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Pharmacology > GI drugs > Flashcards

GI drugs Flashcards

1
Q

Which of the following mechanisms does NOT lead to a an increase in proton-pump activity.

a. Ach stimulating muscarinic receptors
b. Gastrin stimulating CCK2 receptors
c. Histamine stimulating H2 receptors
d. PGE2 stimulating EP3 receptors

A

d. PGE2 stimulating EP3 receptors

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2
Q

What is the main role of prostaglandins in the GI?

A
  • produce more substrates to make up the mucosa to protect stomach lining
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3
Q

What are the 2 ways in which gastrin stimulates the parietal cell? Which one is more common?

A
  • gastrin stimulates ECL cell to produce more histamine*

- gastrin stimulates CCK2 cell

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4
Q

The feedback loop in the GI is mostly mediated by what?

A
  • Gastrin
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5
Q

When are the parietal cells most activate?

A
  • after a meal
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6
Q

What is the difference between lumen pH with an empty stomach and post prandial?

A
  • basal acid = 1-2

- post pandrial = 4-5

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7
Q

What antibiotics may be prone to interactions with antacids?

A
  • FQs
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8
Q

What is the mechanism of Antacids?

A
  • rapid local neutralization of acid in the stomach
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9
Q

What adverse effects are seen with antacids? What elements correlate to each?

A
  • diarrhea = Mg
  • constipation = AI
  • abdominal distension = Ca2+
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10
Q

If a patient is taking an antacid and is complaining of side effects what do you need to do?

A
  • find out exactly what antacid they are taking (ask for the bottle)
  • take home message from the graph
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11
Q

What are the 3 indications for bismuth compounds? (Pepto-Bismol)

A
  • protect stomach lining
  • slow down intestinal transit (diarrhea)
  • can be useful to treat traveler’s diarrhea (antibacterial)
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12
Q

What are the 4 adverse effects listed with bismuth compounds (Pepto-Bismol)?

A
  • constipation
  • darkening of tongue/stool
  • avoid if aspirin allergy
  • drug interactions
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13
Q

Which of the cytoprotectants is prescription only?

  • Bismuth Compounds
  • Sucralfate
  • Misoprostol
A
  • Sucralfate
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14
Q

What are the 2 potential uses for sucralfate?

A
  • acid-peptic disease

- stress ulcer prophylaxis (patient on mechanical ventilator)

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15
Q

Which animal is at risk for stress ulcers?

A

horses

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16
Q

Why may sucralfate be a better drug for stress ulcer prophylaxis then a PPI or H2 antagonist?

A
  • does not change pH in stomach so doesn’t change bacteria in stomach = less risk of aspiration pneumonia in patients who are ventilated
17
Q

What is the most common adverse effect of sucralfate?

A
  • constipation
18
Q

Which patients are at greatest risk of stress ulcer?

A
  • patients intubated in ICU

* give stress ulcer prophylaxis = Misoprostol

19
Q

This cytoprotectant is a prostaglandin E1 analog.

  • Bismuth Compounds
  • Sucralfate
  • Misoprostol
A
  • Misoprostol

* stimulates secretion of mucin and bicarb

20
Q

What is the primary concern in a pregnant patient using misoprostol?

A
  • increased uterine contractility = medical termination OR labor induction
21
Q

What is the major side effect with misoprostol?

A
  • diarrhea
22
Q

What is the mechanism of H2 -receptor antagonists (e.g. cimetidine) ?

A
  • compete with histamine for binding to H2 receptors on parietal cells
23
Q

What are the 3 indications for a H2-receptor antagonist (e.g. cimetidine)?

A
  • uncomplicated GERD
  • gastric/duodenal ulcers
  • stress ulcer prophylaxis
24
Q

What are the 3 side effects unique to cimetidine? (H2 antagonists)

A
  • short acting
  • inhibitor of CYP-450
  • gynecomastia in men; galactorrhea in women
25
Q

What is the reason Ranitidine is not on the market anymore?

A
  • has the potential to form NDMA which is carcinogenic
26
Q

What agents are the most potent of the acid suppressive therapies?

A
  • PPIs (e.g. Omeprazole)

* most potent at raising pH!!

27
Q

When is it best to take PPIs in relation to eating?

A
  • 30 to 60 minutes prior
28
Q

Why is PPIs enteric coated formulations?

A
  • parent compound is unstable in acid
29
Q

What is the mechanism of action of PPIs?

A
  • irreversibly bind to and inactivate H-K ATPase
30
Q

What is the half life, onset, and duration of effect of PPIs (e.g. omeprazole)?

A
  • half life = 1-2 hours
  • onset = 2-5 days
  • duration = 24-48 hours
31
Q

What are the 4 indications for PPIs?

A
  • gastric and duodenal ulcers
  • GERD
  • Barrett’s esophagus
  • Zollinger Ellison syndrome
32
Q

What happens to gastrin with PPI administration?

A
  • gastrin will be hyper-secreted

* can lead to hypertrophy of ECL

33
Q

PPI reduces the absorption of what 3 vitamin/minerals?

A
  • B12
  • Calcium
  • Magnesium
34
Q

What is the association between Clopidogrel (Plavix) and PPIs?

A
  • PPIs inhibit 2C19 enzyme = decrease efficacy of Clopidogrel d/t it being a pro drug
35
Q

What is the major adverse effect of withdrawing PPIs?

A
  • reflex hyperacidity

* need to taper down

36
Q

What is the primary therapy regimen for H. Pylori?

A
  • Bismusth subsalicylate
  • Metronidazole
  • Tetracycline
    (10-14 days)

*plus high dose acid suppressive therapy
(continued 2+ weeks after BMT)

37
Q

What are the adverse effects seen in the primary treatment regiment for H. Pylori (BMT)? (4)

A
  • nausea
  • diarrhea
  • taste disturbances
  • allergic reactions

Pharmacology (6 decks)

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