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pharm > LOCALS > Flashcards

LOCALS Flashcards

1
Q

LAs reversibly block

A

AFFERENT nerve transmission

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2
Q

Order of blockade observed

A
  1. autonomic blockade
  2. somatic sensory blockade
  3. somatic motor blockade
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3
Q

Myelination in PNS is done by

A

Schwann cells

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4
Q

LA cannot easily penetrate myelin so it acts at

A

nodes of ranvier

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5
Q

You need enough LA concentration to block

A

three nodes of ranvier to effectively block a nerve

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6
Q

Pain fibers

A

A-delta, pain/temperature = FAST pain

C - dull pain/temperature = SLOW pain

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7
Q

A-alpha fibers are

A

motor and propioception

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8
Q

A-beta fibers are

A

motor, touch, and pressure.

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9
Q

A-gamma fibers are

A

motor/muscle tone, muscle spindle

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10
Q

A-delta fibers are

A

pain, temperature, touch, FAST pain

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11
Q

B fibers are

A

PREganglionic, myelinated, autonomic

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12
Q

C fibers are

A

dull pain, temperature, touch, POST ganglionic, autonomic, no myelin, SLOW pain

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13
Q

when using LA we typically don’t fully block or block

A

A-alpha or A-beta

A-alpha : motor / proprioception
A-beta : motor, touch, pressure

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14
Q

preganglionic fibers are

A

more readily blocked than any other fiber, even though they’re myelinated

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15
Q

the sensitivity of a peripheral nerve to LA is inversely

A

related to its size (clinically / in-vivo)

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16
Q

unmyelinated fibers are usually at the

A

mantle [[superficial]] part of nerve fibers

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17
Q

clinical sequence of anesthesia with LAs

A

1st. sympathetic block -> C fibers
2nd. loss of pain and temperature, sensation -A delta
3rd. loss of proprioception - a gamma

4th loss of touch and pressure if you have dense enough block - a beta

5th motor blockade A-alphpa (not intentional)

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18
Q

LAs bind at the

A

internal H gate of the VG sodium ion channel at the INACTIVE-closed state

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19
Q

LA easily ACCESS VGNC

A

when they are activated-open

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20
Q

LA easily BINDS to VGNC when

A

they are in inactivated-closed

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21
Q

a resting nerve is less sensitive

A

to LA than a repetitively stimulated one

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22
Q

_____ determines how sensitive the nerve is to an LA in a resting nerve

A

LIPID SOLUBILITY

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23
Q

the cationic charged form of LA interacts preferentially with

A

inactivated state of the Na channel

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24
Q

inter nodal distance of nodes of ranvier increases with

A

fiber diameter

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25
Q

Distance between nodes of ranvier in myelinated fibers contributes to

A

DIFFERENTIAL nerve block /
why? cause big somatic neurons are gonna take a lot of LA to block , so youre alble to block function of pain before getting to the point where you actually block motor

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26
Q

Organic Chemistry Components of an LA

A

lipophilic head (aromatic ring) , intermediate chain * (either an ester or amide) and a hydrophilic tail (tertiary amine)

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27
Q

esters have less of a

A

toxicity risk because they are metabolized faster [[ester hydrolysis]]

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28
Q

increase in the length of the intermediate chain (increase in number of carbons) increases

A

potency and toxicity and alters metabolism rate and DOA

  • cause you’ve made the drugs more lipid soluble
  • intermediate chain here alters DOA and metabolism cause you could potentially change the amide or ester group
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29
Q

increase in length of tertiary amine chain increases

A

potency and toxicity

  • more lipid soluble
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30
Q

Minimum Blocking Concentration =

A

minimum concentration at a nerve required to block it

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31
Q

fiber diameter and minimum concentration

A

directly related

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32
Q

minimum concentration and tissue ph

A

If acidic, require too much LA

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33
Q

Potency and minimum concentration

A

more potent drug = lower minimum concentration, because less molecules of the drug will be needed to block the nerve

34
Q

increased tissue pH or high frequency of nerve stimulation =

A

[alkalosis] or more excitable nerve = decreases minimum concentration

cause frequency dependent block and increase degree of NONionized molecules

35
Q

the more vascular the region

A

the higher the risk of systemic absorption and the higher the risk of plasma toxicity.

36
Q

Top 3 sites of vascular systemic uptake

A

IV
Trachel
intercostal

37
Q

least vascular region

A

subQ , so lowest risk of toxicity

38
Q

All LAs are

A

weak bases
pKa 7.5 - 9

*one exception

39
Q

LAs are packaged in an acidic form to

A

improve solubility and stability, so they don’t precipitate out. Also to preserve epinephrine

40
Q

Adding bicarb increases

A

the onset, enhances the block depth, and increases the spread of the block

41
Q

deceasing temperature reduces

A

drug absorption across the nerve membrane, could delay onset.

42
Q

LAs for labor

A
  1. Ester, cause rapid metabolism

2. Amide that is HIGHLY Protein bound because it will stay local

43
Q

DOA is effected by

A

blood flow (affects uptake)
lipid solubility
protein binding

44
Q

potency in LAs =

A

lipid solubility,

this is an inherent property of the drug, depends on chemical structure

45
Q

Most important factor for DOA =

A

protein binding.

binds to local proteins with great affinity = stay there for a while.

46
Q

Use of vasoconstrictor with LA serves three purposes

A
  1. inhibition of systemic absorption (decreases uptake)
  2. prolongation of the LA effect
  3. detection of IV injection *
47
Q

determinants of of concentration of LA in systemic blood

A 
tissue blood flow 
concentration of LA used 
Pulmonary first pass
metabolism of drug 
vasoconstrictor?
48
Q

when people are allergic to esters they are responding to

A

PABA (metabolite)

49
Q

Esters are metabolized by

A

pseudocholinesterase in the plasma

and some in the liver
less than 5% unchanged in kidneys

50
Q

Cocaine metabolism

A

significantly metabolized in liver (therefore longer DOA)

and 10-12% excreted unchanged in urine

51
Q

metabolism of amides is effected by

A

liver disease! cYP450 = liver
decreased hepatic blood flow,
drugs that interfere with cyp450

52
Q

after systemic absorption, amide LA are

A

more widely distributed in tissues than ester LA

53
Q

muscle twitching especially in face and then extremities indicates

A

imminent onset of seizures, r/t CNS toxicity

54
Q

How to treat seizures in CNS toxicity

A

bicarb/benzo
100%fio2
ventilation

55
Q

SE of cocaine with CNS toxicity include

A

euphoria, restlessness, tremors, seizures

excessive norepinephrine and dopa + CNS

56
Q

Toxic systemic affects are more likely with

A

AMIDES over esters

57
Q

In CNS toxicity seizures are followed by

A

CNS depression

58
Q

CV more resistant to

A

LA toxicity than CNS

59
Q

LA toxicity on heart =

A

hypotension, AV conduction block, myocardial depression,

reduced SVR (HYPOTENSION),
reduced CO (myocardial depression)
widened PRi and QRS (AV conduction block)
CV collapse

60
Q

most CV toxic =

A

bupivocaine

61
Q

cocaine overdose =

A

massive sympathetic outflow
coronary vasospasm
MI

62
Q

Increased risk of CVS effects =

A

pregnancy

have already received other CV modulating drugs

63
Q

treatment of CV collapse with overdose

A
  1. crack chest/ cpr
  2. modified ACLS, no amio no lidocaine,
  3. INTRALIPID 20%
64
Q

Intralipid is more beneficial for drugs that are

A

very lipid soluble

65
Q

TNS

A

Transient neurological symptoms

neuroinflammatory symptoms causes pain I lower back, buttocks, posterior thighs.

presents 6-36 Hours after recovery from block, lasts about a week.

66
Q

Cauda equina is associated with

A

lidocaine 5%, tetracaine, and chloroprocaine

67
Q

Anterior Spinal Artery Syndrome

A

LE paralysis with +/- sensory deficit

unknown cause, vasoconstrictors/PVD/advanced age may increase it

68
Q

allergic reactions are more common with

A

ESTERS -> PABA

69
Q

pseudocholinesterase inhibitors will prolong

A

the actions of ESTERS

70
Q

cimetidine and propanolol

A

decreased hepatic blood flow, decrease clearance of amide LAs and COCAINE

71
Q

Fentanyl, clonoidine, epi ->

A

synergistic effects when added to LA

72
Q

fibers that are more easily blocked have a lower

A

Cm

73
Q

There is a greater fraction of the ionized drug

A

inside the cell rather than outside the cell.

ICF = slightly more acidic than ECF

74
Q

Onset of 0.75% bupivacaine will be faster than 0.2% bupivacaine because

A

higher concentration = more molecules = quicker onset

why chloroprocaine is fast onset despite high pKa

75
Q

Cardiac arrest can occur before seizure with

A

bupivacaine

76
Q

Toxicity is more common with

A

PNB than with epidural anesthesia

77
Q

Factors that increase risk for CNS toxicity

A

hypercarbia, hyperkalemia, metabolic acidosis

78
Q

hypercarbia increases risk for CNS toxicity because

A

hypercarbia / acidosis -> leads to vasodilation in cebereal blood flow leads to increased drug in brain

Hypercarbia also decreases protein binding

79
Q

difficulty of cardiac resuscitation in order

A

bupivacaine > levobupivacaine > ropivacaine > lidocaine

80
Q

EMLA cream is made of

A

50% Lido and 50% prilocaine, therefore risk for methomglobienemia from prilocaine

81
Q

epidural doses per segment

A

1.25 to 1.6 mL/segmente desired block

pharm (4 decks)

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