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Unit 6 > GI pharm > Flashcards

GI pharm Flashcards

1
Q

H2 antagonists (drugs)

A

Cimetidine (major one)

ranitidine

famotidine

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2
Q

H2 antagonists - MOA

A

Works on parietal cells to decrease HCl secretion caused by vagally or gastrin-induced release of histamine from enterochromaffin-like cells

No effect on gastric emptying time

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3
Q

H2 antagonists - uses

A

Less effective the PPIs Used in: PUD, GERD, ZE syndrome

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4
Q

Cimetidine - what is it? Side effect profile?

A

H2 antagonist

SE:

  • major inhibitor of certain cyp450s –> elevated levels of other drugs
  • anti-androgenic effects –> decreases androgens –> gynecomastia and decreased libido
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5
Q

Proton pump inhibitors (PPIs)

A

Omeprazole and related “-prazoles” are irreversible, direct PPIs (K+/H+ antiport) in gastric parietal cell

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6
Q

PPIs - clinical uses

A

More effective than H2 blockers in everything

  • PUD (peptic ulcer disease)
  • GERD
  • ZE syndrome
  • eradication regime for H. pylori
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7
Q

Misoprostol

A

PGE1 analog – cytoprotective increasing mucus and bicarbonate secretion

also decreases HCl secretion

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8
Q

Misoprostol - clinical uses

A

previously used for NSAID-induced ulcers, but PPIs are now used

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9
Q

Sucralfate

A

Polymerizes GI luminal surface to form protective, gel-like coating of ulcer beds – basically coats the ulcer and protects from further damage

Requires acid pH (antacids may interfere)

Uses: increased healing and decreased ulcer recurrence

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10
Q

Sucralfate - biggest problem with this drug?

A

can’t really take it with any other GI drugs (anti-cholinergics, H2 blockers, or PPIs)

Requires an acidic environment to work, so any of the other drugs may interfere with that

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11
Q

Bismuth subsalicylate

A

Similar to sucralfate MOA: binds selectively to ulcer, coating and protecting it from acid and pepsin main component of peptobismol

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12
Q

Bismuth subsalicylate - clinical uses

A

combined with metronidazole and tetracycline to eradicate H. pylori (BMT regimen)

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13
Q

Most rapid way to relieve the pain associated with peptic ulcers

A

Antacids – aluminium hydroxide, magnesium hydroxide or calcium carbonate neutralizes protons in the gut lumen

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14
Q

Antacids

A

aluminium hydroxide, magnesium hydroxide or calcium carbonate neutralizes protons in the gut lumen

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15
Q

ionization states and absorption

A

ionized –> harder to absorb (remember best characteristics of absorption is: small, nonpolar, noncharged)

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16
Q

Antacid + weak base drug || what happens to the absorption?

A

weak base drug is increased. antacid –> increased pH –> neutral form of drug –> increased uptake

17
Q

Antacid + weak acid drug || what happens to the absorption?

A

weak acid drug is decreased. antacid –> increased pH –> ionized form of drug –> decreased uptake

18
Q

Interaction between antacids and tetracyclines or fluoroquinolones

A

Decreased activity of the antibiotics because of chelation. The metals chelate up the antibiotics and are excreted

19
Q

Major 2 receptors in the chemoreceptor trigger zone (CTZ) responsible for vomiting

A

D2

5HT3

20
Q

chemoreceptor trigger zone – receptors

A

D2

5HT3

CB1 (cannaboid receptor 1) – normally inhibitory effect on emesis

21
Q

Emetic pathways

A

Antagonists

  • 5HT3
  • D2
  • M1 (muscarinic)
  • NK1

Agonists

  • CB1 (cannaboid)
22
Q

antiemetic 5HT3 antagonists

A

“-setrons”

  • ondansetron (used in cancer chemotherapy)
  • granisetron
23
Q

antiemetic DA antagonists

A

Work on D2 receptors

  • prochlorperazine (weak anti-psychotic effects)
  • metoclopramide (used in cancer chemo; also prokinetic GI motility in GERD)
24
Q

antiemetic DA antagonists – SE profile

A

anti-psychotic effects –> pseudo Parkingson disease found especially with chronic use

25
Q

antiemetic H1 antagonists

A
  • diphenhydramine
  • meclizine
  • promethazine

first generation anti-histamine have anti-muscarinic effects (and hence are antiemetic)

26
Q

antiemetic muscarinic antagonists

A

Scopolamine (motion sickness)

27
Q

antiemetic cannabinoids

A

Dronabinol –> stimulate CB1 receptors

28
Q

antiemetic NK1-receptor antagonist

A

Aprepitant

29
Q

Opioid analgesics (ie morphine) and their role in emesis

A

Dual action:

  • decreases emesis by activating receptors that decrease pain transmission
  • decrease emesis by activating receptors in the CTZ
30
Q

What receptors are on the parietal cell that can cause acid secretion? (3)

A

gastrin

ACh

histamine (H2)

31
Q

magnesium hydroxide - what is its use? MOA? What SE does it have?

A

antacid – directly neutralizes the acid in the stomach

Overdose can lead to hypermagnesemia –> loss of deep tendon reflexes and respiratory paralysis

32
Q

opioid agonists

A

Loperamide

Diphenoxylate

Dronabinol

33
Q

azathioprine

A

immunosuppressive drug used to prevent relapses of ulcerative colitis

MOA: inhibits the synthesis of purines

34
Q

Aprepitant – how does it work?

A

NK = neurokinin (same family as bradykinin – mediates pain)

These antagonists aim to prevent pain-induced vomiting

Unit 6 (10 decks)

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