Muscle Blockers Flashcards

1
Q

why don’t muscle blockers effect the brain or CNS?

A

polar compounds can’t go thru BBB so must give IV

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2
Q

how long do short acting non depolarizing neuromuscular blockers work? long acting? what is the only long acting neuromuscular blocker?

A

short: 30-60 minutes
long: 60-120 minutes

only long acting: pancuronium

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3
Q

increasing the length of use of non depolarizing muscle blocker does what to duration of action?

A

prolongs it

remember for ICU

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4
Q

how to reverse effects of non depolarizing agent?

A

acetylcolinesterase inhibitors to increase ACh concentration

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5
Q

what mm is last affected by non depolarizing blockers?

A

diaphragm

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6
Q

DOA of succinylcholine?

A

5-10 minutes

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7
Q

MOA of succinylcholine

A

binds & activates the nicotinic receptor once causing one transmission of an impulse to the muscle.

Doesn’t transmit anymore and doesn’t leave the receptor either.

It sits there blocking the channel

Normal closure of the gate is prevented and the blocker moves in and out rapidly

Muscle stays in depolarized state, unable to repolarize while succinylcholine sits there.

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8
Q

how long do fasciculations last after dosing succinylcholine? how long until paralysis?

A

30 seconds of fasciculations

90 seconds until paralysis

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9
Q

CVS affects of nondepolarzing blockers?

A

hypotension (prevent with antihistamines)

tachycardia

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10
Q

CVS affects of depolarizing blockers?

A

arrhythmia when given with other anesthetics

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11
Q

what drug causes hyperkalemia? who does it happen to?

A

succinylcholine if given to pt with burns, nerve damage, neuromuscular disease, or trauma

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12
Q

what drug causes most mm pain after paralysis?

A

succinylcholine

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13
Q

succinylcholine + volatile anesthetics =

A

malignant hyperthermia from abnormal release of Ca from stores in skeletal mm

treatment: dantrolene

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14
Q

muscular blockers + aminoglycosides (Abx) =

A

increased blockade

Abx decrease the release of ACh and can lead to respiratory depression

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15
Q

increased age + NM blockers =

A

increased effect (decrease dose if older than 70)

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16
Q

NM+ myasthenia gravis =

A

increased effect

17
Q

NM + severe burn or UMNL =

A

decreased effect

18
Q

benefits of NM blockers in ventilation

A

increases O2

decreases atelectasis

19
Q

NM blocker + intubation =

A

upper airway muscle relaxation

safer to put tube down first

20
Q

cause of muscle spasticity?

A

increased tonic stretch of reflex (DTR) or flexor mm spasm (increased tone)

often get with mm weakness

caused by spinal injury
CP
MS
stroke

21
Q

MOA of spasmolytics

A

change stretch reflex arc (DTR) or act on mm directly (dantrolene)

decrease pain but don’t fix dysfunction

22
Q

Diazepam MOA

A

increases GABA which hyper polarizes cell (decreases excitability of mm)

23
Q

use of diazepam?

A

any spasticity (spinal cord transection, CNS origin) q

24
Q

SE of diazepam as spasmolytic?

A

CNS sedation

25
Q

Baclofen MOA?

A

agonizes GABA (decreases excitatory NT in brain and substance P in spinal cord)

26
Q

clinical use of baclofen?

A

given PO (intrathecal if severe)

as effective as diazepam w/o sedation

no effect on mm strength like dantrolene

addiction or spasms

27
Q

SE of baclofen?

A

drowsiness (tolerance occurs)

anticholinergic effects

increased seizure potential when drug is stopped (if epileptic)
- withdraw dose slowly

28
Q

MOA of tizanidine?

A

CNS alpha 2 adrenergic agonist (like clonidine)

29
Q

use of tizanidine?

A

spasticity from cerebral or spinal injury (equally effective to the others)

30
Q

SE of tizanidine?

A

drowsiness
hypotension
dry mouth
asthenia (perceived loss of strength)

31
Q

MOA of dantrolene?

A

works in mm fibers
prevents release of calcium in skeletal mm (prevents contraction)

little effect on cardiac/smooth mm

32
Q

clinical uses of dantrolene?

A

spams (CNS or spinal cord), and malignant hyperthermia

33
Q

SE of dantrolene

A

generalized mm weakness, sedation, symptomatic hepatitis (with >800mg/d)

34
Q

what is malignant hyperthermia?

A

prolonged release of Ca from mm leads to massive contraction

increased lactic acid

fever

death

35
Q

use of cyclobenazprine and its look alikes

A

acute mm spasm caused by tissue trauma or strain (not for spasms from spinal cord or brain injuries)

usually nonspecific back pain

36
Q

SE of cyclobenazprine and its look alike?

A

strongly anticholinergic
drowsy
confusion
visual hallucinations

37
Q

drugs used for severe mm spasms due to euro injury?

A

diazepam
baclofen
tizanidine
dantrolene

38
Q

drugs used for mm pain/injury syndromes where spasms is cause of pain or secondary to local mm:

A
ophenadrine
carisoprodol
cyclobenzaprine
metaxalone
methocarbamol
39
Q

what population do u need to be careful with, with spasmolytics?

A

elderly (increased SE)