Hadzics Chapter 2 Flashcards

(41 cards)

1
Q

What is the resting potential range in neurons?

A

–60 to –70 mV

Set by the Na⁺/K⁺ ATPase pump.

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2
Q

What determines the resting potential in neurons?

A

High intracellular K⁺, low intracellular Na⁺

The membrane is more permeable to K⁺, leading to a negative interior.

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3
Q

List the steps of action potential.

A
  • Stimulus → threshold reached
  • Depolarization: Na⁺ influx
  • Repolarization: K⁺ efflux
  • Refractory period: Na⁺ channels reset
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4
Q

What is saltatory conduction?

A

Myelin speeds conduction allowing impulses to ‘jump’ at Nodes of Ranvier

These nodes have high Na⁺ channel density.

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5
Q

How do local anesthetics (LAs) affect nerve conduction?

A

Block Na⁺ entry → stop depolarization → nerve conduction halts

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6
Q

Where do local anesthetics bind?

A

Inside the sodium channel (α-subunit)

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7
Q

What is the process for local anesthetics to bind to the sodium channel?

A

Unionized form crosses lipid membrane → converts to ionized form in axoplasm → binds channel

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8
Q

What is meant by ‘use-dependent block’ in local anesthetics?

A

LAs preferentially bind open and inactivated states during repeated firing

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9
Q

Which nerves are less sensitive to local anesthetics?

A

Resting nerves are less sensitive than active/repeatedly stimulated nerves

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10
Q

What are the three essential components of local anesthetics?

A
  • Aromatic ring (lipophilic)
  • Intermediate chain (ester or amide)
  • Amine group (hydrophilic)
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11
Q

What does the pKa of local anesthetics affect?

A

Proportion of ionized vs unionized forms

Most LAs have a pKa of 7.6–9.0.

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12
Q

How does infection affect local anesthetic efficacy?

A

More ionized drug in acidic tissue → poor block

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13
Q

What is the relationship between lipid solubility and local anesthetics?

A

Lipid solubility = potency and toxicity risk

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14
Q

What determines the duration of action of local anesthetics?

A

Protein binding

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15
Q

What factors influence the onset of local anesthetics?

A

Lower pKa → faster onset

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16
Q

Which local anesthetic has a faster onset, lidocaine or bupivacaine?

A

Lidocaine (pKa 7.8) is faster than bupivacaine (pKa 8.1)

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17
Q

What is the order of nerve fiber sensitivity to local anesthetics?

A
  • Pain (Aδ, C fibers)
  • Temperature
  • Touch & pressure
  • Motor (Aα fibers)
18
Q

Which function typically disappears first when using local anesthetics?

A

Pain disappears first, motor function lasts

19
Q

What is the typical order of recovery from local anesthetic block?

A
  • Motor function (Aα)
  • Proprioception & pressure (Aβ)
  • Touch (Aβ)
  • Temperature (Aδ)
  • Pain (C fibers, Aδ)
20
Q

True or False: Patients regain motor function before feeling temperature or pain after local anesthesia.

21
Q

What are the two main types of local anesthetics?

A

Esters and Amides

Esters have one ‘i’ in the name, while Amides have two.

22
Q

What is the metabolism process for Esters?

A

Plasma cholinesterase metabolism

Esters have a higher allergy risk due to the PABA byproduct.

23
Q

What is the main characteristic of Chloroprocaine?

A

Rapid onset, short duration, very low toxicity

Good for short cases.

24
Q

What is Procaine known for?

A

First synthetic LA, slow onset, short duration, vasodilator

Rarely used now.

25
What are the properties of Tetracaine?
Potent, long-acting, high toxicity risk ## Footnote Commonly used in spinal anesthesia.
26
What is unique about Cocaine as a local anesthetic?
Inhibits catecholamine reuptake → vasoconstriction, abuse potential, ENT use ## Footnote It is the only local anesthetic with these properties.
27
What is the metabolism process for Amides?
Hepatic metabolism ## Footnote Amides have a rare allergy risk.
28
What is Lidocaine known as?
Gold standard local anesthetic ## Footnote It has intermediate duration and versatility in use.
29
How does Mepivacaine compare to Lidocaine?
Similar to lidocaine, less vasodilation, slightly longer duration ## Footnote Both are commonly used local anesthetics.
30
What potential side effect is associated with Prilocaine?
Can cause methemoglobinemia ## Footnote This is due to its metabolite o-toluidine.
31
What is notable about Bupivacaine?
Very potent, long duration, highly cardiotoxic ## Footnote It is advised to avoid large doses.
32
What is Levobupivacaine?
S-enantiomer of Bupivacaine, less cardiotoxic ## Footnote Considered a safer alternative.
33
What are the characteristics of Ropivacaine?
Long-acting, less lipid soluble than bupivacaine → less motor block, less cardiotoxic ## Footnote This makes it a preferred option in certain situations.
34
What is the effect of adding Epinephrine to local anesthetics?
Epinephrine causes vasoconstriction, which decreases absorption, prolongs duration, and lowers toxicity risk. ## Footnote It also serves as a marker for intravascular injection (↑HR, BP).
35
What is the role of Opioids in neuraxial anesthesia?
Opioids provide synergistic analgesia when added to local anesthetics (e.g., morphine, fentanyl).
36
What is Clonidine and its effects when added to local anesthetics?
Clonidine is an α2 agonist that prolongs the block and may cause some hypotension and bradycardia.
37
What is Dexmedetomidine and its effects when added to local anesthetics?
Dexmedetomidine is a more potent α2 agonist that extends the block by approximately 4 hours and can cause sedation and bradycardia.
38
What is Dexamethasone's role in local anesthesia?
Dexamethasone is a corticosteroid that prolongs the block, especially perineural, with a low risk of side effects.
39
What are the early signs of CNS toxicity from local anesthetics?
Early signs include circumoral numbness, tinnitus, metallic taste, and seizures.
40
What are the signs of CV toxicity from local anesthetics?
CV toxicity can manifest as hypotension, arrhythmias, and cardiac arrest, with the worst effects seen with bupivacaine.
41
What is the treatment for severe Local Anesthetic Systemic Toxicity (LAST)?
The treatment for severe LAST is lipid emulsion therapy, also known as 'lipid rescue.'