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Brain and Behavior Exam 2 > Lec 17 Local Anesthetics > Flashcards

Lec 17 Local Anesthetics Flashcards

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1
Q

What is clinical use for local anesthetics?

A
  • produce analgesia in restricted region by inhibiting neurons that transmit nociception
  • blockade not specific to nociceptors so get general loss of sensation
  • ideally do not alter brain activity [unlike general anesthetics]
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2
Q

What is the general structure of local anesthetics?

A

aromatic group + linker + amino group

–> either ester or amide

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3
Q

What are routes of administration of local anesthetics?

A
  • topical [surface]
  • injection near a nerve
  • regional block [iv injection into extremity, tourniquet to reduce systemic distribution
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4
Q

What is primary mech of action of local anesthetics ?

A
  • block voltage-gated sodium channels
  • bind site formed by 3 of the S6 helices that line pore
  • little selectivity for subtypes of Na channel [contributes to adverse effects]
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5
Q

What is a field block?

A
  • injection of local anesthetic near nerve

- anesthetizes region distal to injection

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6
Q

what is a local infiltration?

A

injection of local anesthetic at site to be excised

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7
Q

What is a nerve block?

A

injection near a peripheral nerve or nerve plexus

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8
Q

How is potency of local anesthesia correlated with lipid solubility? molecular size?

A

small molecular size + more lipid soluble = more potent

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9
Q

As a general rule are C nerve fibers carrying pain and temp or larger A fibers more easily blocked?

A
  • smaller fibers blocked first
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10
Q

What are the 3 important structural features of local anesthetics?

A
  • aromatic group [lipophilic]
  • linker [either amide or ester]
  • amino group [hydrophilic, ionizable]
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11
Q

How do you tell if a local anesthetic is an amide or an ester based on its name?

A
  • all amIdes have an I before the “caine”
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12
Q

What form of local anesthetic can traverse cell membrane? what form has higher affinity for binding site in Na channel?

A
  • nonionized form traverses cell membrane

- ionized form has higher affinity for binding site in Na channel

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13
Q

What is pKA of most weak bases?

A

7-9

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14
Q

What is pka?

A

pH at which half of drug is in ionized and half in nonionized

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15
Q

What is henderson hasselbach?

A

log (protonated)/(unprotonated) = pKa - pH

“protonated = more, goes on top”

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16
Q

Which one local anesthetic can only be found in ionized form?

A

benzocaine

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17
Q

How does reduced pH affect ability of local anesthetic to function? in what scenarios do you see this?

A

when low pH –> more of drug is in protonated form –> less avaible that can diffuse into nerve cell

  • reduces effect of a given dose
  • seen in inflamed tissues, infection
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18
Q

What are the two major routes by which local anesthetic accesses channel?

A

major: via intracelluar, drug in cytoplasm enters and blocks open channel
minor: membrane delimited, drug diffused from within lipid bilayer to channel pore

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19
Q

How does carbonation of local anesthetic solution affect its action?

A
  • decreases intracellular pH –> increases prevalence of cationic active form inside the nerve = increase activity
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20
Q

What is use-dependent inhibition?

A

in order for local anesthetic to block channel via major cytoplasmic route, requires channel to be open

means that really active neurons [like those sensing pain] will be blocked faster

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21
Q

What is use-independent inhibition?

A

access to channel from lipid bilayer does not require it to be open

with long enough exposure to drug, even relatively inactive neurons become inhibited this way

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22
Q

Do fibers on inside or outside of nerve get blocked by local anasthetics first?

A

fibers on outside –> easier to get to

outside usually proximal, inside = distal, so proximal blocked before distal

23
Q

How does hydrophobicity of the local anesthetic base corelated with potency?

A
  • highly hydrophobic base accumulates in lipid bilayer –> create reservoir of drug molec that can be pronated at cyto surface to block open channel
  • because more potent, lower concentration used so tend to block more slowly [ b/c lower conc gradient]
24
Q

Which fiber types are most sensitive to local anesthetics?

A

most sensitive = C type fibers

  • sensory = pain
  • motor = sympathetic [a receptors, vasoconstrictors]

A-d also pretty sensitive = pain

large fibers relatively spared but will always have some effect

25
Q

Why are smaller fibers more susceptible?

A
  • AP decays if Na channels block
  • smaller neuron = shorter space constant = more rapid decay
  • same region of block will cause thin fibers to fail first [and not large fiber]
26
Q

given constant region of block and equal diameter, are myelinated or unmyelinated fibers more susceptible?

A

myelinated are more susceptible

27
Q

Are most local anastheticcs vasoconstrictors or vasodilators? 2 exceptions?

A

most are vasodilators [inhibit sympathetic fibers to vasculature]

2 exceptions: cocaine, prilocaine

28
Q

Why do you often give a vasoconstrictor with local anasthetic? which one usually?

A

usually epinephrine

  • administer b/c anesthetics are vasodilators, increase blood flow/permeability which causes drug to distribute away from the target tissue.
  • giving vasoconstrictor increases duration of effect and reduces systemic adverse effects
29
Q

Why shouldn’t you coadminister epinephrin for nerve block in fingers/toes?

A
  • supplied by end-arteries

- may cause ischemia or necrosis

30
Q

How are ester-type local anesthetics metabolized? effect of this?

A
  • enter blood stream

- metabolized by plasma esterases to PABA or derivative

31
Q

Are esters or amides more likely to have local rxn?

A

esters can get local allergic rxn because metabolized locally to PABA that triggers hypersensitivity

32
Q

Are esters or amides more likely to have systemic effects?

A
  • amides

- because local anesthetic effect terminated by systemic distrubution-

33
Q

How are amide-type local anesthetics metabolized?

A
  • by the liver, in part by cyt P450 enzymes

- excreted in metabolized + unchanged form by kidney

34
Q

In what situations is rate of amide anesthetic metabolism decreased?

A
  • patients with liver disease
  • ## co-administration of drugs that interfere with cyt P450 enzymes
35
Q

What are CNS side effects of local anesthetics?

A
  • at low levels –> sedation
  • at high levels –> seizure, loss of consciousness, may reflect blockade of inhibitory neurons

with increased dose: drowsiness –> sensory disturbance –> dizziness –> twitching –> seizures –> coma

36
Q

What are cardiac effects of local anesthetics?

A
  • generally occur at higher dose than CNS symptoms
  • conduction cells most sensitive –> arrhythmia, AV block, ventricular arrest
  • mediated by block of cardiac Na channels, or at very high dose can be due to direct inhibition Ca channels
  • bradycardia, hypotension
37
Q

cocaine

  • ester or amide?
  • What is onsent/duration/metabolism?
  • clinical use?
  • mech?
  • side effects?
A
  • ester
  • onset/duration/metabolism: hepatic metabolism if systemically distributed
  • use: topical use on mucous membranes
  • mech: induces vasoconstriction, inhibits MO re-uptake [including NE]
  • ## effects: euphoria, CNS stim, tachycardia, restlessness, tremors, seizures
38
Q

procaine

  • ester or amide
  • onset/ duration/ met /potency/ etc
  • clinical use
A
  • ester
  • onset/duration/met: rapidly hydrolyzed [short duration], low potency, slow onset, not effective topically
  • use: infiltration anesthesia
39
Q

tetracaine

  • ester or amide
  • onset/ duration
  • clinical use
A
  • ester
  • onset etc: very slow onset, long acting
  • use: spinal block, topical
40
Q

benzocaine

  • ester or amide
  • properties
A
  • ester
    unique struct –> lacks ionizable group, poor aqueous solubility

use: surface anesthesia

41
Q

what is longest acting –> shortest acting between procaine, tetracaine, cocaine

A

tetracaine > cocaine > procaine

42
Q

What is prototypical amide?

A

lidocaine, most commonly used local anesthetic

43
Q

lidocaine

  • ester or amide
  • onset
  • duration
  • clinical use
A
  • amide
  • rapid onset
  • intermediate duration 1-2 hrs
  • use: systemically to treat cardiac arrhythmias
44
Q

What does it mean that lidocaine metabolism is flow-limited?

A
  • clearance is sensitive to changes in hepatic blood flow

- extra caution in pts with liver disease

45
Q

prilocaine

  • ester or amide
  • onset
  • duration
  • clinical use
A
  • ester
  • weak vasodilator so generally don’t need Epinephrine
  • rapid systemic elimination [hepatic + renal]
  • large Vd
  • use: spinal anesthesia
46
Q

What is an adverse affect seen with prilocaine use?

A

methemoglobinemia from its toluidine metabolites

  • Fe3 [ferric] heme rather than normal Fe2 [ferrous]
47
Q

Where do drugs with large Vd end up?

A

in lipid/fat cells

48
Q

bupivacaine

  • ester or amide
  • onset
  • duration
  • clinical use
  • side effects
A
  • amide
  • slow onset, long duration
  • use: blocks sensory over motor, use in labor
  • sustained-release liposomal formulation [24 hr] for post op pain management
  • cardiotoxicity [arrhythmia
49
Q

Which amide local anesthetic has greatest cardiotoxicity? why?

A

bupivacaine

- serious ventricular arrhythmias, myocardial depression

50
Q

What is ropivacaine?

A
  • R- enantiomer of bupivicaine

- less cardiotoxic

51
Q

What measures to minimize likelihood of systemic effects of lidocaine or other local anesthetic?

A
  • give NE or other vasoconstrictor
52
Q

Would pt with local anesthetic induced CNS symptoms also experience direct cardio effects?

A
  • maybe –> CNS effects come first, need higher dose to get cardio effect than CNS effect
53
Q

What chemical characteristic of lidocaine increases likelihood of systemic effects?

A
  • its an amide so metabolized in the liver rather than locally in the plasma so it has to go through systemic circulation first
54
Q

would drug named mepivacaine likely share same chemical characteristics as lidocaine?

A

yes, i before the “caine” means its an amide just like lidocaine

Brain and Behavior Exam 2 (21 decks)

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