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Neuro Round 2 wk 2+ > Local anesthetics > Flashcards

Local anesthetics Flashcards

1
Q

What are the three parts of a local anesthetic organically?

A

lipophilic aromatic group

intermediate chain of ester or amide

hydrophilic amine group

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2
Q

Do ester or amide local anesthetics have a longer duration of action? Why is this?

A

amides

esters are susceptible to esterases that break them down

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3
Q

What form of local anesthetic is required to penetrate the tissues and cell membrane to reach the site of action in the cytoplasm?

A

uncharged form (not ionized)

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4
Q

What is the charged form of local anesthetics required for?

A

to block the voltage-dependent Na channels

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5
Q

Charged LAs bind to…

A

open (active) Nav channels

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6
Q

At physiologic pH, what are LAs doing?

A

switching bt charged and uncharged forms

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7
Q

A decrease in tissue pH (acidosis) will cause an __________ in the amount of ionized drug.

A

increase

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8
Q

Diffusion of LA across the membrane is facilitated by an… pH

A

alkaline

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9
Q

LAs with high lipid solubility generally have the greatest… and …

What is an example of this?

A

potency and longest duration of action

bupivacaine

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10
Q

How can you speed the onset of LA block?

What drugs does this work best for?

A

make the pH of LA more basic (alkalization) by adding bicarbonate

less lipophilic LAs like lidocaine

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11
Q

The degree of Nav block by LA depends on the…

meaning with …

A

frequency of nerve impulses

increased AP frequency there will be increased Nav block

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12
Q

What type of axons are most difficult to block with LA?

A

large diameter myelinated (A type) axons

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13
Q

Anesthesia from a peripheral nerve block first develops ….

A

proximally

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14
Q

longer duration of LA block are achieved with drugs that are more… and in locations …

A

hydrophobic

with less vascularization

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15
Q

What alpha 1 agonists are usually used to prolong the duration of LA? What is their MOA?

A

epi and phenylephrine

vasoconstrictor

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16
Q

When should vasoconstrictors not be used with LAs?

A

in areas lacking collateral blood flow, like digital blocks or ears

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17
Q

Besides prolonging the duration of action of LA, what do vasoconstrictors do when given concurrently with LA?

A

limit LA toxicity by decreasing distribution into systemic circulation

18
Q

Can LAs cross the BBB or placenta?

A

yes

19
Q

How could LAs cause seizures if they are decreasing APs?

A

In the CNS, LAs block GABA before blocking excitatory neurons

increases restlessness and tremors leading to convulsions

20
Q

What do LAs do to the heart if they get into systemic circulation?

A

decrease cardiac electrical excitability, conduction velocity, and force of contraction

21
Q

Most LAs will cause vasodilation, what is the exception to this?

A

cocaine

22
Q

Allergic reactions to LAs are much more likely to … because they are metabolized to …

A

esters

PABA (p-aminobenzoic acid)

23
Q

How can a cardiac rescue be performed if too much LA is used?

A

intralipid - is a lipid emulsion that is typically used as an IV feeding supplement, but txs LA OD

intralipid absorbs the LA like a sponge to reduce the levels to below toxic - Nav channels become unblocked and are able to once again generate APs

24
Q

bupivacaine has a longer duration of action than lidocaine bc it is …

A

more hydrophobic

25
Q

Conventional cardiac resuscitation techniques often fail on pt with LA induced cardiac arrest bc…

A

cardiac APs cannot be generated

26
Q

You want to do a long duration nerve block, but are concerned about cardiac toxicity. The best LA choice is…

A

ropivacaine

27
Q

What are three LAs that can be used topially?

A

lidocaine

cocaine

benzocaine

28
Q

Neuromuscular blocking drugs have no…

A

analgesic or anesthetic properties

29
Q

What is the only depolarizing muscle blocking drug clinically available?

A

succinylcholine

30
Q

What is the MOA of succinylcholine?

A

strong agonist for nAChR

31
Q

Nondepolarizing muscle blocking drugs MOA

A

antagonists for the muscle nAChR

32
Q

What is an AE of succinylcholine upon IV injection?

A

fasciculations which are non-synchronus contractions

33
Q

What component of a succinylcholine block is phase I?

A

depolarizing, rending Nav channels inactive

34
Q

What is phase II of succinylcholine block?

A

non-depolarizing component - desensitization

35
Q

What are some AEs a/w succinylcholine use?

A

cardiac dysrrhythmias, fasciculations, hyperkalemia, myalgia, malignant hyperthermia

36
Q

How do you tx malignant hyperthermia?

A

IV dantrolene

37
Q

What is an AE of pancuronium?

A

increase in CO, HR, and MAP

38
Q

What is an AE of atracurium?

A

histamine release at high doses induces hypotension and tachycardia

39
Q

How do you reverse neuromuscular blockade?

When would this not work but why may it not matter much?

A

neostigmine - inhibits AChE activity (nondepolarizing agents), increasing ACh concentration at the NMJ

does not work for succinycholine, but phase I is enhanced, some reversal of phase II

sucs is such a short duration of action, you probably can just wait instead of reversing it

40
Q

How is the action of succinylcholine terminated?

A

metabolism by plasma esterases

41
Q

The nondepolarizing muscle blocking drug with the fastest onset of action is …

A

rocuronium

42
Q

The bradycardia effect induced by succinylcholine can be blocked by pretx with…

A

atropine

Neuro Round 2 wk 2+ (16 decks)

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