Git Pharmacology

Front 1

What are cimetidine, rantidine, famotidine, nizatidine?

Back 1

H2 blockers

Front 2

What is the mechanism of H2 blockers?

Back 2

Reversible block of histamine H2 receptors --> decrease H+ secretion by parietal cells

Front 3

What is the clinical use of H2 blockers?

Back 3

Peptic ulcer, gastritis, mild esophageal reflux

Front 4

What are the side effects of cimetidine?

Back 4

Potent inhibitor of P-450, antiandrogenic effects (prolactin release, gynecomastia, impotence, decreased libido in males); can cross blood-brain barrier causing confusion, dizzines, headaches; can cross placenta; decrease renal excretion of creatinine

Front 5

What are omeprazole and lansoprazole?

Back 5

Proton pump inhibitors

Front 6

What is the mechanism of proton pump inhibitors?

Back 6

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

Front 7

What is the clinical use of proton pump inhibitors?

Back 7

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

Front 8

What is the mechanism of bismuth, sucralfate?

Back 8

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

Front 9

What is the use of bismuth, sucralfate?

Back 9

Increase ulcer healing, traveler's diarrhea

Front 10

What is the mechanism of misoprostol?

Back 10

PGE1 analog that increases production and secretio nof gastric mucous barrier and decreases acid production

Front 11

What is the use of misoprostol?

Back 11

Prevention of NSAID-induced peptic ulcers, maintenance of a patent ductus arteriosus, induce labor

Front 12

What is the toxicity and contraindications of misoprostol?

Back 12

Diarrhea; contraindicated in women of childbearing potential (abortifacient)

Front 13

What are pirenzepine and propantheline?

Back 13

Muscarinic antagonists

Front 14

What is the mechanism of pirenzepine and propantheline?

Back 14

Block M1 receptors on ECL cells --> decrease histamine secretion and block M3 receptors on parietal cells --> decrease H+ secretion

Front 15

What is the clinical use of pirenzepine and propantheline?

Back 15

Peptic ulcer

Front 16

What are cimetidine, rantidine, famotidine, nizatidine?

Back 16

H2 blockers

Front 17

What is the mechanism of H2 blockers?

Back 17

Reversible block of histamine H2 receptors --> decrease H+ secretion by parietal cells

Front 18

What is the clinical use of H2 blockers?

Back 18

Peptic ulcer, gastritis, mild esophageal reflux

Front 19

What are the side effects of cimetidine?

Back 19

Potent inhibitor of P-450, antiandrogenic effects (prolactin release, gynecomastia, impotence, decreased libido in males); can cross blood-brain barrier causing confusion, dizzines, headaches; can cross placenta; decrease renal excretion of creatinine

Front 20

What are omeprazole and lansoprazole?

Back 20

Proton pump inhibitors

Front 21

What is the mechanism of proton pump inhibitors?

Back 21

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

Front 22

What is the clinical use of proton pump inhibitors?

Back 22

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

Front 23

What is the mechanism of bismuth, sucralfate?

Back 23

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

Front 24

What is the use of bismuth, sucralfate?

Back 24

Increase ulcer healing, traveler's diarrhea

Front 25

What is the mechanism of misoprostol?

Back 25

PGE1 analog that increases production and secretio nof gastric mucous barrier and decreases acid production

Front 26

What is the use of misoprostol?

Back 26

Prevention of NSAID-induced peptic ulcers, maintenance of a patent ductus arteriosus, induce labor

Front 27

What is the toxicity and contraindications of misoprostol?

Back 27

Diarrhea; contraindicated in women of childbearing potential (abortifacient)

Front 28

What are pirenzepine and propantheline?

Back 28

Muscarinic antagonists

Front 29

What is the mechanism of pirenzepine and propantheline?

Back 29

Block M1 receptors on ECL cells --> decrease histamine secretion and block M3 receptors on parietal cells --> decrease H+ secretion

Front 30

What is the clinical use of pirenzepine and propantheline?

Back 30

Peptic ulcer

Front 31

What is the toxicity of pirenzepine and propantheline?

Back 31

Tachycardia, dry mouth, difficulty focusing eyes

Front 32

What are aluminim hydroxide, magnesium hydroxide, and calcium carbonate?

Back 32

Antacids

Front 33

What is the effect of antacids on other drugs?

Back 33

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

Front 34

What can overuse of aluminum hydroxide cause?

Back 34

Constipation and hypophosphatemia, proximal muscle weaness, osteodystrophy, seizures, hypokalemia

Front 35

What can overuse of magnesium hydroxide cause?

Back 35

Diarrhea, hyporeflexia, hypotension, cardiac arrest, hypokalemia

Front 36

What can overuse of calcium carbonate cause?

Back 36

Hypercalcemia, rebound acid increase, hypokalemia

Front 37

What is the mechanism of infliximab?

Back 37

Monoclonal antibody to TNG, proinflammatory cytokine

Front 38

What is the use of infliximab?

Back 38

Crohn's disease, rheumatoid arthritis

Front 39

What is the toxicity of infliximab?

Back 39

Respiratory infection, fever, hypotension

Front 40

What is sulfasalazine and how is it activated?

Back 40

Combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory), activated by colonic bacteria

Front 41

What is the use of sulfasalazine?

Back 41

Ulcerative colitis, Crohn's disease

Front 42

What is the toxicity of sulfasalazine?

Back 42

Malaise, nausea, sulfonamide toxicity, reversible oligospermia

Front 43

What is the mechanism of ondansetron?

Back 43

5-HT3 antagonist, powerful central-acting antiemetic

Front 44

What is the clinical use of ondansetron?

Back 44

Control vomiting postoperatively and in patient undergoing cancer chemotherapy

Front 45

What is the toxicity of ondansetron?

Back 45

Headache, constipation

Front 46

What is the mechanism of cisapride?

Back 46

Acts through serotonin receptors to increase Ach release at the myenteric plexus --> increase esophageal tone, gastric and duodenal contractility therefore improving transit time

Front 47

What is the toxicity of cisapride?

Back 47

No longer used. Causes torsades de pointes with erythromycin, ketoconazole, nefazodone, and fluconazole

Front 48

What is the mechanism of metoclopramide?

Back 48

D2 receptor antagonist --> increases resting tone, contractility, lower esophageal sphincter tone, motility (but not colon transport time)

Front 49

What is the clinical use of metoclopramide?

Back 49

Diabetic and post-surgery gastroparesis

Front 50

What is the toxicity, drug interactions, and contraindications of metoclopramide?

Back 50

Increase parkinsonian effects, restlessness, drowsiness, fatigue, depression, nausea, diarrhea; interacts with digoxin and diabetic agents; contraindicated in patients with small bowel obstruction