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IMSK Exam 2 > Local Anesthetics > Flashcards

Local Anesthetics Flashcards

1
Q

Define transduction

A

the process by which tissue damaging stimuli activate nerve endings

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2
Q

What are the free nerve endings that are stimulated in response to pain?

A

nociceptors

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3
Q

What are nociceptors stimulated by?

A
  • mechanical impulses
  • thermal impulses
  • chemical impulses
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4
Q

Define transmission

A

relay of functions by which message is carried from site of tissue injury to brain regions underlying perception

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5
Q

Describe the nerves fibers of nociceptors

A

A(delta): fast; large diamter, thinly myelinated, evoked by sharp, intense, stinging, cold, temporary localized pain
C: slow, small diameter, unmyelinated, evoked by aching, dull, burning poorly localized pain
A(beta): thickly myelinated, cutaneous mechanoreceptors, free nerve ending that responds to light touch and bending of hairs

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6
Q

Which fibers are going to be most sensitive to a blocking agent?

A

C&raquo_space;» A

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7
Q

What are the voltage-gated NA+ channels associated with pain transmission?

A

Nav1.1, Nav1.6, Nav1.7, Nav1.8, Nav1.9

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8
Q

Define a local anesthetic

A

drug that produces a state of local anesthesia by reversibly blocking the nerve conductances that transmit the feeling of pain from point of administration to the brain

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9
Q

What allows a local anesthetic to inactivate the Na+ channels?

A
  • they are lipophilic which allows them to pass through the membrane
  • after passing thru the membrane, they become hydrophilic and binds the Na+ channels – prolonging the inactivation state
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10
Q

What is the order of loss of for local anesthetics?

A

pain – temperature – touch – pressure

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11
Q

How can local anesthetics block nerve conduction?

A

1) inhibit influx of Na+ through VGSC – impaired AP
2) decrease nerve membrane permeability to sodium
- -both of these increase threshold for excitation

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12
Q

What are the ester local anesthetics?

A

procaine
tetracaine
benzocaine
chloroprocaine

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13
Q

What are the amide local anesthetics?

A

lidocaine
mepiracaine
bupivacaine
ropivacaine

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14
Q

Ester link is more prone to ________; esters usually have a _________ DOA

A

hydrolysis; shorter

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15
Q

Local anesthetics are _____________, available as salts to ____________

A

weak acids; increase solubility and stability

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16
Q

What determines the rate of onset and termination of action?

A

absorption to nerves

  • correlated with relative lipid solubility of uncharged form
  • reduced pH = reduced diffusion = reduced effectiveness (inflamed tissue)
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17
Q

An increase in molecular weight of R-1 and R-2 groups will do what?

A

increase potency and toxicity

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18
Q

Duration of action increases with what?

A

protein binding

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19
Q

An increase in lipid solubility leads to a ______ in potency

A

increase

20
Q

Order the Lidocaine, bupivacaine, mepivacaine, and tetracaine from highest potency to least

A

tetracaine
bupivacaine
lidocaine
mepivacaine

21
Q

__________ pKa = faster time of onset

A

decreasing (getting closer to environmental pH for a given environment)

22
Q

Higher concentration = ______ speed of onset

A

increase

23
Q

Great alkalization with NaHCO3 = ________ time of onset

A

increase

24
Q

What are the DOA, potency, indications, and adverse effects of procaine?

A

DOA: short – 30-60 min
Potency: 1 (low)
Indications: dental procedures
ADR: hypersensitivity, cardiotoxicity

25
Q

What are the DOA, potency, indications, and adverse effects of Tetracaine?

A

DOA: long – 60-200 min
Potency: 8 (high)
Indications: spinal anesthesia
ADR: CNS excitation/toxicity at higher concentrations

26
Q

What are the DOA, potency, indications, and adverse effects of Benzocaine?

A

DOA: very short – 5-10 min
Potency: -
Indications: topical anesthesia
ADR: methemoglobinemia in <2 yo

27
Q

What are the DOA, potency, indications, and adverse effects of Chloroprocaine?

A

DOA: short – 30-60 min
Potency: 1 (low)
Indications: spinal anesthesia
ADR: CNS excitation, local neurotoxicity at higher concentrations

28
Q

Describe the metabolism of of Ester type LAs

A
  • rapid hydrolysis of ester linkage by plasma cholinesterase
  • metabolites are benign (except for PABA allergy)
  • atypical pseudocholinesterase - high incidence of systemic toxicity
29
Q

Why would we not use procaine?

A
  • requires a vasoconstrictor

- no real advantage over lidocaine

30
Q

Describe cocaine and its mode of action and toxicity

A
  • topical ester LA; 1st used in dentistry
  • MOA: vasoconstrictor; inhibits reuptake of norepinephrine into adrenergic nerve terminals; intrinsic sympathomimetic
  • toxicity
    • myocardial ischemia, myocardial infarction, arrhythmias, seizures, hypertension, mania, paranoia
31
Q

What are the DOA, potency, indications, and adverse effects of lidocaine?

A

DOA: short – <60 min
Potency: 2 (int.)
Indications: dental procedures, nerve block
ADR: CV at high concentrations; neurotoxicity at high concentrations*, methemoglobinemia

32
Q

What are the DOA, potency, indications, and adverse effects of Mepivacaine?

A

DOA: moderate – 60-120 min
Potency: 1.5
Indications: spinal anesthesia, nerve block
ADR: ringing of ears, blurred vision, headache

33
Q

What are the DOA, potency, indications, and adverse effects of Bupivacaine?

A

DOA: long – 120-340 min
Potency: 8 (high)
Indications: spinal anesthesia
ADR: CV at high concentrations, increased atrial excitability*

34
Q

What are the DOA, potency, indications, and adverse effects of Ropivacaine?

A

DOA: short – 30-60 min
Potency: 8 (high)
Indications: spinal anesthesia
ADR: N/V, headaches

35
Q

What is the most commonly used amide type LA?

A

lidocaine

36
Q

Describe Lidocaine

A
  • liver metabolism
  • successive N-de-ethylations – glycinexylidide (GX) is more toxic than the parent compound [important when lidocaine is used as IV antiarrhythmic]
37
Q

Describe Benzocaine

A
  • used topically; it needs 20% or greater concenrtation to be effective as local anesthetic topically
  • beware of PABA or sulfonamide allergy – safer alternative may be topical lidocaine
  • found in OTC lotions and ointments including dental preparations
    • risk of methemoglobinemia with oral use
38
Q

What is the “Bier Block”?

A
  • circulation to the limb is blocked and LA injected into the venous vessels distal to the occlusion
  • nerves that travel with blood vessels will be anesthetized
  • useful for surgeries <1 hr on an extremity or for chronic pain
  • prilocaine commonly used
39
Q

What is the most frequent clinical use of LAs?

A

“Bier block”

40
Q

Describe a peripheral nerve blockade

A
  • deliberate interruption of signals traveling along a nerve
  • combination of LA (lidocaine), epinephrine (constricts blood flow), steroid (reduce inflammation), and opioid
  • used for femoral nerve blockade and sciatic nerve blockade — anesthetic for leg surgeries
41
Q

Describe neuraxial anesthesia

A
  • pertains to local anesthesia plasced around the nerves of the CNS (spinal anesthesia)
  • epidural space or spinal
42
Q

What is systemic toxicity determined by?

A
  • local blood flow: most LAs are vasodilators except cocaine
  • addition of vasoconstrictor
  • physiochemistry of LA – increased cardiac and CNS toxicity w/ increased lipid solubility
  • local pH - infection
43
Q

What are the allergic reactions associated with LAs?

A
  • rare (PABA or sulfonamides for a few)

- *Esters are most likely to cause an allergic reaction

44
Q

What toxicities are associated with LAs?

A
  • respiratory acidosis and hypoxemia
  • cardiovascular-arrythmias and BP
  • treat seizures - barbituates or benzodiazepines
  • intralipid (20%) by IV infusion
45
Q

How do vasoconstrictors treat toxicities of LAs?

A
  • decrease peak plasma concentration of LA
  • reduces renal and systemic toxicity
  • decreases blood flow – slows removal of drug from injection site
  • increases DOA
  • no effect on potency
46
Q

What is most commonly used as a vasoconstrictor?

A

epinephrine

47
Q

What is the second most commonly used vasoconstrictor?

A

norepinephrine (and then other proprietary vasoconstrictors)

IMSK Exam 2 (5 decks)

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