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Flashcards in Local anesthetics Deck (23)
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1
Q

What is the role of voltage gated sodium channels?

A

It opens transiently when membrane is depolarised for sodium ions to pass through

2
Q

What is the difference between inactivated and deactivated receptors?

A

Inactivated - ion flow blocked by a gating mechanism

Deactivated - ion flow blocked by closing of channel

3
Q

What is the mechanism of action of LA?

A

Stops axonal conduction by blocking sodium channels in the axonal membrane when applied locally in appropriate concentration → prevent sodium entry → slow down or bring conduction to a halt

4
Q

Does the protonated or non-protonated form of LAs pass through the membrane channel?

A

Non-protonated.

5
Q

Which receptor states do LAs bind most strongly to?

A

Inactivated and activated channels

6
Q

Why does LA work better when in a lot of pain?

A

Use dependency: Passage of train of action potentials cause sodium channels to cycle through open and inactivated states. During this train of action potentials, it is likely that the channel is open more often, then LA can work better

7
Q

Describe use-dependency of LA

A

Depth of LA nerve block increase with action potential frequency because LA molecules gain access to the channel more readily when channel is open and have higher affinity for the inactivated than resting (closed) channels

8
Q

Why are LAs given topical or by injection

A

They are non-selective modifiers of neuronal function (block action potentials in all neurons in which they have access)

9
Q

Factors affecting LA action?

A

More lipid soluble drugs are more potent and act longer
(more hydrophobic: tetracaine, etidocaine, bupivacaine; Less hydrophobic: lidocaine, procaine, mepivacaine)

Nerve factors - size (smaller>bigger), frequency of firing (high>low), position (circumferential>deep), myelination (myelinated>non-myelinated)

pH dependency - alkaline pH → increased LA (low proportion of ionised molecules)

10
Q

Types of LAs

A

Amide (lidocaine, mepivacaine, bupivacaine) and ester (procaine, tetracaine)

11
Q

How are amide and ester LAs metabolised

A

Ester - plasma/tissue non-specific esterases

Amide - hepatic enzymes

12
Q

Which anesthetics have the fastest onset?

A

Those that penetrate the axon most rapidly (small size, high lipid solubility, low ionisation)

13
Q

When does toxicity occur?

A

When unintended large dose of LA is accidentally injected IV/intra-arterial
When there is excessive LA injected locally and subsequently lead to high and toxic blood level following absorption

14
Q

How can you reduce the toxicity of LAs?

A

Combine with epinephrine (reduces vessel diameter, constricting it to reduce blood flow so rate of absorption of LA into systemic circulation is lower)

15
Q

What kind of toxicity does LA give rise to?

A

CNS and CVS toxicity
CVS: reduce cardiac contraction, arteriolar dilation and hypotension, cardiovascular collapse
CNS: sleepiness, convulsion, stoppage of vital functions, death

16
Q

Which is the most cardiotoxic LA?

A

Bupivacaine

17
Q

What are the side effects of cocaine?

A

Vasoconstriction and hypertension (due to blocking noradrenaline uptake)

18
Q

Which LA causes methaemoglobin? How is it reversed?

A

O-toluidine.

Reversed by IV methylene blue or ascorbic acid

19
Q

In which patients should you avoid ester LAs?

A

Those with PABA allergy

dont use procaine and tetracaine

20
Q

How can LAs be delivered?

A

Topical cream, epidural space, directly into nerve fibers, just below surface of the skin

21
Q

Uses of topical LAs (DOGES)

A

Skin - minor burns, wounds
Eye - remove foreign objects
Dental - applied on gum before injection needle
Otorhinolaryngology - insertion of endoscope
Gynecology - episiotomy cuts

22
Q

What anesthetics are used for epidural?

A

Lidocaine, bupivacaine

can combine with fentanyl to reduce dose

23
Q

What anesthetics are used for dental?

A

Lidocaine, bupivacaine