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PHTH 561: Pharmacology > Skeletal Muscle Relaxants Quiz > Flashcards

Skeletal Muscle Relaxants Quiz Flashcards

1
Q

What are skeletal muscle relaxants used to treat?

A

Used to treat conditions associated with hyper excitable skeletal muscle- specifically spasticity and muscle spasms

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2
Q

What is spasticity vs spasm?

A

-Spasticity: velocity dependent increase in muscle tone caused by the increased excitability of the muscle stretch reflex
-Spasms: involuntary muscle contractions

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3
Q

What are common symptoms of severe spasticity?

A

-Muscle stiffness
-Muscle spasms
-Rapid muscle contractions
-Fixed joints: contractures
-Exaggerated muscle jerks
-Pain or tightness around joints

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4
Q

What is the primary goal of skeletal muscle relaxants?

A

-Selective decrease in skeletal muscle excitability
-Decrease pain without causing a profound decrease in muscle function

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5
Q

What are common anti-spasticity drugs?

A

-Baclofen
-Dantrolene
-Tizanidine
-Botulinum toxin
-Gabapentin
-Diazepam (Benzodiazepines)

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6
Q

What are common spasmolytics?

A

-Carisoprodol (Soma)
-Cyclobenzaprine (Flexeril)
-Methocarbamol (Robaxin)
-Orphenadrine (Norflex)

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7
Q

What is the mechanism of Carisoprodol? What is a brand name of this drug?

A

-Its exact mechanism is unknown, but is believed to alter interneuronal activity in the spinal cord and descending reticular formation
-Polysynaptic inhibitor
-Decrease alpha motor neuron excitability
-Soma

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8
Q

What is the mechanism of Cyclobenzaprine? What is a brand name of this drug?

A

-Works centrally, likely by decreasing activity in the brainstem to relieve muscle spasms
-Flexeril

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9
Q

What is the mechanism of Methocarbamol? What is a brand name of this drug?

A

-Central muscle relaxant properties
-Robaxin

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10
Q

What is the mechanism of Orphenadrine? What is a brand name of this drug?

A

-Anticholinergic properties are believed to be responsible for this drugs mechanism
-Norflex

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11
Q

What are the key differences in the mechanisms for anti-spasticity drugs vs spasmolytics?

A

-Anti-spasticity drugs often have more specific targets
-Spasmolytics are less clear and can be diverse

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12
Q

What are the uses of polysynaptic inhibitors?

A

-Adjuncts to rest and PT for relief of muscle spasms associated with acute painful MSK injuries
-The same compounds sometimes incorporated into the same tablet with analgesic (Norgesic)

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13
Q

What are adverse effects of polysynaptic inhibitors?

A

-Drowsiness, dizziness
-Nausea, lightheadedness, vertigo, ataxia, headache
-Tolerance and physical dependence

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14
Q

What are the most common polysynaptic inhibitors?

A

-Carisoprodol (Soma)
-Cyclobenzaprine (Flexeril)
-Methocarbamol (Robaxin)
-Orphenadrine citrate (Norflex)

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15
Q

What is the mechanism of Diazepam (Valium)?

A

-Increases the inhibitory effects at CNS synapses that use GABA
-Binds to GABA A receptors: positive allosteric modulation
-Increases GABA-mediated inhibition of alpha motor neuron ——> less excitability

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16
Q

What are therapeutic uses of Diazepam?

A

-Treats muscle spasms associated with MSK injuries, especially low back strains
-Controls muscle spasms associated with tetanus toxin (inhibits spasms of larynx)

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17
Q

What are adverse effects of Diazepam?

A

-Sedation and a general reduction in psychomotor ability
-Long-term use also limited by tolerance and dependence
-Sudden withdrawal after prolonged use can cause seizures, anxiety, agitation, tachycardia, and even death
-Overdose can result in coma or death

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18
Q

What is an antidote for diazepam?

A

Flumazenil is antidote for Diazepam and other benzodiazepines

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19
Q

What drugs work on GABA A receptors?

A

Benzodiazepines (Valium/diazepam)

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20
Q

What drugs work on GABA B receptors?

A

Baclofen

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21
Q

What drugs work on alpha 2 receptors in the spinal cord?

A

Tizanidine

22
Q

What drugs work directly on the skeletal muscle?

A

Dantrolene

23
Q

What is the chemical name of Baclofen (Lioresal)? What is the mechanism?

A

-Chemical name: beta-(p-choloro-phenyl)-GABA
-Derivative of the central inhibitory GABA
-Binds to GABA B receptors in spinal cord
-Inhibits transmission within the spinal cord at specific synapses causing an inhibitory effect on alpha motor neurons within spinal cord

24
Q

What are common uses of Baclofen?

A

-Administered orally to treat spasticity with spinal cord lesions (paraplegia, quadriplegia, SC demyelination)
-Drug of choice with MS because of fewer side effects
-Does not cause as much generalized muscle weakness as direct-acting relaxants such as Dantrolene

25
Q

What are the adverse effects of Baclofen?

A

-Transient drowsiness which usually disappears within a few days
-Sometimes confusion and hallucinations in patients with CVA or in elderly
-Nausea, muscle weakness
-Headache

26
Q

What are intrathecal injections? What are they used for? What is the benefit?

A

-Spinal injections
-Used in severe spasticity (Baclofen)
-Catheter and “pump” deliver drug to subarachnoid space
-May decrease spasticity with less drug, fewer systemic side effects

27
Q

What is an itrathecal baclofen pump?

A

-Smaller catheter usually implanted surgically
-Open end of the catheter is attached to some type of programmable pump
-Pump is implanted subcutaneously in the abdominal wall
-Adjusted to deliver drug at slow, continuous rate
-Rate of infusion titrated over time to achieve best clinical reduction in spasticity

28
Q

What are adverse effects of intrathecal baclofen?

A

-Disruption in delivery system
-Pump malfunction
-Increased drug delivery can cause overdose
-Abrupt stoppage of drug secondary to pump dysfunction can cause withdrawal syndrome (fever, confusion, delirium, seizures)
-Tolerance with long-term use

29
Q

What is the mechanism of adrenergic alpha-2 receptor agonists? What is the primary agent?

A

-Primary agent: Tizanidine (Zanaflex)
-Stimulate alpha-2 receptors located on spinal interneurons
-Cause inhibition of interneurons which decreases excitatory input onto alpha motor neuron
-Tizanidine decreases excitability by both pre and post synaptic inhibition
-Efficacy similar to Baclofen but with less generalized muscle weakness

30
Q

What are the uses of alpha-2 agonists?

A

-Control spasticity from spinal lesions and central lesions
-As effective in decreasing spasticity as oral baclofen or diazepam
-Milder side effects and less generalized muscle weakness
-Tizanidine is better than Clonidine because it has less cardiovascular side effects and hypotension

31
Q

What are the adverse effects of alpha-2 agonists?

A

Sedation, dizziness, dry mouth

32
Q

What is the mechanism of Gabapentin (Neurontin)?

A

-Calcium channel blocker
-Developed originally as anti-seizure drug
-Enhances GABA effect in spinal cord (exact mechanism unclear)

33
Q

What are the uses of Gabapentin (Neurontin)?

A

-Decrease spasticity associated with SCI and MS
-Best use may be in combination with other anti-spasticity agents (Gabapentin + Baclofen)
-May help in reducing certain types of chronic pain

34
Q

What are adverse effects of Gabapentin?

A

-Sedation and fatigue
-Dizziness
-Ataxia

35
Q

What is the mechanism of Dantrolene (Dantrium)?

A

-Only direct acting muscle relaxant
-Inhibits release of calcium from skeletal muscle sarcoplasmic reticulum

36
Q

What are the uses of Dantrolene?

A

-Effective in treating severe spasticity
-Not prescribed to treat muscle spasms caused by MSK injury

37
Q

What are adverse effects of Dantrolene?

A

-Generalized muscle weakness most common
-Use of Dantrolene therefore can be counterproductive because increased motor function with decreased spasticity is offset by muscle weakness
-Severe hepatotoxicity and fatal hepatitis

38
Q

What is the mechanism of Botulinum Toxin?

A

-Injected locally for severe spasms such as torticollis, laryngospasms
-Increased use in spasticity
-Inhibits release of acetylcholine at neuro-muscular junction

39
Q

Where is Botulinum injected into? How long does it last? How does it help with spasticity?

A

-Injected into skeletal muscle
-Relaxation/paralysis occur within 3-7 days and lasts 2-3 months
-Remove spastic dominance in certain patients
-Volitional motor function can be facilitated
-Improved gait and other functional activities in patients with cerebral palsy or TBI
-Helps to stretch muscle and prevent joint contractures
-Enables patients to wear orthotic devices

40
Q

What are the problems and limitations with Botulinum Toxin?

A

-Local irritation at injection site
-Only a limited number of muscles can be injected during a given treatment
-Must limit total dose (300-400 units of Type A, 2500-5000 units Type B)
-Exceeding recommended dosage can cause immune response which will create antibodies against toxin making subsequent treatments less effective

41
Q

How do effects of Botulinum Toxin wear off?

A

-New presynaptic terminal sprouts from axon that originally effected by toxin
-New motor end plate with new source of acetylcholine
-Another injection needed to block sprout

42
Q

What is the duration of action of carisoprodol (Soma)?

A

4-6 hours

43
Q

What is the duration of action of chlorzoxazone?

A

3-4 hours

44
Q

What is the duration of action of cyclobenzaprine (Flexeril)?

A

12-24 hours

45
Q

What is the duration of action of Diazepam (Valium)?

A

Up to 24 hours

46
Q

What is the duration of action of Metaxalone?

A

4-6 hours

47
Q

What is the duration of action of Methocarbamol (Robaxin)?

A

Unknown

48
Q

What is the duration of action of Orphenadrine citrate (Antiflex, Norflex)?

A

12 hours

49
Q

What are alternatives to skeletal muscle relaxants?

A

-Physical therapy
-Ibuprofen/NSAIDS
-Tramadol
-Opioids

50
Q

What are special concerns for rehab patients who use skeletal muscle relaxants?

A

-Meds are used to compliment PT interventions
-Long term use is not recommended: addiction
-PT can reduce the need for meds
-Possible drastic change in muscle tone over short period of time
-Pt’s sometimes rely on muscle spasms or spasticity for functioning

51
Q

What effects of anti-spastic and spasmolytic drugs can interfere with rehabilitation?

A

-Motor control problems
-Functional decline for daily activities
-Decreased alertness
-Weakness
-Tolerance and physical dependence

52
Q

What are possible PT solutions to effects of anti-spastic and spasmolytic drugs?

A

-Schedule PT for time of day when sedative effects are less marked
-Discuss with pt’s PCP
-In pt’s with spasticity due to neurological injury, use intensive PT to return pt to normal physiologic motor control
-Use intensive therapy for acute MSK injuries
-Improve muscle strength, posture, and flexibility which can decrease need for medications

PHTH 561: Pharmacology (7 decks)

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