GASTROINTESTINAL DRUGS Flashcards
T/F
Gastric acid secretion is a continuous process
T
T/F
The parietal cells secrete hydrochloric acid.
T
FACTORS THAT REGULATE THE SECRETION OF HCl
(3)
NEURONAL
PARACRINE
ENDOCRINE
acetylcholine
A. NEURONAL
B. PARACRINE
C. ENDOCRINE
A
released from postganglionic vagal fibers
A. NEURONAL
B. PARACRINE
C. ENDOCRINE
A.
(acetylcholine)
enterochromaffin-like
cells and gastric-G cells
A. NEURONAL
B. PARACRINE
C. ENDOCRINE
A
(acetylcholine)
acts as paracrine mediator diffusing from its sight of
release to nearby parietal cells where it activates H2 receptors to stimulate gastric acid secretion
A. NEURONAL
B. PARACRINE
C. ENDOCRINE
B
(histamine)
gastrin
A. NEURONAL
B. PARACRINE
C. ENDOCRINE
C
produced by antral G-cells
A. NEURONAL
B. PARACRINE
C. ENDOCRINE
C
(gastrin)
most potent producer of acid secretion
A. NEURONAL
B. PARACRINE
C. ENDOCRINE
C
(gastrin)
T/F
lower esophageal sphincter and mucus are the gastric defenses against acid
T
primary esophageal defense
A. lower esophageal sphincter
B. mucus
A
prevents reflux of gastric acidic contents into the esophagus
A. lower esophageal sphincter
B. mucus
A
protects stomach and gastric epithelial cells by trapping
secreted bicarbonate at the cell-surface
A. lower esophageal sphincter
B. mucus
B
forms an insoluble gel that coats the mucosal surface of the
stomach, slows ion diffusion, and prevents mucosal damage
by macromolecules such as pepsin
A. lower esophageal sphincter
B. mucus
B
mucus production is stimulated by ________ which also directly inhibit gastric acid secretion by the parietal cells; thus, drugs that inhibit prostaglandin formation predispose to the development of acid secretion
prostaglandin E2 or
prostacyclin
follow relatively benign course
A. GERD (GASTROESOPHAGEAL REFLUX DISEASE)
B. peptic ulcers
C. stress-related mucosal injury
A
can be associated with severe erosive esophagitis, Barrett
metaplasia and adenocarcinoma
A. GERD (GASTROESOPHAGEAL REFLUX DISEASE)
B. peptic ulcers
C. stress-related mucosal injury
A
drugs used: o PPIs
o H2 receptor antagonists
A. GERD (GASTROESOPHAGEAL REFLUX DISEASE)
B. peptic ulcers
C. stress-related mucosal injury
A
duodenal or gastric type
A. GERD (GASTROESOPHAGEAL REFLUX DISEASE)
B. peptic ulcers
C. stress-related mucosal injury
B
imbalance between the mucosal defense factors like
bicarbonate, mucus and prostaglandin also nitric oxide and other peptides and growth factors and the injurious effects of the acid and pepsin
A. GERD (GASTROESOPHAGEAL REFLUX DISEASE)
B. peptic ulcers
C. stress-related mucosal injury
B
T/F
PEPTIC ULCER
patients with duodenal ulcer produce more acid particularly at day time
False
(patients with duodenal ulcer produce more acid particularly at NIGHT time)
→ H. pylori and endogenous agents such as NSAIDs act in complex ways to cause an ulcer
A. GERD (GASTROESOPHAGEAL REFLUX DISEASE)
B. peptic ulcers
C. stress-related mucosal injury
B
Bacteria that produce an “ammonia cloud” that will protect them from the acid
H. pylori
→ NSAIDs use
→ H. pylori infection
→ high HCL secretion
→ inadequate mucosal defense against gastric acid
A. GERD (GASTROESOPHAGEAL REFLUX DISEASE)
B. peptic ulcers
C. CAUSATIVE FACTORS
C
T/f
single-antibiotic regimen is ineffective in eradicating H. pylori infection and lead to antibiotic resistance that’s why combination therapy is needed
T
blocker enhances the effectiveness of an antibiotic
PPI or H2
T/F
patients with history of gastric ulcer can influence the choice of therapeutic agent or time of drug administration
T
____ may reduce the absorption of drugs such as Ampicillin
PPIs
____ antagonists inhibit the hepatic metabolism of
Lidocaine
H2 receptor
DRUGS THAT REDUCE INTRAGASTRIC ACIDITY (5)
ANTACIDS
H2 RECEPTOR ANTAGONISTS
PROTON PUMP INHIBITOR (PPI)
PROSTAGLANDINS
ANTIMUSCARINIC AGENTS
the acid neutralizing ability depends on:
o its capacity to neutralize gastric acid (rate of dissolution,
water solubility, rate of reaction with acid)
o whether the stomach is empty or full
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
A
Alka-Seltzer
A. SODIUM BICARBONATE
B. CALCIUM CARBONATE (TUMS)
C. MAGNESIUM HYDROXIDE/ALUMINUM HYDROXIDE
A
What are the antacids?
A. SODIUM BICARBONATE
B. CALCIUM CARBONATE (TUMS)
C. MAGNESIUM HYDROXIDE/ALUMINUM HYDROXIDE
reacts rapidly with acid → CO2 & NaCl
o this CO2 produces gastric distention and belching
A. SODIUM BICARBONATE
B. CALCIUM CARBONATE (TUMS)
C. MAGNESIUM HYDROXIDE/ALUMINUM HYDROXIDE
A
may be taken with Simethicone to avoid gas discomfort
A. SODIUM BICARBONATE
B. CALCIUM CARBONATE (TUMS)
C. MAGNESIUM HYDROXIDE/ALUMINUM HYDROXIDE
A
less soluble & reacts slowly than sodium bicarbonate
A. SODIUM BICARBONATE
B. CALCIUM CARBONATE (TUMS)
C. MAGNESIUM HYDROXIDE/ALUMINUM HYDROXIDE
B
excessive doses of either sodium bicarbonate or calcium carbonate combined with calcium-containing dairy products →
hypercalcemia, renal insufficiency, metabolic alkalosis
A. SODIUM BICARBONATE
B. CALCIUM CARBONATE (TUMS)
C. MAGNESIUM HYDROXIDE/ALUMINUM HYDROXIDE
B
reacts slowly with acid
A. SODIUM BICARBONATE
B. CALCIUM CARBONATE (TUMS)
C. MAGNESIUM HYDROXIDE/ALUMINUM HYDROXIDE
C
adverse effects:
osmotic diarrhea, constipation
A. SODIUM BICARBONATE
B. CALCIUM CARBONATE (TUMS)
C. MAGNESIUM HYDROXIDE/ALUMINUM HYDROXIDE
C
T/ F
All antacids should not be given within 2 hours of a dose of tetracycline or quinolones because they will affect the absorption of these drugs.
T
Histamine-2 receptor antagonists
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
B
Cimetidine, Ranitidine, Famotidine, Nizatidine
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
B
inhibit gastric acid secretion particularly effective against
nocturnal acid secretion
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
B
selective and reversible competitive antagonists
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
B
T/ F
H2 receptors ANTAGONISTS are located on the membrane of parietal cells
T
competitively blocks the binding of histamine to H2 receptors
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
B
if ulcers are caused by NSAIDs or Aspirin, these should be discontinued and a _____ should be given instead of a H2 antagonist
PPI inhibitor
T/F
Peptic Ulcers
if the ulcer is caused by H. pylori, H2 antagonists play no therapeutic role anymore and PPIs are given instead along with antibiotics
T
T/F
Acute Stress Ulcer is given through IV
T
H2 RECEPTOR ANTAGONISTS are?
CIMETIDINE
RANITIDINE
FAMOTIDINE
NIZATIDINE
→ given orally
→ distributed throughout the body
A. CIMETIDINE
B. RANITIDINE
C. FAMOTIDINE
D. NIZATIDINE
A
30% is inactivated by the liver; 70% excreted unchanged in the
urine
A. CIMETIDINE
B. RANITIDINE
C. FAMOTIDINE
D. NIZATIDINE
A
potentiate the action of Warfarin, Diazepam, Phenytoin,
Quinidine, Carbamazepine, Theophylline, Imipramine
A. CIMETIDINE
B. RANITIDINE
C. FAMOTIDINE
D. NIZATIDINE
A
longer acting, 5-10 fold more potent
A. CIMETIDINE
B. RANITIDINE
C. FAMOTIDINE
D. NIZATIDINE
B
minimal side effects; do not produce the anti-androgenic or
prolactin-stimulating effects of Cimetidine
A. CIMETIDINE
B. RANITIDINE
C. FAMOTIDINE
D. NIZATIDINE
B
does not affect the concentration of other drugs
A. CIMETIDINE
B. RANITIDINE
C. FAMOTIDINE
D. NIZATIDINE
B
→ 20-50x more potent than Cimetidine
A. CIMETIDINE
B. RANITIDINE
C. FAMOTIDINE
D. NIZATIDINE
C
3-20x more potent than Ranitidine
A. CIMETIDINE
B. RANITIDINE
C. FAMOTIDINE
D. NIZATIDINE
C
similar to Ranitidine
A. CIMETIDINE
B. RANITIDINE
C. FAMOTIDINE
D. NIZATIDINE
D
metabolized in the liver and eliminated primarily by the kidney
A. CIMETIDINE
B. RANITIDINE
C. FAMOTIDINE
D. NIZATIDINE
D
ADVERSE EFFECTS
gynecomastia, galactorrhea, LOW SPERM COUNT
A. CIMETIDINE
B. RANITIDINE
C. FAMOTIDINE
D. NIZATIDINE
A
Omeprazole, Esomeprazole, Lansoprazole, Pantoprazole
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
C
most potent inhibitors for gastric acid secretion
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
C
drug of choice for treating acid-related GI disorders
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
C
its antagonism is irreversible
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
C
undergo rapid first-pass metabolism & systemic hepatic metabolism
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
C
MODE OF ACTION
→ bind to H/K-ATPase (proton pump) of parietal cell → suppression of secretion of H ions into gastric lumen
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
C
→ prevention of rebleeding from peptic ulcer
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
C
MODE OF ACTION
→ bind to H/K-ATPase (proton pump) of parietal cell → suppression of secretion of H ions into gastric lumen
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
C
DRUG INTERACTIONS
→ inhibit metabolism of warfarin, diazepam, phenytoin
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
C
→ reduce clopidogrel activation and its antiplatelet action
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
C
PROSTAGLANDIN E2
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
D
MISOPROSTOL
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
D
Dicyclomine
A. ANTACIDS
B. H2 RECEPTOR ANTAGONISTS
C. PROTON PUMP INHIBITOR (PPI)
D. PROSTAGLANDINS
E. ANTIMUSCARINIC AGENTS
E
→ produced by gastric mucosa
→ inhibits secretion of HCl
A. PROSTAGLANDIN E2
B. MISOPROSTOL
C. Dicyclomine
A
→ stimulates secretion of mucus & bicarbonate
A. PROSTAGLANDIN E2
B. MISOPROSTOL
C. Dicyclomine
A
→ prevention of ulcer induced by NSAIDs
A. PROSTAGLANDIN E2
B. MISOPROSTOL
C. Dicyclomine
B
mode of action:
o interacts with receptor on parietal cell → inhibits adenyl cyclase → decrease cAMP
A. PROSTAGLANDIN E2
B. MISOPROSTOL
C. Dicyclomine
B
produce uterine contraction
A. PROSTAGLANDIN E2
B. MISOPROSTOL
C. Dicyclomine
B
adjunct in management of ulcer & Z-E syndrome
A. PROSTAGLANDIN E2
B. MISOPROSTOL
C. Dicyclomine
C
MUCOSAL PROTECTIVE AGENTS are?
SUCRALFATE
BISMUTH COMPOUNDS
binds selectively to ulcers or erosions for up to 6 hours and
should not be administered with H2 antagonists or antacids because it requires an acidic pH for activation
A. MUCOSAL PROTECTIVE AGENTS
B. ANTIDIARRHEAL DRUGS
C. LAXATIVES
A.
[SUCRALFATE]
Bismuth subsalicylate
A. MUCOSAL PROTECTIVE AGENTS
B. ANTIDIARRHEAL DRUGS
C. LAXATIVES
A
*actions:
o coats ulcers & erosions
o stimulates prostaglandin, mucus, & bicarbonate secretion
*reduces stool frequency & liquidity in acute infectious diarrhea
A. MUCOSAL PROTECTIVE AGENTS
B. ANTIDIARRHEAL DRUGS
C. LAXATIVES
A.
(Bismuth subsalicylate)
*has direct antimicrobial effect & binds enterotoxins
*uses:
o prevention of Traveler’s disease
o eradication of H. pylori
- decrease fluid secretion in the bowel
A. MUCOSAL PROTECTIVE AGENTS
B. ANTIDIARRHEAL DRUGS
C. LAXATIVES
D. Both a and b
E. Both b and c
D.
(Bismuth subsalicylate)
causes harmless blackening of stools, harmless blackening, of tongue
A. MUCOSAL PROTECTIVE AGENTS
B. ANTIDIARRHEAL DRUGS
C. LAXATIVES
A.
(Bismuth subsalicylate)
Diphenoxylate
A. MUCOSAL PROTECTIVE AGENTS
B. ANTIDIARRHEAL DRUGS
C. LAXATIVES
B
contribute to toxic megacolon
o not used in young children and in patients with severe colitis
A. MUCOSAL PROTECTIVE AGENTS
B. ANTIDIARRHEAL DRUGS
C. LAXATIVES
B
used to promote the evacuation of the bowel:
o enhancing retention of intramural fluid
o decreasing net absorption of fluid
o altering motility by inhibiting non propulsive contraction or
stimulating propulsive contraction
A. MUCOSAL PROTECTIVE AGENTS
B. ANTIDIARRHEAL DRUGS
C. LAXATIVES
D. Both a and b
E. Both b and c
C
may cause electrolyte imbalance when chronically used
A. MUCOSAL PROTECTIVE AGENTS
B. ANTIDIARRHEAL DRUGS
C. LAXATIVES
D. Both a and b
E. Both b and c
C
SENNA
A. MUCOSAL PROTECTIVE AGENTS
B. ANTIDIARRHEAL DRUGS
C. LAXATIVES
D. Both a and b
E. Both b and c
C
BISACODYL
A. MUCOSAL PROTECTIVE AGENTS
B. ANTIDIARRHEAL DRUGS
C. LAXATIVES
D. Both a and b
E. Both b and c
C
CASTOR OIL
A. MUCOSAL PROTECTIVE AGENTS
B. ANTIDIARRHEAL DRUGS
C. LAXATIVES
D. Both a and b
E. Both b and c
C
widely used stimulant laxative
A. SENNA
B. BISACODYL
C. CASTOR OIL
D. Methylcellulose
E. Docusate sodium
A
if combined with Docusate-containing stool softener → useful in treating opioid-induced constipation
A. SENNA
B. BISACODYL
C. CASTOR OIL
D. Methylcellulose
E. Docusate sodium
A
potent stimulant of the colon
A. SENNA
B. BISACODYL
C. CASTOR OIL
D. Methylcellulose
E. Docusate sodium
B
should not be taken with antacids at same time → causes gastric
irritation & pain
A. SENNA
B. BISACODYL
C. CASTOR OIL
D. Methylcellulose
E. Docusate sodium
B
broken down in small intestine to ricinoleic acid which is very irritating to the gut & promptly increases peristalsis
A. SENNA
B. BISACODYL
C. CASTOR OIL
D. Methylcellulose
E. Docusate sodium
C
causes uterine contractions
A. SENNA
B. BISACODYL
C. CASTOR OIL
D. Methylcellulose, Psyllium seeds, bran
E. Docusate sodium
C
used with caution in bed-ridden patients due to potential for
intestinal obstruction
A. SENNA
B. BISACODYL
C. CASTOR OIL
D. Methylcellulose, Psyllium seeds, bran
E. Docusate sodium
F. SALINE & OSMOTIC LAXATIVES
D
Magnesium citrate, Magnesium sulfate, Sodium phosphate, Magnesium hydroxide
A. SENNA
B. BISACODYL
C. CASTOR OIL
D. Methylcellulose, Psyllium seeds, bran
E. Docusate sodium
F. SALINE & OSMOTIC LAXATIVES
F
Lactulose
A. SENNA
B. BISACODYL
C. CASTOR OIL
D. Methylcellulose, Psyllium seeds, bran
E. Docusate sodium
F. SALINE & OSMOTIC LAXATIVES
G. STOOL SOFTENERS
F
Docusate sodium, Docusate calcium, Docusate potassium
A. SENNA
B. BISACODYL
C. CASTOR OIL
D. Methylcellulose, Psyllium seeds, bran
E. Docusate sodium
F. SALINE & OSMOTIC LAXATIVES
G. STOOL SOFTENERS
H. LUBRICANT LAXATIVES
G
should not be taken with mineral oil because of potential for
absorption of mineral oil
A. SENNA
B. BISACODYL
C. CASTOR OIL
D. Methylcellulose, Psyllium seeds, bran
E. Docusate sodium
F. SALINE & OSMOTIC LAXATIVES
G. STOOL SOFTENERS
H. LUBRICANT LAXATIVES
G
mineral oil, Glycerine suppositories
A. SENNA
B. BISACODYL
C. CASTOR OIL
D. Methylcellulose, Psyllium seeds, bran
E. Docusate sodium
F. SALINE & OSMOTIC LAXATIVES
G. STOOL SOFTENERS
H. LUBRICANT LAXATIVES
H
T/F
mineral oil should be taken orally in an downward position to avoid aspiration and potential for lipid pneumonia
F
(mineral oil should be taken orally in an UPRIGHT position to avoid aspiration and potential for lipid pneumonia)
cephalic phase of gastric acid secretion
Acetylcholine
reversible competitive antagonists
H2 RECEPTOR ANTAGONISTS
antagonism is irreversible
PROTON PUMP INHIBITOR (PPI)
