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GI > PHARM: Antacids and H. Pylori Eradication > Flashcards

PHARM: Antacids and H. Pylori Eradication Flashcards

1
Q

What type of drugs are weak bases that neutralize gastric acid?

A

antacids

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2
Q

What are antacids used for?

A

heartburn (quick acting with short duration)

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3
Q

What is the pharmacokinetic difference between systemic and non-systemic antacids?

A

systemic antacids are absorbable, non-systemic antacids are NOT absorbable

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4
Q

What is an example of a systemic antacid?

A

sodium bicarbonate

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5
Q

What is the stipulation for the use of sodium bicarbonate?

A

only for SHORT TERM USE—long term leads to sodium and water retention (altering the systemic acid-base balance)

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6
Q

What are some examples of non-systemic antacids?

A

aluminum, magnesium or calcium salts

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7
Q

What types of non-systemic antacids lead to constipaton?

A

Al- and Ca2+ containing antacids

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8
Q

What are some types of non-systemic antacids that lead to diarrhea?

A

Mg2+ containing antacids

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9
Q

What is the only known physiological role of H2 receptors?

A

stimulate secretion of HCl by the gastric parietal cells

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10
Q

What cells in the stomach release histamine?

A

ECL cells

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11
Q

How do the products of the ECL cells (histamine) get to the H2 receptors in the stomach?

A

paracrine

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12
Q

What does binding of histamine to H2 receptors cause?

A

cAMP cascade that leads to increased acid secretion from the membrane-bound molecules of the H+/K+ ATPase

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13
Q

Why do H2 blockers not solve all the acid problems in the stomach?

A

parietal cells can also be stimulated by neurocrine (vagal) stimulation or endocrine (gastrin) pathways that are NOT affected by these drugs

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14
Q

What do the H2 blockers end with?

A

“tidine”

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15
Q

when do you take H2 receptor blockers?

A

before bed

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16
Q

When do H2 blockers have their peak action

A

during the resting or “basal” state of the stomach (overnight)

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17
Q

Why are H2 blockers not as effective during the day?

A

inhibitory effects are partly overcome by stimulatory effect of food on acid secretion (would need to take multiple pills)

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18
Q

How does physiological tolerance occur in those taking H2 receptor blockers?

A

up-regulation of the receptor develops after a few days of continuous dosing

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19
Q

What H2 receptor blocker poses problems due to CYP inhibiton?

A

cimetidine

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20
Q

Which cimetidine DDIs are of physiological importance? Why is this?

A

phenytoin
warfarin
theophylline

These drugs have narrow therapeutic indexes and their concentrations increase to toxic levels if given with cimetidine

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21
Q

What are the indications for H2 blockers?

A
  • GERD patients with MILD symptoms ONLY

- Is used in seriously ill patients in ICU to prevent stress-related upper GI bleeds

22
Q

Which drug class is a racemic mixture of R- and S- enantiomers that is typically enterically coated (because the drugs are acid labile and must be protected from gastric acid)?

A

PPIs

23
Q

What is the ending of PPIs?

A

“prazoles”

24
Q

Which PPIs are NOT mixtures of R- and S- enantiomers?

A

Esomeprazole (purified S-enantiomer of omeprazole)

Dexlansoprazole (purified R-enantiomer of lansoprazole)

25
Q

What is the name of immediate release omeprazole that is mixed with sodium bicarbonate?

A

Zegerid

26
Q

What is special about Zegerid compared to other PPIs?

A

it is the only PPI that does NOT have an enteric coating

27
Q

What is the path of a PPI after swallowing?

A

enteric coating of drug removed by acid in stomach (delayed release), drug absorbed and distributed within the body, drug preferentially taken up by PARIETAL cells

28
Q

True or false: PPIs have a short elimination half life and a very short duration of action.

A

FALSE: short elimination half-life, but since effect is IRREVERSIBLE, the duration of action is much longer.

29
Q

When do you give a PPI?

A

early morning 30-60 minutes before food

30
Q

Why do H2 blockers and PPIs have a different dosage schedule?

A

PPIs block acid secretion both in the basal state AND in response to food stimulation

31
Q

Does tolerance develop with PPIs?

A

NO

32
Q

How does a PPI work?

A

PPI taken up by parietal cells→ become protonated→ excreted via the luminal aspect of the parietal cells and undergo chemical conversion to sulfenamide→ form covalent –SH bonds with cysteine residues of membrane bound proton pump to IRREVERSIBLY terminate its action

33
Q

When can acid secretion be recovered with PPI use?

A

only after synthesis of new proton pumps

34
Q

Who should get lower doses of PPIs than usual?

A

patients with hepatic dysfunction

35
Q

What is a possible side effect of PPIs?

A

rebound hypersecretion of acid after stopping therapy

36
Q

What is the PPI that leads to CYP- mediated DDIs?

A

omeprazole (CYP inhibitor)

37
Q

What are the two DDIs of omeprazole (CYP-wise)?

A

phenytoin and warfarin

38
Q

Why should you NOT take clopidogrel with omeprazole or esomeprazole?

A

may reduce the anti-platelet effect by slowing the conversion of clopidogrel to its active metabolite

39
Q

What are the indications for PPIs?

A
  • GERD
  • PUD (helps heal duodenal ulcers)
  • NERD
  • Helpful after episode of ulcer bleeding
40
Q

What is the first question that should be asked when a patient has PUD?

A

whether or not the patient is infected with H. pylori.

41
Q

When do people acquire an H. pylori infection?

A

childhood

42
Q

If a patient with PUD is NOT infected with H. pylori, what is the most likely cause?

A

NSAID or aspirin use

43
Q

What drug is used to treat H. pylori negative PUD?

A

PPIs

44
Q

What is REQUIRED to eradicate H. pylori?

A

You need to administer 2 or 3 antibiotics combined with an acid-suppressing drug (which improves the performance of antibiotics)!

45
Q

What is the major type of triple therapy in H. pylori infection?

A

Clarithromycin-based triple therapy (PPI + clarithromycin + amoxicillin (or metronidazole if penicillin allergy)

46
Q

What is the major quadruple therpay for H. pylori infection?

A

Bismuth-based quadruple therapy:

PPI (or H2RA) + bismuth + metronidazole + tetracycline

47
Q

What are the major reasons 25-30% of patients have persistent H. pylori infection after treatment?

A

poor compliance

antimicrobial resistance

48
Q

Which antibiotics are H. pylori always susceptible to?

A

amoxicillin

tetracycline

49
Q

What should you do if a patient fails triple or quadruple therapy?

A

you CANNOT re-prescribe the same combination (but you can use amoxicillin or tetracycline in the new combinations)

50
Q

Which is the antibiotic with the biggest problem with H. pylori resistance?

A

clarithromycin

GI (21 decks)

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