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Pharmacology I > Peptic Ulcer Disease (PUD) and Inflammatory Bowel diseases (IBS) > Flashcards

Peptic Ulcer Disease (PUD) and Inflammatory Bowel diseases (IBS) Flashcards

1
Q

peptic ulcer disease defined

A

epigastric pain that is associated with hyperacidity

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2
Q

gastric ulcers

A

associated with normal or reduced gastric acid output

altered mucosal resistance may be primary factor

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3
Q

duodenal ulcers

A

associated with high gastric acid output, especially at night

inadequate duodenal bicarbonate secretion, and insufficient acid neutralization are significant contributing factors

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4
Q

etiology PUD

A

Generally caused by NSAIDs or Helicobacter pylori infection. Therefore, H. Pylori is regarded as the major infectious cause of PUD.

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5
Q

why is H. pylori resistant to harmful effects of the acidic environment?

A

produce enzyme urease which converts urea in teh stomach juice into ammonia and bicarbonate

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6
Q

goals in treatment of peptic ulcer disease

A
  1. eradication of H. pylori
  2. relief of symptoms
  3. healing of ulceration
  4. prevention of recurrence and complications
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7
Q

antacids MOA

A
  • Are weak bases that chemically neutralize acid. By raising acid pH.
  • They prevent the transformation of pepsinogen to pepsin. (Goal to raise gastric pH >4).
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8
Q

SE aluminum hydroxides

A

constipation

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9
Q

SE magnesium hydroxides

A

diarrhea

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10
Q

Calcium carbonate

A

gas and acid reflux

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11
Q

therapeutic uses of antacids

A
  • Simple dyspepsia
  • Adjuncts to primary therapy with H2 blockers or proton pump inhibitors
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12
Q

simethicone

A

belch

forms plug to prevent regurgitation

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13
Q

H2 antagonists

A

famotidine > nizatidine > cimetidine

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14
Q

MOA of H2 antagonists

A

competitive inhibit (reversible) histamine-mediated acid secretion and also blunt the response to gastrin and Ach

highly selective

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15
Q

H2 histamine receptor antagonists inhibit what

A

basal membrane, food stimulated nocturnal section

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16
Q

cancer causing agent found in?

A

Ranitidine was pulled out from circulation because the drug/or a metabolite is associated with increased levels of N-nitrosodimethylamine (NDMA) a cancer causing agent.

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17
Q

Adverse effects and drug interactions of H2 antagonists

A

infrequent and mild.

may alter the bioavailability of rate of absorption of certain drugs secondary to changes in gastric pH (example aspirin).

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18
Q

cimetidine

A

Inhibits the activity of cytochrome p450 and thus slows the metabolism of many drugs

Thus if drugs interactions are to be avoided, choose an H2 blocker other than cimetidine

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19
Q

proton pump inhibitors (PPI) MOA

A

inhibitors of the H ion pump responsible for secreting HCl into the gastric lumen

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20
Q

proton pump inhibitors specificity

A
  • selective distribution of H+/K+/ATPase are in parietal cells
  • requirement for acidic pH for drug activation (i.e. they need to be ionized)
  • trapping of the drug at its site of action
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21
Q

PPIs are _____ effective than __________ in relieving symptoms of PUD in healing ulcers.

A

more; H2 blockers

22
Q

PPIs are _____ effective than __________ in relieving symptoms of GERN and in healing erosive esophagitis.

A

more; H2 blockers

23
Q

does tolerance develop with PPIs?

A

NO, H2

24
Q

clinical uses of PPI

A

Zollinger-Ellison syndrome and refractory gastric, esophageal and duodenal

25
Q

clinical uses of PPI

A

Zollinger-Ellison syndrome and refractory gastric, esophageal and duodenal

26
Q

what PPI inhibit acid secretion and effectively orally?

A

omeprazole and esomeprazole

27
Q

what PPI is less effective in severe esophagitis?

A

lansoprazole

28
Q

what PPI is metabolized to a much lower extent by the cytochrome P450 system?

A

rabeprazole (aciphex)

29
Q

what can occur after chronic use of PPIs and H2 blockers?

A

decreased absorption of vitamin B12 and → deficiency

30
Q

what are moderate inhibitors of CYP2C19?

A

omeprazole and esomprazole

31
Q

what drug is converted to its active metabolite by CYP2C19?

A

clopidogrel (Plavix) - therefore inhibition of CYP2C19 may interfere with its activation

32
Q

bismuth subslicylate is also called

A

pepto bismol

33
Q

bismuth subslicylate MOA

A
  • enhances secretion of mucus and HCO3-
  • inhibits pepsin activity
  • chelates with proteins at the base of the ulcer crater and forms a protective barrier against acid and pepsin
    • inhibits H. pylori
34
Q

side effect of bismuth subslicylate

A

turns the tongue and stool black and can cause tinnitus

35
Q

sucralfate

A

forms sticky, viscous gel that adheres to gastric epithelial cells protecting them from acid and pepsin

36
Q

what drug is the only one it its class to require an acid pH?

A

sucralfate

given 1 hour before meals and at bedtime to promote gastric healing

37
Q

what drug is provided to bedridden patients?

A

sucralfate

38
Q

misoprostol has what intolerable side effect?

A

diarrhea

39
Q

misoprostol is used for what patients?

A

primarily used for patients who must NSAIDs

also for ABORTION!

40
Q

clairthromycin MOA

A

macrolide that inhibits protein synthesis in microbes

41
Q

amoxicillin MOA

A

effective against gram negative bacilli

contraindicated in patients allergic to penicillin

42
Q

tetracycline MOA

A

second line drug

must stagger its dose when it is given in conjunction with Bismuth

43
Q

metronidazole MOA

A

synthetic ABO against obligate anaerobes

44
Q

furazolidine MOA

A

nitrofuran antibacterial and antiprotozoal

45
Q

if resistance to clarithromycin is suspected, replace it with _________

A

metronidazole

46
Q

if both clarithromycin and metronidazole resistance is suspected, what drugs is substituted?

A

furazolidone or rifabutin

47
Q

what drug is highly active against H. pylori with little resistance?

A

Rifabutin

48
Q

metoclopramide MOA

A

dopamine 2 receptor blocker as well as 5HT4-R agonist, which increases local release of acetyl choline

49
Q

domperidone MOA

A

dopamine 2 receptor blocker only

50
Q

pharm actions of prokinetic

A
  • stimulates GI smooth muscle
  • increases amplitude of esophageal contractions
  • accelerates gastric emptying
  • increases LES pressure

enhance the main anti-reflex mechanism and accelerate gastric emptying

51
Q

prokinetic side effects

A
  • tardive dyskinesia related to central dopaminergic antagonism
  • prescribed for a short time
52
Q

antisecretory drugs

A

no effect on LES (lower esophageal pressure), esophageal peristalsis, or gastric emptying

because they work increase gastric pH

Pharmacology I (7 decks)

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