Muscle Relaxers Flashcards
What are the centrally acting spasmolytics? (5)
Baclofen Carisprodol Cyclobenzaprine Diazepam Tizanidine
Baclofen
MOA
Uses
AE
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)
Carisprodol
MOA
Kinetics
AE
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
Cyclobenzaprine
MOA
Kinetics
AE
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)
Diazepam
MOA
Effects
Diazepam
MOA- promotes GABA binding GABAa-R to inc inhibitory transmission and reduce spasticity
Effects- sedation, m relaxation, antianxiety, and anticonvulsant
Tizanidine
MOA
AE
Tizanidine
MOA- a2-adrenergic agonist dec excitatory input
AE- drowsy, hypotension, dry mouth, m weakness
What are the 2 non-centrally acting spasmolytics?
Dantrolene
Botulinum Toxin
Dantrolene
MOA
Uses
AE
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
Botox
MOA
Uses
AE
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
What are the 4 immuno agents used to treat MS?
Glucocorticoids
Glatiramer acetate
IFN
Mitoxantrone
Glucocorticoids
-how do you use them for MS
Glucocorticoids
Monthly bolus IV of methylprednisolone to treat primary/secondary progressive MS
Glatiramer acetate
MOA
Glatiramer acetate
Activats T lymphocyte suppressor cells specific to myelin Ag a nd interfere w/ Ag presentation
IFN
MOA
Actions
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
Mitoxantrone
MOA
Uses
Mitoxantrone
MOA- intercalates into DNA to form cross-links and cause strand breaks
Uses- anti-neoplastic, MS, AML, prostate cancer
Nondepolarizing Neuromuscular Blockers General nomenclature MOA Kinetics AE
Nondepolarizing NM blockers “Curium” “curines” “curarine” MOA- nAchR antagonists Kinetics- given parenterally AE- histamine mediated effects, hypotension, tachycardia
A, C, D, and M “curiums”
- what type of NM blocking agents are these
- which are short, long, and intermediate acting
Nondepolarizing NM blockers A-curium- intermediate acting C-curium- intermiediate acting D-curium- long-acting (not used often) M-curium- short acting
What are the steroid derivative non-depolarizing neuromusuclar blockers?
Which are intermediate or long acting; which has the fastest onset
Coruniums
V and R coruniums- intermediate
P coruniums- long acting
R corunium- most rapid onset
What is the depolarizing neuromuscular blocker?
Succinylcholine
Succinylcholine Kinetics Dynamics (target, PhaseI and phaseII) Uses AE (CI and black box)
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
How do you treat malignant hyperthermia
Dantrolene
AChE-I
3 subclasses and examples of each
AChE-I
Alcohols- edrop
Carbamic acids- stigmines
Organophosphates- echo
AChE-I Kinetic Classes
Quad charged- CNS distribution? Examples
Tertiary uncharged- CNS? Examples
Quad charged
- NO CNS
- N/P stigmine, edrop, echo, ambenonium
Tertiary uncharged
- CNS distribution
- physostigmine, donepezil, tacrine, r-stigmine, galatamine
AChE-I
MOA
Duration of action based off subclass
AChE-I
MOA- inhibit AChE-I
Alcohols- short acting (10 min)
Carbamic acids- intermediate (30 min-8hr)
Organophosphates- irreversible inhibitors require pralidoxime
Treatment of myasthemia gravis
Drugs
Diagnostic test and results for comparing myasthenic vs cholinergic crisis
Myasthenia gravis
(P/N stigmine and ambenomium)
Edrop test- symptoms improve if m gravis
