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Pharmacology (Dustin, Ben) > B13: Local anesthetics > Flashcards

B13: Local anesthetics Flashcards

1
Q

What is the function of a local anesthetic + how does it achieve this?

(A more general definition from the slides, NOT including molecular targets)

A

A drug causing loss of sensation in a circumscribed area of the body by blocking AP generation and propagation

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2
Q

Very generally…

what are 2 side effects of local anesthetics?

what are 2 general clinical indications?

what are 2 differences from general anesthesia?

(Basics from slides)

A
  • May cause muscle paralysis and somatic/visceral reflex suppression
  • Used for analgesia and complete blockade of sensory modalities
  • In contrast to general anesthesia:
    • LAs administered directly to target organ
    • Systemic circulation only plays a part in termination of effects
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3
Q

What is the main molecular target of local anesthetics?

A

voltage-gated sodium channels (VGSCs)

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4
Q

Name 2 toxins that block the VGSC from the extracellular side.

A

Tetrodotoxin and saxitoxin

(produced by sea microbes + accumulate in fish)

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5
Q

Other than local anesthetics, what 2 types of drugs inhibit VGSCs?

A
  1. Class I Antiarrhythmics
  2. Some antiepileptic medications (carbamazepine, lamotrigine, valproate, topiramate … but not important to know for now)
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6
Q

Generally, what types of nerve fibers are more sensitive to local anesthetics?

Considering this… what is the time order of disappearance of sensation / nerve function upon administration of a LA?

A
  • smaller diameter and less myelinated nerve fibers are most sensitive (so type C fibers are most sensitive, type A are least)
  • Order of nerve function inhibition: pain > temperature > touch > deep pressure > motor function
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7
Q

What is the general structure of the local anesthetic drugs?

(Hint: 3 regions / function groups)

A
  • The “-caine” drugs all contain a lipophilic aromatic region connected by an ester or amide bond to a basic amine side-chain which is ionizable (may be hydrophilic if quaternary, -phobic if tertiary)
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10
Q

What is the difference between the form in which LAs reach their site of action and the form in which they act on their target molecule?

A
  • They reach their (intracellular) site of action in non-ionic (ie unprotonated, lipophilic) form
  • They act on their target molecule (VGSC intracellular domain) in cationic (ie protonated, hydrophilic) form.
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11
Q

At physiological pH, in what form are LAs primarily found?

How does this change in inflammation?

(How is it different for a specific LA with a very different pKa than the rest?)

A
  • At physio pH (~7.4), primarily found in cationic form
  • Inflammation lowers pH in surrounding tissues > more of the LA is protonated (cationic) > less can diffuse into cells > diminished effect
  • In the case of benzocaine, its pKa is 4 (compared to most LAs pKa ~8-9) so it is much less protonated at physio pH > diffuses better but acts on VGSC less
    • remember pKa - pH = log (protonated / non-protonated) for weak bases
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12
Q

What are the 6 types of LA administration methods?

General uses of each method?

A
  1. Surface Anesthesia - inhaled or nasal spray/eye drop/urinary tract/uterus; drug directly applied to surface to be anesthetized
  2. Infiltration Anesthesia - injected into tissues to affect nerve ending/branch; minor surgery
  3. IV Regional - IV injection distal to a pressure cuff; for limb surgery
  4. Nerve block - injected close to nerve trunk to produce peripheral sensation loss; in surgery, dentistry, analgesia
  5. Spinal Anesthesia - injected into subarachnoid space CSF to act on spinal roots + cord; for abdominal/pelvic/leg surgery
  6. Epidural Anesthesia - injected into epidural space to block spinal roots; often used for painless childbirth
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13
Q

Which LA drugs are used for surface anesthesia?

What are the possible adverse effects of surface anesthesia?

A
  • Drugs: lidocaine, tetracaine (AKA amethocaine), dibucaine, benzocaine
  • Adverse effects: systemic toxicity may develop if large areas are anesthetized or high concentrations are used
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14
Q

Which LA drugs are used for infiltration anesthesia?

What is often co-administered and why?

How large of an area can be anesthetized + why?

A
  • Drugs: most of the -caines are used for infiltration anesthesia
  • Often given with epinephrine or felypressin for local vasoconstriction to ↓ absorption from anesthetised site into systemic circ. (contraindicated in fingers/toes where poor circulation already exists)
  • Only small areas, otherwise systemic toxicity risk increases
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15
Q

Which drugs are used for IV regional anesthesia?

What are the risks of this method?

A
  • mainly lidocaine and prilocaine
  • there is a risk of systemic toxicity if the pressure cuff is released too early (before ~20 minutes)
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16
Q

Which LA drugs are used for nerve block anesthesia?

How does it compare to infiltration anesthesia (amt of drug needed, needle placement, onset of action)?

How can duration of nerve block anesthesia be increased?

A
  • Most of the -caines are used for nerve blocks
  • Needs less drug, but more precise needle placement and longer onset than infiltration
  • Duration can be increased with a local vasoconstrictor (epinephrine, etc.)
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17
Q

What kinds of LA drugs are used for spinal anesthesia?

What are some complications of this method?

A
  • Mostly lidocaine
  • Complications: bradycardia / hypotension (sympathetic block); respiratory depression (via phrenic nerve / respiratory center effects); post-op urinary retention (blocked pelvic autonomic outflow)
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18
Q

What are the LA drugs used for epidural anesthesia?

Common side effects?

A
  • Mostly lidocaine and bupivacaine
  • Similar side effects to spinal anesthesia, but less longitudinal spread of the drug along the SC occurs with this method. Post-op urinary retention still common
19
Q

List the 9 local anesthetics.

(Just an overview card, not super important, at least for MCQs)

A
  1. Cocaine
  2. Procaine
  3. Lidocaine (AKA lignocaine)
  4. Benzocaine
  5. Mepivacaine
  6. Tetracaine (AKA amethocaine)
  7. Bupivacaine
  8. Prilocaine
  9. Articaine

super easy, right?

20
Q

List the 4 medium duration LA drugs.

(Give their approx. half-life, tissue penetration + onset speed… maybe not so important)

A
  1. Cocaine - 1 hr T1/2; medium onset; good pen.
  2. Lidocaine - 2 hrs; rapid onset; good pen.
  3. Mepivacaine - 2 hrs; rapid onset; good pen.
  4. Prilocaine - 2 hrs; medium onset; moderate pen.
21
Q

List the 2 short duration LA drugs.

(+ half-life, onset + penetration)

A
  1. Procaine - <1 hr T1/2; medium onset; poor pen.
  2. Articaine - 0.5 hr; rapid onset; good pen.
22
Q

List the 3 long duration LA drugs.

(+ half-life, onset, penetration)

A
  1. Tetracaine - 1 hr T1/2; very slow onset; moderate pen.
  2. Bupivacaine - 2 hr; slow onset; moderate pen.
  3. Benzocaine - ?? T1/2; slow onset; surface anesthesia only (low pKA > exists only as non-ionized base form)
23
Q

Which 3 LA drugs have signifcant CNS side effects?

What are they? Any other side effects?

If they are used clinically, how?

A
  1. Cocaine - CNS and CV effects via amine reuptake inhibition (euphoria, tachycardia etc.); used as surface anesthesia on eye/upper resp.
  2. Procaine - CNS: restlessness, convulsions, respiratory depression; CV: bradycardia + vasodilation > CV “collapse” (not used)
  3. Mepivacaine - similar to procaine; not sure if it’s used but less vasodilation than procaine, so can be given w/o vasoconstrictor
24
Q

What is one of the most widely used drugs for local anesthesia?

What are its side effects?

(Less important: other uses via IV admin?)

A

Lidocaine

  • Similar side effects to procaine (bradycardia, vasodilation) but less tendency to cause CNS effects
  • (via IV, was used for ventricular arrhythmias, not 1st choice anymore)
25
Q

Which LA drug is used mostly for spinal/corneal anesthesia?

Side effects?

A

Tetracaine (AKA amethocaine)

  • side fx similar to lidocaine (bradycardia, vasodilation, low tendency for CNS effects)
26
Q

Which LA is widely used when long duration of activity is needed?

What are its side effects?

What related drug(s) can be used that have better side effect profiles?

A

Bupivacaine

  • similar side fx to lidocaine with greater cardiotoxicitiy
  • Its racemate levobupivacaine causes less CNS depression / cardiotoxicity; another similar LA ropivacaine also has less cardiotoxicity
27
Q

What widely used LA drug is contraindicated in certain patients due to a possible RBC-related side effect?

Which patients + what side effect?

What common LA side effect does it not produce?

A

Prilocaine

  • contraindicated in obstetric analgesia due to risk for neonatal methemoglobinemia
  • does not produce the vasodilation common to many LAs
28
Q

Which LA drug is used almost exclusively in dentristy?

(Extra: what is its duration of action and why?)

A

Articaine

  • similar side fx to lidocaine
  • (a side chain ester group is broken down by esterases in tissue/blood quickly, giving it a 20-30 minute half-life)
29
Q

What are the 2 routes for metabolism of LAs?

Where do they occur?

Are the breakdown products active?

Depending on which one predominates for a given drug, half-life can be shorter or longer… which one has the longer half-life?

A
  • Amide-linked metabolism occurs by N-dealkylation in the liver and often makes active metabolites. Drugs that are mostly N-dealkylated have longer half-lives.
  • Ester-linked metabolism occurs by esterase-catalyzed hydrolysis in plasma + tissues; these drugs have shorter half-lives.
30
Q

What common LA side effect contributes to the development of other side effects + can decrease their desired effects?

How can this be overcome? And when should it not be?

A
  • Vasodilation caused by most LAs (via direct SM interaction and sympatholysis) can increase systemic absorption/toxicity of LAs and decrease local effects
  • Epinephrine or felypressin (short-acting vasopressin analog) can be used to counteract this, but is contraindicated in CV disease
  • Remember: prilocaine has no vasodilator effect
31
Q

CNS side effects of LAs can be broken into 1) early effects, 2) depression effects, and 3) excitation effects.

What are they and when do they occur?

(Long answer, but kind of logical)

A
  1. Early symptoms occur first: oral numbness, tinnitus, vertigo, tremor, facial/limb twitches, confusion
  2. Depression occurs at low plasma conc.: syncope/coma, respiratory depression, CV collapse
  3. Excitation occurs at high plasma conc.: anxiety, restlessness, vomiting, tonic-clonic convulsion
32
Q

What are the cardiovascular side effects of many LA drugs?

Which drug is an exception and how?

A
  • Negative chronotropy: bradycardia; may lead to ventricular fibrillation + cardiac arrest
  • Negative dromotropy: can cause AV block
  • Negative inotropy
  • Vasodilation > decreased BP
  • Eventually may cause CV collapse
  • Cocaine causes tachycardia, and vasoconstriction (increasing BP)
33
Q

How do local anesthetics interact with NMJ-blocking agents (skeletal muscle relaxers)?

Effects are dose-dependent. How?

(What other drugs have these same effects?)

A
  • Smaller doses - facilitate both depolarizing + non-depolarizing relaxant actions by prejunctional VGSC inhibition
  • Larger doses - have an aspecific nAChR blocking effect
  • (Class I anti-arrhythmics also have these effects, because they also inhibit sodium channels)

Pharmacology (Dustin, Ben) (17 decks)

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