Local anaesthetics/dysrhthmics Flashcards

1
Q

What does use dependency mean?

A

The local anaesthetic is more effective when action potentials are conducted with greater frequency. The degree of block is proportional to the rate of nerve stimulation. This is be cause more protonated drugs can enter open sodium channels and cause inactivation.

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2
Q

Does the activated or inactivated form of Na channel have higher affinity for local anaesthetic?

A

Inactivated form has higher affinity for LA

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3
Q

Which types of fibres are blocked more readily?

A

Smaller fibres are blocked before large fibres.
Small myelinated fibres are blocked before small unmyelinated fibres.
pain sensation tends to disappear first.

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4
Q

Why are vasoconstrictors sometimes used with LAs?

A

Adrenaline/NA/vasopressin are added to LA solutions to delay absorption from site of injection, prolonging duration of the LA at the tissues and reducing risk of toxicity.
felypressin is commonly used.

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5
Q

What are the toxic effects of LAs?

A

CNS effects: hyperactivity, manic behaviour, convulsions-> respiratory coma.
CV effects: vasodilation, cardiac slowing, hypotension
Spinal anaesthesia -> local tissue damage
Dangerous allergic reactions are possible

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6
Q

Which segment of the Na channel plays a dominant role in binding to LA?

A

IVS6 segment
Inner cavity pore of Na channel - alpha subunit (aa residues from at least three of the four domains
contribute to the receptor site)

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7
Q

How are amino amides metabolised?

A

They are slowly metabolised by hepatic amidases

eg lidocaine, prilocaine

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8
Q

What is an ester breakdown product which can cause allergic reaction?

A

para-amino benzoate (PABA)

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9
Q

Which drugs may be topically applied?

A

Lidocaine, benzocaine

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10
Q

Which drugs may be used for infiltration anaesthesia?

A

Lidocaine, prilocaine

with vasopressin/adrenaline/felypressin

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11
Q

Which drugs may be used for spinal anaesthesia?

A

Procaine, tetracaine, cinchocaine

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12
Q

What is delayed after-depolarisation?

A

A cause of dysrhythmia.

[Ca]i increased above normal, due to transient inward current possibly carried by Na/Ca exchanger.

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13
Q

What is reentry or disordered conduction?

A

A cause of dysrhythmia.
Damaged myocardium developed unidirectional conduction block, conduction circulates indefinitely in area of heart. the activation wavefront of the anterograde signal interacts with the repolarisation phase of a preceding excitation wave.

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14
Q

What occurs with heart block?

A

Failure of impulse generation in SA node or failure of propagation through AV node.
Ventricular beating is maintained by abnormal pacemaker (e.g. Purkinje system) which is usually slow and unreliable.

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15
Q

What do K+ channel blockers alter?

A

the AP duration, and thus the refractory period

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16
Q

What are the types and mechanisms of class 1 anti-dysrhythmic drugs?

A

1a immediate dissociation Na channel block eg Disopyrimide
1b fast dissociation Na channel block eg Lidocaine
1c slow dissociation Na channel block eg Flecainide

17
Q

What are the classes and mechanisms of anti-dysrhythmic drugs?

A

Ia-c Na channel block
II β-adrenoceptor antagonism eg propranolol
III K channel block eg Amiodarone, Sotalol
IV Ca channel block eg verapamil

18
Q

What are the problems with Vaughan-William’s classifications?

A

many drugs are not wholly selective for Na+, K+ or Ca2+ channels
there are now more drugs and a greater (yet incomplete) understanding of mechanisms

19
Q

How does quinidine work?

A
Causes use-dependent block of voltage-gated Na+ channels
This is class Ia, decreases spontaneous impulse generation in SAN, leaves fewer Na channels "available", slowing rate of depolarisation.
Decreases reentry, slows conduction such that propagating AP is extinguished before it can reexcite
cells in a re-entrant pathway
20
Q

What is an example of a class Ib drug?

A

Lidocaine
associates with and dissociates from Na+ channel rapidly (within single beat), small slowing of AP rise but channels are blocked following peak – so any premature beat is aborted, also bind preferentially to inactivated Na+ channel

21
Q

What are some example of K channel blockers?

A
Amiodarone, sotalol
These are class III, prolong cardiac AP and refractory period. This reduces the time window in the cardiac cycle when dysrhythmias can occur.
22
Q

What are some examples of Ca channel blockers?

A
Verapamil, diltiazem
These are class IV; inhibit slow inward (L-type) Ca2+ current, indirectly reducing TI current -> decrease SA excitability and slow AV conduction
23
Q

What is the action of cardiac glycosides?

A

eg digoxin

Block Na/K ATPase, can cause dysrhythmia by increased Ca, depolarisation. AV block slowed by vagal input.

24
Q

What is long QT syndrome?

A

Disorder with longer ventricular depolarisation.
Can cause fainting, seizures, sudden death. Due to mutated K channels, hypokalemia (low K levels in blood) or drug exposure

25
Q

Which drugs affect the QT interval?

A

Anti-dysrhythmics (I & III): sotalol, quinidine, disopyramide, procainamide, amiodarone
plus
Antibiotics: erythromycin
Antihistamines: astemizole, terfenadine
Psychoactive drugs: lithium, haloperidol, tricyclic antidepressants
Others: amantadine, chloroquine, glibenclamide, salbutamol