GA Flashcards

1
Q

what is the triad of GA use

A

hypnosis, amnesia and analgesia

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2
Q

what are the 3 components of balanced anaesthesia

A

pain relief, unconsciousness, inhibition of reflex

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3
Q

what is the most commonly used class of drug for analgesia

A

opioid and NO

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4
Q

what is the most commonly used class of drug for induction of anaesthesia

A

short acting barbiturates

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5
Q

what is the most commonly used class of drug for muscle relaxation

A

NM blockigjn agents

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6
Q

inhalant GA: the ____ the solubility, the slower the onset

A

higher

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7
Q

what is the proposed MOA for inhalation GA

A

enhance neurotransmission at inhibitory synapses via allosterically increasing GABA receptor sensitivity to GABA

depress neurotransmission at excitatory synapses via blocking glutamate neurotransmitter acting on NMDA receptor–> prevent NMDA receptor activation

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8
Q

low MAC = ____ anaesthetic potency

A

high

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9
Q

what is MAC

A

minimum conc of drug in air needed to produce immobility in 50% of patients exposed to painful stimulus

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10
Q

MAC values alter with…

A

age, condition, conçoivent administration of other drug

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11
Q

to produce therapeutic effect, inhalation anaesthetic has to reach CNS concentration enough to suppress

A

neuronal excitability

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12
Q

3 factors affecting rate of inhalation GA uptake into the blood

A

blood flow to the lungs
solubility of GA
conc of anaesthetic in the air

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13
Q

elimination of inhaled GA is through

A

lungs

minimal hepatic metabolism

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14
Q

which inhalation GA have nephrotoxic metabolites

A

isoflurane, enflurane

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15
Q

does halothane have analgesia before unconsciousness

A

no

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16
Q

does halothane have respiratory depression

A

yes; dose dependent

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17
Q

Halothane ____ BP due to depression of cardiac output

A

decreases

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18
Q

halothane: ____ and ____ may also occur –> hypotension and dysrhythmia

A

bradycardia and arrhythmia

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19
Q

halothane relaxes ____ muscles and potentiates _____

A

skeletal

potentiates skeletal muscle relaxants

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20
Q

halothane: may lead to ___________

A

halothane associated hepatitis

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21
Q

isoflurane has a ____ smell

A

pungent

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22
Q

isoflurane has a ____ rate of onset and recovery

A

medium

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23
Q

What is the advantage of isoflurane vs halothane

A

less hypotension and arrhythmia

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24
Q

how does isoflurane decrease BP

A

decrease in systemic vascular resistance

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25
Q

sevoflurane has a ____ rate of onset and recovery

A

rapid

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26
Q

seveflurane is metabolised in the ___ ti release _____________- which is nephrotoxic

A

liver

inorganic fluoride

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27
Q

sevoflurane is unstable when exposed to _____ in anaesthetic machines –> metabolite is potentially _______

A

CO2 absorbants

nephrotoxic

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28
Q

NO gives ___ and _____ but not complete ____ or surgical anaesthesia

A

analgesia and amnesia

unconsciousness

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29
Q

what is the function of NO

A

supplement the analgesic effect of primary anaesthetic

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30
Q

what is the major concern of NO

A

post op nausea and vomiting

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31
Q

name 5 IV GA

A
thiopentone 4-7mg.kg 
etomidate 0.2-0.3mg/kg
propofol 2-4mg/kg 
ketamine 1.5mg/kg 
midazolam 0.02mg/kg
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32
Q

what are IV GA agents used for

A

induce unconsciousness

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33
Q

what is the caution with IV GA

A

depress respiration

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34
Q

advantages of inhaled + IV anaesthetics

A
  1. permit dosage of the inhalation agent to be reduced

2. produce effects that cannot be achieved with an inhalation alone

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35
Q

Class of thiopentone

A

barbiturate

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36
Q

thiopentone has ________ lipid solubility

A

extremely high

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37
Q

thiopentone enters the brain _________

onset of action _________

A

easily and rapidly

rapid (10-20 s after IV)

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38
Q

single dose of thiopentone redistributes to _______ tissue in ______ duration of action

A

less vascularised
ultra-short
patients wake up in 10 min

39
Q

multiple doses/infusionsof thiopentone: duration of action depends on __

A

clearance

40
Q

thiopentone has a ____ elimination, ____ Vd, ____ metabolite (______)

A

slow, large, active, pentobarbital

41
Q

thiopentone: liver cirrhosis can result in _________

A

prolongation of clinical action

42
Q

thiopentone is extensive bound to ______

A

plasma protein

43
Q

thiopentone MOA

A

CNS depression by potentiating the action of GABA on the GABAa receptor-gated chloride ion channels

44
Q

does propofol need to be reconstituted

A

no

45
Q

induction rate of propofol is ____ to thiopentone and recovery is ____

A

similar, more rapid

46
Q

what is propofol used for

A

induction and maintenance

47
Q

onset of propofol

A

rapid (unconsciousness within 60 seconds)

48
Q

duration of action of propofol

A

short (3-5min)

49
Q

propofol most used in _______

A

day surgery

50
Q

propofol needs _______ for extended effect

A

continuous, low dose infusion

51
Q

advantage of propofol

A

reduced post op vomiting

52
Q

disadvantage of propofol

A

significant CV effect during induction (decrease bp and negative inotropic)

53
Q

caution when using propofol

A

caution in elderly patients, patients with compromised cardiac function, hypovolemic patients

54
Q

ketamine exists as a __________ preparation

A

racemic

55
Q

katmine produces a state known as _________

A

dissociative anaesthesia

56
Q

ketamine can cause (4)

A

sedation, immobility, analgesia and amnesia

57
Q

ketamine has ____ induction

A

rapid

58
Q

ketamine is metabolised in ___ to _____________ metabolite, excreted in ________________

A

liver, less active metabolite

urine and bile

59
Q

ketamine has ___ Vd, ___ clearance –> suitable for _______________ without the lengthening in duration of action

A

large Vd, rapid clearance, continuous infusion

60
Q

SE of ketamine

A

unpleasant psychologic reactions (hallucination, disturbing dreams, delirium) during recovery
risk of psychologic adverse reactions –> may be reduced with premedication of diazepam or midazolam

61
Q

does ketamine possess analgesia?

A

yes

62
Q

name 4 classes of anaesthetic adjuncts / post op care

A

benzo, alpha adrenergic agonist, analgesics, NM blocking agents

63
Q

name the benzodiazepine used for GA

A

midazolam IV

64
Q

what is midazolam used for in GA

A

anxiolytics, amnesia and sedation prior to induction of anaesthesia or used for sedation during procedures not requiring GA

65
Q

midazolam onsent

A

rapid
unconsciousness in 80s
peak 2 min

66
Q

midazolam duration of action

A

sedates about 30 min when used by itself

67
Q

midazolam metabolism

A

liver

elderly more sensitive slower recovery

68
Q

midazolam TI high or low

A

high

69
Q

why is midazolam TI high

A

less CV and resp depressing effect compared to other IV anaesthetics

70
Q

midazolam SE compounded by………..

A

concurrent use of other agents

71
Q

midazolam ADR can be minimised by……

A

injecting slowly over 2 or more minutes, waiting 2 minutes then doing it again

72
Q

alpha 2 adrenergic example drug

A

dexmedetomidine

73
Q

dexmedetomidine selective?

A

yes

74
Q

dexmedetomidine duration of sedation

A

short term <24h

75
Q

what effects does dexmedetomidine have

A

sedation and analgesia

does not produce reliable GA even at max doses

76
Q

dexmedetomidine resp depression?

A

little

77
Q

dexmedetomidine effect on bp and hr?

A

tolerable decrease

78
Q

dexmedetomidine ADR

A

nausea
dry mouth
hypotension
bradycardia

79
Q

what class of drugs is used for analgesia in GA

A

NSAIDs and opioids

80
Q

when are NSAIDs used in GA

A

minor surgical procedures

81
Q

which types of NSAIDs are used

A

COX-2 inhibitors and paracetamol

82
Q

when are opioids used

A

perioperative period

83
Q

opioids site of action for GA

A

mu

84
Q

which drug has a relative potency of 1000x compared to morphine
duration of action

A

sufentanil

~15min

85
Q

which drug has a relative potency of 300x compared to morphine
duration of action

A

remifentanil

~10 min

86
Q

which drug has a relative potency of 80x compared to morphine
duration of action

A

fentanyl

~30min

87
Q

which drug has a relative potency of 15x compared to morphine
duration of action

A

alfentanil

~20min

88
Q

analgesics in GA metabolised through….. except _______

A

liver

remifentanil –> hydrolysed by tissue and plasma esterase’s

89
Q

analgesics excretion

A

urine, bile

90
Q

name a depolarising NM blocker

A

succinylcholine

91
Q

name a non-depolarising NM blocker

A

vecuronium

92
Q

when are NM blockers used

A

induction of anaesthesia to relax muscles of jaw, neck and airway –> facilitate laryngoscopy and endotracheal intubation

93
Q

advantage of NM blockers

A

aids surgical procedures and additional insurance of immobility

94
Q

precaution for NM blockers and barbiturates

A

ppt when mixed –> clear from IV line first