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Pharmacology > MSK: Skeletal Muscle Relaxants > Flashcards

MSK: Skeletal Muscle Relaxants Flashcards

1
Q

What is the root word of all the non-depolarizing neuromuscular blockers?

A

-cur-

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2
Q

What is the only depolarizing neuromuscular blocker?

A

Succinylcholine

-activates receptor so you will see things like muscle fasiculations

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3
Q

What are the centrally acting spasmolytics? (5)

A 
Baclofen
Carisprodol
Cyclobenzaprine
Diazepam
Tizanidine
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4
Q

What are the non-centrally activating spasmolytics? (2)

A

Dantrolene

Botulism toxin

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5
Q

What are the immunologic drugs for MS? (according to Kruse)

A

Glucocorticoids
Glatiramer Acetate
Interferons (beta)
Mitoxantrone

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6
Q

How do the non-depolarizing (-curarines) work to cause muscle paralysis?

A

Prevents acess to ACh as a pure antagonist effect

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7
Q

What is the effect of succinylcholine on muscles?

A

Excess depolarization causes flaccid paralysis

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8
Q

Which neuromuscular blocker is fastest onset, and has shortest duration?

A

Succinylcholine

-used when inducing intubation due to rapid on and off effects

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9
Q

What drugs are the intermediate acting neuromuscular blockers? (4)

A

Atracurium
Cisatracurium
Rocuronium
Vecuronium

Great for adjuncts to general anesthesia to do intermediate duration

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10
Q

Which class of neuromuscular blockers cause the least amount of histamine to be released with them?

A

Steroid derivatives

-Pancuronium, Pipercuronium, Rocuronium, and Vecuronium

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11
Q

How do you reverse the neuromuscular blockade?

A

Cholinesterase inhibitor (-stigmine) + Anticholinergic (atropine, glycopyrrolate) to reduce effects of Ach at mAChRs

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12
Q

Why do some people have prolonged effects from succinylcholine?

A

They have a polymorphism in pseudocholinesterase

  • cannot break down succinylcholine as fast
  • -just wait it out, and eventually they will have less paralysis
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13
Q

Describe the phases of succinylcholine

A

Phase 1=depolarizing
-this phase produces the flaccid paralysis

Phase 2=desensitizing
-nerves become less sensitized, and membrane becomes repolarized

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14
Q

Which phase (1 or 2) can be reversed with cholinesterase inhibitors?

A

Phase 2

-phase 1 is not affected

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15
Q

Ambenonium, Echothiophate, and tacrine MOA?

A

AChE inhibitors

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16
Q

Donepezil, galantamine, and Rivastigmine MOA? Clinical Use?

A

AChE inhibitors used in Alzheimer’s

17
Q

Physostigmine, Pyridostigmine, neostigmine, and edrophonium MOA? clinical use?

A

AChE inhibitors;

  • can be used to reverse pharmacologic paralysis
  • Mysthenia Gravis
  • Antidote to anticholinergic poisoning
18
Q

Baclofen MOA? Adverse effects?

A

GABAb agonist resulting in inhibition of excitatory NT release

Adverse: drowsiness and increased seizure activity in epileptics

19
Q

Carisoprodol Clinical use?

A

Spasmolytic and has anxiolytic effect

20
Q

Adverse effects of carisoprodol?

A

Addictive potential

21
Q

Clinical use of Cyclobenzaprine?

A

Spasmolytic

22
Q

Adverse effects of cyclobenzaprine?

A

Drowsiness, dizziness, xerostomia

23
Q

MOA of diazepam? Adverse effects?

A

MOA: GABAa receptor agonist; decreases excitatory NTs

Adverse: CNS depression

24
Q

MOA of tizanidine? Adverse effects?

A

MOA: a2 agonist used as antispasmotic

Adverse: CNS depression, hypotension, dry mouth

25
Q

MOA of glatiramer acetate for MS?

A

mixture of random polymers of four amino acids thought to induce and activate T-cell supressors specific for a myelin antigen

26
Q

MOA of interferons for MS?

A

Act on blood brain barrier by interfering with T-cell adhesion to endothelium, or by inhibiting T-cell expression of myelin basic protein

27
Q

MOA of mitoxantrone for MS?

A

Intercalates into DNA resulting in cross-links and strand breaks
-decreases immune response by causing apoptosis in lymphocytes

28
Q

Clinical use of diazepam?

A

Sedation, muscle relaxant, anxiolytic, and anti-convulsant (status epilepticus)

29
Q

MOA of Dantrolene

A

Binds to RYR receptor to block release of calcium into muscle cell
-less contraction

30
Q

Clinical use of dantrolene

A

Spasticity and treatment for malignant hyperthermia**

31
Q

MOA of Botulism toxin?

A

cleaves SNARE proteins, prevents release of ACh into synaptic cleft
-reduces muscle spasms

32
Q

Carisoprodol is metabolized into________ to cause it’s anxiolytic effects (in addition to its antispasmodic effects)?

A

Meprobamate

33
Q

Which drug class are useful in paralyzing the diaphragm during surgery?

A

Neuromuscular blocking drugs (both depolarizing and nondepolarizing)

  • curonium or -curare
  • succinylcholine

Pharmacology (50 decks)

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