Gastric acid secretion by parietal cells of the gastric mucosa are stimulated
by - ANSWERS✔✔ *acetycholine, histamine, gastrin
Receptor-mediated binding of acetylcholine, histamine, or gastrin results in -
ANSWERS✔✔ *the activation of protein kinases, which in
turn stimulates the H+/K+-adenosine triphosphatase (ATPase) proton pump
Gastrin and acetylcholine stimulate release of - ANSWERS✔✔ histamine
receptor binding of prostaglandin E2 and
somatostatin diminish - ANSWERS✔✔ gastric acid production
Antacids - ANSWERS✔✔ weak bases that react with gastric acid to
form water and a salt → diminishing gastric acidity
Reduce pepsin activity - pepsin inactive at a pH >4
Wide variety* in chemical composition, acid-neutralizing capacity, sodium
content, palatability, and price
Acid neutralizing ability* of an antacid depends on its capacity to neutralize
gastric HCl and on whether the stomach is full or empty
• food delays stomach emptying, allowing more time for the antacid to react
,Therapeutic uses of antacids - ANSWERS✔✔ • Symptomatic relief of peptic
ulcer disease (PUD) and gastroesophageal reflux (GERD)
• May promote healing of duodenal ulcers, but not
robust evidence for efficacy in Tx of acute gastric
ulcers
• Calcium carbonate preparations
• also used as calcium supplements for the treatment of osteoporosis
Adverse effects of antacids - ANSWERS✔✔ • Aluminum hydroxide tends to be
constipating
• Magnesium hydroxide tends to cause diarrhea
• Binding of phosphate by aluminum-containing antacids →
hypophosphatemia
• Sodium bicarbonate → belching and flatulence, potential for systemic
alkalosis
• Sodium content of antacids → can be important in pts w/ HTN or CHF
• Excessive intake of calcium carbonate along w/ calcium foods →
hypercalcemia
Sucralfate - ANSWERS✔✔ complex of aluminum hydroxide and sulfated
sucrose
• Small, poorly soluble molecule
• Polymerizes in stomach acid → binds to injured tissue, forms physical
barrier coating over ulcer bed- impairs diffusion of HCl and prevents
degradation of mucus by pepsin and acid
• Accelerates healing of peptic ulcers and ↓ recurrence rate
• Stimulates prostaglandin release, mucus and bicarbonate output
• *BIG drawback.... Must be taken qid• used in long-term maintenance
therapy to prevent recurrence
• Requires an acidic pH for activation -should not be administered with H2
antagonists or antacids
• Little of the drug is absorbed systemically, very well tolerated
• Can interfere w/ absorption of other drugs by binding to them
• Does not prevent NSAID-induced ulcers
Bismuth Compounds - ANSWERS✔✔ • Coats ulcers → protective layer against
acid and pepsin
• May stimulate prostaglandin, mucus, and bicarbonate secretion
• Antimicrobial effect- binds enterotoxins
• reduces stool frequency & liquidity in acute infectious diarrhea
• Causes black stools- harmless
, • Avoid in renal insufficiency
In geriatric patients avoid use of - ANSWERS✔✔ - antacids that contain
magnesium in patients with renal failure
- sodium-containing antacids because of fluid
retention
Antacids in Pediatrics - ANSWERS✔✔ Safety not established in children
Antacids during pregnancy and lactation - ANSWERS✔✔ No FDA category
established, although antacids
generally are considered safe for use in pregnancy
H2 Receptor antagonists - ANSWERS✔✔ • MOA
• Acts selectively on H2 receptors in the stomach, blood vessels, and other
sites (no effect on H1 receptors)
• Competitively blocks binding of histamine to H2 receptors
• less effective than PPIs against stimulated secretion
• Four drugs: cimetidine*. ranitidine, famotidine, and nizatidine
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