NURS 8024 PHARM FINAL EXAM NEWEST TEST BANK
COMPLETE 500 QUESTIONS AND CORRECT DETAILED
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 - ANSWER: histamine
receptor binding of prostaglandin E2 and
somatostatin diminish - ANSWER: gastric acid production
Antacids - ANSWER: 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 - 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 - ANSWER: Classes
• 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 - ANSWER: Cytoprotective compounds
Sucralfate
Bismuth Compounds
Cytoprotective Compounds - ANSWER: enhance mucosal protection
mechanisms → preventing mucosal injury, ↓ inflammation, promotes healing of
existing ulcers
Sucralfate - ANSWER: 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 - 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 - ANSWER: Safety not established in children
,Antacids during pregnancy and lactation - ANSWER: No FDA category established,
although antacids
generally are considered safe for use in pregnancy
Antisecretory agents - ANSWER: Histamine-2 receptor antagonists
Proton pump inhibitors
Examples of Histamine-2 receptor antagonists - ANSWER: ranitidine, *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 - ANSWER: H+/K+ ATPase proton pump
Omeprazole - ANSWER: PPI, 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 - ANSWER: PPIs
• 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 - ANSWER: 30 minutes before breakfast (or largest meal of the
day)
If taken with a PPI For best effect an H2 receptor antagonist should be taken -
ANSWER: well 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 - ANSWER: Decreased efficacy
Omeprazole inhibits the metabolism of - ANSWER: warfarin, phenytoin,
diazepam, and cyclosporine
Use of PPIs increases the risk for - ANSWER: osteoporosis
• Modest increase in the risk of hip fracture
COMPLETE 500 QUESTIONS AND CORRECT DETAILED
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 - ANSWER: histamine
receptor binding of prostaglandin E2 and
somatostatin diminish - ANSWER: gastric acid production
Antacids - ANSWER: 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 - 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 - ANSWER: Classes
• 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 - ANSWER: Cytoprotective compounds
Sucralfate
Bismuth Compounds
Cytoprotective Compounds - ANSWER: enhance mucosal protection
mechanisms → preventing mucosal injury, ↓ inflammation, promotes healing of
existing ulcers
Sucralfate - ANSWER: 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 - 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 - ANSWER: Safety not established in children
,Antacids during pregnancy and lactation - ANSWER: No FDA category established,
although antacids
generally are considered safe for use in pregnancy
Antisecretory agents - ANSWER: Histamine-2 receptor antagonists
Proton pump inhibitors
Examples of Histamine-2 receptor antagonists - ANSWER: ranitidine, *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 - ANSWER: H+/K+ ATPase proton pump
Omeprazole - ANSWER: PPI, 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 - ANSWER: PPIs
• 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 - ANSWER: 30 minutes before breakfast (or largest meal of the
day)
If taken with a PPI For best effect an H2 receptor antagonist should be taken -
ANSWER: well 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 - ANSWER: Decreased efficacy
Omeprazole inhibits the metabolism of - ANSWER: warfarin, phenytoin,
diazepam, and cyclosporine
Use of PPIs increases the risk for - ANSWER: osteoporosis
• Modest increase in the risk of hip fracture
