GI Pharmacology 3

Question 1

acute treatment of esophageal variceal hemorrhage

Answer 1

*OCTREOTIDE (splanchnic vasoconstrictor that decreased blood flow + pressure)
*transfusion and fluids
*mechanical interventions

Question 2

octreotide - MOA

Answer 2

*somatostatin analogue that leads to:
-decreased secretion of GI hormones + fluids
-slows GI motility
-decreased portal + splanchnic blood flow

note - octreotide is a splanchnic vasoconstrictor, leading to decreased blood flow and pressure

Question 3

prevention of esophageal variceal hemorrhage

Answer 3

*non-selective beta blocker (decreases cardiac output, which decreases blood flow and pressure)
*mechanical interventions

Question 4

octreotide - uses

Answer 4

-endocrine tumors
-diarrhea
-decreases pancreatic secretion
-GI bleeding (ex. ESOPHAGEAL VARICEAL HEMORRHAGE)

Question 5

octreotide - ADEs

Answer 5

*nausea + vomiting
*abdominal pain
*steatorrhea
*gallbladder sludge + stones
*hypothyroidism
*hyper- or hypo-glycemia

Question 6

non-selective beta blockers - specific drugs

Answer 6

*propranolol
*nadolol
*carvedilol

Question 7

non-selective beta blockers - MOA

Answer 7

*decreased cardiac output, blood flow, and portal pressure

Question 8

non-selective beta blockers - uses

Answer 8

*prevention of esophageal variceal bleeding
*HTN and other cards diseases

Question 9

diuretic treatment of ascites

Answer 9

*SPIRONOLACTONE (competitive aldosterone antagonist)
*furosemide (inhibits sodium reabsorption in the loop of Henle)

note - we use MUCH LARGER DOSES of spironolactone FOR ASCITES than we use for normal diuresis and CHF

Question 10

furosemide

Answer 10

*drug class: loop diuretic
*MOA: inhibits sodium reabsorption in loop of Henle
*uses: ASCITES (+ others)
*ADEs: hypokalemia

Question 11

spironolactone

Answer 11

*drug class: aldosterone antagonist
*MOA: blocks actions of aldosterone in renal tubule
*uses: ASCITES (+ others)
*ADEs: hyperkalemia, gynecomastia, decreased libido

Question 12

treatment for primary spontaneous bacterial peritonitis (SBP)

Answer 12

*acute: ceftriaxone (3rd gen cephalosporin - binds to PBPs to inhibit cell wall synthesis)

*prevention/prophylaxis: ciprofloxacin (fluoroquinolone - inhibits DNA synthesis by binding to topoisomerase)

Question 13

ciprofloxacin

Answer 13

*drug class: fluoroquinolone
*MOA: inhibits DNA synthesis by binding to 2 topoisomerases
*uses: PREVENT SBP; tx traveler’s diarrhea & intrabdominal infections
*ADEs: CNS at high doses; QTc prolongation; GI; tendon rupture?; aortic aneurysm?

Question 14

treatment regimen for hepatic encephalopathy

Answer 14

lactulose or rifaximin

Question 15

lactulose - treating hepatic encephalopathy

Answer 15

*drug class: osmotic cathartic (synthetic disaccharide)
*MOA: traps ammonia in colon; cathartic effect
*uses: HEPATIC ENCEPHALOPATHY; constipation
*ADEs: bloating, diarrhea, epigastric pain, flatulence, nausea

Question 16

why does lactulose help in hepatic encephalopathy

Answer 16

*colonic bacteria degrade lactulose and form lactic acid, acetic acid, and formic acid
*reducing colonic pH “traps” ammonia (NH3) as NH4+, which is not readily absorbed and is therefore excreted in the stool

Question 17

rifaximin - treating hepatic encephalopathy

Answer 17

*drug class: antibiotic
*MOA: inhibits protein synthesis by binding to RNA polymerase (kills ammonia-producing bacteria in HE)
*uses: hepatic encephalopathy, IBS-D, traveler’s diarrhea, SIBO
*ADEs: well-tolerated but expensive

Question 18

treatment of acetaminophen overdose/toxicity

Answer 18

N-acetylcysteine (NAC)

Question 19

N-acetylcysteine (NAC) - MOA

Answer 19

REPLETES LIVER GLUTATHIONE to treat acetaminophen toxicity

Question 20

N-acetylcysteine (NAC) - uses

Answer 20

acetaminophen toxicity

Question 21

N-acetylcysteine - adverse effects

Answer 21

*nausea and vomiting
*diarrhea
*GI reflux
*anaphylactoid reaction (if given IV)
*stinks like rotten eggs

Question 22

treatment recommendations for pancreatitis

Answer 22

*only give ABX if infected (necrotic or have ongoing SIRS)
*treat with:
1. cefepime + metronidazole
OR
2. pip/tazo

Question 23

difference between cefepime and ceftriaxone

Answer 23

*cefepime covers Pseudomonas; ceftriaxone does not

Question 24

pancrelipase

Answer 24

*drug class: pancreatic enzyme replacement
*MOA: replaces lipase, amylase, and protease
*uses: pancreatic insufficiency (cystic fibrosis, chronic pancreatitis)
*ADEs: abdominal pain

Question 25

GLP-1 agonists - specific drugs

Answer 25

-dulaglutide
-exenatide
-semaglutide
-liraglutide

Question 26

GLP-1 agonists - MOA

Answer 26

*increased insulin secretion
*decreased glucagon secretion
*decreased appetite (leads to weight loss)

Question 27

GLP-1 agonists - uses

Answer 27

*DM2
*prophylaxis of cardiac disease in DM2 and/or overweight patients
*obesity

Question 28

GLP-1 agonists - ADEs

Answer 28

*abdominal pain
*constipation or diarrhea
*nausea and vomiting
*medullary thyroid cancer?
*cholelithiasis
*pancreatitis

Question 29

oral vancomycin

Answer 29

*drug class: ABX for C diff
*MOA: binds to D-ala-D-ala terminal group to inhibit cell wall synthesis
*uses: C diff
*ADEs: minimal

note - not absorbed; don’t treat systemic infection with this product

Question 30

fidaxomicin

Answer 30

*drug class: ABX for C diff
*MOA: inhibits protein synthesis by binding to RNA polymerases
*uses: C diff
*ADEs: minimal

note - VERY EXPENSIVE