Depolarizing NMB - SCh Flashcards

1
Q

binds to the alpha subunit of the postsynaptic nicotinic receptor and mimics ACh and causes the muscle cell membrane to depolarize

A

depolarizing NMB

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2
Q

competes with ACh to bind with the alpha subunits to prevent the ion channel from opening and preventing the muscle cell membrane from depolarizing

A

nondepolarizing

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3
Q

two acetylcholine molecules linked by acetate methyl groups

A

SCh

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4
Q

what ACh receptors are affected by SCh

A
  • cholinergic receptors at NMJ
  • parasympathetic nervous system
  • sympathetic ganglions
  • muscarininc receptors in the SA node
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5
Q

Why use SCh?

A
  • rapid intubation

- desire for short duration of action

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6
Q

Causes depolarization – initial contractions (fasciculations) — then paralysis – diffuses away from NMJ — repolarizes for later use

A

Phase I SCh Block

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7
Q
  • Fasciculations
  • decreased single twitch
  • NO FADE W TETANUS/TOF/DOUBLE BURST
  • blockade enhanced by anticholinesterase
  • rapid recovery, short duration of action
A

Characteristics of Phase I SCh block

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8
Q
  • FADE OF TETANUS/TOF/DOUBLE BURST
  • posttetanic twitch
  • prolonged duration
  • reversible with anticholinesterase
A

Phase II SCh block

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9
Q

SCh: You give a small dose of edrophonium (.1-.2 mg/kg) and block becomes weaker. Should you give remainder of reversal dose? Is this indicative of a phase I or Phase II block

A

Give remainder, Phase II block

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10
Q

SCh: You give small dose of endrophonium (.1-.2 mg/kg), block becomes stronger. Should you give remainder of dose and is this indicative of phase I or phase II block?

A

Avoid additional dose and phase I block

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11
Q

What is SCh metabolized by

A

plasma choinesterase at 80 mg/min

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12
Q

what organ is responsible for SCh elimination

A

kidneys

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13
Q

where is pseudocholinesterase produced

A

liver

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14
Q

anticipated in patients with severe liver disease, pregnancy, malignancies, malnutrition, collagen vascular disease, and hypothyroidism

A

deficit of plasma cholinesterase

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15
Q

these patients can decrease plasma cholinesterase activity up to 40%, but at term there is no prolonged effect due to the increase volume of distribution of blood (high plasma volume)

A

pregnant patients

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16
Q

two genes dictate quality and quantity of plasma cholinesterase

A

atypical plasma cholinesterase

17
Q

96% homozygous for normal genes - SCh duration is?

A

5-10 mins

18
Q

3.96% heterozygous atypical - duration of SCh?

A

30 mins

19
Q

.04% homozygous for atypical genes- duration of SCh

A

3 hrs or more

20
Q

How can you test for issues with SCh metabolism

A

dibucaine

21
Q

Inhibits normal plasma cholinesterase activity by 80%

A

dibucaine number of 80

normal 5-10 min duration

22
Q

inhibits homozygous atypical activity by 20%

A

dibucaine number 20

duration 3 hrs or longer

23
Q

inhibits heterozygous atypical activity by 40 to 60%

A

dibucaine number 40-60

duration 30 mins

24
Q

causes a decrease in plasma cholinesterase activity

A

neostigmine and edrophonium (to a lesser degree)

25
Q
  • anticholinesterase drugs used in insecticides
  • treatment of glaucoma
  • myasthenia gravis
  • chemo drugs like nitrogen mustard
  • metoclopramide
A

cause decrease in plasma cholinesterase activity

26
Q

tacrine (cognex), donepezil (aricept), rivastigmine (exelon), galantamine (razadyne)

A

anticholinesterase drugs used to treat alzheimer’s and some forms of dementia that increase ACh levels in the CNS that may prolong SCh

27
Q

tachycardia muscle rigidity
bradycardia prolonged relaxation
hyperkalemia increased IOP
fasciculations increased ICP
myoglobinuria increased intragastric pressure
MH histamine release
sustained muscle contractions

A

complications of SCh

28
Q

what patients should you not use SCh with?

A

damaged muscle membranes, guillain-barre, crush injury, MVA, burns

29
Q

ED95 SCh

A

0.3 mg/kg

30
Q

intubating dose SCh

A

1 mg/kg

1.5 mg/kg with pretreatment

31
Q

IM dose SCh

A

4-5 mg/kg

32
Q

Onset SCh

A

45 to 90 seconds

33
Q

Durations SCh

A

5-10 mins