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Pharmacology II > Acid Peptic Disorders > Flashcards

Acid Peptic Disorders Flashcards

1
Q

H. pylori ulcers

A
  • Location: Duodenum > stomach
  • Epigastric pain
  • Superficial ulcer
  • Less severe GI bleeding
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2
Q

NSAID ulcers

A
  • Location: Stomach>duodenum
  • asymptomatic
  • Deep ulcer
  • More severe GI bleeding
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3
Q

Stress ulcer

A
  • ACUTE!
  • Location: Stomach>duodenum
  • Asymptomatic
  • Superficial ulcer
  • More severe GI bleeding
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4
Q

Parietal cells contain receptors for what 3 things?

A
  1. Gastrin (CCK-B)
    - from G cells
  2. Histamine (H2)
  3. Acetylcholine (muscarinic, M3)
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5
Q

How do antacids work

A

weak bases that react with stomach acid to form a salt and water

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6
Q

How long do antacids typically work?

A

If taken 1 hour after a meal, they effectively neutralize gastric acid for up to 2 hours

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7
Q

Antacids: Sodium Bicarbonate

A

Ex. baking soda, alka Seltzer
-React with gastric acid to form carbon dioxide and sodium chloride

ADE: 1. gastric distension 2. belching**

  • be careful if kidneys don’t work, could cause metabolic alkalosis
  • becareful with NaCl absorption and fluid retention
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8
Q

Antacids: Calcium carbonate

A

Ex. Tums, Os-cal

-Reacts more slowly to form CO2 and CaCl2 (calcium chloride)

ADE: 1. belching 2. metabolic alkalosis 3. milk-alkali syndrome –>hypercalcemia if taken with dairy

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9
Q

Antacids: Magnesium hydroxide and aluminum hydroxide

A

Maalox (contains both magnesium and aluminum)

MOA:: reacts slowly to form magnesium chloride

  • No gas or belching :)
  • metabolic alkalosis uncommon

ADE: unabsorbed magnesium salts may cause diarrhea. Aluminum salts may cause constipation

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10
Q

Because antacids interact and effect the absorption of some medications, which should not be given within 2 hours of antacids?

A
  1. Tetracyclines
  2. Fluroquinolones
  3. Itraconazole
  4. Iron
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11
Q

H2 Receptor Antagonists

A

Ex. Cimetidine, Ranitidine, Famotidine, Nizatidine

-1st pass hepatic metabolism** (except Nizatidine)
Metabolism: hepatic, glomerular filtration, renal tubular secretion

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12
Q

When should H2 receptor blockers be given?

A

Bedtime

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13
Q

Most potent and least potent H2 blockers?

A

Least potent: cimetidine

Most potent: Famotidine

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14
Q

How long do H2 blockers work for?

A

10 hours (prescription strength)

6 hours (OTC)

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15
Q

What is the biggest ADE of H2 blockers?

A

Possible risk of nosocomial PNA in critically ill patients

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16
Q

Cimetidine unique ADEs

A
  • Cytochrom P450 metabolized
  • inhibits dihydrotestosterone to androgen receptors
  • increases serum prolactin levels (galactorrhea in women)
  • gynecomastia/impotence in men
17
Q

PPIs: pharmacokinetics

A

Bioavailability is decreased by about 50% by food

  • Irreversible inactivation of proton pump (H+/K+ ATPase which only exists in stomach)
  • Rapid first-pass systemic hepatic
  • Take 30-60 minutes before eating*
  • Take at breakfast*
18
Q

PPI: ADEs

A
  • Diarrhea*
  • Potentially effects absorption of iron, calcium, magnesium (increased fracture risk)
  • increased risk of C. diff infection
  • Rebound acid hypersecretion
19
Q

PPIs: Drug interactions

A
  • Omeprazole may inhibit metabolism of Warfarin
  • Pantoprazole = no significant drug interactions
  • Clopidogrel is a prodrug and can have reduced activation if used with some PPIs
20
Q

What chemical is important in stimulating mucus and bicarbonate secretion and mucosal blood flow?

A

prostaglandins

21
Q

Mucosal Protective Agents: Sucralfate

A
  • forms physical barrier that restricts caustic damage

- Stimulates mucosal prostaglandin and bicarbonate secretion

22
Q

Sucralfate: ADE

A

Constipation* (due to aluminum salt)

-Can bind to other medications and impair absorption

23
Q

Gastrointestinal mucosa synthesize which prostaglandins?

A

PGE

PGF

24
Q

Misoprostol

A
  • PGE1
  • Short half-life, so take it 3-4 times a day

MOA: inhibit acid, protect mucosa

other: stimulate intestinal electrolyte and fluid secretion, intestinal motility, uterine contractions

25
Q

Misoprostol: ADE

A
  • Diarrhea
  • Cramping abdominal pain
  • DO NOT USE in pregnancy or in women with child bearing potential (unless negative hCG), and on contraception)
26
Q

Bismuth Compounds: types

A
  1. Bismuth subsalicylate (ex. Pepto-Bismol)
    - OTC
  2. Bismuth subcitrate potassium
    - Rx
    - Contains metronidazole and tetracycline for treating H. pylori
27
Q

Bismuth Compounds: metabolism

A
  • 99% of bismuth ends up in stool

- Salicylate dissociates with bismuth in the stomach and is readily absorbed and excreted in the urine.

28
Q

Bismuth compounds: pharmacodynamics

A

Bismuth: creates a protective layer against pepsin and acid
-Bismuth has direct antimicrobial effects —>binds enterotoxins (antimicrobial activity against H. pylori)

Bismuth subsalicylate: reduces stool frequency and liquidity (inhibits intestinal prostaglandins and chloride secretion)

29
Q

Bismuth Compounds: ADE

A
  • blackening of stool
  • darkening of tongue
  • AVOID in renal insufficiency –> bismuth toxicity with encephalopathy, ataxia, headaches, confusion

-Remember that salicylate toxicity can cause tinnitus!

30
Q

H. Pylori: Triple therapy Tx

A

PPI + Clarithromycin + Amoxicillin/Metronidazole

for 14 days

31
Q

H. Pylori: Bismuth quadruple therapy

A

PPI + Bismuth + metronidazole + tetracycline

Pharmacology II (31 decks)

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