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Pharmacology > Muscle relaxants > Flashcards

Muscle relaxants Flashcards

1
Q

Mechanism of skeletal muscle contraction

A

initiation of impulse, release of acetylcholine, activation of nicotinic receptor at motor end plate, opening of ion channel, passage of Na depolarization of end plate, muscle contraction

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2
Q

Drug targets

A

neuromuscular blocking agents interfere with process of signal conduction, also by blocking muscle contraction even if the signal to contract is propogated along the neuron

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3
Q

Skeletal muscle reflex arc

A

increase in Ca causes muscle contraction, signal carried from spinal cord to muscle (efferent neurons), muscles to spinal cord (afferent neurons)

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4
Q

GABA

A

gamma aminobutyric acid inhibitory neurotransmitter in CNS that bind to GABA receptors and decrease efferent firing- stops reflex arc to prevent inappropriate contractions

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5
Q

Muscle spasm

A

a sudden, involuntary muscle contraction, initiated by trauma, tonic or clonic, painful (spasm-pain-spasm etc)

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6
Q

Chronic muscle spasms can result in

A

muscle atrophy

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7
Q

Muscle spasticity

A

increased muscle tone or contraction, stiff awkward movements, caused by nerve damage in CNS, usually permanent (cerebral palsy), not disease but a process

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8
Q

Skeletal muscle relaxants are used to

A

decrease muscle spasms or spasticity, selective for skeletal muscles

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9
Q

Central acting muscle relaxants mostly work by

A

decreasing signalling from the efferent neurons as opposed to directly inhibiting contraction

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10
Q

Skeletal muscle relaxant drugs

A

Baclofen (Lioresal), Cyclobensaprine (Flexeril), Carisoprodol (Soma), Metaxalone (Skelaxin), Methocarbamol (Robaxin), Chlorzoxazone (Parafon Forte), Dantrolene (Dantrium), Orphenadrine (Norflex)

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11
Q

Baclofen (Lioresal) MOA

A

centrally acting GABA agonist on efferent neurons, inhibits transmission of reflexes at spinal cord level, relieving muscle spasticity, also inhibits substance P in spinal cord

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12
Q

Baclofen (Lioresal) clinical uses

A

spasticity, migraine prevention, MS, spinal cord injury, usually long term

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13
Q

Baclofen (Lioresal) ADRs

A

CNS related, drowsiness, sedation, muscle weakness, hypotension, HA, *less sedating than others

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14
Q

Baclofen (Lioresal) boxed warning

A

severe withdrawal from abrupt d/c, causes altered mental status and rebound spasticity

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15
Q

Baclofen (Lioresal) Pearls (5)

A

TID, PO, can be given intrathecal route for spinal cord injury, MS, degenerative myelopathy, CA; caution with seizure pts, older drug

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16
Q

Cyclobenzaprine (Flexeril) MOA

A

centrally-acting, structurally and pharmacologically very similar to TCAs, reduces tonic somatic motor activity

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17
Q

Cyclobenzaprine (Flexeril) Clinical uses

A

muscle spasms associated w/ muscle injury or strain, short term use only, also good for low back spasms

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18
Q

Cyclobenzaprine (Flexeril) ADRs

A

drowsiness, dizziness, sedation, anticholinergic (no BPH, glaucoma, Alzheimer’s)

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19
Q

Cyclobenzaprine (Flexeril) Pearls (4)

A

Only PO, immediate release or long acting (TID/daily), not for use in MS or cerebral palsy, caution in elderly, MAOI pts, or liver failure

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20
Q

Tizanidine (Zanaflex) MOA

A

alpha agonist, similar to clonidine, bu not lipophilic enough to penetrate BBB, causes presynaptic inhibition of motor neurons

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21
Q

Tizanidine (Zanaflex) clinical uses

A

PO and BID-TID, spasticity, unlabeled for tension HA, acute low back pain

22
Q

Tizanidine (Zanaflex) ADRs

A

drowsiness, hypotension, dry mouth, constipation

23
Q

Carisoprodol (Soma) MOA

A

not sure, but is CNS depressant, sedating/anxiolytic properties resulting in muscle relaxation

24
Q

Carisoprodol (Soma) clinical uses

A

Acute management of musculoskeletal pain (2-3 weeks)

25
Q

Carisoprodol (Soma) ADRs

A

drowsiness, sedation!!, dizziness

26
Q

Carisoprodol (Soma) Pearls (6)

A

QID, PO only, result in addiction, caution in elderly/ pt with drug abuse, abrupt d/c= withdrawal, DEA controlled

27
Q

Metaxalone (Skelaxin) MOA

A

not sure, but CNS depressant, breaks spasm-pain cycle, no direct effect on skeletal muscle

28
Q

Metaxalone (Skelaxin) clinical use

A

muscle spasms/discomfort

29
Q

Metaxalone (Skelaxin) ADRs

A

CNS depression, dizziness, drowsiness, sedation

30
Q

Metaxalone (Skelaxin) pearls (4)

A

TID-QID, only PO, caution in renal AND hepatic failure, elderly, pts taking other sedatives and pt with anemia

31
Q

Methocarbamol (Robaxin) MOA

A

CNS depression

32
Q

Methocarbamol (Robaxin) ADRs

A

bradycardia

33
Q

Methocarbamol (Robaxin) Pearls (6)

A

IV, PO, IM, IV contra in renal insufficiency, caution in pt with seizure disorders, usually for long-term

34
Q

Dantrolene (Dantrium) MOA

A

unique in that it is not central acting, acts directly on skeletal muscle, interfering w/ excitation/contraction coupling to produce relaxation, decr amt of Ca released

35
Q

Dantrolen (Dantrium) clinical use

A

acute management of malignant hyperthermia, neuroleptic malignant syndrome (short-term), and cerebral palsy or MS (long-term), Rare, IV and PO

36
Q

Dantrolen (Dantrium) ADRs

A

euphoria, muscle weakness, drowsiness/sedation, hepatotoxic w/ chronic use

37
Q

Other skeletal muscle relaxants

A

Chlorozoxazone (Parafon Forte) PO only and Orphenadrine (Norflex)- centrally acting, euphorigenic and analgesic properties

38
Q

Neuromuscular blockers types

A

depolarizing (Succinylcholine, (Anectine)) and non-depolarizing (Pancuronium, Vecuronium (Norcuron), Rocuronium (Zemuron), Cisatracurium (Nimbex), Atracurium

39
Q

NMBs cause

A

system-wide paralysis, are selective for skeletal muscle not smooth muscle

40
Q

Succinylcholine (Anectine) MOA

A

depolarizing, acetylcholine agonist, binds nicotinic receptors to open the channels and cause immediate depolarization, leave channels open and unable to contract muscle

41
Q

Succinylcholine (Anectine) clinical use

A

1x IVP dose for intubations, very fast onset, short duration

42
Q

Succinylcholine (Anectine) ADRs

A

hyperkalemia, bradycardia, malignant hyperthermia

43
Q

Non-depolarizing NMBs MOA

A

compete with acetylcholine at the nicotinic receptor sites of neuromuscular junction, will not see initial muscle contraction

44
Q

Non-depolarizing NMBs clinical uses

A

intubation, and continuous paralysis in critically ill, paralysis during surgical procedures, in ICU for pts whose respiratory fnc is not improving while on mechaniclal ventilation

45
Q

Non-depolarizing NMBs ADRs

A

hypotension, hyperkalemia (mostly in pts with burns, nerve damage, crush injuries, head injuries), CNS stimulation(Rocuronium), tachy (Pancuronium)

46
Q

Non-depolarizing NMBs Pearls (6)

A

monitor with train of four (2/4), all given parenterally, short T1/2, always via continuous infusion, relative quick onset, not for combative or agitated pts

47
Q

Rocuronium (Zemuron) Pearls (3)

A

fastest onset, avoid in liver failure, DOC in pt w/ renal failure

48
Q

Vecuronium/Pancuronium avoid in

A

pt with renal failure

49
Q

Which has active metabolites that make DOA variable

A

Vecuronium

50
Q

Cisatracurium (Nimbex) pearls

A

$$$, unique metabolism (Hoffman eilimination) that results in spontaneous breakdown of drug

51
Q

NMB consideration

A

T1/2 and duration dictate how that are used, do not use in management of seizures, reversed with acetylcholinesterase inhibitors (Physostigmine, neostigmine), always ensure pt is properly sedated w/ ample analgesia, high risk med!

Pharmacology (61 decks)

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