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Pharm > Local Anesthetics > Flashcards

Local Anesthetics Flashcards

1
Q

What was the first local anesthetic? When was it developed?

A

Procaine (1905)

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2
Q

Clinical applications of local anesthetics:

A
  • anesthesia
  • analgesia
  • acute and chronic pain management
  • decrease perioperative stress
  • improve perioperative outcomes
  • treat cardiac dysrhythmias
  • anti-inflammatory
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3
Q

List the sections of a peripheral nerve from innermost to outermost:

A
  • endoneurium
  • perineurium
  • epineurium
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4
Q

Influx of which ion produces a neuronal action potential?

A

Na+

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5
Q

Influx of which ion generates the wave of depolarization down a nerve axon?

A

Na+

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6
Q

Resting membrane potential of a nerve:

A

-70mV

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7
Q

How many nodes of Ranvier must be blocked to reliably interrupt impulse propagation?

A

3

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8
Q

Define salutatory conduction:

A

in myelinated axons, the AP is conducted only at the nodes of Ranvier, skipping the distance between adjacent nodes

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9
Q

Describe how LAs work:

A
  • reversibly bind to voltage-gated Na+ channels in the nerve’s axon
  • no entrance of Na+ into the cell
  • no depolarization
  • no propagation of the AP down the axon
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10
Q

List the 3 other channels/receptors that local anesthetics block beyond their primary mechanism:

A

1) voltage-dependent K+ channels
2) L-type Ca2+ channels
3) some G-protein coupled receptors

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11
Q

During which states do LAs preferably bind to Na+ channels?

A

activated & inactivated state

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12
Q

Which portion of the LA diffuses through the skin/membrane? Which portion binds to the receptor in the Na+ channel?

A
  • non-ionized/lipid soluble portion diffuses through the membrane
  • ionized portion binds to the receptor inside the voltage-gated Na+ channel; this portion cannot penetrate the cell membrane
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13
Q

What is the order in which nerve fibers are blocked?

A
  • B
  • C
  • A-delta
  • A-gamma
  • A-beta
  • A-alpha
    (Beer & Cheese AnD A Game Are Better than An Apple)
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14
Q

How does diameter of nerve fibers correlate to sensitivity?

A

smaller diameter = most sensitive (C fibers)
larger diameter = least sensitive (A-alpha fibers)

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15
Q

How does myelin affect sensitivity?

A

more myelin = less sensitive

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16
Q

What is the clinical order of loss of function?

A

Pain
Temperature
Touch
Proprioception
Skeletal muscle tone
(Pregnancy TEsts Take PRecise SKills)

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17
Q

Axon diameter is (inversely/proportional) to LA resistance.

A

proportional
Larger diameter = more resistance

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18
Q

Sensory & sympathetic nerves are blocked (first/last).

A

first

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19
Q

Motor nerves are blocked (first/last).

A

last

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20
Q

Define minimum effective concentration:

A

the minimum concentration of LA needed to produce a conduction block of an impulse
*different for different nerve fibers (larger fibers require higher concentrations)

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21
Q

How does tissue pH affect Cm?

A
  • increased tissue pH –> decreased Cm
  • decreased tissue pH –> increased Cm
    (why a typical dose is less effective in acidic/infected tissue)
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22
Q

List bodily tissues from highest to lowest blood flow:
I Think I Can Please Everyone But Susie & Sally

A

Intravenous
Tracheal
Intercostal
Caudal
Paracervical
Epidural
Brachial plexus
Subarachnoid
Subcutaneous

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23
Q

How are ester LAs metabolized? Excreted?

A
  • metabolized: plasma esterases
  • excreted: renal
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24
Q

How are amide LAs metabolized? Excreted?

A
  • metabolized: hepatic enzymes
  • eliminated: renal
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25
Q

LAs are weak (acids/bases), which means they are (more/less) nonionized at physiologic pH.

A
  • weak bases
  • more nonionized at physiologic pH
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26
Q

When the pKa of a drug is closer to physiologic pH, more of the drug exists as…

A

lipid-soluble, uncharged, base

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27
Q

Compare the pKa, ionization, and onset of Lidocaine and Procaine:

A

Lidocaine
- pKa 7.9
- 3:1 ionized:unionized
- 2-3 min onset

Procaine
- pKa 8.9
- 32:1 ionized:unionized
- 6-12 min onset

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28
Q

How is onset related to pKa?

A

the closer the drug is to physiologic pH, the more of the drug exists in the unionized/active state and the faster it works

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29
Q

Which factors, in addition to pKa, affect onset?

A

dose & concentration
(higher dose/concentration = faster onset d/t more molecules given)

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30
Q

Which LA is an outlier when it comes to pKa and onset?

A

Choloroprocaine;
really high pKa so should have a slower onset BUT it is not very potent so a large dose must be given –> more molecules –> rapid onset

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31
Q

Describe how LAs work in infected tissue?

A

infected tissue has a lower pH; many LAs are bases and thus more ionized/less active at low pH; poor penetration of nerve tissue and less effective nerve block

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32
Q

How is potency related to lipid solubility?

A

More lipid soluble the drug, the easier it is to diffuse through the epineurium

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33
Q

How does the vasodilating effect of LA affect potency?

A

greater vasodilating effects = faster vascular uptake = less potent as the drug is not sequestered to the area it was injected into.

34
Q

How is duration of action of LAs related to protein binding?

A
  • drug bound to tissue proteins acts as a reservoir that extends the DOA
  • LAs = weak bases that primarily bind to AAG (secondary binding to albumin)
35
Q

What other characteristics of LAs affect duration of action?

A
  • lipid solubility (more soluble = longer DOA)
  • vasodilating effect (increases rate of vascular uptake = shorter DOA)
  • addition of vasoconstrictors (decreases ability of drugs to diffuse away = longer DOA)
36
Q

Which LAs have low potency and short DOA?

A

Procaine (Novocaine)
Choloroprocaine (Nesacaine)

37
Q

Which LAs have intermediate potency and DOA?

A

Mepivacaine (Carbocaine)
Lidocaine (Xylocaine)

38
Q

Which LAs have high potency and a long DOA?

A

Bupivacaine (Marcaine)
Ropivacaine (Naropin)
Tetracaine (Pontocaine)

39
Q

2 structural classes of LAs:

A
  • aminoester
  • aminoamide
40
Q

How do you differentiate between the 2 structural classes of LAs?

A
  • amino esters has one “i” and one “i” in the generic names
  • amino amides has 2 “i”s and 2 “i”s in the generic names
41
Q

Differences in metabolism of 2 classes of LAs:

A

amino esters = hydrolysis in the plasma
amino amides = biotransformation in the liver

42
Q

Which structural class of LAs is more stable and associated with fewer allergic reactions?

A

amino amides

43
Q

4 facts about Procaine:

A

1) amino ester LA
2) earliest developed injectable LA
3) unstable, potential for allergic reactions
4) spinal procaine –> increased nausea

44
Q

4 facts about Tetracaine:

A

1) amino ester LA
2) commonly used for spinal anesthesia
3) more slowly metab than Procaine/Choloroprocaine
4) rarely used for epidurals or PNBs

45
Q

Which LA is rarely used for epidurals or PNBs? Why?

A

Tetracaine

  • slow onset
  • profound motor blockade
  • potential toxicity
46
Q

4 facts about Chloroprocaine:

A

1) amino ester LA
2) popular epidural anesthetic d/t short duration
3) rapid hydrolysis = minimal risk to fetus
4) often used to quickly load epidural for crash C-sections

47
Q

What characteristic is important when considering drugs being used in the intrathecal space?

A

preservative-free

48
Q

4 facts about Lidocaine:

A

1) amino amide LA
2) most commonly used & most versatile
3) potential neurotoxicity (cauda equina syndrome) w/ continuous spinal use
4) Transient Neurological Symptoms (TNS) with spinal use

49
Q

4 facts about Mepivacaine:

A

1) amino amide LA
2) less vasodilation than other LAs (slightly longer DOA)
3) similar uses as Lidocaine except ineffective topically
4) lower incidence of TNS than Lidocaine

50
Q

4 facts about Prilocaine:

A

1) amino amide LA
2) metabolite = ortho-toludine
3) rapid metabolism
4) 40% less CNS toxicity than Lidocaine

51
Q

Effects of the metabolite of Prilocaine:

A

ortho-toludine
- converts Hgb to methemoglobin
- may spontaneously subside
- OR may be reversed with Methylene Blue

52
Q

Prilocaine is rapidly metabolized & has low acute toxicity (40% less than Lidocaine). Why is it not widely used?

A

metabolite (ortho-toludine)

53
Q

4 facts about Bupivacaine:

A

1) amino amide LA
2) most commonly used LA for labor epidurals and PO pain mgmt
3) also used for PNBs and spinals
4) SE = refractory cardiac arrest

54
Q

Describe how Bupivacaine can lead to refractory cardiac arrest:

A
  • prolonged recovery from Bupivacaine blockade makes it more potent in depressing the maximum upstroke velocity of cardiac AP and ventricular cardiac muscle
    *dilute solutions for epidural, small doses for spinal reduce this risk
55
Q

4 facts about Ropivacaine:

A

1) amino amide LA
2) S(-) enantiomer of the homolog of Bupiv & Mepiv
3) less pronounced motor block, C fibers preferentially blocked, may produce greater differential block
4) lower lipid-solubility = less potent than Bupiv
$$$$$

56
Q

4 facts about Levobupivacaine:

A

1) amino amide LA
2) S (-) enantiomer of Bupiv
3) less cardiotoxic than Bupiv
4) no advantage over Bupiv r/t differential blockade

57
Q

When is it most advantageous to utilize Ropivacaine or Levobupivacaine?

A

cases in which relatively high doses of anesthetic are administered

58
Q

Patients who receive Exparel should not receive any other form of Lido for ___ hours

A

96 hours

59
Q

Describe how Liposomal Bupivacaine works:

A
  • Bupivacaine is encapsulated by liposomes
  • nearly identify to cell membranes (made of phospholipids)
  • deliver drug via diffusion
60
Q

Dose/onset/duration of Exparel:

A
  • dose = max of 266mg
  • onset = 15min-2hours
  • DOA = up to 72 hours
61
Q

What % solution is a solution containing 1 gram of drug per 1 mL of fluid?

A

100% solution

62
Q

What % solution is a solution containing 10 mg/mL?

A

1%
1000mg in 100mL
1g in 100mL

63
Q

What % solution is a solution containing 1mg/mL?

A

0.1%
100mg in 100mL
0.1g in 100mL

64
Q

What % is a solution with a 1:100 dilution?

A

1% solution

65
Q

How many mg are in 1 mL of a 0.6% solution?

A

6mg/mL

66
Q

Describe tumescent anesthesia:

A
  • plastic surgeon technique during liposuction
  • subcutaneous injection of large volumes of dilute LA + epi
  • may peak up to 20 hours after infusion
67
Q

List the potential adverse effects of LAs:

A
  • allergic reaction
  • direct neurotoxicity
  • intraneural injection
  • local anesthetic systemic toxicity (LAST)
  • methemoglobinemia
  • transient neurologic syndrome (TNS)
68
Q

Allergic reactions to LAs:

A
  • very uncommon
  • more common with amino esters d/t metabolism to paraminobenzoic acid (PABA)
  • cross sensitivity between groups is absent
69
Q

Describe cauda equina syndrome (CES):

A
  • bowel/bladder dysfunction with bilat LE weakness and sensory impairment
  • d/t supranormal doses of intrathecal LA OR maldistribution of LA spread within intrathecal space
  • Chloroprocaine (large dose)
  • Lidocaine (continuous spinal anesthesia)
70
Q

Describe Transient Neurologic Symptoms (TNS):

A
  • back & LE pain x5 days postop
  • burning, aching, crampy, radiating pain in anterior & posterior thighs
  • d/t spinal Lidocaine?
  • surgical positioning?
  • treat symptomatically and include NSAIDS
71
Q

Describe methemoglobinemia:

A
  • Ferrous Hgb (Fe2+) oxidized to Ferric form (Fe3+)
  • reduced O2 carrying capacity
  • shifts oxyhemoglobin curve to the L
  • common culprits: Bezocaine, Procaine, Dapsone, Nitrites
  • treat with methylene blue (1-2mg/kg) over 3-10 min
  • level >70 may need transfusion or dialysis
72
Q

Clinical signs of methemoglobinemia:

A
  • hypoxia not improved with increased FiO2
  • abnormal blood coloration
  • saturation gap (blood gas paO2 is OK but low pulse ox)
  • new-onset cyanosis or hypoxia after ingestion of an oxidative agent
73
Q

Causes of LAST:

A
  • inadvertent intravascular injection of LA
  • absorption of large amounts of LA
  • continuous infusion/accumulation of drug + metabolites x several days
74
Q

Effects of LAST:

A
  • depression of voltage-gated Na+, K+, and Ca2+ channels in excitable tissues of CNS and cardiac system
  • depression of inhibitory CNS neurons –> seizures
  • decreased cardiac contractility, several arrhythmias
75
Q

Describe the progression of symptoms of LAST:

A
  • numbness of tongue (2-4mcg/mL)
  • dizziness/tinnitus (4-6mcg/mL)
  • visual problems (6-8mcg/mL)
  • muscle cramps (8-10mcg/mL)
  • seizures (12-16mcg/mL)
  • decreased consciousness (16-18mcg/mL)
  • coma (16+mcg/mL)
  • respiratory/cardiovascular arrest (24+mcg/mL)
76
Q

LAST treatment:

A
  • stop injecting the LA
  • lipid emulsion therapy
  • manage airway
  • control seizures
  • treat hypotension & bradycardia
77
Q

How does addition of opioids to LA affect blocks?

A
  • increased duration
  • increased quality of surgical anesthesia & analagesia
78
Q

How does addition of Dexamethasone affect blocks?

A

increases duration

79
Q

How does addition of clonidine or dexmedetomidine affect blocks?

A
  • multiple sites of action
  • increase duration of block
  • increase anesthesia
80
Q

How does bicarbonate affect blocks?

A
  • increases % of nonionized drug
  • increases membrane penetration
  • decreases onset time
  • reduces pain during SQ infiltration

Pharm (19 decks)

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