Gastrointestinal Pharmacology Flashcards

1
Q

name the H2 blockers

A

-dine

Cimetidine

ranitidine

famotidine

nizatidine

“Take H2 blockers before you dine. Think ‘table for 2’ to remember H2.”

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2
Q

H2 blockers–mechanism

A

reversible block of histamine H2 receptors –> decrease H+ secretion by parietal cells

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3
Q

H2 blockers–use

A

peptic ulcer

gastritis

mild esophageal reflux

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4
Q

cimetidine–toxicity

A

(H2 blocker)

potent inhibitor of cytochrome P-450

antiandrogenic effects–prolactin release, gynecomastia, impotence, dec libido in males

can cross blood brain barrier–confusion, dizziness, headaches

can cross placenta

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5
Q

name the proton pump inhibitors

A

omeprazole

lansoprazole

esomeprazole

pantoprazole

dexlansoprazole

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6
Q

proton pump inhibitors–mechanism

A

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

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7
Q

proton pump inhibitors–use

A

peptic ulcer

gastritis

esophageal reflux

Zollinger-Ellison syndrome

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8
Q

proton pump inhibitors–toxicity

A

inc risk of C. difficile infection, pneumonia

decrease serum Mg2+ with long term use

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9
Q

how does antacid usage affect other drugs?

A

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

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10
Q

name 3 types of antacids

A

aluminum hydroxide

calcium carbonate

magnesium hydroxide

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11
Q

what can all antacids cause?

A

hypokalemia

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12
Q

aluminum hydroxide–toxicity

A

contipation

hypophosphatemia

proximal muscle weakness

osteodystrophy

seizures

“Aluminimum amount of feces”

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13
Q

calcium carbonate–toxicity

A

hypercalcemia–milk alkali syndrome

rebound acid increases

can chelate and decrease effectiveness of other drugs (ie. tetracycline)

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14
Q

magnesium hydroxide–toxicity

A

diarrhea

hyporeflexia

hypotension

cardiac arrest

Mg2+ = Must go to the bathroom”

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15
Q

bismuth, sucralfate–mechanism

A

bind to ulcer base which protects it and allows HCO3- secretion to reestablish pH gradient in the mucous layer

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16
Q

bismuth, sucralfate–use

A

inc ulcer healing

travelers’ diarrhea

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17
Q

misoprostol–mechanism

A

a PGE1 analog

inc production and secretion of gastric mucous barrier

dec acid production

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18
Q

misoprostol–use

A

prevention of NSAID induced peptic ulcers (NSAIDs block PGE1 production)

maintenance of a patent ductus arteriosis

also used off label for induction of labor–ripens cervix

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19
Q

misoprostol–toxicity

A

diarrhea

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20
Q

contraindication for misoprostol

A

women of childbearing potential (abortifacient)

21
Q

name the stimulant laxatives

A

Bisacodyl (DULCOLAX)

Senna (SENOKOT)

Castor Oil

22
Q

Examples of saline laxatives

A

Magnesium hydroxide (MILK OF MAGNESIA)

Magnesium sulfate (EPSOM SALTS)

Magnesium citrate

Sodium phosphate (FLEET’S PHOSPHOSODA)

23
Q

Saline laxative MOA

A

draw water into the intestinal lumen

24
Q

name the osmotic laxatives

A

magnesium hydroxide

magnesium citrate

polyethylene glycol

lactulose

25
Q

osmotic laxatives–mechanism

A

provide osmotic load to draw water into the GI lumen

26
Q

osmotic laxatives–use

A

constipation

27
Q

lactulose–use and specific mechanism

A

(osmotic laxative)

helps treat hepatic encephalopathy since gut flora degrade it into metabolites (lactic acid and acetic acid) that promote nitrogen excretion as NH4+

28
Q

osmotic laxatives–toxicity

A

diarrhea

dehydration

may be abused by bulimics

29
Q

sulfasalazine–mechanism

A

combination of sulfapyridine (antibacterial) and 5-aminosalicyclic acid (anti-inflammatory)

activated by colonic bacteria

30
Q

sulfasalazine–use

A

ulcerative colitis

Crohn disease (colitis component)

31
Q

sulfasalazine–toxicity

A

malaise

nausea

sulfonamide toxicity

reversible oligospermia

32
Q

loperamide–mechanism

A

agonist at mu-opioid receptors

slows gut motility

poor CNS penetration (low addictive potential)

33
Q

loperamide–use

A

diarrhea

34
Q

loperamide–toxicity

A

constipation

nausea

35
Q

ondansetron–mechanism

A

5-HT3 antagonist

decrease vagal stimulation

powerful central acting antiemetic

36
Q

ondansetron–use

A

control vomiting postop and in patients undergoing cancer chemotherapy

“at a party but feeling queasy? Keep on dancing with ondansetron”

37
Q

ondansetron–toxicity

A

headache

constipation

QT interval prolongation

38
Q

metoclopramide–mechanism

A

D2 receptor antagonist

inc resting tone, contractility, LES tone, motility

does not influence colon transport time

39
Q

metoclopramide–use

A

diabetic and postsurgery gastroparesis

antiemetic

40
Q

metoclopramide–toxicity

A

inc Parkinsonian effects, tardive dyskinesia

restlessness

drowsiness

fatigue

depression

diarrhea

41
Q

what is a possible drug interaction with metoclopramide?

A

digoxin

diabetic agents

42
Q

what is a contraindication for metoclopramide?

A

patients with small bowerl obstruction or Parkison disease (due to D2 receptor blockade)

43
Q

What drugs/classes of drugs can lower lower esophageal sphingter tone increasing risk of reflux?

A

Anticholinergics

Benzodiazepines

Caffeine

Calcium channel blockers (dihydropyridines)

Estrogen/progesterone

Nicotine

Nitrates

Theophylline

Tricyclic antidepressants

44
Q

What is important patient teaching when prescribing a PPI?

A

uDo not crush or chew capsules

uTake before meals – preferably breakfast

uLong term users (>6 months) need to taper off

uRebound gastric hypersecretion is common

45
Q

which class of anti-emetics is most frequently prescribed for motion sickness?

A

anticholingerics/antihistamines

46
Q

ursodiol (ursodeoxycholic acid)–mechanism

A

non toxic bile acid

inc bile secretion

dec cholesterol secretion and reabsorption

47
Q

ursodiol (ursodeoxycholic acid)–use

A

primary biliary cirrhosis

gallstone prevention or dissolution

48
Q

Common side effects of phenothiazines (compazine and phenergan)

A

Blurred vision, Dry mouth, Dizziness, Restlessness, Seizures, Extrapyramidal effects - Tardive dyskinesia (long term treatment)

49
Q

What is the difference between pre and probiotics?

A