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NMSP Exam III*** > 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
Which AE of Succinylcholine may be seen when administered during halothane anesthesia?
**Cardiac arrhythmias**
26
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
27
How can the potential negative inotropic (contraction strength) and chronotropic (heart rate) effects of Succinylcholine be attenuated?
Administration of an **anticholinergic** i.e., **Atopine**
28
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**
29
Succinylcholine may cause increased pressure in which 2 locations as an AE?
↑ **intraocular pressure** and ↑ **intragastric pressure**
30
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**
31
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
32
The combination of Succinylcholine and volatile anesthetics can result in what; how is this treated?
**Malignant hyperthermia** (rare); tx with **Dantrolene**
33
What are 4 major uses of neuromuscular blocking drugs?
- **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
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**
35
Which 5 AChE inhibitors are tertiary/uncharged; well absorbed from all sites and have **CNS distribution**?
**Physostigmine** + **Donepezil + Tacrine + Rivastigmine + Galantamine**
36
Which AChE inhibitor of the organophosphate type is charged and does not have CNS distribution?
**Echothiophate**
37
What is the effect on arteries/veins with normal dose of AChE inhibitor vs. high-dose?
- **Normal**: dilation (via EDRF) - **High-dose**: constriction
38
What are the 3 standard AChE inhibitors used in the symptomatic tx of myasthenia gravis; why?
- **Pyridostigmine**, **neostigmine**, and **ambenonium** - Do not cross BBB
39
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**
40
Which AChE inhibitor is commonly used to reverse neuromuscular blocking drug-induced paralysis?
**Neostigmine**
41
Which 3 AChE inhibitors are used to tx Alzheimers and Dementia associated with Parkinsons?
**Donepezil**, **Rivastigmine**, and **Galantamine**
42
Which AChE inhibitor is preferred as an antidote for anticholinergic intoxication?
**Physostigmine** - can _cross_ the BBB
43
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
44
AChE inhibitors may enhance which effect of beta-blockers?
**Bradycardia**
45
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_
46
What are the dominant initial signs of AChE intoxication?
Those of **_mAChR stimulation_**: **miosis**, **salivation**, **sweating**, **bronchial constriction**, **vomiting**, and **diarrhea**
47
What is the MOA of the centrally-acting spasmolytic, Baclofen?
**GABAB** receptor **agonist**; results in **hyperpolarization** (due to ↑ **K+** conductance) and **inhibition** of excitatory NT release in **brain** and **spinal cord**
48
Which centrally-acting spasmolytic is as effective as diazepam in reducing spasticity and causes less sedation?
**Baclofen**
49
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
50
The precise MOA for the centrally-acting spasmolytic, Carisprodol, is unknown but it acts as what?
**CNS depressant**
51
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
52
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
53
The centrally-acting spasmolytic, Carisprodol, is metabolized to what; why is this useful?
**Meprobamate**, which has **_anxiolytic_** and **_sedative effects_** (used to manage **anxiety** disorders)
54
What is the action of the centrally-acting spasmolytic, Cyclobenzaprine?
_Reduces_ tonic **somatic motor activity** by influencing both **alpha** and **gamma motor neurons**
55
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_**
56
What is significant about the metabolism of the centrally-acting spasmolytic, Cyclobenzaprine?
Metabolized by **CYP450**; use with caution with CYP inhibitors
57
What are 3 AE's of the the centrally-acting spasmolytic, Cyclobenzaprine?
**Drowsiness + dizziness + _xerostomia_**
58
What is the MOA of Diazepam?
Promotes binding of **GABA** to **GABAA receptor** = **↑ frequency** of channel openings --\> **↑ inhibitory transmission** and **↓ spasticity**
59
What 4 effects does Diazepam have?
- **Sedation** - **Muscle relaxation** - **Anxiolytic** - **Anticonvulsant**
60
What are the effects of the α2-adrenergic agonist, Tizanidine?
**Drowsiness + hypotension + dry mouth + asthenia/muscle weakness**
61
What is the MOA of Dantrolene?
**- Inhibits** the **ryanodine receptor (RyR)** --\> _prevents_ release of **Ca2+** from _sarcoplasmic reticulum_ - Impaired **skeletal** muscle contraction; cardiac and smooth m. unaffected
62
What are 3 AE's associated with Dantrolene?
- Generalized muscle weakness - **Sedation** - Occasionally **hepatitis**
63
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
64
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
65
What is Glatiramer Acetate and it's MOA?
- 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
What is the MOA of interferon-beta-1a and beta-1b used for MS?
_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
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**
68
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)

NMSP Exam III*** (20 decks)

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