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ED Primary Exam > Week 7 Pharmacology - Anaesthestics/Sedation + Antipsychotics + Antidepressants > Flashcards

Week 7 Pharmacology - Anaesthestics/Sedation + Antipsychotics + Antidepressants Flashcards

1
Q

What are common amide local anaesthetics?

A

Lignocaine, Ropivocaine, Buprivocaine, Prilocaine

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2
Q

What is the major clinical difference in amide vs ester local anaesthetics?

A

Amides are metabolised in liver (p450 complex)

Esters metabolised by pseudocholinesterase in plasma

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3
Q

What is the mechanism of action of local anaesthetics?

A

Na+ channel blockade, increased with activated channels. Causes reduced amplitude and eventually failure to generate AP –> block impulse conduction along axon

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4
Q

What is the duration of action of lignocaine?

A

1-2 hours
2-4 hours with adrenaline

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5
Q

What are the CNS effects of LA toxicity?

A

perioral and tongue numbness
Lightheadedness
Nystagmus
Tinnitus
Visual disturbance
Seizure
Sedation

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6
Q

What are the CVS effects of LA toxicity?

A

Cardiovascular collapse/hypotension
Bradycardia
Arrhythmia

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7
Q

What is the MAC?

A

Minimal alveolar concentration

Minimum alveolar concentration at which 50% of population do not respond to surgical incision

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8
Q

What is the blood partition co-efficient?

A

Describes solubility of inhalational agent –>gases need to exert a partial pressure to cross BBB, and the higher the solubility, the higher the amount of gas needed to be dissolved in blood before it can exert that partial pressure.

Therefore gases with low partition co-efficient are generally preferred.

This is because larger co-efficient means longer onset and offset of effect

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9
Q

What is FA and FI?

A

FA = alveolar concentration of gas

FI = inspired concentration of gas

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10
Q

What is the practical application of FA/FI ration?

A

The greater the difference between the two, the slower the induction

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11
Q

What factors affect alveolar anaesthetic gas concentration?

A

Solubility in blood
Alveolar blood flow
Difference in partial pressure in venous blood and alveolar gas

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12
Q

What is the difference between gaseous and volatile inhaled anaesthetic agents?

A

Refers to matter state at room temperature.

Volatile have low vapour pressure and high boiling point and are liquids at room temperature

Gaseous inhaled have high vapour pressure and low boiling point, are gases at room temperature

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13
Q

What are examples of volatile inhaled anaesthetics?

A

Sevoflurane
Isoflurane
Halothane
Desflurane

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14
Q

What are examples of gaseous inhaled anaesthetics?

A

Nitrous oxide
Xenon

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15
Q

How are inhaled anaesthetics generally eliminated?

A

Via ventilation - particularly true for agents with low blood gas partition co-efficient, as being poorly soluble, it will not be taken up into tissues, and instead will be removed by increasing ventilation.

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16
Q

What is the mechanism of action of NO?

A

NMDA receptor antagonist, similar to ketamine –> able to produce analgesia

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17
Q

What is the mechanism of action of inhalational anaesthetics?

A

Unclear, but likely potentiation of GABA inhibitory signalling and attenuation of excitatory channels

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18
Q

What factors affect the uptake of inhalational agents?

A

Solubility
Cardiac output –> greater distribution and peripheral uptake
Alveolar –> venous partial pressure difference

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19
Q

What volatile anaesthetic is primarily metabolised in the liver?

A

Halothane - H for hepatic

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20
Q

Does propofol have analgesic effect?

A

No

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21
Q

Why is propofol formulated in emulsion of soybean, glycerol, lecithin, egg yolk?

A

Poorly soluble in water

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22
Q

What is the time to recovery after induction dose of propofol?

A

8-10 mins

23
Q

What is the mechanism of action of propofol?

A

Potentiation of chloride current mediated through GABAa receptor complex

24
Q

What are the pharmacokinetics of propofol?

A

A: IV
D: 2-10L/kg, 97% protein bound!
M: 3-8 duration of action, rapidly metabolised in liver to water soluble compound
E: Renal excreted

25
Q

What is the benefit of propofol over thiopental in induction for intubation?

A

Propofol blunts airway reflexes
Thipentone also can cause intermittent porphyria

26
Q

What are the adverse effects of propofol?

A

Hypotension (Decreased systemic vascular resistance)
Pain on injecting
No analgesia

27
Q

Compare cerebral blood flow between ketamine and propofol?

A

Propofol = decreased cerebral blood flow and cerebral metabolic rate

Ketamine = increases cerebral blood flow and metabolic rate. Transient increase in HR and blood pressure.

28
Q

What is the caution in using ketamine in patients who are shocked?

A

Due to increased sympathetic activity - if patient has already had massive catecholamine discharge, it can cause hypotension/worsened shock state

29
Q

What is the mechanism of action of ketamine?

A

NMDA receptor antagonist

30
Q

How is ketamine metabolised?

A

Hepatically, then renal excretion

31
Q

What common neurotransmitter do all neuromuscular blocking drugs bear resemblance to?

A

Acetylcholine

32
Q

What is the prototype depolarising NM blocker?

A

Succinylcholine - (Suxamethonium)

33
Q

What is the mechanism of action of suxamethonium?

A

Phase 1: reacts with nicotinic receptors to open channel and cause depolarisation. Then maintains membrane depolarisation as not metabolised effectively, doesn’t respond to further impulses. Not reversed by cholinesterase inhibitors.

Phase II: prolonged exposure leads to desensitisation, this phase can be reversed by cholinesterase inhibitors

34
Q

How is suxamethonium metabolised?

A

Plasma and hepatic cholinesterase

35
Q

What effect does suxamethonium have on cardiac function?

A

Negative isotropy and chronotropy

36
Q

What are the adverse effects of suxamethonium?

A

Hyperkalaemia due to fasciculations
Increased IOP, contraindicated if ruptured globe
Increased intragastric pressure due to fasciculations
Malignant hyperthermia

37
Q

What are the two main categories of non depolarising NM blockers?

A

Isoquinoline:
- Atracurium
- Cistracurium
- Tubocurarine

Steroid:
- Pancuronium
- Rocuronium
- Vecuronium

38
Q

What is the mechanism of action of non depolarising NM blockers?

A

Competitive antagonists of nicotinic receptors by competing with acetylcholine.

Also can block pre-junctional sodium channels and reduce mobilising ACh from nerve ending

39
Q

Compare metabolism of atracurium and rocuronium?

A

Atracurium = Hoffman elimination in plasma
Rocuronium = 90% hepatic

40
Q

What is the duration of action of atracurium and rocuronium?

A

20-35 mins

41
Q

What is the mechanism of action of suggamadex?

A

Binds to the drug itself and prevents antagonism at receptors, it is the reversal agent for rocuronium and vecuronium

42
Q

What is the mechanism of action of benzodiazepines?

A

GABA potentiation via binding to GABAa site on GABA ion channels and causing Cl- influx

43
Q

What is the half life of diazepam?

A

49 hours, Vd1L, highly protein bound

44
Q

What is the structure of the GABA chloride channel?

A

5 subunits arranged concentrically around ion channel

45
Q

What is the general rule regarding metabolism of anti-epileptic/convulsant medications?

A

Largely hepatic clearance, long half lives, many inducers of liver enzymes, and lots of interactions!

46
Q

What is the mechanism of action of carbamazepine and phenytoin?

A

Targets presynaptic membrane voltage gated sodium channels to reduce glutamate release from nerve terminals

47
Q

What is the mechanism of valproate?

A

Blocking NMDA receptor mediated excitation and enhancing GABA transmission

48
Q

What is the biogenic amine theory of depression?

A

Brain amines (NA, 5-HT) function as mood neurotransmitters and their functional decrease manifests as mood disorder. Based on premise of therapies which increase amine availability in CNS

49
Q

How are antipsychotics classified?

A

Typical:
- Haloperidol
- Chlorpromazine

Atypical: - Also 5HT activity
- Quetiapine
- Risperidone
- Olanzapine

50
Q

What are the prominent side effects of each category of antipsychotics?

A

Typical = EPSE
Atypical = metabolic

51
Q

What is the dopaminergic hypothesis of schizophrenia?

A

Relative excess of dopamine neurotransmission leads to symptoms of schizophrenia

52
Q

What are the dopaminergic tracts of the brain?

A

Mesocortical and mesolimbic –> mentation and mood
Nigrostriatal = Extrapyramidal function

53
Q

What are the two major effects of acute overdose in anti-psychotics?

A

Hypotension - usually responsive to fluids
Seizure via lowering seizure threshold

54
Q

What are side effects/toxicity of antipsychotics?

A

Neuroleptic malignant syndrome (treatment with dantrolene as with malignant hyperthermia)
EPSE: bradykinesia, rigidity, tremor
Tardive dyskinesia

ED Primary Exam (46 decks)

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