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4. Pharm III > 1- Local Anesthetics > Flashcards

1- Local Anesthetics Flashcards

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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
Local distribution of an LA can be described in what 3 ways?
Hyperbaric, isobaric, hypobaric
26
What factors affect systemic absorption of an LA?
Dosage, site of injection, drug-tissue binding, chemical properties of drug, local BF, vasoconstricting agents (Epi)
27
What is the affect of vasoconstricting agents such as Epi on the systemic absorption of LAs?
Decreases drug diffusion = prolonged duration of action
28
Amides are metabolized by what?
CYP450s
29
In what populations is amide toxicity more likely?
Hepatic disease/ reduced hepatic BF
30
Esters are metabolized by what?
Butyrylcholinesterase in plasma (mutations can impact ester LA metabolism)
31
What is a differential block and how do you reverse it?
Block is not limited to intended site, reversed with Etidocaine
32
What factors affect LA action?
Differential block, anatomic arrangement, intrinsic susceptibility of nerve fibers, order of sensitvity
33
How does anatomic arrangement affect LA action?
Closer to injection site affected more
34
With respect to intrinsic susceptibility of nerve fibers to the block, what factors affect LA action and how?
* Diameter- smaller diameter fibers more sensitive than larger diameter fibers * Myelinated less sensitive than unmyelinated * Faster conduction veloctity = less sensitive (more drug needed
35
What is the order of sensitivity for LA action?
SNS \> sensory (pain) \> touch \> motor
36
What are the common CV SEs of LAs?
Arrhythmias, vasodilation, hypotension
37
What are the common CNS SEs of LAs? (7)
Sedation, visual/ auditory disturbances, circumoral numbness, nystagmus, muscle twitching, convulsions, death (large doses)
38
What are the common "blood" SEs of LAs?
Prilocaine metabolite may produce methemoglobinemia
39
What are the common peripheral NS SEs of LAs?
Prolonged sensory and motor deficit (high doses)
40
What are the common localized toxicity SEs of LAs?
Neural injury, transient neurological sxs (TNS)- transient pain, dysesthesia (a/w lido for spinal anesthesia)
41
What is the duration of action for Procaine?
Short (10-20 min)
42
What is the MOA of Procaine?
Ester
43
What is the use for Procaine?
Infiltration anesthesia and dx nerve blocks (ex. colonoscopy)
44
What are the pharmacokinetics of Procaine?
Injection (no topical)
45
What are the SEs of Procaine?
Hypersensitivity (PABA metabolite)
46
What is the duration of action of Cocaine?
Medium
47
What is the MOA of Cocaine?
Ester (inhibits Na+ channels), ↑ DA in CNS/ periphery
48
What is the use of Cocaine?
Topical anesthesia of mucous membranes (UR tract), decrease bleeding (dental procedures)
49
Cocaine is metabolized by what?
Butyrylcholinesterase
50
What are the SEs of Cocaine?
SNS and CVs
51
What are the cautions with use of Cocaine?
Addicts, drugs that increase catecholamines
52
What is the duration of action of Lidocaine?
Medium
53
What is the use for Lidocaine?
Infiltration blocks and epidural anesthesia
54
What is the onset of action for Lidocaine?
Rapid (more potent/ longer vs Procaine)
55
What are the SEs of Lidocaine?
TNS (do not use for spinal blocks)
56
What is the duration of action of Prilocaine?
Medium
57
What is the MOA of Prilocaine?
Amide
58
What is the use for Prilocaine?
Limited to dentistry
59
What are the important pharmacokinetics of Prilocaine?
Highest clearance (one of the safest) of amide drugs
60
What is the SE of Prilocaine?
Methemoglobinemia (excessive methemoglobin in blood → chocolate color)
61
What are the SEs/ treatment for methemoglobinemia?
SX: SOB, fatigue, dizziness, dysrhythmias, seizures, coma, death TX: Reversed w/ methylene blue
62
What are the contraindications for Prilocaine?
Pts w/ methemoglobinemia, cardiac & respiratory disease
63
What is the duration of action of Mepivacaine?
Medium
64
What is the MOA for Mepivacaine?
Amide
65
What is the use of Mepivacaine?
Peripheral nerve blocks (not typically used)
66
What is the contraindication to use of Mepivacaine?
Labor anesthesia
67
What is the duration of action of Tetracaine?
Long (2-3 hrs)
68
What is the MOA for Tetracaine?
Ester
69
What is the use of Tetracaine?
Preferred for ophthalmological use, spinal anesthesia (combined with dextrose = hyperbaric)
70
What are the important pharmacokinetics of Tetracaine?
Slow onset of action (\>10 min), 16x more potent and toxic (vs procaine), metabolized by butyrylcholinesterase
71
Severe toxicity of Tetracaine can be seen when?
High # of peripheral blocks
72
What is the mechanism of action of Bupivacaine?
Amide
73
What is the use of Bupivacaine?
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
What is the important pharmacokinetic property of Bupivacaine?
More potent sensory block than motor block
75
What is the SE of Bupivacaine?
CV (greater than other amides) → reverse w/ IV lipids
76
What is the duration of action of Ropivacaine?
Long
77
What is the MOA of Ropivacaine?
Amide
78
What is the use of Ropivacaine?
Peripheral and epidural blocks (not preferred for childbirth), vasoconstricting effects at clinical doses (do not need to add Epi)
79
What is the important pharmacokinetics of Ropivacaine?
S-enantiomer of Bupivacaine (less lipid soluble and cleared more rapidly → fewer adverse events/ CV toxicity)
80
What are the SEs of Ropivacaine?
Drug interactions (CYP3A4)
81
What is the MOA for Benzocaine?
Ester, lipophilic (non-ionized)
82
What is the use of Benzocaine?
Sunburn, minor burns, pruritus (topical skin conditions)
83
What are the pharmacokinetics of Benzocaine?
Topically only, metabolized by butyrylcholinesterase
84
What are the SEs of Benzocaine?
Methemoglobinemia
85
What is the duration of action of Etidocaine?
Long
86
What is the MOA for Etidocaine?
Amide
87
What is the use of Etidocaine?
Inverse differential block (may cause motor block before or without sensory block)
88
What is the MOA of Articaine?
Amide + additional ester group
89
What is the use of Articaine?
Dental medicine - boost anesthetic action (able to use throughout procedure)
90
What is the important pharmacokinetic property of Articaine?
Decreased half life and potential for toxicity (b/c amide and ester properties)
91
What is the (RARE) SE of Articaine?
Persistent paresthesias
92
What is the MOA for Dibucaine?
Amide
93
What is the use of Dibucaine?
Topical in US, spinal anesthetic outside of US
94
What is the general use of centrally acting muscle relaxants (spasmolytics)?
Used for relief of spastic muscle disorders
95
↑ in tonic stretch reflexes + flexor muscle spasms + muscle weakness is defined as what?
Spasticity
96
What are the target proteins for centrally acting muscle relaxants?
GABAA, GABAB, 𝜶2, Ca channels
97
What are the centrally acting muscle relaxants?
Diazepam (Valium), Baclofen, Tizanidine
98
What are the direct acting muscle relaxants?
Dantrolene and Botulinum
99
What is the MOA of Diazepam?
Acts on GABAA (but affect all receptor subtypes) → GABA mediated presynaptic inhibition in the spinal cord
100
What is the use of Diazepam?
Local muscle trauma, adjunct in spasticity
101
What is the SE of Diazepam?
Heavy sedation
102
What is the MOA of Baclofen?
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
What are the pharmacokinetics of Baclofen?
Oral, 3-4 hr t1/2
104
What are the SEs of Baclofen?
Drowsiness, weakness, increased seizure activity, respiratory depression
105
What is the MOA for Tizanidine?
a2 receptor agonist → pre and postsynaptic inhibition of spinal cord synaptic activity to ↓ muscle spasticity, inhibits pain transmission to dorsal horn
106
What is the use of Tizanidine?
Acute and chronic muscle spasms (muscle weakness limited)
107
What are the SEs of Tizanidine?
Sedation, dry mouth, weakness, falls in elderly, hepatotoxicity (monitor liver function)
108
What is the MOA for Dantrolene?
Inhibits Ca @ NMJ
109
What is the use of Dantrolene?
Neuroleptic malignant syndrome, malignant hyperthermia
110
What are the SEs of Dantrolene?
Weakness, sedation (less vs centrally acting)
111
What is the MOA of Botulinum?
Inhibits ACh release from NMJ
112
What is the use for Botulinum?
Small amounts injected locally to control muscle spasms following stroke or neuro injury
113
How long do the effects of Botulinum last?
Weeks to months
114
What are the SEs of Botulinum?
Large amounts = toxic → spread of toxin to unwanted areas (CNS)
115
What drugs are used for acute local muscle spasms?
Cyclobenzaprine and Carisoprodol
116
What is the result of a brain stem sedative?
↓ neuronal activity in the spinal cord
117
What is the general use of acute local muscle spasm drugs?
Used for acute spasm caused by local tissue trauma/muscle strain (Limited effectiveness but may alter perception of pain)
118
What is the SE of acute local muscle spasm drugs?
Significant sedation
119
What is important to know about Cyclobenzaprine?
* Centrally acting * Antimuscarinic activity- sedation, confusion, hallucinations
120
What is important to know about Carisoprodol?
* Similar to barbiturates * Popular drug of abuse → caution in recovering addicts

4. Pharm III (16 decks)

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