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Anesthesia Pharmacology Medications > Week 7: GI Meds > Flashcards

Week 7: GI Meds Flashcards

1
Q

Scopolamine

  1. Mechanism of action
  2. Use
  3. Side Effects
A
  1. Anticholinergic
  2. Prevention of motion sickness and PONV
  3. Sedation, cyclopegia, aniscoria, and drying of secretions -> central anticholinergic syndrome: restlessness, hallucinations, somnolence, unconsciousness
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2
Q

Metoclopramide

  1. Mechanism of action
  2. Use
  3. Key points
A
  1. Benzamide: Dopamine antagonist: stimulates GI tract via cholinergic mechanism-> increases gastric and small intestinal motility
  2. PONV, pre-operatively to decrease gastric contents in a patient that is not NPO, is obese, trauma, DM or parturients (needs 20-30 minutes to work)
  3. **DO NOT use with Parkinson’s Disease or Restless Leg Syndrome because of effects on Dopamine pathway
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3
Q

Droperidol

  1. Mechanism of action
  2. Use
  3. Key points
A
  1. Butyrophenone: effects dopamine pathway
  2. PONV (rescue or intra-op)
  3. Black box warning for long QT: need previous 12 lead
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4
Q

Dexamethasone

  1. Mechanism of action
  2. Use
  3. Key points
A
  1. Corticosteroid: mechanism not fully known
  2. PONV
  3. Synergistic effect with zofran; Caution with diabetic patients; Use low dose (4mg) for antiemetic effects
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5
Q

Ondansetron

  1. Mechanism of action
  2. Use
  3. Metabolism
  4. Dose
A
  1. 5-HT3 receptor antagonist: receptors in GI tract (vagus) and Brain (CTZ)
  2. Nausea
  3. Metabolized in liver, excreted in urine and stool
  4. 4mg IV or 8mg oral dis

**Half life is 4 hours and is BETTER at the end -> give at the end of the case

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6
Q

Granisetron

  1. Mechanism of action
  2. Use
  3. Metabolism
  4. Dose
A
  1. 5-HT3 receptor antagonist: receptors in GI tract (vagus) and Brain (CTZ)
  2. Nausea
  3. Metabolized in liver, excreted in urine and stool
  4. 1mg
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7
Q

Palenosetron

  1. Mechanism of action
  2. Use
  3. Metabolism
  4. Dose
    * *Advantages
A
  1. 5-HT3 receptor antagonist: receptors in GI tract (vagus) and Brain (CTZ)
  2. Nausea
  3. Metabolized in liver, excreted in urine and stool
  4. .075 mg, .25 mg
  • *Newest, greatest affinity for 5HT3, WORKS FOR 72 hours (give at beginning of case)
  • **NO QT prolongation
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8
Q

Promethazine

  1. Mechanism of Action
  2. Use
  3. Cons
A
  1. Histamine Receptor Antagonist
  2. Rescue for nausea or for motion sickness due to high number of histamine receptors in vestibular center
  3. Sedating, Drying

**BAD if infiltrates in IV

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9
Q

Diphenhydramine

  1. Mechanism of Action
  2. Pros
  3. Cons
A
  1. Histamine Receptor Antagonist
  2. Rescue for nausea or for motion sickness due to high number of histamine receptors in vestibular center
  3. Sedating, Drying
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10
Q

Dimenhydrinate

  1. Mechanism of Action
  2. Pros
  3. Cons
A
  1. Histamine Receptor Antagonist
  2. Rescue for nausea or for motion sickness due to high number of histamine receptors in vestibular center
  3. Sedating, Drying
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11
Q

Aprepitant

  1. Mechanism of Action
  2. Pros
  3. Cons
A
  1. Neurokinin-1 antagonist
  2. Lasts up to 48 hours, as effective as zofran
  3. Must be taken PRE-OP (3 hrs before anesthesia), expensive and not covered by insurance, not a rescue
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12
Q

Propofol Key Points

A
  • Subhypnotic doses have been shown to have antiemetic effect for PONV
  • Mostly due to helping decrease use of volatiles (risk factor for PONV)
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13
Q

Clonidine

  1. Use
  2. Mechanism
A
  1. PONV
  2. Alpha 2 Agonist: Decreases opioid need, decreased PONV risk VS. direct effect??
    * *Use with dexmedetomidine for a weak short lived antinausea effect
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14
Q

Midazolam

  1. Use
  2. Timing
A
  1. Some antiemetic effect

2. Can be given at end of case to decrease PONV -> subhypnotic dose during case was as effective as propofol use

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15
Q

Gabapentin

  1. Use/Mechanism
  2. Dose/Timing
A
  1. PONV due to opioid sparing effect

2. 600-800mg 2 hours pre-op

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16
Q

Sodium Bicarb

  1. Mechanism of action
  2. Key points
A
  1. Increases pH (neutralizes HCl)
  2. -Caution in renal patients
    - Neutralization increases gastric motility and LES tone
17
Q

Milk of Magnesia

  1. Mechanism of action
  2. Key points
A
  1. Neutralizes HCl to increase pH
  2. **Unique to MOM = NO ACID REBOUND
    - prominent laxative effect
    - systemic absorption can lead to neurologic, neuromuscular and cardiac effects
18
Q

Ca++ Carbonate

  1. Mechanism of action
  2. Key points
A
  1. Neutralizes HCl
  2. Acid rebound
    - Can increase plasma Ca++ levels transiently
    - Can cause hypophosphatemia
19
Q

Aluminum Hydroxide

  1. Mechanism of action
  2. Key points
A
  1. Neutralizes HCl

2. Acid rebound; Minimal systemic absorption

20
Q

Na+ Citrate

  1. Mechanism of action
  2. Key points
A
  1. Neutralizes HCl

2. Non-particulate (aka clear)-> less risk of aspiration

21
Q

Chlorpheniramine and Diphenhydramine

  1. Mechanism of action
  2. Side effects
A
  1. First generation selective H1 antagonist: act on muscarinic cholinergic and alpha adrenergic receptors
  2. Dry mouth, blurred vision, tachycardia, long QT, Sedation
22
Q

Hydroxyzine

  1. Mechanism of action
  2. Side effects
A
  1. First generation selective H1 antagonist: act on muscarinic cholinergic and alpha adrenergic receptors
  2. Dry mouth, blurred vision, tachycardia, long QT, Sedation
23
Q

Loratidine

  1. Mechanism of action
  2. Advantages
A
  1. Second generation highly selective H1 antagonist: act on muscarinic cholinergic and alpha adrenergic receptors
  2. NO CNS effects
24
Q

Arivastine

  1. Mechanism of action
  2. Advantages
A
  1. Second generation highly selective H1 antagonist: act on muscarinic cholinergic and alpha adrenergic receptors
  2. NO CNS effects
25
Q

Azelastine

  1. Mechanism of action
  2. Advantages
A
  1. Second generation highly selective H1 antagonist: act on muscarinic cholinergic and alpha adrenergic receptors
  2. NO CNS effects
26
Q

Cimetidine

  1. Mechanism of Action
  2. Use
  3. SE
A
  1. H2 antagonist: selective, reversible inhibition of H2 receptor mediated secretion of hydrogen ions from parietal cells
  2. Prevent aspiration in at risk individuals (not routine for everyone)
  3. HA, somnolence, confusion, bradycardia, hypotension

**Many drug interactions

27
Q

What drugs increase Cimetidine plasma concentrations?

A
  • Warfarin, propranolol, nifedipine, lidocaine, meperidine, procainamide
    (even more)
28
Q

Famotidine

  1. Mechanism of Action
  2. Use
  3. SE
A
  1. H2 antagonist: selective, reversible inhibition of H2 receptor mediated secretion of hydrogen ions from parietal cells
  2. Prevent aspiration in at risk individuals (not routine for everyone)
  3. HA, somnolence, confusion, bradycardia, hypotension
29
Q

Ranitidine

  1. Mechanism of Action
  2. Use
  3. SE
A
  1. H2 antagonist: selective, reversible inhibition of H2 receptor mediated secretion of hydrogen ions from parietal cells
  2. Prevent aspiration in at risk individuals (not routine for everyone)
  3. HA, somnolence, confusion, bradycardia, hypotension
30
Q

Omeprazole

  1. Mechanism of Action
  2. Use
  3. SE
A
  1. Proton pump inhibitor: block hydrogen movement to suppress stomach acid
  2. PONV
  3. Crosses BBB so can cause HA, agitation, confusion; also bacterial overgrowth due to acid suppression; Calcium leaching (should supplement)
31
Q

Pantoprazole

  1. Mechanism of Action
  2. Use
  3. SE
A
  1. Proton pump inhibitor: block hydrogen movement to suppress stomach acid
  2. PONV
  3. Crosses BBB so can cause HA, agitation, confusion; also bacterial overgrowth due to acid suppression; Calcium leaching (should supplement)
32
Q

Lansoprazole

  1. Mechanism of Action
  2. Use
  3. SE
A
  1. Proton pump inhibitor: block hydrogen movement to suppress stomach acid
  2. PONV
  3. Crosses BBB so can cause HA, agitation, confusion; also bacterial overgrowth due to acid suppression; Calcium leaching (should supplement)

Anesthesia Pharmacology Medications (9 decks)

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