Anti-Ulcer Drugs

Question 1

Preferred penicillin for H. pylori

Answer 1

amoxicillin

not ampicillin

Question 2

Preferred macrolide for H. pylori

Answer 2

clarithromycin

Question 3

Preferred tetracycline for H. pylori

Answer 3

tetracycline

Question 4

Amoxicillin

MOA

Tox

Answer 4

amoxocillin

MOA: transpeptidation inhibitor ⇒ bacteriocidal

Tox: hypersensitivity

Question 5

Clarithromycin

MOA

Tox

Answer 5

clarithromycin

MOA: binds 23S of 50S, prevents ribosome translocation ⇒ bacteriostatic

Tox: MACRO–GI motility, arrythmia from long QT, cholestatic hepatitis, rash, eosinophilia

Question 6

Tetracycline

MOA

Tox

Answer 6

tetracycline

MOA: binds 30S, prevents tRNA attachment ⇒ bacteriostatic

Tox: GI, photosensitivity, discoloration of teeth

Question 7

Rifabutin

MOA

Tox

Answer 7

rifabutin

MOA: inhibits DNA-dependent RNA-Pol

Tox: red fluids, CYP450 ramping, hypersensitivity, hepatotoxicity

Question 8

Metranidazole

MOA

Tox

Answer 8

metranidazole

MOA:? in this case, 25-35% resistance

Tox: GI, CNS tox, disulfuram-like rxn, teratogenic

Question 9

Tinidazole

MOA

Tox

Answer 9

tinidazole

MOA:?

Tox: decreased side effects compared to metronidazole, decreased dosing

_**inhibit CYP2CP ⇒ same as warfarin and H2 blockers**_

Question 10

Bismuth subsalicylate

MOA

Tox

Answer 10

busmuth subsalicylate

MOA: disrupt cell wall → prevents adhesion, may inhibit urease, protects surface by coating and increasing secretion of mucus, PG, HCO₃^-

Tox: black tongue and stool, vomiting, emesis, tinitus, confusion, hyperthermia, resp. acidosis → metabolic alkalosis

Question 11

Atropine, Pirenzipine

MOA

Tox

Answer 11

atropine, pirenzipine

MOA: mAChR antagonists, M1 and M3 (atropine), M1 (pirenzipine)

Tox: ABCD’s, anorexia, blurry vision constipation, confusion, dry mouth, stasis

Question 12

Atropine overdose

Answer 12

CNS (hallucinations)

tachycardia

hot, dry skin

Question 13

-DINEs

cemetidine, fomatidine, nizatidine, ranitidine

MOA

PK

Tox

Answer 13

MOA: H₂ receptor antagonists ⇒ decrease cAMP

PK: short t_1/2, liver metabolism, renal secretion, competes with weak bases (metranidazole) for tubular secretion

Tox: rapid IV → bradycardia, teratogenic (not for pregnant women)

Question 14

Cimetidine

toxicity

Answer 14

decreased binding of DHT to androgen receptors

decrease estrogen metabolism

increase prolactin

⇒ gynecomastia in males

⇒ galactorrhea in females

Question 15

Esomeprazole/omeprazole

lansoprazole

Pantoprazole

Robeprazole

MOA

PK

Tox

Answer 15

MOA: PPIs, inhibit H⁺/K⁺ ATPase in parietal cells

PK: acid labile → pass to small intestine and delivered to acidic areas (parietal cells) via blood

Tox: headache, diarrhea, nausea, rash

Question 16

Timing of PPI therapy

Answer 16

need to give in fasting state

30 min before meal

⇒ highest concentration at this time

Question 17

Long-term concerns of PPI use

Answer 17

• decreased B12, Fe, Ca²⁺, Zn ⇒ increased risk of hip fractures
• increase in resp and enteric infections (because less acid being secreted)
  
  • ECL hyperplasia ⇒ neuroendocrine tumors (?)

Question 18

4 antacids

Answer 18

Al(OH)₃

Mg(OH)₂

CaCO₃

NaHCO₃

Question 19

Toxicity of Al(OH)₃

Answer 19

constipation

Question 20

Toxicity of Mg(OH)₂

Answer 20

pugative (laxative)

Question 21

Drug interactions with antacids

Answer 21

changes in pH, gastric and systemic

Question 22

Sucralfate

MOA

TU

PK

Tox

Answer 22

sucralfate Al(OH)₃ and sulfonated sucrose

MOA: H⁺ converts it to thick paste → stick to and protect ulcer surface

TU: stress-induced ulcers in ICU

PK: requires acid, no co-admin w/ H₂ blockers or PPIs

Tox: constipating, drug-drug

Question 23

Misoprostol

MOA

TU

PK

Tox

Answer 23

misoprostol

MOA: PGE1 agonist, acts in opposition to H2 by decreasing cAMP

TU: NSAID-induced ulcers

PK: rapid absorption and metabolism, excreting in urine

Tox: bad–diarrhea, severe nausea, cramping, abdominal pain, abortifacent**

Question 24

Strong CYP2CP inhibitor

Answer 24

Tinidazole

substitute for metronidazole