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Flashcards in GI therapy Deck (13):
1

H2 blockers

Names: cimetidine, ranitidine, famotidine, nizatidine

mechanism: reversible block of histamine H2 receptors leading to decreased H+ secretion by parietal cells

clinical use: peptic ulcer, gastritis, mild esophageal reflux

Toxicity: cimeditine is a potent inhibitor of cytochrome P-450 (multiple drug interactions); antiandrogenic effects; can cross BBB and placenta; cimetidine and ranitidine decrease renal excretion of creatinine

2

Proton pump inhibitors

Names: omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole

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

Clinical use: peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome

Toxicity: increased risk of C diff infection, pneumonia; hip fractures, decreased serum Mg2+ with long-term use

3

Bismuth, sucralfate

Mech: bind to ulcer base, providing physical protection and allowing bicarb secretion to reestablish pH gradient in mucous layer

Clinical use: increase ulcer healing, traveler's diarrhea

4

Misoprostol

Mech: A PGE1 analog, increases production and secretion of gastric mucous barrier, decreases acid production

Clinical use: prevention of NSAID-induced peptic ulcers; maintenance of a patent ductus arteriosis. Also used to induce labor (ripens cervix)

Toxicity: diarrhea. contraindicated in women of childbearing potential (abortifacient)

5

Octreotide

mech: long-acting somatostatin analog

clinical use: acute variceal bleeds, acromegaly, VIPoma, carcinoid tumors

Toxicity: nausea, cramps, steatorrhea

6

Aluminum hydroxide

Antacid

Toxicity: constipation and hypophosphatemia; proximal muscle weakness, osteodystrophy, seizures

7

Magnesium hydroxide


Antacid

Toxicity: diarrhea, hyporeflexia, hypotension, cardiac arrest

8

Calcium carbonate

Hypercalcemia, rebound acid increased

9

Osmotic laxatives

Names: magnsium hydroxide, magnesium citrate, polyethylene glycol, lactulose

mech: provide osmotic load to draw water out; lactulose also treats hepatic encephalopathy since gut flora degrade it into metabolites (lactic acid and acetic acid) that promote nitrogen excretion as ammonia

clinical use: constipation

toxicity: diarrhea, dehydration, may by abused by bulimics

10

Infliximab

mech: monoclonal antibody to TNF-alpha

clinical use: Crohn's disease, UC, RA

Toxicity: infection (including reactivation of TB), fever, hypotension

11

Sulfasalazine

mechanism: a combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory), activated by colonic bacteria

Clinical use: UC, Crohn's

Toxicity: malaise, nausea, sulfonamide toxicity, reversible oligospermia

12

Ondansetron

Mechanism: 5-HT3 antagnois. Powerful central-acting antiemetic

Clinical use: Control vomiting postop and in pts undergoing chemo

Toxicity: headache, constipation

13

Metoclopramide

mechanism: D2 receptor antagonist, increased resting tone, contractility, LES tone, motility. Does not influence colon transport time

Clinical use: diabetic and post-surgery gastroparesis, antiemetic

toxicity: increased parkinsonism effects. Restlessness, drowsiness, fatigue, depression, nausea, diarrhea. Drug interaction with digoxin and diabetic agents. Contraindicated in patients with small bowel obstruction or Parkinson's disease.

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