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Pharmaco > Gastro-intestinal > Flashcards

Gastro-intestinal Flashcards

1
Q

What is the mechanism of action of antacids (= AlOH, CaCO3, MgOH)

A

Decrease pepsin activity, bind to bile acids in the stomach, stimulate PGE2 synthesis.
Likely don’t have a strong enough buffering capacity to truly decrease the pH.

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2
Q

How does the efficiency of H2 antagonists / proton pump inhibitors change over time?

A
  • H2 antagonists: efficiency decreases because of tolerance within 3 days
  • Proton pump inhibitors: efficiency increases over the first 2-5 days because extra proton pumps are synthesized initially and need to be blocked as well + PPIs inhibit cytochrome P450 (-> decreased metabolism)
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3
Q

Why is the co-administration of H2 antagonists and PPIs not recommended

A

PPIs need to be in an acidic environment to inhibit the proton pump

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4
Q

Do PPIs / H2 antagonists need to be tapered

A

PPIs should be tapered if administered for > 3-4 weeks

H2 antagonists should be tapered (tolerance develops early)

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5
Q

Name examples of drugs whose absorption will be decreased by the use of PPIs

A
  • Antifungals (except liquid itraconazole and fluconazole)
  • Mycophenolate
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6
Q

Mechanism of action of cyproheptadine

A

5-hydroxytryptamine (5-HT2) antagonist & anti-histamine

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7
Q

Mechanism of action of mirtazapine

A

5-HT-2C receptor antagonist (-> blocks anorexic stimuli) + H1-receptor antagonist (histamine decreases appetite)

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8
Q

How frequently should mirtazapine be dosed in otherwise healthy cats? In dogs? What can prolong its half life?

A

Daily in healthy cats, potentially twice daily in dogs

Half life prolonged by older age, kidney disease, liver disease

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9
Q

Name 3 appetite stimulants

A
  • Cyprohepatdine (5-HT agonist, H1 antagonist)
  • Mirtazapine (5-HT-2C antagonist, H1 antagonist)
  • Capromorelin (ghrelin receptor agonist)
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10
Q

Absorption / metabolism and mechanism of action of PPIs

A
  • Absorbed in the duodenum (can be lysed by gastric acidity so better to give SQ initially or with bicarbonate / in enteric-coated formulation)
  • First-pass hepatic metabolism
  • Part of the drug not metabolized -> concentrated in parietal cells ; activated in acidic environment -> irreversible inhibition of H+/K+ transporter (proton pump)
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11
Q

Mechanism of action of sucralfate

A

Sucrose + aluminum hydroxide

Binds to epithelial cells in acidic environment, mostly at the base of erosions / ulcers -> physical barrier against pepsin and bile acids + stimulates local production of prostaglandins and epidermal growth factor

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12
Q

Name 1 competitive and 1 non-competitive inhibitor of gastric acid secretion

A
  • Competitive: H2-receptor antagonists
  • Non-competitive: PPIs
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13
Q

What H2 receptor antagonist causes marked inhibition of cytochrome P450 enzymes

A

Cimetidine

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14
Q

Mechanism of action of misoprostol

A

Prostaglandin E1 analog ->stimulates mucus secretion and bicarbonate secretion, increases gastric mucosal blood flow + inhibits H+ secretion from parietal cells (in response to food, gastrin, histamine)

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15
Q

Mechanism of action of maropitant and its different effects

A

Neurokinin 1 inhibitor -> blocks actions of substance P in CNS and peripherally (GI tract)

-> antiemetic
-> other: antitussive, antiinflammatory, neuroptotectant, hepatoprotectant, analgesic (visceral pain), MAC reducer in anesthesia

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16
Q

Mechanism / sites of action of ondansetron

A

5-HT3 antagonist

-> inhibits 5-HT3 receptors peripherally (in gut, responsible for vagal afferent input) and centrally (in CRTZ and medullary vomiting center)

17
Q

Mechanism of action of metoclopramide

A
  1. Dopaminergic D2 receptor antagonist:
    - in the gut -> increased motility
    - in CRTZ -> decreased vomiting
  2. 5-HT3 receptor antagonist:
    - in CRTZ -> decreased vomiting
  3. 5-HT4 receptor agonist:
    - in the gut -> increased motility
  4. +/- muscarinic receptor antagonist
18
Q

What H2 receptor antagonist has a pro-motility effect? By what mechanism?

A

Ranitidine

Acetylcholinesterase inhibitor

19
Q

What promazine derivatives can be used as antiemetics? What is their mechanism of action? Side effects?

A

Chlorpromazine, prochlorperazine

Anti-dopaminergic and anti-histamine in CRTZ (+/- medullary vomiting center)

Also alpha-adrenergic antagonists (same as acepromazine) -> can cause hypotension
+ can cause sedation

20
Q

What anticholinergic agent could be used as an antiemetic

A

Aminopentamide

21
Q

What sedative / anesthetic agents could have anti-emetic properties

A
  • Opioids (can be both emetic and anti-emetic ; butorphanol shown to prevent vomiting)
  • Propofol
22
Q

What are the different types of pro-kinetic drugs and their preferential sites of actions in the GI tract

A
  1. 5-HT4 serotoninergic agonists (cisapride)
    -> lower esophageal sphincter, stomach, small intestine, colon
  2. Motilin agonists (eyrthromycin)
    -> lower esophageal sphincter, stomach, small intestine +/- colon (mostly in dogs)
  3. Cholinomimetic drugs (true cholinomimetic = betanechol / acetylcholinesterase inhibitor = ranitidine)
    -> diffuse GI for betanechol, mostly stomach +/- colon for ranitidine
  4. Metoclopramide = D2 dopaminergic antagonist and 5-HT4 serotoninergic agonist + may increase sensitivity of small intestinal smooth muscle to ACh
    -> LES, stomach, duodenum
23
Q

Which GI drug can moderately reduce MAC of sevoflurane during GA?

A

Maropitant

24
Q

What is an adverse effect of metoclopramide when overdosed? Which group of patients is at risk?

A

Extrapyramidal signs (behaviour changes, apparent hallucinations, hyperactivity…)

Patients with renal dysfunction (excreted by kidneys)

25
Q

True or false: Cisapride can be used to improve esophageal motility

A

False: ineffective on striated muscle

26
Q

Which pro kinetic stimulates motilin receptors?

A

Erythromycin

27
Q

Between metoclopramide and cisapride, which is the most effective?

28
Q

Other than its gastroprotectant effects, what is another property of misoprostol?

A

Enhances colonic motility

29
Q

For each of the following GI recpetors, indicated which medication acts on it and whether it has an agonist or antagonist effect:

  1. 5 HT2
  2. 5 HT2c
  3. 5 HT3
  4. 5 HT4
  5. H1
  6. H2
  7. H+ K+ - ATPAS
  8. NK-1
  9. Muscarinic
  10. Motilin receptor
A
  1. 5 HT2 –> Cyproheptadine - ANTagonist
  2. 5 HT2c –> Mirtazapine - ANTagonist
  3. 5 HT3 –> Metoclopramide & ondansetron - ANTagonist
  4. 5 HT4 –> cisapride - agonist
  5. H1 –> Mirtazapine - ANTagonist
  6. H2 –> famotidine - ANTagonist
  7. H+ K+ - ATPase –> PPI - ANTagonist
  8. NK-1 –> Maropitant - ANTagonist
  9. Muscarinic –> Bethanecol - agonist
  10. Motilin receptor –> erythromycin - agonist

Pharmaco (7 decks)

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