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GI/Liver: Pharmacology > PUD > Flashcards

PUD Flashcards

1
Q

What is the goal when treating PUD and other disorders of chronic inflammation (GERD, Gastritis, etc)?

A

Goal is to reduce inflammation

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2
Q

What are the protective cells of GI tract?

A

Surface epithelial, mucosal neck, and stem cells

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3
Q

What are the digestive cells of GI?

A

Parietal, chief, and endocrine cells

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4
Q

Describe direct pathway of acid secretion

A

Ach, gastrin, histamine directly stimulate parietal cells to secrete acid

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5
Q

Describe the indirect pathway of acid secretion

A

Ach and gastrin stimulate ECL cells –> histamine release –> acid secretion

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6
Q

Half of this lecture is stuff we know from phys, micro, & path. Should you review these subjects for the test?

A

Yes.. So now we will move on to pharm stuff

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7
Q

Whats the overall goal of PUD tx? (3)

A
  1. Eradicate H. pylori with antibiotics
  2. Relieve symptoms with anti-secretory drugs or antacids
  3. Heal ulcers with PGs, bismuth, sucrasulfate
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8
Q

What do antacids do?

A

Neutralize acid in the stomach (duh)

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9
Q

What is the goal for antacid tx?

A

pH > 4

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10
Q

What are the antacid drugs?

A
  1. Maalox (Mg-Al hydroxide)
  2. Gaviscon (Maalox + algenic acid)
  3. Calcium carbonate (Tums)
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11
Q

What are antacids used for?

A
  1. Simple dyspepsia

2. Adjunctive with H2 blockers or PPIs

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12
Q

When are antacids taken?

A

A few hours post meal or before bedtime

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13
Q

What is probably the biggest consideration when prescribing antacids?

A

They can SIGNIFICANTLY affect the absorption of other drugs (b/c the increase the pH of the stomach). So you dont want to take them within a few hours of other drugs*****

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14
Q

Maalox is a combo of Mg hydroxide and Al hydroxide. What do these things do?

A

Mg hydroxide causes diarrhea. Al hydroxide causes constipation. You mix them together to balance the AEs. (Mg: M for Mudbutt)

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15
Q

What do H2 antagonists do? (3)

A
  1. Block histamine receptors.
  2. Inhibit basal, cephalic, and nocturnal gastric acid secretion.
  3. Reduces volume and [H+] of gastric acid
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16
Q

Name the H2 antagonists

A
  • Cemetidine: 1x potency
  • Ranitidine & Nizatidine: 4-10x potency
  • Famotidine: 20-50x potency
  • *All have same efficacy
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17
Q

Are the H2 antagonist specific for the stomach or not?

A

Yes! Thats good because few AEs

18
Q

Unique thing about Cemetidine?

A

Inhibits CYPs –> drug interactions

19
Q

Unique thing about Ranitidine?

A

Alters other drug’s bioavailability via an unknown mechanism

20
Q

Unique thing about Famotidine?

A

Leads to decreased Theophylline clearance

**Theophylline treats COPD

21
Q

What do PPIs do?

A

Inhibit H+ pump at apical surface of parietal cells

  • *More effective than H2 blockers b/c it is the final common pathway so can block 90% of acid secretion**
  • *All orally active pro-drugs with long duration of action
22
Q

Name the PPIs

A

The prazoles: Omeprazole, Esomepraole, Lansoprazole

23
Q

How do these drugs get to their place of action?

A

Drug has enteric coating which allows release of prodrug into SI (in neutral pH of SI, PPI is stable) –> PPIs then absorbed into blood stream (lipid soluble) –> Carried in blood to parietal cells where acid pH ionizes & traps them –> Ionized drug irreversibly binds to H/K ATPase

24
Q

What is the result of PPIs binding to H/K ATPase?

A

Achlorhydria & no gastric acid secretion. The parietal cell must make new H/K ATPases (proton pumps)

25
Q

All PPIs inhibit which CYP? Which PPI is the weakest inhibitor of said CYP?

A

CYP2C19. Pantoprazole is the weakest inhibitor of the CYP

26
Q

What does the CYP inhibition do?

A
  1. Decreases Clopidogrel efficacy

2. Decreases bioavailability of anti-retrovirals

27
Q

Clinical uses of PPIs? (4)

A
  1. Short term for active PUD
  2. Managing ZE syndrome
  3. Managing refractory GI ulcers
  4. Management of GERD
    * *Basically all letters: PUD, ZE, GERD
28
Q

Name the cytoprotective agents (think BS)!

A
  1. Bismuth subsalicylate

2. Sucralfate

29
Q

What does Bismuth subsalicylate do? (4 things)

A
  1. Increases mucous & HCO3 secretion
  2. Decreases pepsin activity
  3. Chelates protein at base of ulcer to form protective barrier from GA and pepsin
  4. Inhibits H. pylori
30
Q

What is Bismuth subsalicylate effective for? (4 things)

A

“TUG- Diarrhea”: Travelers diarrhea, Ulcers, GERD, diarrhea

31
Q

What does Sucralfate do?

A

Forms sticky gel that adheres to gastric epithelium protecting it from GA and pepsin
**Think sucralfate = sucrose = sticky gel

32
Q

What is unique about Sucrasulfate as far as activity?

A

It is the only agent that requires ACIDIC pH for activity so it can protect against ulcers without need for alkalinization (alkalinizatoin can lead to bacterial overgrowth)

33
Q

What is unique about Sucrasulfate as far as who to use it on?

A

Bedridden pts!

34
Q

What antibiotics treat H. pylori

A

Clarithromycin, Amoxicillin, Tetracycline, Metronidazole, Furazolidine

35
Q

Clarithromycin MOA?

A

protein synthesis inhibitor (50S subunit)

36
Q

Amoxicillin MOA?

A

B-lactamase resistant B-lactam (watch for Pcn allergy)

37
Q

Metronidazole MOA?

A

Inh nucleic acid synthesis. It is a synthetic antibiotic for obligate anaerobes

38
Q

Furazolidone MOA?

A

Nitrofuran anti-bacterial and anti-protozoal

39
Q

Describe the triple or quad therapy for treating H. pylori

A

Give:

  1. PPI
  2. H2 blocker
  3. Bismuth subsalicylate
  4. One or two antibiotics
    * *For 10-14 days
40
Q

If Clarithromycin resistant, switch to?

A

Metronidazole

41
Q

If Metronidazole resistant, switch to?

A

Furazolidine

GI/Liver: Pharmacology (19 decks)

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