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Week 3 (Neuro 2) > PHARM - General Anesthesia > Flashcards

PHARM - General Anesthesia Flashcards

1
Q

what is the MOA of most general anesthetics?

what are the exceptions? and what are their MOAs?

A
  • potentiation of GABAa channel activity
    • exceptions:
      • N2O: blocks NDMA receptor
      • ketamine: blocks NMDA receptor
      • dexmedetomidine: activates a2 adrenergic receptors
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2
Q

which anesthetics have an additional MOA on top of GABA potentiation?

what is this MOA?

A

volatile agents (sevoflurane)

also enhance the activity of 2-pore K+ channels

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3
Q

what is the role of hyponotics in general anthesia?

which barbituate?

A

barbituates - methohexital, specifically

for induction of electroconculsive therapy

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4
Q

what is the role of anxiolytics in general anesthesia?

A

benzodiazepines - midazolam, specifically

can be used for preoperative sedation & seizure suppresion

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5
Q

general anesthetics come in what two routes of adminstration?

A
  • intravenous
  • inhaled
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6
Q

propofal

  • clinical use
  • advantages
  • AEs
A
  • clinical use: IV sedation (w/ no analgesia) - inducation & maintenance
  • advantages
    1. NO post-op nausea & vomitting
    • pt wakes up 8-10 min post injection w no hangover d/t
      • rapid clearance and recovery
      • low context sensitive T1/2
  • AEs: CV & respiratory depression
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7
Q

etomidate

  • clinical use
  • advantages
  • AEs
A
  • clnical use: IV sedation (w/ no analgesia) - induction, but NOT continuous infusion!
  • advantages: less CV / respiratory affects - good for unstable cardiac patients ​
  • AEs
    • nausea and vomitting
    • ​adrenocortial suppresion - no second dose
    • myoclonus
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8
Q

which two IV sedative are hyponotic agents without analgesia?

how do their properties differ?

A
  • propofal - for induction AND maintenace
    • no N&V
    • but, CV / resp depression
    • other: no hangover
  • etomaidate - for induction ONLY
    • causes N&V
    • but less CV / resp depression - good for CV unstable patients
    • other: adrenocortiosuppresion
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9
Q

ketamine

  • clinical use
  • MOA
  • advantages
  • AE/CI
A
  • clinical use: IV sedation + profound analgesia
  • MOA: blocks NDMA receptor
  • advantages:
    • profound analgesia
    • CV stimulation via indirect sympathomimetics
      • good for shock patients
  • AE: disorientation / illusions on emergenace
  • CI: in pts with ischemic heart disease
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10
Q

dexmedetomidine

  • clinical use
  • MOA
  • advantages
  • MOA
A
  • clinical use: IV sedation + mild analgesia
  • MOA: a2 receptor agonist. inhibits inhibitors of VLPO -> GABA release
  • advantages: more like physiologic sleep than other agents
  • AE: severe CV & respiratory depression - hypoTN, bradycardia
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11
Q

what is the role of opioids in general anesthesia?

A

fentanyl can be used for perioperative anesthesia

is rapid onset and causes profound analgesia

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12
Q

which IV sedatives have important CV effects and what are they?

A
  • etomidate: provides cardiovascular stability
  • ketamine: cardiovascular stimulant
  • propofal & dexmedetomidine: cardiovasculature depression
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13
Q

which IV sedative is C/I in patients with ischemic heart disease?

conversely, what is it useful for?

A

ketamine (CV stimulant)

common used for shock / severely hypotensive patients

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14
Q

which IV sedative is useful in hemodynamically unstable patients?

why?

A

etomidate

causes minimal CV or respiratory suppression

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15
Q

which IV sedative is anti-emetic?

A

propofal

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16
Q

which IV sedative is the most severe CV depressant?

A

dexmedtomidine

17
Q

the rate of induction of inhaled anesthesics depends on which four factors?

A
  1. inspired gas concentration
  2. alveolar ventilation rate
  3. pulmonary blood flow
  4. solubility - inversely
18
Q

how is the concentration of inspired anesthetic controlled?

A

by modifying the alveolar partial pressure (PP) of the gas containing the anesthetic

at equilibrium the PP in the lungs, blood and brain will all be the same, so the concentration of anesthetic in the lungs = concentation of anesthetic in the brain

19
Q

what determines the solubility of anesthesia?

how is solubility related to to the anesthesia’s rate of induction?

A
  • determined by: blood gas partition coefficient
  • is inversely related to the rate of induction
20
Q

list the induction speeds of the inhaled anesthetics from slowest to fastest

A

halothane -> isoflurane -> sevoflurane -> desflurane -> NO

  • halothane = most soluble, slowest induction
  • NO = least soluble, fastest onset
21
Q

describe the metabolism of inhaled anesthetics

A

most are not metabolized and are immediately exhaled by the lung.

volatile agents (esp halothane) undergo some hepatic metabolism

22
Q

what is MAC?

A

minimum alveolar concentration

lowest concentration of anesthetic at which 50% of patients will not remove in response to a surgical excision

the higher the potency of the anesthetic, the lower the MAC value

23
Q

which inhaled anesthetics have the lowest and highest MAC values?

what does this mean?

A
  • halothane: lowest MAC (< 10%) = highest potency
  • NO: highest MAC (> 100%) = lowest potency
24
Q

NO

  • what kind of drug
  • pharmokinetic properties
  • advantages
  • AEs
A
  • inhaled anesthetic used in combo w/ other agents to reduce their dosage requirements
  • PK properties
    • fastest induction (least soluble)
    • lowest potency (highest MAC) - why it cant be used alone*
  • advantages:
    • little affect on CV / respiratory system
    • NO malignant hyperthermia!!
  • AE: hematotoxicity - via inactivation of Vit B-12 dependent enzymes
25
Q

halogenated agents

  • what kind of drugs?
  • includes what drugs
  • pharmokinetic properties
  • AEs
A
  • inhaled anesthetics
  • includes: halothane, desflurane, sevoflurane, isoflurance methoxyflurane
  • PK properties: overall - slower induction & higher potency than NO
    • potency: halothane > isoflurance > sevoflurane > desflurane
    • induction: halothane < isoflurance < sevoflurance < desflurane
  • AE:
    • CV depression
    • malignant hyperthermia
26
Q

malignant hyperthermia

  • cause
  • presentation
  • triggers
  • treatment
A
  • cause: mutation of ryanodine receptor leads to Ca++ release from SR
  • presentation: muscle rigidity + rapid rise in body temp
  • triggers:
    • volatile anesthetics (- fluranes)
    • succinylcholine (depolarizing NMB)
  • treatment: dantrolene
27
Q

what is the treatment of malignant hyperthermia?

how does it work?

A

dantrolene

blocks release of Ca++ from the SR

28
Q

what anesthetics can be given if there is a concern for malignant hyperthermia?

A

non volatile agents - NO, propofal

29
Q

which anesthetic is especially good for inducing anesthesia?

why?

A

sevoflurane

low pungency

30
Q

which inhaled anesthetic has the most rapid onset?

A

NO

31
Q

which anesthetic is highly pungent?

what does this mean?

A

desflurance

means it is NOT good for inducing anesthesia

Week 3 (Neuro 2) (5 decks)

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