Gastrointestinal Flashcards Preview

Step 1 Pharmacology > Gastrointestinal > Flashcards

Flashcards in Gastrointestinal Deck (43):
1

What are the H2 blockers?

Cimetidine, ranitidine, famotidine, nizatidine

2

What is the mechanism of H2 blockers?

Reversible block of histamine H2-receptors → ↓ H+ secretion by parietal cells

3

What is the clinical use of H2 blockers?

Peptic ulcer, gastritis, mild esophageal reflux

4

What are the toxicities of H2 blockers?

Cimetidine is a potent inhibitor of cytochrome P-450 (multiple drug interactions); it also has antiandrogenic effects (prolactin release, gynecomastia, impotence, ↓ libido in males); can cross blood-brain barrier (confusion, dizziness, headaches) and placenta. Both cimetidine and ranitidine ↓ renal excretion of creatinine. Other H2 blockers are relatively free of these effects.

5

What are the Proton Pump Inhibitors?

Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole

6

What is the mechanism of Proton Pump Inhibitors?

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

7

What is the clinical use of Proton Pump Inhibitors?

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

8

What are the toxicities of Proton Pump Inhibitors?

Increased risk of C. difficile infection, pneumonia. Hip fractures, ↓ serum Mg2+ with long-term use.

9

What is the mechanism of Bismuth and sucralfate?

Bind to ulcer base, providing physical protection and allowing HCO3– secretion to reestablish pH gradient in the mucous layer.

10

What is the clinical use of Bismuth and sucralfate?

↑ ulcer healing, travelers’ diarrhea.

11

What is the mechanism of Misoprostol?

A PGE1 analog. ↑ production and secretion of gastric mucous barrier, ↓ acid production.

12

What is the clinical use of Misoprostol?

Prevention of NSAID-induced peptic ulcers (NSAIDs block PGE1 production); maintenance of a PDA. Also used to induce labor (ripens cervix).

13

What are the toxicities of Misoprostol?

Diarrhea. Contraindicated in women of childbearing potential (abortifacient).

14

What is the mechanism of Octreotide?

Long-acting somatostatin analog

15

What is the clinical use of Octreotide?

Acute variceal bleeds, acromegaly, VIPoma, and carcinoid tumors

16

What are the toxicities of Octreotide?

Nausea, cramps, steatorrhea

17

What are the key features of Antacid use?

Can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.
All can cause hypokalemia.
Overuse can also cause the following problems.

18

Antacid - What is the clinical use of Aluminum hydroxide?

Constipation and hypophosphatemia; proximal muscle weakness, osteodystrophy, seizures

19

Antacid - What is the clinical use of Calcium carbonate?

Hypercalcemia, rebound acid ↑
Can chelate and ↓ effectiveness of other drugs (e.g., tetracycline)

20

Antacid - What is the clinical use of Magnesium hydroxide?

Diarrhea, hyporeflexia, hypotension, cardiac arrest

21

What are the osmotic laxatives?

Magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose

22

What is the mechanism of osmotic laxatives?

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 NH4+.

23

What is the clinical use of osmotic laxatives?

Constipation

24

What are the toxicities of osmotic laxatives?

Diarrhea, dehydration; may be abused by bulimics

25

What is the mechanism of Infliximab?

Monoclonal antibody to TNF-α

26

What is the clinical use of Infliximab?

Crohn disease, ulcerative colitis, rheumatoid arthritis, ankylosing spondylitis, psoriasis

27

What are the toxicities of Infliximab?

Infection (including reactivation of latent TB), fever, hypotension

28

What is the mechanism of Sulfasalazine?

A combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory).
Activated by colonic bacteria.

29

What is the clinical use of Sulfasalazine?

Ulcerative colitis, Crohn disease

30

What are the toxicities of Sulfasalazine?

Malaise, nausea, sulfonamide toxicity, reversible oligospermia

31

What is the mechanism of Ondansetron?

5-HT3 antagonist; ↓ vagal stimulation. Powerful central-acting antiemetic

32

What is the clinical use of Ondansetron?

Control vomiting postoperatively and in patients undergoing cancer chemotherapy.

33

What are the toxicities of Ondansetron?

Headache, constipation

34

What is the mechanism of Metoclopramide?

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

35

What is the clinical use of Metoclopramide?

Diabetic and post-surgery gastroparesis, antiemetic

36

What are the toxicities of Metoclopramide?

↑ parkinsonian effects. Restlessness, drowsiness, fatigue, depression, nausea, diarrhea. Drug interaction with digoxin and diabetic agents. Contraindicated in patients with small bowel obstruction or Parkinson disease (D1-receptor blockade).

37

What does atropine do in a GI context?

Atropine blocks vagal stimulation of parietal cells. Vagal stimulation of G cells is unaffected as a different transmitter (gastrin-releasing peptide, or GRP) is used, not ACh.

38

What is the treatment for Crohn's disease?

Corticosteroids, azathioprine, methotrexate, infliximab, adalimumab

39

What is the treatment for Ulcerative colitis?

ASA preparations (sulfasalazine), 6-mercaptopurine, infliximab, colectomy

40

What is the treatment for Hepatic encephalopathy?

Lactulose (↑ NH4+ generation), low-protein diet, and rifamixin (kills intestinal bacteria)

41

What is the treatment for Crigler-Najjar syndrome, type I?

Type II is less severe and responds to phenobarbital, which ↑ liver enzyme synthesis.

42

What do you treat Wilson's disease (hepatolenticular degeneration) with?

Pencillamine or trientine

43

What do you treat Hemochromatosis with?

Hereditary hemochromatosis: repeated phlebotomy, deferasirox, deferoxamine.