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My Notes > GI pharm > Flashcards

GI pharm Flashcards

1
Q

What do -prazole drugs do?

A

proton pump inhibitors (e.g. omeprazole)

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2
Q

Which pathways agonize and antagonize the H+/K+ ATPase in the stomach?

A

Agonists: H2 (Gs); vagus M3 and gastrin (Gq)
Antagonists: PG and somatostatin (Gi)

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3
Q

What drug suffix denotes H2 antagonists used for peptic ulcer disease?

A

-tidine e.g. cimetidine

Get a table for 2 [H2] before you dine

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4
Q

Why don’t we target the parasympathetic pathway as a target for the treatment of PUD?

A

muscarinic antagonists are in the atropine family and thus would have atropine-like side effects (hot, mad, dry, red, blind)

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5
Q

What are the 3 effects of prostaglandins in the stomach?

A
  1. ↓ proton pump activity
  2. promote secretion of mucus which protects stomach
  3. enhance bicarb secretion to neutralize acid
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6
Q

What drug is the direct antidote to NSAID induced PUD?

A

MisoPROSTol (a PROSTaglandin PGE1 analog)

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7
Q

What treatments are available for gastrinomas (e.g. ZES)?

A

There are no gastrin antagonists, we use PPIs

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8
Q

How does sucralfate work in the tx of PUD?

A

it is a sticky gel that coats the ulcer crater, protecting it from further erosion by acids

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9
Q

What are antacids?

A

bases that neutralize free protons in the stomach

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10
Q

What two stimuli cause histamine release from ECL cells? Which receptors are involved?

A
  1. Gastrin (CCK-B receptor)

2. Vagal (M1)

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11
Q

Do H2 blockers affect gastric emptying time?

A

no

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12
Q

What are 3 applications for H2 inhibitors?

A
  1. PUD (both gastric and duodenal; less effective than PPIs)
  2. GERD
  3. ZES
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13
Q

What is the main mechanism by which cimetidine → side effects? What are they?

A

Inhibition of cyt p450 → anti-androgen effects → gynecomastia and ↓ libido in ♂
Note: cimetidine is also associated with confusion in the elderly

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14
Q

Are PPIs reversible or irreversible, and competitive or non-competitive inhibitors of the H+/K+ ATPase?

A

Irreversible; non-competitive → ↑ effectiveness

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15
Q

Besides outperforming H2 blockers in the treatment of GERD, PUD, and ZES, what is an additional application of PPIs?

A

part of treatment regimen for H. pylori

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16
Q

What is the treatment for H. pylori?

A

Omeprazole

Clarithromycin +/- Amoxicillin

17
Q

What is the primary treatment of GERD?

A

PPIs

18
Q

Is omeprazole a p450 inhibitor?

A

yes, though it is not in the mnemonic

19
Q

What is the primary contraindication of misoprostol?

A

Anything with -prost- = prostaglandin = contraindicated in pregnancy → induce contractions → abortion by triggering labor

20
Q

What should not be given with sucralfate for ulcers? Why?

A

don’t give antacids b/c sucralfate is a prodrug that requires acidic environment to turn into a protective gel lining

21
Q

What is the medical term for pepto bismol?

A

bismuth subsalicylate

22
Q

What is the mechanism of action of bismuth?

A

binds selectively to ulcer, coating and protecting it from acid and pepsin

23
Q

When is bismuth primarily used?

A

as part of BMT regimen to eradicate H. pylori and prevent ulcer recurrence
BMT = bismuth, metronidazole, and tetracycline

24
Q

What is the side effect of aluminum containing drugs? Mg2+ containing drugs?

A

Al: constipation
Mg: diarrhea

25
Q

What are the drug interactions of antacids?

A
  1. ↑ pH of gut → ↑ absorption of drugs that are weak bases (deionizes them; e.g. quinidine)
  2. ↑ pH of gut → ↓ absorption of weak acids (ionizes them; e.g. warfarin)
  3. tetracycline chelates ions (e.g. Ca2+, Al+, Mg2+) in antacids → ionizing tetracycline → ↓ absorption of tetracycline and interfering with benefit of antacid
26
Q

Which receptors does the vagus activate on ECL cells? on parietal cells?

A

M1 on ECL cells and M3 on parietal cells

27
Q

Where is the chemoreceptor trigger zone (CTZ) in the brain? What is it responsible and what is special about its blood supply?

A

area postrema at the floor of the 4th ventricle; projectile vomiting; no good BBB as a circumventricular organ → drugs can readily reach receptors here

28
Q

What 3 receptors are located in the chemoreceptor trigger zone (area postrema)?

A

agonists: D2 and 5HT3
antagonist: CB1 (cannabinoid)

29
Q

What are the inputs into the vomiting center in the brain?

A
  1. chemoreceptor trigger zone
  2. vestibular system (CN VIII)
  3. pain afferents via spinal cord
30
Q

How does the vestibular system interact with the vomiting center?

A

Motion → ACh release from CN VIII → M1 receptors in vomiting center

31
Q

How does pain trigger vomiting?

A

Visceral/GI pain especially → GI afferents → release substance P → NK1 receptors in dorsal horn of spinal cord → stimulate vomiting center

32
Q

How does ondansetron work?

A

antagonizes 5HT3 receptors in the CTZ

33
Q

When is ondansetron used?

A

prevent vomiting in chemotherapy (esp. cisplatin), radiotherapy, and post-op

34
Q

What is metocloparamide? What are its applications in the GI system?

A

D2 receptor antagonist; antiemetic in cancer chemotherapy, diabetic and post-op gastroparesis, prokinetic in GERD (before PPIs)

35
Q

What drugs are used to treat motion sickness? What are the side effects?

A
  1. H1 antagonists (diphenhydramine, meclizine, promethazine) – not used b/c H1 blocking but b/c antimuscarinic
  2. Scopolamine - antimuscarinic
    Side effects: atropine-like, sedation, anterograde amnesia
36
Q

Which drug agonizes the CB1 receptor in the CTZ to prevent vomiting?

A

cannabinoids: dronabinol (THC)

37
Q

Which drug antagonizes NK1 receptors (part of pain mediated vomiting path) in the spine?

A

aprepitant

38
Q

What are neurokinins?

A

inflammatory mediators such as substance P and bradykinin that can also cause pain

39
Q

How could octreotide theoretically be used in the treatment of ulcers?

A

It is a somatostatin analog that binds to the ST2 receptor on ECL cells, inhibiting histamine release

My Notes (23 decks)

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