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RUSVM Pharmacology > Sedative And Anesthetics > Flashcards

Sedative And Anesthetics Flashcards

1
Q

______________induces a state of behavioral change where anxiety is relieved and the patient is relaxed, but aware of their surroundings

A

Tranquilizer (neuroleptic)

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2
Q

____________ induces a state characterized by CNS depression and drowsiness, decreased awareness of surroundings

A

Sedative

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3
Q

__________ induces sleep

A

Hypnotic

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4
Q

_____________ attenuated nocicpetive input leading to reduced rain

A

Analgesic

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5
Q

______________ decreases central sensitization to pain

A

Antihyperalgesics

do not block transmission of stimulus

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6
Q

_______________ diminishes ability to perceive pain

A

Antinocipcetion

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7
Q

____________ induces analgesia and stupor bordering on anesthesia

A

Narcotic

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8
Q

________________ causes analgesia and amnesiac state produced by admin of a neuroleptic and narcotic

A

Neuroleptanalgesia

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9
Q

________________ are drugs given before a medical, surgical, or invasive produced to induce sedation, analgesic, ad relieve anxiety

A

Premedication

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10
Q

What makes up the blood brain barrier?

A

Tight capillary endothelial junctions
Glial cells
Active transport for removal of organic acids or bases
CSF into venous drainage

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11
Q

What re the excitatory neurotransmitters?

A 
Glutamate (NMDA receptor) 
ACh 
Epi/ Norepi 
Dopamine
Serotonin 
Histamine
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12
Q

What are the inhibitory neurotransmitters?

A

GABA

Glycine (spinal cord)

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13
Q

Neuroleptics (tranquilizer) can be classified into

A

Phenothiazine derivative

Benzodiazepine derivative

Butyrophenone derivative

A2 agonists

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14
Q

What are the main effects of neuroleptics

A

Sedation and hypnosis
Emotional quietness
Dissociation from surroundings

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15
Q

What are the only group of neuroleptics to have analgesic effects?

A

A2 agonists

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16
Q

T/F: none of the neuroleptics have true anesthetic effects

A

T

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17
Q

What is the most common phenothiazine?

A

Acepromazine

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18
Q

What is the MOA of phenothiazines?

A

Competitively antagonize excitatory dopamine receptors in the CNS

Inhibit vomiting
Prolactin release
Muscle relaxation

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19
Q

How are phenothiazines administered?

A

IV, IM,SQ, PO

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20
Q

What is the oral bioavailability of phenothiazines in dogs?

A

Low

About 20%

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21
Q

Where are phenothiazines metabolized

A

Liver, excreted in urine

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22
Q

What effects do phenothiazines have in the CNS?

A

Sedation (dopamine receptor)
Decreased spontaneous motor activity
Hypothermia and hyperprolactinemia (hypothalamus)
Anti-emetic (alpha 2 receptor)

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23
Q

What are the effects of phenothiazines on the CVS?

A

Block alpha 1 receptor

Vasodilation-> hypotension ‘epinephrine reversal’

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24
Q

What breeds are more susceptible to the CVS effects of phenothiazines

A

Boxers/brachydephalics

Large breed dogs and sighthounds

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25
Q

What effects do phenothiazines have on the respiratory system

A

Minimal at therapeutic dose

Depression at hight dose or with other opioids

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26
Q

What effects do phenothiazines have on skeletal muscle

A

Moderate relaxation

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27
Q

What are the precautions to using phenothiazines?

A

Boxers/brachycephalic/large dog/sighthounds.MDR1 mutations

When vasodilation is contraindicated

Stallions: penile prolapse
Cattle: not approved ->ruminal regurgitation
Aggressive dog: increase aggression
Excited animals : reduced sedative effect

Toxins: extrapyramial effect
Liver disease: hepatotoxic
Concurrent epinephrine use

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28
Q

What two phenothiazines are used as anti-emetics

A

Prochlorperazine and chlorpromazine

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29
Q

What phenothiazine is used as a antihistamine

A

Trimeprazine

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30
Q

What are the benzodiazepines

A

Agonists:
Diazepam
Midazolam
Alprazolam

Antagonist:
Flumazenil

Partial agonist:
Imepitoin

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31
Q

What is the MOA of benzodiazepines?

A

Bind and active benzodiazepine binding site on GABA receptor to cause hyperpolarization of neurons

(GABA is main inhibitory NT in CNS)

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32
Q

What is the distribution of benzodiazepine

A

Lipid soluble
Wide distribution
Cross BBB
Protein bound

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33
Q

What benzodiazepine is given IV

A

Diazepam

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34
Q

What benzodiazepine is given IM

A

Midazolam

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35
Q

What benzodiazepine is given orally

A

Alprazolam (diazepam has short duration and can cause hepatic necrosis in cats)

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36
Q

What are the clinical uses for benzodiazepines?

A

Anxiolytics (behavioral modifiers)

Anticonvulsant

Premedication (combine with other agents)

Sedation (not reliable on its own!) -> most reliable in ruminants

Muscle relaxation -> central effect but short lived

Appetite stimulation

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37
Q

What is used for specific reversal of benzodiazepines?

A

Flumazenil

Competing antagonist on GABA receptor

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38
Q

What are contraindications to using benzodiazepine

A

CAT: hepatotoxicity with oral diazepam

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39
Q

What are precautions to use in benzodiazepine ?

A

Horse: muscle fasciculations seen (ataxia at high dose)

Paradoxical excitement (fear/aggressive animals)

Propylene glycol (diazepam injection-> pain IM and hypotension IV

Pregnancy -teratogenic

Hepatic and renal disease - altered metabolism and excretion

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40
Q

T/F: acepromazine has tranquilizer going and analgesic effects

A

F

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41
Q

What is the most important cardiovascular side effect of acepromazine ?

A

Hypotension

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42
Q

Why is oral diazepam contraindicated in cats

A

Hepatotoxicity

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43
Q

What are the A2 agonist neuroleptics

A

Dexmedatomidine
Medetomidine
Xylazine
Yohimbine

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44
Q

Where is the pain pathway will A2 agonist have and effect

A

Perception
Modulation
Transmission

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45
Q

Dexmedetomidine is used in what species

A

Dogs
Cat
Exotic

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46
Q

Xylazine is used in what species

A

Horse, deer, elk

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47
Q

What is the reversal agent for dexmedetomidine

A

Atipamezole

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48
Q

What is the reversal agent to xylazine

A

Yohimbine

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49
Q

What is the MOA of Xylazine and dexmedetomidine ?

A

Competitive a2 agonism

  • > Brian (sedation)
  • > dorsal horn (analgesic and muscle relaxation)

Competitive agonism of a1 receptors
-> vasoconstriction

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50
Q

Activation of a2 receptors stimulates what pathway of action

A

G(inhibitory) protein receptor pathway

  • > negative coupling to reduce adenylyl cyclase and decrease cAMP
  • > increase outward flow of K+

Hyperpolarization
Inhibit neurons
Decrease NE release

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51
Q

What are the a2 agonists from most to least selective

A

Dexmedatomidine
Romifidine
Detomidine
Xylazine

52
Q

How are a2 agonists administered?

A

IV or IM
Oral transmucosal
Epidural

53
Q

T/F: a2 agonists are widely distributed and can cross the BBB

54
Q

How does the onset and duration of action differ between xylazine and medetomidine/detomidine?

A

Xylazine rapid onset (15min) sedation 1-2hrs analgesia 15-30min

Medetomidine and detomidine have slightly longer action

55
Q

What are the main effects of A2 agonists on the CNS

A

Sedation
Pain modulation and analgesia
Muscle relaxation
Emesis

56
Q

What is the emetic of choice in cats

57
Q

What are the main effects of a2 agonists on the CVS?

A

Bi-phasic effect

  1. peripheral phase (peripheral vasocontriction)
    Mediated by a1 receptors
    -systemic vascular resistance causes increase in BP=> reflex bradycardia (to maintain constant cerebral perfusion pressure)
  2. Central phase
    Mediated by a2 receptors
    -decreased sympathetic tone -> heart rate stays low => hypotension AND bradycardia
58
Q

When after giving A2 agonists, you see bradycardia and increased BP, should we give anticolinergics to help maintain HR?

A

No

Phase 1 of biphasic effect
Contraindicated because increased workload of heart against high vascular resistance will exacerbate pre-existing heart disease or worsen arrhythmias

59
Q

When after giving A2 agonists, you see bradycardia and decreased BP, should we give anticolinergics to help maintain HR?

A

Yes

Phase 2 of Biphasic response
Clinical for cardiovascular depression

60
Q

What effect will A2 agonists have on the respiratory system?

A

Decreased respiratory rate (cats may be more sensitive)

Sheep, goat, and horse > increase respiratory rate and airway pressure=> increased CO2

61
Q

What effect with A2 agonist have on the GI system

A

Decrease motility

Decrease acid secretion

62
Q

What effects can a2 have on the uterus

A

Stimulate myometrial contractions -> may cause abortion in ruminants

63
Q

What effect will A2 have on blood sugar

A

Hyperglycemia
Decrease insulin release (transient)
More pronounced in horse and ruminant

64
Q

Clinically, what are a2 agonists used for?

A

Sedation
Pre-anesthetic/premedication
Analgesia

Emetic
Behavioral
Chemical ejaculation in stallions

65
Q

What are precautions to using A2 agonists ?

A 
Cardiovascular disease/instability 
Emesis 
Liver disease
Kidney disease 
Seizure disorder (increased ICP) 
Intra-arterial injection 
Late pregnancy in cattle and sheep
66
Q

When is A2 agonist use contraindicated?

A

Critically ill and patients with shock

67
Q

How should I administer competitive A2 antagonist (reversal agents)

A

IM -> greater possibility of side effects when give IV

68
Q

What are the main effects of A2 antagonists?

A

CNS effects reversed (sedation and analgesia)

Cardiovascular depression reversed

Respiratory depression reversed

GI side effect: salivation and diarrhea

69
Q

When should I use A2 antagonists?

A

To reverse a2 agonist toxicity
Mitoban toxicity
Amitraz tick collars

70
Q

What drug is the most selective to the A2 receptor

A

Dexmedetomidine

71
Q

Alpha 2 agonists often cause bradycardia and bradyarrhythmias, what is the most common arrhythmia it causes?

A

Atrioventricular block

72
Q

What is anesthesia

A

Drug induced central CNS depression in unconsciousness in which the patient cannot be arose by painful stimuli, and sensory motor and autonomic reflex functions are attenuated

73
Q

What is dissociated anesthesia ?

A

Drug induced dissociation of the thalamocrotical and limbic systems in a catatonic state

74
Q

What are the stages of anesthesia?

A

Analgesia -> voluntary motor excitement and state of analgesia

Excitement phase -> characterized by involuntary excitation or delirium

Surgical anesthesia -> plane of surgical anesthetic depth is reached

Medullary paralysis -> characterized by paralysis of vital centers in medulla

Death -> respiratory failure and collapse of resuscitative

75
Q

What are the depths of surgical anesthesia

A

Consciousness, pain sensation and most neuromuscular reflexes are abolished

1 and 2 => light
1 and 3=> deep

76
Q

What is the MOA of dissociative anesthetics

A

Non competitive NMDA receptor antagonist

Inhibits activation by glutamate of ligand-gated ion channels

77
Q

What part of the pain pathway does dissociative anesthetics work?

A

Modulation

78
Q

What is the distribution of anesthetics?

A

Wide
Lipid soluble
Crosses BBB

79
Q

How are anesthetics excreted?

A

Urine

Cats have more renal excretion than other species -> caution in renal insufficiency

80
Q

What is the onset, duration and recovery of anesthetics??

A

Induction - fast
Duration - 20-45min
Recovery - 2-10hrs (very long)

81
Q

What are the main effects of dissociative anesthetics on the CNS?

A
  1. depress thalamocortical system (sensory )
  2. activate limbic system -> dissociation (emotion/behavioral/memory)

Anesthesia, amnesia, and catalepsy

82
Q

What is catalepsy?

A

Muscle tone maintained to hypertonic -> need to be used in combo with muscle relaxant

83
Q

What are the main effects of dissociative anesthetics on the CVS?

A

Centrally mediated CV stimulation

Increase sympathetic tone (positive inotrope).
Decreased parasympathetic tone

84
Q

What are the main effects of dissociative anesthetics on the respiratory system?

A

Stimulate respiration (low dose)
Bronchodilation (good for asthmatic patients)
Increased secretions

Depress respiration (very high dose)

85
Q

What is the main effect dissociative anesthetics will have on the GI system

A

Stimulate salivary secretion

86
Q

At low doses, ketamine primarily will act on?

A

CNS hypersensitization (suppress)

87
Q

Can ketamine be used as a sole analgesic

A

No

Used at subanesthetic dose in combo with opioid to manage acute main

88
Q

What is the recovery time for tiletamine/Zolazepam and what part of it is reversible

A

Tiletamine -> dissociative
Zolazepam (benzodiazepine )

LONG recovery (hours) 
Only the zolazepam is reversible
89
Q

What are the clinical uses for dissociative anesthetics?

A

Chemical restrain and anesthetic for minor procedure
Induction of anesthesia
Part of triple drip in large animals
Analgesia (CRI)

90
Q

What is ‘Kitty magic’ for induction of anesthesia ?

A

Ketamine + Dexmedtomidine + Buprenorphine

91
Q

What is the triple drip in large animals?

A

Form of total intravenous anesthetia (TIVA)

Guaifenesin + Xylazine + Ketamine

92
Q

What is used in combination to a dissocative anesthetic to produce analgesic effects

A

Fentanyl + Lidocaine + Ketamine (FLK)

Morphine + Lidocaine + Ketamine (MLK)

93
Q

What role does a dissociative anesthetic play in acute pain

A

Reduce post-op pain hypersensitivity
Reduce short term tolerance to opioids
Prevent opioid-induced hyperalgesia
Reduce dose in post operative opioids

94
Q

What are disadvantages to using ketamine?

A

Irreversible
Cannot be used alone -> use with opioid
Inappropriate in cardiac disease patient
Increase ICP
Pain with IM injection
Risk of corneal ulceraction and substance abused

95
Q

That are precautions to using dissociative anesthetics ?

A

Pain with IM injection (good in cats but less good IM in dogs)

Eyes remain open-> lubricate /blink
Respiratory depression at high dose

96
Q

When should ketamine not be used

A

If increased ICP or IOP is contraindicated
Seizure
Myelography
Certain cardiac disease or hyper tension
Hepatic insufficiency
Renal disease/failure in cats

97
Q

What is the sequence of dose dependent sedation induced by GABA agonists

A

Sedation -> hypnosis -> anesthesia -> coma -> death

98
Q

What part of the pain pathway do GABA agonist analgesics have an effect?

A

General anesthesia -> perception

Anticonvulsant -> modulation

99
Q

What is the MOA of GABA agonists

A

Bind GABA receptor

Barbiturates: Increase the amount of time that GABA remains on the binding site and at high doses are reported to be able to activate chloride channels without GABA present

Main effect -> sedation and hypnosis

100
Q

What are the GABA agonist drugs?

A

Barbiturates :
Thiopental

Non-barbiturates :
Propofol
Alflaxalone
Etomidate

101
Q

How are barbiturates administered?

A

IV and Oral.

Not SQ or IM -> injection causes tissue damage

102
Q

How are barbiturates metabolized?

A

Hydroxylation in the liver

Thiobarbituaes are inactivated in the brain and the kidney

103
Q

What is the main effect of barbiturates on the CNS?

A

Nonselective dose-dependent depression
Sedation, hypnosis, and anesthesia
Poor analgesia unless anesthetized

Anticonvulsant

Decrease ICP
Increase threshold for spinal reflex

104
Q

Why are barbiturates good for head trauma cases?

A

Barbiturates decrease brain metabolism -> neuroprotective for a poorly perfused brain

105
Q

What are the main effects of barbiturates on the cardiovascular system

A

Hypotension ( due to cardiac depression)
-> reflex tachycardia

Thiobarbituates sensitize myocardium to catecholamine-induced arrhythmias
Intra-arterial injection causes vasoconstriction and gangrene

106
Q

What are the main effects of barbiturates on the respiratory system?

A

Dose dependent respiratory depression (cats are more sensitive)

VERY important -> most common cause of death due to poor dosing/monitoring

107
Q

What effect with barbiturates have on skeletal muscle

A

Inhibit sensitivity of motor endplate to ACH

Abdominal relaxation incomplete

108
Q

What effect with barbiturates have on body temp?

A

Hypothermia -> decreased basal metabolic rate

109
Q

What effect with barbiturates have on the kidney?

A

Oliguria and Anura due to decreased blood pressure -> reduced GFR
Stimulate ADH

110
Q

Repeated use of propoflo can cause what in cats?

A

Blood dyscrasia

Heinz body anemia

111
Q

Propoflo is administered how?

112
Q

What is the distribution of propoflo?

A 
Widely distributed (lipid soluble) 
Redistributed to muscle then fat
113
Q

What are the main effects of propofol on CNS

A

Dose dependent CNS depression

114
Q

What are the main effects of propofol on the cardiovascular system?

A

Vasodialation without reflex tachycardia

Splenic engorgement cab be observed

115
Q

What are the main effects of propofol on the respiratory system

A

Dose dependent depression

Rate dependent apnea

116
Q

_________________ GABA agonist is an analog of progesterone

A

Alfaxalone neurosteroid

117
Q

How is alfaxalone administered?

A

Labeled IV only

Sometimes used IM (unlike propofol)

118
Q

T/F: alfaxalone and propofol provide significant analgesia

119
Q

Myoclonus can be seen during induction (and by non-IV on recovery) with admin of what drug?

A

Alfaxalone

120
Q

What is the MOA of Etomidate

A

Depress the CNS by enhancing GABA

121
Q

What anesthetic is indicated in patients with significant cardiac disease?

A

Etomidate

-> least amount of cardiac depression

122
Q

T/F: etomidate has no analgesic effects

123
Q

What are the main effects of etomidate

A

Sedative, hypnotic and anesthetic effects
Dose dependent respiratory depression
Decreased ICP and IOP
Inhibits cortisol synthesis

Rapid recovery with no accumulation

124
Q

Use of ___________ in animals with hypoadreanal cortisol crisis is contraindicated

A

Etomidate

Causes relative adrenal insufficiency by inhibiting cortisol synthesis by the adrenal gland -> critical illness

125
Q

What anesthetic should be avoided in patients with traumatic brain injury?

A

Ketamine

-> increased ICP

126
Q 
Which of the following is not considered and IV anesthetic induction agent?
Ketamine 
Propofol 
Alfaxalone 
Fentanyl
127
Q 
Which of the following causes the least amount of cardiovascular depression 
Ketamine 
Propofol 
Etomidate 
Alfaxalone
A

Ketamine -> causes cardiac stimulation

RUSVM Pharmacology (18 decks)

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