Week 1 Neuroanatomy 2 of 4 Flashcards

1
Q

What is the spread of depolarization?

A

Opening of Na+ channels generates local current circuit that depolarizes adjacent membrane, opening more Na+ channels

Picture:

at rest

stimulated (depolarization)

spread of depolarization

spread of depolarization

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2
Q

Saltatory conduction: node to node jumping of depolarization

A
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3
Q

Un-ionizes form enter and ionized form blocks

A
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4
Q
A
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5
Q

Explain the action potential of local anesthetics.

A

Local anesthetics slow the rate of depolarization of the nerve action potential such that the threshold potential is not reached. As a result, an action potential cannot be propagated in the presence of local anesthetic and conduction blockade results.

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6
Q

Examples of Local Anesthetics.

A

A.Procaine, cocaine, lidocaine, bupivacaine

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7
Q

Mechanism of Action of local anesthetics.

A
  1. Local anesthetics are weak bases present in un-ionized form (LA) and ionized form (LAH+)
  2. Un-ionized form (LA) penetrates the cell membrane.
  3. The pH is slightly acidic inside the cells -> more ionized form (LAH+) produces.
  4. Ionized form (LAH+) blocks the Na+ channels (from inside)
  5. Inhibit conduction of pain impulses from periphery to CNS (afferent fibers)
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8
Q

When using local anesthetics how many nodes of Ranvier be blocked to stop nerve conduction?

A

A.For myelinated axon, 2-3 nodes of Ranvier must be blocked to stop the nerve conduction.

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9
Q

______ the frequency of action potential, the _____ the nerve is blocked by LA

A

D.Greater the frequency of action potential, the faster the nerve is blocked by LA

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10
Q

LA must attach to the ____________ when it is in the inactivated state

A

D.LA must attach to the sodium channel when it is in the inactivated state

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11
Q

____________ fibers are more sensitive to LA.

A

D.Small diameter fibers are more sensitive to LA.

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12
Q

_________ are relatively resistant to LA

A

D.C-fibers are relatively resistant to LA

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13
Q

What are LA normally used in?

A

D.Uses: minor surgical procedures, spinal anesthesia

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14
Q

Height of Sensory Versus Motor Block After Subarachnoid (spinal) injection of Local Anesthetic

A

A.Sympathetic block is 2-6 dermatomes higher than sensory block

B.Motor block is 2 dermatomes lower than sensory block

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15
Q

What pH are agents with lower pKa are more un-ionized?

A

A.Agents with lower pKa are more un-ionized at pH=7.4

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16
Q

A.Un-ionized form is lipid soluble and can easily penetrate axon cell membrane –> faster conduction block

A

Look at slide 28 on Regional ANesthesia Neuroanatomy (couldnot copy and paste table)

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17
Q

What blocks sodium channels which will inturn block nerve conduction?

A

A.LA blocks sodium channels –> block nerve conduction

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18
Q

More lipid solubility means what?

A

B.More lipid solubility –> more easier to cross cell membrane

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19
Q

When local anesthetics are highly protein bound they will have what kind of duration?

A

C.LA that are highly protein bound will have prolong duration of action

20
Q

What does pKa of a local anesthetic determine?

A

D.pKa of a LA determines the speed of onset

1.Lower pKa = faster onset

21
Q

In regards to potency of local anesthetics, the greater the oil: water coeffcient __________________

A

A.Greater the oil : water coefficient, the greater the lipid solubility

22
Q

The more lipid solubility of the LA; the greater its _______

A

B.The more lipid solubility of the LA; the greater its potency

23
Q

Potency depends on what 5 things?

A

C.Potency also depends on

  1. Fiber size
  2. Myelination
  3. pH (acidic pH antagonizes block)
  4. Frequency of nerve stimulation
  5. Electrolyte balance ( hypokalemia and hypercalcemia antagonize block)
24
Q

Potency of LA

A

look at slide 31 in Regional Anesthesia under Neuroanatomy (unable to paste chart)

25
Q

What is the duration of action determined by (two properties)?

A

A.Duration of action of a LA is determined by two properties

  1. The degree of protein binding
    a. Most important factor
    b. Mainly alpha-1 acid glycoprotein (AAG)
    c. Greater the protein binding, the longer the duration of action
    d. Protein bound LA acts as reservoir of LA; maintaining slow release

ProtLAH D Prot - + LAH+ D LA + H+

  1. Lipid solubility
    a. Greater the lipid solubility, longer the duration of action
    b. Lipids act as reservoir of LA; maintaining the nerve block
26
Q

Duration of Action of Local Anesthetics

Agents that are most ________ and have the greatest protein binding are ________

A

Agents that are most lipid soluble and have the greatest protein binding are longest acting

Look at slide 33 in NeuroAnatomy

27
Q

What 5 things determine blood concentration of LA?

A

A.Blood concentration of LA is determined by

  1. Presence or absence of a vasoconstrictor
    a. Epinephrine INCREASES duration of action of spinal anesthesia by 75-100% by alpha adrenergic action (vasoconstriction DECREASES the rate of absorption)
  2. Alpha-2 agonist INCREASES blocks
  3. Tissue Blood Flow
  4. .Concentration injected
    a. Greater the concentration of injected LA, longer the duration of action
  5. Number and frequency of injections
28
Q

What is the blood flow ranking?

REMEMBER:

In Time I Can Please Everyone But Susie & Sally.

A

Tissue blood flow

a. Higher the blood flow, faster the absorption and wash away from injection site –> decrease the duration of action
b. Blood flow ranking :
1) Intravenous
2) Tracheal
3) Intercostal
4) Caudal
5) Paracervical
6) Epidural
7) Brachial Plexus
8) Subarachnoid , Sciatic, Femoral
9) Subcutaneous

29
Q

Esters are LA that are metabolized by what?

A

A.Ester local anesthetics are metabolized by plasma pseudocholinesterase (or plasma cholinesterase)

  1. That’s why do not accumulate in blood
  2. Esters are derived from benzoic acid
30
Q

What are amides metabolized by?

A

A.Amides are metabolized by liver P-450 enzyme system

  1. Abnormal liver function –> toxicity
  2. Very little excretes by kidneys
31
Q

What can benzocaine cause?

A

A.Benzocaine can cause methemoglobinemia

32
Q

What is the agent of choice for obstetrics and why?

A

A.Chloroprocaine is agent of choice for obstetrics because it is rapidly metabolized. This prevents toxic effects to fetus. (Remember LA cross the placental barrier)

33
Q

________ is slowly metabolized, increases likelihood of toxicity

A

A.Tetracaine is slowly metabolized, increases likelihood of toxicity

34
Q

What is system toxicity determine by in local anesthetics?

A

A.Systemic toxicity is determined by the concentration of LA achieved in the blood

35
Q

Toxic manifestations of lidocaine (2-4 mg/ml is therapeutic concentration) are:

A

Plasma Conc. of Lidocaine

Toxic Manifestations for any Local Anesthetic

3 mg/ml Circumoral and tongue numbness

4 mg/ml Lightheadedness and tinnitus

6 mg/m Visual disturbance

8 mg/ml Muscular twitching

10 mg/ml Unconsciousness

12 mg/ml Convulsions

15 mg/ml Coma

20 mg/ml Respiratory arrest

26 mg/ml Cardiovascular collapse

36
Q

Esters how have many i’s while amides have how many i’s?

A

1.Esters have one ‘i’ (procaine, chloroprocaine) while amides have two ‘i’ (prilocaine, lidocaine, etidocaine)

37
Q

What patients may have a prolong duration of LA?

A

2.Patient with atypical pseudocholinesterase have prolong duration of action

38
Q

Chronic therapy with what prolongs the action of ester LA?

A

1.Chronic therapy with acetylcholinesterase inhibitors ( edrophonium, physostigmine, echothiophate) prolongs the action of ester LA

39
Q

___________ is a metabolic end-product of ester metabolism may cause hypersensitivity reaction

A

2.Para-aminobenzoic acid (PABA) is a metabolic end-product of ester metabolism may cause hypersensitivity reaction

40
Q

What depresses the activity of pseudocholinesterase by 80% ?

A

3.Dibucaine depresses the activity of pseudocholinesterase by 80% (Dibucaine number)

41
Q

_________ may cause methemoglobinemia.

A

Prilocaine may cause methemoglobinemia

42
Q

Toxic dose of lidocaine with epinehrine?

A

5.With epinephrine toxic dose of lidocaine is 6 mg/kg

43
Q

What is responsible for hypotension in LA?

A

6.Sympathetic blockade is responsible for hypotension

−Vasodilatation –> decrease preload –> hypotension

44
Q

If beta adrenergic effects are not required what med would you add?

A

7.Add phenylephrine instead of epinephrine if beta adrenergic affects are not required

45
Q
A