Wk2 Acid/Peptic disease drugs Flashcards

1
Q

Metronidazole inhibits which enzyme causing drug interactions?

A

CYP2C9

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2
Q

Major drug interactions due to metronidazole’s inhibition of CYP2C9:

A

potentiates warfarin

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3
Q

Cimetidine’s effect on metronidazole?

A

decreases clearance –> potentiates effects

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4
Q

bacterioCIDAL

cell wall inhibitor (beta-lactam)

hypersensitivity

A

amoxicillin

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5
Q

Why clarithromycin vs azithromycin for H. pylori?

A

MIC90 of .06 vs .25

more acid stable

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6
Q

bacterioSTATIC

protein synthesis inhibitor (binds to 50s ribosomal RNA to prevent translocation)

GI irritation, drug interactions (both a substrate and an inhibitor of CYP3A4)

A

clarithromycin

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7
Q

Two ways antimuscarinics decrease H+ secretion:

A
  1. Block M3 receptors on ECL cells preventing their release of histamine (–> parietal cell stimulation)
  2. directly block M3’s on parietal cells
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8
Q

IRREVERSIBLY block the final common pathway in acid secretion — H+/K+ ATPase.

A

PPIs

“-Prazoles”

**make sure there is a P

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9
Q

sulfate-aluminum hydroxide complex that attaches to the basement membrane of the ulcer

constipation

requires acidic environment to become paste

A

sucralfate

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10
Q

direct (but limited) antimicrobial activity against H. pylori
disrupts cell wall, causing lysis

prevents adhesion

inhibits urease

protects ulcer surface

coats ulcer surface, protecting it from acid and pepsin
stimulates prostaglandin, mucous and bicarbonate secretion

A

Bismuth

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11
Q

blackening of stool and tongue

A

Bismuth

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12
Q

(PGE1) drug of choice for treatment of ulcers induced by NSAIDs

side effects and the need for frequent dosing limit its use.

It is abortifacient. CONTRAINDICATED in pregnancy.

A

misoprostol

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13
Q

Abx that get chelated and is less effective when taken with antacids:

A

tetracycline

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14
Q

highly selective, competitive inhibitor of parietal cell H2 receptors

reduce intracellular cAMP

A

cimetidine

FAMOTIDINE, NIZATIDINE, RANITIDINE, ROXATIDINE

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15
Q

Two antimuscarinics:

A

atropine

pirenzipine

**no longer used due to big side fx

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16
Q

Time for PPIs to take full effect:

A

3-4 days

17
Q

Fart blocker

A

simethicone

18
Q

rapid onset but short duration of action

no prevention of ulcer recurrence

useful for intermittent dyspepsia

A

antacids

19
Q

relatively rapid onset

intermediate duration, some prevention

many uses

A

H2 blockers

20
Q

slow onset of action

very long duration of action

excellent prevention

drugs of choice for Zollinger-Ellison syndrome and GERD, as well as ulcer treatment

A

PPIs

21
Q

excessive consumption of high calcium foods with certain antacids, over a long period of time

A

milk-alkali syndrome

22
Q

Antacid

efficient

low systemic absorption

constipation

not very effective when given alone

osteomalacia (RARE)

A

Aluminum hydroxide

23
Q

Antacid

efficient

low systemic absorption

osmotic diarrhea

(RARE) renal insufficiency → hypermagnesemia → CNS & cardio-toxicity

A

Magnesium hydroxide

24
Q

Antacid

rapid onset of action

long duration

belching, gastric distension

rebound acid secretion

(RARE) mild systemic alkalosis

(RARE) hypercalcemia in patients with impaired renal function if taken with dairy products (milk-alkali syndrome)

A

Calcium carbonate

25
Q

Antacid

extremely rapid onset of action

belching, gastric distension

short duration of action

systemic absorption

RARE
severe metabolic alkalosis
alkalinizes urine
hypercalcemia in patients with impaired renal function if taken with dairy products (milk-alkali syndrome)
absorption of NaCl → fluid retention in patients with heart failure, hypertension or renal insufficiency

A

Sodium bicarbinate

26
Q

Parietal cell receptor that increases cAMP

A

H2

27
Q

Parietal cell receptors that increase Ca++

A

M3, gastrin (CCK)