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GI Drugs Flashcards

1
Q

H2 blockers

A

Cimetidine, Ranitidine, Famotidine, Nizatidine

*Take before you DINE, Table for 2”

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2
Q

Mechanism of H2 blockers

A

reversibly block histamine (H2) receptors on parietal cell

decreases H+ secretion by parietal cells

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3
Q

Clinical use of H2 blockers

A

peptic ulcer
gastritis
mild GERD

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4
Q

toxicity of H2 blockers

A

Most H2 blockers are relatively free of S/E
Ranitidine– decreases renal excretion of creatinine

Cimetidine–
potent inhibitor of p450 = multiple drug interactions
antiandrogenic effects (inc PRL release = gynecomastia, impotence & dec libido in males)
can cross BBB (confusion, dizzy, HA) & placenta
decreases renal excretion of creatinine

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5
Q

Proton Pump Inhibitors

A 
Omeprazole
lansoprazole
pantoprazaole
esomeprazole
dexlansoprazole

(-prazole)

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6
Q

Mechanism of PPI’s

A

irreversibly inhibit H/K ATPase in stomach parietal cells

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7
Q

Clinical use of PPIs

A

Peptic Ulcer
Gastritis
GERD
Zollinger-Ellison syndrome

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8
Q

toxicity of PPIs

A

inc risk of C. diff infxn & pneumonia
Hip fx
dec serum Mg with long-term use

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9
Q

Bismuth & Sucralfate MOA

A

bind to ulcer base = physical protection

allows HCO3 secretion to re-establish pH gradient in the mucus layer

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10
Q

clinical use of bismuth & sucralfate

A

traveler’s diarrhea

ulcer healing

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11
Q

Misoprostol MOA

A

PGE1 analog (prostaglandin)
increases production & secretion of gastric mucous barrier
decreases acid production

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12
Q

clinical use of Misoprostol

A 
prevents NSAID-induced peptic ulcers
maintains PDA
induces labor (ripens cervix)
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13
Q

Toxicity of Misoprostol

A

Diarrhea

CONTRA if childbearing potential (abortifacient)

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14
Q

Octreotide MOA

A

long-acting somatostatin analog (inhibits GF)

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15
Q

Clinical use of Octreotide

A

Acute variceal bleeds
VIPoma
carcinoid tumor

(and tx acromegaly)

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16
Q

toxicity of Octreotide

A

nausea, cramps, steatorrhea

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17
Q

Antacid types

A

Aluminum Hydroxide
Magnesium Hydroxide
Calcium Carbonate

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18
Q

MOA & S/E of all antacids

A

affects absorption, bioavailability or urinary excretion of other drugs by altering gastric & urinary pH, or by delaying gastric emptying.
causes hypokalemia

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19
Q

Aluminum hydroxide S/E

A 
constipation (MINIMUM feces)
hypophosphatemia
proximal muscle weakness
osteodystrophy
seizures
20
Q

Magnesium hydroxide S/E

A

Diarrhea (Must Go)
hyporeflexia
hypotension
cardiac arrest

21
Q

Calcium carbonate S/E

A

hypercalcemia
rebound acid increase
decreases other drug effectiveness (chelates)– esp tetracycline

22
Q

Osmotic Laxatives

A

magnesium hydroxide
magnesium citrate
polyethylene glycol
lactulose

23
Q

MOA of osmotic laxatives

A

provide osmotic load = draws water out into lumen
lactulose also treats hepatic encephalopathy– since gut flora degrade it into metabolites of lactic acid & acetic acids (promote nitrogen excretion as NH4+)

24
Q

clinical use of osmotic laxatives

A

constipation

25
Q

toxicity of osmotic laxatives

A

diarrhea
dehydration
*abused by bulimics

26
Q

Infliximab MOA

A

monoclonal antibody to TNF-alpha

-mab = monoclonal Ab

27
Q

use of Infliximab

A

Crohn’s Dz
Ulcerative colitis
Rheumatoid arthritis

28
Q

Toxicity of Infliximab

A

infection (reactivation of latent TB)
fever
hypotension

29
Q

Sulfasalazine MOA

A

combo of sulfapyridine (antibacterial) & 5-aminosalicylic acid (anti-inflammatory)
activated by colonic bacteria

30
Q

Use of Sulfasalazine

A

Ulcerative Colitis

Crohn’s

31
Q

Toxicity of Sulfasalazine

A

Malaise
Nausea
reversible oligospermia
sulfonamide toxicity

32
Q

Ondansetron MOA

A

5-HT3 antagonist

powerful centrally-active antiemetic

33
Q

Clinical Use of Ondansetron

A

control vomiting postop

chemotherapy pts

34
Q

S/E of Ondansetron

A

HA, constipation

35
Q

Metoclopramide MOA

A

D2 receptor antagonist
increases resting tone, contractility, LES tone, motility.
does NOT influence colon transport time

36
Q

Clinical use of Metaclopramide

A

Diabetic
Post-surgery gastroparesis
Antiemetic

37
Q

Toxicity of Metaclopramide

A

Inc parkinsonian effects
restlessness, drowsiness, fatigue, depression, nausea, diarrhea
*drug interaction w/ digoxin & diabetic tx
*CONTRA in pts with small bowel obstruction & parkinson’s disease

38
Q

What is octreotide used for?

A

Esophageal varices

39
Q

How does octreotide work in treating esophageal varices?

A

Decreases glucagon and VIP which vasodilate splanchnic vessels.
Causes vasoconstriction of splanchnic vessels thereby diverting blood flow to the systemic circulation.
Does not cause systemic circulation vasoconstriction

40
Q

What is pentagastrin?

A

A gastrin analog used to screen for carcinoid syndrome and medullary carcinoma of the thyroid

41
Q

What over the counter drug may reduce the risk of adenomatous polyp formation in the colon?

A

aspirin - some colon adenomas have shown over expression of COX2

42
Q

What is diphenoxylate?

A

An opiate anti-diarrheal structurally related to meperidine.

43
Q

What is the MOA of diphenoxylate?

A

Binds mu receptors in the GI tract and causes slower motility.

44
Q

What are the side effects of diphenoxylate?

A

Bloating and mild sedation

Can cause euphoria and physical dependence

45
Q

What is diphenoxylate combined with to prevent abuse?

A

Atropine - causes dry mouth, blurry vision and nausea at higher doses.
Atropine + diphenoxylate = lomotil

46
Q

What are the drugs that target secretory diarrhea?

A

Bismuth salicylate
Probiotics
Octreotide

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