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MSK II Exam 2 > Pharm: Skeletal Muscle Relaxants > Flashcards

Pharm: Skeletal Muscle Relaxants Flashcards

1
Q

Non-depolarizing neuromuscular blocking agents must be administered how?

A

Parenterally; they are highly polar

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2
Q

As a general rule which muscles are more resistant to blockade from neuromuscular blocking agents and which recover more rapidly?

A
  • Larger muscles (abdominal, trunk, paraspinous, diaphragm) = more resistant and recover quicker

*Diaphragm = last to be paralyzed and quickest to recover

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3
Q

The effects of nondepolarizing neuromuscular blocking agents are reversed how?

A

Addition of an acetylcholine esterase (AChE) inhibitors

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4
Q

Which agents are co-administered with AChE inhibitors during reversal of the effects of neuromuscular blocking agents to minimize adverse cholinergic effects?

A

Anticholinergic agents i.e., Atropine, Glycopyrrolate –> minimize DUMBBELSS

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5
Q

Which AE’s may be seen with large doses of the neuromuscular blocking agent, Tubocurarine?

A

AChR blockade at autononic ganglia (adrenal medulla) –> HYPOtension + tachycardia

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6
Q

Why has the clinical use of the neuromuscular blocking agent, d-tubocurarine, declined in favor of other agents?

A

Causes significant histamine release and has very long duration of action

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7
Q

Which drugs potentiate the neuromuscular blockage produced by nondepolarizing muscle relaxants in a dose-dependent fashion; list 6 drugs in this class in order of greatest to least effect?

A

Inhaled anesthetics: isoflurane >> sevoflurane = desflurane = enflurane = halothane > nitrous oxide

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8
Q

Which class of antibiotics have been shown to enhance neuromuscular blockade?

A

Aminoglycosides: gentamicin, tobramycin, streptomycin, neomycin, kanaymycin, paromycin, ntilmicin, spectinomycin

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9
Q

List 3 agents that block signaling at the NMJ which can enhance the actions of nondepolarizing agents?

A

Tetrodotoxin, local anesthetics, and botulinum toxin

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10
Q

In which 2 conditions are patients resistant to non-depolarizing muscle relaxants (due to ↑ expression of nAChRs)?

A

Severe burns and upper motor neuron dz

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11
Q

Prolonged duration of action from nondepolarizing muscle relaxants occurs in which patient population?

A

Elderly patients with ↓ hepatic and renal function

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12
Q

Which non-depolarizing muscle relaxant is inactivated by a form of spontaneous breakdown known as Hofmann elimination and causes less histamine release than others in this class?

A

Atracurium

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13
Q

Which non-depolarizing muscle relaxant can be used in pt’s with significant renal and hepatic impairment?

A

Cisatracurium

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14
Q

Which non-depolarizing muscle relaxant is not often used because of long-lasting effects as well as high degree of elimination by the kidney?

A

Doxacurium

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15
Q

Which non-depolarizing muscle relaxant, in large doses, is associated with histamine release and is the only one associated with CV effects?

A

Mivacurium

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16
Q

Which 2 intermediate-acting steroid muscle relaxants undergo biliary excretion or hepatic metabolism for elimination and are more likely to be used clinically?

A

Vecuronium and Rocuronium

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17
Q

Neuromuscular blocking agents with which chemical structure (steroid/isoquinoline) have the least tendency to cause histamine release?

A

Steroidal: Pancuronium, Pipercuronium, Rocuronium, and Vecuronium

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18
Q

Which steroid muscle relaxant has the most rapid time of onset (60-120 sec.) and is an alternative to succinylcholine?

A

Rocuronium

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19
Q

Prolonged neuromuscular blockade after a dose of succinylcholine can occur in pt’s with genetically abnormal what?

A

Variant of plasma cholinesterase

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20
Q

What occurs in the Phase I block after dose of Succinylcholine?

A
  • Activates nAChR –> depolarization of motor end plate: muscle contraction
  • Membranes remain depolarized and unresponsive to subsequent impusles; flaccid paralysis results
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21
Q

What occurs if cholinesterase inhibitors are given during the phase I depolarizing block of Succinylcholine?

A

Potentiate the block; not reversal

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22
Q

What occurs during the Phase II block after dose of Succinylcholine?

A
  • Initial end plate depolarization ↓ and membrane is repolarized; BUT:
  • Unable to depolarize because the receptor is desensitized; ACh receptors are available but don’t work.
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23
Q

How is the Phase II desensitizing block by Succinylcholine reversed?

A

Acetylcholinesterase inhibitors

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24
Q

Succinylcholine is often used in what 2 scenarios?

A
  • For rapid sequence induction i.e., emergency surgery when the objective is to secure the airway rapidly and prevent soiling of the lungs with gastric contents
  • For quick surgical procedures where an ultrashort acting neuromuscular blocker is practical
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25
Q

Which AE of Succinylcholine may be seen when administered during halothane anesthesia?

A

Cardiac arrhythmias

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26
Q

How do the cardiac effects of Succinylcholine differ from regular doses to high doses?

A
  • Regular: stimulates nAChRs and mAChRs to produce negative inotropic (contraction strength) and chronotropic (heart rate) effects
  • Large: can cause positive inotropic and chronotropic effects
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27
Q

How can the potential negative inotropic (contraction strength) and chronotropic (heart rate) effects of Succinylcholine be attenuated?

A

Administration of an anticholinergic i.e., Atopine

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28
Q

Patients with what underlying conditions may respond to Succinylcholine by releasing K+ into the blood, which on rare occasions can lead to cardiac arrest?

A

Pt’s with burns, nerve damage, or neuromuscular disease, closed head injury or other trauma

29
Q

Succinylcholine may cause increased pressure in which 2 locations as an AE?

A

↑ intraocular pressure and ↑ intragastric pressure

30
Q

List 3 contraindications for using Succinylcholine?

A
  • Personal or family hx of malignant hyperthermia
  • Myopathies associated w/ ↑ CPK values
  • Acute phase of injury following: major burns, multiple trauma, extensive denervation of skeletal m. or upper motor neuron injury
31
Q

What is the black box warning associated with Succinylcholine?

A
  • Acute rhabdomyolysis w/ hyperkalemia –> ventricular dysrhythmia, cardiac arrest, and death can occur after administration to apparently healthy children
  • Usually males <8 y/o but also reported in adolescents
32
Q

The combination of Succinylcholine and volatile anesthetics can result in what; how is this treated?

A

Malignant hyperthermia (rare); tx with Dantrolene

33
Q

What are 4 major uses of neuromuscular blocking drugs?

A
  • Surgical relaxation
  • Tracheal intubation
  • Control of ventilation: for adequate gas exchange and prevents atelectasis in pt’s who have ventilatory failure; reduce chest wall resistance and improve thoracic compliance
  • Tx of convulsions: of status epileptics or local anesthetic toxicity
34
Q

How does the pharmacokinetics of quaternary (charged) AChE inhibitors differ from the tertiary (uncharged) type?

A
  • Quaternary: relatively insoluble (parenteral administration), no CNS distribution i.e., neostigmine, pyridostigmine, edrophonium, echothiophate
  • Tertiary: well absorbed from all sites, CNS distribution i.e., physostigmine donpezil tacrine, rivastigmine, galantamine
35
Q

Which 5 AChE inhibitors are tertiary/uncharged; well absorbed from all sites and have CNS distribution?

A

Physostigmine + Donepezil + Tacrine + Rivastigmine + Galantamine

36
Q

Which AChE inhibitor of the organophosphate type is charged and does not have CNS distribution?

A

Echothiophate

37
Q

What is the effect on arteries/veins with normal dose of AChE inhibitor vs. high-dose?

A
  • Normal: dilation (via EDRF)
  • High-dose: constriction
38
Q

What are the 3 standard AChE inhibitors used in the symptomatic tx of myasthenia gravis; why?

A
  • Pyridostigmine, neostigmine, and ambenonium
  • Do not cross BBB
39
Q

How can an AChE inhibitor (edrophonium) delineate between myasthenic crisis and cholinergic crisis?

A
  • If pt is in myasthenic crisis the sx’s will improve
  • If pt is in cholinergic crisis, the sx’s will remain unchanged or worsen
40
Q

Which AChE inhibitor is commonly used to reverse neuromuscular blocking drug-induced paralysis?

A

Neostigmine

41
Q

Which 3 AChE inhibitors are used to tx Alzheimers and Dementia associated with Parkinsons?

A

Donepezil, Rivastigmine, and Galantamine

42
Q

Which AChE inhibitor is preferred as an antidote for anticholinergic intoxication?

A

Physostigmine - can cross the BBB

43
Q

AChE inhibitors typically diminish the blockade of non-depolarizing neuromuscular blocking agents, which drug is an exception to this?

A

Mivacurium (metabolized by plasma AChE) –> AChE inhibitors will prolong the blockade of this agent

44
Q

AChE inhibitors may enhance which effect of beta-blockers?

A

Bradycardia

45
Q

What is the tx for AChE inhibitor intoxication?

A
  • Atropine in combo w/ maintenance of vital signs (respiration) and decontamination; will only be effective at mAChRs
  • To regenerate AChE at NMJ, give pralidoxime
  • Atopine + pralidoxime + benzodiazepine are typically combined
46
Q

What are the dominant initial signs of AChE intoxication?

A

Those of mAChR stimulation: miosis, salivation, sweating, bronchial constriction, vomiting, and diarrhea

47
Q

What is the MOA of the centrally-acting spasmolytic, Baclofen?

A

GABAB receptor agonist; results in hyperpolarization (due to ↑ K+ conductance) and inhibition of excitatory NT release in brain and spinal cord

48
Q

Which centrally-acting spasmolytic is as effective as diazepam in reducing spasticity and causes less sedation?

A

Baclofen

49
Q

What are some of the AE’s associated with Baclofen?

A
  • Drowsiness
  • ↑ seizure activity in epileptic pt’s (withdrawl must be done slowly)
  • Vertigo + dizziness
  • Psychiatric disturbances + insomnia + slurred speech + ataxia
  • Hypotonia + muscle weakness
50
Q

The precise MOA for the centrally-acting spasmolytic, Carisprodol, is unknown but it acts as what?

A

CNS depressant

51
Q

Why must the centrally-acting spasmolytic, Carisprodol, be used only for short term; what are some AE’s?

A
  • Schedule IV controlled due to addictive potential
  • AE’s: dizziness and drowsiness
52
Q

The centrally-acting spasmolytic, Carisprodol, is metabolized how; must be careful using in whom?

A

Metabolized by CYP2C19; use in caution with pt on CYP inhibitors

53
Q

The centrally-acting spasmolytic, Carisprodol, is metabolized to what; why is this useful?

A

Meprobamate, which has anxiolytic and sedative effects (used to manage anxiety disorders)

54
Q

What is the action of the centrally-acting spasmolytic, Cyclobenzaprine?

A

Reduces tonic somatic motor activity by influencing both alpha and gamma motor neurons

55
Q

The centrally-acting spasmolytic, Cyclobenzaprine, is structurally related to which other class of drugs; how does this influence its AE’s?

A
  • TCA antidepressants and produces antimuscarinic AE’s:
  • Significant sedation + confusion + transient visual hallucinations
56
Q

What is significant about the metabolism of the centrally-acting spasmolytic, Cyclobenzaprine?

A

Metabolized by CYP450; use with caution with CYP inhibitors

57
Q

What are 3 AE’s of the the centrally-acting spasmolytic, Cyclobenzaprine?

A

Drowsiness + dizziness + xerostomia

58
Q

What is the MOA of Diazepam?

A

Promotes binding of GABA to GABAA receptor = ↑ frequency of channel openings –> ↑ inhibitory transmission and ↓ spasticity

59
Q

What 4 effects does Diazepam have?

A
  • Sedation
  • Muscle relaxation
  • Anxiolytic
  • Anticonvulsant
60
Q

What are the effects of the α2-adrenergic agonist, Tizanidine?

A

Drowsiness + hypotension + dry mouth + asthenia/muscle weakness

61
Q

What is the MOA of Dantrolene?

A

- Inhibits the ryanodine receptor (RyR) –> prevents release of Ca2+ from sarcoplasmic reticulum

  • Impaired skeletal muscle contraction; cardiac and smooth m. unaffected
62
Q

What are 3 AE’s associated with Dantrolene?

A
  • Generalized muscle weakness
  • Sedation
  • Occasionally hepatitis
63
Q

What is Dantrolene used for?

A
  • Tx spasticity assoc. w/ UMN disorders (i.e., spinal cord injury, stroke, cerebral palsy, or MS)
  • Malignant hyperthermia
  • Neuroleptic malignant syndrome i.e., toxicity of antipsychotic drugs
64
Q

How are glucocorticoids used for tx of MS?

A

Monthly bolus IV glucocorticoids (typically methylprednisolone) used for tx of 1’ or 2’ progressive MS alone or in combo w/ other immunomodulatory/immunosuppressive meds

65
Q

What is Glatiramer Acetate and it’s MOA?

A
  • Mix of polymers of 4 AA’s (L-alanine, L-glutamic acid, L-lysine, and L-tyrosine) antigenically similar to myelin basic protein
  • Induces and activates T-lymphocyte suppressor cells specific for myelin antigen
  • Also interference w/ antigen-presenting function of certain immune cells opposing pathogenic T-cell function
66
Q

What is the MOA of interferon-beta-1a and beta-1b used for MS?

A

Interferes w/ T-cell adhesion to the endothelium at BBB by binding VLA-4 on T cells or by inhibiting T-cell expression of MMP

67
Q

What are the benefits of using interferon-beta-1a and beta-1b to tx MS?

A
  • Reduction of relapses by 1/3
  • Reduction of new MRI T2 lesions and the volume of enlarging T2 lesions
  • Reduction in the number and volume of Gd-enhancing lesions
  • Slowing of brain atrophy
68
Q

What is the MOA of Mitoxantrone used for MS?

A

Antineoplastic agent; works by intercalating into DNA –> cross-links and strand breaks (related to anthracycline antibiotics)

MSK II Exam 2 (10 decks)

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