GI Pharm

Question 1

H2 blocker examples

Answer 1

Cimetidine, ranitidine, famotidine, nizatidine

Question 2

Mechanism of H2 blockers

Answer 2

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

Question 3

Clinical use of H2 blockers

Answer 3

Peptic ulcer, gastritis, mild esophageal reflux

Question 4

Inhibitor of P450 H2 blocker

Answer 4

Cimetidine

Question 5

Other effects of cimetidine

Answer 5

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

Question 6

H2 blockers that decrease renal excretion of creatinine

Answer 6

Ranitine, cimetidine

Question 7

PPI examples

Answer 7

Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole

Question 8

Mechanism of PPIs

Answer 8

Irreversibly inhib H/K ATPase in stomach parietal cells

Question 9

CLinical use of PPIs

Answer 9

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

Question 10

Adverse effects of PPIs

Answer 10

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

Question 11

Consideration with antacids

Answer 11

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

Question 12

Overuse of aluminum hydroxide

Answer 12

Constipation and hypophosphatemia, prox muscle weakness, osteodystrophy, seizures

Question 13

Antacids

Answer 13

Aluminum hydroxide, Ca carbonate, mg hydroxide

Question 14

Calcium carbonate overuse

Answer 14

Hypercalcemia (milk alkali syndrome), rebound acid increase

Question 15

MG hydroxide overuse

Answer 15

Diarrhea, hyporeflexia, hypotension, caridac arrest

Question 16

Bismuth and sulcralfate mechanism

Answer 16

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

Question 17

Clinical use of bismuth and sucralfate

Answer 17

Ulcer healing, travelers diarrhea

Question 18

Misoprostol mechanism

Answer 18

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

Question 19

Clinical use of misoprostol

Answer 19

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

Question 20

Adverse effects of misoprostol

Answer 20

Diarrhea, CI in women of childbearing potential (abortifacent)

Question 21

Octerotide mechanism

Answer 21

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

Question 22

Clinical use of octreotide

Answer 22

Acute variceal bleeds, acromegaly, VIPoma, carcinoid tumors

Question 23

ADE of octreotide

Answer 23

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

Question 24

Mechanism of sulfasalazine

Answer 24

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

Question 25

Sulfasalazine clinical use

Answer 25

UC and colitis Crohns

Question 26

Sulfasalazine ADE

Answer 26

Malaise, nausea, sulfonamide tox, reversible oligospermia

Question 27

Loperamide mechanism

Answer 27

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

Question 28

Loperamide clinical use

Answer 28

Diarrhea

Question 29

ADE of loperamide

Answer 29

Constipation, nausea

Question 30

Ondansetron mechanism

Answer 30

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

Question 31

Ondansetron clinical use

Answer 31

Postoperative vomiting, chemo

Question 32

ADE of ondansetron

Answer 32

Headache, constipation, QT interval prolongation, serotonin syndrome

Question 33

Metoclopramide mechanism

Answer 33

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

Question 34

Clinical use of metaclopramide

Answer 34

Diabetic and postsurg gastroparesis, antiemetic, persisitent GERD

Question 35

ADE of metoclopramide

Answer 35

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)

Question 36

Orlistate mechanism

Answer 36

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

Question 37

Clinical use of orlistat

Answer 37

Wt loss

Question 38

ADE of orlistat

Answer 38

Steatorrhea, less absorption of fat soluble vitamins

Question 39

Bulk forming laxative examples

Answer 39

Psyllium, methylcellulose

Question 40

Mechanism of bulk forming laxatives

Answer 40

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

Question 41

ADE of bulk forming laxatives

Answer 41

BLoating

Question 42

Osmotic laxative examples

Answer 42

MG hydroxide, Mg citrate, polyethylene glycol, lactulose

Question 43

Osmotic laxative mechanism

Answer 43

Provide osmotic load to draw water into GI lumen

Question 44

Lactulose also tx...and why

Answer 44

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

Question 45

Osmotic laxatives ADE

Answer 45

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

Question 46

Stimulants example

Answer 46

Senna

Question 47

Senna mechanism

Answer 47

Enteric nerve stimulation --> colonic contraction

Question 48

ADE of senna

Answer 48

Diarrhea, melanosis coli

Question 49

Emolients example

Answer 49

Docusate

Question 50

Docusate mechanism

Answer 50

Promotes incorporation of water and fat into stool

Question 51

Docusate ADE

Answer 51

Diarrhea

Question 52

Aprepitant mechanism

Answer 52

Supstance P antagonist, blocks NK1 receptors in brain

Question 53

Aprepitant clinical use

Answer 53

Antiemetic for chemo induced NV