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NMSP Exam III > Pharm: Skeletal Muscle Relaxants > Flashcards

Pharm: Skeletal Muscle Relaxants Flashcards

1
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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2
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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3
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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4
Q

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

A

Malignant hyperthermia (rare); tx with Dantrolene

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5
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
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6
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
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7
Q

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

A

Donepezil, Rivastigmine, and Galantamine

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8
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)

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9
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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10
Q

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

A

Physostigmine + Donepezil + Tacrine + Rivastigmine + Galantamine

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11
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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12
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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13
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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14
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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15
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

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16
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
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17
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

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18
Q

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

A

Drowsiness + dizziness + xerostomia

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19
Q

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

A

Cardiac arrhythmias

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20
Q

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

A

↑ intraocular pressure and ↑ intragastric pressure

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21
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

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22
Q

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

A

Physostigmine - can cross the BBB

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23
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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24
Q

What are 3 AE’s associated with Dantrolene?

A
  • Generalized muscle weakness
  • Sedation
  • Occasionally hepatitis
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25
Why has the clinical use of the neuromuscular blocking agent, d-tubocurarine, declined in favor of other agents?
Causes _significant_ **histamine** release and has **very long duration of action**
26
What is the tx for AChE inhibitor intoxication?
- **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_
27
What is the effect on arteries/veins with normal dose of AChE inhibitor vs. high-dose?
- **Normal**: dilation (via EDRF) - **High-dose**: constriction
28
How are glucocorticoids used for tx of MS?
**Monthly bolus IV glucocorticoids** (typically methylprednisolone) used for tx of **1'** or **2'** _progressive_ **MS** alone or in combo w/ other immunomodulatory/immunosuppressive meds
29
Prolonged duration of action from nondepolarizing muscle relaxants occurs in which patient population?
**Elderly patients** with ↓ **hepatic** and **renal** function
30
Which AChE inhibitor of the organophosphate type is charged and does not have CNS distribution?
**Echothiophate**
31
The precise MOA for the centrally-acting spasmolytic, Carisprodol, is unknown but it acts as what?
**CNS depressant**
32
List 3 contraindications for using Succinylcholine?
- 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**
33
What are the benefits of using interferon-beta-1a and beta-1b to tx MS?
- _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**
34
How can the potential negative inotropic (contraction strength) and chronotropic (heart rate) effects of Succinylcholine be attenuated?
Administration of an **anticholinergic** i.e., **Atopine**
35
Which non-depolarizing muscle relaxant is not often used because of long-lasting effects as well as high degree of elimination by the kidney?
Doxacurium
36
Patients with what underlying conditions may respond to Succinylcholine by releasing K+ into the blood, which on rare occasions can lead to cardiac arrest?
Pt's with **burns**, **nerve damage**, or **neuromuscular disease**, **closed head injury** or other **trauma**
37
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?
**Atracurium**
38
What are the effects of the α2-adrenergic agonist, Tizanidine?
**Drowsiness + hypotension + dry mouth + asthenia/muscle weakness**
39
The effects of nondepolarizing neuromuscular blocking agents are reversed how?
Addition of an **acetylcholine esterase (AChE) inhibitors**
40
AChE inhibitors may enhance which effect of beta-blockers?
**Bradycardia**
41
Which non-depolarizing muscle relaxant, in large doses, is associated with histamine release and is the only one associated with CV effects?
Mivacurium
42
What are some of the AE's associated with Baclofen?
- Drowsiness - ↑ seizure activity in epileptic pt's (withdrawl must be done slowly) - Vertigo + dizziness - Psychiatric disturbances + insomnia + slurred speech + ataxia - Hypotonia + muscle weakness
43
What is the MOA of Diazepam?
Promotes binding of **GABA** to **GABAA receptor** = **↑ frequency** of channel openings --\> **↑ inhibitory transmission** and **↓ spasticity**
44
What is Dantrolene used for?
- 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
45
What are the 3 standard AChE inhibitors used in the symptomatic tx of myasthenia gravis; why?
- **Pyridostigmine**, **neostigmine**, and **ambenonium** - Do not cross BBB
46
Which non-depolarizing muscle relaxant can be used in pt's with significant renal and hepatic impairment?
**Cisatracurium**
47
What is the MOA of Mitoxantrone used for MS?
Antineoplastic agent; works by **intercalating** into **DNA** --\> **cross-links** and **strand breaks** (related to anthracycline antibiotics)
48
Why must the centrally-acting spasmolytic, Carisprodol, be used only for short term; what are some AE's?
- **Schedule IV** controlled due to _addictive_ potential - **AE's**: dizziness and drowsiness
49
The centrally-acting spasmolytic, Carisprodol, is metabolized how; must be careful using in whom?
Metabolized by **CYP2C19**; use in caution with pt on CYP inhibitors
50
AChE inhibitors typically diminish the blockade of non-depolarizing neuromuscular blocking agents, which drug is an exception to this?
**Mivacurium** (metabolized by plasma AChE) --\> AChE inhibitors will _prolong_ the blockade of this agent
51
Which centrally-acting spasmolytic is as effective as diazepam in reducing spasticity and causes less sedation?
**Baclofen**
52
The centrally-acting spasmolytic, Cyclobenzaprine, is structurally related to which other class of drugs; how does this influence its AE's?
- **TCA antidepressants** and produces **antimuscarinic** AE's: - **Significant _sedation_ + _confusion_** + transient **_visual hallucinations_**
53
How can an AChE inhibitor (edrophonium) delineate between myasthenic crisis and cholinergic crisis?
- 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**
54
What are the dominant initial signs of AChE intoxication?
Those of **_mAChR stimulation_**: **miosis**, **salivation**, **sweating**, **bronchial constriction**, **vomiting**, and **diarrhea**
55
What 4 effects does Diazepam have?
- **Sedation** - **Muscle relaxation** - **Anxiolytic** - **Anticonvulsant**
56
How do the cardiac effects of Succinylcholine differ from regular doses to high doses?
- **Regular**: stimulates nAChRs and mAChRs to produce **_negative_** _inotropic_ (contraction strength) and _chronotropic_ (heart rate) effects - **Large**: can cause **_positive_** inotropic and chronotropic effects
57
Neuromuscular blocking agents with which chemical structure (**steroid/isoquinoline**) have the least tendency to cause histamine release?
**Steroidal:** Pancuronium, Pipercuronium, Rocuronium, and Vecuronium
58
As a general rule which muscles are more resistant to blockade from neuromuscular blocking agents and which recover more rapidly?
- **Larger muscles** (abdominal, trunk, paraspinous, diaphragm) = _more_ resistant and recover _quicker_ \***Diaphragm** = last to be paralyzed _and_ quickest to recover
59
Which AChE inhibitor is commonly used to reverse neuromuscular blocking drug-induced paralysis?
**Neostigmine**
60
Which AE's may be seen with large doses of the neuromuscular blocking agent, Tubocurarine?
AChR blockade at _autononic ganglia (adrenal medulla)_ --\> **HYPOtension** + **tachycardia**
61
How is the Phase II desensitizing block by Succinylcholine reversed?
Acetylcholinesterase inhibitors
62
What occurs during the Phase II block after dose of Succinylcholine?
- 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.
63
Non-depolarizing neuromuscular blocking agents must be administered how?
**Parenterally**; they are _highly polar_
64
How does the pharmacokinetics of quaternary (charged) AChE inhibitors differ from the tertiary (uncharged) type?
- **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**
65
List 3 agents that block signaling at the NMJ which can enhance the actions of nondepolarizing agents?
**Tetrodotoxin**, **local anesthetics**, and **botulinum toxin**
66
What is the black box warning associated with Succinylcholine?
- **Acute rhabdomyolysis** w/ **hyper**kalemia --\> **ventricular dysrhythmia**, **cardiac arrest**, and **death** can occur after administration to apparently healthy children - Usually **males** \<**8 y/o** but also reported in adolescents
67
Which class of antibiotics have been shown to enhance neuromuscular blockade?
**Aminoglycosides**: gentamicin, tobramycin, streptomycin, neomycin, kanaymycin, paromycin, ntilmicin, spectinomycin
68
What is significant about the metabolism of the centrally-acting spasmolytic, Cyclobenzaprine?
Metabolized by **CYP450**; use with caution with CYP inhibitors

NMSP Exam III (20 decks)

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