Muscle Relaxers

Question 1

What are the centrally acting spasmolytics? (5)

Answer 1

Baclofen
Carisprodol
Cyclobenzaprine
Diazepam
Tizanidine

Question 2

Baclofen
MOA
Uses
AE

Answer 2

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)

Question 3

Carisprodol
MOA
Kinetics
AE

Answer 3

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

Question 4

Cyclobenzaprine
MOA
Kinetics
AE

Answer 4

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)

Question 5

Diazepam
MOA
Effects

Answer 5

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

Question 6

Tizanidine
MOA
AE

Answer 6

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

Question 7

What are the 2 non-centrally acting spasmolytics?

Answer 7

Dantrolene

Botulinum Toxin

Question 8

Dantrolene
MOA
Uses
AE

Answer 8

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

Question 9

Botox
MOA
Uses
AE

Answer 9

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

Question 10

What are the 4 immuno agents used to treat MS?

Answer 10

Glucocorticoids
Glatiramer acetate
IFN
Mitoxantrone

Question 11

Glucocorticoids

-how do you use them for MS

Answer 11

Glucocorticoids

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

Question 12

Glatiramer acetate

MOA

Answer 12

Glatiramer acetate

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

Question 13

IFN
MOA
Actions

Answer 13

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

Question 14

Mitoxantrone
MOA
Uses

Answer 14

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

Question 15

Nondepolarizing Neuromuscular Blockers
General nomenclature
MOA
Kinetics
AE

Answer 15

Nondepolarizing NM blockers
“Curium” “curines” “curarine”
MOA- nAchR antagonists
Kinetics- given parenterally
AE- histamine mediated effects, hypotension, tachycardia

Question 16

A, C, D, and M “curiums”

• what type of NM blocking agents are these
• which are short, long, and intermediate acting

Answer 16

Nondepolarizing NM blockers
A-curium- intermediate acting
C-curium- intermiediate acting
D-curium- long-acting (not used often)
M-curium- short acting

Question 17

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

Answer 17

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

Question 18

What is the depolarizing neuromuscular blocker?

Answer 18

Succinylcholine

Question 19

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

Answer 19

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

Question 20

How do you treat malignant hyperthermia

Answer 20

Dantrolene

Question 21

AChE-I

3 subclasses and examples of each

Answer 21

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

Question 22

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

Answer 22

Quad charged

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

Tertiary uncharged

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

Question 23

AChE-I
MOA
Duration of action based off subclass

Answer 23

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

Question 24

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

Answer 24

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

Question 25

What drug is used to reverse neuromuscular blocking drug induced paralysis

Answer 25

N-stigmine

Question 26

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

Answer 26

Physostigmine

Question 27

AE of AChE-I

What is used to treat AChE-I AE

Answer 27

Miosis, salivation, sweating, bronchoconstriction

Treat w/ atropine