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BMSc - Neuropharmacology and Behaviour > Clinical Anaesthesia > Flashcards

Clinical Anaesthesia Flashcards

1
Q

What are GAs?

A

A reversible, drug induced state of unconsciousness (including muscle relaxation and analgesia)

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2
Q

What are the different stages of anaesthesia?

A

Stage 1 = state of analgesia or disorientation
Stage 2 = stage of excitement or delirium
Stage 3 = state of surgical anaesthesia
Stag 4 = medullary paralysis - ultimately cardio/resp arrest

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3
Q

Describe the triad of GA

A

Narcosis
Muscle Relaxation
Analgesia
== balanced GA

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4
Q

Describe the different narcosis agents

A

Inhalational (induction and maintenance) - isoflurane, sevoflurane (sweet smelling, smooth induction, good for children), desflurane (low blood/gas solubility co-efficient, rapid onset and offset, highly irritant to airways, useful for maintenance and rapid wakeup)

IV anaesthetics (smooth and rapid induction):

  • Propofol (often with midazolam to produce synergistic action, allowing for a reduced dose of each agent, reducing SE)
  • Thiopentone
  • Etomidate
  • Ketamine (dissociative)

Frequent bolus for maintenance - total intravenous general anaesthesia

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5
Q

How are inhalational anaesthetics produced?

A

Must be vaporised

Pass anaesthetic gases such as oxygen, NO or air over the liquid anaesthetic, transferred to patient

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6
Q

Describe the drawbacks of IV anaesthetic induction

A

Although a smooth induction, there are significant SE

Propofol; hypotension, resp depression

Thiopentone; hypotension (less so than Propofol), resp depression

Etomidate; cardiovascular smooth induction but can produce pain on injection

Ketamine; unusual form of anaesthesia, dissociative

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7
Q

How is muscle relaxation achieved in GA?

A

NMJ agents that target NAChARs on post synaptic membrane on skeletal muscle

These are different from general muscle relaxants (BZD, baclofen)

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8
Q

What are the 2 groups of NMJs in GA?

A

Depolarizing - suxamethonium

Non-depolarizing - atracurium, vecuronium, rocuronium

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9
Q

Within the dorsal horn, where do the nociceptor fibres terminate in the laminae of rexed

A

Layer 1 and 2 (C fibres)

Layers 1 and 5 (A-delta)

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10
Q

Where is the substantia gelatinosa located?

A

Layer 2 of laminae of rexed

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11
Q

How is pain controlled in the peri-op period?

A

Pain assessment is used to guide analgesia (visual analogue scale)
WHO pain ladder
Other techniques; LA (local infiltration or regional block), centrally acting (non-opioid); amitriptyline, gabapentinoids
Non-pharma; TENS, acupuncture (release of endogenous opioids)
Psychological

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12
Q

Describe the ideal analgesic drug

A

Suppressive of all pain types (MSK, visceral, dull, shooting)

Inexpensive

Does not inhibit other sensations e.g. motor block

Good oral bioavailability/ easily metabolised and excreted

Non-toxic

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13
Q

Describe opioids

A

Mixture of alkaloids from opium poppy

Phenanthrene derivative
2 planar rings and 2 aliphatic rings
Morphine derivatives; based on substitution at C3 and C6 to OH and N17

Semi-synthetic opioids:

  • Methadone (long half life)
  • Piperidines (pethidine, fentanyl; short half life with high potency)
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14
Q

Describe the central effects of opioids

A 
Analgesia 
Sedation 
Euphoria (dependence) 
Respiratory depression (careful titration) 
Anti-tussive 
N+V (use antiemetics) 
Pupillary constriction
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15
Q

Describe the peripheral effects of opioids

A

Hypotension (direct CVS depression, vasodilation, alongside central effect)

Increases sphincter tone and reduces gastric motility = constipation, nausea

Urinary retention

Histamine release = itch (pseudoallergic effect)

Immunosuppressant effect - poorer outcomes after surgery

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16
Q

Describe the opioid receptors

A

Mu (OP3/ MOR)
Kappa (OP2/ KOR)
Delta (OP1/ DOR)
Sigma (not true opioid receptor)

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17
Q

Where can the mu receptors exert analgesic effects?

A

Supra-spinal
Spinal
Peripheral

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18
Q

Describe the different endogenous ligands?

A

Mu; beta endorphin, endomorphin
Delta; enkephalin (met and leu enkephalin)
Kappa; dynorphin

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19
Q

Describe the MOA of opioids

A

Act via Gi/o
Inhibit calcium entry via N and P/Q channels (also R)
Facilitate potassium efflux via IR channels (GIRK)
Inhibits cAMP
Inhibit nT release

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20
Q

What are the advantages and disadvantages of PCA?

A

Up to 12 mg of morphine per hour

Ad:

  • Dose matches need
  • Reduced nursing workload coordination
  • Patient autonomy

Disad:

  • Expensive
  • Cooperation and breakthrough pain
21
Q

What are other routes of opioid administration (not IV, IM)

A

Oral; not immediately after major abdo surgery, not suitable for NBM or PONV (peri-op nausea and vomiting)

Sublingual; limited to buprenorphine (partial agonist)

Transdermal (fentanyl); highly lipophilic therefore well absorbed, useful for chronic pain

22
Q

What are the benefits to a spinal and epidural opioid injection?

A

Excellent analgesia
Spinal - directly into CSF into substantia gelatinosa

SE:

  • Resp depression
  • Urinary retention (men)
  • Itching +++
  • N+V
23
Q

What is the bioavailability of opioids?

A

Ratio of a drug that reaches the systemic circulation in comparison with IV injection

Oral morphine = extensive first pass metabolism (only 30% reaches systemic)

Synthetic morphine 6 glucuronide achieves bioavailability of up to 50%

Topical/ sublingual - increased bioavailability

IV/ spinal/ epidural analgesia

24
Q

Describe the metabolism and excretion of opioids

A

Converted to polar metabolites (liver) and excreted via kidney

Hydroxyl groups are conjugated with glucuronide (e.g. morphine)

Esters are hydrolysed by esterase’s (pethidine)

N-demethylation also occurs (methadone) - this is why methadone has a long half life

25
When are NMJ drugs needed?
Tracheal intubation Mechanical ventilation Surgery where muscle relaxation is required
26
Describe the basic physiology of the neuromuscular junction
Motor nerves extend form brainstem (cranial nerves) or spinal cord to the skeletal muscle Insulated with myelin, speeding conduction to 50-100 m/s (saltatory conduction) Axon terminates in motor end plate
27
Describe the most common subtype of nicotinic ACh receptors
2 alpha 1 Beta 1 Epsilon Delta Forms a pentameric structure around a central pore ACh binds to alpha 1; conformational change, allowing Na+ influx into the post synaptic endplate = endplate potential
28
What is the action of botulinum toxin?
Reduces the release of ACh | Flaccid paralysis
29
What do NMJ blockers target?
Nicotinic ACh receptors on post synaptic membrane
30
What is the only depolarising NMB?
Suxamethonium - quaternary ammonium compound (2 ACh molecules) Each ACh moiety binds to an alpha subunit - opening the channel Clinically: - Fasciculation then relaxation (refractory period) - Rapid onset (60-90 secs) - Rapid offset (3-5 mins) due to plasma cholinesterase's
31
Describe the different phases of suxamethonium NMJ blockade
Despite initial activation of nicotinic ACh receptors, the ongoing activation leads to inactivation = paralysis Phase 1 block: - Persistent activation of endplate nicotinic receptors - Prolonged depolarisation of endplate - Inactivation of voltage-gated sodium channels Phase 2 blocks: - Desensitization of endplate nicotinic receptors - Repolarization of endplate - Receptor desensitization maintains blockade
32
How is sux metabolised?
Plasma pseudocholinesterase's Gene encoding plasma cholinesterase's is E1u 3 abnormal genes: E1a (atypical), E1s (silent), E1f (fluoride-resistant) associated with decreased enzymatic activity 94% of population are heterozygous for usual gene (normal response to sux); E1a homozygotes in 0.03% of population, E1s in 0.001% and E1f in 0.0003% = all remain apnoeic for 1-2 hours - suxamethonium apnoea
33
What are the SE of suamethonium?
Muscle pains Increased intraocular/ intragastric (regurgitation = aspiration pneumonia) / intrathoracic pressure Increased ICP Hyperkalaemia (issue in elderly, or renal issues) Increased vagal tone (incr parasymp activation) - brady Anaphylaxis (quaternary ammonium compound) Prolonged apnoea (plasma cholinesterase deficiency) Trigger for malignant hyperpyrexia (inherited condition due to mutation within ryanodine (sarcoplasmic reticulum) resulting in intense muscle spasms and hyperthermia
34
Describe non-depolarizing NMJ agents
Competitive nicotinic receptor antagonists at NMJ Highly ionised/ water soluble 2 main classes: - Benzylisoquinolinium; tubocurarine/ atracurium/ mivacurium - Aminosteroids; vecuronium, rocuronium
35
What is the half life of tubocurarine?
100 mins | Causes twitch-tension
36
What is a feature of all non-depolarizing muscle agents?
Post-tetanic fade Twitch height after sustained tetanus is reduced following administration Fade due to blockade of pre-synaptic ACh receptors
37
Describe atracurium
Quaternary ammonium compound broken down by Hoffman Degradation (temp and pH dependent) and plasma esterase's Undergoes spontaneous hydrolysis; not reliant on normal hepatic and/or renal metabolism
38
What is the benefit of Hoffman Degradation of Atracurium?
Provides a safety net for patients (especially those with hepato-renal failure) Duration; 20-30 mins No direct cardiac effects (c.f. suxamethonium) Histamine release (local - itch, wheals. Systemic; hypotension, bronchospasm)
39
Describe vecuronium
Aminosteroids Possess a quaternary ammonium ion attached to the steroid nucleus (androstane) and an acetate ester Minimal histamine release, mild bradycardia and moderately rapid onset Active metabolites (50-70% of parent drug activity) Reversal; largely through redistribution, elimination t1/2 is about 60 mins Prepared as a powder with mannitol
40
Describe rocuronium
Rapid onset curonium, desacetoxy analogue of vec Similar onset time as sux; 60-90 secs Metabolised in liver; t1/2 = 40-60 mins Novel reversal agent; sugammadex
41
How can the reversal of NMJB be achieved?
For non-depolarizing agents; increase ACh within the synaptic cleft to act as competition. This is achieved by blocking activity of acetylcholinesterase
42
Describe the action of anticholinesterases in the reversal of non-depolarizing NMJB
Inhibit acetylcholinesterases to prolong half life of ACh Short acting = edrophonium Medium acting = neostigmine/ pyridostigmine Irreversible = dyflos
43
Describe ACh
nT at NMJ (nicotinic AChRs) and also parasympathetic nervous system/ ganglia (muscarinic AChRs), and therefore when using anticholinesterases co-administration with atropine of glycopyrrolate (anti-muscarinic) is required to prevent unwanted muscarinic effects (parasympathetic NS): - Brady - Hypotension - Bronchoconstriction - Incr peristaltic activity - Hypersalivation - Incr lacrimation
44
Describe irreversible anticholinesterases
Pentavalent organo-phosphorous compound Used as insecticides and chemical weapons; dyflos or parathion Relies on synthesis of new enzyme s(days/ weeks) Chronic exposure = neurological symptoms Prophylactic (medium acting) carbamates and atropine (anti muscarinic) may prevent poisoning Centrally acting agents have potential use in Alzheimer's disease
45
Describe sugammadex
Modified gamma-cyclodextran Eight neg charged carboxy thio-ethers binds to the quaternary nitrogen of rocuronium (and vecuronium) Rapid reversal of mod or deep paralysis (1-2 mins) Minima risk of residual paralysis Avoids autonomic SE assoc with neostigmine and muscarinic antagonists Cost prohibits widespread use
46
Compare non depolarizing drugs from depolarizing drugs
Non-depolarizing = competitive muscle relaxants compete with ACh for receptor sites at NMJ, with action reversal with anticholinesterases such as neostigmine Non-depolarizing have a slower onset of action than sux Non-depolarizing; classified by duration of action (short = 15-30 mins, intermediate (30-40 mins) and long (60-120 mins), although duration of action is dose-dependent Short/ intermediate = atracurium, vecuronium Long duration of action = pancuronium Non-depolarizing agents have no sedative or analgesic effects, and furthermore do not trigger malignant hyperthermia Patients in intensive care or tracheal intubation/mechanical ventilation = non-depolarizing agent is chosen according to onset of action - Rocuronium due to rapid onset can facilitate intubation - Atracurium or cisatacurium are suitable for long term NMJ blockade because duration of action is not dependent on elimination by liver or kidneys
47
Describe atracurium
Benzylisoquinolinium NMJB with intermediate duration of action Undergoes non-enzymatic metabolism which is independent of liver or kidney function, thus allowing use in patients with hepatic or renal impairment CV effects are assoc with significant histamine release; which can be minimised by slow administration or divided doses over 1 min
48
Describe rocuronium
Effect within 2 mins, most rapid onset of non-depolarizing NMJ drugs Aminosteroids with intermediate duration of action Minimal CV effects; high doses produce mild vagolytic activity
49
Describe sux
Most rapid onset of action of all NMJBs Ideal if fast onset and brief duration of action are required e.g. tracheal incubation (RSI) Action cannot be reversed and recovery is spontaneous; anticholinesterases such as neostigmine potentiate the NMJ block Should not be given after anaesthetic induction because paralysis is usually preceded by painful muscle fasciculation's Tachycardia occurs with single use, bradycardia occurs with repeated doses Premed with atropine reduced bradycardia as well as excessive salivation assoc with sux Prolonged paralysis may occur in dual block, which occurs with repeated or high doses of sux Development of non-depolarising block following initial depolarising block. Myasthenia gravis = resistant to sux but may develop dual block = delayed recovery

BMSc - Neuropharmacology and Behaviour (27 decks)

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