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Pharmacology > GI Drugs > Flashcards

GI Drugs Flashcards

1
Q
  • tidine drugs mechanism
A

reversible block of H2 receptors –> decreased H+ secretion by parietal cells (no translocation of K+/H+ exchange pump to apical membrane)

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2
Q
  • tidine drugs clinical use
A
  • peptic ulcers
  • gastritis
  • mild GERD
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3
Q
  • tidine drugs SEs
A
  • antiandrogenic - prolactin release, gynecomastia, impotence, decreased libido
  • crosses BBB (confusion, dizziness, HA) and placenta
  • decrease renal excretion of creatinine
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4
Q

-prazole drugs mechanism

A

irreversible inhibitor of H+/K+ ATPase on apical membrane of stomach parietal cells

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5
Q

-prazole drugs clinical use

A
  • peptic ulcers
  • gastritis
  • GERD
  • Zollinger-Ellison syndrome
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6
Q

-prazole drugs SEs

A
  • increased risk of C. difficile, pneumonia (bugs don’t have low pH to kill them)
  • decreased GI absorption of Ca 2+, Mg 2+ due to higher gastric pH –> osteoporosis
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7
Q

In terms of onset of action and efficacy, _____ are faster and more efficacious to treat GERD.

A

PPIs (-prazole)

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8
Q

Bi, sucralfate mechanism

A
  • insoluble salt that binds to ulcerated sites or breaks in mucosa to provide physical protection and allow HCO3- secretion to reestablish pH gradient in the mucous layer
  • enhances mucosal defense/repair
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9
Q

Bi, sucralfate clinical use

A
  • ulcer healing

- traveler’s diarrhea

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10
Q

Bi, sucralfate SEs

A
  • due to binding of GI mucosa, may decrease absorption of other drugs –> avoid this by timing meds properly and taking Bi, sucralfate by itself
  • hyperpigmented stool
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11
Q

misoprostol mechanism

A

PGE1 analogue - increases production/secretion of gastric mucous and decreases gastric acid production

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12
Q

misoprostol clinical use

A
  • to prevent NSAID-induced peptic ulcers (NSAIDs block endogenous PGE1 production)
  • to keep patent ductus arteriosus open
  • to induce labor
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13
Q

misoprostol SEs

A
  • diarrhea
  • abortifacient
  • ab. cramps
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14
Q

antacids mechanism

A
  • neutralize gastric acid, but has no role in prevention or healing
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15
Q

antacids SEs

A
  • can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH
  • delayed gastric emptying
  • hypokalemia
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16
Q

Al(OH)3 SEs

A

constipation

17
Q

Ca3(CO3)2 SEs

A

hypercalcemia

18
Q

Mg(OH2) SEs

A
  • diarrhea

- avoid in CKD to prevent hypermagnesemia

19
Q

Maalox

A

Al + Mg hydroxide - SEs cancel each other out!

20
Q

MgOH, Mg-citrate, polyethylene glycol, and lactulose are all:

A

osmotic laxatives - draw water into GI lumen from intravascular and interstitial compartments of ECF

21
Q

clinical use of osmotic laxatives

A
  • constipation

- lactulose used for hepatic encephalopathy since gut flora degrade it into metabolites that promote NH4+ excretion

22
Q

SEs of osmotic laxatives

A
  • diarrhea
  • dehydration
  • metabolic acidosis
23
Q

mechanism of sulfasalazine

A
  • combo of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory)
  • cleaved to release 5-ASA by colonic bacteria
24
Q

clinical use of sulfasalazine

A

ulcerative colitis, Crohn’s disease colitis

25
Q

SEs sulfasalazine

A
  • malaise, nausea, sulfonamide toxicity (hemolytic anemia, agranulocytosis), oligospermia (from sulfapyridine portion)
  • nephritis (from 5-ASA portion)
26
Q

mechanism of rifamixin

A

gut-directed antibiotic that simply wipes out gut flora non-specifically

27
Q

clinical use of rifamixin

A
  • used before probiotics to repopulate gut flora (any dz in which gut flora is out of whack like symptomatic IBS)
28
Q

lubiprostone

A

fatty acid derived from PGE1 that activates and opens luminal Cl- channels causing GI luminal secretion (laxative)

29
Q

methylnaltrexone

A

blocks opiate receptors in GI tract, so good for opiate-induced constipation

30
Q

linaclotide

A

peptide agonist of guanalyl cyclase that reduces activation of colonic sensory neurons and activates colonic motor neurons (used in IBS)

31
Q

budesonide

A

corticosteroid effective for short-term IBD managemenT

32
Q

mechanism of azathioprine/6-MP

A
  • aza –> 6-MP

- purine analogue that via pseudofeedback prevents purine synth and also disrupts DNA/RNA synthesis

33
Q

clinical use of azathioprine/6-MP

A

maintenance of IBD

34
Q

SEs of azathioprine/6-MP

A
  • GI disturbances
  • hepatotoxicity
  • infxns
  • pancreatitis
  • BM suppression
  • malignancy (lymphoma)
35
Q

mechanism of methotrexate

A

folic acid analogue that competitively inhibits dihydrofolate reductase –> decreased DNA synthesis

36
Q

clinical use of methotrexate

A

maintenance of Crohn’s dz

37
Q

mechanism of infliximab

A

anti-TNF monoclonal ab

38
Q

clinical use of infliximab

A

treats IBD flairs and fulminant dz

39
Q

SEs of infliximab

A
  • autoimmunogenicity
  • CHF
  • hepatotoxicity
  • malignancy (lymphoma)
  • demyelinating dz
  • infxn
  • DM suppression

Pharmacology (22 decks)

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