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Pharmacology. > 12. Induction agents > Flashcards

12. Induction agents Flashcards

1
Q

What is propofol full name?

Draw propofol.

A

2, 6, diisopropylphenol.

(Page 2 of diagrams sheet)

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2
Q

How does propofol work?

A

Enhances GABA at GABAa and NMDA receptors.

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3
Q

What is the preparation of propofol?

A

1 or 2% lipid emulsion containing egg lecithin, soya bean and glycerol.

Disodium edetate added to chelate bacterial growth

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4
Q

What is the metabolism of propofol?

A

In the liver. 40% glucuronide conjugation and 60% metabolised to quinol

No active metabolites

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5
Q

How is propofol excreted?

A

As glucuronide and sulphate conjugates in the urine

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6
Q

Do the table of induction agents

A

Table 3 in reference table document

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7
Q

How can drug extravasation cause compartment syndrome?

A

Osmolarity over 290 exert osmotic pressure causing compartment syndrome.

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8
Q

What does propofol do to the CNS?

A

Hypnotic

Reduces CPP, ICP and cerebral O2 requirement

Occasional dystonias

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9
Q

What does propofol do to the GI system?

A

D2 receptor antagonist so an antiemetic

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10
Q

What causes propofol injection pain?

What happens to urine.

A

Early = direct irritation

Late = bradykinin mediated

Can go green from phenol derivatives.

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11
Q

What level of propofol TCI do people normally go to sleep at?

A

Effect site concentration of 2.5-3mcg

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12
Q

What causes propofol infusion syndrome?

Risk factors?

Volumes of propofol?

S/S?

Treatment?

A

Genetic predisposition plus critical illness.
Low carb state causes catecholamine induced lipolysis. increased free fatty acids, decreased utilisation and mitochondrial impairment of beta oxidation. Causes increased FFS’s and acyl carnitine complexes (pro arrhythmia)

Risks: kids, head injury, sepsis and high steroids/catecholamines

Over 4mg/kg/hr for 24h.

See: metabolic acidosis, brugada, rhabdo, and high triglycerides.

Rx: stop propofol, supportive and monitor Ck.

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13
Q

What do we do during a manually controlled infusion of propofol?

A

Aim for blood concentration of 3mcg/ml.

Induction 1mg/kg, then 10mg/kg for 10m, then 8 for 10 and 6 after.

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14
Q

What are kids propofol TCI models?

A

Peadfusor for 1-16y and 5-61kg

Kataria 3-16y and 15-61kg

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15
Q

What is the basic structure of benzo’s?

A

Benzene ring attached to a Halogen, with a diazepine ring attached to a carbonyl group

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16
Q

What are the 5 general actions of benzo’s?

A

Sedation, amnesia, anti-convulsant, anxiolysis and muscle relaxation

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17
Q

What is the general mechanism of benzo’s?

What receptors do they work on?

What do these do?

A

Enhance GABAa, binding between alpha and gamma subunits.

19 different types of receptor and BDZ’s have different affinities for each.
BZ1 = cord and cerebellum = anxiolysis
BZ2 = cord, hippocampus and cortex = sedation and anticonvulsant

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18
Q

What are the different categories of BDZ’s and what are the drugs?

A

Short acting: midazolam and alprazolam
Medium: tempazepam, clonazepam and lorazepam
Long: diazepam and chlordiazepoxide

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19
Q

What is the protein binding, lipid solubility and metabolism common to BDz’s?

A

All strongly protein bound and lipid soluble

All metabolised in the liver.

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20
Q

Do BDZ table

A

Page 2 of reference table documents

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21
Q

What pH is midazolam and what pH does it undergo ring closure?

A

PH 3.5 = ionised
Over pH 4 = unionised.

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22
Q

What does midazolam do to sleep?

A

Reduced REM and slow wave sleep

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23
Q

What does midazolam do to the respiratory system?

A

Reduced TV
Slight increased RR
Reduced CO2 sensitivity
Apnoea in high doses

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24
Q

What does midazolam do to the CV system?

A

Reduced SVR, preload, CO and BP.
Obtunds presser response to laryngoscopy

25
Q

What dose do we use for midazolam infusion for status and why can we use this?

A

High clearance rate so less CSHT

Use 1-20mg/h

26
Q

What does midazolam do in pregnancy?

A

Crosses placenta and increases cleft palate. Excreted in milk to variable degrees.

27
Q

What is flumazenil?

Dose?

Contraindications?

S/E?

A

Imidazobenzodiazepine used to reverse benzo’s

Give 0.1mg boluses to a max of 2g.

Contra: BDZ addiction, seizures, long QT

S/E: vomiting, anxiety, sweating, flushing and HTN.

28
Q

What is the basic structure of all barbiturates?

Basic properties?

A

Derived from barbituric acid (condensation of urea and malonic acid)

Not CNS depressants on own, but with added functional groups.

29
Q

What are the two categories of barbiturates and their properties?

A

Thiobarbiturates = more lipid soluble and protein bound
Oxybarbiturates = less lipid soluble and protein bound

30
Q

How to barbiturates work?

A

Mimic gaba at gaba a
Block glutamate receptors decreasing post synaptic excitatory impulses
Block voltage gated na and Ca channels (neuroprotective)
Block K and nicotinic receptors

31
Q

What condition should we avoid barbiturates in?

A

Porphyria

32
Q

What is the preparation of thiopental?

A

Racemic mixture.

Weakly acidic pale yellow powder with 6% anhydrous sodium carbonate in an atmosphere of nitrogen. Nitrogen stops precipitation of free acids through acidification with atmospheric CO2 and oxidisation.

33
Q

How is thio prepared and what mix does this give?

A

500mg prepared in 20ml of water to give a 2.5% solution.

SC keeps the pH at between 10-11, keeping the solution in the more water soluble -enrol form.

34
Q

What happens to thio when injected?

What would happen in acidosis?

A

Weak acid.

PKa is 7.6 so is 99% ionised in solution (-enrol form) (pH 10-11)

Once injected, pH of 7.4 causes formation of an unstable unionised protonated sulphide, which rapidly isomerisms into the stable lipid soluble -keto form.

Acidosis would cause more lipid solubility (more unionised), causing increased clinical effect

35
Q

What is the metabolism of thio?

A

Metabolised to inactive in the liver
Causes enzyme induction

36
Q

What does thio interact with?

A

Acidic or oxidising agents can cause precipitation

E.g. vec, roc, lidocaine, morphine and calcium

Make sure flush after

37
Q

What is a thio induction like?

A

Smooth with a clear end point in 20s
No unwanted movements e.g. coughing or hiccuping

May taste onion or garlic

38
Q

What thio doses do we use for status?

Why is it helpful?

A

Boluses of 250mg up to 5g to produce a normal EEG
Then maintenance infusion of 4-10mg/kg/h

Reduced CMRO by 55%, reduced blood flow by 50% and dose dependent reduction in ICP. Auto regulation maintained. (Also reduces intra ocular pressure)

39
Q

What are the respiratory effects of thio?

A

Apnoea, resp depression, depressed medullary response to hypoxia and hypercapnoea. No suppression of laryngeal reflexes.

40
Q

What are the CVS effects of thio?

A

Transient fall in CO and BP.
Dose dependent reflex tachy
High rapid doses can cause myocardial depression

41
Q

What are the disadvantages of thio?

A

Low therapeutic index
Reduced arterial pressure and CO
Slow metabolism
Porphyria
Histamine release

Extravasation/arterial injection

42
Q

What can extravasation of thio cause?

Why?

A

Ulceration and tissue necrosis

High pH and precipitation of drugs

43
Q

What happens with inadvertent arterial injection of thio?

Why?

A

Physiological pH transfers it to keto form, which is fat soluble and acid crystals precipitate out of solution.

Normally not a problem in veins as is constantly diluted by new blood flow

When in an artery the crystals can stick and cause severe vasospasm

44
Q

What is the treatment for inter-arterial thio?

A

Stop injecting but don’t remove cannula

500ml warmed fluids to dilute crystals
1% lignocaine for analgesia +/- other analgesia
500 - 1000 units of heparin through the cannula to reduce the risk of thrombosis (may need 14 days)
Papeverine for arterial spasm (smooth muscle relaxant)

Can do a block e.g. Stellare ganglion or brachial plexus to vasodilation/give analgesia

45
Q

What is methohexital?

Preparation?

Uses?

Comparison to thio?

A

Induction agent. White powder with 6% sodium carbonate, with a pH of 11.
Bacteriostatic

PKa of 7.9, more unionised at physiological pH than thio and less protein bound.
More respiratory depression and laryngospams
Less CVS disturbance
Shorter acting
Same issues with extravasation etc. but slight less damage

Ultra short acting so usually ECT or field

46
Q

What is phenobarbital?

Preparation?

Kinetics?

Effect?

A

Longest acting induction agent

Odourless white crystalline powder which is a weak acid

50% protein bound and potent enzyme inducer

Sedative hypnotic and anti-seizure (not absence)

Causes resp and CVS depression in OD

Can cause megaloblastic anaemia, mild hypersensitivity and osteomalacia. Behavioural disturbances and hyperkinesia

47
Q

What kind of drug is etomidate?

How is it prepared?

What does it target?

A

Imidazole derivative Induction agent

Weak base. Colourless solution of 20mg in 10ml of 35% propylene glycol (2mg/ml or 0.2%) or a Lipura mix.

R entantiomer ten times more potent than S. Binds between alpha and beta on GABAa receptors with B2 (sedative) and 3 (anaesthetic) subunits.

At higher concentrations it can elicit currents without GABA

48
Q

How quickly does etomidate work and how long does it last?

A

Works in 30-60s and peaks at 60

Lasts 3-5 minutes

49
Q

How is etomidate metabolised?

Excreted?

A

Mainly hepatic ester hydrolysis to carboxylic acid and ethanol, with main metabolite being inactive.

85% renally excreted

50
Q

What are the effects of etomidate?

Resp?
CVS?
CNS?
ECR?

A

Maintained reflexes, hyperventilation then brief apnoea. No histamine release

CVS: slight hypotension and tachycardia

CNS: hypnosis. Maintained CPP, but decreased CMRO by 45%, ICP down by 50% and reduced ICF production at high doses. High myoclonus due to loss of cortico-inhibition during induction.

ECR: reversible 11b hydroxylase inhibition causing decreased cortisol and mineralcorticoids (72h)

51
Q

What are the advantages and disadvantages of etomidate and what is it used for?

Contraindications?

A

Good: high therapeutic index, minimal resp depression, cerebral protection, no histamine release and rapid recovery

Bad: pain on injection (less with lipuro), steroid inhibition, superficial thrombophlebitis, myoclonus and N&V.

Uses: cardiac surgery to avoid is haemia during bypass, neurosurgery and trauma, ECT (doesn’t increase seizure threshold but increases duration).

Contra: sepsis and critically ill, adrenal sufficiency and porphyria

52
Q

What kind of drug is ketamine?

Preparation?

A

Phencyclidine derivative

Racemic originally but now a single isomer. S has 4x NMDA affinity and 3x anaesthetic potency. Reduced recovery time and lower dose requirement.

colourless solution with benzathonium hydrochloride of 10, 50 and 100mg/ml.

53
Q

What does ketamines pKa of 7.5 mean?

What is its lipid solubility compared to thio?

A

7.5, meaning lots lipid soluble at physiological pH. 5-10x more lipid soluble than thio.

54
Q

What receptors does ketamine work on?

A

Non competitive of NMDA receptors.

Also opioid particularly mu and kappa

Also targets: thalamoneocortical projection, antagonises: MAO, cholinergic, purigenic and adrenoreceptors

Targets neuronal Na channels giving an LA like effect at high doses

55
Q

What routes can ketamine be delivered by?

Bioavailability?

A

IV,
IM (93%)
Nasal 25-50%
Oral 20-25%

56
Q

What is the metabolism of ketamine?

What is the excretion?

A

In the liver undergoing demethylation and hydroxylation to metabolites norketamine (20% relative activity)

Conjugated and excreted in urine

57
Q

What are the effects of ketamine?

Resp?
CVS?
CNS?

A

Resp: transient apnoea if rapid IV, salivation (worse in kids, can cause spasm. Can give glyco). Bronchodilator

CVS: positive chronotrope and direct negative inotrope (increased sympathetic stimulation overrides this), raised BP and increased cardiac work. Can use for cardiostable induction in shock.

CNS: dissociative state due to uncoupling of thalamic/neocortical and limbic systems. EEG = characteristic loss of alpha waves and dominant theta activity. Maintains MAP and CPP. Clinically can see cataplexy, slow beat nystagmus, dilated pupils, lacrimation, altered tone and movements.

58
Q

What is ketamine emergence phenomena?

A

Effects 5-30%, gives a range of mood disturbance and vivid dreams to severe delirium. Can trigger psychosis in mentally ill.

59
Q

What are the contraindications to ketamine?

A

Allergy, porphyria, disposition to spasm/apnoea, severe CVS disease, CSF obstruction, psychosis, hyperthyroidism (tachy), raised IOP and pre-eclampsia.

Pharmacology. (22 decks)

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