Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology II > Local Anesthetics > Flashcards

Local Anesthetics Flashcards

1
Q

Neurophysiology of pain involves what three things?

A

initiation

propagation

perception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define local/peripheral analgesics

A

analgesia close to the source of the pain

ie) Novocaine, cocaine, NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define central analgesics

A

analgesia through supraspinal and spinal sites

ie) morphine, NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define general anesthetics

A

Loss of consciousness, amnesia, +/- analgesia

ie) propofol, etomidate, barbituates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are pain receptors also called?

A

Nociceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Provide an example of a pain receptor

A

TRP channels

(transient receptor potential)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the two types of pain fibers?

A

C fibers and alpha delta fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What NT is released at synapse of alpha delta fibers?

A

Glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the NT released at the synapse of C fibers?

A

Substance P

(and a little bit of glutamate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Are C fibers unmyelinated or myelinated?

Do they have fast or slow AP propagation?

A

Unmyelinated

Slow propagation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Are alpha delta fibers unmyelinated or myelinated?

Do they have fast or slow AP propagation?

A

myelinated

fast, saltatory conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Character of first pain?

What fiber is responsible for first pain?

A

Sharp, Stinging, High Intensity Pain

fast alpha delta fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Character of second pain?

What fiber is responsible for second pain?

A

Dull, Aching, Low Intensity Pain

slow C fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do NSAIDs work to decrease sensitization of C and alpha delta fibers?

A

NSAIDs inhibit production of PGs by blocking COX2 in proinflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is TTX?

A

tetrodotoxin

from pufferfish

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does TTX work?

A

it blocks Na+ channel via the extracellular side

extracellular Na+ channel blockage

THUS, since it is bound to the outer pore,

it blocks Na+ entry no matter what stage/state Na+ channel is in (resting, activated, inactivated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do local anesthetics bind differently than TTX to the Na+ channels?

A

local anesthetics are lipophilic so they get into cell and then wait around inside cell until Na+ channel is activated and then LAs go in and bind to Na+ channel and block Na+

So intracellular channel blockage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Blockage of Na+ channel occurs in what state for TTX?

resting and/or activated and/or inactivated

A

resting &

activated &

inactivated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Blockage of Na+ channel occurs in what state for local anesthetics?

resting and/or activated and/or inactivated

A

Blockade occurs when channel is in activated state

(M gate opens up and allows LA to gain entry into inner Na+ channel and block it)

Blockade can also occur during inactivated state

(LA can gain access to this inner pore of Na+ channel and block during inactivated state too)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why do local anesthetics (and not TTX) lead to use-dependent blockade?

A

local anesthetics cannot bind and block during resting state

they can bind and block only in activated and inactivated states

21
Q

Graph of use-dependent blockade of Na+ currents by local anesthetics

A

See picture

22
Q

In the presence of TTX, the Na+ current trace following the 1st stimulation of the neuron would look like?

See Picture

A

trace 25

23
Q

True or false:

Increased lipophilicity of local anesthetic means greater potency of local anesthetic and earlier onset of action of local anesthetic

A

true

24
Q

What local anesthetics are esters?

Do they have a short or long duration of action?

A

See picture

25
Q

What local anesthetics are amides?

Do they have a short or long duration of action?

A

See picture

26
Q

True or false:

For every 10 local anesthetics that form as cationic,

one forms as uncharged and

can cross the membrane and block Na+ channels

A

True

27
Q

Infected tissue has lower pH leading to more charged local anesthetic, so this anesthetic is more or less able to cross the cell membrane?

A

less

So less potency in these areas and takes longer to work/onset of action

28
Q

The charged or uncharged local anesthetic can cross the membrane?

A

uncharged

29
Q

The charged or uncharged local anesthetic blocks the Na+ channel?

A

charged

30
Q

Small or large diameter fibers are blocked most easily by local anesthetics?

A

small

31
Q

myelinated or unmyelinated fibers (of the same diameter) are blocked more readily?

A

myelinated fibers are blocked more readily

32
Q

True or false:

The more the fiber fires, the more it is blocked by local anesthetics

A

True

use dependent thing

33
Q

Are fibers in the interior or exterior more or less readily blocked by local anesthetics?

A

fibers in interior are less readily blocked by local anesthetics and fibers on the exterior are more blocked by local anesthetics

34
Q

Name six routes of administration of local anesthetics

A

topical

infiltration

bier block

peripheral nerve block

epidural

spinal

35
Q

When does systemic toxicity occur with local anesthetics?

A

when the LAs get absorbed into the vasculature and reach high enough concentrations in the heart and/or brain to disrupt cardiac and CNS function

probablility of this happening increases when LAs are administered into tissues with dense vasculature

(high vascularization) intercostal > caudal > epidural > brachial plexus > sciatic nerve (low vascularization)

36
Q

Symptoms of systemic toxicity of brain

A

anxiety

confusion

tremors

convulsions

37
Q

Symptoms of systemic toxicity of cardiovascular system

A

depressed myocardial contractility

bradycardia

vasodilation

hypotension

(exception: cocaine: tacycardia, vasoconstrction, and hypertension due to its abilit to block catecholamine reuptake at sympathetic nerve termini: that revolving door NET: NE transporter)

38
Q

Administration of what reduces the likelihood of systemic toxicity by causing vasoconstrction and consequently prolongs duration of action of local anesthetics?

A

Epinephrine

(many LA formulations contain epinephrine)

39
Q

What can direct injection into vasculature of local anesthetics cause?

A

temporary blindness

aphasia

hemiparesis

convulsions (treated with benzodiazepines)

respiratory depression

coma

cardiac arrest

40
Q

What are some local adverse reactions to local anesthetics?

A

range from pain to tissue necrosis at site of injection

41
Q

What are allergies most associated with, esters or amides?

A

rare but most associated with esters

(It is the PABA: para-aminobenzoic acid derivatives produced by metabolism of local anesthetic through pseudocholinesterases)

42
Q

What drug given in adjunct therapy to reduce pain transmition?

A

Clonidine

See picture

43
Q

Highlights of Cocaine

A

ester

used in nose and throat procedures

high abuse potential

can cause tachycardia

can cause vasoconstriction

44
Q

Highlights of Procaine (Novocaine)

A

first sythetic local anesthetic

ester

slow onset

short duration

relatively low systemic toxicity

commonly used for infiltration and peripheral nerve blocks

45
Q

Highlights of Lidocaine (Xylocaine)

A

most commonly used

amide

xylidine derivative

rapid onset

intermediate duration

causes vasodilation and is therefore combined with epinephrine

this compound is also used as a class 1B anti-arrhythmic due to its capacity to inhibit cardiac Na+ channels

46
Q

Highlights of Ropivacaine (Naropin)

A

synthesized in only the S-isomer

S-isomer has low affinity for cardiac Na+ channels

(R-isomer has high affinity for cardiac Na+ channels)

lower cardiac toxicity compared to other local anesthetics

47
Q

Drug Summary Table

A

See picture

48
Q

Drug summary table

A

See picture

Pharmacology II (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions