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1
Q

MOA of local anaesthetics?

A

they block the voltage-dependant Na+ channels that depolarise the neutron
ore than 90% of channels must be affected to stop nerve conduction

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2
Q

which drugs are most likely to cause malignant hyperthermia?

A

volatile anaetshetics
suxamethonium

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3
Q

CI to suxamethonium?

A

penetrating eye injuries or acute narrow angle glaucoma, as suxamethonium increases intra-ocular pressure

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4
Q

moa of depolarising vs non-depolarising neuromuscular blocking drugs

A

depolairisng: Binds to nicotinic acetylcholine receptors resulting in persistent depolarization of the motor end plate
non-depolarising: Competitive antagonist of nicotinic acetylcholine receptors

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5
Q

what factors influence LA action?

A

local concentration of LA
size of nerve fibre
nerve myelination
length of nerve exposed to LA

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6
Q

which nerve fibres transmit pain?

A

myelinated A delta and small non-myelinated C fires

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7
Q

why is ketamine often used as an induction agent in emergency surgeries?

A

as it doesn’t drop the bp

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8
Q

LA action of myelinated and non-myelinated nerves?

A

myelinated - LA penentrates at nodes of Ranvier and must block at least 3 consecutive nodes
unmyelinated nerves must be blocked over a sufficient length and around the full circumference of the nerve

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9
Q

which neuromuscular blocking drug causes muscle fasciculations?

A

suxamethonium

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10
Q

what is the potency of a LA directly related to?

A

its lipid solubility

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11
Q

do LAs exist as acids or bases?

A

weak bases

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12
Q

what is pKa? what is it for lidocaine?

A

the pH at which the ionised and non-ionised forms are equal
7.8

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13
Q

what happens when the pKa of a LA = the physiological PH?

A

there will be a higher concentration of non-ionised base and a faster onset

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14
Q

in which form is the water solubility of local anaesthetics greatest?

A

in the ionised form (this is why injectable preparations are formulated as hydrochloride salts with a pH of 5-6 as it keeps the LA in its ionised form)

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15
Q

what are the implications of LAs with high pKa?

A

a larger proportion of the drug will be more ionised at physiological pH = less molecules in non-ionised state = less lipophilic = so speed of onset is slower BUT once inside a higher proportion of LA is in the ionised state = produce a more effective blockade

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16
Q

what does use-dependance mean?

A

the more channels that are opened, the greater the block becomes

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17
Q

common LAs?

A

lidocaine
bupivacaine
tetracaine
prilocaine

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18
Q

max concentration of a topical anaesthesia?

A

up to 10%

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19
Q

what can LA be mixed with in peripheral nerve blocks to increase speed of onset and duration of action?

A

Bicarbonate for speed
epinephrine for duration

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20
Q

how much LA is given in a spinal?

A

1.5-2.5ml

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21
Q

where is a spinal anaesthetic inserted?

A

between L3 and L4

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22
Q

why can adrenaline be given alongside a LA?

A

as most LAs cause vasodilation so adrenaline causes vasoconstriction to reduce their removal

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23
Q

what does the spread of the LA within the subarachnoid space in a spinal depend on?

A

density of sollution
posture of person during the first 10-15 mins

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24
Q

what are the amide-linked drugs?

A

lidocaine
prilocaine
bupivacaine
etidocaine
mepivacaine
ropivacaine

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25
what are the ester-linked drugs?
tetracaine choroprocaine cocaine procaine
26
how are ester-linked LAs metabolised?
rapidly hydrolysed by plasma cholinesterase = short half life
27
how are amide-linked LAs metabolised?
metabolised in the liver by N-dealkylation metabolites are often pharmacologically active
28
Local SE of LA?
irritation and inflammation ischaemia from use of vasoconstrictor agents
29
systemic SE of LA?
myocardial depression vasodilation hypotension arrhythmias agitation confusion tremors convulsions respiratory depression
30
how is LA toxicity treated?
with IV 20% lipid emulsion
31
drug interactions for lidocaine?
Beta blockers, ciprofloxacin, phenytoin
32
dose of lidocaine without and with adrenaline?
3 and 7
33
dose of bupivicaine with and without adrenaline?
2and 2
34
dose of prilocaine without and with adrenaline?
6 and 9
35
when is adding adrenaline to LA CI?
in pts taking MAOIs or TCAs
36
which has a longer duration of action bupivicaine or lidocaine?
bupivicaine (has a higher pKa)
37
4 stages of anaesthesia?
analgesia excitation surgical anaesthesia medullary depression
38
MOA of etomidate?
binds to GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.
39
MOA of propofol?
positive modulation of the inhibitory function of the neurotransmitter gama-aminobutyric acid (GABA) through GABA-A receptors.
40
MOA of thiopental?
binds to GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.
41
MOA of NO?
Exact mechanism of action unknown. May act via a combination of NDMA, nACh, 5-HT3, GABAA and glycine receptors
42
MOA of ketamine?
interacts with NMDA, opioid, monoaminergic, muscarinic and voltage sensitive Ca ion channels
43
MOA of sevoflurane?
Exact mechanism of action unknown. May act via a combination of GABAA, glycine and NDMA receptors
44
MOA of isoflurane?
Exact mechanism of action unknown. May act via a combination of GABAA, glycine and NDMA receptors
45
MOA of desflurane?
Exact mechanism of action unknown. May act via a combination of GABAA, glycine and NDMA receptors
46
what factors affect inhalation anaesthesia?
Absorption across alveolar membranes Solubility of the anaesthetic in the blood Cardiac output – circulation time Relative concentration of the anaesthetic in the brain and blood at equilibrium
47
what is MAC?
a measure of potency. its the minimum concentration at which 50% of th population will fail to respond to a single noxious stimuli e.g. first surgical skin incision
48
what is the Meyer-Overton correlation for anaesthetics?
a graph showing the MAC against the olive oil:gas partition coefficient it shows tan the lower the blood:gas ratio the more GA will arrive at the brain i.e. the higher the MAC
49
what Is the blood:gas partition coefficient?
a measure of solubility of GA in the blood it determines the rate of induction and recovery of inhalation anaesthesia the higher the blood: gas coefficient the slower the induction and recovery i.e. the lower the MAC the potency of an anaesthetic increases as its solubility in oil increases
50
which innhalational anaesthetic agents have the highest blood: gas partition coefficients?
isoflurane and halothane (this means they have the lowest MAC - halothane is no longer used in the UK)
51
what is NO used for?
it is not sufficiently potent to be used alone Is used part of a combination of drugs to allow a significant reduction in dosage (with other inhalational anaesthetics or intravenous anaesthetics) used for maintenance of anaesthesia or In sub-anaesthetic concentrations for analgesia – e.g. Entonox® – 50:50 mixture with oxygen
52
MAC of NO?
105%
53
54
what factors influence elimination of inhalational anaesthetics?
ventilation rate bod:gas partition coefficient duration of inhalation extent of tissue equilibration
55
examples of IV anaesthetics?
etomidate ketamine propofol thiopental
56
why has propofol largely replaced thiopental as an induction agent?
more rapid recovery and less hangover effect
57
why is etomidate not used as a continuous infusion?
due to toxicity on adrenals and adenocortical suppression
58
what is dissociative anaesthesia nd what causes it?
ketamine marked sensory loss and analgesia with amnesia but without complete loss of consciousess the analgesia outlasts the anaesthesia
59
examples of non-depolarising neuromuscular blockers?
atracurium cisatracurium mivacurium pancuronium rocuronium vecuronium
60
adverse effects of depolarising neuromuscular blocking drugs?
malignant hyperthermia hypekalaemia
61
examples of depolarising neuromuscular blockers?
suxamethonium
62
what is an important but rare adverse event with suxamethonium?
a very prolonged paralysis occurs in 1 in 2000 people who have a genetic deficiency of pseudocholinesterase
63
reversal agent for non-depolarising neuromuscular blockers? what is given with it?
neostigmine (not with depolarising neuromuscular blockers!) and an antimuscarinic such as atropine or glycopyrrolate is given immediately before to prevent bradycardia or excessive salivation
64
universal donor blood?
O neg
65
monitoring when giving blood transfusion?
observations at 0, 15, 30 mins and then hourly and then again on completion
66
1 unit should increase Hb by xg/L
10
67
when is a platelet transfusion indicated?
if plt <10 if <30 with grade 2 clinically significant bleeding <100 with grade 3/4 bleeding 50-100 if having invasive procedure
68
daily requirements of water, Na+, K+, Cl-. glucose?
water 25-30mls/kg Na+ 1 mmol/kg K+ 1 mmol/kg Cl- 1 mmol/kg glucose 50-100g
69
what does adrenaline interact with?
amitryptiline beta blockers MAOI
70

ACUTE (18 decks)

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