NURS8024 Pharm Exam 1 Questions &
Answers
Gastric acid secretion by parietal cells of the gastric mucosa are stimulated by -
ANSWER*acetycholine, histamine, gastrin
Receptor-mediated binding of acetylcholine, histamine, or gastrin results in -
ANSWER*the activation of protein kinases, which in
turn stimulates the H+/K+-adenosine triphosphatase (ATPase) proton pump
Gastrin and acetylcholine stimulate release of - ANSWERhistamine
receptor binding of prostaglandin E2 and
somatostatin diminish - ANSWERgastric acid production
Antacids - ANSWERweak 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 - ANSWER• 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
Commonly used antacid drugs - ANSWERClasses
• Calcium salts: calcium carbonate: Tums/Rolaids
• Sodium bicarbonate: Alka-Seltzer
• Aluminum salts - Aluminum hydroxide: Amphojel; Aluminum carbonate: Basaljel
• Magnesium salts/ magnesium oxide: Milk of Magnesia
• Combination products
• Aluminum hydroxide and magnesium hydroxide (Maalox, Mylanta)
• Alginic acid, magnesium trisilicate, calcium stearate
,(Gaviscon)
Adverse effects of antacids - ANSWER• 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
Mucosal Protective Agents - ANSWERCytoprotective compounds
Sucralfate
Bismuth Compounds
Cytoprotective Compounds - ANSWERenhance mucosal protection
mechanisms → preventing mucosal injury, ↓ inflammation, promotes healing of existing
ulcers
Sucralfate - ANSWERcomplex 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 - ANSWER• 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 - ANSWER- antacids that contain magnesium in
patients with renal failure
- sodium-containing antacids because of fluid
retention
Antacids in Pediatrics - ANSWERSafety not established in children
,Antacids during pregnancy and lactation - ANSWERNo FDA category established,
although antacids
generally are considered safe for use in pregnancy
Antisecretory agents - ANSWERHistamine-2 receptor antagonists
Proton pump inhibitors
Examples of Histamine-2 receptor antagonists - ANSWERranitidine, *cimetidine,
famotidine, nizatidine
Examples of Proton pump inhibitors - ANSWER• omeprazole, esomeprazole
• Lansoprazole, pantoprazole
• rabeprazole
H2 Receptor antagonists - ANSWER• 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
• Can inhibit > 90% basal, food-stimulated and nocturnal secretion of gastric acid after a
single dose
• Main clinical use is to inhibit gastric acid secretion
• particularly effective against nocturnal acid secretion
H2 Receptor antagonist ADEs - ANSWER• H2 antagonists very safe
• ADE < 3% of patients - diarrhea, h/a, fatigue, myalgias, constipation
• Drugs such as ketoconazole, which depend on an acidic medium for gastric
absorption, may not be efficiently absorbed if taken w/ H2 blocker
• Not used for NSAID-induced ulcers
• Better healing and prevention with PPIs
Cimetidine - ANSWER• Inhibits cytochrome P450 and can slow metabolism -
potentiating the action of other drugs
• warfarin, diazepam, phenytoin, quinidine,
carbamazepine, theophylline, and imipramine
• Cimetidine can have endocrine effects, acts as a
nonsteroidal antiandrogen. (effects include gynecomastia, galactorrhea, and reduced
sperm count)
Proton pump inhibitors inhibit - ANSWERH+/K+ ATPase proton pump
Omeprazole - ANSWERPPI, the first of a class of drugs that bind to the H+/K+- ATPase
enzyme system (proton pump) of the parietal cell
, • Suppresses secretion of hydrogen ions into the gastric lumen (membrane-bound
proton pump is the final step in the secretion of gastric acid)
lansoprazole, rabeprazole, pantoprazole,
esomeprazole, dexlansoprazole - ANSWERPPIs
• Agents are pro-drugs w/ acid-resistant enteric coating to protect them from premature
degradation by gastric acid
Absorption/Action of PPIs - ANSWER*Coating is removed* in the alkaline duodenum,
and the prodrug, a weak base, is absorbed and transported to the parietal cell
canaliculus → Converted to the active form
All PPIs inhibit both basal and stimulated gastric acid secretion by > 90%
• Onset of gastric acid suppression w/i 1 to 2 hrs post first dose of lansoprazole and
slightly earlier with omeprazole
Metabolism/Actions of PPIs - ANSWER
Therapeutic uses of PPIs - ANSWER• Superiority of PPIs over H2 antagonists for
gastric acid suppression and healing peptic ulcers - preferred therapy
• Preferred drugs for treating erosive esophagitis, active duodenal ulcer, long-term tx of
pathologic hypersecretory conditions
• Approved for the treatment of GERD.
• *Studies demonstrate that PPIs reduce bleeding risk from *aspirin and other NSAID
related ulcers
• Used w/ ATB in treatment of H. pylori related disease
PPIs should be taken - ANSWER30 minutes before breakfast (or largest meal of the
day)
If taken with a PPI For best effect an H2 receptor antagonist should be taken -
ANSWERwell before a PPI
H2 Receptors reduce activity of the proton pump
Concerns r/t long term use of PPIs - ANSWER• Increased gastric bacterial
concentration → Possible higher risk of aspiration pneumonia
• *Higher risk of CKD (chronic kidney disease)*
• Prolonged tx w/ PPIs and H2 antagonists, can cause low vitamin B12 - (acid required
for B12 absorption)
• 2-3 x increased risk for hospital & community-acquired Clostridium difficile infection in
patients taking PPIs
Plavix and use of PPIs - ANSWERDecreased efficacy
Omeprazole inhibits the metabolism of - ANSWERwarfarin, phenytoin,
diazepam, and cyclosporine
