Succinylcholine Flashcards

1
Q

Plasma cholinesterase abnormalities seen with

A

Profound liver disease (decreased production)

Drug induced

Genetically atypical

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2
Q

Cardiac dysrhythmia with succ due to succ action at _____________________

A

Cardiac muscarinic cholinergic receptors where succ mimics Ach

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3
Q

Succ and MH

First sign

Last sign

A

Increase in ETCO2

Hyperyrexia

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4
Q

____________ gives succ small Vd

A

Poor lipid solubility

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5
Q

NMJ has 3 types of _____________ receptors. Breakdown

A

Cholinergic nicotinic receptors

2 post synaptic on skeletal muscle
1 presynaptic on nerve endings

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6
Q

Why fast twitch muscles equilibrate first

A

More Ach receptor sites

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7
Q

Succ and cardiac rhythm- causes

A

Stimulates autonomic ganglia and muscarinic receptors causing change in cardiac rhythm (bradycardia) including cardiac arrest

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8
Q

Obesity and succ

A

Have greater plasma cholinesterase activity so require larger dose

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9
Q

______ of succ excreted unchanged in urine

A

10%

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10
Q

Risk of hyperkalemia in 4 contraindicated pt peaks

A

7-10 days after injury

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11
Q

How to somewhat prevent occurrence of cardiac dysrhythmia with succ

A

Pretreat with non depolarizer

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12
Q

Single twitch response give what type of data

A

Post junctional

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13
Q

4 factors influencing development of phase 2 block

A

Duration of drug exposure

Drug exposure

Muscle type (fast or slow)

Interaction with anesthetics

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14
Q

NTS at NMJ for muscle contraction

A

Acetylcholine

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15
Q

IV succ in children may result in deadly arrhythmias due to

A

Undiagnosed underlying myopathy

Rhabo and hyperkalemia

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16
Q

Only with ___________ is plasma cholinesterase production too low to prolong succ

A

Severe liver disease

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17
Q

Succinylmonocholine broken down into

A

Succinic acid and choline

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18
Q

Succ pharmacokinetics (3)

A

Highly ionized

Water soluble at body pH

Poorly lipid soluble

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19
Q

Dose required to block at diaphragm

A

2 times required to block adductor pollis and orbicularis oculi

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20
Q

Succ pharmacological effect

A

Interrupt nerve impulse transmission at NMJ by mimicking Ach at NMJ

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21
Q

Succ effect on IOP

Onset

Duration

Causes

A

Maximally increases 2-4 minutes

Lasts 5-10 minutes

Contraction of extraocular muscles and increased resistance to aqueous humor flow

INCREASES IOP

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22
Q

Anticholinesterase typically used to reverse succ

Why

A

Endrophonium

Shortest duration of action

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23
Q

Avoid succ in ESRD bc

A

Risk of hyperkalemia

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24
Q

Basis of NM transmission

A

Flow of ions

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25
Q

Succ MOA

A

Combines with cholinergic receptors of motor end plates causing depolarization then inhibits subsequent NM transmission

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26
Q

If pretreat with non depolarizer then give succ will get

A

More profound response to succ

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27
Q

Sites of action for succ

A

2 alpha subunits of nicotinic receptors

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28
Q

Muscle to monitor for diaphragm

A

Adductor pollicis

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29
Q

Fasiculations are caused by

A

Succ initially causes depolarization of skeletal muscle fibers

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30
Q

Due to hyperkalemia risk Succ is contraindicated in what 4 pt populations

A

Major burns
Multiple traumas
Extensive denervation of muscle
Upper motor neuron injury

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31
Q

Dibucaine # 40-60

A

Prolonged succ block up to 30 minutes

Heterozygous for atypical plasma cholinesterase

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32
Q

Depolarizing block is a ______ block

A

Phase 1

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33
Q

CV effects of succ enhanced by

A

Halogenated anesthetics

34
Q

If give neostigmine to reverse pt with phase 1 block

A

It will worsen block to phase 2 bc less plasma cholinesterase

35
Q

Initial sign of phase 2 block

A

Tachyphylaxix

36
Q

Plasma cholinesterase low activity due to

A
Neostigmine
Insecticides
Glaucoma 
Myasthenia Gravis drugs
Chemo
37
Q

In these 2 circumstances succ can induce serious cardiac arrhythmias due to hyperkalemia

A

Electrolyte abnormalities

Dig toxicity

38
Q

Muscle damage with fasiculations causes

A

Hyperkalemia and muscle pains

39
Q

Succ __________ cross lipid membranes like (4)

A

DOES NOT

  • BBB
  • renal tubulular epithelium
  • GI
  • placenta
40
Q

TOF with succ

A

Each twitch decreased equally in size

NO FADE

41
Q

Succ short duration of action is due to __________ made in _______

A

Hydrolysis by plasma cholinesterases

Liver

42
Q

Changes in rhythm with succ result from

A

Vagal stimulation or hyperkalemia

43
Q

Succ effect on myocardium

A

No direct effect

44
Q

Myoglobinuria with succ seen with

A

MH

Rhabdo

Stains

Muscle disease

45
Q

Myasthenia gravis patients and succ

A

More resistant to succ to due lower number of fx Ach receptors

Have to give more

46
Q

Succ metabolism

Compared to Ach

A

Hydrolysis by psudocholinesterases

Slower than Ach

47
Q

Succ and GI

A

Causes inconsistent increase in intragastric pressure r/t fasiculations

Increases risk of aspiration of gastric contents

48
Q

Cause of increased serum K+ levels with succ

A

Sustained receptor ion channel opening causes K+ leakage out of cell

49
Q

TOF to check fast twitch

A

Orbicularis oculi

Laryngeal

50
Q

Adverse reactions of succ are due to

A

Ability to work on numerous sites of action bc similar to Ach which binds to several receptors

51
Q

Plasma cholinesterase affects succ duration of action by

A

Controlling amounts hydrolysis before reaching NMJ

52
Q

If use anticholinergic drug to reverse phase 2 block should be accompanied by

A

Anticholinergic drug

53
Q

Treatment for hyperkalemia

A

IV Calcium
Bicarbonate
IV insulin
Hyperventilation

54
Q

Succ dose for laryngospasm

A

0.1 mg/kg

55
Q

Pretreatment with non-depolarizer may prevent (4)

But not

A
  • dysrhythmia (bradycardia)
  • myalgia
  • increased intragastric pressure
  • increased IOP

DOES NOT PREVENT HYPERKALEMIA

56
Q

Huge plasma cholinesterase capacity causes

A

Most succ hydrolyzed before reaching NMJ

57
Q

TOF check for slow twitch muscles

A

Adductor polices

58
Q

Dibucaine # is indicator of

A

Quality of plasma cholinesterase not quantity

59
Q

__________ muscles equilibrate more rapidly with plasma succ

A

Fast twitch muscles- laryngeal muscles

Orbicularis oculi

60
Q

Succ. IV

Dose

Onset

Duration

A

1-1.5mg/kg

30-60 seconds

3-5 minutes

61
Q

Diagnosis of phase 2 block

A

Peripheral nerve stimulator

62
Q

Phase 2 block resembles

Implication

A

Non-depolarizer block

Why should ensure recovery from succ before giving non-depolarizer

63
Q

Initial metabolite of succ

A

Succinylmonocholine

Very weak NM activity

64
Q

Ach binding with NMJ post junctional receptors causes

A

Opening of K+ receptors allowing ion flow

65
Q

Succ causes increase of serum K+ by

A

0.5 mEq/L

66
Q

When Ach released it binds to ____________ receptors on post synaptic membranes

A

Nicotinic cholinergic

67
Q

Dibucaine # 20

A

20% inhibition of plasma cholinesterase activity

Single dose of succ can last longer

Homozygous for atypical plasma cholinesterase variant

68
Q

Succ IM

Dose

Onset

A

3-4 mg/kg

1-2 minutes

69
Q

Dibucaine # of 80 means

A

80% inhibition of plasma cholinesterase activity

Normal

70
Q

Tx for phase 2 block

A

Propofol gtt and leave on the vent until worn off

71
Q

Plasma cholinesterase abnormalities cause

A

Slow to absent hydrolysis and prolongation of NMB

72
Q

Pretreatment dose of non-depolarizer

A

1/10 intubating dose

73
Q

Succ and open globe injuries

A

AVOID

74
Q

Thought to be a cause of fasiculations with succ

A

Binding of succ to both alpha subunits on nicotinic cholinergic post synaptic receptors simultaneously

75
Q

Cause of prolonged paralysis with succ

A

Plasma cholinesterase levels or atypical cholinesterases

76
Q

Succ and preganancy

A

Plasma cholinesterase levels are decreased in pregnancy and several days postpartum

More sensitive to succ

77
Q

Last muscles paralyzed with succ

First to recover

A

Intercostals and diaphragm last paralyzed and first to recover

78
Q

Incidence of succ induced myalgia

A

About 50%

79
Q

Ending of succ NMJ blockade due to

A

Diffusion away from NMJ bc low plasma cholinesterase level at NMJ

80
Q

THE NM jx NTS

A

Acetylcholine