GI Drugs Flashcards

1
Q

Name the H2 blockers

A

“-tidine”

cimetidine, ranitidine, famotidine, nizatidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mechanism of H2 blockers

A

reversible block of the histamine H2 receptors –> decrease H+ secretion by parietal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Use of H2 blockers

A

peptic ulcer, gastritis, mild GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Toxicity of cimetidine specifically

A
inhibits cytochrome p450 (multiple drug interactions)
antiandrogenic effects (prolactin release, gynecomastia, impotence, decreased libido in males)
can cross BBB (cause confusion, dizziness, headaches) and can cross placenta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Toxicity of cimetidine and ranitidine

A

decrease renal excretion of creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name the proton pump inhibitors

A

“-prazole”

omeprazole, lansoprazole, esmeprazole, pantoprazole, dexlansoprazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Mech of PPIs

A

irreversibly inhibit H+/K+ ATPase in stomach parietal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Use of PPIs

A

peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Toxicity of PPIs

A

increased risk of C. difficile infection, pneumonia

decreased serum Mg2+ with long-term use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Mechanism of bismuth and sucralfate

A

bind to ulcer base, providing physical protection and allowing HCO3- secretion to reestablish pH gradient in the mucous layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Use of bismuth and sucralfate

A

increase ulcer healing, travelers diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Mechanism of misoprostol

A

a PGE1 analog

increases production and secretion of gastric mucous barrier, decreases acid production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Use of misoprostol

A

prevention of NSAID-induced peptic ulcers (NSAIDs block PGE1 production); maintenance of a PDA

also off label for induction of labor (ripens cervix)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Toxicity of misoprostol

A

diarrhea

contraindicated in women of childbearing potential (abortifactant)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mechanism of octreotide

A

long-acting somatostatin analog; inhibits actions of many splanchnic vasodilatory hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Use of octreotide

A

acute variceal bleeds, acromegaly, VIPoma, carcinoid tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Toxicity of octreotide

A

nausea, cramps, steatorrhea

18
Q

Concern with use of antacids

A

can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying

cause hypokalemia

19
Q

Toxicity of aluminum hydroxide

A

constipation and hypophosphatemia
proximal muscle weakness
osteodystrophy
seizures

20
Q

Toxicity of calcium carbonate

A

hypercalcemia

rebound acid

21
Q

Toxicity of magnesium hydroxide

A

diarrhea
hyporeflexia
hypotension
cardiac arrest

22
Q

Name the osmotic laxatives

A

Magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose

23
Q

Mechanism of osmotic laxatives

A

provide osmotic load to draw water into the GI lumen

24
Q

Use of osmotic laxatives

A

constipation

25
Toxicity of osmotic laxatives
diarrhea, dehydration; may be abused by bulimics
26
Specific use of lactulose
treats hepatic encephalopathy since gut flora degrade it into metabolites (lactic acid and acetic acid) that promote nitrogen excretion as NH4+
27
Mechanism of sulfasalazine
combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory) activated by colonic bacteria
28
Use of sulfasalazine
ulcerative colitis, Crohn disease (colitis component)
29
Toxicity of sulfasalazine
malaise, nausea, sulfonamide toxicity, reversible oligospermia
30
Mechanism of ondansetron
5-HT3 antagonist decreases vagal stimulation powerful central-acting antiemetic
31
Use of ondansetron
control vomiting postoperatively and in pts receiving cancer chemotherapy
32
Toxicity of ondansetron
headache, constipation, QT interval prolongation
33
Mechanism of metoclopramide
D2 receptor antagonist increases resting tone, contractility, LES tone, motility does NOT influence colon transport time
34
Use of metoclopramide
diabetic and postsurgery gastroparesis, antiemetic
35
Toxicity of metoclopramide
increased parkinsonian effects, tardive dyskinesia | restlessness, drowsiness, fatigue, depression, diarrhea
36
Drug interaction of metoclopramide
with digoxin and diabetic agents
37
Contraindication of metoclopramide use
in patients with small bowel obstruction or Parkinson disease (due to D1 receptor blockade)
38
Mechanism of orlistat
inhibits gastric and pancreatic lipase --> decreased breakdown and absorption of dietary fats
39
Use of orlistat
weight loss
40
Toxicity of orlistat
steatorrhea, decreased absorption of fat soluble vitamins