Depolarizing NMB - SCh Flashcards

(33 cards)

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?

18
Q

3.96% heterozygous atypical - duration of SCh?

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

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
- anticholinesterase drugs used in insecticides - treatment of glaucoma - myasthenia gravis - chemo drugs like nitrogen mustard - metoclopramide
cause decrease in plasma cholinesterase activity
26
tacrine (cognex), donepezil (aricept), rivastigmine (exelon), galantamine (razadyne)
anticholinesterase drugs used to treat alzheimer's and some forms of dementia that increase ACh levels in the CNS that may prolong SCh
27
tachycardia muscle rigidity bradycardia prolonged relaxation hyperkalemia increased IOP fasciculations increased ICP myoglobinuria increased intragastric pressure MH histamine release sustained muscle contractions
complications of SCh
28
what patients should you not use SCh with?
damaged muscle membranes, guillain-barre, crush injury, MVA, burns
29
ED95 SCh
0.3 mg/kg
30
intubating dose SCh
1 mg/kg | 1.5 mg/kg with pretreatment
31
IM dose SCh
4-5 mg/kg
32
Onset SCh
45 to 90 seconds
33
Durations SCh
5-10 mins