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Flashcards in Muscle Relaxers Deck (27)
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1
Q

What are the centrally acting spasmolytics? (5)

A
Baclofen
Carisprodol
Cyclobenzaprine
Diazepam
Tizanidine
2
Q

Baclofen
MOA
Uses
AE

A

Baclofen
MOA- GABAb-R agonist causes hyperpolarization and inhibits release of excitatory NT
Uses- reduce spasticity w/o causing sedation
AE- dizzy, drowsy, seizure in epileptics (withdraw slowly)

3
Q

Carisprodol
MOA
Kinetics
AE

A

Carisprodol
MOA- CNS depressant
Kinetics- metabolized by cyp2c so use w/ caution if using cyp inhibitors; metabolized into meprobamate which can manage anxiety disorders
AE- addictive (use only short term), dizzy, drowsy

4
Q

Cyclobenzaprine
MOA
Kinetics
AE

A

Cyclobenzaprine
MOA- reduces tonic somatic motor activity by acting on alpha/gamma motor neurons
Kinetics- metabolized by cyp450 so use w/ caution in pt on cyp inhibitors
AE- similar to TCAs (sedation, visual hallucinations), drowsy, dizzy, xerostomia (dry mouth)

5
Q

Diazepam
MOA
Effects

A

Diazepam
MOA- promotes GABA binding GABAa-R to inc inhibitory transmission and reduce spasticity
Effects- sedation, m relaxation, antianxiety, and anticonvulsant

6
Q

Tizanidine
MOA
AE

A

Tizanidine
MOA- a2-adrenergic agonist dec excitatory input
AE- drowsy, hypotension, dry mouth, m weakness

7
Q

What are the 2 non-centrally acting spasmolytics?

A

Dantrolene

Botulinum Toxin

8
Q

Dantrolene
MOA
Uses
AE

A

Dantrolene
MOA- inhibitors ryanadine R to block Ca release and m contraction w/o affecting cardiac or smooth m
Uses- UMN spasticity assoc w/ spinal injury, stroke, cerebral pasly, and MS; and malignant hyperthermia
AE- weakness and sedation

9
Q

Botox
MOA
Uses
AE

A

Botox
MOA- cleaves snare proteins involved in exocytosis to prevent release of Ach
Uses- strabismus, wrinkles, cervical dystonia, hyperhidrosis, chronic migraines
AE- weakness that can last months

10
Q

What are the 4 immuno agents used to treat MS?

A

Glucocorticoids
Glatiramer acetate
IFN
Mitoxantrone

11
Q

Glucocorticoids

-how do you use them for MS

A

Glucocorticoids

Monthly bolus IV of methylprednisolone to treat primary/secondary progressive MS

12
Q

Glatiramer acetate

MOA

A

Glatiramer acetate

Activats T lymphocyte suppressor cells specific to myelin Ag a nd interfere w/ Ag presentation

13
Q

IFN
MOA
Actions

A

IFN a and b
MOA- act on BBB by binding VLA4 on T cells and inhibiting T cell expression of MMP( blocks T cell adhesion)
Actions- reduces relapse, reduces new MRI T2 lesions and volume of T2 lesions, reduces Gd enhancing lesions, and slows brain atrophy

14
Q

Mitoxantrone
MOA
Uses

A

Mitoxantrone
MOA- intercalates into DNA to form cross-links and cause strand breaks
Uses- anti-neoplastic, MS, AML, prostate cancer

15
Q
Nondepolarizing Neuromuscular Blockers
General nomenclature
MOA
Kinetics
AE
A
Nondepolarizing NM blockers
“Curium” “curines” “curarine”
MOA- nAchR antagonists
Kinetics- given parenterally
AE- histamine mediated effects, hypotension, tachycardia
16
Q

A, C, D, and M “curiums”

  • what type of NM blocking agents are these
  • which are short, long, and intermediate acting
A
Nondepolarizing NM blockers
A-curium- intermediate acting
C-curium- intermiediate acting
D-curium- long-acting (not used often)
M-curium- short acting
17
Q

What are the steroid derivative non-depolarizing neuromusuclar blockers?
Which are intermediate or long acting; which has the fastest onset

A

Coruniums
V and R coruniums- intermediate
P coruniums- long acting
R corunium- most rapid onset

18
Q

What is the depolarizing neuromuscular blocker?

A

Succinylcholine

19
Q
Succinylcholine
Kinetics
Dynamics (target, PhaseI and phaseII)
Uses
AE (CI and black box)
A

Succinylcholine
Kinetics- very short duration of action
Dynamics- nAchR agonist
Phase1- activate nAchR->depolarize->flaccid paralysis
Phase2- desensitizes receptor preventing membrane depolarization; reverse w/ AchE-I
Uses- emergency surgery and quick surgery
AE- arrhythmias, hyperkalemia, inc intraocular and gastric pressure
CI- FH of malignant hyperthermia and w/ acute injury
Black box- cardiac arrest risk due to acute rhabdomylolysis and hyperkalemia in kids w/ skeletal myopathy

20
Q

How do you treat malignant hyperthermia

A

Dantrolene

21
Q

AChE-I

3 subclasses and examples of each

A

AChE-I
Alcohols- edrop
Carbamic acids- stigmines
Organophosphates- echo

22
Q

AChE-I Kinetic Classes
Quad charged- CNS distribution? Examples
Tertiary uncharged- CNS? Examples

A

Quad charged

  • NO CNS
  • N/P stigmine, edrop, echo, ambenonium

Tertiary uncharged

  • CNS distribution
  • physostigmine, donepezil, tacrine, r-stigmine, galatamine
23
Q

AChE-I
MOA
Duration of action based off subclass

A

AChE-I
MOA- inhibit AChE-I
Alcohols- short acting (10 min)
Carbamic acids- intermediate (30 min-8hr)
Organophosphates- irreversible inhibitors require pralidoxime

24
Q

Treatment of myasthemia gravis
Drugs
Diagnostic test and results for comparing myasthenic vs cholinergic crisis

A

Myasthenia gravis
(P/N stigmine and ambenomium)
Edrop test- symptoms improve if m gravis

25
Q

What drug is used to reverse neuromuscular blocking drug induced paralysis

A

N-stigmine

26
Q

What is the preferred AChE-I used as an antidote to anticholinergic agents

A

Physostigmine

27
Q

AE of AChE-I

What is used to treat AChE-I AE

A

Miosis, salivation, sweating, bronchoconstriction

Treat w/ atropine