood flow. The resulting decrease in blood pressure affects diastolic blood pressure more than systolic, and affects both supine and standing blood pressure. The activity of Prazosin on the alpha-adrenergic receptors of the prostate allows it to be used in the treatment of benign prostatic hyp http://www.virtualmedicalcentre.com/drugs/pressin/2759 Prazosin is an alpha-adrenergic antagonist. Blockade of arteriolar alpha-adrenergic receptors results in vasodilation and an overall decrease in total peripheral resistance. Selectivity of Prazosin for alpha1 receptors means there is no reflex tachycardia, increase in cardiac output or increase in renal blood flow. The resulting decrease in blood pressure affects diastolic blood pressure more than systolic, and affects both supine and standing blood pressure. The activity of Prazosin on the alpha-adrenergic receptors of the prostate allows it to be used in the treatment of benign prostatic hyp http://www.virtualmedicalcentre.com/drugs/prinivil/2760 Lisinopril is a long acting angiotensin converting enzyme inhibitor. It is a peptidyl dipeptidase inhibitor, which inhibits the angiotensin converting enzyme (ACE) that catalyses the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased concentrations of plasma angiotensin II which results in decreased vasopressor activity and decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium. http://www.virtualmedicalcentre.com/drugs/ramace/2762 ACE inhibitor. Following absorption from the gut, Ramipril is hydrolysed in the liver to the active metabolite, ramiprilat. Ramipril and ramiprilat inhibit angiotensin converting enzyme, the enzyme responsible for catalysing the conversion of angiotensin I to angiotensin II. Angiotensin II has vasocontrictor activity and stimulates aldosterone release from the adrenal cortex. It is believed that the chief mechanism by which Ramipril lowers blood pressure is through suppression of the renin / angiotensin / aldosterone system, however Ramace still exerts an antihypertensive effect in patient http://www.virtualmedicalcentre.com/drugs/renitec/2763 Enalapril maleate is a prodrug which when administered orally is hydrolysed to release the active converting enzyme inhibitor enalaprilat. The liver appears to be the main site for this conversion. Administration of enalapril to patients with hypertension results in a reduction of both supine and standing blood pressure without a significant increase in heart rate. http://www.virtualmedicalcentre.com/drugs/captopril-terry-white-chemists/2766 Captopril is an angiotensin converting enzyme (ACE) inhibitor. ACE-inhibitors block the conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. Angiotensin II induces vasoconstriction, and aldosterone release from the adrenal cortex resulting in renal sodium and fluid reabsorption. By reducing the formation of Angiotensin II, ACE-inhibitors produce vasodilatation and increased sodium and fluid loss from the kidneys resulting in a subsequent drop in blood pressure. The decrease in blood pressure produced by ACE-inhibitors has a minimal effect on heart rat http://www.virtualmedicalcentre.com/drugs/enalapril-terry-white-chemists/2767 Enalapril maleate is a prodrug which when administered orally is hydrolysed to release the active converting enzyme inhibitor enalaprilat. The liver appears to be the main site for this conversion. Administration of enalapril to patients with hypertension results in a reduction of both supine and standing blood pressure without a significant increase in heart rate. http://www.virtualmedicalcentre.com/drugs/lisinopril-terry-white-chemists/2769 Lisinopril is a long acting angiotensin converting enzyme inhibitor. It is a peptidyl dipeptidase inhibitor, which inhibits the angiotensin converting enzyme (ACE) that catalyses the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased concentrations of plasma angiotensin II which results in decreased vasopressor activity and decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium. http://www.virtualmedicalcentre.com/drugs/prazosin-terry-white-chemists/2770 Prazosin is an alpha-adrenergic antagonist. Blockade of arteriolar alpha-adrenergic receptors results in vasodilation and an overall decrease in total peripheral resistance. Selectivity of Prazosin for alpha1 receptors means there is no reflex tachycardia, increase in cardiac output or increase in renal blood flow. The resulting decrease in blood pressure affects diastolic blood pressure more than systolic, and affects both supine and standing blood pressure. The activity of Prazosin on the alpha-adrenergic receptors of the prostate allows it to be used in the treatment of benign prostatic hyp http://www.virtualmedicalcentre.com/drugs/teveten/2771 Eprosartan is a non-biphenyl nontetrazole angiotensin II receptor (AT1 subtype) antagonist It blocks the vasoconstricting and aldosterone secreting effects of angiotensin II by antagonizing the angiotensin II (AT1 subtype) receptor: this renin angiotensin system is involved in the pathophysiology of hypertension. Eprosartan inhibits the vasoconstrictive effects of angiotensin II which leads to a reduction in systemic vascular resistance. http://www.virtualmedicalcentre.com/drugs/topace/2772 Captopril is an angiotensin converting enzyme (ACE) inhibitor. ACE-inhibitors block the conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. Angiotensin II induces vasoconstriction, and aldosterone release from the adrenal cortex resulting in renal sodium and fluid reabsorption. By reducing the formation of Angiotensin II, ACE-inhibitors produce vasodilatation and increased sodium and fluid loss from the kidneys resulting in a subsequent drop in blood pressure. The decrease in blood pressure produced by ACE-inhibitors has a minimal effect on heart rat http://www.virtualmedicalcentre.com/drugs/tritace/2774 Tritace (Ramipril) is an angiotensin converting enzyme (ACE) inhibitor, which blocks the conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. As a result, they reduce the effects of angiotenisn II-induced vasoconstriction, sodium retention and the release of aldosterone. They also decrease the effect of angiotensin on the sympathetic nervous system and as a growth factor.1,2 http://www.virtualmedicalcentre.com/drugs/vasocardol-cd/2775 -Diltiazem is a slow calcium channel blocker. -It inhibits the influx of calcium ions during membrane depolarisation of cardiac and vascular smooth muscle. -Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/veracaps-sr/2776 Calcium channel blockers block the inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L-type calcium channels. Verapamil acts mainly on the heart to reduce contractility, slow the heart rate and slow conduction but has less effect on vascular smooth muscle. http://www.virtualmedicalcentre.com/drugs/zestril/2779 Lisinopril is a long acting angiotensin converting enzyme inhibitor. It is a peptidyl dipeptidase inhibitor, which inhibits the angiotensin converting enzyme (ACE) that catalyses the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased concentrations of plasma angiotensin II which results in decreased vasopressor activity and decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium. http://www.virtualmedicalcentre.com/drugs/anselol/2780 Atenolol, a type of beta-1-selective-beta-Blocker, competitively blocks beta- adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver. The antihypertensive effect works by reducing cardiac output without reflex increase in peripheral vascular resistance; CNS effect and reduced renin secretion may also contribute. The antianginal effect is due to reductionin left ventricular work and oxygen use, resulting from decrease in heart rate and contractility. The antiarrhythmic properties are due to antisympathetic effects: depression of sinus nod http://www.virtualmedicalcentre.com/drugs/atehexal/2781 Atenolol, a type of beta-1-selective-beta- Blocker, competitively blocks beta- adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver. The antihypertensive effect works by reducing cardiac output without reflex increase in peripheral vascular resistance; CNS effect and reduced renin secretion may also contribute. The antianginal effect is due to reduction in left ventricular work and oxygen use, resulting from decrease in heart rate and contractility. The antiarrhythmic properties are due to antisympathetic effects: http://www.virtualmedicalcentre.com/drugs/atenolol-bc/2782 Atenolol is a beta-Adrenoceptor blocking agent that acts preferentially on beta-receptors in the heart. It reduces raised blood pressure by an unknown mechanismAtenolol prevents angina by decreasing the heart rate and the force of contractility of the heart subsequently reducing the cardiac workload and the myocardial oxygen requirementsAtenolol also has an antisympathetic effect which is thought to be responsible for its antiarrhythmic actions. Atenolol depresses the function of the sinus node and the atrioventricular node and also prolongs the refractory periods in the atria. http://www.virtualmedicalcentre.com/drugs/barbloc/2783 Pindolol is a non-selective beta-blocker that blocks beta-adrenergic receptors and also has intrinsic sympathomimetic activity. Pindolol slows the heart rate, reduces the force of cardiac contraction and reduces cardiac output all of which result in a decreased in the myocardial demand for oxygen making an attack of angina less likely to occur. The mechanism by which Pindolol reduces blood pressure is unknown. Peak plasma concentrations of Pindolol are reached 1-2 hours after oral ingestion and therapeutic levels are established quickly. http://www.virtualmedicalcentre.com/drugs/betaloc/2784 Metoprolol is a cardioselective beta-adrenoreceptor blocker that has no intrinsic sympathomimetic activity. At therapeutic dosses it acts on beta 1 receptors located in the heart without acting on the beta-2- receptors located in the bronchi and peripheral vessels. Metoprolol reduces blood pressure in both the erect and supine position and reduces the rise in blood pressure that occurs with physical and mental stress. Metoprolol reduces the frequency and severity of attacks in patients with angina pectoris and increases these patients exercise tolerance. Metoprolol has also been http://www.virtualmedicalcentre.com/drugs/bicor/2785 Bisoprolol is a beta-1-selective adrenoceptor blocker that has very low affinity to the beta-2-receptors of the bronchiolar and vascular smooth muscle. However, at doses greater than the maximum recommended dose of 10 mg, Bisoprolol may also inhibit these beta-2-receptors Bisoprolol reduces the heart rate, cardiac output and blood pressure both at rest and when exercising. http://www.virtualmedicalcentre.com/drugs/brevibloc/2786 Esmolol selectively blocks beta-1-adrenoreceptors in the cardiac muscle. It works quickly and its duration of action is short By blocking the beta-1-adrenoreceptors in the heart, esmolol decreases the heart rate. Esmolol has no significant intrinsic sympathomimetic or membrane stabilising activity at therapeutic dosages. At high doses Esmolol will begins to inhibit beta-2-receptors located chiefly in the bronchial and vascular smooth muscle. http://www.virtualmedicalcentre.com/drugs/chem-mart-atenolol-film-coated-tablets/2787 Atenolol is a beta-Adrenoceptor blocking agent that acts preferentially on beta-receptors in the heart. It reduces raised blood pressure by an unknown mechanism. Atenolol prevents Angina by decreasing the heart rate and the force of contractility of the heart subsequently reducing the cardiac workload and the myocardial oxygen requirements. Atenolol also has an antisympathetic effect which is thought to be responsible for its antiarrhythmic actions. Atenolol depresses the function of the sinus node and the atrioventricular node and also prolongs the refractory periods in the atria. http://www.virtualmedicalcentre.com/drugs/chem-mart-metoprolol/2788 Atenolol, a type of beta-1-selective-beta-Blocker, competitively blocks beta- adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver.The antihypertensive effect works by reducing cardiac output without reflex increase in peripheral vascular resistance; CNS effect and reduced renin secretionmay also contribute.The antianginal effect is due to reductionin left ventricular work and oxygen use, resulting from decrease in heart rate and contractility.The antiarrhythmic properties are due to antisympathetic effects: depression ofsinus node function and http://www.virtualmedicalcentre.com/drugs/corbeton/2789 Oxprenolol is a non-selective beta-adrenoreceptor antagonist. By blocking cardiac beta-adrenoreceptor oxprenolol produces a reduction in heart rate and reduced myocardial oxygen requirements. Oxprenolol also possesses membrane stabilising ability, which contributes to its antiarrhythmic action. http://www.virtualmedicalcentre.com/drugs/deralin/2790 Propranolol is a beta-adrenoreceptor blocker and acts on both beta1 and beta2 adrenoreceptors. Propranolol inhibits excessive sympathetic nervous system stimulation to the heart resulting in a reduction in heart rate, reduced force of cardiac contraction and reduced cardiac output. These effects combined, result in a significant reduction in reduction in left ventricular workload and in myocardial oxygen demand. The mechanism by which Propranolol lowers blood pressure is unknown. Propranolol has negative inotropic effects and is thus contraindicated in congestive heart failure. http://www.virtualmedicalcentre.com/drugs/dilatrend/2791 Dilatrend is indicated for the treatment of patients with symptomatic mild to severe (NYHA class II-IV) congestive heart failure (CHF) as an adjunct to conventional treatments, e.g. diuretics, digoxin, ACE inhibitors and vasodilators. Carvedilol is used in the treatment of hypertension. Carvedilol non-electively blocks beta adrenoreceptors, selectively blocks alpha1-adrenoreceptors and also has antioxidant and membrane stabilising properties 5. Alpha1-adrenoreceptor blockade causes vasodilatation and a reduction in peripheral vascular resistance resulting in a subsequent drop in blood p http://www.virtualmedicalcentre.com/drugs/genrx-atenolol/2792 Atenolol is a beta-Adrenoceptor blocking agent that acts preferentially on beta-receptors in the heart. It reduces raised blood pressure by an unknown mechanismAtenolol prevents angina by decreasing the heart rate and the force of contractility of the heart subsequently reducing the cardiac workload and the myocardial oxygen requirementsAtenolol also has an antisympathetic effect which is thought to be responsible for its antiarrhythmic actions. Atenolol depresses the function of the sinus node and the atrioventricular node and also prolongs the refractory periods in the atria. http://www.virtualmedicalcentre.com/drugs/genrx-metoprolol/2793 Atenolol, a type of beta-1-selective-beta-Blocker, competitively blocks beta- adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver.The antihypertensive effect works by reducing cardiac output without reflex increase in peripheral vascular resistance; CNS effect and reduced renin secretionmay also contribute.The antianginal effect is due to reductionin left ventricular work and oxygen use, resulting from decrease in heart rate and contractility. The antiarrhythmic properties are due to antisympathetic effects: depression of sinus node function a http://www.virtualmedicalcentre.com/drugs/healthsense-atenolol/2794 Atenolol is a beta-Adrenoceptor blocking agent that acts preferentially on beta-receptors in the heart. It reduces raised blood pressure by an unknown mechanismAtenolol prevents angina by decreasing the heart rate and the force of contractility of the heart subsequently reducing the cardiac workload and the myocardial oxygen requirementsAtenolol also has an antisympathetic effect which is thought to be responsible for its antiarrhythmic actions. Atenolol depresses the function of the sinus node and the atrioventricular node and also prolongs the refractory periods in the atria. http://www.virtualmedicalcentre.com/drugs/healthsense-metoprolol/2795 Atenolol, a type of beta-1-selective-beta-Blocker, competitively blocks beta- adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver.The antihypertensive effect works by reducing cardiac output without reflex increase in peripheral vascular resistance; CNS effect and reduced renin secretionmay also contribute.The antianginal effect is due to reductionin left ventricular work and oxygen use, resulting from decrease in heart rate and contractility.The antiarrhythmic properties are due to antisympathetic effects: depression ofsinus node function and http://www.virtualmedicalcentre.com/drugs/kredex/2797 Carvedilol is a nonselective beta-blocking agent. It is active on beta1 and beta2 adrenoceptors, but also has activity on alpha1-adrenoceptors, which are thought to be primarily responsible for its vasodilatory effect. The beta-blockade is responsible for reduction of cardiac output and suppression of the renin/angiotensin system. These effects combine to reduce blood pressure and help in the treatment of congestive heart failure. http://www.virtualmedicalcentre.com/drugs/lopresor/2798 Metoprolol is considered a cardioselective beta-blocker, i.e. it acts preferentially on beta1 receptors (located chiefly in the heart) at lower doses. It has little membrane stabilising or partial agonist activity below the plasma level threshold for beta blockade. Metoprolol reduces the stimulant effect of catecholamines on the heart causing a decrease in heart rate, cardiac contractility and cardiac output. It is not associated with orthostatic or electrolyte disturbances. Hypertension: metoprolol lowers elevated blood pressure in both the standing and lying position, and limits rises http://www.virtualmedicalcentre.com/drugs/metohexal/2799 Atenolol, a type of beta-1-selective-beta-Blocker, competitively blocks beta- adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver.The antihypertensive effect works by reducing cardiac output without reflex increase in peripheral vascular resistance; CNS effect and reduced renin secretionmay also contribute.The antianginal effect is due to reductionin left ventricular work and oxygen use, resulting from decrease in heart rate and contractility.The antiarrhythmic properties are due to antisympathetic effects: depression ofsinus node function and http://www.virtualmedicalcentre.com/drugs/metolol/2800 -Atenolol, a type of beta-1-selective-beta-Blocker, competitively blocks beta- adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver. -The antihypertensive effect works by reducing cardiac output without reflex increase in peripheral vascular resistance; CNS effect and reduced renin secretionmay also contribute. -The antianginal effect is due to reductionin left ventricular work and oxygen use, resulting from decrease in heart rate and contractility. -The antiarrhythmic properties are due to antisympathetic effects: depression ofsinus n http://www.virtualmedicalcentre.com/drugs/metoprolol-bc/2801 Atenolol, a type of beta-1-selective-beta-Blocker, competitively blocks beta- adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver.The antihypertensive effect works by reducing cardiac output without reflex increase in peripheral vascular resistance; CNS effect and reduced renin secretion may also contribute. The antianginal effect is due to reductionin left ventricular work and oxygen use, resulting from decrease in heart rate and contractility.The antiarrhythmic properties are due to antisympathetic effects: depression ofsinus node function a http://www.virtualmedicalcentre.com/drugs/minax/2802 Atenolol, a type of beta-1-selective-beta-Blocker, competitively blocks beta- adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver. The antihypertensive effect works by reducing cardiac output without reflex increase in peripheral vascular resistance; CNS effect and reduced renin secretionmay also contribute. The antianginal effect is due to reductionin left ventricular work and oxygen use, resulting from decrease in heart rate and contractility. The antiarrhythmic properties are due to antisympathetic effects: depression ofsinus node http://www.virtualmedicalcentre.com/drugs/noten/2803 Atenolol, a type of beta-1-selective-beta- Blocker, competitively blocks beta- adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver. The antihypertensive effect works by reducing cardiac output without reflex increase in peripheral vascular resistance; CNS effect and reduced renin secretion may also contribute. The antianginal effect is due to reduction in left ventricular work and oxygen use, resulting from decrease in heart rate and contractility. The antiarrhythmic properties are due to antisympathetic effects: http://www.virtualmedicalcentre.com/drugs/tenormin/2804 Atenolol, a type of beta-1-selective-beta- Blocker, competitively blocks beta- adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver. The antihypertensive effect works by reducing cardiac output without reflex increase in peripheral vascular resistance; CNS effect and reduced renin secretion may also contribute. The antianginal effect is due to reduction in left ventricular work and oxygen use, resulting from decrease in heart rate and contractility. The antiarrhythmic properties are due to antisympathetic effects: http://www.virtualmedicalcentre.com/drugs/tensig/2805 Atenolol, a type of beta-1-selective-beta- Blocker, competitively blocks beta- adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver. The antihypertensive effect works by reducing cardiac output without reflex increase in peripheral vascular resistance; CNS effect and reduced renin secretion may also contribute. The antianginal effect is due to reduction in left ventricular work and oxygen use, resulting from decrease in heart rate and contractility. The antiarrhythmic properties are due to antisympathetic effects: http://www.virtualmedicalcentre.com/drugs/atenolol-terry-white-chemists/2806 Atenolol is a beta-Adrenoceptor blocking agent that acts preferentially on beta-receptors in the heart. It reduces raised blood pressure by an unknown mechanism. Atenolol prevents angina by decreasing the heart rate and the force of contractility of the heart subsequently reducing the cardiac workload and the myocardial oxygen requirements. Atenolol also has an antisympathetic effect which is thought to be responsible for its antiarrhythmic actions. Atenolol depresses the function of the sinus node and the atrioventricular node and also prolongs the refractory periods in the atria. http://www.virtualmedicalcentre.com/drugs/metoprolol-terry-white-chemists/2807 Atenolol, a type of beta-1-selective-beta-Blocker, competitively blocks beta- adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver.The antihypertensive effect works by reducing cardiac output without reflex increase in peripheral vascular resistance; CNS effect and reduced renin secretionmay also contribute.The antianginal effect is due to reductionin left ventricular work and oxygen use, resulting from decrease in heart rate and contractility.The antiarrhythmic properties are due to antisympathetic effects: depression ofsinus node function and http://www.virtualmedicalcentre.com/drugs/visken/2808 Competitive non selective beta-Adrenergic antagonist with intrinsic sympathomimetic activity, though with only minor membrane stabilising activity. Absorption: completely absorbed from the small intestine with peak plasma concentrations reached within 1-2 hours. Metabolism Excretion: approximately 60% of the drug is metabolised, mostly by conjugation, with a half life averaging 3.3 hours, and then excreted by the kidneys. http://www.virtualmedicalcentre.com/drugs/aldactone/2809 Spironolactone is an aldosterone antagonist, and competitively binds to receptors at the aldosterone dependent sodium-potassium exchange site in the distal convoluted renal tubule. By binding to these receptors Spironolactone causes increased amounts of sodium and water to be excreted, while potassium is retained. Spironolactone also treats ascites, oedema and hypertension in primary and secondary aldosteronism (secondary causes include congestive heart failure, hepatic cirrhosis and the nephrotic syndrome) by competing for the aldosterone receptor sites. Aldactone also has moderate an http://www.virtualmedicalcentre.com/drugs/amizide/2810 Amizide consists of amiloride hydrochloride and hydrochlorothiazide. Amizide produces diuretic and antihypertensive effects, which are principally due to hydrochlorothiazide. Hydrochlorothiazide affects electrolyte reabsorption in the renal tubules and increases the excretion of sodium and chloride with some accompanying potassium and bicarbonate loss. Amiloride has only weak diuretic and antihypertensive activity however it has a potassium conserving actions to prevent the excessive potassium loss that hydrochlorothiazide can cause. Amiloride interferes with the exchange of sodium ions fo http://www.virtualmedicalcentre.com/drugs/aprinox/2811 Bendrofluazide is a thiazide diuretic that acts on the renal tubules to reduce the reabsorption of sodium and chloride ions by the tubules, increasing excretion of these ions and thereby increasing water excretion. The fluid loss will reduce the amount of oedema and lower the blood pressure. Bendrofluazide does not produce a rapid or prolonged diuresis making it suitable in a patient who wants to be able to continue living a normal life. The majority of the diuresis is over within 12 hours. Bendrofluazide is suitable for long-term therapy. The effect on the blood pressure will be evident http://www.virtualmedicalcentre.com/drugs/burinex/2812 Bumetanide is a loop diuretic that has a rapid onset and a short duration of action. Bumetanide acts at the ascending limb of the loop of Henle where it inhibits the resorption of sodium and chloride causing them to be excreted. Potassium excretion is also increased and uric acid excretion is decreased leading to an increase in serum uric acid. The diuretic effect of bumetanide is dose related and patient’s who do not respond to an initial dose will usually responds when the dose is increased. Diuresis begins within 30 minutes after oral administration and lasts for 3 to 4 hours. After http://www.virtualmedicalcentre.com/drugs/chem-mart-frusemide/2813 Frusemide is a potent loop diuretic that acts by inhibiting sodium and chloride absorption in the ascending limb of the loop of Henle and in both the proximal and the distal tubule. This results in increased salt and water excretion from the body. The greatest effect of Frusemide occurs within the first or second hour following administration and its effects last for 6-8 hours. http://www.virtualmedicalcentre.com/drugs/edecrin/2815 - Ethacrynic acid causes and increased excretion of salt and water from the kidneys. - It inhibits active sodium reabsorption in the ascending limb of the loop of Henle and other areas of the nephron. - This disrupts the normal solute gradient in the nephron and results in larger excretion of urine. http://www.virtualmedicalcentre.com/drugs/frusehexal/2816 Frusemide is a potent loop diuretic that acts by inhibiting sodium and chloride absorption in the ascending limb of the loop of Henle and in both the proximal and the distal tubule. This results in increased salt and water excretion from the body. The greatest effect of Frusemide occurs within the first or second hour following administration and its effects last for 6-8 hours. http://www.virtualmedicalcentre.com/drugs/frusemide-injection-bp/2817 Frusemide is a potent loop diuretic that acts by inhibiting sodium and chloride absorption in the ascending limb of the loop of Henle and in both the proximal and the distal tubule. This results in increased salt and water excretion from the body. The greatest effect of Frusemide occurs within the first or second hour following administration and its effects last for 6-8 hours. http://www.virtualmedicalcentre.com/drugs/frusemide-bc/2818 Frusemide is a potent loop diuretic that acts by inhibiting sodium and chloride absorption in the ascending limb of the loop of Henle and in both the proximal and the distal tubule. This results in increased salt and water excretion from the body. The greatest effect of Frusemide occurs within the first or second hour following administration and its effects last for 6-8 hours. http://www.virtualmedicalcentre.com/drugs/frusid/2819 Frusemide is a potent loop diuretic that acts by inhibiting sodium and chloride absorption in the ascending limb of the loop of Henle and in both the proximal and the distal tubule. This results in increased salt and water excretion from the body. The greatest effect of Frusemide occurs within the first or second hour following administration and its effects last for 6-8 hours http://www.virtualmedicalcentre.com/drugs/genrx-frusemide/2820 Frusemide is a potent loop diuretic that acts by inhibiting sodium and chloride absorption in the ascending limb of the loop of Henle and in both the proximal and the distal tubule. This results in increased salt and water excretion from the body. The greatest effect of Frusemide occurs within the first or second hour following administration and its effects last for 6-8 hours http://www.virtualmedicalcentre.com/drugs/healthsense-frusemide/2823 Frusemide is a potent loop diuretic that acts by inhibiting sodium and chloride absorption in the ascending limb of the loop of Henle and in both the proximal and the distal tubule. This results in increased salt and water excretion from the body. The greatest effect of Frusemide occurs within the first or second hour following administration and its effects last for 6-8 hours http://www.virtualmedicalcentre.com/drugs/hygroton/2825 Chlorthalidone is a benzothiazide diuretic. It acts on the distal renal tubules, where it inhibits sodium chloride reabsorption and promotes Ca2+ reabsorption. These mechanisms enhance the delivery of Na+ and water to the cortical collecting tubule and diuresis. Secretion and excretion of potassium and hydrogen ions is also increased. The diuretic effect of Chlorthalidone is dose dependent, and occurs whether or not oedema is present in the patient. The diuresis induced by Hygroton decreases plasma volume, cardiac output and systemic blood pressure. The antihypertensive action may be blunted http://www.virtualmedicalcentre.com/drugs/kaluril/2826 Amiloride is a potassium sparing diuretic. It acts on the distal convoluted tubule of the kidney, where it interferes with the sodium/potassium exchange. The exact mechanism of action is not fully understood, but a lack of relationship to aldosterone suggests a direct cellular action. Sodium excretion increases moderately, accounting for the mild diuretic and antihypertensive activity of Kaluril. Due to its potassium-sparing actions, Kaluril’s main use is to conserve potassium in patients receiving kaliuretic diuretic agents (eg: thiazide diuretics).Chloride excretion remains unchanged or incr http://www.virtualmedicalcentre.com/drugs/lasix/2827 -Lasix is a powerful diuretic and may promote diuresis in patients apparently resistant to other diuretics. It inhibits the absorption of sodium and chloride in the ascending limb of the loop of Henle and in the proximal and the distal tubules. Its action on the distal tubule is independent of any inhibitory effect on carbonic anhydrase or aldosterone, and contributes to its high efficacy. It has no significant pharmacological effects other than on renal function. -Onset of diuresis following oral administration is within 1 hour, with a peak effect occurring within 1-2 hours and a duration http://www.virtualmedicalcentre.com/drugs/midamor/2829 Amiloride is a potassium sparing diuretic. It acts on the distal convoluted tubule of the kidney, where it interferes with the sodium/potassium exchange. The exact mechanism of action is not fully understood, but a lack of relationship to aldosterone suggests a direct cellular action. Sodium excretion increases moderately, accounting for the mild diuretic and antihypertensive activity of Kaluril. Due to its potassium-sparing actions, Kaluril’s main use is to conserve potassium in patients receiving kaliuretic diuretic agents (eg: thiazide diuretics).Chloride excretion remains unchanged or incr http://www.virtualmedicalcentre.com/drugs/moduretic/2830 Moduretic contains two active ingredients, Amiloride and Hydrochlorothiazide. Hydrochlorothiazide is a thiazide diuretic. It works in the distal tubules of the kidney, where it changes the balance of sodium chloride and calcium ions. These changes in balance promote water excretion (diuresis), and potassium and hydrogen ions are also excreted. The diuresis caused by Hydrochlorothiazide causes a reduced plasma volume, reduces work on the heart and lowers blood pressure. The blood pressure lowering effect of Hydrochlorothiazide is generally gentle, as the body’s compensatory mechanisms dull p http://www.virtualmedicalcentre.com/drugs/spiractin/2832 Spironolactone is an aldosterone antagonist. It competitively binds receptors at the aldosterone dependent sodium-potassium exchange site in the distal convoluted tubule of the nephron leading to an increased amount of sodium and water excretion, whilst retaining potassium. Spironolactone also has moderate antiandrogenic effects by inhibiting the interaction between dihydrotestosterone and the intracellular androgen receptor- this may lower plasma levels of testosterone. http://www.virtualmedicalcentre.com/drugs/frusemide-terry-white-chemists/2833 Frusemide is a potent loop diuretic that acts by inhibiting sodium and chloride absorption in the ascending limb of the loop of Henle and in both the proximal and the distal tubule. This results in increased salt and water excretion from the body. The greatest effect of Frusemide occurs within the first or second hour following administration and its effects last for 6-8 hours. http://www.virtualmedicalcentre.com/drugs/uremide/2834 Frusemide is a potent loop diuretic that acts by inhibiting sodium and chloride absorption in the ascending limb of the loop of Henle and in both the proximal and the distal tubule. This results in increased salt and water excretion from the body. The greatest effect of Frusemide occurs within the first or second hour following administration and its effects last for 6-8 hours. http://www.virtualmedicalcentre.com/drugs/urex-urex-m-urex-forte/2835 Frusemide is a potent loop diuretic that acts by inhibiting sodium and chloride absorption in the ascending limb of the loop of Henle and in both the proximal and the distal tubule. This results in increased salt and water excretion from the body. The greatest effect of Frusemide occurs within the first or second hour following administration and its effects last for 6-8 hours. http://www.virtualmedicalcentre.com/drugs/adenocor/2836 Adenosine slows conduction through the atrioventricular node interrupting re-entry circuits involving the atrioventricular node such as Wolff-Parkinson-White syndrome slowing the heart rate and restoring normal sinus rhythm. By slowing atrioventricular conduction adenosine can also aid the diagnosis of complex tachyarrhythmias and can be used as an adjunct to clinical and ECG observations. http://www.virtualmedicalcentre.com/drugs/amiodarone-hydrochloride-injection-concentrate-dbl/2837 Amiodarone is a Class III antiarrhythmic agent that acts by prolonging the action potential duration and consequently increased the refractory period of atrial, nodal and ventricular tissues. Amiodarone decreases sinus automaticity in the sinus node and increases the refractory period of the atrial cells gives excellent control of atrial tachyarrhythmias. Amiodarone reduces the speed of conduction and increases the refractory period of the atrioventricular node and by doing this allows control of nodal tachycardias caused by re-entry through the atrioventricular node such as Wolf-Parkinson-Whi http://www.virtualmedicalcentre.com/drugs/aratac/2838 Amiodarone is a Class III antiarrhythmic agent that acts by prolonging the action potential duration and consequently increased the refractory period of atrial, nodal and ventricular tissues. Amiodarone decreases sinus automaticity in the sinus node and increases the refractory period of the atrial cells gives excellent control of atrial tachyarrhythmias. Amiodarone reduces the speed of conduction and increases the refractory period of the atrioventricular node and by doing this allows control of nodal tachycardias caused by re-entry through the atrioventricular node such as Wolf-Parkinson-Whi http://www.virtualmedicalcentre.com/drugs/cardinorm/2839 Amiodarone is a Class III antiarrhythmic agent that acts by prolonging the action potential duration and consequently increased the refractory period of atrial, nodal and ventricular tissues. Amiodarone decreases sinus automaticity in the sinus node and increases the refractory period of the atrial cells gives excellent control of atrial tachyarrhythmias. Amiodarone reduces the speed of conduction and increases the refractory period of the atrioventricular node and by doing this allows control of nodal tachycardias caused by re-entry through the atrioventricular node such as Wolf-Parkinson-Whi http://www.virtualmedicalcentre.com/drugs/cardol/2840 Sotalol is a non-selective beta-adrenoreceptor antagonist that also has class III antiarrhythmic activity. By blocking beta-adrenoreceptors Sotalol causes decreased heart rate and reduced force of contraction of the heart leading to a reduction in cardiac work and myocardial oxygen demand. Sotalols antiarrhythmic effect involves prolongation of the refractory periods in the atria, ventricles and accessory pathways. http://www.virtualmedicalcentre.com/drugs/amiodarone/2841 Amiodarone is a Class III antiarrhythmic agent that acts by prolonging the action potential duration and consequently increased the refractory period of atrial, nodal and ventricular tissues. Amiodarone decreases sinus automaticity in the sinus node and increases the refractory period of the atrial cells gives excellent control of atrial tachyarrhythmias. Amiodarone reduces the speed of conduction and increases the refractory period of the atrioventricular node and by doing this allows control of nodal tachycardias caused by re-entry through the atrioventricular node such as Wolf-Parkinson-Whi http://www.virtualmedicalcentre.com/drugs/chem-mart-sotalol/2842 Sotalol is a non-selective beta-adrenoreceptor antagonist that also has class III antiarrhythmic activity. By blocking beta-adrenoreceptors Sotalol causes decreased heart rate and reduced force of contraction of the heart leading to a reduction in cardiac work and myocardial oxygen demand. Sotalol?s antiarrhythmic effect involves prolongation of the refractory periods in the atria, ventricles and accessory pathways. http://www.virtualmedicalcentre.com/drugs/cordarone-x/2843 Amiodarone is a Class III antiarrhythmic agent that acts by prolonging the action potential duration and consequently increased the refractory period of atrial, nodal and ventricular tissues. Amiodarone decreases sinus automaticity in the sinus node and increases the refractory period of the atrial cells gives excellent control of atrial tachyarrhythmias. Amiodarone reduces the speed of conduction and increases the refractory period of the atrioventricular node and by doing this allows control of nodal tachycardias caused by re-entry through the atrioventricular node such as Wolf-Parkinson-Whi http://www.virtualmedicalcentre.com/drugs/flecatab/2844 Flecainide acetate is a class I antiarrhythmic drug - i.e. membrane stabilising agent. Flecainide acetate inhibits fast sodium channels that are responsible for the rapid upstroke of the myocardial action potential which hence stabilizes cardiac rhythm. This drug is also known to depress electrical conduction in all parts of the heart and in particular the His-Purkinje system. http://www.virtualmedicalcentre.com/drugs/genrx-amiodarone/2845 Amiodarone is a Class III antiarrhythmic agent that acts by prolonging the action potential duration and consequently increased the refractory period of atrial, nodal and ventricular tissues. Amiodarone decreases sinus automaticity in the sinus node and increases the refractory period of the atrial cells gives excellent control of atrial tachyarrhythmias. Amiodarone reduces the speed of conduction and increases the refractory period of the atrioventricular node and by doing this allows control of nodal tachycardias caused by re-entry through the atrioventricular node such as Wolf-Parkinson-Whi http://www.virtualmedicalcentre.com/drugs/genrx-sotalol/2846 Sotalol is a non-selective beta-adrenoreceptor antagonist that also has class III antiarrhythmic activity. By blocking beta-adrenoreceptors Sotalol causes decreased heart rate and reduced force of contraction of the heart leading to a reduction in cardiac work and myocardial oxygen demand. Sotalol’s antiarrhythmic effect involves prolongation of the refractory periods in the atria, ventricles and accessory pathways. http://www.virtualmedicalcentre.com/drugs/healthsense-amiodarone/2847 Amiodarone is a Class III antiarrhythmic agent that acts by prolonging the action potential duration and consequently increased the refractory period of atrial, nodal and ventricular tissues. Amiodarone decreases sinus automaticity in the sinus node and increases the refractory period of the atrial cells gives excellent control of atrial tachyarrhythmias. Amiodarone reduces the speed of conduction and increases the refractory period of the atrioventricular node and by doing this allows control of nodal tachycardias caused by re-entry through the atrioventricular node such as Wolf-Parkinson-Whi http://www.virtualmedicalcentre.com/drugs/healthsense-sotalol/2848 Sotalol is a non-selective beta-adrenoreceptor antagonist that also has class III antiarrhythmic activity. By blocking beta-adrenoreceptors Sotalol causes decreased heart rate and reduced force of contraction of the heart leading to a reduction in cardiac work and myocardial oxygen demand. Sotalol’s antiarrhythmic effect involves prolongation of the refractory periods in the atria, ventricles and accessory pathways. http://www.virtualmedicalcentre.com/drugs/isoptin-injection/2849 Calcium channel blockers block the inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L-type calcium channels. Verapamil acts mainly on the heart to reduce contractility, slow the heart rate and slow conduction but has less effect on vascular smooth muscle. http://www.virtualmedicalcentre.com/drugs/kinidin-durules/2850 Quinidine blocks fast sodium channels in the cardiac conducting cells reducing the rate of rise in the action potential, increasing the duration of the action potential and the effective refractory period. This results in slowed conduction reduced automaticity and reduced excitability in the atria, atrioventricular node and ventricles. The effect of quinidine on the fast sodium channels is diminished when the extracellular potassium concentration is reduced and is enhanced when it is increased. Quinidine has a negative inotropic action which is of no significance at therapeutic plasma c http://www.virtualmedicalcentre.com/drugs/lignocaine-hydrochloride-injection/2851 Lignocaine is a class I (membrane-stabilising) antiarrhythmic agent. In cardiac tissue, lignocaine decreases automaticity by reducing the rate of diastolic (phase 4) depolarisation. It produces a blockage of sodium channels, thereby decreases the action potential duration and shortens the refractory period. http://www.virtualmedicalcentre.com/drugs/mexitil-capsules/2852 Mexiletine hydrochloride is structurally similar to the local anaesthetic lignocaine. Mexiletine hydrochloride however can be absorbed in the gastrointestinal tract and also has a longer duration of action. Mexiletine hydrochloride is classified as a class I antiarrhythmic drug as it depresses the maximum rate of myocardial depolarization without affecting the myocyte resting potential. Mexiletine hydrochloride may also exhibit a minor negative iontropic effect. http://www.virtualmedicalcentre.com/drugs/pronestyl/2853 Class IA (membrane stabilising) cardiac antiarrhythmic agent. Procainamide reduces myocardial excitability in response to electrical stimulation in the atria, and also His-Purkinje system and ventricles. Damaged myocardium may experience slightly reduced cardiac output. Therapeutic levels may exert vagolytic activity. Supratherapeutic levels can prolong atrioventricular conduction time with possible atrioventricular block and spontaneous firing. Following intramuscular injection, Pronestyl reaches peak plasma levels 15-60 minutes. Intravenous Pronestyl achieves therapeutic levels within min http://www.virtualmedicalcentre.com/drugs/rythmodan/2854 Antiarrhythmic agent: Class Ia (sodium channel blocker with membrane stabilising activity) Disopyramide reduces automaticity in cardiac Purkinje fibres by prolonging phase 4 diastolic depolarisation; slows atrial, atrioventricular nodal, Purkinje fibre and ventricular muscle conduction velocity by prolonging phase 0 depolarisation in these fibres; extends atrial, Purkinje fibre and ventricular muscle action potential and refractory period duration; and depresses excitability of atrial and ventricular myocytes. Disopyramide invokes a slight and transient depressant effect on the heart. H http://www.virtualmedicalcentre.com/drugs/solavert/2855 Sotalol is a non-selective beta-adrenoreceptor antagonist that also has class III antiarrhythmic activity. By blocking beta-adrenoreceptors Sotalol causes decreased heart rate and reduced force of contraction of the heart leading to a reduction in cardiac work and myocardial oxygen demand. Sotalol’s antiarrhythmic effect involves prolongation of the refractory periods in the atria, ventricles and accessory pathways. http://www.virtualmedicalcentre.com/drugs/sotacor/2857 Sotalol is a non-selective beta-adrenoreceptor antagonist that also has class III antiarrhythmic activity. By blocking beta-adrenoreceptors Sotalol causes decreased heart rate and reduced force of contraction of the heart leading to a reduction in cardiac work and myocardial oxygen demand. Sotalol’s antiarrhythmic effect involves prolongation of the refractory periods in the atria, ventricles and accessory pathways. http://www.virtualmedicalcentre.com/drugs/sotahexal/2858 Sotalol is a non-selective beta-adrenoreceptor antagonist that also has class III antiarrhythmic activity. By blocking beta-adrenoreceptors Sotalol causes decreased heart rate and reduced force of contraction of the heart leading to a reduction in cardiac work and myocardial oxygen demand. Sotalol’s antiarrhythmic effect involves prolongation of the refractory periods in the atria, ventricles and accessory pathways. http://www.virtualmedicalcentre.com/drugs/sotalol-bc/2859 Sotalol is a non-selective beta-adrenoreceptor antagonist that also has class III antiarrhythmic activity. By blocking beta-adrenoreceptors Sotalol causes decreased heart rate and reduced force of contraction of the heart leading to a reduction in cardiac work and myocardial oxygen demand. Sotalol’s antiarrhythmic effect involves prolongation of the refractory periods in the atria, ventricles and accessory pathways. http://www.virtualmedicalcentre.com/drugs/tambocor/2860 Class I antiarrhythmic agent: sodium channel blocker with membrane stabilising activity. Reduces rate of rise of action potential (phase 0) without greatly affecting duration, and also lengthens effective refractory period. The peak plasma levels are achieved within 3 hours for most patients (range 1-6 hours) The mean plasma half life after multiple oral doses is approximately 20 hours. http://www.virtualmedicalcentre.com/drugs/amiodarone-terry-white-chemists/2861 Amiodarone is a Class III antiarrhythmic agent that acts by prolonging the action potential duration and consequently increased the refractory period of atrial, nodal and ventricular tissues. Amiodarone decreases sinus automaticity in the sinus node and increases the refractory period of the atrial cells gives excellent control of atrial tachyarrhythmias. Amiodarone reduces the speed of conduction and increases the refractory period of the atrioventricular node and by doing this allows control of nodal tachycardias caused by re-entry through the atrioventricular node such as Wolf-Parkinson-Whi http://www.virtualmedicalcentre.com/drugs/sotalol-terry-white-chemists/2862 Sotalol is a non-selective beta-adrenoreceptor antagonist that also has class III antiarrhythmic activity. By blocking beta-adrenoreceptors Sotalol causes decreased heart rate and reduced force of contraction of the heart leading to a reduction in cardiac work and myocardial oxygen demand. Sotalol’s antiarrhythmic effect involves prolongation of the refractory periods in the atria, ventricles and accessory pathways. http://www.virtualmedicalcentre.com/drugs/xylocard/2863 - Lignocaine is a membrane stabilising agent, local anaesthetic and antiarrhythmic agent - It depresses the slow spontaneous depolarization of Purkinje fibres, shortens the action potential period and refractory period of Purkinje and ventricular cells and depresses membrane responsiveness (hence cardiac conduction velocity) in Purkinje fibres and the ventricular myocardium http://www.virtualmedicalcentre.com/drugs/anginine/2864 Anginine is a vasodilator, which relieves the pain of angina pectoris, which is believed to be the result of myocardial ischaemia secondary to coronary artery disease. Anginine also causes vasodilation in coronary arteries that are in spasm. Anginine is thought to cause vasodilation by its nitric oxide activating guanylate cyclase in the vascular smooth muscle cells, which results in an increased synthesis of cyclic guanosine monophosphate, which leads to smooth muscle relaxation. In the relief of acute anginal pain the effect of Anginine occurs 2-3 minutes after administration and lasts for u http://www.virtualmedicalcentre.com/drugs/cardizem/2866 -Diltiazem is a slow calcium channel blocker. -It inhibits the influx of calcium ions during membrane depolarisation of cardiac and vascular smooth muscle. -Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/chem-mart-diltiazem/2867 Diltiazem acts by inhibiting the influx of calcium ions during membrane depolarisation of cardiac and vascular smooth muscle Diltiazem inhibits coronary artery spasm by vasodilating epicardial and subendocardial coronary arteries. It also increases exercise tolerance by reducing myocardial oxygen demand and increasing oxygen supply to the myocardium by reducing the heart rate and blood pressure (by decreasing the peripheral vascular resistance through vasodilation) and by dilating coronary arteries. http://www.virtualmedicalcentre.com/drugs/chem-mart-isosorbide-mononitrate/2868 Isosorbide mononitrate reduces the end diastolic pressure and volume leading to an improvement in the subendocardial blood flow. The net result is reduced workload for the heart by producing venous and arterial dilatation and an improvement in oxygen supply. Natural initiator of vascular relaxation is endothelium derived relaxing factor, which has the characteristics of nitric oxide. Organic nitrates are metabolised to nitric oxide and they are thought to be the physiological substitute for endothelium derived relaxing factor. http://www.virtualmedicalcentre.com/drugs/coras/2869 Diltiazem acts by inhibiting the influx of calcium ions during membrane depolarisation of cardiac and vascular smooth muscle Diltiazem inhibits coronary artery spasm by vasodilating epicardial and subendocardial coronary arteries. It also increases exercise tolerance by reducing myocardial oxygen demand and increasing oxygen supply to the myocardium by reducing the heart rate and blood pressure (by decreasing the peripheral vascular resistance through vasodilation) and by dilating coronary arteries. http://www.virtualmedicalcentre.com/drugs/diltahexal/2870 -Diltiazem is a slow calcium channel blocker. -It inhibits the influx of calcium ions during membrane depolarisation of cardiac and vascular smooth muscle. -Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/diltiazem-bc/2871 Diltiazem acts by inhibiting the influx of calcium ions during membrane depolarisation of cardiac and vascular smooth muscle Diltiazem inhibits coronary artery spasm by vasodilating epicardial and subendocardial coronary arteries. It also increases exercise tolerance by reducing myocardial oxygen demand and increasing oxygen supply to the myocardium by reducing the heart rate and blood pressure (by decreasing the peripheral vascular resistance through vasodilation) and by dilating coronary arteries. http://www.virtualmedicalcentre.com/drugs/dilzem/2872 Diltiazem is a slow calcium channel blocker. It inhibits the influx of calcium ions during membrane depolarisation of cardiac and vascular smooth muscle. Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/duride/2873 Pharmacology. Isosorbide mononitrate is an active metabolite of isosorbide dinitrate. It has qualitatively similar effects. Isosorbide mononitrate reduces the workload of the heart by producing venous and arterial dilatation. It lowers intramural pressure by reducing the end diastolic pressure and volume. This leads to an improvement in the subendocardial blood flow. When isosorbide mononitrate is administered, the net effect is therefore a reduced workload for the heart and an improvement in the oxygen supply/ demand balance of the myocardium. Nitrates are highly effective in the prophylaxis http://www.virtualmedicalcentre.com/drugs/genrx-diltiazem/2874 Diltiazem is a slow calcium channel blocker. It inhibits the influx of calcium ions during membrane depolarisation of cardiac and vascular smooth muscle. Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/genrx-isosorbide-mononitrate/2875 Isosorbide mononitrate reduces the end diastolic pressure and volume leading to an improvement in the subendocardial blood flow. The net result is reduced workload for the heart by producing venous and arterial dilatation and an improvement in oxygen supply. Natural initiator of vascular relaxation is endothelium derived relaxing factor, which has the characteristics of nitric oxide. Organic nitrates are metabolised to nitric oxide and they are thought to be the physiological substitute for endothelium derived relaxing factor. http://www.virtualmedicalcentre.com/drugs/glyceryl-trinitrate-for-injection-dbl/2876 GTN acts on vascular smooth muscle causing arterial and venous dilatation with venous dilation predominating over arteriolar dilation. Venous dilation decreases venous return to the heart, reducing left ventricular end diastolic pressure and preload. Arteriolar relaxation reduces systemic vascular resistance and arterial pressure. Myocardial oxygen requirements are reduced by the effects of GTN on both the arterial and venous vessels. When therapeutic doses of IV GTN are systolic, diastolic and mean arterial blood pressure will all be reduced. Glyceryl trinitrate also has a short http://www.virtualmedicalcentre.com/drugs/healthsense-diltiazem/2877 Diltiazem acts by inhibiting the influx of calcium ions during membrane depolarisation of cardiac and vascular smooth muscle Diltiazem inhibits coronary artery spasm by vasodilating epicardial and subendocardial coronary arteries. It also increases exercise tolerance by reducing myocardial oxygen demand and increasing oxygen supply to the myocardium by reducing the heart rate and blood pressure (by decreasing the peripheral vascular resistance through vasodilation) and by dilating coronary arteries. http://www.virtualmedicalcentre.com/drugs/healthsense-isosorbide-mononitrate/2878 Isosorbide mononitrate reduces the end diastolic pressure and volume leading to an improvement in the subendocardial blood flow. The net result is reduced workload for the heart by producing venous and arterial dilatation and an improvement in oxygen supply. Natural initiator of vascular relaxation is endothelium derived relaxing factor, which has the characteristics of nitric oxide. Organic nitrates are metabolised to nitric oxide and they are thought to be the physiological substitute for endothelium derived relaxing factor. http://www.virtualmedicalcentre.com/drugs/ikorel/2879 Ikoril has a dual mechanism of action. Its first action is to open ATP-dependent potassium channels in vascular smooth muscle causing hyperpolarisation of the smooth muscle cells which leads to arterial dilatation and a reduction in afterload. Its second action is to relax vascular smooth muscle by increasing the intracellular cyclic guanosine monophosphate. This effect occurs predominantly in the venous vasculature causing a decrease in preload. These two actions improve blood flow and oxygen supply to the myocardium. http://www.virtualmedicalcentre.com/drugs/imdur-durules/2880 Isosorbide mononitrate reduces the end diastolic pressure and volume leading to an improvement in the subendocardial blood flow. The net result is reduced workload for the heart by producing venous and arterial dilatation and an improvement in oxygen supply. Natural initiator of vascular relaxation is endothelium derived relaxing factor, which has the characteristics of nitric oxide. Organic nitrates are metabolised to nitric oxide and they are thought to be the physiological substitute for endothelium derived relaxing factor. http://www.virtualmedicalcentre.com/drugs/imtrate-sr/2881 - Isosorbide mononitrate causes venous and arterial dilatation and thus reduces workload on the heart - End diastolic pressure and volume is reduced in the heart , hence intramural pressure (inside the heart tissue) is also reduced which improves subendocardial blood flow - The net effect of isosorbide mononitrate is an improvement in oxygenation of the myocardium and a reduced workload on the heart - The way in which nitrates dilate blood vessels is not yet completely understood but it is thought that they are a substitute for the endogenously derived endothelium derived relaxing factor (E http://www.virtualmedicalcentre.com/drugs/isomonit/2882 Isosorbide mononitrate reduces the end diastolic pressure and volume leading to an improvement in the subendocardial blood flow. The net result is reduced workload for the heart by producing venous and arterial dilatation and an improvement in oxygen supply. Natural initiator of vascular relaxation is endothelium derived relaxing factor, which has the characteristics of nitric oxide. Organic nitrates are metabolised to nitric oxide and they are thought to be the physiological substitute for endothelium derived relaxing factor. http://www.virtualmedicalcentre.com/drugs/isordil/2883 - Isosorbide dinitrate is an organic nitrate ester which relaxes vascular smooth muscle which causes vasodilatation. This in turn encourages venous pooling which reduces venous return, left ventricular filling pressure and pulmonary artery and capillary pressures - Arterial dilatation also occurs which reduces afterload - This vascular relaxation also reduces oxygen demand on the myocardium - The net effect is an increase in cardiac output and reduction in myocardial oxygen demands http://www.virtualmedicalcentre.com/drugs/isosorbide-mononitrate-bc/2884 Isosorbide mononitrate produces relaxation of the smooth muscle in the blood vessels causing venous and arterial dilatation. This has several effects on the heart including improved subendocardial blood flow leading to an increased oxygen supply to the myocardium, and reduced workload of the heart. This reduces the risk of an attack of angina pectoris occurring. Tablets contain a slow release formulation of isosorbide mononitrate. After a tablet is taken it slowly releases isosorbide mononitrate over approximately ten hours. http://www.virtualmedicalcentre.com/drugs/minitran/2885 Glyceryl trinitrate relaxes smooth muscle throughout the body. Its mechanism of action is based on an increase in venous capacitance leading to decreased return of blood to the heart. This results in decrease in left ventricular end-diastolic pressure (preload), which leads to decreased myocardial oxygen requirement at rest and during exercise. It also causes redistribution of coronary blood flow to ischaemic subendocardium by selectively dilating large epicardial vessels. http://www.virtualmedicalcentre.com/drugs/monodur/2886 Isosorbide mononitrate reduces the end diastolic pressure and volume leading to an improvement in the subendocardial blood flow. The net result is reduced workload for the heart by producing venous and arterial dilatation and an improvement in oxygen supply. Natural initiator of vascular relaxation is endothelium derived relaxing factor, which has the characteristics of nitric oxide. Organic nitrates are metabolised to nitric oxide and they are thought to be the physiological substitute for endothelium derived relaxing factor. http://www.virtualmedicalcentre.com/drugs/nitrodur/2887 Glyceryl trinitrate relaxes smooth muscle throughout the body. Its mechanism of action is based on an increase in venous capacitance leading to decreased return of blood to the heart. This results in decrease in left ventricular end-diastolic pressure (preload), which leads to decreased myocardial oxygen requirement at rest and during exercise. It also causes redistribution of coronary blood flow to ischaemic subendocardium by selectively dilating large epicardial vessels. http://www.virtualmedicalcentre.com/drugs/nitrolingual-pumpspray/2888 Glyceryl trinitrate relaxes smooth muscle throughout the body. Its mechanism of action is based on an increase in venous capacitance leading to decreased return of blood to the heart. This results in decrease in left ventricular end-diastolic pressure (preload), which leads to decreased myocardial oxygen requirement at rest and during exercise. It also causes redistribution of coronary blood flow to ischaemic subendocardium by selectively dilating large epicardial vessels. http://www.virtualmedicalcentre.com/drugs/pexsig/2889 Studies suggest Pexsig (perhexiline) spares oxygen use in the heart inhibiting myocardial fatty acid catabolism and increases glucose utilisation. This results in increased myocardial efficiency, and reduces potential for impaired myocardial function during ischaemia. Perhexiline has cardiac membrane activity similar to Class I antiarrhythmic agents, reducing exercise induced tachycardia without reducing resting heart rate. Perhexiline has also been shown to have mild diuretic activity. Perhexiline is 80% absorbed from the gut after oral administration, although complete data on bioavai http://www.virtualmedicalcentre.com/drugs/sorbidin/2890 Sorbidin (isosorbide dinitrate) is an organic nitrate ester, and acts to relax vascular smooth muscle. Venodilatation causes venous pooling, reducing venous return, left ventricular filling pressure, pulmonary artery and capillary pressures, and reduces myocardial oxygen requirements. Arteriolar dilation promotes afterload reduction. These effects correspond clinically in heart failure patients as increases in cardiac output, and reductions in the symptoms of pulmonary vascular congestion and ischaemic chest pain. Nitrates may promote redistribution of coronary blood flow to ischaemic areas http://www.virtualmedicalcentre.com/drugs/diltiazem-terry-white-chemists/2891 Diltiazem acts by inhibiting the influx of calcium ions during membrane depolarisation of cardiac and vascular smooth muscle. Diltiazem inhibits coronary artery spasm by vasodilating epicardial and subendocardial coronary arteries. It also increases exercise tolerance by reducing myocardial oxygen demand and increasing oxygen supply to the myocardium by reducing the heart rate and blood pressure (by decreasing the peripheral vascular resistance through vasodilation) and by dilating coronary arteries. http://www.virtualmedicalcentre.com/drugs/isosorbide-mononitrate-terry-white-chemists/2892 Isosorbide mononitrate reduces the end diastolic pressure and volume leading to an improvement in the subendocardial blood flow. The net result is reduced workload for the heart by producing venous and arterial dilatation and an improvement in oxygen supply. Natural initiator of vascular relaxation is endothelium derived relaxing factor, which has the characteristics of nitric oxide. Organic nitrates are metabolised to nitric oxide and they are thought to be the physiological substitute for endothelium derived relaxing factor. http://www.virtualmedicalcentre.com/drugs/transiderm-nitro/2893 Glyceryl trinitrate relaxes smooth muscle throughout the body. Its mechanism of action is based on an increase in venous capacitance leading to decreased return of blood to the heart. This results in decrease in left ventricular end-diastolic pressure (preload), which leads to decreased myocardial oxygen requirement at rest and during exercise. It also causes redistribution of coronary blood flow to ischaemic subendocardium by selectively dilating large epicardial vessels. http://www.virtualmedicalcentre.com/drugs/vasocardol-tablets/2894 -Diltiazem is a slow calcium channel blocker. -It inhibits the influx of calcium ions during membrane depolarisation of cardiac and vascular smooth muscle. -Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/ausgem/2895 Gemfibrozil decreases serum triglycerides and total cholesterol and very low density lipoprotein cholesterol (VLDL) and increases high density lipoprotein cholesterol (HDL). It inhibits peripheral lipolysis and decreases hepatic extraction of free fatty acids , reducing hepatic triglyceride production. It also inhibits synthesis and increases clearance of apolipoprotein B, a carrier of VLDL, leading to a decrease in VLDL production. http://www.virtualmedicalcentre.com/drugs/chem-mart-gemfibrozil/2896 Gemfibrozil decreases serum triglycerides and total cholesterol and very low density lipoprotein cholesterol (VLDL) and increases high density lipoprotein cholesterol (HDL). It inhibits peripheral lipolysis and decreases hepatic extraction of free fatty acids , reducing hepatic triglyceride production. It also inhibits synthesis and increases clearance of apolipoprotein B, a carrier of VLDL, leading to a decrease in VLDL production. http://www.virtualmedicalcentre.com/drugs/colestid-granules/2897 - Colestipol binds bile acids (of which cholesterol is the main precursor) and this forms a complex which causes increased faecal loss of bile acids. This leads to an increased oxidation of cholesterol to bile acids, a decrease in LDL levels and decreased serum cholesterol levels http://www.virtualmedicalcentre.com/drugs/gemfibrozil-bc/2898 Gemfibrozil decreases serum triglycerides and total cholesterol and very low density lipoprotein cholesterol (VLDL) and increases high density lipoprotein cholesterol (HDL). It inhibits peripheral lipolysis and decreases hepatic extraction of free fatty acids, reducing hepatic triglyceride production. It also inhibits synthesis and increases clearance of apolipoprotein B, a carrier of VLDL, leading to a decrease in VLDL production. http://www.virtualmedicalcentre.com/drugs/gemhexal/2899 Gemfibrozil decreases serum triglycerides and total cholesterol and very low density lipoprotein cholesterol (VLDL) and increases high density lipoprotein cholesterol (HDL). It inhibits peripheral lipolysis and decreases hepatic extraction of free fatty acids , reducing hepatic triglyceride production. It also inhibits synthesis and increases clearance of apolipoprotein B, a carrier of VLDL, leading to a decrease in VLDL production. http://www.virtualmedicalcentre.com/drugs/genrx-gemfibrozil/2900 Gemfibrozil decreases serum triglycerides and total cholesterol and very low density lipoprotein cholesterol (VLDL) and increases high density lipoprotein cholesterol (HDL). It inhibits peripheral lipolysis and decreases hepatic extraction of free fatty acids , reducing hepatic triglyceride production. It also inhibits synthesis and increases clearance of apolipoprotein B, a carrier of VLDL, leading to a decrease in VLDL production. http://www.virtualmedicalcentre.com/drugs/healthsense-gemfibrozil/2901 Gemfibrozil decreases serum triglycerides and total cholesterol and very low density lipoprotein cholesterol (VLDL) and increases high density lipoprotein cholesterol (HDL). It inhibits peripheral lipolysis and decreases hepatic extraction of free fatty acids , reducing hepatic triglyceride production. It also inhibits synthesis and increases clearance of apolipoprotein B, a carrier of VLDL, leading to a decrease in VLDL production. http://www.virtualmedicalcentre.com/drugs/jezil/2902 Gemfibrozil decreases serum triglycerides and total cholesterol and very low density lipoprotein cholesterol (VLDL) and increases high density lipoprotein cholesterol (HDL). It inhibits peripheral lipolysis and decreases hepatic extraction of free fatty acids , reducing hepatic triglyceride production. It also inhibits synthesis and increases clearance of apolipoprotein B, a carrier of VLDL, leading to a decrease in VLDL production. http://www.virtualmedicalcentre.com/drugs/lescol/2903 Fluvastatin inhibits the enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase competitively.1-3 This is the rate-limiting enzyme in cholesterol synthesis. It converts HMG-CoA to Mevalonate a precursor for cholesterol.1-3 The reduction in the production of cholesterol in the liver causes an increase in cholesterol uptake from blood which leads to a reduction of total cholesterol, LDL and triglyceride levels in the blood.1-3 http://www.virtualmedicalcentre.com/drugs/lipazil/2904 Gemfibrozil decreases serum triglycerides and total cholesterol and very low density lipoprotein cholesterol (VLDL) and increases high density lipoprotein cholesterol (HDL). It inhibits peripheral lipolysis and decreases hepatic extraction of free fatty acids , reducing hepatic triglyceride production. It also inhibits synthesis and increases clearance of apolipoprotein B, a carrier of VLDL, leading to a decrease in VLDL production. http://www.virtualmedicalcentre.com/drugs/lipex/2905 Lipex (simvastatin) is 3-hydroxy-3-methlyglutarly coenzyme A (HMG-CoA) reductase (a rate limiting enzyme in the synthesis of cholesterol) inhibitor. Lipex works to competitively inhibit HMG-CoA. This results in the increase of hepatic cholesterol uptake from blood, reduction in the concentration of total cholesterol, LDL and triglyceride, and producing a slight increase in HDL concentrations.1,2 http://www.virtualmedicalcentre.com/drugs/lipitor/2906 The active ingredient in Lipitor, atorvastatin, works to lower lipid levels by inhibiting HMG-CoA reductase, an enzyme which converts 3-hydroxy-3-methyl-glutaryl-coenzyme A to mevalonate, in the cholesterol production pathway. This inhibits the synthesis of cholesterol in the liver. It also increases the activity of low-density lipoprotein (LDL) receptors in the liver and thus increases LDL catabolism and reduces circulating LDL levels.1 http://www.virtualmedicalcentre.com/drugs/lopid/2907 Gemfibrozil decreases serum triglycerides and total cholesterol and very low density lipoprotein cholesterol (VLDL) and increases high density lipoprotein cholesterol (HDL). It inhibits peripheral lipolysis and decreases hepatic extraction of free fatty acids , reducing hepatic triglyceride production. It also inhibits synthesis and increases clearance of apolipoprotein B, a carrier of VLDL, leading to a decrease in VLDL production. http://www.virtualmedicalcentre.com/drugs/nicotinic-acid/2908 Nicotinic acid is normally derived from the diet and serves as a coenzyme to metabolise a large number of proteins that catalyse oxidation-reduction reactions that are essential for tissue respiration. http://www.virtualmedicalcentre.com/drugs/pravachol/2909 Pravastatin belongs to the HMG-CoA reductase inhibitors. These are competitive inhibitors of 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase, enzyme catalysing early rate limiting step in cholesterol synthesis, conversion of HMG-CoA to mevalonate. Due to its action, pravastatin results in an increase in number of low density lipoprotein (LDL) receptors and enhanced clearance of circulating LDL. It also inhibits hepatic synthesis of very low density lipoprotein (VLDL), the LDL presursor. http://www.virtualmedicalcentre.com/drugs/questran-lite/2910 Cholesterol is the sole precursor of bile acids in the body. Cholestyramine is an ion exchange resin that combines with bile acids to form an insoluble complex in the small intestine. This complex is then excreted unchanged in the faeces and the bile acids are permanently removed from the body. Removing bile acids from the body leads to an increased amount of cholesterol being converted to bile acids and a resulting decrease in low-density lipoproteins (LDLs) in the blood. Cholestyramine has been found to increase hepatic production of cholesterol, but the overall result is still a reduction i http://www.virtualmedicalcentre.com/drugs/gemfibrozil-terry-white-chemists/2911 Gemfibrozil decreases serum triglycerides and total cholesterol and very low density lipoprotein cholesterol (VLDL) and increases high density lipoprotein cholesterol (HDL). It inhibits peripheral lipolysis and decreases hepatic extraction of free fatty acids , reducing hepatic triglyceride production. It also inhibits synthesis and increases clearance of apolipoprotein B, a carrier of VLDL, leading to a decrease in VLDL production. http://www.virtualmedicalcentre.com/drugs/zocor/2913 Zocors (Simvastatin) chief metabolite is a HMG-CoA reductase inhibitor, and therefore restricts the rate limiting step in cholesterol biosynthesis. Zocor only partially blocks cholesterol synthesis at an early stage, and so allows the production of the necessary amounts of cholesterol for biological functions, and is not expected to cause an accumulation of potentially toxic sterols. Simvastatin is well absorbed after oral administration and undergoes extensive first pass metabolism with CYP3A4. Maximum plasma concentrations of active metabolites occur within 1.3-2.4 hours post dose. http://www.virtualmedicalcentre.com/drugs/lanoxin/2914 Digoxin is a positive inotrope that increases force of myocardial contraction. It also decreases AV nodal conduction via a vagotonic effect on the heart. http://www.virtualmedicalcentre.com/drugs/sigmaxin/2916 Digoxin is a positive inotrope that increases force of myocardial contraction. It also decreases AV nodal conduction via a vagotonic effect on the heart. http://www.virtualmedicalcentre.com/drugs/adrenaline-hydrochloride-injection/2917 Adrenaline is a directly-acting sympathomimetic agent. It also has vasopressor, antihistaminic and bronchodilator effects. It acts rapidly and for only a very short time (half life 5-10 minutes). By stimulating adrenoceptors, adrenaline causes tachycardia, increased systolic blood pressure, reduced diastolic blood pressure, hyperglycaemia and hypokalaemia. http://www.virtualmedicalcentre.com/drugs/adrenaline-injection/2918 Sympathomimetic amine. Pharmacology. Adrenaline acts on both alpha- and beta-adrenergic receptors of tissues innervated by sympathetic nerves, except the sweat glands and arteries of the face. It is the most potent alpha-receptor activator. Adrenaline stimulates the heart to increased output; raises the systolic blood pressure; lowers diastolic blood pressure; relaxes bronchial spasm and mobilises liver glycogen, resulting in hyperglycaemia and possibly glycosuria. Pharmacokinetics. Parenterally administered adrenaline has a rapid onset and short duration of action. The circulating drug is met http://www.virtualmedicalcentre.com/drugs/dobutamine-hydrochloride-injection/2920 Dobutamine is a directly acting ionotrope with effects primarily on the beta-adrenergic receptors of the heart with low hypertensive, arrhythmogenic and vasodilative effects. Facilitation of atrioventricular conduction has been observed in human studies in patients with atrial fibrillation. The onset of action of dobutamine is within one to two minutes; however, as much as ten minutes may be required to obtain the peak effect of a particular infusion rate. Metabolism is in tissues and the liver to form substances that are excreted into the urine. http://www.virtualmedicalcentre.com/drugs/dobutamine-hydrochloride-injection-dbl/2921 Dobutamine is a directly acting ionotrope with effects primarily on the beta-adrenergic receptors of the heart with low hypertensive, arrhythmogenic and vasodilative effects. Facilitation of atrioventricular conduction has been observed in human studies in patients with atrial fibrillation. The onset of action of dobutamine is within one to two minutes; however, as much as ten minutes may be required to obtain the peak effect of a particular infusion rate. Metabolism is in tissues and the liver to form substances that are excreted into the urine. http://www.virtualmedicalcentre.com/drugs/dopamine-concentrate-sterile-dbl/2923 Dopamine stimulates alpha, beta and dopamine receptors. At low levels (0.5 to 2 mcg/kg/minute), only dopamine receptors are activated causing vasodilation, most crucially in the renal and mesenteric arteries. At higher levels (2 to 10 mcg/kg/minute), beta-1 and beta-2 receptors are activated causing increased cardiac output and increased systolic blood pressure. At even higher levels (above 10 mcg/kg/minute), alpha receptors are activated causing peripheral vasoconstriction and raising both the systolic and diastolic blood pressures. Dopamine does not cross the blood brain barrier and so does http://www.virtualmedicalcentre.com/drugs/ephedrine-sulfate-injection-dbl/2924 Sympathomimetic. Ephedrine sulfate causes the release of noradrenaline from storage sites and stimulates α and β adrenoceptors, resulting in: a rise in systolic and diastolic blood pressure via an increase in cardiac output and peripheral vasoconstriction; bronchial smooth muscle relaxation; and cardiac stimulation. Other effects of Ephedrine sulfate are: stimulation of the central nervous system; sphincter contraction; relaxation of the detrusor muscle and bladder wall; decreased activity and motility in the intestine; and decreased muscular activity in the uterus. http://www.virtualmedicalcentre.com/drugs/epipen/2925 Adrenaline is a sympathomimetic drug that acts on both alpha- and beta-adrenoceptors. It is not only a potent cardiac stimulant but also a bronchodilator, vasopressor and an antihistamine. It results in the increased systolic blood pressure, reduced diastolic pressure, tachycardia, hypokalaemia and hyperglycaemia. The onset of action is rapid and of short duration. After intravenous infusion the half-life is approximately five to ten minutes. Adrenaline is rapidly distributed to the heart, spleen, several glandular tissues and adrenergic nerves. Large proportions of adrenaline are bou http://www.virtualmedicalcentre.com/drugs/levophed/2927 Levophed stimulates alpha-receptors and beta-receptors in the heart, resulting in peripheral vasoconstriction, dilatation of coronary arteries and a positive inotropic effect on the heart. Levophed therefore increases systemic blood pressure and coronary artery blood flow. http://www.virtualmedicalcentre.com/drugs/neo-synephrine-1andpermil-injection/2928 Phenylephrine is a synthetic sympathomimetic agent related to adrenaline and ephedrine. It is a powerful stimulator of post-synaptic alpha receptors, which causes vasoconstriction and a resulting increase in total peripheral resistance. When administered parenterally, Phenylephrine causes a rise in systolic and diastolic blood pressure due to constriction of most vascular beds. Because it doesnt affect the beta receptors of the heart, Phenylephrine does not cause an accompanying rise in heart rate, in fact reflex bradycardia usually occurs. This can be combated with atropine, after which Phen http://www.virtualmedicalcentre.com/drugs/dibenyline/2929 Phenoxybenzamine is an alpha-adrenergic receptor blocking agent that causes vasodilatation and decreased peripheral resistance and a subsequent decrease in blood pressure. By this mechanism phenoxybenzamine can prevent episodes of paroxysmal hypertension that can occur in patients with phaeochromocytoma due to high levels of circulating catecholamines. Phenoxybenzamine also blocks of alpha-adrenoreceptors on the smooth muscle of the bladder neck and distal urethral sphincter reducing smooth muscle tone and thereby reducing the resistance that can prevent urine outflow. http://www.virtualmedicalcentre.com/drugs/ismelin/2930 Guanethidine inhibits the peripheral sympathetic nervous system by two mechanisms. Guanethidine depletes noradrenaline storing vesicles and eliminates their capacity to store noradrenaline resulting in a depleted of noradrenaline in sympathetically innervated organs. Guanethidine also selectively inhibits release of the neurotransmitter noradrenaline subsequently blocks the activity of noradrenergic neurones. Guanethidine has strong polarity which prevents it from crossing the blood-brain barrier and acting on the central nervous system. http://www.virtualmedicalcentre.com/drugs/catapres-100/2934 Catapres 100 is an antihypertensive that is thought to act centrally by stimulating alpha2-adrenergic receptors which results in the inhibition of cardioacceleration and sympathetic vasoconstriction centres, hence decreasing central sympathetic outflow. It also stimulates increased vagal activity that decreases heart rate and there is also an increase in baroreceptor activity. Alpha1-adrenergic receptors are also transiently stimulated peripherally. For migraine prophylaxis and menopausal flushing the action of Catapres 100 seems to be important in its modification of the response of periph http://www.virtualmedicalcentre.com/drugs/dihydergot/2936 Dihydergot has complex pharmacological effects. It possesses affinity for both alpha-adrenergic and serotonergic receptors with both stimulating and blocking properties.2Dihydergot exerts its effect in orthostatic hypotension by selective constriction of capacitance vessels. This increases venous tone which leads to a redistribution of blood preventing excessive venous pooling.2In migraine attacks, Dihydergotnbsp;compensates the decreased 5-hydroxytryptamine (5HT) plasma level vianbsp;stimulating the effect of 5HT and hence counteracts the loss of tone of the extracranial vasculature.2nbsp; http://www.virtualmedicalcentre.com/drugs/zomig/2943 Zolmitriptan is a 5HT1 agonist that constricts cranial blood vessels by selectively binding to 5HT1B/1D receptors. http://www.virtualmedicalcentre.com/drugs/aggrastat/2944 Aggrastat is a non-peptide antagonist of the platelet glycoprotein (GP) IIb/IIIa receptor, the major platelet surface receptor involved in platelet aggregation. Aggrastat prevents binding of fibrinogen to GP IIb/IIIa, hence blocking the crosslinking of platelets and platelet aggregation.2 http://www.virtualmedicalcentre.com/drugs/arixtra/2945 Fondaparinux is a synthetic inhibitor of activated factor X (Xa). Fondaparinux binds selectively to Antithrombin III and potentiates the action of Antithrombin III. Antithrombin III neutralises factor Xa, interrupting the coagulation cascade and thus preventing the formation of thrombin and subsequent thrombus development. Fondaparinux does not inactivate thrombin and has no effects on platelet aggregation. When given at the recommended dose it will not affect fibrinolytic activity or bleeding times. http://www.virtualmedicalcentre.com/drugs/asasantin-sr/2946 Asasantin SR contains two active ingredients namely aspirin (25mg) and dipyridamole (200 mg). Together these drugs have additive effects to reduce the risk of thrombotic events. Aspirin irreversibly inhibits cyclo-oxygenase, reducing synthesis of thromboxane A2 and subsequently inhibiting platelet aggregation.1 Dipyridamole inhibits phosphodiesterases, subsequently causing inhibition of platelet adhesion and aggregation. Dipyridamole tend to act best in diseased states where platelets are excessively adhesive, thus it is of particular benefit in preventing thrombus formation.1 As fore ment http://www.virtualmedicalcentre.com/drugs/astrix-100-capsules/2947 Aspirin inhibits the activity of an enzyme called cyclo-oxygenase, which is responsible for the formation of thromboxane. Thromboxane is found on circulating platelets in the bloodstream and causes platelets to group together and from blood clots so by blocking thromboxane synthesis, aspirin reduces the formation of blood clots. Aspirin acetylates cyclo-oxygenase and consequently inhibits the synthesis of prostaglandins, thromboxane and prostacyclin. Thromboxane is a vasoconstrictor and induces platelet aggregation so by blocking the synthesis of thromboxane, Aspirin reduces thrombus http://www.virtualmedicalcentre.com/drugs/cartia/2950 Aspirin inhibits the activity of an enzyme called cyclo-oxygenase, which is responsible for the formation of thromboxane. Thromboxane is found on circulating platelets in the bloodstream and causes platelets to group together and from blood clots so by blocking thromboxane synthesis, aspirin reduces the formation of blood clots. Aspirin acetylates cyclo-oxygenase and consequently inhibits the synthesis of prostaglandins, thromboxane and prostacyclin. Thromboxane is a vasoconstrictor and induces platelet aggregation so by blocking the synthesis of thromboxane, Aspirin reduces thrombus f http://www.virtualmedicalcentre.com/drugs/clexane/2951 As a low molecular weight heparin (LMWH) Clexane (enoxaparin) achieves its effect by binding to antithrombin III. This results in thenbsp;inactivation of the major clotting factor Xa. Enoxaparin also inhibits the production and activity of thrombin (factor IIa). LMWHs have greater effect on factor Xa then unfractionated heparins. As a result, LMWHs have been shown to be more effective than heparin or warfarin in the prevention of thromboembolism after orthopaedic surgery.1,2 http://www.virtualmedicalcentre.com/drugs/coumadin/2952 Coumadin acts by inhibiting the synthesis of the vitamin K dependent coagulation factors VII, IX, X and II. By inhibiting these factors Coumadin prevents further extension of clots that have formed and also reduces the risk of thromboembolic complications. http://www.virtualmedicalcentre.com/drugs/heparin-injection-bpdbl/2955 Heparin potentiates the action of naturally occurring inhibitors of coagulation, antifactor Xa and antithrombin III. Normally there is balance between fibrinogen deposition and fibrinolysis which prevents the formation of thrombi. In the settings of trauma, surgery and immobilisation there is an increased predisposition to thrombus formation. By potentiating the actions of antifactor Xa and antithrombin III Heparin lessens the risk of the formation of new thrombi however it has no effect on thrombi that are already present http://www.virtualmedicalcentre.com/drugs/heparin-injection-bp-dbl/2956 Heparin potentiates the action of naturally occurring inhibitors of coagulation, antifactor Xa and antithrombin III. Normally there is balance between fibrinogen deposition and fibrinolysis which prevents the formation of thrombi. In the settings of trauma, surgery and immobilisation there is an increased predisposition to thrombus formation. By potentiating the actions of antifactor Xa and antithrombin III Heparin lessens the risk of the formation of new thrombi however itnbsp;has no effect on thrombi that are already present. http://www.virtualmedicalcentre.com/drugs/heparin-sodium-injection/2957 Heparin potentiates the action of naturally occurring inhibitors of coagulation, antifactor Xa and antithrombin III. Normally there is balance between fibrinogen deposition and fibrinolysis which prevents the formation of thrombi. In the settings of trauma, surgery and immobilisation there is an increased predisposition to thrombus formation. By potentiating the actions of antifactor Xa and antithrombin III Heparin lessens the risk of the formation of new thrombi however it has no effect on thrombi that are already present http://www.virtualmedicalcentre.com/drugs/heparinised-saline/2958 Heparin potentiates the action of naturally occurring inhibitors of coagulation, antifactor Xa and antithrombin III. Normally there is balance between fibrinogen deposition and fibrinolysis which prevents the formation of thrombi. In the settings of trauma, surgery and immobilisation there is an increased predisposition to thrombus formation. By potentiating the actions of antifactor Xa and antithrombin III Heparin lessens the risk of the formation of new thrombi however it has no effect on thrombi that are already present http://www.virtualmedicalcentre.com/drugs/iscover/2960 Clopidogrel is a potent inhibitor of platelet aggregation. Clopidogrel inhibits the binding of adenosine diphosphate (ADP) to its platelet receptor by irreversibly altering the platelet ADP receptor. ADP is needed for activation of the GPIIb/IIIa complex which is involved in platelet aggregation so by preventing the binding of ADP Clopidogrel inhibits platelet aggregation. As Clopidogrel irreversibly modifies the platelet ADP receptor, platelets that are exposed to Clopidogrel are affected for the remainder of their lifespan. The return of normal platelet function will occur only with the http://www.virtualmedicalcentre.com/drugs/marevan/2961 Warfarin inhibits the synthesis of vitamin K (II, IIV, IX, X) dependant clotting factors. Thereby acting as an anticoagulant. http://www.virtualmedicalcentre.com/drugs/orgaran/2962 The Orgaran (Danaparoid) anticoagulant profile is characterised by a high ratio of anti Factor Xa to antithrombin activity, giving effective inhibition of thrombin generation and formation, with minimal bleeding enhancing activity, through with negligible effects on haemostatic plug formation, platelet function and platelet aggregation. The anti-Xa activity is mediated by antithrombin III and is not inactivated by endogenous heparin neutralising factors. With the therapeutic dose range, the risk of haemorrhage with danaparoid is not related to plasma anti-Xa activity. No specific chemical ass http://www.virtualmedicalcentre.com/drugs/persantin/2963 Persantin inhibits platelet adhesion and aggregation, particularly in hypercoagulable states. The suggested mechanism of antiplatelet action is the weak inhibition of cAMP and cGMP. Persantin also causes coronary artery vasodilatation. http://www.virtualmedicalcentre.com/drugs/persantin-sr/2964 Persantin inhibits platelet adhesion and aggregation, particularly in hypercoagulable states. The suggested mechanism of antiplatelet action is the weak inhibition of cAMP and cGMP. Persantin also causes coronary artery vasodilatation. http://www.virtualmedicalcentre.com/drugs/plavix/2965 Clopidogrel is a potent inhibitor of platelet aggregation.1-3 It prevents the binding of adenosine diphosphate (ADP) to its platelet receptor. This prevents the activation glycoprotein IIb/IIIa complex mediated by ADP which in turn prevents platelet aggregation.1-3 http://www.virtualmedicalcentre.com/drugs/thrombotrol-vf/2967 Thrombotrol-VF is made from human plasma. The active pharmacological component is ATIII. ATIII is normally present in human plasma and is the major plasma inhibitor of thrombin, it also inactivates other components of the coagulation cascade, including factors IXa. Xa. XIa, XIIa and plasmin.The neutralisation of serine proteases by ATIII is greatly accelerated in the presence of heparin. However, as the antithrombotic effect of heparin is mediated by ATIII, the absence of ATIII in plasma greatly reduces the anticoagulant activity of heparin.The half life of ATIII is between 2.8 and 3.2 days. http://www.virtualmedicalcentre.com/drugs/kogenate-fs/2975 Kogenate FS contains octocog á, which has the same biological activity as human plasma-derived factor VIII. However, Kogenate FS lacks von Willebrand factor. http://www.virtualmedicalcentre.com/drugs/novoseven/2980 NovoSeven is a recombinant coagulation factor VIIa.nbsp;It binds to tissue factor to initiate the coagulation cascade, resulting in the formation of a haemostatic plug. Factor VIIa is practically inactive unless it binds to tissue factor to form a complex. These tissue factors are expressed at the site of damage to the vessel, thus the activity of NovoSeven is localised.1,2 http://www.virtualmedicalcentre.com/drugs/actilyse/2988 This drug converts plasminogen to plasmin, which then catalyses the breakdown of fibrin Alteplase belongs to a group of medicines known as fibrinolytics. 1 http://www.virtualmedicalcentre.com/drugs/actilyse-50-mg/2990 Alteplase is a tissue plasminogen activator that is made by recombinant DNA technology. When given intravenously Alteplase binds to fibrin in a thrombus and converts entrapped plasminogen to plasmin. Plasmin then initiates local fibrinolysis. The action of Alteplase is fibrin dependent and in the absence of fibrin Alteplase produces only minimal conversion of plasminogen to plasmin. The action of Alteplase is relatively selective and the drug produces minimal systemic effects. This is due to several factors including the high affinity of tissue Alteplase for fibrin, the fibrin dependent activa http://www.virtualmedicalcentre.com/drugs/metalyse/2991 Tenecteplase is an intravenously administered recombinant plasminogen activator that binds to the fibrin component of the thrombus, converting plasminogen to plasmin, and breaking down the fibrin matrix of the clot. Compared to native tPA, Tenecteplase has a higher fibrin specificity and greater resistance to inactivation by its endogenous inhibitor. Tenecteplase is chiefly distributed to and cleared by the liver. However, tenectaplase shows less affinity for hepatic receptors than native tPA, delaying it?s metabolism and increasing its half life. The initial, dominant half-life is 24 +/- http://www.virtualmedicalcentre.com/drugs/rapilysin/2992 Reteplase is a recombinant plasminogen activator that catalyses the cleavage of endogenous plasminogen to generate plasmin. Plasmin is an endogenous agent that degrades fibrin and fibrinogen which are the major components of thrombi. This degradation of fibrin and fibrinogen breaks down the thrombus thus improving circulation. http://www.virtualmedicalcentre.com/drugs/streptase/2993 Streptase (streptokinase) and plasminogen form an activator complex that converts plasminogen to plasmin. The activator complex has a half life of about 23 minutes, and is partly inactivated by anti-streptococcal antibodies. Plasmin degrades fibrin clots both superficially and from within the thrombus, and also degrades fibrinogen and some other plasma proteins. Plasmin is inactivated by circulating inhibitors (e.g. alpha-2-plasmin inhibitor or alpha-2-plasmin macroglobulin) that are rapidly consumed at high doses of streptokinase. Intravenous infusions of streptokinase increase fibrinolyti http://www.virtualmedicalcentre.com/drugs/xigris/2994 Xigris (dogrecogin alfa) is human activated protein C engineered with recombinant DNA technology, it has similar properties to endogenous human activated protein C. Activated protein C exhibits anti-thrombotic, profibrinolytic and anti-inflammatory properties. 90% of the steady state condition is achieved within two hours of commencing an infusion. After the completion of an infusion, activated protein C concentrations exhibit a biphasic half life with a rapid intial phase of 13 minutes, and a slower second phase of 1.6 hours. The mechanism by which activated protein C is cleared from the http://www.virtualmedicalcentre.com/drugs/adenoscan/2995 Adenosine slows conduction through the atrioventricular node interrupting re-entry circuits involving the atrioventricular node such as Wolff-Parkinson-White syndrome slowing the heart rate and restoring normal sinus rhythm. By slowing atrioventricular conduction adenosine can also aid the diagnosis of complex tachyarrhythmias and can be used as an adjunct to clinical and ECG observations http://www.virtualmedicalcentre.com/drugs/flolan/2998 Flolan consists of an active ingredient known as epoprostenol, which is a prostacyclin agent with two major pharmacological actions: Direct vasodilatation of pulmonary and systemic arterial vascular beds.1,2,3 Anti-platelet aggregating effects1,2,3 Animal studies have shown that epoprostenol through its vasodilatory effects can reduce left and right ventricular after-load and increase cardiac output and stroke volume1,2. Additionally, the effect of epoprostenol on heart rate in animals varies with dose. For instance, at low doses a vagally mediated bradycardia is present, but at higher dos http://www.virtualmedicalcentre.com/drugs/indocid-pda/2999 Exact mechanism of action is not known, but it is believed to be a potent inhibitor of prostaglandin synthesis. In human newborns with certain congenital heart malformations, PGE2 dilates ductus arteriosus. http://www.virtualmedicalcentre.com/drugs/persantin-ampoules/3003 Persantin inhibits platelet adhesion and aggregation, particularly in hypercoagulable states. The suggested mechanism of antiplatelet action is the weak inhibition of cAMP and cGMP. Persantin also causes coronary artery vasodilatation. http://www.virtualmedicalcentre.com/drugs/intal-spincaps-dpi/3011 Act by inhibiting release of inflammatory mediators from mast cells http://www.virtualmedicalcentre.com/drugs/chemists-own-decongestant-nasal-spray/3013 Produce vasoconstriction in nasal mucosa; decrease nasal blood flow and congestion Maximal effect lasts for 6 hours http://www.virtualmedicalcentre.com/drugs/otrivin-nasal-mist-junioradult/3014 Produce vasoconstriction in nasal mucosa; decrease nasal blood flow and congestion Maximal effect lasts for 6 hours http://www.virtualmedicalcentre.com/drugs/nyal-decongestant-elixir/3015 Act on alpha adrenoreceptors on vascular smooth muscle in the respiratory tract, producing vasoconstriction of dilated nasal vessels, reducing tissue swelling and nasal congestion http://www.virtualmedicalcentre.com/drugs/sudafed-12-hour-relief/3016 Act on alpha adrenoreceptors on vascular smooth muscle in the respiratory tract, producing vasoconstriction of dilated nasal vessels, reducing tissue swelling and nasal congestion http://www.virtualmedicalcentre.com/drugs/seretide-mdi-cfc-free/3018 Salmeterol component: Relax bronchial smooth muscle by stimulating beta 2 adrenoreceptors1 Long duration of action (12hours) Onset of action: 10 to 20 minutes Fluticasone component: This has glucocorticoid activity in the airways reducing bronchial mucosal inflammation and bronchial hyper-reactivity. This improves symptoms, allows reduction of other drugs, such as rescue bronchodilators, and may limit the risk of decline in lung function over time.3 Fluticasone has few systemic effects. Both forms of seretide (accuhaler DPI and MDI) have produced similar outcomes in clinical trials. http://www.virtualmedicalcentre.com/drugs/celapram/3020 Selective inhibition of pre-synaptic uptake of serotonin (5- hydroxytryptamine, 5-HT) SSRIs inhibit Cytochrome P450 enzymes, thus potentially interacting with those drugs by decreasing their metabolism http://www.virtualmedicalcentre.com/drugs/clopixol-depot-inj/3021 Antipsychotic actions are thought to be mediated (at least in part) by blockade of dopaminergic transmission in various parts of the brain (in particular, the limbic system). Although all antipsychotics block D2 receptors, there is some evidence to suggest that blockade of other dopamine receptors (e.g. D1) may influence therapeutic and adverse effects. http://www.virtualmedicalcentre.com/drugs/clopixol-acuphase-inj/3022 Antipsychotic actions are thought to be mediated (at least in part) by blockade of dopaminergic transmission in various parts of the brain (in particular, the limbic system). Although all antipsychotics block D2 receptors, there is some evidence to suggest that blockade of other dopamine receptors (e.g. D1) may influence therapeutic and adverse effects. http://www.virtualmedicalcentre.com/drugs/atrovent-autohaleratrovent-forte/3023 Promote bronchodilation by inhibiting cholinergic bronchomotor tone Ipratropium is as effective as inhaled beta 2 agonists in maintenance treatment of COPD. It is also indicated for severe acute asthma in addition to short-acting beta 2 agonists Duration of action of Ipratropium is approximately 6 hours, thus it can be used to augment the duration of bronchodilatation achieved with beta 2 agonist therapy. Ipratropium has shorter duration of action than the other anticholinergic bronchodilator, Tiotropium. Anticholinergic effects such as dry mouth occur less often with Ipratropium than Tiot http://www.virtualmedicalcentre.com/drugs/proladone/3024 Proladone is an opioid analgesic. Opioids mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems to produce analgesia. Opioids prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioids also produce respiratory depression and constipation. http://www.virtualmedicalcentre.com/drugs/compufen/3025 Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Ibuprofen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/proven/3026 Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Ibuprofen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/di-gesic/3027 Di-Gesic contains dextropropoxyphene and paracetamol. Dextropropoxyphene is a centrally acting, synthetic opioid analgesic that is structurally related to methadone. Dextropropoxyphene binds to opioid receptors at many sites within the central nervous system to reduce the bodys perception of pain. Paracetamol is a non-opioid analgesic that acts by inhibition ofnbsp;prostaglandin synthesis in the central nervous system and by blocking the generation of pain impulses in the periphery. When dextropropoxyphene and paracetamol are combined they produce a greater analgesia than would be produced b http://www.virtualmedicalcentre.com/drugs/allosig/3028 Allopurinol inhibits xanthine oxidase the enzyme responsible for uric acid production. Allopurinol is metabolised to oxypurinol, which also inhibits xanthine oxidase. By reducing uric acid production allopurinol and oxypurinol lower the plasma and urinary urate concentrations http://www.virtualmedicalcentre.com/drugs/actiq/3029 Opioid action. http://www.virtualmedicalcentre.com/drugs/nufloxib/3030 Microbiology. Norfloxacin is a broad spectrum, synthetic fluoroquinolone antibiotic. It is bacteriostatic and bactericidal. Norfloxacin shows in vitro activity against the following organisms: Urinary tract infection pathogens: Aerobic bacteria. Gram positive bacteria including S.faecalis, S.aureus, S.epidermidis, S.saprophyticus. Gram negative bacteria including E.coli, E.cloacae, K.oxytoca, K.pneumoniae, P.mirabilis, P.aeruginosa, C.diversus, C.freundii. Gastrointestinal tract infection pathogens: Shigella, E.coli, S.typhi. Others: N.gonorrhoea. The development of resistance duri http://www.virtualmedicalcentre.com/drugs/eryc/3031 Erythromycin is produced by a strain of Streptomyces erythreus, belongs to the macrolide antibiotic group, and inhibits bacterial protein synthesis. It is bacteriostatic at low concentrations and bactericidal at high concentrations. It is especially active against Gram positive cocci and bacilli. Erythromycin is usually active against the following microorganisms although not all strains are sensitive: S.pyogenes, alpha haemolytic Streptococci (viridans group), S.pneumoniae, S. aureus, M.pneumoniae, H.influenzae, L.pneumophilia, T.pallidum, N.gonorrhoeae, C.diphtheriae, C.minitissiumum, L.m http://www.virtualmedicalcentre.com/drugs/ciprofloxacin-bc/3033 Ciprofloxacin is a synthetic, broad-spectrum, quinolone antibiotic. Its bactericidal action is due interference with the bacterial enzyme, DNA gyrase. Ciprofloxacin exerts reliable activity against the following organisms in vitro: Gram negative: E.coli; Klebsiella sp; Enterobacter sp; Citrobacter sp; Salmonella sp; Shigella sp; P.mirabilis; P.vulgaris; Providencia stuartii; Providencia rettgeri; Morganella morganii; Serratia sp; P.aeruginosa; P.fluorescens; Campylobacter sp; H.influenzae; N.gonorrhoea; M.catarrhalis. Gram positive: S.aureus, coagulase negative Staphylococcus, S.pyoge http://www.virtualmedicalcentre.com/drugs/capastat/3034 Microbiology. Capreomycin is active against Mycobacterium tuberculosis. Cross resistance is common between capreomycin and viomycin, and occasional between capreomycin and kanamycin and neomycin. Cross resistance has not been seen between capreomycin and isoniazid, aminosalicylic acid, cycloserine, streptomycin ethioamide and ethambutol. Pharmacokinetics. Following intramuscular injection peak serum levels are reached 1-2 hours after administration, and half of the dose in excreted in urine, virtually unchanged, within 12 hours. http://www.virtualmedicalcentre.com/drugs/amoxycillin-bc/3035 Amoxicillin is a broad spectrum antibiotic with similar bactericidal activity to ampicillin. It acts by inhibiting cell wall mucopeptide biosynthesis. It is active against both Gram positive and negative pathogens, including P.mirabilis, H.influenzae, alpha beta haemolytic Streptococci, S.pneumoniae, S.faecalis, non-penicilliase producing Staphylococci, N.gonorrhoea, N.meningitidis. However, some organisms are only susceptible to amoxicillin at concentrations achieved in the urine, and gonococci strains relatively resistant to benzylpenicillin are likely to be resistant to amoxicillin. A http://www.virtualmedicalcentre.com/drugs/murelax/3036 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/temtabs/3037 Benzodiazepines potentiate the inhibitory effects of gamma aminobutyric acid (GABA throughout the CNS, resulting in anxiolytic, sedative hypnotic, muscle relaxant and antiepileptic effects http://www.virtualmedicalcentre.com/drugs/ultac/3038 Ranitidine acts by competitively blocking H2 receptors on gastric parietal cells thereby reducing gastric acid secretion. http://www.virtualmedicalcentre.com/drugs/azapin/3039 Azathioprine is metabolised to form mercaptopurine which through altering purine synthesis impairs cellular immunity, depresses cell proliferation and inhibits cellular inflammatory responses http://www.virtualmedicalcentre.com/drugs/panafcort/3040 Corticosteroids act by binding to intracellular cytoplasmic receptors, regulating the expression of corticosteroid-responsive genes. By regulating these genes corticosteroids suppress the normal physiological inflammation and immune responses. Prednisone has predominantly glucocorticoid activity with minimal mineralocorticoid activity. http://www.virtualmedicalcentre.com/drugs/fluoxetine-dp/3044 Fluoxetine exerts its antidepressant and antiobsessional effects by inhibiting the CNS neuronal uptake of serotonin. http://www.virtualmedicalcentre.com/drugs/pegasys/3045 The conjugation of a polyethylene glycol chain (PEG) reagent to interferon alpha-2a forms pegylated interferon alpha-2a (Pegasys). Interferon alpha-2a is biosynthetically produced using recombinant DNA, and is the product of a cloned human leucocyte gene inserted into and expressed in Escherichia coli. The structure of the PEG moiety directly affects the clinical pharmacology of Pegasys, defining its absorption, distribution and elimination characteristics. Pegasys possesses the in vitro antiviral and antiproliferative activities of the interferon alpha-2a. Interferons bind to cell surfa http://www.virtualmedicalcentre.com/drugs/genrx-lactulose/3046 Actilax is taken orally and reaches the large bowel without being absorbed into the bloodstream. Here, it is degraded by the normal bacteria found in the bowel, and this changes the pH, making it more acidic. This has two effects: one is to increase the amount of water in the bowel, which makes the stools softer and allows defecation to occur. The other is to remove harmful ammonia from the system and expel it in faeces, preventing the brain from being exposed to it as happens in PSE. http://www.virtualmedicalcentre.com/drugs/red-seal-liquid-calcium-capsules/3047 Calcium carbonate neutralises excess acid produced by the stomach, thereby reducing the burning symptoms associated with indigestion. Sustained calcium levels in the blood also help to prevent excess bone resorption associated with osteoporosis. http://www.virtualmedicalcentre.com/drugs/zantac-relief-extra-strength/3048 Ranitidine is a histamine H2-receptor antagonist with no action at H1-receptors and works to prevent gastric acid secretion in the stomach. Acid secretion in response to basal stimulation, histamine, food and other stimulatory factors is prevented equally. A plasma Ranitidine concentration of 50ng/ml will reduce gastric acid secretion by 50%. Gastric acid secretion stimulated by pentagastrin is inhibited according to Ranitidine dose. Secretion of gastric mucus and pancreatic enzymes is not affected by Ranitidine, and bacterial growth is not affected by the decreased acid levels in the stomach. http://www.virtualmedicalcentre.com/drugs/alimta/3052 The active ingredient in Alimta is pemetrexed which is an antifolate, antineoplastic agent. Pemetrexed behaves as a multi-targeted antifolate by inhibiting thymidylate synthase, dihydrofolate reductase and glycinamide ribonucleotide formyltransferase. These are all key folate-dependent enzymes involved in de novo biosynthesis of thymidine and purine nucleotides which are essential for cell replication. Both reduced folate carrier and membrane folate binding protein transport systems are thought to be involved in pemetrexed transport into cells.1 Following entry to a cell, pemetrexed is conver http://www.virtualmedicalcentre.com/drugs/enalapril-dp/3053 Enalapril maleate is a prodrug which when administered orally is hydrolysed to release the active converting enzyme inhibitor enalaprilat. The liver appears to be the main site for this conversion. Administration of enalapril to patients with hypertension results in a reduction of both supine and standing blood pressure without a significant increase in heart rate. http://www.virtualmedicalcentre.com/drugs/colifoam-rectal-foam/3054 The topical medication is applied to the rectal mucosa where the active ingredient, hydrocortisone acetate, has an anti-inflammatory effect. The medication has a mucoadherent base which keeps it inside the rectum, allowing the patient to continue with daily activities immediately. Up to 50% of the topical dose may be absorbed systemically where it is bound to plasma proteins and metabolised hepatically and renally. http://www.virtualmedicalcentre.com/drugs/cordilox-sr/3055 Calcium channel blockers block the inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L-type calcium channels. Verapamil acts mainly on the heart to reduce contractility, slow the heart rate and slow conduction but has less effect on vascular smooth muscle. http://www.virtualmedicalcentre.com/drugs/diltahexal-cd/3057 -Diltiazem is a slow calcium channel blocker. -It inhibits the influx of calcium ions during membrane depolarisation of cardiac and vascular smooth muscle. -Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/dilzem-cd/3058 -Diltiazem is a slow calcium channel blocker. -It inhibits the influx of calcium ions during membrane depolarisation of cardiac and vascular smooth muscle. -Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/genrx-diltiazem-cd/3059 -Diltiazem is a slow calcium channel blocker. -It inhibits the influx of calcium ions during membrane depolarisation of cardiac and vascular smooth muscle. -Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/adefin/3060 Nifedipine is a calcium channel blocker. It inhibits the slow inward calcium ion channels -It is a relaxant of vascular smooth muscle and an inhibitor of coronary artery spasm thus improving myocardial oxygen supply. -It inhibits the influx of calcium ions causing relaxation and peripheral vasodilatation, which in turn reduces the afterload against which the heart works. -It directly decreases myocardial oxygen consumption. -Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/adefin-xl/3061 -Nifedipine is a calcium channel blocker. It inhibits the slow inward calcium ion channels -It is a relaxant of vascular smooth muscle and an inhibitor of coronary artery spasm thus improving myocardial oxygen supply. -It inhibits the influx of calcium ions causing relaxation and peripheral vasodilatation, which in turn reduces the afterload against which the heart works. -It directly decreases myocardial oxygen consumption. -Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/nypine/3062 -Nifedipine is a calcium channel blocker. It inhibits the slow inward calcium ion channels -It is a relaxant of vascular smooth muscle and an inhibitor of coronary artery spasm thus improving myocardial oxygen supply. -It inhibits the influx of calcium ions causing relaxation and peripheral vasodilatation, which in turn reduces the afterload against which the heart works. -It directly decreases myocardial oxygen consumption. -Reduction in blood pressure is mediated by relaxation of vascular smooth muscle and resultant decrease in peripheral vascular resistance. http://www.virtualmedicalcentre.com/drugs/gliadel-implant/3063 Carmustine is an alkylating agent. Alkylating agents work on DNA in three different ways to disrupt its function and result in cell death. Firstly, they add alkyl groups to the bases making up the DNA. As normal repair enzymes try to replace the alkylated bases, the DNA is fragmented. Secondly, alkylating agents form cross-links between DNA strands, which prevents the strands from separating and undergoing replication. The final mechanism by which alkylating agents disrupt DNA is by causing mismatching of DNA bases. The alkylated bases are different from the original bases, and may pair incorr http://www.virtualmedicalcentre.com/drugs/fasturtec/3066 Lysis of large numbers of tumour cells following chemotherapy results in an acute increase in plasma uric acid levels.2,4 This can lead to renal damage and renal failure.2-4 Fasturtec is a recombinant urate-oxidase enzyme, which converts uric acid into the more easily excreted metabolite, allantoin.1-4 This decreases the risk of renal damage due to tumour lysis syndrome.1-4 http://www.virtualmedicalcentre.com/drugs/iressa/3068 Gefitinib is a specific inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase. EGFR tyrosine kinase is commonly expressed in solid tumours of epithelial origin. By inhibiting this important molecule, Gefitinib suppresses the growth of the tumour and enhances the antineoplastic activity of other chemotherapeutic agents, radiotherapy and hormonal therapy. 1,2,3 http://www.virtualmedicalcentre.com/drugs/kytril-tablets/3069 Granisetron is a 5HT3-receptor antagonist. 5HT3-receptors are found on preganglionic and postganglionic neurones and neurones of the sensory and enteric nervous systems. Importantly, they are also found in the area postrema, a chemoreceptor trigger zone in the fourth ventricle associated with vomiting. Chemotherapy agents cause vomiting by releasing serotonin from enterochromaffin cells of the small intestine, which is detected by vagal afferents. Granisetrons antagonism of 5HT3-receptors at vagal and central sites helps prevent and treat this nausea and vomiting2 http://www.virtualmedicalcentre.com/drugs/eligard/3070 Leuprorelin works by lowering the level of testosterone in the body. The testes only make testosterone if told to do so by a hormone known as luteinising hormone, which is produced by a part of the brain known as the pituitary gland. Leuprorelin reduces the production of luteinising hormone, which lowers the levels of testosterone. This may result in shrinkage of the tumour or a slowing down of its growth. There may be a brief increase in testosterone levels in the first few days or weeks of starting treatment. Tumour flare Leuprorelin may temporarily increase the levels of testosterone http://www.virtualmedicalcentre.com/drugs/genrx-methylphenidate/3072 Proposed mode of action of psychostimulants in ADHD is enhancement of dopaminergic and noradrenergic neurotransmission. http://www.virtualmedicalcentre.com/drugs/lorentin/3073 Proposed mode of action of psychostimulants in ADHD is enhancement of dopaminergic and noradrenergic neurotransmission. http://www.virtualmedicalcentre.com/drugs/anagraine/3074 Metoclopramide is an antiemetic agent. It stimulates the motility of the upper gastrointestinal tract without increasing secretions of the stomach, gallbladder or pancreas. Although its mechanism of action is not fully understood, Metoclopramide appears to sensitise tissues to the actions of acetylcholine. This increases the tone and amplitude of gastric contractions and increases peristalsis of the duodenum and jejunum, facilitating gastric emptying. It also increases the resting tone of the oesophageal sphincter, preventing upward movement of stomach contents. Metoclopramide is unlikely to c http://www.virtualmedicalcentre.com/drugs/lycinate/3075 Glyceryl trinitrate relaxes smooth muscle throughout the body. Its mechanism of action is based on an increase in venous capacitance leading to decreased return of blood to the heart. This results in decrease in left ventricular end-diastolic pressure (preload), which leads to decreased myocardial oxygen requirement at rest and during exercise. It also causes redistribution of coronary blood flow to ischaemic subendocardium by selectively dilating large epicardial vessels. http://www.virtualmedicalcentre.com/drugs/sevredol/3076 Morphine is an opioid analgesic. Opioid medications mimic endogenous opioids by binding to opioid receptors in the central and peripheral nervous systems. Here, they prevent transmission of the pain impulse by acting on presynaptic terminals to reduce the release of neurotransmitters and by reducing the activity of postsynaptic neurones in the spinal cord. As well as relieving pain, opioid analgesics also cause respiratory depression via direct activity on brainstem respiratory centres, and have many direct gastrointestinal effects due to action on organs containing smooth muscle. http://www.virtualmedicalcentre.com/drugs/liprace/3077 Lisinopril is a long acting angiotensin converting enzyme inhibitor. It is a peptidyl dipeptidase inhibitor, which inhibits the angiotensin converting enzyme (ACE) that catalyses the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased concentrations of plasma angiotensin II which results in decreased vasopressor activity and decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium. http://www.virtualmedicalcentre.com/drugs/lisinopril/3078 Lisinopril is a long acting angiotensin converting enzyme inhibitor. It is a peptidyl dipeptidase inhibitor, which inhibits the angiotensin converting enzyme (ACE) that catalyses the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased concentrations of plasma angiotensin II which results in decreased vasopressor activity and decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium. http://www.virtualmedicalcentre.com/drugs/ceftriaxone-sodium-for-injection-dbl/3093 Ceftriaxone is a semisynthetic broad spectrum antibiotic of the cephalosporin family. Its bactericidal effect is due to inhibition of bacterial cell wall synthesis. Ceftriaxone is a third generation cephalosporin, therefore has a high degree of stability against beta-lactamase (type I, II and III) producing organisms. It has activity against the following microorganisms: - Enterobacter aerogenes - Enterobacter cloacae - Escherichia coli - Haemophilus influenzae - Klebsiella spp. (including K. pneumoniae) - Neisseria gonorrhoeae - N. meningitidis - Proteus mirabilis - P. vulgaris - Mo http://www.virtualmedicalcentre.com/drugs/ural/3094 Ural works as a gastric and urinary alkaliniser.1,2nbsp; nbsp;nbsp;nbsp; http://www.virtualmedicalcentre.com/drugs/adenoscan/3095 Adenosine slows conduction through the atrioventricular node interrupting re-entry circuits involving the atrioventricular node such as Wolff-Parkinson-White syndrome slowing the heart rate and restoring normal sinus rhythm. By slowing atrioventricular conduction adenosine can also aid the diagnosis of complex tachyarrhythmias and can be used as an adjunct to clinical and ECG observations. http://www.virtualmedicalcentre.com/drugs/chemists-own-period-pain-tablets/3097 http://www.virtualmedicalcentre.com/drugs/eazydayz-tablets/3098 Naproxen is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase an enzyme involved in the pathway of prostaglandin synthesis. By inhibiting prostaglandin synthesis Naproxen has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and promote early restoration of joint mobility. http://www.virtualmedicalcentre.com/drugs/chem-mart-diclofenac/3100 Diclofenac is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain, inflammation and fever by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit cyclooxygenase (COX) an enzyme involved in the pathway of prostaglandin synthesis. There are two form of COX – COX1 and COX2. Diclofenac inhibits both of these COX enzymes By inhibiting prostaglandin synthesis Diclofenac has anti-inflammatory, analgesic and antipyretic properties and is able to provide prompt symptomatic relief of inflammation and pain and prom http://www.virtualmedicalcentre.com/drugs/chem-mart-gliclazide/3101 Gliclazide is a hypoglycaemic agent from the sulfonylurea class. It requires some residual islet cell function to have its effect. It stimulates insulin secretion from pancreatic islet cells and also increases the sensitivity of these islet cells to a glucose stimulus. Gliclazide restores the first-phase insulin secretion that has become diminished in non-insulin dependent diabetic (NIDDM) patients. Gliclazide has also been shown to have extrapancreatic effects, including improvement in insulin-mediated glucose utilisation and potentiation of postreceptor insulin sensitive pathways. It is th http://www.virtualmedicalcentre.com/drugs/chem-mart-piroxicam-capsules/3102 The mode of action of Piroxicam has not been fully established however it is known that piroxicam acts in several ways to diminish immune and inflammation responses. Piroxicam is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit Cyclo-oxygenase (COX), an enzyme involved in the pathway of prostaglandin synthesis. There are two forms of Cyclo-oxygenase, COX-1 and COX-2. Piroxicam inhibits both forms Piroxicam inhibits neutroph http://www.virtualmedicalcentre.com/drugs/chem-mart-piroxicam-dispersible-tablets/3103 The mode of action of Piroxicam has not been fully established however it is known that piroxicam acts in several ways to diminish immune and inflammation responses. Piroxicam is a non-steroidal anti-inflammatory drug (NSAID). NSAIDs relieve pain and inflammation by inhibiting the synthesis of prostaglandins, which are important mediators of inflammation, pain and fever. NSAIDs inhibit Cyclo-oxygenase (COX), an enzyme involved in the pathway of prostaglandin synthesis. There are two forms of Cyclo-oxygenase, COX-1 and COX-2. Piroxicam inhibits both forms Piroxicam inhibits neutroph http://www.virtualmedicalcentre.com/drugs/genrx-gliclazide/3104 Gliclazide is a hypoglycaemic agent from the sulfonylurea class. It requires some residual islet cell function to have its effect. It stimulates insulin secretion from pancreatic islet cells and also increases the sensitivity of these islet cells to a glucose stimulus. Gliclazide restores the first-phase insulin secretion that has become diminished in non-insulin dependent diabetic (NIDDM) patients. Gliclazide has also been shown to have extrapancreatic effects, including improvement in insulin-mediated glucose utilisation and potentiation of postreceptor insulin sensitive pathways. It is th http://www.virtualmedicalcentre.com/drugs/gliclazide-terry-white-chemists/3105 Gliclazide is a hypoglycaemic agent from the sulfonylurea class. It requires some residual islet cell function to have its effect. It stimulates insulin secretion from pancreatic islet cells and also increases the sensitivity of these islet cells to a glucose stimulus. Gliclazide restores the first-phase insulin secretion that has become diminished in non-insulin dependent diabetic (NIDDM) patients. Gliclazide has also been shown to have extrapancreatic effects, including improvement in insulin-mediated glucose utilisation and potentiation of postreceptor insulin sensitive pathways. It is th http://www.virtualmedicalcentre.com/drugs/mellihexal/3106 Gliclazide is a hypoglycaemic agent from the sulfonylurea class. It requires some residual islet cell function to have its effect. It stimulates insulin secretion from pancreatic islet cells and also increases the sensitivity of these islet cells to a glucose stimulus. Gliclazide restores the first-phase insulin secretion that has become diminished in non-insulin dependent diabetic (NIDDM) patients. Gliclazide has also been shown to have extrapancreatic effects, including improvement in insulin-mediated glucose utilisation and potentiation of postreceptor insulin sensitive pathways. It is th http://www.virtualmedicalcentre.com/drugs/chem-mart-gabapentin/3108 - The way in which gabapentin exerts its anticonvulsant effect is unknown - The drug is structurally related to the neurotransmitter GABA (gamma-aminobutyric acid) but its mechanism of action differs to other drugs that interact with GABA synapses - The binding site of gabapentin is yet to be established - It also does not affect sodium channels, a means by which other anticonvulsants may work http://www.virtualmedicalcentre.com/drugs/gabahexal/3109 - The way in which gabapentin exerts its anticonvulsant effect is unknown - The drug is structurally related to the neurotransmitter GABA (gamma-aminobutyric acid) but its mechanism of action differs to other drugs that interact with GABA synapses - The binding site of gabapentin is yet to be established - It also does not affect sodium channels, a means by which other anticonvulsants may work http://www.virtualmedicalcentre.com/drugs/gabapentin-terry-white-chemists/3110 - The way in which gabapentin exerts its anticonvulsant effect is unknown - The drug is structurally related to the neurotransmitter GABA (gamma-aminobutyric acid) but its mechanism of action differs to other drugs that interact with GABA synapses - The binding site of gabapentin is yet to be established - It also does not affect sodium channels, a means by which other anticonvulsants may work http://www.virtualmedicalcentre.com/drugs/nupentin/3111 - The way in which gabapentin exerts its anticonvulsant effect is unknown - The drug is structurally related to the neurotransmitter GABA (gamma-aminobutyric acid) but its mechanism of action differs to other drugs that interact with GABA synapses - The binding site of gabapentin is yet to be established - It also does not affect sodium channels, a means by which other anticonvulsants may work http://www.virtualmedicalcentre.com/drugs/phenobarbitone-elixir-15mg5ml/3112 - Phenobarbitone is a central nervous system (CNS) depressant that it mainly used for the management of seizures - The complete mechanism by which this drug exerts its action is not known however, it may act by enhancing or mimicking the synaptic action of the neurotransmitter gamma aminobutyric acid (GABA) - Seizure control is thought to occur due to the reduction of synaptic transmission and the increase in threshold for electrical stimulation to the motor cortex (responsible for producing gross movement) of the brain http://www.virtualmedicalcentre.com/drugs/metformin-terry-white-chemists/3113 Biguanides are orally active hypoglycaemic agents that do not require functioning B cells. Their action is complex and incompletely understood. Metformin works by increasing the biological efficacy of insulin, thereby increasing peripheral uptake of glucose. Metformin does not stimulate insulin release but does require the presence of insulin to exert its antihyperglycaemic effect. Its possible mechanisms of action include inhibition of gluconeogenesis in the liver, delay in glucose absorption from the gastrointestinal tract and an increase in peripheral uptake of glucose. Metformin also ha http://www.virtualmedicalcentre.com/drugs/metoclopramide-injection-bp/3115 Metoclopramide is an antiemetic agent. It stimulates the motility of the upper gastrointestinal tract without increasing secretions of the stomach, gallbladder or pancreas. Although its mechanism of action is not fully understood, Metoclopramide appears to sensitise tissues to the actions of acetylcholine. This increases the tone and amplitude of gastric contractions and increases peristalsis of the duodenum and jejunum, facilitating gastric emptying. It also increases the resting tone of the oesophageal sphincter, preventing upward movement of stomach contents. Metoclopramide is unlikely to c http://www.virtualmedicalcentre.com/drugs/aspen-fisamox/3116 Amoxil belongs to the penicillin group of antibiotics, and has a similar gram positive and gram negative spectrum to ampicillin. Its action is bactericidal against sensitive strains, and is thought to act by inhibiting the synthesis of cell wall mucopeptide. http://www.virtualmedicalcentre.com/drugs/kineret/3117 Anakinra blocks the activity of interleukin-1 (IL-1) by competitively inhibiting the binding of IL-1 to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 is produced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. http://www.virtualmedicalcentre.com/drugs/humira/3118 Adalimumab binds to and inhibits the activity of tumour necrosis factor (TNF), which is a cytokine involved in immune and inflammatory processes. TNF is found in increased concentrations in the affected tissues of patients with rheumatoid conditions. http://www.virtualmedicalcentre.com/drugs/neulasta/3119 Neulasta is a recombinant human granulocyte colony stimulating factor with a long duration of action. It increases the number neutrophils in peripheral blood counts by upregulating the release of neutrophils from the bone marrow. Neulasta improves the quality of neutrophils released as well as the quantity. Neutrophils released whilst a patient undergoes Neulasta therapy show enhanced chemotactic and phagocytic function. http://www.virtualmedicalcentre.com/drugs/kytril-injection/3120 Granisetron is a 5HT3-receptor antagonist. 5HT3-receptors are found on preganglionic and postganglionic neurones and neurones of the sensory and enteric nervous systems. Importantly, they are also found in the area postrema, a chemoreceptor trigger zone in the fourth ventricle associated with vomiting. Chemotherapy agents cause vomiting by releasing serotonin from enterochromaffin cells of the small intestine, which is detected by vagal afferents. Granisetrons antagonism of 5HT3-receptors at vagal and central sites helps prevent and treat this nausea and vomiting.1,2 http://www.virtualmedicalcentre.com/drugs/tester/3123 tester http://www.virtualmedicalcentre.com/drugs/avastin/3124 Avastin is a new class of therapy known as an angiogenesis inhibitor, which targets tumour angiogenesis (the growth of a network of blood vessels that supply nutrients and oxygen to cancerous tissues). This therapy uses a vastly different mode of action to chemotherapy. While chemotherapy targets the tumour itself, Avastin targets a naturally occurring protein called VEGF (Vascular Endothelial Growth Factor), which is a key mediator for angiogenesis. Tumours release VEGF when they reach a certain size and in order to grow further they need their own blood supply. By inhibiting VEDG, Avasti http://www.virtualmedicalcentre.com/drugs/salofalk-foam-enemas/3125 Mesalazine has been identified as the active component of sulfasalazine in the treatment of inflammatory bowel disease. The mechanism of action is not yet fully known. However, it is thought to act in multiple ways against several inflammatory mediators. For example, the effects of mesalazine on prostaglandin concentration in the intestinal mucosa has been demonstrated. Also it has been found to have influence in leukotriene production. From investigations, mesalazine has a role in lipoxygenase inhibition. It may also function as a radical scavenger of reactive oxygen compounds. http://www.virtualmedicalcentre.com/drugs/hepsera/3126 Adefovir is an acyclic nucleotide analogue of adenosine monophosphate with activity against human hepatitis B virus (HBV). It is phosphorylated to the active metabolite, adefovir diphosphate, by cellular kinases. Adefovir diphosphate inhibits HBV DNA polymerase (reverse transcriptase) by competing with the natural substrate deoxyadenosine triphosphate and by causing DNA chain termination after its incorporation into viral DNA. http://www.virtualmedicalcentre.com/drugs/pegatron-combination-therapy/3127 Peginterferon alfa-2b, when bound to the cell membrane receptors, initiates a complex intracellular enzymatic cascade that results in inhibition of virus replication in virus infected cells, suppression of cell proliferation and such immunomodulating activities as enhancement of the phagocytic activity of macrophages and augmentation of the specific cytotoxicity of lymphocytes for target cells. Ribavirin is a synthetic nucleoside analogue that has been shown to have some activity against some RNA and DNA viruses through an unknown mechanism. However, used in combination with peginterferon a http://www.virtualmedicalcentre.com/drugs/thalidomide-pharmion/3130 The exact mechanism of action of thalidomide is unknown. However, it is known that thalidomide decreases production and increases clearance of circulatingnbsp;tumour necrosis factor alpha (TNF-alpha). The reduction in TNF-alpha decreases inflammatory activity. In addition, thalidomide has positive effects on CD4+ T cells, and has anti-angiogenic activity.1,2 http://www.virtualmedicalcentre.com/drugs/salofalk-granules/3132 Mesalazine has been identified as the active component of sulfasalazine in the treatment of inflammatory bowel disease. The mechanism of action is not yet fully known. However, it is thought to act in multiple ways against several inflammatory mediators. For example, the effects of mesalazine on prostaglandin concentration in the intestinal mucosa has been demonstrated. Also it has been found to have influence in leukotriene production. From investigations, mesalazine has a role in lipoxygenase inhibition. It may also function as a radical scavenger of reactive oxygen compounds. http://www.virtualmedicalcentre.com/drugs/litak/3133 Litak is a synthetic antineoplastic agent. It contains cladribine as active ingredient, a purine nucleoside analogue (cytostatic agent) that acts as an antimetabolite. Cladribine is a prodrug, rapidly taken up into cells and phosphorylated intracellularly to the active nucleotide 2-chlorodeoxyadenosine-5-triphosphate (CdATP).The active CdATP is accummulated mainly in lymphocytes and other haemopoietic cells. The mechanism in which Litak acts is that the CdATP is incorporated into DNA strands to block DNA synthesis in rapidly dividing cells, and to inhibit DNA repair mechanisms. CdATP also inh http://www.virtualmedicalcentre.com/drugs/ferriprox/3134 Deferiprone is an active synthetic iron chelator. It is taken orally and absorbed in the upper part of the gastrointestinal tract. Depending on the patients fasting status, the peak serum concentration of deferiprone is reported from 45 minutes to 2 hours.In the blood stream, deferiprone binds to iron in 3:1 molar ratio and removes excess iron from the body. Based on clinical studies, deferiprone is effective in promiting iron excretion and can lower serum ferritin levels and tissue iron stores in transfusion-dependent thalassaemia patients. However, the exact mechanism of action is unknown. http://www.virtualmedicalcentre.com/drugs/tetrabenazine/3135 Tetrabenazine has a central amine depleting effect which resembles that of reserpine. However, Tetrabenazine is shorter acting (lasts 24 hours, with a more specific central action than reserpine). http://www.virtualmedicalcentre.com/drugs/vsl3/3137 VSL#3 contains 8 strains of bacteria. These include: 4 strains of lactobacilli (L. casei, L. plantarum, L. acidophilus, L. delbrueckii subspecies bulgaricus); 3 strains of bifidobacteria (B. longum, B. breve, B. infantis); and 1 strain of streptococcus (S. salivarius subspecies thermophilus). These strains were chosen for their synergy (co-operative activity) and ability to colonise the lower intestine. VSL#3 acts through probiotic therapy. It strives to establish the balance between the number and proportion of different bacterial species present in the gastrointestinal tract. The gastrointes http://www.virtualmedicalcentre.com/drugs/abelcet/3138 The pharmacokinetic properties of Abelcet and conventional amphotericin B are different. Amphotericin B when administered as Abelcet is rapidly distributed to tissues, especially the spleen, liver and lung. Abelcet may be fungistatic or fungicidal, depending on its concentration and on fungal susceptibility. It probably acts by binding to ergosterol in the fungal cell membrane and causing subsequent membrane damage. Leakage of cell contents from the fungal cell then leads to cell death. Binding of the drug to sterols in human cell membranes may result in toxicity, but amphotericin B has greate http://www.virtualmedicalcentre.com/drugs/vytorin/3140 Plasma cholesterol homeostasis depends on the balance between intestinal absorption and endogenous synthesis. Vytorin contains ezetimibe and simvastatin, two lipid-lowering compounds with complementary mechanisms of action. Vytorin reduces elevated total-C, LDL-C, Apo B, TG, and non-HDL-C, and increases HDL-C through dual inhibition of cholesterol absorption and synthesis.2,4 Ezetimibe: Ezetimibe inhibits the intestinal absorption of cholesterol. Ezetimibe is orally active and has a mechanism of action that differs from other classes of cholesterol reducing compounds (e.g. statins, bile http://www.virtualmedicalcentre.com/drugs/colazide/3141 Balsalazide is a prodrug of the active metabolite, mesalazine, which is linked to a carrier molecule via an azo bond. It is believed that mesalazine is released in the colon by a process of azo reduction by colonic bacteria.3 This ensures the active moiety reaches the appropriate site of action and minimises systemic side effects. Mesalazine is a 5-aminosalicylic acid compound that has anti-inflammatory effects on the colonic mucosa, however its precise mechanism of action is unknown.1 http://www.virtualmedicalcentre.com/drugs/keppra/3142 The precise mechanism of action by which levetiracetam induces seizure protection is unknown, but appears unrelated to the mechanisms of other antiepileptic drugs currently available. The mechanism of action may relate to an interaction with a specific and stereoselective binding site that is only found within the central nervous system.1,3 Other proposed mechanisms include inhibition of voltage-dependent N-type calcium channels; blockade of GABA-ergic inhibitory transmission; reduction of delayed rectifier potassium current; or binding to synaptic proteins which modify neurotransmitter releas http://www.virtualmedicalcentre.com/drugs/lyrica/3143 Pregabalin is an analogue of the neurotransmitter (NT) gamma-aminobutyric acid (GABA) with analgesic and anticonvulsant activity.1 In vitro studies show that pregabalin bind to the voltage-gated calcium channels in the central nervous system.1,3,4 In doing so, it reduces the calcium influx at nerve terminals and decreases the release of several neurotransmitters including glutamate, noradrenaline and substance P.1-4 The significance of these effects for the clinical pharmacology of pregabalin is not known.1 http://www.virtualmedicalcentre.com/drugs/lignocaine-injection/3144 Lignocaine is a class I (membrane-stabilising) antiarrhythmic agent. In cardiac tissue, lignocaine decreases automaticity by reducing the rate of diastolic (phase 4) depolarisation. It produces a blockage of sodium channels, thereby decreases the action potential duration and shortens the refractory period. http://www.virtualmedicalcentre.com/drugs/inspra/3147 Eprelenone is a mineralocorticoid receptor antagonist which acts to inhibit the action of aldosterone. It has only weak action at glucocorticoid, androgen and progesterone receptors meaning that the drug is relatively selective.1 As a result of this inhibiton at the mineralocorticoid receptor you get increased levels of aldosterone and renin due to loss of regulatory negative feedback. However this increase in levels of aldosterone and renin do not overcome the effects of eplerenone on blood pressure.1 http://www.virtualmedicalcentre.com/drugs/truvada/3148 This drug has two components, Tenefovir disoproxil fumarate and emtricitabine. Tenefovir disoproxil fumarate is a nucleoside inhibitor of reverse transcriptase and it works to stop viral replication of the HIV-1 virus by causing DNA chain termination by competing with the natural substrate. The emtricitabine component of the drug works in much the same way.2 These drugs are also weak inhibitors of mammalian DNA polymerase.1 There is evidence that these two drugs when used in combination with one another act synergistically.1 http://www.virtualmedicalcentre.com/drugs/minirin-tablets/3150 Desmopressin acetate is a synthetic structural analogue of the natural pituitary hormone arginine vasopressin (anti-diuretic hormone). Vasopressin regulates water retention and excretion.nbsp;Desmopressin has a considerably longer period of action and does not induce pressor effects in clinical doses.1 http://www.virtualmedicalcentre.com/drugs/symbicort/3151 Symbicort Turbuhaler contains budesonide and and eformetorol. These have different modes of action, and show additive effects in terms of reduction of asthma exacerbations. Pharmacology2 Budesonide is a glucocorticosteroid with a high local anti-inflammatory effect. When inhaled, it has a rapid and dose dependent anti-inflammatory action in the airways, resulting in reduced symptoms and fewer asthma exacerbations. Inhaled budesonide has less severe adverse effects than systemic corticosteroids. The exact mechanism responsible for the anti-inflammatory effect of glucocorticosteroids is unk http://www.virtualmedicalcentre.com/drugs/pentasa/3154 Mesalazine is a member of the 5-aminosalicylate class of drugs. 1 This group of drugs acts to inhibit the production of prostaglandins via the cyclooxygenase pathway and leukotrienes via the lipooxygenase pathway. 2 The inhibition of the lipooxygenase pathway results in reduced: 2 leukocyte chemotaxis cytokine scavenging for free radicals leukotriene production. Inhibition of the cyclooxygenase pathway results in a reduced production of prostaglandins which have proinflammatory effects. 2 Mesalazines effect is mainly due to its local effects on the inflamed rectal tissue, which is why http://www.virtualmedicalcentre.com/drugs/alvesco/3155 Alvesco reduces asthma symptoms through its anti-inflammatory effect in the airways. Inflammation of the small and large airways is associated with increased sensitivity to inhaled stimuli, and bronchial inflammation plays a key role in the pathogenesis of asthma. Alvesco has been shown to reduce airway reactivity and inflammatory markers.1 Ciclesonide, the active ingredient in Alvesco, is an ester pro-drug belonging to a new class of on-site activated non-halogenated inhaled glucocorticosteroids. It has approximately 100-fold lower affinity for the glucocorticosteroid receptor than its activ http://www.virtualmedicalcentre.com/drugs/ezetrol/3159 Ezetrol (ezetimibe) is a relatively new hypolipidaemic agent with a mechanism of action that differs from other classes of cholesterol- reducing compounds such as statins which inhibit hepatic cholesterol synthesis and bile-acid binding resins which lead to an increase in bile excretion. The exact molecular action of ezetimibe is not known but it is thought to act in the brush border of the small intestine to inhibiting the transport of both biliary and dietary cholesterol across the intestinal wall.1,4 This subsequently reduces the amount of cholesterol delivered to the liver, reduces hepatic http://www.virtualmedicalcentre.com/drugs/didronel/3160 Didronel acts primarily on bone. It modifies the crystal growth of calcium hydroxyapatite in vitro by chemisorption onto the crystal surface. Depending on concentration, the drug inhibits either crystal resorption or crystal growth. In addition to that, it may also directly affect cellular metabolic processes in vivo. When administered at daily doses of 10mg/kg/day or above, Didronel has also been observed to cause serum phosphate elevations. This appears to be the result of increased tubular reabsorption of phosphate by the kidney. No adverse effects of Didronel-induced hyperphosphataemia http://www.virtualmedicalcentre.com/drugs/erbitux/3163 Erbitux is a recombinant, human/mouse chimeric monoclonal antibody. It works by binding to its target protein human epidermal growth factor receptor (EGFR) (specifically to the extracellular domain) which is over-expressed on the surface of colorectal cancer cells.2 This competitively inhibits the natural occurring EGF from binding to the receptor thus inhibiting the normal signaling process for cells to divide.1 This inhibits the unregulated growth of the cancer and leads to apoptosis of cancer cells. http://www.virtualmedicalcentre.com/drugs/prexige-no-longer-available/3164 http://www.virtualmedicalcentre.com/drugs/rilutek/3165 The pathogenesis of amyotrophic lateral sclerosis is currently unknown. However there are a number of hypotheses that exist as to how the condition develops. 2 One hypothesis is that there is excess injury to motor neurons as a result of an excess of glutamate. 2 It is hypothesized that genetic and/or environmental factors predispose certain individuals to this glutamate excess. 2 It is thought that riluzole acts by the inhibition of voltage gated sodium channels and as a result causes an impairment in glutaminergic neurotransmission. 2 http://www.virtualmedicalcentre.com/drugs/levitra/3166 During sexual stimulation, nitric oxide (NO) is released from the nerve endings in the corpus carvenosum. NO activates the enzyme guanylate cyclase, resulting in an increased level of cyclic guanosine monophosphate (cGMP) in the corpus cavernosum. Elevation of cGMP level relaxes smooth muscle, thus allowing increased blood flow into the penis andnbsp;resulting in erection. The degradation of cGMP level is regulated by the rate of synthesis via the guanylate cyclase and the rate of degradation via cGMP hydrolysing phosphodiesterases (PDEs).nbsp;nbsp;nbsp;Levitra works by inhibiting PDE5, th http://www.virtualmedicalcentre.com/drugs/cialis/3167 The active ingredient in Cialis isnbsp;tadalafil,nbsp;a phosphodiesterase type 5 (PDE5) inhibitor that specifically targets cyclic guanosine monophosphate (cGMP). Tadalafil exerts its PDE-5 inhibition effect only in response to the local release of nitric oxide catalysed by sexual stimulation. When this occurs, PDE-5 inhibition results in increased levels of cGMP in the corpus cavernosum, which in turn increases smooth muscle relaxation, increasing blood flow to the penile tissues and enhancing erection.1 http://www.virtualmedicalcentre.com/drugs/caverject-impulse/3168 Caverject Impulse contains the naturally occurring compound prostaglandin E1 (alprostadil) that is normally present in various areas throughout the body.2,3 This agent has numerous pharmacological effects, the most important of which are vasodilation and inhibition of platelet aggregation. When injected into the penis, alprostadil induces an erection in patients with erectile dysfunction by relaxing smooth muscle within the corpus cavernosum and spongiosum and dilating cavernosal arteries. This leads to engorgement of blood within the penis which becomes trapped due to the compression of venul http://www.virtualmedicalcentre.com/drugs/lantus/3169 Insulin lowers blood sugar levels by increasing or enhancing the ability of the body to metabolise glucose. Insulin enhances cellular glucose uptake, inhibits hepatic glucose production and inhibits lipolysis in adipocytes.1, 3 Lantus (insulin glargine) is a human insulin analogue specifically designed to be slowly absorbed from the site of subcutaneous injection. It has a prolonged duration of action and a smooth (peakless) time/concentration profile, allowing once-daily dosing.1 http://www.virtualmedicalcentre.com/drugs/vidaza/3170 Vidaza is believed to exert its antineoplastic effects through hypomethylation of DNA and direct cytotoxicity on abnormal haematopoietic cells in the bone marrow. The cytotoxic effects of Vidaza cause the death of rapidly dividing cells, including cancer cells that are no longer restricted by physiological control mechanisms. Non-proliferating cells are relatively unaffected. http://www.virtualmedicalcentre.com/drugs/refludan/3171 Lepirudin is a recombinant hirudin. It acts as a highly specific direct inhibitor of thrombin, binding to and blocking thrombins pro-coagulant activity. It acts independently of antithrombin III.2 http://www.virtualmedicalcentre.com/drugs/tykerb/3175 Following oral administration, Tykerb (lapatinib) has incomplete and variable absorption. However, once at a significant serum concentration it exerts its metabolic effects by entering the cell and blocking the function of specific proteins. (This contrasts to other chemotherapy drugs such as trastuzumab which targets proteins from outside the cell). Lapatinib is a 4-anilinoquinazoline kinase inhibitor which works through both Epidermal Growth Factor Receptor (EGFR and Human Epidermal Receptor Type 2 (HER2 receptors, to disrupt growth signals in tumour cells. Thus this leads to reduced tumou http://www.virtualmedicalcentre.com/drugs/tarceva/3176 The active ingredient in Tarceva, erlotinib, has been shown to inhibit tumour growth and induce tumour apoptosis. It is known to inhibit phosphorylation of HER1/EGFR tyrosine kinase within cells, but the exact mechanism of its anti-tumour action has not been determined.1 http://www.virtualmedicalcentre.com/drugs/vectibix/3177 http://www.virtualmedicalcentre.com/drugs/concerta-extended-release-tablets/3178 Concerta contains the active ingredient methylphenidate, a central nervous system stimulant. Its mode of pharmacological action remains unclear. The drug is believed to increase the release of dopamine and noradrenaline in the extraneuronal space and inhibit their reuptake in the presynaptic neuron.1,2 http://www.virtualmedicalcentre.com/drugs/survanta/3179 Survanta (Beractant) mimics the action of endogenous pulmonary surfactants to reduce the surface tension on the alveoli during respiration.1,3 In addition surfactant stabilizes the resting transpulmonary pressures to prevent atelectasis 3 and increase lung compliance.2 Survanta is a natural bovine lung extract containing phospholipids, fatty acids and surfactant associated proteins to which stabilizing proteins are added and suspended in 0.9% saline. 1 http://www.virtualmedicalcentre.com/drugs/pariet/3180 Rabeprazolenbsp;suppresses gastric acid secretion by the specific inhibition of the H+/K+ ATPase enzyme (proton pump) at the secretory surface of the gastric parietal cell, thereby blocking the final step of acid production. This effect is dose-related and leads to inhibition of both basal and stimulated acid secretion irrespective of the stimulus. Animal studies indicate that, after administration, rabeprazole sodium rapidly disappears from both the plasma and gastric mucosa.3 Oral administration of a 20 mg dose of Pariet provides rapid and effective reduction of gastric acid secretion. The http://www.virtualmedicalcentre.com/drugs/velcade/3181 Velcade reversibly inhibits the 26S proteasome (which degrades intracellular ubiquitinated proteins, including multiple components of signalling cascades involved in cell cycle control and growth) impairing cell growth and leading to apoptosis. Velcade is cytotoxic to a variety of cancer cell types in vitro.1,2,4 http://www.virtualmedicalcentre.com/drugs/risperdal-oral-solution/3182 Risperdal belongs to a new class of antipsychotic drugs known as the benzisoxazole derivatives. Risperdal is a selective monoaminergic antagonist with a high affinity for serotonin and dopamine receptors. Risperdal also binds to alpha1-adrenergic receptors and, with lower affinity, to H1-histamine and alpha2-adrenergic receptors. Risperdal is thought to act against the positive symptoms of schizophrenia mainly through central dopamine D2-receptor antagonism. The serotonin and dopamine antagonism may work together to extend the therapeutic activity against the negative and affective symptoms of http://www.virtualmedicalcentre.com/drugs/risperdal-oral-quicklet/3183 Risperdal belongs to a new class of antipsychotic drugs known as the benzisoxazole derivatives. Risperdal is a selective monoaminergic antagonist with a high affinity for serotonin and dopamine receptors. Risperdal also binds to alpha1-adrenergic receptors and, with lower affinity, to H1-histamine and alpha2-adrenergic receptors. Risperdal is thought to act against the positive symptoms of schizophrenia mainly through central dopamine D2-receptor antagonism. The serotonin and dopamine antagonism may work together to extend the therapeutic activity against the negative and affective symptoms of http://www.virtualmedicalcentre.com/drugs/risperdal-oral-tablets/3184 Risperdal belongs to a new class of antipsychotic drugs known as the benzisoxazole derivatives. Risperdal is a selective monoaminergic antagonist with a high affinity for serotonin and dopamine receptors. Risperdal also binds to alpha1-adrenergic receptors and, with lower affinity, to H1-histamine and alpha2-adrenergic receptors. Risperdal is thought to act against the positive symptoms of schizophrenia mainly through central dopamine D2-receptor antagonism. The serotonin and dopamine antagonism may work together to extend the therapeutic activity against the negative and affective symptoms of http://www.virtualmedicalcentre.com/drugs/risperdal-consta/3185 Risperdal Consta is an extended release microspheres formulation of risperidone, micro-encapsulated in polyglactin for intramuscular injection, in strengths of 25 mg, 37.5 mg and 50 mg when suspended in 2 mL diluent. Risperdal belongs to a new class of antipsychotic drugs known as the benzisoxazole derivatives. It is a selective monoaminergic antagonist with a high affinity for serotonin and dopamine receptors. Risperdal also binds to alpha1-adrenergic receptors and, with lower affinity, to H1-histamine and alpha2-adrenergic receptors. Risperdal is thought to act against the positive symptoms http://www.virtualmedicalcentre.com/drugs/anzatax/3186 Paclitaxel exerts its antineoplastic effect by inhibiting the cell cycle in the G2 and M phases.1,2 Paclitaxel is an antimicrotubule agent; it promotes the formation of stable, nonfunctional microtubules through the polymerization of tubulin and inhibits their disassembly.1 It is a member of the taxane family of chemotherapeutics.2 http://www.virtualmedicalcentre.com/drugs/topamax-tablets/3187 Topamax is an anticonvulsant. Several mechanisms of action are thought to contribute to the anticonvulsant effect:1,2 Stabilization of presynaptic neuronal membranes by blocking voltage-dependent sodium channels. Enhancement of the activity of GABA on postsynaptic chloride channels.Antagonism of kainates ability to activate the kainite/AMPA subtype excitatory receptor.The mechanism of action of Topamax in migraine prophylaxis is not known.2 http://www.virtualmedicalcentre.com/drugs/topamax-sprinkle-capsules/3188 Topamax is an anticonvulsant. Several mechanisms of action are thought to contribute to the anticonvulsant effect: Stabilization of presynaptic neuronal membranes by blocking voltage-dependent sodium channels.1 Enhancement of the activity of GABA on postsynaptic chloride channels.1 Antagonism of kainates ability to activate the kainite/AMPA subtype excitatory receptor.2The mechanism of action of Topamax in migraine prophylaxis is not known.2 http://www.virtualmedicalcentre.com/drugs/prograf-injection/3191 Tacrolimus is a macrolide lactone (found initially in fungus, but made by a Streptomyces species) immunosuppressive. Tacrolimus appears to inhibit the formation of cytotoxic lymphocytes, preventing a cell mediated response to allograft. Tacrolimus: suppresses T-cell activation;suppresses T-helper-cell-dependent B-cell proliferation;suppresses production of cytokines including Il-2, Il-3 and y-interferon; anddownregulates Il-2 receptor.Intracellularly, the effects of tacrolimus appear to be mediated by binding to FKBP (FK-506 Binding Protein; FK-506 is a formerly used name of tacrolimus). A com http://www.virtualmedicalcentre.com/drugs/abilify/3192 Pharmacodynamics Unlike other antipsychotic agents, Abilify has an entirely different chemical structure and unique pharmacological properties. Its exact mechanism of action remains unknown but has been proposed to exert partial agonist activity at both dopamine D2 and serotonin 5-HT1A receptors and antagonistic effect at serotonin 5-HT2A receptors.2 Abilify also interacts with other receptor subtypes which may explain other clinical effects. Pharmacokinetics Abilify has oral bioavailability of 87% and administration with food does not affect its absorption. However, food may delay its Tmax by http://www.virtualmedicalcentre.com/drugs/videx/3194 Videx is a synthetic purine nucleoside analogue. In vivo, it is converted by cellular enzymes to the active antiviral metabolite dideoxyadenosine triphosphate (ddATP). The intracellular half-life of ddATP varies from 8 to 24 hours. Videx is rapidly degraded at acidic pH. Hence, it is protected against degradation by administration with antacids to increase the pH of the gastric environment. The pharmacokinetic profile of Videx buffered tablet is different from that of Videx EC capsule. The time to peak plasma concentration (Tmax) of Videx is 0.67 hours for Videx buffered tablets as compare http://www.virtualmedicalcentre.com/drugs/videx-ec/3195 Videx EC is a synthetic purine nucleoside analogue. In vivo, it is converted by cellular enzymes to the active antiviral metabolite dideoxyadenosine triphosphate (ddATP). The intracellular half-life of ddATP varies from 8 to 24 hours. Videx EC is rapidly degraded at acidic pH. It is formulated as an enteric coated capsule. The enteric coating dissolves when the beadlets empty in to the small intestine. The absolute bioavailability of Videx EC is approximately 40%. The peak plasma concentration (Cmax) of Videx EC capsules is reduced approximately 40% relative to Videx buffered tablets. http://www.virtualmedicalcentre.com/drugs/sensipar/3196 Cinacalcet reduces PTH (parathyroid hormone) while simultaneously lowering Ca x P (serum calcium-phosphorus product), calcium and phosphorus levels in chronic kidney disease in patients receiving dialysis.4 Secondary hyperparathyroidism (HPT) is a progressive disease, which occurs in patients with chronic kidney disease (CKD) and manifests as increases in PTH levels and derangements in calcium and phosphorus metabolism. Increased PTH stimulates osteoclastic activity resulting in cortical bone resorption and marrow fibrosis. The calcium sensing receptor on the surface of the chief cell of the http://www.virtualmedicalcentre.com/drugs/somatuline-autogel/3199 Somatuline Autogel consists of an active ingredient known as lanreotide, which acts as an inhibitory peptide (somastostain analogue) suppressing the release of a number of endocrines, neuroendocrine, exocrine and paracrine hormones (1,2,3). It has a marked affinity and selectivity for the peripheral somatostatin receptor and long duration of action than that of the natural somastostain (1,2,3). The pharmacological features of this drug make it a suitable candidate for treatment of acromegaly. http://www.virtualmedicalcentre.com/drugs/nexavar/3201 Nexavar consists of an active ingredient known as sorafenib tosylate, which is multikinase inhibitor that targets several serine/ threonine and receptor tyrosine kinases 1-3. Some examples of targets that are abnormally activated in tumour cells are Raf-1 (CRAF), BRAF, V600E BRAF, KIT and FLT-3, and in the tumour vasculature includes Raf-1 (CRAF), VEGFR-2, VEGFR-3 and PDGFR-beta 1,2. By targeting specific tyrosine and Raf kinases, sorafenib has been shown to inhibit tumour cell survival, proliferation, growth and angiogenesis.1-3 As a result Nexavar helps to prolong the survival rate of pat http://www.virtualmedicalcentre.com/drugs/renagel-tablets/3203 Renagel contains an active agent known as sevelamer hydrochloride, a non-absorbed phosphate-binding polymer, free of metal and calcium. It contains multiple amines, which become partially protonated in the intestine and interact with phosphorous molecules through ionic and hydrogen bonding 1. Through binding dietary phosphate in the gastrointestinal tract, absorption of phosphate is reduced thus decreasing serum phosphate concentration 1,2 Renagel decreases the incidence of hypercalcaemic episodes compared to patients using the calcium based phosphate binders alone 1 Renagel treatment also http://www.virtualmedicalcentre.com/drugs/reductil/3204 Sibutramine is a serotonin and noradrenaline reuptake inhibitor (SNRI). It reduces calorie intake by increasing post-ingestion satiety, and increases energy expenditure by increasing the treated individuals resting metabolic rate.1 http://www.virtualmedicalcentre.com/drugs/lamogine/3206 The precise mechanism of the anticonvulsant action of lamotrigine is not certain. The results of neurochemical and electrophysiological studies with various in vitro and in vivo preparations indicate that lamotrigine can inhibit voltage gated sodium channels and reduce the release of glutamate, an excitatory amino acid implicated in the pathophysiology of epilepsy. It is possible that these effects underlie inhibition of the sustained repetitive firing of action potentials characteristic of neurons in epileptic foci, thereby limiting the spread of seizures.1,2 http://www.virtualmedicalcentre.com/drugs/lamictal/3208 The precise mechanism of the anticonvulsant action of lamotrigine is not certain. The results of neurochemical and electrophysiological studies with various in vitro and in vivo preparations indicate that lamotrigine can inhibit voltage gated sodium channels and reduce the release of glutamate, an excitatory amino acid implicated in the pathophysiology of epilepsy. It is possible that these effects underlie inhibition of the sustained repetitive firing of action potentials characteristic of neurons in epileptic foci, thereby limiting the spread of seizures.1,2 http://www.virtualmedicalcentre.com/drugs/elmendos/3209 The precise mechanism of the anticonvulsant action of lamotrigine is not certain. The results of neurochemical and electrophysiological studies with various in vitro and in vivo preparations indicate that lamotrigine can inhibit voltage gated sodium channels and reduce the release of glutamate, an excitatory amino acid implicated in the pathophysiology of epilepsy. It is possible that these effects underlie inhibition of the sustained repetitive firing of action potentials characteristic of neurons in epileptic foci, thereby limiting the spread of seizures.1,2 http://www.virtualmedicalcentre.com/drugs/lamitrin/3210 The precise mechanism of the anticonvulsant action of lamotrigine is not certain. The results of neurochemical and electrophysiological studies with various in vitro and in vivo preparations indicate that lamotrigine can inhibit voltage gated sodium channels and reduce the release of glutamate, an excitatory amino acid implicated in the pathophysiology of epilepsy. It is possible that these effects underlie inhibition of the sustained repetitive firing of action potentials characteristic of neurons in epileptic foci, thereby limiting the spread of seizures.1,2 http://www.virtualmedicalcentre.com/drugs/neo-recormon/3212 Pharmacodynamics1,2 Neo-Recormon, erythropoietin beta, is a glycoprotein that stimulates the production of erythrocytes in the same way as erythropoietin. Neo-Recormon is identical in its amino acid and carbohydrate composition to erythropoietin that has been isolated from the urine of anaemic patients. It leads to increased haemoglobin formation and accelerated cell maturation by reducing the cell cycle time. This, therefore, accelerates recticulocyte maturation and increases reticulocyte level in the bloodstream. Pharmacokinetics1 Neo-Recormon administered subcutaneously has a variable http://www.virtualmedicalcentre.com/drugs/forteo/3213 Teriparatide is the active fragment of the endogenous parathyroid hormone (PTH) that binds to PTH receptors on target cells. It therefore has similar activity for regulating calcium and phosphate metabolism in the kidney and bones as PTH. Its activity includes1,2,3: Renal tubular reabsorption of calcium and phosphate Regulation of bone metabolism Increase calcium absorption from the intestinal wall. http://www.virtualmedicalcentre.com/drugs/levemir/3214 Insulin Detemir is a long acting insulin which has an onset of action within 60 minutes of administration and lasts for a duration of 12 to 23 hours. The action of Insulin Detemir takes approximately 3- 14 hours to peak.1,2,3 Insulin Detemir has a mode of action similar to insulin which is to enhance or re-establish the glucose metabolising capacity by: improving the uptake of glucose into cells; and inhibiting endogenous glucose output and lipolysis.1,2,3 The rys abbreviation in Insulin Detemir (rys) is used to specify the genetic engineering technique used to produce it. http://www.virtualmedicalcentre.com/drugs/humalog-injection-vial-humalog-injection-cartridge/3215 Insulin Lispro is a rapid acting (ultra-short acting) insulin which has an onset of action within 15 minutes of administration and lasts for a duration of 4 to 5 hours. The action of Insulin Lispro takes approximately 1 hour to peak.1,2,3 Insulin Lispro has a mode of action similar to insulin which is to enhance or re-establish the glucose metabolising capacity by: improving the uptake of glucose into cells; and inhibiting endogenous glucose output and lipolysis.1,2,3 http://www.virtualmedicalcentre.com/drugs/emend/3216 Aprepitant is a selective and high affinity antagonist of substance P neurokinin 1 (NK1) receptor1,2,3. Studies have shown that aprepitant has at least 3,000-fold selectivity for the NK1-receptor over other enzyme transporter ion channel and receptor sites, including the dopamine and serotonin (5HT3) receptors, which are also targets for existing chemotherapy-induced nausea and vomiting1,2. Aprepitant studies in animal models have shown to inhibit emesis induced by cytotoxic chemotherapeutic agents, such as cisplatin, via central action1,3. Preclinical studies show that aprepitant has a l http://www.virtualmedicalcentre.com/drugs/crestor/3217 Crestor consists of an active ingredient known as rosuvastatin, which is a synthetic competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. HMG-CoA reductase is a rate-limiting enzyme that converts HMG-CoA to mevalonate, a precursor of cholesterol. Rosuvastatin produces its lipid modifying therapeutic effects using two methods: Increases the number of hepatic low density lipoprotein (LDL) receptors on the cell surface leading to enhanced uptake and catabolism of LDL.Inhibits the hepatic synthesis of very low-density lipoprotein (VLDL), thereby reducing the total nu http://www.virtualmedicalcentre.com/drugs/ultiva-for-injection/3218 Ultiva consists of an active ingredient known as remifentanil hydrochloride, which is a potent opioid with analgesic and sedative properties.1-3 Remifentanil hydrochloride, analogues of fentanyl, acts as short-acting mu-opioid receptor agonists.3 Ultiva has a rapid onset of action, blood-brain equilibration half time of 1 +/-1 minutes, and a very short duration of action.1-3 http://www.virtualmedicalcentre.com/drugs/sutent/3219 Sutent contains the active ingredient sunitinib. Sunitinib is a tyrosine kinase inhibitor that targets multiple receptor tyrosine kinases implicated in tumour cell growth, angiogenesis and metastasis. By inhibiting receptor tyrosine kinase, sunitinib has been shown to inhibit cancer cell proliferation and metastasis.1 http://www.virtualmedicalcentre.com/drugs/cervarix/3221 The primary cause of cervical cancer and most precursor lesions is persistant infection with oncogenic HPV types; of these, HPV types 16 and 18 are responsible for approximately 70% of invasive cervical cancers.1 Cervarix is a recombinant vaccine prepared from non-infectious virus-like particles (VLPs) of the major L1 protein of HPV types 16 and 18. Since VLPs contain no viral DNA, they cannot infect cells or reproduce. VLPs are thought to work through cell mediated immunity.1 It is thought that the primary mechanism of protection against infection is through transudation of antiHPV IgG an http://www.virtualmedicalcentre.com/drugs/systane/3222 Systane acts as an artificial tear supplement to provide ocular lubrication.1,2 Dry eye damages the structures on the eye, exposing the ocular surface. The borate system in Systane crosslinks with the hydroxypropyl guar upon contact with the tear film, forming a protective three dimensional gel-like network. Hydroxypropyl guar helps tonbsp;keep the demulcent system on the surface of the eye for longer.2 http://www.virtualmedicalcentre.com/drugs/olmetec/3223 Olmesarten competitively antagonises the action of angiotensin II specifically at type 1 angiotensin (AT1) receptors.1-3 This complex results in reduced sodium reabsorption, aldosterone release and vasoconstrictive properties of angiotensin.1-3 http://www.virtualmedicalcentre.com/drugs/micardis-plus/3224 Micardis Plus is a combination of an angiotensin II receptor antagonist, Telmisartan, and a thiazide diuretic, hydrochlorothiazide.1-3 Telmisartan competitively antagonises the action of angiotensin II specifically at type 1 angiotensin (AT1) receptors. This complex results in reduced sodium reabsorption, aldosterone release and vasoconstrictive properties of angiotensin.1-3 Hydrochlorothiazide is a benzothiadiazine (thiazide) diuretic that inhibits the reabsorption of sodium and chloride in the proximal part of the distal convulated tubule.1-3 http://www.virtualmedicalcentre.com/drugs/norspan/3225 Pharmacodynamics2 Buprenorphine is a partial opioid agonist, acting at the mu-opioid receptor. It also has antagonistic activity at the kappa-opioid receptor. The mu receptor is the primary site of the analgesic effects of opioid drugs. The opioid agonist activities of buprenorphine are dose related. However, a ceiling effect to analgesia is well documented. This means that above a certain dose there is no further analgesic effect. Buprenorphine binds to and dissociates from the receptor slowly, which may account for the prolonged duration of analgesia. nbsp;Pharmacokinetics2 Each Norspan Tra http://www.virtualmedicalcentre.com/drugs/lucentis/3226 The active ingredient in Lucentis, ranibizumab, is a humanised recombinant monoclonal antibody fragment that targets human vascular endothelial growth factor A (VEGF-A). It binds to VEGF-A, and in so doing prevents VEGF-A binding to its receptors VEGF-1 and VEGF-2. Preventing VEGF-A binding to these receptors prevents proliferation of endothelial cells, neovascularisation and neovascular leakage, all of which appear to contribute to age-related macular degeneration of neovascular origin and to macular oedema causing visual impairment in diabetes and retinal vein occlusion.1 http://www.virtualmedicalcentre.com/drugs/spiriva/3227 Tiotropium is a long-acting anti-cholinergic agent. It promotes bronchodilatation by inhibiting cholinergic bronchomotor tone.1 It has similar antagonistic affinity to muscarinic receptor subtypes M1 to M5. Inhibition by tiotropium of M3-receptors at the smooth muscle results in relaxation of the airways. The long duration of acting is likely to be due to its slow dissociation from M3-receptors.2 http://www.virtualmedicalcentre.com/drugs/testogel/3228 The active ingredient in Testogel is a semi-synthetic testosterone. Exogenous administration has the effect of increasing serum testosterone levels.1 Exogenous testosterone performs the same functions as endogenously produced testosterone, primarily development of the male genitals and development of secondary sex characteristics (regulation of the male sex drive, body fat distribution, hair growth). Testosterone also plays a role in protein anabolism and regulating urinary nitrogen, sodium, potassium, chloride and phosphate and water excretion.1 http://www.virtualmedicalcentre.com/drugs/byetta/3229 Byetta exerts its effects via three mechanisms:1 Firstly, gastric emptying is slowed leading to a lower rate of glucose from meal appearing in blood. Secondly, Byetta produces actions similar to glucagon-like-peptide-1 (GLP-1) which causes an increase of insulin synthesis and secretion. Thirdly, glucagon secretion is suppressed causing reduced glucose output from the liver. http://www.virtualmedicalcentre.com/drugs/reandron/3231 The active ingredient in Reandron, testosterone undecanoate, is converted to testosterone through cleavage following injection. The effect is an increase in serum testosterone levels within a day of administration. Exogenous testosterone plays the same role as endogenous testosterone, including developing the male genitals and secondary sex characteristics (e.g. hair growth, body fat distribution).1 http://www.virtualmedicalcentre.com/drugs/triasyn/3232 Ramipril is an angiotensin converting enzyme inhibitor (ACEI) which works by reducing vasoconstriction (by reducing activation of the sympathetic nervous system) and also by antagonizing the renin-angiotensin system.1 Felodopine is a dihydropyridine calcium channel blocker which exerts its action by reducing vascular resistance particularly exerting its effect on the arteriolar smooth muscle.1 http://www.virtualmedicalcentre.com/drugs/exjade/3233 Exjade binds to non-transferrin-bound iron to reduce iron overload toxicity.1 http://www.virtualmedicalcentre.com/drugs/gardasil/3234 HPV can affect cutaneous and mucosal epithelial tissues.3nbsp;HPV 16 and 18 are oncogenic, while HPV 6 and 11 are known to cause most genital warts and are less oncogenic.1-3Gardasil is a quadrivalent human papillomavirus recombinant vaccine (types 6, 11, 16, 18). The vaccine contains 4 recombinant virus-like particles, eachnbsp;of whichnbsp;carry a unique capsid L1 protein of the respective virus type (types 6, 11, 16, 18).nbsp; The body develops a humoral immune response against the L1 proteins.2 The vaccine is unable to reproduce or infect an individual, as it does not contain any viral http://www.virtualmedicalcentre.com/drugs/zaditen/3236 Ketotifen is a non-specific anti-inflammatory agent and a mast cell stabiliser. It has an inhibitory effect on phosphodiesterase, resulting in increased levels of cyclic adenosine monophosphate. This is thought to contribute to ketotifens cell stabilising effect. The medication also decreases chemotaxis,nbsp;activation and degranulation ofnbsp;eosiniphils.1,2 http://www.virtualmedicalcentre.com/drugs/stalevo/3237 The rationale for drug therapy in Parkinsons disease is to provide symptomatic relief only - no pharmacological agent has been shown to slow the progression of Parkinsons disease. Stalevo is a combination product containing levodopa (a precursor to dopamine), carbidopa (a dopa decarboxylase inhibitor), and entacapone (a catechol-O-methyl transferase inhibitor). The aim of pharmacological treatment in Parkinsons disease is to replace depleted physiological dopamine levels in the substantia nigra of the central nervous system, thus improving the balance between dopaminergic and cholingeric ne http://www.virtualmedicalcentre.com/drugs/refresh-eye-drops/3238 Refresh eye drops increase the production of tears and stabilize the tear form.1 http://www.virtualmedicalcentre.com/drugs/femtran/3239 Femtran releases oestradiol into the body, which acts as annbsp;oestrogen replacement therapy and thus relieves symptoms suffered by oestrogen-deficient people.1,2 http://www.virtualmedicalcentre.com/drugs/caduet/3244 Caduet contains amlodipine and atorvastatin.1,2 Amlodipine is a diyhdropyridine calcium channel blocker. It blocks the inward current of calciumnbsp; via L-type calcium channelsnbsp;into vascular smooth muscle cells.1,2 The result is a reduction in peripheral vascular resistance, and therefore a reduction in blood pressure.1,2nbsp;Amlodipine has been shown to dilate peripheral arterioles as well as block constriction of coronary arteries.1,2 It also has a lessernbsp;effect on myocardial cells.1,2 Atorvastatin competitively inhibits the enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) http://www.virtualmedicalcentre.com/drugs/pv-carpine/3246 Pilocarpine stimulates cholinergic receptors in the eye,nbsp;causing contraction of the iris sphincter (leading to miosis) and ciliary muscle (leading to increased accommodation).1-3 The result is an increase in aqueous humour outflow through the trabecular meshwork,nbsp;and thusnbsp;a reduced intraocular pressure.1-3 http://www.virtualmedicalcentre.com/drugs/difflam-cream/3247 Benzydamine is an anti-inflammatory agent that chemically differs from other non-steroidal anti-inflammatory drugs (NSAIDs). Like all NSAIDs, benzydamine possesses analgesic, antipyretic and anti-inflammatory activity. Although the exact mechanism of benzydamine is yet to be elucidated, its pharmacological properties are likely related to the inhibition of prostaglandin biosynthesis.1 In addition, benzydamine possesses local anaesthetic activity at concentrations used for topical administration. When applied topically, benzydamine is well absorbed into the skin and accumulates in inflamed tiss http://www.virtualmedicalcentre.com/drugs/difflam-gel/3248 Benzydamine is an anti-inflammatory agent that chemically differs from other non-steroidal anti-inflammatory drugs (NSAIDs). Like all NSAIDs, benzydamine possesses analgesic, antipyretic and anti-inflammatory activity. Although the exact mechanism of benzydamine is yet to be elucidated, its pharmacological properties are likely related to the inhibition of prostaglandin biosynthesis.1 In addition, benzydamine possesses local anaesthetic activity at concentrations used for topical administration. When applied topically, benzydamine is well absorbed into the skin and accumulates in inflamed tiss http://www.virtualmedicalcentre.com/drugs/difflam-anti-inflammatory-lozenges-with-cough-suppressant/3249 Difflam Anti-Inflammatory Lozenges with Cough Suppressant contain the active ingredients benzydamine, cetylpyridinium and pholcodine. Benzydamine is an anti-inflammatory agent that chemically differs from other non-steroidal anti-inflammatory drugs (NSAIDs). Like all NSAIDs, benzydamine possesses analgesic, antipyretic and anti-inflammatory activity. Although the exact mechanism of benzydamine is yet to be elucidated, its pharmacological properties are likely related to the inhibition of prostaglandin biosynthesis. In addition, benzydamine possesses local anaesthetic activity at concentrations http://www.virtualmedicalcentre.com/drugs/difflam-mouth-gel/3250 Benzydamine is an anti-inflammatory agent that chemically differs from other non-steroidal anti-inflammatory drugs (NSAIDs). Like all NSAIDs, benzydamine possesses analgesic, antipyretic and anti-inflammatory activity. Although the exact mechanism of benzydamine is yet to be elucidated, its pharmacological properties are likely related to the inhibition of prostaglandin biosynthesis.1,2 In addition, benzydamine possesses local anaesthetic activity at concentrations used for topical administration. When applied topically, benzydamine is well absorbed into the oral mucosa and accumulates in infl http://www.virtualmedicalcentre.com/drugs/seretide-mdi/3251 Salmeterol component:2,3 Stimulates beta;2-adrenoreceptors, causing relaxation of bronchial smooth muscleLong duration of action ( gt;12 hours)Onset of action: 10-30 minutesFluticasone component:1,3 Glucocorticoid activity in the airways reduces bronchial mucosal inflammation and hyper-reactivityImproves symptoms, allows reduction of other drugs (eg. rescue bronchodilators) and may limit the risk of decline in lung function over time http://www.virtualmedicalcentre.com/drugs/auralgan/3253 The dehydrated glycerol helps to absorb moisture, and thenbsp;phenazone and benzocaine have analgesic effects during acute stages of otitis media and Swimmers ear.1,2 http://www.virtualmedicalcentre.com/drugs/rhinocort/3254 Budesonide is a corticosteroid, therefore it produces a local anti-inflammatory effect causing vasoconstriction in the nasal mucosa, andnbsp;reducing capillary permeability and mucous production.1-3 Onset of action occurs within 3-7 hours, with an optimum effect after several days of regular use. It is also effective on an as-needed basis.2 http://www.virtualmedicalcentre.com/drugs/difflam-anti-inflammatory-throat-spray/3255 Benzydamine is an anti-inflammatory agent that chemically differs from other non-steroidal anti-inflammatory drugs (NSAIDs). Like all NSAIDs, benzydamine possesses analgesic, antipyretic and anti-inflammatory activity. Although the exact mechanism of benzydamine is yet to be elucidated, its pharmacological properties are likely related to the inhibition of prostaglandin biosynthesis. In addition, benzydamine possesses local anaesthetic activity at concentrations used for topical administration.1,2 http://www.virtualmedicalcentre.com/drugs/difflam-c-anti-inflammatory-antiseptic-solution/3256 Difflam-C Anti-inflammatory Antiseptic Solution contains the active ingredients benzydamine and chlorhexidine.nbsp;nbsp;Benzydamine is an anti-inflammatory agent that chemically differs from other non-steroidal anti-inflammatory drugs (NSAIDs). Like all NSAIDs, benzydamine possesses analgesic, antipyretic and anti-inflammatory activity.nbsp; Although the exact mechanism of benzydamine is yet to be elucidated, its pharmacological properties are likely related to the inhibition of prostaglandin biosynthesis. In addition, benzydamine possesses local anaesthetic activity at concentrations used http://www.virtualmedicalcentre.com/drugs/mabcampath/3257 Alemtuzumab is a humanized IgG monoclonal antibody designed specifically to target the CD52 antigen (a cell surface glycoprotein) present on neutrophils and B- and T-lymphocytes.1-3 In addition, the CD52 antigen has been found to be expressed on monocytes, thymocytes, macrophages, sperm cells, certain epithelial cells and a small percentage of granulocytes. The CD52 antigen has not been identified on erythrocytes and platelets.1,2 Alemtuzumab is non-selective in targeting both normal and malignant lymphocytes in the body. Mechanistically, alemtuzumab has been shown to induce cell death in mali http://www.virtualmedicalcentre.com/drugs/strattera/3258 Pharmacodynamicsnbsp;Atomoxetine selectively inhibits presynaptic noradrenaline reuptake in the CNS.1 It has moderate affinity for 5HT2 and GABAA receptors but poor affinity for most other receptors. The main hydroxyatomoxetine metabolite is equipotent to the parent compound at the noradrenaline transporter and a more potent inhibitor of the 5HT transporter than the parent compound. 2 Pharmacokinetics1,2Atomoxetine is rapidly and almost completely absorbed after oral dosing. Strattera can be administered with or without food. A standard high fat meal did not seem to affect the extent of oral http://www.virtualmedicalcentre.com/drugs/dimetapp-12-hour-nasal-spray/3259 Oxymetazoline is a sympathomimetic with high alpha-adrenergic action. When applied locally it acts as a decongestant by causing vasoconstriction in the nasal membranes, thereby reducing blood flow and associated swelling.1,2 http://www.virtualmedicalcentre.com/drugs/duro-tuss-chesty-cough-liquid-plus-nasal-decongestant/3260 Bromhexine is a mucolytic agent that reduces mucous viscosity by fragmenting acid mucopolysaccharide fibres found in mucoid sputum. This facilitates its removal by ciliary action or expectoration.1 Pseudoephedrine (a stereoisomer of ephedrine) is a sympathomimetic agent that possesses both alpha;- and beta;-adrenergic receptor agonistic properties. In the respiratory tract, stimulation of alpha;1-adrenergic receptors on vascular smooth muscle cells produces vasoconstriction of dilated vessels, reducing tissue swelling and nasal congestion. Pseudoephedrine also stimulates heart rate and card http://www.virtualmedicalcentre.com/drugs/duro-tuss-dry-cough-liquid-plus-nasal-decongestant/3261 Pholcodine is a drug chemically related to morphine, which possesses cough suppressant activity but no analgesic action. Pholocdine acts directly on the cough centre in the medulla of the CNS, suppressing the cough reflex. Pholcodine is as effective as codeine in its antitussive actions, and has a longer half-life. Unlike codeine, pholcodine acts selectively on the cough centre without causing respiratory depression, constipation, euphoria and dependence.1,3 Pseudoephedrine (a stereoisomer of ephedrine) is a sympathomimetic agent that possesses both alpha;- and beta;-adrenergic receptor agon http://www.virtualmedicalcentre.com/drugs/duro-tuss-chesty-cough-liquid-regular/3262 Bromhexine is a mucolytic agent that reduces mucous viscosity by fragmenting acid mucopolysaccharide fibres found in mucoid sputum. This facilitates its removal by ciliary action or expectoration.1 http://www.virtualmedicalcentre.com/drugs/duro-tuss-chesty-cough-liquid-forte/3263 Bromhexine is a mucolytic agent that reduces mucous viscosity by fragmenting acid mucopolysaccharide fibres that are found in mucoid sputum. This facilitates its removal by ciliary action or expectoration.1 Guaifenesin is an expectorant that loosens and reduces the viscosity of mucoid sputum, facilitating its removal by expectoration.1 http://www.virtualmedicalcentre.com/drugs/difflam-anaesthetic-antibacterial-and-anti-inflammatory-lozenges/3264 Benzydamine is an anti-inflammatory agent that chemically differs from other non-steroidal anti-inflammatory drugs (NSAIDs). Like all NSAIDs, benzydamine possesses analgesic, antipyretic and anti-inflammatory activity.nbsp; Although the exact mechanism of benzydamine is yet to be elucidated, its pharmacological properties are likely related to the inhibition of prostaglandin biosynthesis. In addition, benzydamine possesses local anaesthetic activity at concentrations used for topical administration.1,2nbsp; Lignocaine is an amide-linked local anaesthetic agent that non-specifically and rever http://www.virtualmedicalcentre.com/drugs/duro-tuss-dry-cough-liquid-regular/3265 Pholcodine is a drug chemically related to morphine, which possesses cough suppressant activity but no analgesic action. Pholcodine acts directly on the cough centre in the medulla of the CNS, suppressing the cough reflex. Pholcodine is as effective as codeine in its antitussive actions, and has a long half-life. Unlike codeine, pholcodine acts selectively on the cough centre without causing respiratory depression, constipation, euphoria and dependence.1,3 http://www.virtualmedicalcentre.com/drugs/duro-tuss-dry-cough-liquid-forte/3266 Pholcodine is a drug chemically related to morphine, which possesses cough suppressant activity but no analgesic action. Pholcodine acts directly on the cough centre in the medulla of the CNS, suppressing the cough reflex. Pholcodine is as effective as codeine in its antitussive actions, and has a long half-life. Unlike codeine, pholcodine acts selectively on the cough centre without causing respiratory depression, constipation, euphoria and dependence.1,3 http://www.virtualmedicalcentre.com/drugs/duro-tuss-cough-liquid-expectorant/3267 Pholcodine is a drug chemically related to morphine, which possesses cough suppressant activity but no analgesic action. Pholcodine acts directly on the cough centre in the medulla of the CNS, suppressing the cough reflex. Pholcodine is as effective as codeine in its antitussive actions, and has a long half-life. Unlike codeine, pholcodine acts selectively on the cough centre without causing respiratory depression, constipation, euphoria and dependence.1,3 Bromhexine is a mucolytic agent that reduces mucous viscosity by fragmenting acid mucopolysaccharide fibres that are found in mucoid sputum http://www.virtualmedicalcentre.com/drugs/duro-tuss-sugar-free-lozenges/3268 Pholcodine is a drug chemically related to morphine, which possesses cough suppressant activity but no analgesic action. Pholocdine acts directly on the cough centre in the medulla of the CNS, suppressing the cough reflex. Pholcodine is as effective as codeine in its antitussive actions, and has a long half-life. Unlike codeine, pholcodine acts selectively on the cough centre without causing respiratory depression, constipation, euphoria and dependence.1,3Cetylpyridinium is an antibacterial agent. The clinical efficacy of an antibacterial agent in lozenges in reducing the duration or severity http://www.virtualmedicalcentre.com/drugs/champix/3269 Champix (Varenicline tartrate) exhibits both antagonistic and agonistic effects at the alpha;4beta;2 neuronal nicotinic receptors. Champix selectively binds to these receptors and in doing so exerts a partial agonistic effect, stimulating the receptor enough to diminish the symptoms of withdrawal. While at the same time, due to its high affinity for the recptor, Champix acts as an antagonist blocking the binding of nicotine and thus reducing the enjoyment and gratification of smoking.1,2 http://www.virtualmedicalcentre.com/drugs/tasigna/3270 Tasigna is a next generation Bcr-Abl inhibitor for Ph+ CML. Tasigna was specifically designed to be a highly selective inhibitor of Bcr-Abl which isnbsp;the key cause and driver of Ph+ CML, and its mutations. Tasigna thus blocks thenbsp;over production of white blood cells.1nbsp; http://www.virtualmedicalcentre.com/drugs/diabex-xr/3272 Metformin is an oral biguanide antihyperglycaemic agent which increases sensitivity of the available exogenous and endogenous insulin.1 It increases the peripheral uptake of glucose and reduces hepatic glucose production. It does not stimulate insulin release but does require presence of insulin to exert its blood glucose lowering effect.2 http://www.virtualmedicalcentre.com/drugs/zeldox/3273 Ziprasidone shares similar receptor activity with most of the other atypical antipsychotics.2 As with the other medications that are indicated for schizophrenia and/or bipolar disorder, the mechanism of action is still unknown.1 However, it has been suggested thatnbsp;its efficacy is throughnbsp;antagonisingnbsp;both dopamine D2 receptors and serotonin 5HT2A.1So far, Ziprasidone is the only atypical neuroleptic that antagonises serotonin 5HT1D, agonises serotonin 5HT1A and inhibits reuptake of both noradrenaline and serotonin.2 http://www.virtualmedicalcentre.com/drugs/canesoral/3275 Fluconazole is a bis-triazole antifungal that inhibitsnbsp;fungal cytochrome P450 sterolnbsp;C-14 alpha-demethylation. It is a selective inhibitor becausenbsp;mammalian cell methylation has significantly less sensitivity to fluconazole inhibition. The loss of sterolsnbsp;causes 14 alpha-methyl sterols to accumulate in fungi and hence eliciting the fungistatic action of fluconazole.1 http://www.virtualmedicalcentre.com/drugs/invega/3279 Paliperidone is a key active metabolite of risperidone and hence acts on the same receptors. Like all other drugs indicated for schizophrenia, the mode of action of paliperidone is unknown. However, it has been suggested that it works through antagonism of dopamine D2 and serotonin 5HT2A receptors. http://www.virtualmedicalcentre.com/drugs/levonorgestrel/3280 http://www.virtualmedicalcentre.com/drugs/valette/3282 The chief mechanisms of action of Valette are suppression of gonadotrophins and hence inhibition of ovulation as well as alterations of the cervical secretions which impedes access of sperm into the uterus.Due to its positive properties, Valette can also help make womenrsquo;s cycles more regular, less painful and bleed lighter. This may help reduce the chance of iron deficiency occurring. Dienogest also has an anti-androgenic action which helps to reduce acne lesions and sebum production. http://www.virtualmedicalcentre.com/drugs/voltaflex-plus/3284 Voltaflex Plus (Glucosamine and Chondroitin) consists of two natural substances of cartilage. Glucosamine is important in providing proper joint function. Its role is in the formation, repair and maintenance of the cartilage and joint fluid. On the other hand, Chondroitin is an important structural substance of cartilage, which provides elasticity and strength to the cartilage, which helps to improve the flexibility of joints. In patients suffering from osteoarthritis, supplementation with glucosamine and chondroitin has been shown to produce clinical benefits.1nbsp; http://www.virtualmedicalcentre.com/drugs/dihydergot-injection/3286 Dihydergot has complex pharmacological effects. It possesses affinity for both alpha-adrenergic and serotonergic receptors with both stimulating and blocking properties.2Dihydergot exerts its effect in orthostatic hypotension by selective constriction of capacitance vessels. This increases venous tone which leads to a redistribution of blood preventing excessive venous pooling.2In migraine attacks, Dihydergotnbsp;compensates the decreased 5-hydroxytryptamine (5HT) plasma level vianbsp;stimulating the effect of 5HT and hence counteracts the loss of tone of the extracranial vasculature.2 http://www.virtualmedicalcentre.com/drugs/prezista/3287 Prezista inhibits HIV-1 protease and ultimately prevents formation of infectious mature viral particles. http://www.virtualmedicalcentre.com/drugs/revatio/3288 The active ingredient of Revation is sildenafil citrate. Revatio selectively inhibits cyclic guanosine monophosphate (cGMP) specific phosphodiesterase type-5 in the smooth muscles of the pulmonary vasculature. This results in increased cGMP in the vascular smooth muscles of the lungs, and hence relaxation/vasodilatation.1,2 http://www.virtualmedicalcentre.com/drugs/fosamax-plus/3291 Fosamax Plus contains alendronate sodium (a biphosphonate) and cholecalciferol.1,2Alendronate sodium preferentially distributes to sites of bone resorption to hinder osteoclastic bone resorption.1,2 Cholecalciferol eventually works to increase absorption of calcium and phosphate from the intestines. It is also implicated in the regulation of serum calcium, renal calcium, phosphate excretion, bone formation and bone resorption.1,2 http://www.virtualmedicalcentre.com/drugs/dramamine-junior/3295 Dramamine Juniornbsp;blocks histamine H1 receptors. It alsonbsp;displays additional anticholinergic and sedative properties which enhance antiemetic activity and directly acts on the vestibular system.1nbsp;The site of action of Dramamine Junior remainsnbsp;unclear. However, it is thought thatnbsp;Dramamine Junior acts either on the overstimulated labyrinth, depresses transmission of nerve stimuli centrallynbsp;or at the chemoreceptor trigger zone.2 http://www.virtualmedicalcentre.com/drugs/dramamine-junior-liquid/3296 Dramamine Juniornbsp;Liquid blocks histamine H1 receptors. It alsonbsp;displays additional anticholinergic and sedative properties which enhance antiemetic activity and directly acts on the vestibular system.1nbsp;The site of action of Dramamine Junior Liquidnbsp;remainsnbsp;unclear. However, it is thought thatnbsp;Dramamine Junior Liquid acts either on the overstimulated labyrinth, depresses transmission of nerve stimuli centrallynbsp;or at the chemoreceptor trigger zone.2 http://www.virtualmedicalcentre.com/drugs/menevit/3299 Menevit maintains optimal male physiological functions and has been specially formulated to support male fertility by maintaining sperm health. This may then help to support conception.1 http://www.virtualmedicalcentre.com/drugs/yaz/3300 2 Yaz is a combined oral contraceptive (COC) that contains a synthetic progestogen (drospirenone) and synthetic oestrogen (ethinyloestradiol). Yaz works via various mechanisms, the primary one seen as inhibition of ovulation. Other mechanisms include alterations to the cervical mucus and altering uterine lining to make it less receptive to implantation. http://www.virtualmedicalcentre.com/drugs/somac-heartburn-relief/3301 The active ingredient of Somac Heartburn Tablets is pantoprazole, a proton pump inhibitor; that is, a medication which inhibits the enzyme (H+/K+-ATPase) which secretes gastric acid. H+/K+-ATPase is found in the parietal cells of the stomach. Pantoprazole is converted to an active form (sulphenamide) in the acidic environment of the parietal cells and binds to H+/K+-ATPase. This results in proton pump inhibition and long lasting suppression of gastric acid secretion, regardless of whether acid secretion is stimulated by acetylcholine, histamine or gastrin.1 The proton pump inhibition effect o http://www.virtualmedicalcentre.com/drugs/abraxane/3302 Paclitaxel, the active ingredient in Abraxane, is a naturally occurring anti-microtubule agent which interferes with cell mitosis. Paclitaxel induces the abnormal organisation of microtubules within cells, which prevents depolymerisation and cell mitosis.1nbsp; http://www.virtualmedicalcentre.com/drugs/somac-granules-40mg-on-prescription/3303 The active ingredient in Somac is pantoprazole, a proton pump inhibitornbsp;(PPI). PPIs inhibit the enzyme (H+/K+-ATPase) responsible for the secretion of gastric acid, a process which occurs in the parietal cells of the stomach. Pantoprazole enters and accumulates in the parietal cells in its inactive form as a substituted benzimidazole. It is converted to an active from (sulphenamide) in the acidic environment of the parietal cells and binds to H+/K+-ATPase. This results in proton pump inhibition and long-lasting suppression of gastric acid secretion, regardless of whether acid secretion is http://www.virtualmedicalcentre.com/drugs/cerezyme/3304 Cerezyme contains the active ingredient imiglucerase, an analogue of glucocerebrosidase producednbsp;by recombinant DNA technology using mammalian cell culture. Glucocerebrosidase isnbsp;the enzyme deficient in Gaucher disease. It is needed to catalyse the hydrolysis of glucocerebroside to glucose and ceramide.1 http://www.virtualmedicalcentre.com/drugs/panvax-h1n1-vaccine-swine-flu-vaccine/3305 Panvax is a purified, inactivated, split virion vaccine, prepared from virus propagated in the allontoic fluid of fertilised chicken eggs. It induces an antibody response involving the glycoproteins haemaggluttin and neuraminidase.1 http://www.virtualmedicalcentre.com/drugs/panvax-h1n1-vaccine-junior-child-swine-flu-vaccine/3306 The active ingredient in Panvax is a purified, inactivated, split virion, prepared from influenza virus propagated in the allontoic fluid of fertilised chicken eggs. It induces an antibody response involving the glycoproteins haemagglutintin and neuraminidase, which protect against infection.1 http://www.virtualmedicalcentre.com/drugs/circadin-prolonged-release-tablets/3307 Melatonin is an endogenous human hormone, structurally similar to serotonin, levels of which decrease as an individual ages. It is secreted by the pineal gland according to a circadian rhythm, with secretion commencing in the evening, peaking in the early hours of the morning (2ndash;4 am) and diminishing in the remainder of the night.1 Endogenous (and exogenous) melatonin functions to control the bodys circadian rhythm and response to the dark-light cycle. It induces a hypnotic effect and increases sleepiness, due to its effect on MT1 and MT2 receptors. These receptors control the circadia http://www.virtualmedicalcentre.com/drugs/aloxi/3308 Aloxi functions to prevent nausea and vomiting by selectively inhibiting serotonin subtype 3 (5HT3) receptors. These receptors, located in the nerve terminals of the vagus, are activated when serotonin is released from the small intestine, andnbsp;initiate the vomiting reflex. Chemotherapeutic agents are thought to induce nausea and vomiting in this way.1 http://www.virtualmedicalcentre.com/drugs/tramal-solution-for-injection-50-mg1ml-100-mg2ml/3311 The active ingredient in Tramal is tramadol hydrochloride, a synthetic analgesic from the aminocyclohexanol group. This group of medications act on the central nervous system and relieve pain in a similar manner to opioid analgesics. However, tramadol hydrochloride is not chemically related to opioids and is produced from synthetic materials.1 The exact action of Tramal is not fully understood, though at least two pain-relieving mechanisms have been identified. The mechanisms are similar to those of opioid analgesics. Tramadol hydrochloride binds with low affinity to micro;-opioid receptors, http://www.virtualmedicalcentre.com/drugs/tramal-immediate-release-capsules-50-mg/3312 The active ingredient in Tramal is tramadol hydrochloride, a synthetic analgesic from the aminocyclohexanol group. This group of medications act on the central nervous system and relieve pain in a similar manner to opioid analgesics. However, tramadol hydrochloride is not chemically related to opioids and is produced from synthetic materials.1 The exact action of Tramal is not fully understood, though at least two pain-relieving mechanisms have been identified. The mechanisms are similar to those of opioid analgesics. Tramadol hydrochloride binds with low affinity to micro;-opioid receptors, http://www.virtualmedicalcentre.com/drugs/tramal-oral-drops-100-mgml/3313 The active ingredient in Tramal is tramadol hydrochloride, a synthetic analgesic from the aminocyclohexanol group. This group of medications act on the central nervous system and relieve pain in a similar manner to opioid analgesics. However, tramadol hydrochloride is not chemically related to opioids and is produced from synthetic materials.1 The exact action of Tramal is not fully understood, though at least two pain-relieving mechanisms have been identified. The mechanisms are similar to those of opioid analgesics. Tramadol hydrochloride binds with low affinity to micro;-opioid receptors, http://www.virtualmedicalcentre.com/drugs/elonva-solution-for-injection/3314 Elonva is a gonadotrophin hormone that promotes enhanced follicular development by the same mechanism as FSH. Its action is sustained for a period of seven days.1 http://www.virtualmedicalcentre.com/drugs/mezavant-gastro-resistant-prolonged-release-tablets/3315 Mezavant tablets have a gastro-resistant film coating encasing a multi-matrix core containing the active ingredient mesalazine. The formulation enables sustained release of the active ingredient once the tablet reaches the colon. Systemic absorption is limited.1 The exact effects of mesalazine are not well understood. The drug appears to exert an anti-inflammatory effect on the colons epithelium. A possible mode of action is by blocking cyclooxygenase and inhibiting prostaglandin production in the colon. More recently, it has been proposed that impairment of PPAR-gamma; nuclear receptors ( http://www.virtualmedicalcentre.com/drugs/zostavax-powder-for-injection/3316 Zostavax boosts immunity to herpes zoster virus, commonly known as shingles, by increasing immunity to varicella zoster virus.1 Herpes zoster infection occurs secondary to varicella infection, when varicella-specific antibodies begin to wane. This is typically in older individuals aged gt;50 years, who experience more frequent and severe herpes zoster infections compared to their younger counterparts.1 The risk of herpes zoster infection is thought to increase as varicella-specific immunity declines. Zostavax increases varicella-specific immunity, and in doing so is thought to protect indiv http://www.virtualmedicalcentre.com/drugs/pradaxa/3323 The active ingredient in Pradaxa, dabigatran etexilate, is a prodrug which is rapidly absorbed by the liver where it is metabolised. The primary metabolite of dabigatran etexilate in plasma is dabigatran, a competitive and reversible direct thrombin (serine protease) inhibitor. It inhibits the action of free thrombin, fibrin-bound thrombin and thrombin-induced platelet aggregation.1 Thrombin plays a key role in coagulation pathways. Specifically, it enables the conversion of fibrinogen to fibrin during blood clotting and induces platelet aggregation. Thrombin inhibition prevents the formation http://www.virtualmedicalcentre.com/drugs/minirin-melt/3327 Desmopressin acetate is a synthetic structural analogue of the natural pituitary hormone arginine vasopressin (anti-diuretic hormone). Vasopressin regulates water retention and excretion. Desmopressin has a considerably longer period of action and does not induce pressor effects in clinical doses.1 http://www.virtualmedicalcentre.com/drugs/minirin-spray/3329 Desmopressin acetate is a synthetic structural analogue of the natural pituitary hormone arginine vasopressin (anti-diuretic hormone). Vasopressin regulates water retention and excretion. Desmopressin has a considerably longer period of action than vasopressin, which is thought to be due to resistance to inactivation. In animal models, pressor activity with desmopressin is 0.1% of that which occurs with vasopressin.1 Desmopressin acetate acts on the renal collecting tubule to increase its permeability to water reabsorption. This drug also has coagulant effects.1 http://www.virtualmedicalcentre.com/drugs/stelara/3332 Stelara is a monoclonal antibody that inhibits the activity of cytokines interleukin 12 (IL-12) and 23 (IL-23). This agent binds to the p40 subunit integral to both of these cytokines2 preventing their binding to receptors expressed on the surface of immune cells.4 This, in turn, inhibits subsequent signalling pathways, cell differentiation and cytokine formation central to the pathogenesis of psoriasis.1 http://www.virtualmedicalcentre.com/drugs/omnaris/3333 The active ingredient in Omnaris, ciclesonide, is a pro-drug which, following intranasal administration, is metabolised to the pharmacologically active form C21-desisobutyryl-ciclesonide (des-ciclesonide). Des-ciclesonide is an anti-inflammatory substance with high affinity (120-times that of the ciclesonide form) for the glucocorticoid receptor. The precise mechanism of action by which the metabolite works to prevent allergic rhinitis has not been identified. However, as a class, glucocorticoids are known to affect a wide range of cells involved in inflammatory responses, including mast cells