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Flashcards in GI Drugs Deck (39):
1

- tidine drugs mechanism

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

2

- tidine drugs clinical use

- peptic ulcers
- gastritis
- mild GERD

3

- tidine drugs SEs

- antiandrogenic - prolactin release, gynecomastia, impotence, decreased libido
- crosses BBB (confusion, dizziness, HA) and placenta
- decrease renal excretion of creatinine

4

-prazole drugs mechanism

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

5

-prazole drugs clinical use

- peptic ulcers
- gastritis
- GERD
- Zollinger-Ellison syndrome

6

-prazole drugs SEs

- 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

7

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

PPIs (-prazole)

8

Bi, sucralfate mechanism

- 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

9

Bi, sucralfate clinical use

- ulcer healing
- traveler's diarrhea

10

Bi, sucralfate SEs

- 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

11

misoprostol mechanism

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

12

misoprostol clinical use

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

13

misoprostol SEs

- diarrhea
- abortifacient
- ab. cramps

14

antacids mechanism

- neutralize gastric acid, but has no role in prevention or healing

15

antacids SEs

- can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH
- delayed gastric emptying
- hypokalemia

16

Al(OH)3 SEs

constipation

17

Ca3(CO3)2 SEs

hypercalcemia

18

Mg(OH2) SEs

- diarrhea
- avoid in CKD to prevent hypermagnesemia

19

Maalox

Al + Mg hydroxide - SEs cancel each other out!

20

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

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

21

clinical use of osmotic laxatives

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

22

SEs of osmotic laxatives

- diarrhea
- dehydration
- metabolic acidosis

23

mechanism of sulfasalazine

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

24

clinical use of sulfasalazine

ulcerative colitis, Crohn's disease colitis

25

SEs sulfasalazine

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

26

mechanism of rifamixin

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

27

clinical use of rifamixin

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

28

lubiprostone

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

29

methylnaltrexone

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

30

linaclotide

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

31

budesonide

corticosteroid effective for short-term IBD managemenT

32

mechanism of azathioprine/6-MP

- aza --> 6-MP
- purine analogue that via pseudofeedback prevents purine synth and also disrupts DNA/RNA synthesis

33

clinical use of azathioprine/6-MP

maintenance of IBD

34

SEs of azathioprine/6-MP

- GI disturbances
- hepatotoxicity
- infxns
- pancreatitis
- BM suppression
- malignancy (lymphoma)

35

mechanism of methotrexate

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

36

clinical use of methotrexate

maintenance of Crohn's dz

37

mechanism of infliximab

anti-TNF monoclonal ab

38

clinical use of infliximab

treats IBD flairs and fulminant dz

39

SEs of infliximab

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