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
sevoflurane has a ____ rate of onset and recovery
rapid
26
seveflurane is metabolised in the ___ ti release _____________- which is nephrotoxic
liver | inorganic fluoride
27
sevoflurane is unstable when exposed to _____ in anaesthetic machines --> metabolite is potentially _______
CO2 absorbants | nephrotoxic
28
NO gives ___ and _____ but not complete ____ or surgical anaesthesia
analgesia and amnesia | unconsciousness
29
what is the function of NO
supplement the analgesic effect of primary anaesthetic
30
what is the major concern of NO
post op nausea and vomiting
31
name 5 IV GA
``` thiopentone 4-7mg.kg etomidate 0.2-0.3mg/kg propofol 2-4mg/kg ketamine 1.5mg/kg midazolam 0.02mg/kg ```
32
what are IV GA agents used for
induce unconsciousness
33
what is the caution with IV GA
depress respiration
34
advantages of inhaled + IV anaesthetics
1. permit dosage of the inhalation agent to be reduced | 2. produce effects that cannot be achieved with an inhalation alone
35
Class of thiopentone
barbiturate
36
thiopentone has ________ lipid solubility
extremely high
37
thiopentone enters the brain _________ | onset of action _________
easily and rapidly | rapid (10-20 s after IV)
38
single dose of thiopentone redistributes to _______ tissue in ______ duration of action
less vascularised ultra-short patients wake up in 10 min
39
multiple doses/infusionsof thiopentone: duration of action depends on __
clearance
40
thiopentone has a ____ elimination, ____ Vd, ____ metabolite (______)
slow, large, active, pentobarbital
41
thiopentone: liver cirrhosis can result in _________
prolongation of clinical action
42
thiopentone is extensive bound to ______
plasma protein
43
thiopentone MOA
CNS depression by potentiating the action of GABA on the GABAa receptor-gated chloride ion channels
44
does propofol need to be reconstituted
no
45
induction rate of propofol is ____ to thiopentone and recovery is ____
similar, more rapid
46
what is propofol used for
induction and maintenance
47
onset of propofol
rapid (unconsciousness within 60 seconds)
48
duration of action of propofol
short (3-5min)
49
propofol most used in _______
day surgery
50
propofol needs _______ for extended effect
continuous, low dose infusion
51
advantage of propofol
reduced post op vomiting
52
disadvantage of propofol
significant CV effect during induction (decrease bp and negative inotropic)
53
caution when using propofol
caution in elderly patients, patients with compromised cardiac function, hypovolemic patients
54
ketamine exists as a __________ preparation
racemic
55
katmine produces a state known as _________
dissociative anaesthesia
56
ketamine can cause (4)
sedation, immobility, analgesia and amnesia
57
ketamine has ____ induction
rapid
58
ketamine is metabolised in ___ to _____________ metabolite, excreted in ________________
liver, less active metabolite | urine and bile
59
ketamine has ___ Vd, ___ clearance --> suitable for _______________ without the lengthening in duration of action
large Vd, rapid clearance, continuous infusion
60
SE of ketamine
unpleasant psychologic reactions (hallucination, disturbing dreams, delirium) during recovery risk of psychologic adverse reactions --> may be reduced with premedication of diazepam or midazolam
61
does ketamine possess analgesia?
yes
62
name 4 classes of anaesthetic adjuncts / post op care
benzo, alpha adrenergic agonist, analgesics, NM blocking agents
63
name the benzodiazepine used for GA
midazolam IV
64
what is midazolam used for in GA
anxiolytics, amnesia and sedation prior to induction of anaesthesia or used for sedation during procedures not requiring GA
65
midazolam onsent
rapid unconsciousness in 80s peak 2 min
66
midazolam duration of action
sedates about 30 min when used by itself
67
midazolam metabolism
liver | elderly more sensitive slower recovery
68
midazolam TI high or low
high
69
why is midazolam TI high
less CV and resp depressing effect compared to other IV anaesthetics
70
midazolam SE compounded by...........
concurrent use of other agents
71
midazolam ADR can be minimised by......
injecting slowly over 2 or more minutes, waiting 2 minutes then doing it again
72
alpha 2 adrenergic example drug
dexmedetomidine
73
dexmedetomidine selective?
yes
74
dexmedetomidine duration of sedation
short term <24h
75
what effects does dexmedetomidine have
sedation and analgesia | does not produce reliable GA even at max doses
76
dexmedetomidine resp depression?
little
77
dexmedetomidine effect on bp and hr?
tolerable decrease
78
dexmedetomidine ADR
nausea dry mouth hypotension bradycardia
79
what class of drugs is used for analgesia in GA
NSAIDs and opioids
80
when are NSAIDs used in GA
minor surgical procedures
81
which types of NSAIDs are used
COX-2 inhibitors and paracetamol
82
when are opioids used
perioperative period
83
opioids site of action for GA
mu
84
which drug has a relative potency of 1000x compared to morphine duration of action
sufentanil | ~15min
85
which drug has a relative potency of 300x compared to morphine duration of action
remifentanil | ~10 min
86
which drug has a relative potency of 80x compared to morphine duration of action
fentanyl | ~30min
87
which drug has a relative potency of 15x compared to morphine duration of action
alfentanil | ~20min
88
analgesics in GA metabolised through..... except _______
liver | remifentanil --> hydrolysed by tissue and plasma esterase's
89
analgesics excretion
urine, bile
90
name a depolarising NM blocker
succinylcholine
91
name a non-depolarising NM blocker
vecuronium
92
when are NM blockers used
induction of anaesthesia to relax muscles of jaw, neck and airway --> facilitate laryngoscopy and endotracheal intubation
93
advantage of NM blockers
aids surgical procedures and additional insurance of immobility
94
precaution for NM blockers and barbiturates
ppt when mixed --> clear from IV line first