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Anaesthesia > Anaesthetic Pharmacology > Flashcards

Anaesthetic Pharmacology Flashcards

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1
Q

What is the anaesthetic dose for propofol?

A

2 mg/kg (normal anaesthetic dose)
3 mg/kg (RSI dose)

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2
Q

Describe the mechanism of action of propofol in regards to its anaesthetic properties.

A

Anaesthetic mechanism: Propofol is a GABAA receptor agonist, causing an influx of calcium into post-synaptic cells resulting in hyperpolarisation, and inhibits depolarisation

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3
Q

What are the clinical effects of propofol that make it a useful anaesthetic agent? (5)

A
  1. Hypnosis
  2. Antipruritic
  3. Antiemetic
  4. Decreased cerebral metabolic consumption rate of O2 (CMRO2)
  5. Decreased airway reflexes
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4
Q

What are the effects of propofol on the circulatory system?

A
  1. Decreased preload (2* sympathetic inhibition causing decreased vascular tone)
  2. Decreased afterload (also 2* sympathetic inhibition)
  3. Stable cardiac output (contractility maintained)
  4. Hypotension (from sympathetic inhibition and vasodilation rather than direct inotropic effects)
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5
Q

How is propofol metabolised and excreted?

A

Hepatic metabolism, renal excretion. Excretion not impaired by renal or hepatic disease

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6
Q

What is the mechanism of action of Ketamine? (3)

A
  1. Non-competitive antagonist at NMDA + Glutamate receptors
  2. Muscarinic Ach recptor agonist
  3. Opioid receptor
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7
Q

What are the clinical effects of ketamine that make it a useful anaesthetic agent? (5)

A
  1. Dissociative anaesthesia
  2. Amnesia
  3. Analgesia
  4. Bronchodilation
  5. Cardiac stable agent (relatively)
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8
Q

What are the main side effects of propofol? (4)?

A
  1. Hypotension
  2. Pain on injection
  3. Propofol infusion syndrome
  4. Respiratory depression
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9
Q

What are the main effects of propofol infusion syndrome? (3)

A
  1. Metabolic acidosis
  2. Rhamdomyolysis
  3. Cardiac failure
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10
Q

What is the effect of ketamine on the CVS?

A

Decreased re-uptake of adrenaline and noradrenaline, causing increased SNS activity

Mild direct myocardiac depression

=> overall relatively stable fro CVS perspective

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11
Q

What are the adverse effects of ketamine? (4)

A
  1. Emergence phenomena
  2. Involuntary movements
  3. Increased tracehobronchial secretions
  4. PONV
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12
Q

What is the mechanism of action of midazolam?

A

GABA-A receptor agonist, causing membrane hyper-polarisation and subsequent inhibitory effects of GABA on CNS

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13
Q

What are the clinical effects of midazolam that make it a useful anaesthetic agent? (5)

A
  1. Anxiolysis
  2. Sedation
  3. Anterograde amnesia
  4. Depression of upper airway reflexes
  5. Skeletal muscle relaxation
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14
Q

What are the adverse effects of midazolam?(2)

A
  1. Respiratory depression
  2. Decreased SVR => decreased MAP
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15
Q

What are the 2 broad types of muscle relaxants?

A

Depolarising, Non-depolarising

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16
Q

What is the chemical structure of suxamethonium and how does it result in neuromuscular blockage

A

It has 2 molecules of acetylcholine, linked by their acetyl groups

One or both of these molecules binds to the nicotinic-Ach receptor in the post-synapatic junction, thus causing depolarisation and competitive inhibition of further Ach

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17
Q

Which neurotransmitters and receptors are involved in the activation of skeletal muscle

A

Acetylcholine crosses the NMJ and binds to the nicotinic acetylcholine receptors found in the post-synaptic NMJ.

This causes depolarisation and thus muscle activation

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18
Q

What is the mechanism of action of suxamethonium

A

Depolarising muscle relaxant

It binds to one or both of the post-synaptic nicotinic-Ach receptor subunits, causing depolarisation

As there is no plasma acetylcholinesterase in the NMJ, depolarisation is blocked until the suxamethonium diffuses out of the NMJ

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19
Q

What the the side effects of suxamethonium? (8)

A
  1. Anaphylaxis
  2. MH
  3. Sux apnoea
  4. Myalgia
  5. Masseter spasm
  6. Hyperkalaemia
  7. Increased salivation/secretions
  8. Phase 2 block
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20
Q

What are the risks of repeated or prolonged use of suxamethonium?

A

Phase 2 block, where the post-junctional receptor repolarises but is unable to respond to further Ach

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21
Q

Why does suxamethonium not cause paralysis of smooth muscle?

A

Suxamethonium binds to the nicotinic Ach receptors, whereas smooth muscle contains muscarinic receptors

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22
Q

What is the mechanism of action of non-depolarising muscle relaxants?

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A

Competitive binds to post-synaptic nicotinic-Ach receptors, without causing depolarisation

There is dynamic binding with repeated association and dissociation

Ach will begin to bind to the receptor once Ach levels outcompete the levels of the medication

23
Q

What is the mechanism of action of non-depolarising muscle relxants?

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A

Competitive antagonism with the post-synaptic nicotininic Ach receptors

They bind to one or both alpha subunits of the receptor, do not cause conformational change, and inhibit Ach binding

There binding is dynamic with repeated association and dissociation

24
Q

What are the main drug factors that affect onset of NDMRs? (4)

Study These Flashcards
A
  1. Dose
  2. Potency
  3. ‘Priming principle’ -> if 10% of dose is given a few minutes before the complete dose
  4. Drug interactions
25
What are the main patient factors affecting onset of NDMRs? (5)
1. Cardiac output 2. Skeletal muscle bloodflow 3. Age (younger people tend to have higher CO, and hence distribute the drug more rapidly) 4. Site of injection (IV faster than IM) 5. Myasthenia Gravis/Neuromuscular diseases
26
What is the sequence of paralysis when using muscle relaxants?
Small and central muscles first, peripheral muscles last (eg finger twitch)
27
What physiological factors prolong the duration of NDMRs? (5)
1. Acidosis (prolonged) 2. Hypothermia (prolonged) 3. Hypokalaemia (prolonged) 4. Hypocalcaemia (prolonged) 5. Hypermagnesaemia
28
What sort of conditions/diseases need to be considered when delivering muscle relaxants?
Neuromuscular conditions
29
What is the intubating doses of rocuronium, and their onset of action?
0.6mg/kg for intubation. Onset in 60-90 seconds 1.2mg/kg for RSI. Onset in 60 seconds
30
What is the approximate duration of rocuronium?
30-40 minutes
31
How is rocuronium metabolised?
Minimally metabolised, excreted in urine and bile
32
Describe the mechanism of action of sugammadex?
It is a donut shaped molecule which binds to NDMRs in the plasma (during the dissociation from the receptor) Chelates the NDMR, which then is excreted in urine
33
Is there need for anticholinergics when administering sugammadex?
No
34
What is the dose of sugammadex?
2-4mg/kg after 0.6mg/kg rocuronium 8-16mg/kg for deeper levels of blockade
35
How can NDMRs be reversed?
Amino-steroid compounds can be reversed with sugammadex All NDMR's can be reversed with anticholinesterases
36
What is the mechanism of action of anticholinesterases in regards to reversal of NDMRs?
Forms covalent bonds with estaeratic site of acetylcholine-esterases, thus inhibiting plasma cholinesterase Thus there is more circulating Ach, which competitively binds to the Ach receptors to which NDMRs are bound
37
What is the dose of neostigmine for reversal of NDMRs?
50mcg/kg IV
38
What is the side effect of neostigmine, and what needs to be done about it?
Neostigmine and other anticholinesterases cause inhibition of cholinesterases, which results in excessive plasma Ach levels This can cause bradycardia and increased secretions. By also giving atropine or glycopyrrolate (competitively binds to muscarinic Ach receptors), the effects of excessive muscarinic activation are avoided, whilst still alowing reversal of NDMRs on the nicotinic receptors
39
What is the initial distribution half life of propofol?
1-3 minutes
40
What is the difference between opium, opiates, and opioids?
Opium: a mixuture of alkaloids from the poppy plant Opiates: all naturally occuring substance with morphine-like properties Opioids: subtances which bind to the opioid receptors
41
What is the MOA of opioid agonists?
Opioid receptors are G-protein coupled receptors, located in the brain and spinal cord When opioids bind to the receptor in substantia gelatinosa in the spinal cord, there are 2 main effects: 1. Inactivation of voltage-gated Ca2+ channel on the A-delta fibre (presynaptic), causing inhibition on neurotransmitter release (Substance P, glutamate), and hence decreasing the pain signal 2. Activation of the K+ channels in the post-synaptic neuron (secondary neuron) which causes hyperpolarisation and thus decreased neuronal excitability
42
What are the main opioid receptor subtypes? (3)
Mu Kappa Delta
43
What are the main effects of the Mu opioid receptor? (5)
1. Analgesia 2. Euphoria 3. Sedation 4. Respiratory depression 5. Constipation
44
What are the main effects of the Kappa opioid receptor? (1)
Dysphoria via reduction of dopamine release
45
What are the main effects of the Delta opioid receptor? (2)
1. Hallucinogenic effects 2. Constipation
46
What are the CNS effects of opioids? (6)
1. Analgesia 2 Euphoria 3. Dysphoria 4. Sedation 5. Anxiolysis 6. Decreased MAC
47
What are the respiratory effects of opioids? (6)
1. Respiratory depression 2. Dose dependent decreased response to hypercapnia 3. Decreased ventilatory response to hypoxia 4. Suppression of the cough reflex 5. Depression of upper airway reflexes 6. Bronchospasm
48
What the the CVS effects of opioids? (4)
1. DecreasedSVR, causing hypotension 2. Decreased HR 3. Inhibition of broreceptor reflex 4. Myocardial depression
49
Describe the pharmacokinetics of IV morphine
Onset of action after 1 minute Peak effect after 5-20 minutes
50
What features of fentanyl make it useful in anaesthesia? (6)
1. Blunting of airway reflexes 2. Relatively cardiac stable 3. No significant histamine release 4. Analgesia 5. Sedation/anxiolysis 6. Decreased MAC
51
Describe the pharmacokinetics of IV fentanyl
Onset of action in 30 seconds Peak effect in 3-5 minutes
52
Describe the pharmacokinetics of IV alfentanil
Onset of action in < 30 seconds Peak effect in 1-2 minutes
53
What is the use case for Remifentanil? (3)
Remifentanil is an ultra-short acting opioid, an as such can be used in instances where there are discrete but intensely painful stimuli It can also be used in instances where there needs to be tight blood pressure control (eg. neurosurgery) It can be used together with propofol for induction without use of musce relaxant
54

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