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Sem 5 > Introduction to Anaesthetics > Flashcards

Introduction to Anaesthetics Flashcards

1
Q

What is unusual compared to other drugs about the physicochemical interaction of major inhalational anaesthetics at their target sites?

A

need high conc (millimolar range) to have an effect, so a slight reduction causes effects reversal. IMPORTANT, as want to reverse therapy quickly once anaesthetic effect no longer required.

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2
Q

what single pharmacokinetic factor in inhalational anaesthetics determines their active concentration at their targets in the CNS?

A

alveolar concentration

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3
Q

what does a lower minimal alveolar concentration of an anesthetic mean in terms of its potency?

A

greater potency, as less drug needed to put patient to sleep

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4
Q

reversible effects of anaesthesisa?

A

sedation up to unconsciousness (thalamus)
amnesia (hippocampus- part of temporal lobe)
muscular relaxation
reflex suppression and immobilisation (SC)
anxiolysis- treat anxiety e.g. benzodiazepines
analgesia

NO single agent able to produce all these effects, so POLYPHARMACY- principle anaesthetic and range of adjuvants.

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5
Q

example of regional anaesthesia?

A

epidural- given during labour
below L2 vertebral level as this marks end of SC= conus medullaris. Then continues as cauda equina to S2. *syndrome= pathological.

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6
Q

which channel is propofol (IV) considered to exert its main sedative effect?

A

GABA A activated Cl- channel

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7
Q

anaesthetic effects mediated by action on neuronal nicotinic ACh receptors?

A

analgesia and amnesia, rather than sedation

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8
Q

anaesthetics exerting primary pharmacological action on NMDA (glutamate) receptors?

A 
nitrous oxide (inhalational)
ketamine (IV)
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9
Q

how do anaesthetics work by acting on neuronal nicotinic ACh receptors?

A

inhibition to reduce excitatory Na+ currents caused by Ach binding.

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10
Q

how do anaesthetics work by acting on NMDA receptors?

A

inhibition: reduce Ca2+ current

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11
Q

how do anaesthetics work by acting on GABA A and glycine ligand gated ion channels?

A

stimulation: increase sensitivity to GABA A and glycine once bound, so increase Cl- currents and hyperpolarise neurone, decreasing excitability.

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12
Q

define the minimal alveolar concentration (MAC)

A

% of inhaled anaesthetic that abolishes response to surgical incision in 50% of patients
Lower value= more potent, as MAC closely related to its lipid solubility

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13
Q

how can MAC of individual agents be significantly reduced to reduce dosing?

A

give in combination with nitrous oxide, or the opiate fentanyl

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14
Q

what is the degree of absorption of an inhaled anaesthetic across alveoli into blood defined by?

A

the blood:gas coefficient
this describe the vol of gas in L that can dissolve in 1 L of blood.
e.g. isoflurane= 1.4, so 1.4 litres of isoflurane could be dissolved in 1 L of blood.
Higher coefficient= more readily enters blood.

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15
Q

what does the distribution of an anaesthetic around the body depend on?

A

relative b.supply to each organ/tissue and specific tissue uptake capacity for anaesthetic

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16
Q

how does isoflurane partition in the body?

A 
most absorbed by adipose tissue, fat:blood partition coefficient=45=very large reservoir that can redistribute during recovery phase- longer time for obese patients to recover from anaesthetic*
then muscle =2.9
then CNS ( where we want it!)= 1.6
fat and muscle less perfused so anesthetic will move out into venous supply more gradually.
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17
Q

what is duration of recovery from inhaled anaesthetics directly related to?

A

length of procedure and degree of loading of muscle and fat compartments with anaesthetic

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18
Q

in relation to flurane distribution, why might its free plasma levels be affected by other drugs?

A

compete for protein binding as protein binding high at 98%

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19
Q

what is unusual about the elimination of propofol?

A

undergoes both hepatic and extra-hepatic met. so t1/2 about 2 hrs, and doesn’t contribute to prolonged post procedural ‘hangover’ during recovery.

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20
Q

in addition to increasing potency of glycine and GABA A, how else do anaesthetics targeting inhibitory ligand-gated ion channels act?

A

increase efficacy of GABA or glycine so that binding at any 1 channel allows more Cl- current to flow. May be due to stabilising effect of anaesthetic on ‘open’ state of channel.
=+ve allosteric modulation= increases efficacy of NT by binding at site other than main receptor site for GABA and glycine.

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21
Q

describe how potency and efficacy are affected by anaesthetics acting on excitatory ligand-gated ion channels

A

EC50/potency unaffected but efficacy of excitatory ligand decreases
non-competitive allosteric effect of anaesthetic, so once bound, it inactivates the receptor, reducing efficacy but ligand binding affinity of remaining unbound receptors is unchanged, and the inward movement of excitatory currents is reduced. -ve allosteric modulation?

22
Q

how do benzodiazepines e.g. midazolam, exert their anaesthetic effect?

A

induce anxiolysis and amnesia by stimulating inhibitory GABA A receptors.

23
Q

what is the agent of choice for rapid IV induction of anesthesia?

A

propofol- rapid induction of deep initial sedation via stimulation of GABA A receptors.

24
Q

what is nitrous oxide used to achieve in anaesthesia?

A

analgesia and reduce main inhalational agent MAC e.g. flurane, so less dose required
action on NMDA exitatiory receptors- inhibits them, so decreases Ca2+ current
also has rapid controlled pulmonary elimination so good at minimising recovery time

25
Q

why is fentanyl preferred to morphine as an opiate used to produce an analgesia in anaesthetics?

A

fentanyl= 100X more potent than morphine, inducing analgesia almost immediately and acts over 30-60 mins, allowing for finer control of analgesic effect relative to morphine during surgery.

26
Q

what agents are used to abolish reflexes and induce muscle relaxation in anaesthesia?

A

neuromuscular blocking agents=
competitive N ACh receptor antagonsits e.g. tubocurarine or pancuronium
or N ACh receptor depolarising agents e.g. succinycholine- end up with insufficient Na+ current for AP as membrane continually depolarised but not quite to threshold?*
Fluranes via CNS action also potentiate neuromuscualar relaxation

27
Q

ADRs of fluranes?

A

cardiovascular and resp depression with reduced neuronal activity in medulla- resp depres also occurs with opiates and benzodiazepines-flumazenil is used to antagonise the effects of benzodiazepines
arrhythmia and hypotension as reduced vascular resistance from direct effect on arteriorlar smooth muscle
increased IC pressure as cerebral b.flow increases with reduced vascular resitance
coughing and laryngospasm as a.way irritants
malignant hyperthermia- muscle tetany due to massive flurane induced sarcoplasmic Ca2+ release via ryanodine receptor- excessive heat produced with muscle contractions, can treat with a muscle relaxant e.g. dantrolene- blocks Ca2+ release from SR.

28
Q

ADRs of nitrous oxide?

A

expansion of a.way cavities e.g. sinuses and middle ear, as because gas, enters alveolar space much faster than nitrogen, which is dangerous in those with a pneumothorax, IC air or where vascular air emboli present.

29
Q

describe what happens in recovery from nitrous oxide

A

it diffuses very rapidly out of blood into alveoli, decreasing alveolar O2 conc= diffusion hypoxia- important if patient has compromised resp function
offset by increasing partial pressure of inspired O2 at onset of recovery when surgery completed.

30
Q

ADRs of propofol (IV)?

A

CVS and resp depression via action on medullary control centres

31
Q

ADRs of benzodiazepines and opioids?

A

resp depression

opioids: constipation, tolerance, dependence, nausea and vomiting post op

32
Q

describe the assessment of a patient that takes place during surgery in relation to anaesthesia given

A

pre-surgical review: anaesthetist directly assesses- age, BMI, PMH and surgical hist, current med. , history of drug abuse, fasting time, away assessment.
peri-surgical monitoring: anaesthetic and adjuvant delivery- direct control and monitoring of gaseous mixture, and rate of mechanical ventilation.
systemic physi monitoring: ECG, BP, pulkse oximetry, expired CO2, temp- core will drop with prolonged anaesthesia so must be aware of increase- maybe fever or malignat hyperthermia, EEG monitoring.

33
Q

3 main stages of anaesthesia?

A

induction- normally propofol and beginning of inhalational agents
maintenance-adjuvants kept in balance to maintain adequate depth. propofol may be used.
recovery-agents withdrawn and physiological function monitored closely. Antidotes may be given to keep depth within therapeutic window.

34
Q

why are delirium and aggressive behaviour in stage 2 of anaesthetic depth now uncommon?

A

induction so rapid with use of propofol

35
Q

what is dissociative anaesthesia?

A

use agents such as ketamine (IV) that inhibit transmission of nerve impulses between higher and lower centres of brain.
Mainly used in children and elderly for short procedures, as they appear less susceptible to its post op hallucinogenic effects.

36
Q

Overview of the different drugs required in anaesthesia from a practical viewpoint?

A

premed- hypnotic e.g. benzodiazepine
induction- usually IV e.g. propofol, maybe inhalational (volatile)
IO analgesia- opioid
muscle paralysis- must make patient relaxed to be able to intubate and hence ventilate- necessary as opiate can causer esp depression
maintenance- IV and/or inhalational
reversal of muscle paralysis and recovery, including post op analgesia, neostigmine- reverse muscle relax, anti-emetic- cover nausea from opioid.

37
Q

what are the 4 stages a patient encounters with anaesthesia, and what name is given to these signs?

A

Guedel’s signs
Stage 1: analgesia and consciousness
2: unconscious, breathing erratic but delirium could occur (less likely now with propofol causing rapid induction), leading to an excitement phase.
3: surgical anaesthesia with profound CNS depression, skeletal muscles fully relaxed. 4 levels of increasing depth until breathing weak.
4: resp paralysis and death

38
Q

what affects MAC?

A 
Age (High in infants lower in elderly)
Hyperthermia (increased); hypothermia 
(decreased) 
Pregnancy (increased)
Alcoholism (increased)
Central stimulants (increased)
Other anaesthetics and sedatives (decreased)
Opioids (decreased)
39
Q

which drugs are the exception to all anaesthetics potentiating GABA A mediatied Cl- conductance to depress CNS activity?

A

nitrous oxide (N2O)
ketamine
xenon

40
Q

3 desirable effects in anaesthetics of potentiating GABA activity?

A

sedation
anxiolysis
anaesthesia

41
Q

systems target by aneasthetics?

A

Reticular formation (hindbrain, midbrain and thalamus)
depressed.
Reticular system often called “activating system” due to
ability to increase arousal. (*spinoreticular tract= indirect tract for pain, increases arousal and wakefulness.)
Thalamus transmits and modifies sensory information.
Hippocampus depressed (memory).
Brainstem depressed (respiratory and some CVS).
Spinal cord-depress dorsal horn (analgesia) and motor
neuronal activity (MAC).

42
Q

main IV anaesthetics?

A

propofol (rapid effect)
barbiturates (rapid)
ketamine (slower)
‘induction’.
Can be used as sole anaesthetic in TIVA (Total
IntraVenous Anaesthesia).
All potentiate GABA A except ketamine- acts on NMDA ligand-gated ion channels to inhibit Ca2+ current.

43
Q

how is IV anaesthetic potency described?

A

Plasma concentration to achieve a specific end

point e.g. loss of eyelash reflex.

44
Q

examples of when local anaesthesia is used?

A 
Dentistry
Obstetrics
Regional surgery (patient awake)
Post-op (wound pain) 
Chronic pain management (PHN)
45
Q

characteristics of local anaesthetics e.g. lidocaine?

A

Lipid solubility – potency (higher=greater potency)
Dissociation constant (pKa) – time of onset. Lower pKa=
faster onset
Chemical link – metabolism
Protein binding – duration (higher= for longer duration)

46
Q

mechanism of action of local anaesthetics?

A

use dependent block of VO Na+ channels

47
Q

why can adrenaline prolong duration of action of local anaesthetics?

A

causes vasoconstriction so prevents anaesthetic from escaping

48
Q

ADRs of general anaesthesia?

A

post op nausea and vomiting, and cognitive dysfunction
hypotension
chest infection

49
Q

ADRs of local anaesthetics?

A

CVS toxicity

50
Q

how does the oil/gas partition coefficient of an inhaled aneasthetic relate to its potency?

A

greater= more potent, causes anaesthesia at lower partial pressures
smaller blood/gas coefficient= shorter induction time.

51
Q

why does nitrous oxide not achieve full anaesthesia when used alone?

A

low oil/gas partition coefficient, so low potency, hence high MAC so due to need to maintain an acceptable pO2, this prevents attainment of full anaesthesia using nitrous oxide alone.
but good in combination as lowers MAC of other inhaled agents, and can be rapidly removed by ventilation during recovery-quick

52
Q

examples of adjuvant drugs used in surgery to provide desirable effects not neccessarily provided by general anaesthetics?

A

benzodiazepines e.g. diazepam- anxiolytic and amnesic
opioids e.g. fentanyl- analgesia
nAChR blockers e.g. tubocurarine- muscle relaxation

Sem 5 (35 decks)

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