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Pharmacology > Anaesthetics > Flashcards

Anaesthetics Flashcards

1
Q

What is the difference between local and general

A

General loses sense of consciousness aswell as sensation/pain

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2
Q

What 2 types of general anaesthetics are there

A

Inhalation

IV

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3
Q

What is the lipid theory to how anaesthetics work

A

They interact with the lipid bilayer and cause membrane expansion which disrupts protein signalling

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4
Q

What is the ion channel theory

A

They target ligand channels like gaba and nmda

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5
Q

What does blood/gas partition coefficient mean for inhaled anaesthetics

A

How blood soluble the anaesthetic is

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6
Q

What does it mean if a drug has high blood/gas partition coefficient

A

They are very soluble in blood

Causing slow induction and recovery

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7
Q

What happens if a drug has a lower blood gas partition coefficient

A

Faster induction (less drug needed) and also fast recovery

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8
Q

What is oil/gas partition coefficient mean for inhalation anaesthetics

A

How lipid soluble the drug is

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9
Q

What happens if anaesthetics have a higher oil/gas partition coefficient

A

High lipid solubility = high potency of drug

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10
Q

How does vascularisation determine levels of Anaesthesia

A

If somewhere in highly vascularised like the brain = higher levels

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11
Q

Does ventilation rate affect induction and removal of inhalation anaesthetics?

A

Yes

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12
Q

How are inhaled anaesthetics removed

A

Via veins back to the alveoli and exhaled

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13
Q

Where does some anaesthetics (inhaled) get metabolised into toxic waste

A

Kidney

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14
Q

What is the effect of inhaled anaesthetics of respiration

A

Depression of respiratory rate

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15
Q

What is the CVS effect of inhaled anaesthetics

A

Decreased BP (hypotension)

Via decreased cardiac output

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16
Q

Are IV general anaesthetics fast induction?

A

Yes

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17
Q

What are the names of the IV anaesthetics which are GABA agonists (hyperpolarisation)

A

Thiopental and etomidate and propofol

18
Q

Why is etomidate a good GABA agonist / IV anaesthetic

A

It has a large TI

19
Q

Why is propofol GABA modulator bad

A

Has rapid metabolism and therefore fast elimination

Also has a low TI

20
Q

What are propofol, thiopentol and etomidate

A

Allosteric modulators of GABA

21
Q

What is the only IV anaesthetic which is an NMDA antagonist

A

Ketamine

22
Q

Why is ketamine rarely used as IV anaesthetic

A

Causes hallucinations and psychosis

23
Q

Do IV anaesthetics like thiopentol and etomidate cause hypotension

A

Yes — they also lower BP like inhalation ones do

24
Q

Which channel is targeted by local anaesthetics to stop AP

A

Voltage gated na channels

25
Q

Which subunit do local anaesthetics bind to at voltage na channels

A

A subunit

26
Q

What do B1 and B2 subunits on the na channels do

A

Hold the a subunit in the membrane 4 pass

27
Q

What happens when voltage changes to the a subunit

A

Changes position causing opening and influx of na

28
Q

Which state must local anaesthetics be in to bind to a subunit

A

Ionised

29
Q

Which state must local anaesthetics be in first to pass myelin sheath

A

Unionised state

30
Q

What are the 3 components of local anaesthetics

A

Aromatic ring

Amide or ester bond

Side chain (alkaline)

31
Q

What determines duration of action of local anaesthetics

A

Hydrolysis of ester or amide bond

32
Q

Where are amide bonds metabolised and do they have a longer half life than esters?

A

In the liver Via CYP

They do have a longer half life

33
Q

Why are anaesthetics unionised when they enter via injection

A

They are weak bases which cause increased PH so causes unionisation

The base is then released

34
Q

Where is the free base from anaesthetics ionised due to lower ph

A

At the axon

35
Q

Which part can then when ionised at the acidic axon cause blocking of a subunit

A

The alkaline side chain

36
Q

How can the body restrict site of action of anaesthetics

A

Via vasoconstriction at A1

37
Q

How does the alkaline side chain cause faster induction

A

Faster absorption into the tissue being unionised

38
Q

Which fibres are the most sensitive to local anaesthetics

A

Small diameter and myelinated

39
Q

Why does increased AP firing cause better blockage via local anaesthetics

A

Channels are more in their open or inactive state rather than testing

The anaesthetic has higher affinity for these stages

40
Q

What are the negatives of local anaesthetics if they get into the circulation

A

In the brain they’d cause confusion

In the heart they lower BP (hypotension)

41
Q

How do inhalation anaesthetics cause increased BV

A

Stop glomerular filtration and less urine released

Pharmacology (24 decks)

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