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Pharmacology > 3: Muscle Relaxants > Flashcards

3: Muscle Relaxants Flashcards

1
Q

primary goal

A

selective decrease skeletal muscle excitability

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2
Q

primary uses

A

1) muscle spasms

2) spasticity

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3
Q

injury usually to muscle or peipheral nerve

A

muscle spasm

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4
Q

tonic contraction in paraspinals, traps, etc.

A

muscle spasms

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5
Q 
injury to CNS-- 
CNS lesions (SCI, CP, CVA, etc)
A

spasticity

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6
Q

exaggerated stretch reflex

A

spasticity

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7
Q

agents used to treat muscle spasms

A

1) centrally acting anti-spasm drugs

2) Diazepam (Valium)

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8
Q

muscle spasm agent: diverse group of drugs

A

centrally-acting antispasm drugs

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9
Q

muscle spasm agent: used commonly in back, neck spasms; other orthopedic injuries

A

centrally-acting antispasm drugs

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10
Q

centrally-acting antispasm drugs: enhances GABA inhibition in brain (GABA A effect)

A

Carisoprodol

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11
Q

centrally-acting antispasm drugs: might increase serotonin in brainstem

A

Cyclobenzaprine

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12
Q

all centrally-acting antispasm drugs are

A

strong sedatives

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13
Q

centrally-acting antispasm drugs primary effect

A

strong sedatives

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14
Q

antispasm drugs: short term use may be beneficial for…

A

acute muscle spasms

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15
Q

antispasm drugs: patients may decide to take only when? why?

A

bedtime bc it’s a strong sedative

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16
Q

antispasm drugs: should be combined with what?

A

aggressive physical therapy

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17
Q

antispasm drugs: when should drugs be decreased?

A

ASAP- discontinue drups (3-4 days) while continuing PT

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18
Q

muscle spasm agent: developed originally as an anti-anxiety drug

A

diazepam (valium)

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19
Q

Diazepam (Valium) is a ( ) agent

A

Benzodiazepine

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20
Q

How does Diazepam work in CNS?

A

increases inhibitory effects of GABA

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21
Q

Benzodiazepine receptors in phospholipid bilayer also have receptors for

A

GABA and barbituates

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22
Q

How does GABA cause inhibition?

A

Cl- channels open in protein and becomes more negative whice inhibits

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23
Q

Valium causes GABA to do what?

A

GABA binds stronger –> more Cl- enters –> more inhibition

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24
Q

Valium increases ( ) inhibition of the alpha motor neuron

A

GABA-mediated

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25
Q

spasticity agent: acts in CNS, increases GABA mediated inhibition

A

Diazepam

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26
Q

spasticity agent: Valium long term use also limited by ( )

A

tolerance and dependence

27
Q

spasticity agent: may be helpful if patient has spasticity AND anxiety

A

Diazepam

28
Q

spasticity agent: systhetic GABA

A

Baclofen

29
Q

spasticity agent: stimulates GABA receptors in spinal cord (GABA B agonist)

A

Baclofen

30
Q

Baclofen decreases excitation of what?

A

alpha motor neuron

31
Q

How can Baclofen be administered?

A

intrathecally

32
Q

Intrathecal injections mean what?

A

spinal injections

33
Q

Baclofen intrathecal into what area of cord?

A

subarachnoid space (B/W Pia mater and arachnoid mater)

34
Q

how to see if intrathecal injection works well for patient?

A

trial injection- PT monitors how they’re reacting

35
Q

when is intrathecal baclofen used?

A

in severe spasticity

36
Q

when is intrathecal baclofen used?

A

in severe spasticity

37
Q

where is intrathecal baclofen pump usually put on body?

A

lower abdomen

38
Q

Alpha-2 agonists primary agent

A

tizanidine (Zanaflex)

39
Q

spasticity agent: stimulates alpha-2 receptors located on spinal interneurons

A

alpha-2 agonists

40
Q

alpha-2 agonists causes inhibition of what?

A

interneurons

41
Q

alpha-2 agonists causes inhibition of interneurons…what does this mean exactly?

A

decreases excitatory input onto alpha motor neuron

42
Q

spasticity agent: efficacy similar to oral baclofen but less generalized muscle weakness

A

alpha-2 agonists

43
Q

spasticity agent: develped originally as antiseizure drug

A

Gabapentin (Neurontin)

44
Q

spasticity agent: inhibits Ca++ entry presynaptic terminals

A

Gabapentin

45
Q

By inhibiting Ca++ entry presynapic terminials, what dees Gabapentin do?

A

decreases release of glutamate, other excitatory NTs

46
Q

when is Gabapentin primarily used?

A

MS, SC; may cause sedation, dizziness, ataxia

47
Q

spasticity agent: only direct-acting muscle relexant

A

Dantrolene sodium (Dantrium)

48
Q

spasticity agent: inhibits release of calcium from skeletal muscle SR

A

Dantrolene sodium (Dantrium)

49
Q

Dantrolene sodium: problems with liver?

A

liver toxicity- unsure why

50
Q

spasticity agent: muscle paralytic

A

Botulinum toxin

51
Q

spasticity agent: injected locally for severe spasms such as torticollis, laryngospasms, etc

A

Botulinum toxin

52
Q

Botulinum toxin has 7 serotypes, but which 2 are for clinical use?

A

1) Type A (Botox, Dysport, Zeomin)

2) Type B (Myobloc)

53
Q

Botulinum toxin mechanism:

A

inhibits ACh release at skeletal NMJ

54
Q

spasticity agent: injected into selected muscle(s)

A

Botulinum toxin

55
Q

Botulinum: when does relazation/paralysis occur? how long does it last?

A
  • occurs within 3-7 days

- lasts 2-3 months

56
Q

Botulinum reduces spastic dominace which may allow:

A

1) increased residual function

2) improved ADL, braching, etc.

57
Q

As BTX possible retrograde transmission

A

may be transported via alpha motor neuron to CNS

58
Q

what effect could retrograde transmission have on BTX?

A

may produce carry-over and long-term effects on reflex activity in cord and brain

59
Q

BTX probs: ( ) at injection site

A

local irritation

60
Q

BTX probs:potential for ( ) production

A

antibody

61
Q

must limit totatl BTX dose to:

A
  • 300-400 units/tx (BTX type A)

- 2500-5000 units/tx (BTX type B)

62
Q

BTX probs: watch for OD signs…

A

1) drooping eyes
2) difficultly speaking/swallowing
3) general muscle weakness
4) respiratory distress

63
Q

muscle relaxants: rehab concerns

A

1) generalized weakness
2) sedation
3) possible drastic change in muscle tone over relatively short time span

Pharmacology (6 decks)

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