what is the pathophysiology of gastroesophageal reflux disease (GERD)?
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what is the pathophysiology of peptic ulcers?
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what causes it? (GERD top box, ulcers bottom box)
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occurs when contents of stomach and duodenum backflow into oesophagus, causing inflammation of the oesophageal mucosa (oesophagitis)
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an ulcer in an area where the mucosa is saturated in HCl and pepsin of the gastric juices
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if there is too much pressure on the stomach or the sphincter muscle is dysfunctional
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bacteria (H.pylori) or overuse of NSAIDs
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what are the drug types used to treat GERD & peptic ulcers?
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what is an example of each?
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what is the mechanism of action of each?
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antacids
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lots of over-the-counter drugs
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neutralises stomach acid, thereby increasing pH of stomach and allowing mucous layer time to repair itself
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proton pump inhibitors
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omeprazole, lansoprazole, etc
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irreversibly inhibits the hydrogen-potassium ATPase proton pump that controls H+ secretion from parietal cells, reducing gastric acid production
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H2 receptor antagonists
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cimetidine, ranitidine, etc
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competitively blocks H2 histamine receptors, which stimulate gastric acid secretion from parietal cells, to reduce stomach acidity
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M1 muscarinic receptor antagonists
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pirenzepine, hyoscyamine, etc
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M1 muscarinic receptor antagonism, blocking acetylcholine
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prostaglandins
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misoprostol
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binds to E1 G-protein coupled receptors on parietal cells, inhibiting adenyl cyclase and decreasing cAMP, blocking acid production
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mucosal strengtheners
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sucralfate, bismuth chelate, etc
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polymerise in the acid environment of the stomach, then binds to the damaged tissue and forms a protective coating over the ulcer beds
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