Neuro Exam 2: Local Anesthetics

Front 1

What is a local anesthetic?

Back 1

a substance that temporarily blocks propogation of APs along a nerve fiber to render a SPECIFIC SITE insensitive to noxious stimuli

Front 2

What is nociception?

Back 2

recognition and transmission of painful stiumuli

Front 3

Where are nociceptors located?

Back 3

free afferent nerve endings of myelinated A delta and unmyelinated C fibers

Front 4

What is the ideal local anesthetic?

Back 4

lidocaine (xylocaine)

Front 5

What do A-delta fibers mediated?

Back 5

pain, temp and touch --> fast pain receptors

Front 6

What provides the upstroke of the AP?

Back 6

VG Na channel

Front 7

What is the primary active site of local anesthesia action?

Back 7

VG Na channel

Front 8

If pH = pKa -->

Back 8

50% of drug is in charged drug and 50% in uncharged form

Front 9

If pH > pKa -->

Back 9

more drug is in uncharged form

Front 10

if pH < pKa -->

Back 10

more drug is in charged form

Front 11

T or F: Charged drugs can enter Na channel

Back 11

FALSE

Front 12

Which form of a drug is more membrane permeable (charged or uncharged)?

Back 12

uncharged

Front 13

Which form is a better blocker (charged or uncharged)?

Back 13

charged

Front 14

How do Locals block Na channels?

Back 14

the uncharged form enters the cell via the channel. It becomes charged again and binds its receptor site on the inside of the Na channel and block the channel

Front 15

What are some factors that determine susecptibility to locals?

Back 15

localization w/ in the nerve
diameter
myelination

Front 16

Small unmyelinated fibers --> aka __

Back 16

C fibers

Front 17

T or F: small, unmyelinated fibers (C fibers) are blocked at lower concentrations of LA than large myelinated fibers?

Back 17

TRUE

Front 18

T or F: Slow pain fibers are (C fibers) are blocked at the lowest concentration?

Back 18

TRUE

Front 19

Which fibers are blocked at the highest concentation of LA?

Back 19

touch, motor, proprioception

Front 20

What are the three parts of the LA?

Back 20

lipophilic, hydrocarbon chain, and hydrophilic

Front 21

What is an amide LA?

Back 21

lidocaine (xylocaine)

Front 22

What is an example of an ester LA?

Back 22

procaine

Front 23

Amides have what in their names?

Back 23

they have an I in the first part of their names

Front 24

What are the 2 main classes of LA?

Back 24

amides and esters

Front 25

How are amides metabilized?

Back 25

CYP450 in hepatic microsomal enzymes

Front 26

How are esters metabolized?

Back 26

hydrolysis by plasma cholinesterases

Front 27

What determines the onset of local anesthesia?

Back 27

the pKa of the drug

Front 28

What are the pKas of most LAs?

Back 28

7.6-8.9

Front 29

What is physiological pH?

Back 29

7.4

Front 30

What does the addition of sodium bicarb do to LAs?

Back 30

hasten the onset of action by raising the pH so more of the drug is non-ionized (more lipid soluble)

Front 31

what is the pH of inflamed tissue relative to healthy tissue?

Back 31

it is acidic (lower pH) --> more drug protonated --> can't cross the membrane

Front 32

Anesthesia of inflamed tissue is __ than that of normal tissue

Back 32

slower

Front 33

What is the major determining factor of how long a LA acts?

Back 33

how well it binds to proteins

Front 34

What does Epi do when added to a LA?

Back 34

causes peripheral vasoconstriction leading to decreased system absorption and prolongs the duration of action

Front 35

When do you avoid adding vasoconstrictors to LA?

Back 35

areas that lack collateral blood flow.

Front 36

What determines the potency of LA?

Back 36

lipid solubility

Front 37

What is the protein binding of Procaine? What is the duration?

Back 37

5% --> very short duration

Front 38

What is the protein binding of Lidocaine? What is the duration?

Back 38

65% --> intermediate duration

Front 39

What is the protein binding of Bupivacaine? What is the duration?

Back 39

95% --> very long duration

Front 40

What are some toxic targets of LA?

Back 40

VG channels in locations other than the peripheral nervous system (CNS and cardiac)

Front 41

What is a prime determinant of an LAs intrinsic toxic potential?

Back 41

lipid solubility

Front 42

What are some factors related to redistribution of an LA from the injection site?

Back 42

inadvertent intravascular injection
vascularity of tissue at injection site
composition of injection site
use of vasoconstrictors
tissue uptake

Front 43

From more to less, what are the vascularities of some body sites?

Back 43

intercostal > caudal > epidural > brachial plexus > sciatic block > subcutaneous

Front 44

What is the CC/CNS ratio?

Back 44

the ratio of agent plasma concentration at which CNS sx occur to the conc at which cardiovascular collapse occurs

Front 45

T or F: The maximum doses are derived from scientific studies and are hard and fast?

Back 45

FALSE

Front 46

T or F: Pts always have neuro sx before cardiac arrest occurs

Back 46

FALSE!!! Bupivicaine has cardiac arrest w/o neuro sx

Front 47

Which LA can accumulate inside myocardiocytes?

Back 47

bupivacaine

Front 48

T or F: Bupivacaine dissociates more slowly during diastole (when the Na channel is in resting phase)

Back 48

TRUE

Front 49

What are some low level CNS toxicities of LA?

Back 49

sedatin, anticonulsant activity, light-headedness, izziness, anxiety, perioral numbness, tinnitus

Front 50

What are some sx of excitement phase CNS toxicities?

Back 50

muscle tremors, tonic-clonic seisures

Front 51

What are some EKG findins in cardiac toxicity?

Back 51

bradycardia, widened QRS, polymorphic V tach, vent. fib

Front 52

What cells in the heart are preferentially blocked in the heart?

Back 52

conduction system cells (AV node, Purkinje system)

Front 53

What are some other rxns of LA?

Back 53

Tachyphylaxis, Methemaglobinemia, Allergic Reactions

Front 54

What is tachyphylaxis?

Back 54

an acute (sudden) decrease in the response to a drug after its administration