NURS8024 Pharm Exam 1
Unlock Your Potential with NURS8024 Exam Prep
Current Updated Exam Study Guide 2025/2026.
Gastric acid secretion by parietal cells of the gastric mucosa are stimulated by -
ans*acetycholine, histamine, gastrin
Receptor-mediated binding of acetylcholine, histamine, or gastrin results in - ans*the
activation of protein kinases, which in
turn stimulates the H+/K+-adenosine triphosphatase (ATPase) proton pump
Gastrin and acetylcholine stimulate release of - anshistamine
receptor binding of prostaglandin E2 and
somatostatin diminish - ansgastric acid production
Antacids - answeak 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 - ans• 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 - ansClasses
• 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 - ans• 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 - ansCytoprotective compounds
Sucralfate
Bismuth Compounds
,NURS8024 Pharm Exam 1
Unlock Your Potential with NURS8024 Exam Prep
Current Updated Exam Study Guide 2025/2026.
Cytoprotective Compounds - ansenhance mucosal protection
mechanisms → preventing mucosal injury, ↓ inflammation, promotes healing of existing
ulcers
Sucralfate - anscomplex 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 - ans• 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 - ans- antacids that contain magnesium in patients with renal
failure
- sodium-containing antacids because of fluid
retention
Antacids in Pediatrics - ansSafety not established in children
Antacids during pregnancy and lactation - ansNo FDA category established, although
antacids
generally are considered safe for use in pregnancy
Antisecretory agents - ansHistamine-2 receptor antagonists
Proton pump inhibitors
Examples of Histamine-2 receptor antagonists - ansranitidine, *cimetidine, famotidine,
nizatidine
Examples of Proton pump inhibitors - ans• omeprazole, esomeprazole
• Lansoprazole, pantoprazole
• rabeprazole
H2 Receptor antagonists - ans• 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
,NURS8024 Pharm Exam 1
Unlock Your Potential with NURS8024 Exam Prep
Current Updated Exam Study Guide 2025/2026.
• 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 - ans• 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 - ans• 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 - ansH+/K+ ATPase proton pump
Omeprazole - ansPPI, 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 - ansPPIs
• Agents are pro-drugs w/ acid-resistant enteric coating to protect them from premature
degradation by gastric acid
Absorption/Action of PPIs - ans*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 - ans
Therapeutic uses of PPIs - ans• 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 - ans30 minutes before breakfast (or largest meal of the day)
, NURS8024 Pharm Exam 1
Unlock Your Potential with NURS8024 Exam Prep
Current Updated Exam Study Guide 2025/2026.
If taken with a PPI For best effect an H2 receptor antagonist should be taken - answell before
a PPI
H2 Receptors reduce activity of the proton pump
Concerns r/t long term use of PPIs - ans• 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 - ansDecreased efficacy
Omeprazole inhibits the metabolism of - answarfarin, phenytoin,
diazepam, and cyclosporine
Use of PPIs increases the risk for - ansosteoporosis
• Modest increase in the risk of hip fracture
• Prolonged increase in gastric pH increases potential for incomplete absorption of calcium
carbonate products
• Option would be to use *calcium citrate* as a source of calcium by patients taking
prolonged acid-suppressing medications
• Absorption of the citrate salt is not affected by gastric pH
Indications for H2 Receptor antagonist meds - ans• Duodenal ulcer treatment and
maintenance
• Gastric ulcer treatment
• Gastroesophageal reflux disease (GERD)
• Pathologic hypersecretory conditions
Indications for use of PPIs - ansGastric and duodenal ulcers
• GERD
• Pathologic hypersecretory conditions
• *Helicobacter pylori*
gastroesophageal reflux disease (GERD) - ansdevelops when reflux of stomach contents
causes
symptoms or complications
Symptoms: *Heartburn, dyspepsia* "Atypical" symptoms: asthma, chronic cough, chronic
laryngitis, sore throat, chest pain & sleep disturbances
Pathophysiology of GERD - ans• Delayed gastric emptying → common after meals and when
reclining
• Increased acidity
• Loss of lower esophageal sphincter (LES) tone
• Loss of secondary peristalsis w/ LES relaxation
• Hiatal hernia
• Truncal obesity → presumably due to ↑ intra-abdominal pressure
Non-pharmacologic treatment of GERD - ans• Untreated →→ severe esophagitis & Barrett
esophagus
Unlock Your Potential with NURS8024 Exam Prep
Current Updated Exam Study Guide 2025/2026.
Gastric acid secretion by parietal cells of the gastric mucosa are stimulated by -
ans*acetycholine, histamine, gastrin
Receptor-mediated binding of acetylcholine, histamine, or gastrin results in - ans*the
activation of protein kinases, which in
turn stimulates the H+/K+-adenosine triphosphatase (ATPase) proton pump
Gastrin and acetylcholine stimulate release of - anshistamine
receptor binding of prostaglandin E2 and
somatostatin diminish - ansgastric acid production
Antacids - answeak 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 - ans• 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 - ansClasses
• 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 - ans• 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 - ansCytoprotective compounds
Sucralfate
Bismuth Compounds
,NURS8024 Pharm Exam 1
Unlock Your Potential with NURS8024 Exam Prep
Current Updated Exam Study Guide 2025/2026.
Cytoprotective Compounds - ansenhance mucosal protection
mechanisms → preventing mucosal injury, ↓ inflammation, promotes healing of existing
ulcers
Sucralfate - anscomplex 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 - ans• 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 - ans- antacids that contain magnesium in patients with renal
failure
- sodium-containing antacids because of fluid
retention
Antacids in Pediatrics - ansSafety not established in children
Antacids during pregnancy and lactation - ansNo FDA category established, although
antacids
generally are considered safe for use in pregnancy
Antisecretory agents - ansHistamine-2 receptor antagonists
Proton pump inhibitors
Examples of Histamine-2 receptor antagonists - ansranitidine, *cimetidine, famotidine,
nizatidine
Examples of Proton pump inhibitors - ans• omeprazole, esomeprazole
• Lansoprazole, pantoprazole
• rabeprazole
H2 Receptor antagonists - ans• 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
,NURS8024 Pharm Exam 1
Unlock Your Potential with NURS8024 Exam Prep
Current Updated Exam Study Guide 2025/2026.
• 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 - ans• 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 - ans• 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 - ansH+/K+ ATPase proton pump
Omeprazole - ansPPI, 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 - ansPPIs
• Agents are pro-drugs w/ acid-resistant enteric coating to protect them from premature
degradation by gastric acid
Absorption/Action of PPIs - ans*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 - ans
Therapeutic uses of PPIs - ans• 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 - ans30 minutes before breakfast (or largest meal of the day)
, NURS8024 Pharm Exam 1
Unlock Your Potential with NURS8024 Exam Prep
Current Updated Exam Study Guide 2025/2026.
If taken with a PPI For best effect an H2 receptor antagonist should be taken - answell before
a PPI
H2 Receptors reduce activity of the proton pump
Concerns r/t long term use of PPIs - ans• 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 - ansDecreased efficacy
Omeprazole inhibits the metabolism of - answarfarin, phenytoin,
diazepam, and cyclosporine
Use of PPIs increases the risk for - ansosteoporosis
• Modest increase in the risk of hip fracture
• Prolonged increase in gastric pH increases potential for incomplete absorption of calcium
carbonate products
• Option would be to use *calcium citrate* as a source of calcium by patients taking
prolonged acid-suppressing medications
• Absorption of the citrate salt is not affected by gastric pH
Indications for H2 Receptor antagonist meds - ans• Duodenal ulcer treatment and
maintenance
• Gastric ulcer treatment
• Gastroesophageal reflux disease (GERD)
• Pathologic hypersecretory conditions
Indications for use of PPIs - ansGastric and duodenal ulcers
• GERD
• Pathologic hypersecretory conditions
• *Helicobacter pylori*
gastroesophageal reflux disease (GERD) - ansdevelops when reflux of stomach contents
causes
symptoms or complications
Symptoms: *Heartburn, dyspepsia* "Atypical" symptoms: asthma, chronic cough, chronic
laryngitis, sore throat, chest pain & sleep disturbances
Pathophysiology of GERD - ans• Delayed gastric emptying → common after meals and when
reclining
• Increased acidity
• Loss of lower esophageal sphincter (LES) tone
• Loss of secondary peristalsis w/ LES relaxation
• Hiatal hernia
• Truncal obesity → presumably due to ↑ intra-abdominal pressure
Non-pharmacologic treatment of GERD - ans• Untreated →→ severe esophagitis & Barrett
esophagus
