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ACUTE > PPT > Flashcards

PPT Flashcards

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
Q

what are the ester-linked drugs?

A

tetracaine
choroprocaine
cocaine
procaine

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26
Q

how are ester-linked LAs metabolised?

A

rapidly hydrolysed by plasma cholinesterase = short half life

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27
Q

how are amide-linked LAs metabolised?

A

metabolised in the liver by N-dealkylation
metabolites are often pharmacologically active

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28
Q

Local SE of LA?

A

irritation and inflammation
ischaemia from use of vasoconstrictor agents

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29
Q

systemic SE of LA?

A

myocardial depression
vasodilation
hypotension
arrhythmias
agitation
confusion
tremors
convulsions
respiratory depression

30
Q

how is LA toxicity treated?

A

with IV 20% lipid emulsion

31
Q

drug interactions for lidocaine?

A

Beta blockers, ciprofloxacin, phenytoin

32
Q

dose of lidocaine without and with adrenaline?

A

3 and 7

33
Q

dose of bupivicaine with and without adrenaline?

A

2and 2

34
Q

dose of prilocaine without and with adrenaline?

A

6 and 9

35
Q

when is adding adrenaline to LA CI?

A

in pts taking MAOIs or TCAs

36
Q

which has a longer duration of action bupivicaine or lidocaine?

A

bupivicaine (has a higher pKa)

37
Q

4 stages of anaesthesia?

A

analgesia
excitation
surgical anaesthesia
medullary depression

38
Q

MOA of etomidate?

A

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
Q

MOA of propofol?

A

positive modulation of the inhibitory function of the neurotransmitter gama-aminobutyric acid (GABA) through GABA-A receptors.

40
Q

MOA of thiopental?

A

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
Q

MOA of NO?

A

Exact mechanism of action unknown. May act via a combination of NDMA, nACh, 5-HT3, GABAA and glycine receptors

42
Q

MOA of ketamine?

A

interacts with NMDA, opioid, monoaminergic, muscarinic and voltage sensitive Ca ion channels

43
Q

MOA of sevoflurane?

A

Exact mechanism of action unknown. May act via a combination of GABAA, glycine and NDMA receptors

44
Q

MOA of isoflurane?

A

Exact mechanism of action unknown. May act via a combination of GABAA, glycine and NDMA receptors

45
Q

MOA of desflurane?

A

Exact mechanism of action unknown. May act via a combination of GABAA, glycine and NDMA receptors

46
Q

what factors affect inhalation anaesthesia?

A

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
Q

what is MAC?

A

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
Q

what is the Meyer-Overton correlation for anaesthetics?

A

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
Q

what Is the blood:gas partition coefficient?

A

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
Q

which innhalational anaesthetic agents have the highest blood: gas partition coefficients?

A

isoflurane and halothane (this means they have the lowest MAC - halothane is no longer used in the UK)

51
Q

what is NO used for?

A

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
Q

MAC of NO?

A

105%

53
Q
A
54
Q

what factors influence elimination of inhalational anaesthetics?

A

ventilation rate
bod:gas partition coefficient
duration of inhalation
extent of tissue equilibration

55
Q

examples of IV anaesthetics?

A

etomidate
ketamine
propofol
thiopental

56
Q

why has propofol largely replaced thiopental as an induction agent?

A

more rapid recovery and less hangover effect

57
Q

why is etomidate not used as a continuous infusion?

A

due to toxicity on adrenals and adenocortical suppression

58
Q

what is dissociative anaesthesia nd what causes it?

A

ketamine
marked sensory loss and analgesia with amnesia but without complete loss of consciousess
the analgesia outlasts the anaesthesia

59
Q

examples of non-depolarising neuromuscular blockers?

A

atracurium
cisatracurium
mivacurium
pancuronium
rocuronium
vecuronium

60
Q

adverse effects of depolarising neuromuscular blocking drugs?

A

malignant hyperthermia
hypekalaemia

61
Q

examples of depolarising neuromuscular blockers?

A

suxamethonium

62
Q

what is an important but rare adverse event with suxamethonium?

A

a very prolonged paralysis occurs in 1 in 2000 people who have a genetic deficiency of pseudocholinesterase

63
Q

reversal agent for non-depolarising neuromuscular blockers? what is given with it?

A

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
Q

universal donor blood?

A

O neg

65
Q

monitoring when giving blood transfusion?

A

observations at 0, 15, 30 mins and then hourly and then again on completion

66
Q

1 unit should increase Hb by xg/L

A

10

67
Q

when is a platelet transfusion indicated?

A

if plt <10
if <30 with grade 2 clinically significant bleeding
<100 with grade 3/4 bleeding
50-100 if having invasive procedure

68
Q

daily requirements of water, Na+, K+, Cl-. glucose?

A

water 25-30mls/kg
Na+ 1 mmol/kg
K+ 1 mmol/kg
Cl- 1 mmol/kg
glucose 50-100g

69
Q

what does adrenaline interact with?

A

amitryptiline
beta blockers
MAOI

70
Q
A

ACUTE (18 decks)

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