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PDA Block 3 > Local Anesthetics > Flashcards

Local Anesthetics Flashcards

1
Q

local anesthetics

A
  • bind reversibly to a site within a pore of voltage gated Na channels; blocking sodium entry when the channel is open
  • because of the role of these channels in action potential initiation and generation, local anesthetics reversibly block nerve conduction
  • cause sensory loss and motor paralysis of the innervated area
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2
Q

topical anesthesia

A
  • applied to skin, mucous membranes, or ulcerated surfaces

- opthalmic- to produce anesthesia of the cornea and conjunctiva

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3
Q

local infiltration anesthesia

A
  • local injection of an agent without consideration of the course of cutaneous nerves
  • provides regional anesthesia around the sites of injection
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4
Q

nerve block anesthesia

A

-injection of a local anesthetic around the individual nerves or nerve plexi that include sensory nerves from the operative site

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5
Q

spinal and epidural anesthesia

A

-inserting it into the epidural space or into the CSF

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6
Q

mechanism of action of the local anesthetics

A
  • act directly on nerve cells to block their ability to conduct impulses
  • act on every type of nerve fiber
  • block AP initiation and propagation on nociceptive neurons to eliminate pain sensation
  • completely reversible, no nerve damage
  • binding site is on the intracellular side of the voltage dependent channel protein
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7
Q

describe the binding of the local anesthetics to the channels

A
  • binding site is on the intracellular side of the voltage dependent sodium channel protein
  • all are weak bases
  • bind in the BH+ form, but must be unionized (B) to cross the nerve memebrane
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8
Q

inhibition of voltage gated sodium channels results in:

A
  • slowed rate of depolarization
  • reduced height of action potential (AP)
  • reduced rise of action potential
  • slowed axonal conduction
  • prevents propagation of the AP
  • increases threshold potential
  • no change in resting membrane potential (Na channels are not involved)
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9
Q

local anesthetics are frequency and voltage gated

A
  • drugs gain access to the channel binding site more easily when the channel is open ( BH+ can slip in)
  • have higher affinity for the inactive channel than the unopened channel (remember unopened then activated then inactive)
  • therefore:
  • resting nerves are less sensitive to local anesthetic block
  • nerves with positive membrane potential are more sensitive to blcok
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10
Q

efficacy is decreased or influenced y pH explain

A

-efficaicy decreased when tissue pH is deacreased such as during inflammation. too little drug can get to site of action (too little is in form B)

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11
Q

pKa of lidocaine and what percentage of the drug is unchanged at pH is 6.8 and what percent is uncharged at pH is 24

A

lidocaine pKa is 7.9

so 7.4% is uncharged at pH 6.8 and 24% is charged at pH 7.4

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12
Q

pKa of Bupivacaine and what percentage of the drug is unchanged at pH is 6.8 and what percent is uncharged at pH is 24

A

bupivacaine pKa is 8.1

so 4.8% is uncharged at pH 6.8 and 16.6% is uncharged at pH 7.4

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13
Q

pKa of Chloroprocaine and what percentage of the drug is unchanged at pH is 6.8 and what percent is uncharged at pH is 24

A

pKa of chloroprocaine is 9.1

so 0.55 IS CHARGED AT PH=6.8 AND 2.0% IS CHARGED AT pH 7.4

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14
Q

what i the effect o administering . local anesthetic with a vasoconstrictor

A

-decreases rate of absorption into the circulation
*increases depth and duration of anesthesia
8less potential for systemic toxicity; so th maximal dose that can be give is higher
-epinephrine an phenyleprhine are use for this purpose

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15
Q

explain the order of neurons blocked

A

Autonomic fibers, small non-myelinated C fibers (mediating pain sensation), and small myelinated Aδ fibers (mediating pain and temperature sensation) are blocked before larger myelinated Aδ, Aβ, and Aα fibers (mediating postural, touch, pressure sensations and motor information)

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16
Q

order of block of nerve conduction

A
  1. pain
  2. cold
  3. warm
  4. touch
  5. deep pressure
  6. motor

so recovery occurs in the reverse order

17
Q

toxicity and adverse effects of local anesthetics

A
  • interfere with the function of all organs in which conduction or transmission of impulse occurs (CNS, ganglia, NMJ, muscle)
  • systemic toxicity reactions are related to high concentration of the local anesthetic in the circulation
  • intraneuronal injection can produce irreversible damage

-S-enantiomer is less toxic than the R_enentiomer in local anesthetics with chiral centers

18
Q

Describe the CNS toxicity of local anesthetics

A
  • CNS stimulation is seen first, sue to depression of cortical inhibitory neurons restlessness, tremors, convulsion
  • CNS depression at higher doses, drowsiness, general depression, respiratory depression and potentially respiratory arrest
  • death associated with sever toxicity usually caused by respiratory depression
19
Q

cardiovascular toxicity of local anesthetics

A
  • general depression of the CV system usually seen after CNS effects develop
  • decrease myocardial contractility leads to decreased BP
  • decreased rate of conductance leads to decreased HR and AV block and arrhythmiaa
  • arteriolar vasodilation

-can develop hypotension and arrhytmias leading to cardiac arrest

20
Q

where are local anesthetic amides metabolized

A

liver

21
Q

where are local anesthetic esters metabolized

A

plasma cholinesterases

22
Q

hypersensitivity to local anesthetics

A
  • rare individuals exhibit hypersensitivity (allergic dermatitis or anaphylactic type reaction)
  • must distinguish from effects of co-administered vasoconstrictors
  • more frequent with ester local anesthetics
  • sometimes associted with preservatives
23
Q

metabolism of local anesthetics

A
  • toxicity depends on the balance between the rate of absorption into the systemic circulation and elimination
  • ester local anesthetic inactivated by plasma esterases
  • amide local anesthetics metabolized in the liver
  • used with caution in patients with sever liver disease
24
Q

Cocaine (ester)

A
  • local anesthetic, but also blocks uptake of NE into presynaptic adnrenergic nerves
  • potent vasoconstrictor
  • used for topicl anesthesia of the upper respiratory tract
25
Q

Procaine (ester)

A
  • short acting; first synthetic local anesthetic
  • supplanted by newer agents but still used for infiltration anesthesia
  • low potency, slow onset, short duration of action
26
Q

Tetracaine (ester)

A
  • long acting ester local anesthetic
  • more potent and longer duration of action than procaine
  • widely used in spinal analgesia and in topical and ophthalmic preparations; not for peripheral nerve block
27
Q

Benzocaine (ester)

A
  • anesthetic with low water solubility, therefore too slowly absorbed when applied topically to be toxic
  • applied to wounds and ulcerated surfaces where it provides relief for long periods of time
28
Q

Lidocaine (amide)

A
  • intermediate duration of action
  • produces faster, more intense, longer lasting, and more extensive anesthesia compared to procaine
  • often used with vasoconstrictors to decrease toxicity
  • wide range of clinical uses
29
Q

Bupivicaine (amide)

A
  • long acting amide local anesthetic
  • capable of producing prolonged anesthesia
  • provides more sensory than motor block
  • more cardiotoxic than equi-effective doses of lidocaine
  • S-enantiomer is available (levobupivacaine) that is less toxic
30
Q

Ropivacaine

A
  • long acting amide local anesthetic consisting of the S-enantiomer
  • anesthetic actions similar to bupivicaine with less cardiotoxicity
  • suitable for epidural and regional anesthesia
  • even more motor-sparing than bupivacaine
31
Q

following a deposition of drug in the tissue near a nerve…..

A

-local anesthetics inhibit pain sensation by blocking voltage dependent sodium channels

32
Q

in general how do vasoconstrictors help local anesthetics

A

they increase duration of action and decrease toxicity

PDA Block 3 (16 decks)

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