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STEP > GI Pharm > Flashcards

GI Pharm Flashcards

1
Q

H2 blocker examples

A

Cimetidine, ranitidine, famotidine, nizatidine

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2
Q

Mechanism of H2 blockers

A

Reverisble block of H2 receptors –> less H secretion by parietal cells

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3
Q

Clinical use of H2 blockers

A

Peptic ulcer, gastritis, mild esophageal reflux

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4
Q

Inhibitor of P450 H2 blocker

A

Cimetidine

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5
Q

Other effects of cimetidine

A

Antiadrogenic (prolactin release, gynecomastia, impotence, less libido in males); can cross BBB –> confusion, dizziness, headaches and placenta

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6
Q

H2 blockers that decrease renal excretion of creatinine

A

Ranitine, cimetidine

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7
Q

PPI examples

A

Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole

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8
Q

Mechanism of PPIs

A

Irreversibly inhib H/K ATPase in stomach parietal cells

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9
Q

CLinical use of PPIs

A

Peptic ulcer, gastritis, esophageal reflux, ZE syndrome, part of therapy for H pylori, stress ulcer prophylaxis

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10
Q

Adverse effects of PPIs

A

Higher risk of C diff infxn, pneumonia, lower serum Mg w/ long term use

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11
Q

Consideration with antacids

A

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

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12
Q

Overuse of aluminum hydroxide

A

Constipation and hypophosphatemia, prox muscle weakness, osteodystrophy, seizures

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13
Q

Antacids

A

Aluminum hydroxide, Ca carbonate, mg hydroxide

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14
Q

Calcium carbonate overuse

A

Hypercalcemia (milk alkali syndrome), rebound acid increase

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15
Q

MG hydroxide overuse

A

Diarrhea, hyporeflexia, hypotension, caridac arrest

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16
Q

Bismuth and sulcralfate mechanism

A

Bind to ulcer base –> physical protection and allowing bicarb secretion to reestablish pH gradient in mucous laye r– requires acidic environment so not given w/ PPIs/H2 blockers

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17
Q

Clinical use of bismuth and sucralfate

A

Ulcer healing, travelers diarrhea

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18
Q

Misoprostol mechanism

A

PGE1 analog –> increased prodxn and secretino of gastric mucous barrier and less acid prodxn

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19
Q

Clinical use of misoprostol

A

Prevent NSAID peptic ulcers – off label to induce labor (ripens cervix)

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20
Q

Adverse effects of misoprostol

A

Diarrhea, CI in women of childbearing potential (abortifacent)

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21
Q

Octerotide mechanism

A

Long lasting somatostating analog – inhib secretion of various splanchnic vasodilatory hormones

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22
Q

Clinical use of octreotide

A

Acute variceal bleeds, acromegaly, VIPoma, carcinoid tumors

23
Q

ADE of octreotide

A

Nausea, cramps, steatorrhea, higher risk of cholelithiasis due to CCK inhib

24
Q

Mechanism of sulfasalazine

A

Combo of sulfapyridine (antibacterial) and 5ASA (anti inflam), activated by colonic bacteria

25
Q

Sulfasalazine clinical use

A

UC and colitis Crohns

26
Q

Sulfasalazine ADE

A

Malaise, nausea, sulfonamide tox, reversible oligospermia

27
Q

Loperamide mechanism

A

Agonist at mu opioid receptors; slows gut motility – low CNS penetration (low addictive potential)

28
Q

Loperamide clinical use

A

Diarrhea

29
Q

ADE of loperamide

A

Constipation, nausea

30
Q

Ondansetron mechanism

A

5HT3 antagonist –> less vagal stim, powerful central active antiemetic

31
Q

Ondansetron clinical use

A

Postoperative vomiting, chemo

32
Q

ADE of ondansetron

A

Headache, constipation, QT interval prolongation, serotonin syndrome

33
Q

Metoclopramide mechanism

A

D2 receptor antagonist –> increased resting tone, contractility, LES tone, motility, promotes gastric emptying – does not influence colon transport time

34
Q

Clinical use of metaclopramide

A

Diabetic and postsurg gastroparesis, antiemetic, persisitent GERD

35
Q

ADE of metoclopramide

A

Increased parkinsonian effects, tardive dyskinesia, restlessness, drowsiness, fatigue, depression, diarrhea,;
Interacts w/ dig and diabetic agents
CI in pts w/ SI obstruction of Parkinsons disease (D2 blockade)

36
Q

Orlistate mechanism

A

Inhibits gastric and pancreatic lipase –> less breakdown/absorption of dietary fats

37
Q

Clinical use of orlistat

A

Wt loss

38
Q

ADE of orlistat

A

Steatorrhea, less absorption of fat soluble vitamins

39
Q

Bulk forming laxative examples

A

Psyllium, methylcellulose

40
Q

Mechanism of bulk forming laxatives

A

Soluble fibers – draws water into gut lumen –> viscous liquid that promotes peristalsis

41
Q

ADE of bulk forming laxatives

A

BLoating

42
Q

Osmotic laxative examples

A

MG hydroxide, Mg citrate, polyethylene glycol, lactulose

43
Q

Osmotic laxative mechanism

A

Provide osmotic load to draw water into GI lumen

44
Q

Lactulose also tx…and why

A

Heptaic encehalopathy – gut flora degrade it into metabolites (lactic acid, acetic acid) that promote nitrogen excretion as NH4

45
Q

Osmotic laxatives ADE

A

Diarrhea, dehydration; can be abused by people w/ bulemia

46
Q

Stimulants example

A

Senna

47
Q

Senna mechanism

A

Enteric nerve stimulation –> colonic contraction

48
Q

ADE of senna

A

Diarrhea, melanosis coli

49
Q

Emolients example

A

Docusate

50
Q

Docusate mechanism

A

Promotes incorporation of water and fat into stool

51
Q

Docusate ADE

A

Diarrhea

52
Q

Aprepitant mechanism

A

Supstance P antagonist, blocks NK1 receptors in brain

53
Q

Aprepitant clinical use

A

Antiemetic for chemo induced NV

STEP (15 decks)

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