GI Drugs

Question 1

• tidine drugs mechanism

Answer 1

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

Question 2

• tidine drugs clinical use

Answer 2

• peptic ulcers
• gastritis
• mild GERD

Question 3

• tidine drugs SEs

Answer 3

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

Question 4

-prazole drugs mechanism

Answer 4

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

Question 5

-prazole drugs clinical use

Answer 5

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

Question 6

-prazole drugs SEs

Answer 6

• 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

Question 7

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

Answer 7

PPIs (-prazole)

Question 8

Bi, sucralfate mechanism

Answer 8

• 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

Question 9

Bi, sucralfate clinical use

Answer 9

• ulcer healing

- traveler’s diarrhea

Question 10

Bi, sucralfate SEs

Answer 10

• 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

Question 11

misoprostol mechanism

Answer 11

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

Question 12

misoprostol clinical use

Answer 12

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

Question 13

misoprostol SEs

Answer 13

• diarrhea
• abortifacient
• ab. cramps

Question 14

antacids mechanism

Answer 14

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

Question 15

antacids SEs

Answer 15

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

Question 16

Al(OH)3 SEs

Answer 16

constipation

Question 17

Ca3(CO3)2 SEs

Answer 17

hypercalcemia

Question 18

Mg(OH2) SEs

Answer 18

• diarrhea

- avoid in CKD to prevent hypermagnesemia

Question 19

Maalox

Answer 19

Al + Mg hydroxide - SEs cancel each other out!

Question 20

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

Answer 20

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

Question 21

clinical use of osmotic laxatives

Answer 21

• constipation

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

Question 22

SEs of osmotic laxatives

Answer 22

• diarrhea
• dehydration
• metabolic acidosis

Question 23

mechanism of sulfasalazine

Answer 23

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

Question 24

clinical use of sulfasalazine

Answer 24

ulcerative colitis, Crohn’s disease colitis

Question 25

SEs sulfasalazine

Answer 25

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

Question 26

mechanism of rifamixin

Answer 26

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

Question 27

clinical use of rifamixin

Answer 27

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

Question 28

lubiprostone

Answer 28

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

Question 29

methylnaltrexone

Answer 29

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

Question 30

linaclotide

Answer 30

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

Question 31

budesonide

Answer 31

corticosteroid effective for short-term IBD managemenT

Question 32

mechanism of azathioprine/6-MP

Answer 32

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

Question 33

clinical use of azathioprine/6-MP

Answer 33

maintenance of IBD

Question 34

SEs of azathioprine/6-MP

Answer 34

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

Question 35

mechanism of methotrexate

Answer 35

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

Question 36

clinical use of methotrexate

Answer 36

maintenance of Crohn's dz

Question 37

mechanism of infliximab

Answer 37

anti-TNF monoclonal ab

Question 38

clinical use of infliximab

Answer 38

treats IBD flairs and fulminant dz

Question 39

SEs of infliximab

Answer 39

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