La Test #1

Front 1

How do LA work?

Back 1

By blocking sodium channels, which doesn't allow membrane depolarization.
It slows the impulse conduction, thereby decreasing the action potential.
It then increases the threshold for excitation until no action potential can be generated.

Front 2

What does LA potency correlate with?

Back 2

Lipid solubility

Front 3

What does local onset of action correlate with?

Back 3

lipid solubility (less soluble = faster onset)
Local concentration (higher concentration = faster onset)
pKa (lower pKa = faster onset)
addition of NaHCO3 (increases onset)

Front 4

What does LA duration of action correlate with?

Back 4

Lipid solubility (high solubility = long duration)
Addition of epinephrine, neosynephrine, clonidine

Front 5

How are esters metabolized?

Back 5

pseudocholinesterase / plasma cholinesterase
(temperature & pH dependent)

Front 6

How are Amides metabolized?

Back 6

P-450 enzyme of the liver

Front 7

What are the early signs of local toxicity?

Back 7

circumoral numbness, tongue paresthesia, dizziness, tinnitus, blurred vision.

Front 8

The resting membrane potential in excitable tissues is determined by what?

Back 8

potassium, all other ions are impermeable in the resting neuron because sodium and calcium channels are closed.

Front 9

What is the treatment of methemoglobinemia?

Back 9

Methylene blue (1-2mg/kg IV)

Front 10

What are the risk factors for transient neurolgic symptoms?

Back 10

Lidocaine, lithotomy position, obesity, outpatient status

Front 11

What are the predisposing risk factors for bupivacaine induced cardiovascular toxicity?

Back 11

Pregnancy, hypoxemia, respiratory acidosis, young children

Front 12

What are the differences between bupivacaine and ropivacaine?

Back 12

Ropivacaine is less lipid soluble and has less motor blockade. It has a larger therapeutic range and is 70% less likely to cause severe cardiac arrhythmias

Front 13

What are LAs impact on ND-neuromuscular blockers?

Back 13

LA potentiate them.

Front 14

What is the preferred drug treatment for LA induced ventricular tachyarrhythmias?

Back 14

Amioderone or bretylium

Front 15

In what state do LA "lock" the sodium channel thereby preventing the impulse?

Back 15

When the sodium channels are in the inactivated state after depolarization. Its called the Absolute Refractory Period.

Front 16

What is the likely site of nerve entrence for local anesthetics in myelinated nerves?

Back 16

the nodes of Ranvier.

Front 17

Which two LAs cause vasoconstriction?

Back 17

Ropivacaine and cocaine

Front 18

How does epinephrine increase the duration of action of LAs?

Back 18

The vasoconstricting properties reduce the rate of vascular absorption.

Front 19

Which class of locals has a greater potential to cause an allergic reaction?

Back 19

Esters, because of the metabolite para-aminobenzoic acid (PABA).

Front 20

What physiological factors antagonize local blockade?

Back 20

Acidic pH, hypokalemia, hypercalcemia

Front 21

What is tachyphylaxis?

Back 21

It is the decreased efficacy of drugs when giving repeated doses.

Front 22

Which patients are at increased risk for local toxicity with esters?

Back 22

Those with abnormal psudocholinesterase / plasma cholinesterase

Front 23

List these amides in order of duration of action: lidocaine, bupivacaine, ropivacaine, prilocaine, mepivacaine.

Back 23

Prilocaine, Lidocaine, Mepivacaine, Ropivacaine, Bupivacaine

Front 24

Which drugs may cause methemoglobinemia?

Back 24

Prilocaine & Benzocaine

Front 25

How many mg of 0.75% Bupivacaine is in 2 mls?

Back 25

15mg

Front 26

What is the maximum dose of Lidocaine with and without epi?

Back 26

4mg/kg without epi
7mg/kg with epi

Front 27

What concentrations does lidocaine come in?

Back 27

0.25% - 4%

Front 28

What is the OOA & DOA of Lidocaine?

Back 28

Fast onset
intermediate duration (60-120min)

Front 29

What is the OOA & DOA of Mepivacaine?

Back 29

Fast onset
intermediate duration (90-180min)

Front 30

What is the OOA and DOA of Etidocaine?

Back 30

Fast onset (??slow)
Long duration (4-8hrs)

Front 31

Which LAs are commonly used for epidurals?

Back 31

Lidocaine, Bupivacaine, Ropivacaine, Chlorprocaine

Front 32

Which LAs are commonly used for spinals?

Back 32

Bupivacaine, Tetracaine

Front 33

What is the OOA and DOA of Prilocaine?

Back 33

Fast onset (??slow)
Intermediate duration (60-120min)

Front 34

What is the OOA and DOA of Bupivacaine?

Back 34

intermediate onset
Long duration (4-8hrs)

Front 35

WHat is the maximum dose of Prilocaine?

Back 35

600mg single injection

Front 36

What is the maximum dose of Bupivacaine?

Back 36

3mg/kg or 175mg single dose w/o epi
225mg single does w/epi

Front 37

What is the OOA and DOA of Ropivacaine?

Back 37

Slow onset
Long duration (4-8hrs)

Front 38

What is the maximum single dose of Ropivacaine?

Back 38

200mg

Front 39

What is the OOA and DOA of Cocaine?

Back 39

Fast onset
Short duration

Front 40

What is the mechanism of action of cocaine?

Back 40

blocks the reuptake of norepinephrine and dopamine

Front 41

How is cocaine metabolized?

Back 41

by plasma cholinesterase

Front 42

What is the OOA and DOA of Procaine (Novacaine)?

Back 42

Slow onset
Short duration (45-60min)

Front 43

What is the OOA and DOA of Chloroprocaine (Nesacaine)?

Back 43

Fast onset
Short duration (30-45min)

Front 44

What is the benefit of using Chlorprocaine for urgent c-sections?

Back 44

It has a very rapid onset for epidural use, but must be followed with a longer acting local. The can start cutting sooner.

Front 45

What is the OOA and DOA of Tetracaine?

Back 45

Slow onset
Long duration (1-3hrs)

Front 46

What is the maximum single dose of tetracaine?

Back 46

20mg

Front 47

What is the OOA and DOA of Benzocaine?

Back 47

Fast onset
Short duration (30-60min)

Front 48

At doses greater than 300mg Benzocaine can cause what?

Back 48

Methemoglobinemia

Front 49

Which local is the only one that is a weak acid vs. being a weak base?

Back 49

Benzocaine, all others are weak bases.
That is why it is only used for topical anesthesia.

Front 50

Which two LAs are generally used in EMLA cream?

Back 50

Prilocaine and Lidocaine

Front 51

What is the concentration and dose of epinephrine that is used in LAs to prolong DOA?

Back 51

1:200,000
0.2mg

Front 52

What is the procedure for a Bier Block?

Back 52

Start IV in distal extremity
Inflate tourniquet (should not be able to draw blood from IV)
0.5% Lidocaine is injected into IV (3mg/kg)
After min. of 20min tourniquet is released

Front 53

What are the principle sites of action for Spinal Anesthesia?

Back 53

The superficial layers of the spinal cord and the preganglionic fibers

Front 54

In local toxicity the seizure threshold is inversly related to what?

Back 54

PaCO2, hyperventilation decreases CO2 thereby increaseing the seizure threshold (less likely to have seizures)

Front 55

What does hypokalemia and hyperkalemia do LA toxicity?

Back 55

Hypokalemia decreases toxicity
Hyperkalemia increases toxicity

Front 56

List the following in order of first occuring to last occuring with local toxicity: Circumoral & tongue numbness, convulsions, CVS depression, Visual disturbances, Coma, Muscle twitiching, Respiratory arrest, unconsiousness

Back 56

circumoral & tongue numbess
visual disturbances
muscle twitiching
convulsions
unconsiousness
coma
respiratory arrest
CVS depression

Front 57

What is the dose of lipid for cardiotoxicity treatment?

Back 57

20% Lipids - 1.5ml/kg bolus
then 0.25ml/kg
* can repeat bolus 2 times at 5min intervalls
* can increase infusion to 0.5ml/kg

Front 58

What nerve fibers carry pain signals to the brain?

Back 58

Afferent nerve fibers. A-delta and C fibers

Front 59

What is the resting membrane potential in the neuron?

Back 59

-70mV

Front 60

What occurs with the sodium channels during depolarization?

Back 60

Sodium channel snaps open and sodium flows inward.

Front 61

What part of the alph subunit do locals bind to?

Back 61

H subunit