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Cognition & Senses - wk 3 > anesthetic drugs (injectible) > Flashcards

anesthetic drugs (injectible) Flashcards

1
Q

what are the elements of the anesthetic state

A
  • unconsciousness (hypnosis)
  • amnesia
  • analgesia (not same as antinociception) (inhibition but may not be sippression or reflex responses to noxious stimulation)
  • immobility (skeletal muscle relaxation)
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2
Q

what are the 4 stages of anethesia

A
  1. analgesia
  2. excitement
  3. surgical anesthesia
  4. medullary paralysis
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3
Q

CNS sites of action

A
  • cerebral cortex
  • reticular activating system
  • others (thalamus, substantia nigra, vestibular system, cerebellum, spinal cord)
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4
Q

cellular sites of action

A

interference with synaptic mechanisms

  • NT synthesis
  • NT release
  • NT clearance
  • NT receptor binding
  • postsynaptic membrane potential
  • inhibition of axonal nerve impulse conduction
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5
Q

molecular sites of action: membrane protein channels

A

interaction of anesthetics with specific NT receptor proteins (GABAa receptor)

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6
Q

injectable anesthetics in clinical use

A
  • barbituates (thiopental)
  • phenols (propofol)
  • steroids (alfaxalone)
  • imidazoles (etomidate)
  • cyclohezanones (ketamine, tiletamine)
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7
Q

what is the main molecular mechanism of action of “classical” injectable anethetics

A
  • allosteric modulation of the GABAa receptor (increase affinity)
  • synergism with benzodiazepines
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8
Q

what are the main mechanims of action of dissociative anethetics

A
  • blockade of the NMDA receptor at subanesthetic dose (use-dependent block and closed channel block)
  • decrease in central glutamatergic activity -> analgesia and anesthesia
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9
Q

what is the common pharmacokinetic feature of all highly lipophilic injectable anesthetics

A

redistribution of drug from CNS to peripheral tissues causes the animal to wake up (needs to go below threshold)

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10
Q

what are phenols

A
  • sedative-hypnotic drug unrelated to barbituates
  • risk of microbial growth in the vehicle (intralipid)
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11
Q

gradual depression of CNS activity with phenols

A

titration of effect possible by increasing the dose: sedation -> hypnosis -> anesthesia

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12
Q

general anesthesia pharmacologic effects of phenol

A
  • rapid onset after IV bolus injection
  • rapid recovery without residual CNS depression
  • maintenance with repeated IV boluses or CRI
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13
Q

IV, long-term sedation pharmacologic effects of phenols

A

low risk for drug accumulation

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14
Q

non-hypnotic CNS effects of phenols

A
  • decrease in CBF, ICP, CMRO2
  • antiemetic effects
  • none or no clinically relevant analgesic effect per se
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15
Q

what systems effects are most severe upon administration at > 1 mg/kg/min

phenol

A
  • respiratory
  • cardiovascular
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16
Q

respiratory system adverse effects

phenol

A
  • central respiratory depression (Vt decreases, RR decreases)
  • bronchodilation
  • inhibition of laryngeal reflexes
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17
Q

cardiovascular system adverse effects

phenol

A
  • hypotension
  • centrally (sympathetic vasomotor tone decreases)
  • peripherally (neg. inotropic effect & direct vasodilation)
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18
Q

excitatory effects (transient)

phenol

A
  • 10% of dogs and cats
  • limb paddling, nystagmus, muscle twitching, myoclonus, and opisthotonus
19
Q

why is there reduced elimination in cats

A

reduced conjugation capacity -> oxidative injury to feline RBCs -> Heinz body formation

20
Q

using propofol with caution

A
  • patients with cardiovascular dysfunction
  • patients that cannot be ventilated b/c not intubated
  • patients with sepsis/systemic infections
  • cats with anemia
21
Q

combining propofol with other preanethetic drugs

A

increases induction dose and makes it safer

22
Q

what is neurosteroid: Alfaxalone

A
  • water soluble compound suitable for IM injection
  • CNS depressant and hypnotic effects as origionally described for progesterone and its congeners in rats
23
Q

biotransformation and elimination of phenols

A
  • extensive hepatic matabolism
  • hydroxylation via CYP450 system
  • glucuronide conjugation
24
Q

main effects of alfaxalone - progressive suppression of brain activity

A
  • increasing doses of alfaxalon causes: sedation -> hyposis -> general anesthesia
  • none or no clinically relevant analgesic effect per se
25
Q

main effects of alfaxalone as a general anethetic

A
  • rapid onset of effect after IV bolus injection
  • relatively short anesthetic effect
  • prolongation of anesthesia with repeated bolus administration or with CRI
  • however, not rarely central excitation during recovery, particuarly in cats
26
Q

main effects of alfazalone - IM sedation

A
  • effective to sedate non-cooperating animals or animal patients at higher risk of anesthetic complications such as trauma patients, cat with FUS, anxious animals
  • effective muscle relaxation when combined with benzodiazepines
27
Q

adverse effects of alfaxalone

A

respiration

  • centrally mediated depression (Vt decreased, RR decreased)
  • less than with propofol, if injected slowly IV to effect
  • suppression of swallow reflexes (-> intubate animal)
  • excitatory signs in recovery period if: (NOT combined with sedatives and/or analgesics/opioids)

cardiovascular system

  • unlike, propofol, somewhat lesser side effects
28
Q

pharmacokinetics of alfaxalone

A
  • fast hepatic metbolism
  • no risk for accumulation in cats or sighthounds
29
Q

principle pharmacologic effect of imidazoles (etomidate)

A
  • ultra-rapid onset of CNS depression with hypnosis in < 20sec
  • no antionociception/no analgesic effect per se
  • non-hypnotic CNS effects (decrease in EEG activity, decrease in CBF - direct cerebral vasoconstriction, decrease in ICP and CMRO2)
30
Q

adverse effects of etomidate

A
  • none or minimal respiratory and cardiovascular effects
  • occasionally CNS excitatory effects
  • inhibition of adrenal steroid genesis (11B-hydrozylase) - responsible for cortisol production
  • hemolysis due to high osmolality of solution
  • pain upon IV injection
31
Q

pharmacokinetics of etomidate

A
  • 76% plasma albumin binding
  • ~25% total plasma protein binding
  • incomplete placental transfer
  • fast decline in fetal plasma levels
32
Q

biotransformation and elimination of etomidate

A
  • extensive hepatic metabolism
  • extrahepatic metabolism (plasma ester hydrolysis)
  • renal elimination of metabolites
33
Q

use of etomidate in clinical practice

A

cautious use in patients with:

  • adrenal insufficiency (addison’s disease)
  • severe stress syndrome
34
Q

cyclohezanones produce anethesia-like state called:

A

“dissociative anesthesia”

  • intense analgesia, light sleep, amnesia and catalepsy
35
Q

ketamine is a racemic mixture of two optical isomers:

A
  • S(+) isoform 3-4 times more potent than R(-)
  • S(+) isoform twice as long active as R(-)
  • dysphoria: S(+) < R(-)
36
Q

what are the principle pharmacologic effects of ketamine

A

dissociative anesthesia

  • selective suppression of thalamoneocortical projection system -> disconnection of thalamoneocortical from limbic and other subcortical areas

analgesia

  • at subanesthetic doses
37
Q

what are the typical features of dissociative anethesia

A
  • loss of consciousness despite neuronal activity outside neocortex
  • catalepsy
  • maintenance of protective reflexes
  • skeletal muscle movements
38
Q

what are the CNS adverse effects of ketamine

A
  • increased EEG activity associated with myoclonus and seizure-like activity
  • increase in CBF (cerebral vasodilation)
  • emergence delirium (dysohoria)
39
Q

respiratory adverse effects of ketamine

A
  • mild, transient decrease in RR and Vt
  • apneustic, shallow, and irregular breathing pattern
  • breath-holding at peak of inspiration
  • bronchodilation
40
Q

cardiovascular adverse effects of ketamine

A
  • indirect stimulation -> increase HR, CO, MAP
  • direct negative inotropic and vasodilatory action -> relevant in cases of compromised CVS
  • pro-arrhythmogenic effects
41
Q

digestive system adverse effects of ketamine

A

increased salivation

42
Q

neuromuscular system adverse effects of ketamine

A
  • increased muscle rigidity (catatonia)
  • decreased nerve conduction
43
Q

biotransformation and elimination of ketamine

A
  • extensive hepatic (CYP450) metabolism
  • N-demethylation to norketamine (20-30% rest activity)
  • exception cat: no metabolism to inactivate compounds

Cognition & Senses - wk 3 (13 decks)

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