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23 spring anesthesia > Test 1: 10 + 11: injectable inductions > Flashcards

Test 1: 10 + 11: injectable inductions Flashcards

1
Q

CNS sites of action of anesthetics

A

cerebral cortex
reticular activating system

thalamus
substantia nigra
vestibular system
cerebellum
spinal cord

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2
Q

cellular site of action of anesthesia

A

interfer with:

neuotransmitter release
neurotransmitter receptor binding
postsynaptic membrane potential

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3
Q

molecular site of action of anesthetics

A

Classic: propofol, alfaxalone, Etomidate
sedation no analgesia
bind to membrane bound ion channels
allows GABA to attaches to GABA receptor longer and allows Cl into the cell

Dissociative: Ketamine,Tiletamine
intense analgesia, light sedation, catalepsy
block NMDA receptor= inhibitory to cell

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4
Q

what are some rapidly acting anesthetics

A

(Barbiturates (Thiopental))
Phenols (Propofol)
Steroids (Alfaxalone)
Imidazoles (Etomidate)
Cyclohexanones (Ketamine, Tiletamine)

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5
Q

what are some slower acting anesthetics

A

potent opioids

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6
Q

classical injectable anesthetics works by

A

bind to GABA receptor and increase GABA binding, leading to longer opening and Cl into the cell

allosteric modulation of the GABA A receptor

synergism with benzodiazepine

classic injectables: thioental, propofol, alfaxalone, amidate (etomidate)

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7
Q

what are some dissociative anesthetics

A

ketamine
tiletamine

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8
Q

how do dissociate anesthetics work

A

cyclohexanones like ketamine and tiletamine

block NMDA receptors and prevent binding of glutamate or glycine

this stops the AP

causes analgesia and anesthesia

ketamine needs to work with other drugs to cause anesthesia

glutamate is an excitatory neurotransmitter: binds to NMDA, Kainate or AMPA receptors and cause K out and Na in

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9
Q

most anesthetics are lipophilic how does this effect distribution in the body

A

will go to brain and viscera first and cause sedation

but then levels in brain drop as drugs are redistributed into the fat

patient wakes up, but drug still in system

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10
Q

— is a phenol anesthetic

A

propofol

causes depression of the CNS activity: sedation→hypnosis →anesthesia

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11
Q

propofol has a — onset and a — recovery with —

A

rapid
rapid
without residual CNS depression

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12
Q

non hypnotic CNS effects of propofol

A
  • decreases cerebral blood flow, intracranial pressure and cerebral metabolic rate or consumption of oxygen
  • antiemetic
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13
Q

adverse effects of propofol on the respiratory system

A

respiratory depression (↓ tidal volume and ↓RR)
bronchodilation
inhibition of laryngeal reflexes- need to intubate

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14
Q

adverse effects of propofol on CV system

A

hypotension
* centrally (↓SYMP vasomotor tone)
* peripherally (negative inotropic effect and direct vasodilation)

NO change in HR

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15
Q

in 10 % of dogs and cats that are given propafol what adverse reaction can happen

A

excitaory- Limb paddling, nystagmus, muscle twitching, myoclonus, and opisthotonus

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16
Q

pts with hypoalbuminemia will need to — the dose of propofol

A

decrease

97-99% of propofol binds to albumin - if there is less albumin to bind to then there is increased free propofol- ↑ effects

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17
Q

propofol is metabolized in the

A

kidneys
lungs
liver

(can use med in pt with liver failure)

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18
Q

what animals can have difficultly metabolizing propofol

A

sight hounds- have problem with liver metabolism (hydroxylation via CYP450)

cats- can’t metabolize drug by glucuronide conjugation, but can still metabolize in the kidney and lungs →heinz body formation

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19
Q

when not to use propofol

A

Patients with cardiovascular dysfunction
* Cardiac failure (low cardiac contractility)
* Hypovolemia
* Hypotension

Patients with sepsis/systemic infections

Cats with anemia→heinz bodies

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20
Q

how to give alfaxalone

A

IV or IM

rapid onset, bolus or CRI

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21
Q

effects of alfaxalone

A

NO analgesia

suppression of brain activity: Sedation → Hypnosis → General anesthesia

22
Q

central excitation during recovery can occur in cats with the use of — sedation

A

alfaxalone

this does not happen if you combine with sedatives and/or analgesics (opioids)

23
Q

— is an effective IM sedation for non-cooperating animals or animals at higher risk of anesthetic complications

A

alfaxalone

24
Q

adverse effects of alfaxalone on respiratory system

A

less effects than propofol when injected slowly

causes central respiratory depression (↓ tidal volume, and ↓RR)

↓ swallow reflex- need to intubate

can cause excitatory signs during recovery if not combined with sedative and/or analgesics

25
Q

Adverse effects of alfaxalone on the CV system

A

unlike propofol, minimal side effects

26
Q

metabolism of alfaxalone

A

liver

can be used in sighthounds and cats, unlike propofol

propofol causes the formation of heinz bodies in cats

27
Q

when not to use alfaxalone

A

animals with respiratory problems ( alfaxalone causes ↓RR)

animals you can not intubate- (alfaxalone ↓ swallowing reflex, needs to be intubated)

animals with heart disease (even though alfaxalone has minimal effect on CV system)

28
Q

— is a ultra short acting anesthetic with high therapeutic index

A

etomidate (imidazole)

29
Q

nonhypnotic CNS effects of Etomidate

A

↓EEG activity
↓ cerebral blood flow- direct cerebral vasoconstriction
↓ intracranial pressure and cerebral metobolic rate or consumption of O2

30
Q

onset of etomidate

A

CNS depression in < 20 sec (ultra rapid onset)

NO Pain relief

31
Q

adverse effects of etomidate on respiratory system

A

none or minimal

32
Q

adverse effects of etomidate on CV system

A

none or minimal

33
Q

adverse effects of etomidate

A

Inhibition of adrenal steroid genesis (11β- hydroxylase)

Hemolysis due to high osmolality of solution

NO respiratory or CV effects

occasional excitatory effects: myoclonus, vomiting, opisthotonus

34
Q

etomidate distribution and elimination rates

A

rapid onset, rapid peak CNS 3 mins

elimination 3 hrs

35
Q

do you need to decrease dose of etomidate if you have hypoalbuminemia?

A

No only binds 76%

unlike propofol which binds 97-99%

36
Q

how is etomidate metabolized

A

liver
plasma ester hydrolysis

renal elimination of metabolities

37
Q

when to use etomidate

A

pts with heart failure, shock or sepsis

pts with increased intracranial pressure or seizures

has no CV or respiratory effects unlike propofol or alfaxalone

38
Q

when not to use etomidate

A

addisons (↓ adrenal function)
severe stress syndrome

etomidate causes the ↓ production of steroids

39
Q

effect of cyclohexanones

A

dissociative anesthesia

intense analgesia
light sleep
amnesia
catalepsy- rigid muscles

cyclohexanones cause dissociative anesthesia: ketamine, tiletamine

40
Q

how does ketamine work

A

block NMDA glutamate receptors → analgesia and anesthesia

block nicotonic ACh receptors: (excitatory receptors)

interact with central opioid receptors, monoaminergic (NA, DA, serotonin) receptors and muscarinic ACh receptors

also block NE re-uptake
block voltage gated Ca channels in the heart
block peripheral nerve conduction

41
Q

why dissociate anesthesia for ketamine

A

Selective suppression of thalamoneocortical projection system → disconnection of thalamoneocortical from limbic and other subcortical areas

42
Q

clinical signs of dissociative anesthesia

A
  • Loss of consciousness despite neuronal activity outside neo-cortex
  • Catalepsy (catatonia)
  • Maintenance of protective reflexes
  • Skeletal muscle movements

ketamine + tiletamine

43
Q

adverse effects of ketamine on CNS

A

increased EEG activity
increased cerebral blood flow (cerebral vasodilation)
emergence delirium(dysphoria) → violent recovery (horses)

opposite effect of classic anesthetics

cyclohexanones cause dissociative anesthesia: ketamine, tiletamine

44
Q

adverse effect of ketamine on respiratory system

A

mild decrease in RR and tidal volume

cause apneustic, shallow and irregular breathing patterns, breath holding at peak inhale

bronchodilation

cyclohexanones cause dissociative anesthesia: ketamine, tiletamine

45
Q

adverse effects of ketamine on CV system

A

indirect stimulation: ↑ SYMP and ↓NE reuptake causes ↑HR, ↑CO and ↑MAP

Can cause direct negative inotropic and vasodilatory actions in old or CV compromised patients

pro-arrhythmic

46
Q

adverse effect of ketamine on digestive system

A

↑ salivation: may make intubation harder

47
Q

adverse effects of ketamine on neuromusclar system

A

causes increased muscle ridigity- bad in pts with bone breaks

decreased nerve conduction

cyclohexanones cause dissociative anesthesia: ketamine, tiletamine

48
Q

metabolism of ketamine

A

Extensive hepatic (CYP 450) metabolism
* N-demethylation to norketamine (20-30 % rest activity)
* then forms inactive compounds that go through glucuronide conjugation

cats no metabolism to inactive compounds

49
Q

when not to use ketamine

A

Animals with cardiovascular dysfunction
* Cardiac failure (low cardiac contractility)
* Decompensated shock (ketamine causes vasodilation)
* Tachyarrhythmias

Animals with pheochromocytoma
Animals with hyperthyroidism
Animals with CNS excitatory signs (ketamine causes dysphoria)

50
Q

Tiletamine can cause severe— therefore it is combined with zolazepam

A

catalepsy and convulsions

cyclohexanones cause dissociative anesthesia: ketamine, tiletamine

23 spring anesthesia (40 decks)

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