principles of pharmacology Flashcards

1
Q

what is a general anaesthetic

A

loss of consciousness and global lack of awareness

achieved using general anaesthetic agents

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2
Q

what is a regional anaesthetic

A

producing insensibility in an area or region of the body

local anaesthetics applies to nerves supplying relevant area

e.g. nerve and plexus blocks incl. central neuraxial block (spinal and epidural)

effect is remote from the injection

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3
Q

what is local anaesthetic

A

insensibility in only the relevant area of the boy

applied directly to the tissues

effect is at the site of inkection

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4
Q

GA vs sedation

A

GA - patient is completely unaware of what is occurring

sedation - some awareness but not necessarily recall

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5
Q

regional anaesthesia vs analgesia

A

regional anaesthesia - little to no sensation of any sort from the blocked area

regional analgesia - only pain sensation need be removed or reduced, other sensations may be retained to varying extents

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6
Q

functions of modern anaesthetic machine

A

regulation of fresh gases and mixing to deliver precise concentrations of gaseous agents

addition of precise concentrations of inhaled anaesthetic gases

CO2 removal to allow recirculation of inhaled gases

mechanical ventilation

monitoring is integrated

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7
Q

safety of anaesthesia

A

overall operative mortality 4% - includes all anaesthetic and surgical mortality from all emergency and elective surgery and all patient groups, includes all deaths within 30 days of surgery

anaesthetic mortality 0.00024%

ASA system - mortality is concentrated in ASA groups 3-5

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8
Q

3 components of anaesthesia

A

hypnosis
analgesia
relaxation

an individual anaesthetic may consist of varying contributions from all 3 but doesn’t require all 3

different drugs do different jobs, some do more than one:

GA agents - relaxation, hypnosis (analgesia)
opiates - hypnosis, analgesia
muscle relaxants - muscle relaxants
LA agents - analgesia, relaxation

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9
Q

3 components of anaesthesia - hypnosis

A

unconsciousness

necessary component of any GA

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10
Q

3 components of anaesthesia - analgesia

A

removal of pain and perception of unpleasant stimulus

if patient is unconscious and unaware of pain, still required to suppress reflex autonomic responses to painful stimulus

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11
Q

3 components of anaesthesia - relaxation

A

skeletal muscle relaxation

necessary to provide immobility for certain procedures, allow access to body cavities and permit artificial ventilation

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12
Q

what is balanced anaesthesia and what are the benefits

A

different drugs do different jobs

great degree of control over the individual components of the triad

titrate doses separately and therefore more accurately to meet individual requirements

avoid over dosage of individual drugs

enormous flexibility

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13
Q

problems with balanced anaesthesia

A

polypharmacy - drug interactions, reactions, allergies

muscle relaxation - requirement for artificial ventilation and airway control

separation of relaxation and hypnosis - awareness (possibility of being awake and paralysed and unable to communicate)

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14
Q

general anaesthetic agents - what do they do

A

inhaled and IV

provide unconsciousness as well as a small degree of muscle relaxation

may to differing extents provide analgesia - negligible for all except ketamine

potent drugs - separates them from sedatives - low doses of a potent agent e.g. propofol may be used to provide sedation

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15
Q

how do general anaesthetic agents work

A

suppress neuronal activity in a dose dependent fashion

open chloride channels which hyperpolarise the neurons - suppresses excitatory synaptic activity

neurons become reversibly hyperpolarised and therefore less able to likely to reach their threshold potential and fire

–> globally suppressed neuronal activity

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16
Q

how do IV and inhalational GA agents work

A

inhalational agents - dissolve in membranes, direct physical effects

IV agents - allosteric binding, GABA receptors - open chloride channels

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17
Q

loss of function with GA

A

cerebral function lot from top down

  • most complex processes interrupted first
  • LOC early, hearing later
  • more primitive functions lost later

spinal reflexes relatively spared - primitive and small number of synapses

allows unconscioussness while preserving some autonomic and automatic functions e.g. respiration and BP homeostasis (impaired in dose dependent fashion)

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18
Q

management of a patient under GA

A
ABC - long drawn out resuscitation 
mandates airway management 
impairment of resp function and control of breathing 
CV impact 
care of the unconscious patient
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18
Q

management of a patient under GA

A
ABC - long drawn out resuscitation 
mandates airway management 
impairment of resp function and control of breathing 
CV impact 
care of the unconscious patient
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19
Q

IV anaesthesia - unconsciousness and recovery

A

rapid onset unconsciousness
1 arm - brain circulation time

rapid recovery - due to disappearance of drug from circulation, redistribution V’s metabolism

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20
Q

how do IV anaesthetic agents work so rapidly

A

highly fat soluble drugs and cross basement membranes extremely quickly

cross the blood brain barrier rapidly and get into neural tissues very quickly

leave the circulation very quickly - a bolus only causes temporary unconsciousness

metabolism contributes very little to the immediate termination of action when given as a bolus

21
Q

examples of IV GA agents

A

thiopentone

propofol

22
Q

IV anaesthetics - blood concentration over time

A

brain concentration (effect of the drug) follows blood concentration very closely

blood level is very high initially but falls quickly as drug moves into highly perfused tissues

Muscle picks up the drug more slowly but the effect is large because of the relative high mass of skeletal muscle in the body.

Fatty tissue picks up drug even more slowly but given lengthy enough exposure can store large amounts due to the high fat solubility - large amounts stored after a length procedure, leaches out slowly over a long time period

23
Q

what is a TCI pump system

A

target controlled infusion pump system

with total IV anaesthesia (TIVA) we can’t measure the drug conc in real time so use calculations to make estimates

allows very accurate infusion to achieve specific blood or brain concentrations of agents - calculations and assumptions about physiology based on age, sex and size

24
Q

what are inhalational anaesthetics

A

halogenated hydrocarbons

25
Q

uptake and excretion of inhalational anaesthetics

A

uptake and excretion via lungs

partial pressure gradient - lungs > blood > brain (patient given a relatively high concentration of the agent at induction to breath in, gas moves down pressure gradient to produce unconsciousness)

cross alveolar BM easily

arterial PP equates closely to alveolar PP

26
Q

what is MAC

A

minimum alveolar concentration

the concentration of the drug required in the alveoli to produce anaesthesia with any particular agent i.e. measure of potency

low MAC value = potent agent

e.g. halothane (MAC 0.8%) is more potent than desflurane (6%) because it takes less concentration of the agent to produce the same effect

27
Q

process of inhalational anaesthetics

A

induction - slow, can be good when this is desirable

maintenance of anaesthesia - prolong duration, very flexible

awakening - stop inhalational admin, washout - reversal of conc grad

28
Q

when can a slow induction with inhalational anaesthesia be desirable

A

e.g. potentially obstructing airway

29
Q

what is the main role of inhalational agents

A

extension or continuation of anaesthesia

patient breathes gas mixture containing inhalational agent for duration of procedure and will remain unconscious for as long as the anaesthetic is administered

30
Q

metabolism of inhalational agents

A

undergo very little actual metabolism in the bdoy

breathed back out again almost completely unchanged

31
Q

sequence of GA

A

induction - IV/inhalational
maintenance - inhalational

more modern agents allow IV maintenance (propofol, opiate - remifentanil) - better recovery

+/- additional regional anaesthesia/analgesia

32
Q

physiology of GA: CVS - central effects

A

adverse effects are almost universally depressant (ketamine is the exception)

central effects arise due to depressant effects of the agent on CV centres and nuclei in brainstem

reduced symp nerve activity
direct -ve chronotropic and inotropic effects on the heart
reduced vasoconstrictor tone –> venous and arterial vasodilation

33
Q

physiology of GA: CVS - direct effects

A

direct effects of anaesthetic on vascular smooth muscle and myocardium - compounds the effects of the reduced symp activity

vasodilation –> decreased peripheral resistance
venodilation - decreased venous return, decreased CO

-vely inotropic - worsen the fall in CO

34
Q

physiology of GA: resp

A

all anaesthetic agents are resp depressants (excl ketamine) - reduce hypoxic and hypercarbic drive (depression of brainstem resp centres), decreased tidal volume and increase rate

paralyse cilia

decrease FRC - lower lung vol, VQ mismatch

35
Q

opiate resp depression

A

preserves tidal vol

low resp rate

36
Q

why is post-op oxygen often required

A

fall in lung vol due to anaesthetic and VQ mismatch persists into post-op period

can persist for several days so patients can require post-op O2 for several days

37
Q

what are muscle relaxants and what is required at the same time

A

paralyse skeletal muscle

indiscriminate - resp and airway muscles are also affected

unconsciousness must also be provided with systemic muscle relaxants

38
Q

indications for muscle relaxants

A

ventilation and intubation
when immobility is essential e.g. microscopic surgery, neurosurgery
body cavity surgery - access

39
Q

problems with muscle relaxants

A

awareness - due to the separation of unconsciousness from relaxation in the triad

incomplete reversal - airway obstruction, ventilatory insufficiency in immediate post-op period, unlikely to persist

apnoea - dependence on airway and ventilatory support

40
Q

analgesia in anaesthesia - what is used alongside it

A

if analgesia is good enough then there is no need for unconsciousness e.g. regional anaesthesia which can be used alone or part of a combined technique

most commonly used in conjunction w/ unconsciousness as part of a balanced GA technique w/ or w/o relaxation

Regional techniques usually provide reasonable muscle relaxation by blocking motor nerves so spinal or epidural analgesia may not require additional muscle relaxation.

41
Q

why is intra-operative analgesia used

A

prevention of arousal from pain of surgery
opiates contribute to hypnotic effect of GA
suppression of reflex responses to painful stimuli

e.g. tachycardia, HT, gross movement

regional anaesthesia has no direct sedative effect but can allow lighter levels of GA to be used

42
Q

examples of opiate analgesics

A

fentanyl

morphine, oxycodone

remifentanil

43
Q

fentanyl uses

A

short acting

potent

intra-operative analgesia

44
Q

morphine, oxycodone and conventional opiate uses

A

intra-operative analgesia which we want to continue into the post-op period

45
Q

remifentanil uses

A

very highly potent and extremely short acting

has to be given by infusion

high potency - allows use as a very potent adjunct to inhalation and IV agents, allowing them to be used in lower doses - faster recovery

doesn’t provide any post-op analgesia

46
Q

examples of local anaesthetics

A

lignocaine

bupivacaine

ropivacaine

47
Q

how do local anaesthetics work

A

analgesia w/o hypnosis

block Na+ channels and prevent axonal AP from propagating

effects on every tissue, toxic if delivered wrong (e.g. IV)

48
Q

effects of local and regional anaesthesia

A

retain awareness/consciousness

lack of global effects of GA

derangement of CVS physiology - proportional to site of anaesthetised area

relative sparing of resp function - preferred technique in pts w/ concomitant resp problems

49
Q

US guided regional anaesthesia

A

US used to guide needle placement

safer and more effective delivery of LA drug w/ less likelihood of going intravenously or direct nerve/vascular injury