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Pharmacology III > Local Anesthetics (Exam #1) > Flashcards

Local Anesthetics (Exam #1) Flashcards

1
Q

In what two ways do Esters differ from Amides?

A

ESTERS have…

  • Shorter DOA
  • MORE systemic toxicity
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2
Q

How are local anesthetics transported across cell membranes?

A
  • Non-ionized form to cross

- Ionized form to bind intracellularly

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3
Q

What type of base are most local anesthetics, and at physiological pH, what form dominates?

How would this change their activity if the extracellular pH is more acidic? More basic?

A

LAs = weak bases
- At pH of 7.4, ionized form dominates

  • If more ACIDIC environment = ionized dominates, so LESS activity because can’t cross membrane
  • If more BASIC environment = non-ionized dominates, so MORE activity because more crosses and then becomes ionized → can bind
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4
Q

What is the exception to the pKa/pH rule for local anesthetics, and what does this mean for its use?

A

Benzocaine has pKa of 3.5 and NON-ionized dominates

- Topical use only because unable to bind within cell

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5
Q

What is the MOA for all local anesthetics?

A

Block Na channels

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6
Q

What type of axon are blocks more effective in? How do elevated Ca vs. elevated K affect the block?

A

Block MORE effective in rapidly firing axons (NOT resting)

  • High Ca = block diminished (channels in resting state)
  • High K = block enhanced (channels in open/firing state)
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7
Q

How is duration of action determined for local anesthetics?

A

DOA = time at site of action

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8
Q

Which local anesthetic is SHORT duration of action? Which is INTERMEDIATE? Which three are LONG?

A
  • Short: Procaine
  • Intermediate: Lidocaine
  • Long: TBR (Tetracaine, Bupivicaine, Ropivicaine)
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9
Q

How are amides metabolized? How are esters metabolized?

A
  • Amides = CYP450s (liver)

- Esters = butyrylchlolinesterases

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10
Q

What is a differential block, and what are two examples of different blocks? What is the order of sensitivity from most to least sensitive?

A

Differential block: different degrees of sensory and motor blocks
- Bupivacaine = sensory before motor (epidural)
- Etidocaine = motor before sensory (inverse diff. block)
Sympathetic > Sensory > Touch > Motor

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11
Q

What characteristic of fibers makes them MORE sensitive? Which two characteristics make them LESS sensitive?

A
  • More sensitive: smaller diameter

- Less sensitive: myelinated, faster conduction velocity

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12
Q

What AE differs between esters and amides?

A

Esters are MORE likely to cause hypersensitivity

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13
Q

What local anesthetic has an AE of increased CV toxicity?

A

Bupivacaine (amide)

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14
Q

What local anesthetic has an AE of methemoglobinemia, and how might this present?

A

Prilocaine (amide)

- Chocolate colored skin

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15
Q

Is Procaine an ester or amide? What is its DOA, and what is its primary use?

A

ESTER
- SHORTEST duration of action

Used for diagnostic blocks

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16
Q

Is Tetracaine an ester or amide? What is its DOA, and what does this mean for its use?

What is its primary use?

A

ESTER
- LONG duration of action = more potent and more AEs

Used for ophthalmology

17
Q

Is Benzocaine an ester or amide? What is its primary use, and why is this important?

A

ESTER

Used topically ONLY bc exception to pH rule

18
Q

Is Cocaine an ester or amide? What is its MOA, and in what two ways might it be used?

A

ESTER
- Increase DA → block Na channels

Can be used as topical anesthesia or for dental procedures to reduce bleeding

19
Q

Is Lidocaine an ester or amide? What is its DOA, and what are its two primary uses? What is it NOT used for?

A

AMIDE
- INTERMEDIATE duration of action

GO-TO: used for infiltration blocks and epidural anesthesia
- NOT spinal blocks

20
Q

Is Prilocaine an ester or amide?

A

AMIDE

21
Q

What is an important note about Prilocaine compared to other amides?

A

Prilocaine has the highest rate of clearance of all amides = SAFER

22
Q

Is Bupivacaine an ester or amide? What is its DOA? What is its primary use, and why is this?

A

AMIDE
- LONG duration of action

Used for epidural blocks in labor/childbirth because more potent SENSORY block than motor

23
Q

What is the primary AE associated with Bupivacaine? What similar drug can be used as an alternative, and why?

A

Cardiac toxicity

- Ropivacaine is the enantiomer of Bupivacaine and is LESS lipid soluble/cleared more rapidly than Bupivacaine

24
Q

What two reasons might Ropivacaine be used?

A
  • Vasoconstriction effects (most other LAs are vasodilating)

- Less cardiac toxicity than Bupivacaine

25
Q

What drug is associated with an inverse differential block, and what does this mean?

A

Etidocaine

- Motor nerves acted on before sensory nerves

26
Q

Which drug is both an amide AND an ester, and what is its primary use?

A

Articaine

- Used in dental medicine (allows for multiple injections throughout procedure if needed)

27
Q

What drug can be used to evaluate for butyrylchlinesterase mutations?

A

Dibucaine

28
Q

Is Dibucaine an ester or amide? What is its primary use?

A

AMIDE

- Dibucaine Number Test = butyrylchlinesterase mutations

29
Q

What is the MOA of Diazepam, and what does this mean? What type of a muscle relaxant is it?

A

Acts on GABA A rec. → inhibits Cl channels

- Centrally-acting

30
Q

What is the MOA of Baclofen, and what does this mean? What type of a muscle relaxant is it?

A

Acts on GABA B rec. → inhibits Ca influx via Gi proteins

- Centrally-acting

31
Q

What is the MOA of Tizanidine? What type of a muscle relaxant is it?

A

a2 receptor agonist

- Centrally-acting

32
Q

What is the MOA of Dantrolene, and what does this mean? What type of a muscle relaxant is it?

A

Inhibits Ca release → interferes with excitation-contraction coupling (actin/myosin)
- Direct-acting

33
Q

What is the MOA of Botulinum Toxin? What type of a muscle relaxant is it?

A

Inhibits ACh release

- Direct-acting

34
Q

What PK property regulates AEs/toxicity?

A

Half life

Pharmacology III (25 decks)

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