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Neurology 1- M2 > 08 29 2014 Local Anesthetics > Flashcards

08 29 2014 Local Anesthetics Flashcards

1
Q

Esters

A 
Cocaine
Tetracaine
Benzocaine
Procaine
Chlorprocaine
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2
Q

Amides

A 
Lidocaine
Mepivacaine
Priolocaine
Bupivacaine
Bupivacaine SR
Proivacaine
EMLA
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3
Q

Local anesthetic

A

drug that reversibly blocks impulse conduction – blocks voltage gated sodium channels

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4
Q

what are characteristics of a perfect local anesthetic?

A
  • non-irritating
  • transient effect
  • low systemic toxicity
  • quick onset
  • action to span duration of surgery

(lidocaine is close to perfect right now)

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5
Q

Structure Activity Relationship

A
  • aromatic ring (lipophilic group)
  • Intermediate chaine
    • ester: -COO-CH2-CH2-N
    • aminde: - NH-CO-CH2-N
  • ionizable group (usually a 3 degree amine)
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6
Q

pH/pKA for local anesthetic

A

-weak bases
log (BH+)/(B)= pka-pH

  • more acidic the pH = increase in BH+
  • more basic pH = more B

Neural form required to diffuse to side of activation, but charged form is required for activity.

NOTE: infection decreases pH (more acidic)
-can’t inject local anesthetic into an inflamed area.

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7
Q

Path of Anesthetic to receptor sites

A

LA + H+ = LAH+

  1. extracellular – slightly basic
    - LA travels through bilayer– and contacts sodium channel and blocks it.
  2. Intracellular – slightly more acidic
    - once LA enters the cell, there is a shift in charge = LAH+
    - trapped here
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8
Q

Mechanism of Action of Local anesthestics

A

Modulated Receptor Hypothesis: LA binding changes conformational state of the channel.

Affinity for activated and inactivated states vs. resting state.

  • fibers that fire at a faster rate are more susceptible to the effects of local anesthetics
    1. neutral form enters membrane, binding site is on the cytoplasmic face of channel.
    2. Charged LA required for binding to channel site.
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9
Q

Frequency dependent block

A

repeated depolarizatioins produce more effective anesthetic binding— after rate are more susceptible to effects of local anesthetics

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10
Q

Important properties of local anesthestics

A
  1. highly lipophilic
    - helps LA diffuse and stay in fatty membrane
    - helps with potency and duration
    - slower onset of action
  2. High pkA = slows onset of action – more ionized at same pH vs. another anestethic.
  3. High Protein Binding = duration (not metabolized/excreted quickly)
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11
Q

Epidural

A

Neuraxial Block

–just short of the Dura

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12
Q

Spinal block

A

Neuraxial block

- enter subarachnoid space

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13
Q

Caudal block

A

Neuraxial block

-epidural space in caudal canal

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14
Q

Clinical uses

A
  1. Topical
  2. Infiltrate (local – numb a specific area on surface)
  3. Regional Anesthesias and Analgesia
    A. - Peripheral blocks
    -plexus anesthesis – single injection or continuous infusion.
    • Individual nerve block (ex femoral)
    • IV regional (Bier Block)– Turnicate and hurts A LOT!!!
      B. -Neuraxial Blocks
      -spinal (low volume), epidural/caudal (high volume)
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15
Q

Incremental increase in the concentration of LA administered during a Neuraxial Block can cause a loss of what nerves and in which order:

A
  1. Autonomic Pain – C-fibers
  2. Sensory
  3. Motor
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16
Q

Effect of a Peripheral block (what goes first? and what follows).

A

motor block occurs before proximal sensory loss (which occurs before distal sensory loss).

Last thing ppl lose is sensation in fingers

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17
Q

Why do they use vasoconstrictors with local anesthetic?

A

-decreases absorption irrespective of the site of injection
-increases tissue binding for duration of action of long acting drugs
(increase time that locals are at site of action)

BEWARE OF HITTING A VESSEL WITH epinephrine/ Phenylephrine.
- use a low does to test if epinephrine is injected intravascularly – in 2 min the heart starts beating like crazy!

18
Q

Elimination of Esters?

A

plasma pseudocholinesterase

Metabolite produced: PABA and derivatives

  • PABA is allergenic
  • Enzyme deficiency may lead to potentiation of action
19
Q

Elimination of Amides

A

Liver CYP450, water soluble metabolites – urinary excretion.

-low blood flow to liver (portal hypertension, CHF) decrease delivery of LA’s to liver– decreasing amide LA metabolism and increasing halftime and serum concentration.

20
Q

Adverse Effects?

A
  1. Systemic toxicity
  2. Local (neural tissue) toxicity
  3. Allergic reactions
  4. Methemoglobin formation
21
Q

How does systemic toxicity occurs when using LAs?

A

LA acting on other excitatory tissue vs. target nerves.

Range of effects is proportional to LA concentration.

Manifest first as CNS toxicity and then cardiotoxicity

22
Q

Presentation of CNS toxicity from LAs?

A

tinnitus, perioral numbness, blurred vision, metallic taste, change in mental status, convulsions.

23
Q

Presentationm of Cardiotoxicity from LAs?

And drugs that are cardiotoxic?

A

Depression of excitability and conduction (prolonged QRS)

Arteriolar dilation (Ca channel effect)

Systemic acidosis –> increases sensitivity to LA toxicity (remember pH/pka formula)

Pregnancy increases sensitivity to toxic effects

DRUGS that are cardiotoxic:

Bupivacaine ( amide) is very cardiotoxic (R+)

Ropivacaine less toxic (L+)

24
Q

How can you try to rescue system from cardiotoxicity form an LA?

A

IV Lipid Emulsion
- propofol
VERY LIPOPHILIC – takes LA away with it.

25
Q

What happens during local (neural tissue) toxicity from using LAs?

A
  1. Neural injury:
    High concentrations for extended period of time can lead to nervous tissue destruction – membrane damage, cytoskeleton disruption

Motor and sensory loss are seen (Ex. caudal equine syndrome)

Paralysis and paresis may result

  1. Transient Neurologic Symptoms (TNS)
    associated with spinally administered Lidocaine and certain surgical positions (lithotomy).

associated with pain or sensory abnormalities in the lower back, buttock, or lower extremities. The symptoms of burning pain and dysethesthia in the L5 and S1 dermatomes usually start after the effects of spinal anesthesia have concluded and may last up to hours to four days

NOT ASSOCIATED WITH MOTOR OR SENSORY LOSS

A self-limited neuropathic pain syndrome

26
Q

Why does Methemoglobinemia occur?

  • Drugs that can cause it?
  • Plus-oximeter reading?
  • Treatment?
A

-Prilocaine metabolites: O-toluidine act as an oxidizing agent to convert Hb 2+ –> Hb 3+

Benzocain can do this too

Causes chocolate colored blood.
Plus oximeter = 85% saturation

Treatment: methylene blue (reducing agent)

27
Q

Allergic reactions with Esters

A

PABA –> Hapten Formation –> True IG3 Mediated Allergy

28
Q

Allergic reactions with Amides

A

Allergic reactions are rare.

29
Q

Methylparaben

A

preservative that can cause allergic reactions regardless of LA type

30
Q

Cocaine (quick facts)

A

stimulant, vasoconstrictor

31
Q

Benzocaine

A

primarily topical, MetHb potential

32
Q

Tetracaine

A

long duration
potent ester –> spinal anesthesia
toxic at relatively low doses (except for short acting ester rule)

33
Q

Procaine

A 
aka Novocaine
quick onset
short duration
hypersensitivity rxns
TNS implication (rarely used)
34
Q

Chlorprocaine

A

quick onset
short duration LA
-used to have a bad rep

35
Q

Lidocaine

A

quick onset, moderate duration and toxicity, TNS explication

DONT USE ON SPINE!

36
Q

Mepivacaine

A
  • longer duration than lidocaine
  • lowest pKa of injectable La’s
  • Acts as a vasoconstrictor
37
Q

Prilocaine

A
  • Associated with methemoglobinemia

- component of EMLA

38
Q

Bupivacaine

A

long duration La with devastating potential for cardiac toxicity

Sensory block > motor block

39
Q

Bupivacaine SR

A

liposomally encapsulated for delivery up to 72hrs/dose.

Use mostly for spinals because you only need to inject a few ccs.

40
Q

Ropivacaine

A
  • long duration with properties similar to bupivacaine but with less cardiotoxicity
  • vasoconstriction.
41
Q

EMLA

A

Eutectic (melting point of compound is less than mp of other ingredients) Mixture of LA prilocaine/ lidocaine for topical anesthesia.

Neurology 1- M2 (22 decks)

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