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4. Pharm III > 1- Local Anesthetics > Flashcards

1- Local Anesthetics Flashcards

1
Q

Esters and amides are both local anesthetics. How do they compare?

A

Esters have a shorter duration of action and increased systemic toxicity

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2
Q

How are esters and amides administered to increase stability and solubility?

A

As salts

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3
Q

At physiologic pH, LAs are predominantly in what form and what effect does this have?

A

Predominantly ionized → membrane transport increases (smaller, more lipophilic) → faster onset of action

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4
Q

What form must a local anesthetic be in to cross the cell membrane?

A

Non-ionized (crosses via hydrophobic pathway)

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5
Q

Once a local anesthetic crosses the cell membrane in the non-ionized from, what happens?

A

Become ionized and binds to Na+ channel

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6
Q

Lidocaine has a faster what than Bupivacaine?

A

Onset of action (but not necessarily duration of action)

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7
Q

Which LA is always non-ionized, making it an “exception”, and what does this indicate for its use?

A

Benzocaine, topical application only

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8
Q

How does inflammation affect membrane transport?

A

Decreases it, due to increased acidification

(need to increase dose to have same effect)

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9
Q

Bicarb makes pH more basic and increases what drug concentrations?

A

Increases non-ionized drug concentrations = ↑ degree of LA transport

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10
Q

The route of administration for LAs are based on what?

A

Duration of action

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11
Q

What route of administration for LAs are applied to the skin, eye, throat, and mucous membranes?

A

Topical

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12
Q

What route of administration goes into peripheral nerve endings (blocks)?

A

Injection

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13
Q

What type of anesthesia is into the tissue?

A

Infiltration anesthesia

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14
Q

What are the advantages/ disadvantages of infiltration anesthesia?

A

Adv: does not disrupt normal body function

Disad: requires large amounts of drug

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15
Q

What type of anesthesia is into the axillary artery?

A

IV regional anesthesia (Bier’s block)

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16
Q

What is the MOA for LAs?

A

Block Na+ channels and inhibit neuronal firing

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17
Q

How does a LA achieve a complete block?

A

Drug binding to most/ all Na channels (rate of AP declines)

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18
Q

Extent of the block (by LA) is dependent on what?

A

Voltage (potential) and time (firing)

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19
Q

What type of channels do LAs have a high and low affinity for?

A

High- activated (inactivation gate open) and inactivated (inactivation gate closed)

Low- closed/ resting channels (inactivation gate open but channel closed)

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20
Q

Due to differences in affinity, a block is more effective in what type of axons?

A

Rapidly firing axons (compared to resting axons)

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21
Q

What factors affect the MOA (block Na+ channels and inhibit neuronal firing) of LAs?

A
  • Elevated Ca2+ → ↑ channels in resting state → block is diminished
  • Elevated K+ → ↑ channels in inactivated state → block is enhanced
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22
Q

The duration of action and potency of LAs are based on what?

A

Lipid solubility

(more lipid soluble = stays at site of application longer = longer duration of action)

(unrelated to t1/2)

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23
Q

The toxic effects of LAs are dependent on what?

A

t1/2

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24
Q

When does systemic absorption occur with LAs?

A

As drug diffuses

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25
Q

Local distribution of an LA can be described in what 3 ways?

A

Hyperbaric, isobaric, hypobaric

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26
Q

What factors affect systemic absorption of an LA?

A

Dosage, site of injection, drug-tissue binding, chemical properties of drug, local BF, vasoconstricting agents (Epi)

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27
Q

What is the affect of vasoconstricting agents such as Epi on the systemic absorption of LAs?

A

Decreases drug diffusion = prolonged duration of action

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28
Q

Amides are metabolized by what?

A

CYP450s

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29
Q

In what populations is amide toxicity more likely?

A

Hepatic disease/ reduced hepatic BF

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30
Q

Esters are metabolized by what?

A

Butyrylcholinesterase in plasma

(mutations can impact ester LA metabolism)

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31
Q

What is a differential block and how do you reverse it?

A

Block is not limited to intended site, reversed with Etidocaine

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32
Q

What factors affect LA action?

A

Differential block, anatomic arrangement, intrinsic susceptibility of nerve fibers, order of sensitvity

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33
Q

How does anatomic arrangement affect LA action?

A

Closer to injection site affected more

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34
Q

With respect to intrinsic susceptibility of nerve fibers to the block, what factors affect LA action and how?

A
  • Diameter- smaller diameter fibers more sensitive than larger diameter fibers
  • Myelinated less sensitive than unmyelinated
  • Faster conduction veloctity = less sensitive (more drug needed
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35
Q

What is the order of sensitivity for LA action?

A

SNS > sensory (pain) > touch > motor

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36
Q

What are the common CV SEs of LAs?

A

Arrhythmias, vasodilation, hypotension

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37
Q

What are the common CNS SEs of LAs? (7)

A

Sedation, visual/ auditory disturbances, circumoral numbness, nystagmus, muscle twitching, convulsions, death (large doses)

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38
Q

What are the common “blood” SEs of LAs?

A

Prilocaine metabolite may produce methemoglobinemia

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39
Q

What are the common peripheral NS SEs of LAs?

A

Prolonged sensory and motor deficit (high doses)

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40
Q

What are the common localized toxicity SEs of LAs?

A

Neural injury, transient neurological sxs (TNS)- transient pain, dysesthesia (a/w lido for spinal anesthesia)

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41
Q

What is the duration of action for Procaine?

A

Short (10-20 min)

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42
Q

What is the MOA of Procaine?

A

Ester

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43
Q

What is the use for Procaine?

A

Infiltration anesthesia and dx nerve blocks (ex. colonoscopy)

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44
Q

What are the pharmacokinetics of Procaine?

A

Injection (no topical)

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45
Q

What are the SEs of Procaine?

A

Hypersensitivity (PABA metabolite)

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46
Q

What is the duration of action of Cocaine?

A

Medium

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47
Q

What is the MOA of Cocaine?

A

Ester (inhibits Na+ channels), ↑ DA in CNS/ periphery

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48
Q

What is the use of Cocaine?

A

Topical anesthesia of mucous membranes (UR tract), decrease bleeding (dental procedures)

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49
Q

Cocaine is metabolized by what?

A

Butyrylcholinesterase

50
Q

What are the SEs of Cocaine?

A

SNS and CVs

51
Q

What are the cautions with use of Cocaine?

A

Addicts, drugs that increase catecholamines

52
Q

What is the duration of action of Lidocaine?

A

Medium

53
Q

What is the use for Lidocaine?

A

Infiltration blocks and epidural anesthesia

54
Q

What is the onset of action for Lidocaine?

A

Rapid (more potent/ longer vs Procaine)

55
Q

What are the SEs of Lidocaine?

A

TNS (do not use for spinal blocks)

56
Q

What is the duration of action of Prilocaine?

A

Medium

57
Q

What is the MOA of Prilocaine?

A

Amide

58
Q

What is the use for Prilocaine?

A

Limited to dentistry

59
Q

What are the important pharmacokinetics of Prilocaine?

A

Highest clearance (one of the safest) of amide drugs

60
Q

What is the SE of Prilocaine?

A

Methemoglobinemia (excessive methemoglobin in blood → chocolate color)

61
Q

What are the SEs/ treatment for methemoglobinemia?

A

SX: SOB, fatigue, dizziness, dysrhythmias, seizures, coma, death

TX: Reversed w/ methylene blue

62
Q

What are the contraindications for Prilocaine?

A

Pts w/ methemoglobinemia, cardiac & respiratory disease

63
Q

What is the duration of action of Mepivacaine?

A

Medium

64
Q

What is the MOA for Mepivacaine?

A

Amide

65
Q

What is the use of Mepivacaine?

A

Peripheral nerve blocks (not typically used)

66
Q

What is the contraindication to use of Mepivacaine?

A

Labor anesthesia

67
Q

What is the duration of action of Tetracaine?

A

Long (2-3 hrs)

68
Q

What is the MOA for Tetracaine?

A

Ester

69
Q

What is the use of Tetracaine?

A

Preferred for ophthalmological use, spinal anesthesia (combined with dextrose = hyperbaric)

70
Q

What are the important pharmacokinetics of Tetracaine?

A

Slow onset of action (>10 min), 16x more potent and toxic (vs procaine), metabolized by butyrylcholinesterase

71
Q

Severe toxicity of Tetracaine can be seen when?

A

High # of peripheral blocks

72
Q

What is the mechanism of action of Bupivacaine?

A

Amide

73
Q

What is the use of Bupivacaine?

A

Analgesia for post-op pain control, spinal anesthesia, infiltration blocks/ epidural anesthesia, preferred as epidural during labor and childbirth (higher degree of differential block - no paralyzation)

74
Q

What is the important pharmacokinetic property of Bupivacaine?

A

More potent sensory block than motor block

75
Q

What is the SE of Bupivacaine?

A

CV (greater than other amides) → reverse w/ IV lipids

76
Q

What is the duration of action of Ropivacaine?

A

Long

77
Q

What is the MOA of Ropivacaine?

A

Amide

78
Q

What is the use of Ropivacaine?

A

Peripheral and epidural blocks (not preferred for childbirth), vasoconstricting effects at clinical doses (do not need to add Epi)

79
Q

What is the important pharmacokinetics of Ropivacaine?

A

S-enantiomer of Bupivacaine (less lipid soluble and cleared more rapidly → fewer adverse events/ CV toxicity)

80
Q

What are the SEs of Ropivacaine?

A

Drug interactions (CYP3A4)

81
Q

What is the MOA for Benzocaine?

A

Ester, lipophilic (non-ionized)

82
Q

What is the use of Benzocaine?

A

Sunburn, minor burns, pruritus (topical skin conditions)

83
Q

What are the pharmacokinetics of Benzocaine?

A

Topically only, metabolized by butyrylcholinesterase

84
Q

What are the SEs of Benzocaine?

A

Methemoglobinemia

85
Q

What is the duration of action of Etidocaine?

A

Long

86
Q

What is the MOA for Etidocaine?

A

Amide

87
Q

What is the use of Etidocaine?

A

Inverse differential block (may cause motor block before or without sensory block)

88
Q

What is the MOA of Articaine?

A

Amide + additional ester group

89
Q

What is the use of Articaine?

A

Dental medicine - boost anesthetic action (able to use throughout procedure)

90
Q

What is the important pharmacokinetic property of Articaine?

A

Decreased half life and potential for toxicity (b/c amide and ester properties)

91
Q

What is the (RARE) SE of Articaine?

A

Persistent paresthesias

92
Q

What is the MOA for Dibucaine?

A

Amide

93
Q

What is the use of Dibucaine?

A

Topical in US, spinal anesthetic outside of US

94
Q

What is the general use of centrally acting muscle relaxants (spasmolytics)?

A

Used for relief of spastic muscle disorders

95
Q

↑ in tonic stretch reflexes + flexor muscle spasms + muscle weakness is defined as what?

A

Spasticity

96
Q

What are the target proteins for centrally acting muscle relaxants?

A

GABAA, GABAB, 𝜶2, Ca channels

97
Q

What are the centrally acting muscle relaxants?

A

Diazepam (Valium), Baclofen, Tizanidine

98
Q

What are the direct acting muscle relaxants?

A

Dantrolene and Botulinum

99
Q

What is the MOA of Diazepam?

A

Acts on GABAA (but affect all receptor subtypes) → GABA mediated presynaptic inhibition in the spinal cord

100
Q

What is the use of Diazepam?

A

Local muscle trauma, adjunct in spasticity

101
Q

What is the SE of Diazepam?

A

Heavy sedation

102
Q

What is the MOA of Baclofen?

A

GABAB receptor agonist → opens K+ channels → inhibition of Ca influx → inhibits AC and cAMP formation → decreases release of excitatory transmitters in brain/ spinal cord

103
Q

What are the pharmacokinetics of Baclofen?

A

Oral, 3-4 hr t1/2

104
Q

What are the SEs of Baclofen?

A

Drowsiness, weakness, increased seizure activity, respiratory depression

105
Q

What is the MOA for Tizanidine?

A

a2 receptor agonist → pre and postsynaptic inhibition of spinal cord synaptic activity to ↓ muscle spasticity, inhibits pain transmission to dorsal horn

106
Q

What is the use of Tizanidine?

A

Acute and chronic muscle spasms (muscle weakness limited)

107
Q

What are the SEs of Tizanidine?

A

Sedation, dry mouth, weakness, falls in elderly, hepatotoxicity (monitor liver function)

108
Q

What is the MOA for Dantrolene?

A

Inhibits Ca @ NMJ

109
Q

What is the use of Dantrolene?

A

Neuroleptic malignant syndrome, malignant hyperthermia

110
Q

What are the SEs of Dantrolene?

A

Weakness, sedation (less vs centrally acting)

111
Q

What is the MOA of Botulinum?

A

Inhibits ACh release from NMJ

112
Q

What is the use for Botulinum?

A

Small amounts injected locally to control muscle spasms following stroke or neuro injury

113
Q

How long do the effects of Botulinum last?

A

Weeks to months

114
Q

What are the SEs of Botulinum?

A

Large amounts = toxic → spread of toxin to unwanted areas (CNS)

115
Q

What drugs are used for acute local muscle spasms?

A

Cyclobenzaprine and Carisoprodol

116
Q

What is the result of a brain stem sedative?

A

↓ neuronal activity in the spinal cord

117
Q

What is the general use of acute local muscle spasm drugs?

A

Used for acute spasm caused by local tissue trauma/muscle strain

(Limited effectiveness but may alter perception of pain)

118
Q

What is the SE of acute local muscle spasm drugs?

A

Significant sedation

119
Q

What is important to know about Cyclobenzaprine?

A
  • Centrally acting
  • Antimuscarinic activity- sedation, confusion, hallucinations
120
Q

What is important to know about Carisoprodol?

A
  • Similar to barbiturates
  • Popular drug of abuse → caution in recovering addicts

4. Pharm III (16 decks)

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