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Week 3 (Neuro 2) > PHARM - Local Anesthesia > Flashcards

PHARM - Local Anesthesia Flashcards

1
Q

briefly - how do local anesthesics relieve pain?

A

by reverisbly blocking nerve conduction

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2
Q

describe the structural components of local anesthetics (LA) & their importance

A
  • lipophillic portion: directs the LA to the proper location
  • hydrophillic portion: blocks the Nav channels
    • can be charged or uncharged
  • hydrocarbon chain: joins lipophillic & hydrophillic components
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3
Q

what are the two variations of LA structures?

why is this relevant pharmacologically?

A
  • esters: ester bond connects lipophillic part to hydrophobic chain
  • amides: amide bond connects lipophillic part to hydrophobic chain

esters are degraded by circulating esterases, and thus have a shorter duration of action than amides. amides are more commonly used

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4
Q

which LAs are esters?

A
  • procaine
  • chloroprocaine
  • tetracaine
  • benzocaine
  • cocaine
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5
Q

which LAs are amides?

A
  • lidocaine
  • mepivacaine
  • bupivacaine
  • ropivacaine
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6
Q

LA - MOA

A
  • LA are activated (open state) sodium channel blockers
    • i.e, they only work on Na+ channels that are open, which - in a pain state - many are d/t noxious stimuli stimulating nerve terminals
      • LA must be uncharged to enter channel (achieved by buffering)
      • LA must be charged (once inside channel) to block Na+ entry
    • Na+ blockage decreases rate of firing
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7
Q

the degree of blockage provided by LAs depends on…?

A

the frequency of nerve impulses (rate of firing)

high frequency = high blok

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8
Q

what happens when LAs become trapped in closed or inactivated channels?

A

the unblock from the anesthesia is slow

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9
Q

which physiochemical factors influence the onset of action of LAs?

A
  • the pH of the environment (tissue) LA is injected
  • the pH of the solution containing the LA
  • the lipid solubility of the LA
  • the protein content of the LA
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10
Q

how does tissue pH affect onset LA onset of action?

A
  • lidocaine has a pkA of 7.4
    • at physiological pH (7.8), it is mostly charged (cationic)
    • after enough time, the body buffers lidocaine so that more molecules are neutral (non-ionized), & can thus enter Na channels.
    • but this buffering capacity is affected by the pH of the surrounding tissue
      • low pH [acidosis]
        • lidocaine gets protonated (becoming charged)
        • takes longer to buffer drug & produce neutral moleccules
        • longer onset of action
      • high pH [alkalosis]
        • lidocaine gets deprotonated (becoming neutral)
        • takes less time drug & produce neutral moleccules
        • shorter onset of action
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11
Q

how does acidosis affect LA onset of action?

what is an example of acidosis?

A

delays onset of action

infection / inflammation (releases H+)

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12
Q

how does alkalosis affect LA onset of action?

A

faster onset of action

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13
Q

lidocaine can be administered in which formulations?

why is this pharmacologically relevant

A
  • 2% lidocaine solution - pH of 3.9
  • 2% lidocaine + EPI solution - pH of 6.0
  • soution + bicarbonate = higher pH

acidic LA solutions (that don’t have bicarb) contain drug in mostly in charged state, and will take longer to buffer = faster onset of action

more basic LA solutions (come with bicarb) contain drug mostly in a neutral state, and will take less time to buffer = faster onset of action

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14
Q

what are the disadvantages of low pH LAs?

A
  • pain on injection (H+ stimulates ASIC channels)
  • tissue injury (H+ is inflammatory)
  • slow onset of analgesia (5-10 min)
  • litte / no analgesia in low pH tissues (infections)
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15
Q

what are the advantages of buffered LAs (bicarbonate added)?

A
  • reduced pain on injection
  • reduced risk of tissue damage
  • faster onset (1-2 minutes)
  • the ability fo obtain analgesia in infected tissue
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16
Q

how does LA lipid solubility affect duration of action?

A

higher solubility = longer duration of action

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17
Q

which LA is the most lipophillic?

A

bupivacaine

18
Q

how does the protein binding capacity of LAs affect the duration of action?

A

higher protein binding = longer duration of action

19
Q

how does anesthesia spread anatomically?

why is this the case?

A
  • anesthetizes proximal areas before distal areas
  • b/c mantle (outer nerve) fibers are blocked before core (inner nerve) fibers
20
Q

to which locations can LAs distribute?

A
  • brain
  • lungs
  • fat
  • placenta
21
Q

LAs - metabolism

A
  • amides - by liver microsomal enzymes
  • esters - rapidly by plasma / liver esterases

esters metabolized faster, have a much shorter duration of action than amides

22
Q

what is the role of epinephrine in EPI-containing LA formulations?

A

vasoconstricts the vasculature near the injection site, limiting flow to & from the site. this “traps” LA at the site, which

  • prolongs its duration of action
  • limits its systemic aborption & thus its systemic toxicity
23
Q

what are the disadvantages of epinephrine in EPI-containg LA formulations?

A
  • locally: ischemia d/t vasoconstriction, esp in areas with low collateral blood flow: digits, ears
  • systemically: could increase BP, affect HR
24
Q

how are the actions of LAs terminated?

A

by eventual removal from the injection site by the circulatory system

this is why vasoconsriction from EPI containing formulation prolong DUA

25
Q

which LAs come in a formulation with EPI?

A
  • both amides:
    • bupivicaine: epi
      • 1:200,000
    • lidocaine: epi
      • 1:200,000
      • 1:100,000
      • 1:50,000

the 1 represents EPI, and the 2nd # represents the LA: the higher the second number, the less EPI the formulation contains

26
Q

how much EPI is “necessary” to optimize LA duration of action?

A
  • 1:200,000
    • available in both lidocaine & buprivacaine formulations
    • gets duration of action to ~ 90 min
    • beyond this, adding more EPI just inc risk of systemic AEs
27
Q

LAs can lead to what systemic AEs?

A
  • CNS:
    • restlessness / tremors / seizures -> depression & coma
      • ​this is b/c inhibitory interneurons are anesthetized first
    • TNS (transient neurological symptoms):
      • ​pain
      • dystheisa
  • CV:
    • ​heart collapse d/t decreased
      • contractie force
      • conduction velocity
      • ​excitability
    • vasculature
      • vasodilation
      • hypotension
  • allergies
28
Q

local anesthetics are C/I in a patient taking what other drugs?

A

methemoglobin causing drugs

  • nitroglycerine
  • phenytoin
29
Q

which LA is the most likely to cause TNS?

A

lidocaine (is the most neurotoxic)

pain, dysthesia

30
Q

which LA is most likely to cause CV collapse?

  • how is this treated? why?
  • which drug can be used as an alternative?
A

bupivacaine

  • tx = ACLS + IV infusion of intralipid
    • ACLS often insufficient to tx bupivacaine-induced CV arrest
    • intralipid = a supplement that can bind & the highly lipophillic bupivacaine, negating its affects
  • ropivicane can be used an an alternative
31
Q

which LA is most likely to induce allergic reactions?

why?

A

the ester LAs: procaine, cholorproctain, benzocaine

this is because the are metaoblized to PABA, an allergen to certain patients

32
Q

how most LAs affect the vasculature?

why is the exception?

A

vasodilate -> hypotension

exception is cocaine (which vasoconstricts)

33
Q

list the uses of each amide LA

A
  • all: local infusion, nerve blocks, epidural
    • mepivacaine, bupivacaine, ropivacaine - spinal
    • lidocaine - topical, IV
34
Q

lidocaine

  • is the only amide LA that can has what anesthetic use?
  • cannot be used for? why?
A
  • only amide used for topical or IV anesthesia
  • no longer used for spinal anesthesia - b/c it is neurotoxic and poses a high risk for TNS
35
Q

describe the onset and duration of each amide LA

A
  • lidocaine: rapid osnet, intermediate duration
  • mepivacaine: rapid onset, long duration
  • bupivacaine: slow onset, long duration
  • ropivacaine: slow onset, long duration
36
Q

which amide can be effectively used as an alternative to bupivicaine?

when might this be useful?

A
  • ropivacaine - has the same onset, duration and uses as bupivacaine
  • can be used to avoid the _cardiotoxic affect_s of bupivacaine
37
Q

what are the clinical uses for neuromuscular blocking drugs (NMBs)?

A

procedures that require muscle paralysis

38
Q

the NMBs work primarily via which methods?

A
  • two major MOAs
    • non-depolarization agents: competitive antagonists of AChR at NMJ
    • depolarization agents: agonists of AChR that work in two phases
      • phase I: continous AChR stimulation = strong depolarization
      • phase II: desentitization of AChRs to any more AChR -> no AP
39
Q

succinylcholine

  • what kind of drug
  • clinical use
  • MOA
  • onset
  • AEs
A
  • drug: is an NMB
  • clinical use: tracheal intubation
  • MOA: depolarization agent (AChR agonist)
  • onset: 1-2 minutes
  • AE
    • malignant HTN
    • cardiac dysarthmia - cardiac / sinus arrest
    • fasciculations
    • kyperkalemia
40
Q

rocuroniom

  • what kind of drug
  • clinical use
  • MOA
  • AEs
A
  • drug: is an NMB
  • clinical use: tracheal intubation
  • MOA: non-depolarizating agent (AChR antagonist)
  • onset: 1-2 minutes
  • AEs: none significant
41
Q

how are neuromuscular blocks by non-depolarizing NMBs reversed?

why?

A
  • via AChE inhibitors - endophonium, neostigmine
  • AChE inhibitors inc ACh concentrations, so ACh can outcompete the competitive AChR antagonists (i.e., rocuronium)
42
Q

how are neuromuscular blocks by depolarizing NMBs reversed?

why?

A

by waiting for recovery in 5-10 minutes

AChE inhibitors wont work: increased ACh at the synapse wont work on desensitized receptors (i.e., succinylcholine)

Week 3 (Neuro 2) (5 decks)

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