Pharm - Muscle Relaxants Flashcards

1
Q

compare MOA between non-depolarizing and depolarizing neuromuscular blocking agents

A

non-depolarizing: antagonists of nAChR

depolarizing: excess of depolarizing agonist (e.g. excess acetylcholine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

list the long acting non-depolarizing neuromuscular blocking agents

A

doxacurium, pancuronium, pipecuronium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

list the intermediate acting non-depolarizing neuromuscular blocking agents

A

atracurium, cisatracurium, rocuronium, vecuronium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

list the short acting non-depolarizing neuromuscular blocking agents

A

mivacurium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how are non-depolarizing neuromuscular blocking agents reversed

A

addition of acetylcholine using an AChE inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

adverse effects non-depolarizing neuromuscular blocking agents

A
  • some produce histamine –> bronchospasm, hypotension, bronchial and salivary secretion
  • large doses tubocurarine –> acetylcholine receptor blockade at autonomic anglia and adrenal medulla –> fall in blood pressure and tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

drug-drug interactions with non-depolarizing neuromuscular blocking agents

A

inhaled anesthetics potentiate the neuromuscular blockade

antibiotics (aminoglycosides)

other agents that block signaling at NMJ (tetrodotoxin, local anesthetics, botulinum toxin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

which inhaled anesthetic has the worse drug-drug interaction with non-depolarizing neuromuscular blocking agents

A

isoflurane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

in what patients is there enhancement of the effects of non-depolarizing neuromuscular blocking agents

A
  • elderly pts with reduced hepatic and renal function

- pts with myasthenia gravis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what patients are resistant to non-depolarizing neuromuscular blocking agents

A

pts with severe burns and those with upper motor neuron dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe phase I and phase II of succinylcholine action

A

phase I: activates nAChR –> muscle contraction –> membranes stay depolarized and unresponsive to subsequent impulses –> flaccid paralysis results

phase II: continued exposure to succinylcholine –> membrane becomes re-polarized –> membrane unable to de-polarize b/c desensitization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

indications succinylcholine

A

rapid sequence induction and quick procedures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

adverse effects succinylcholine

A

CV: arrhythmias, negative inotropic and chronotropic effects

metabolic: hyperkalemia

CNS: increase intraocular pressure, muscle pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

contraindications succinylcholine

A

fmhx malignant hyperthermia

myopathies with elevated CPK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

black box warning for succinylcholine

A

acute rhabdomyolysis w/ hyperkalemia followed by ventricular dysrhythmias, cardiac arrest, and death

**seen in children w/ undiagnosed skeletal muscle myopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

drug-drug interactions succinylcholine

A

volatile anesthetics –> malignant hyperthermia

antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the three subgroups of acetylcholinesterase inhibitors

A

alcohols, carbamic acid esters, organophosphates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

compare the duration of action between the acetylcholinesterase inhibitors

A

alcohols: 2-10 minutes

carbamic acid esters: 30m-8hours

organophosphates: bind covalently and reversal of binding requires rapid administration of pralidoxime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

tx for myasthenia gravis

A

pyridostigmine, neostigmine, ambenonium

20
Q

the edrophonium test is used to test for

A

myasthenia gravis

21
Q

what all are AChE inhibitors indicated for

A

1) myasthenia gravis
2) reversal of pharmacologic paralysis
3) glaucoma
4) dementia
5) antidote

22
Q

in what conditions are AChE inhibitors used for reversal of pharmacological paralysis

A

paralytic ileus

atony of urinary bladder

congenital megacolon

23
Q

drug-drug interactions with AChE inhibitors

A

non-depolarizing neuromuscular blocking agnets

succinylcholine (AChEI enhances phase I and antagonizes phase II)

cholinergic agonists (AChEI enhances them)

beta blockers (AChEI enhances bradycardia)

24
Q

treatment for AChE inhibitors overdose

A

atropine

cholinesterase regenerators are administered to regenerate AChE at the NMJ

25
Q

what is the cholinesterase regenerator used to regenerate AChE at the NMJ

A

pralidoxime

26
Q

MOA baclofen

A

GABA-A agonist

27
Q

adverse effects baclofen

A

drowsiness, increased seizure activity in epileptic pts, vertigo, dizziness, psych problems, insomnia, slurred speech, ataxia

28
Q

adverse effects carisoprodol

A

dizziness and drowsiness

29
Q

metabolism carisoprodol

A

CYP2C19

30
Q

MOA chlorzoxazone

A

depresses polysynaptic reflexes in spinal cord

31
Q

MOA cyclobenzaprine

A

reduces tonic somatic motor activity by influencing alpha and gamma motor neurons

32
Q

metabolism cyclobenzaprine

A

CYP450

33
Q

adverse effects cyclobenzaprine

A

drowsiness, dizziness, xerostomia (dry mouth)

34
Q

MOA tizanidine

adverse effects

A

alpha 2 agonist

drowsiness, hypotension, dry mouth, muscle weakness

35
Q

MOA dantrolene

A

inhibition of RyR –> blocks release of Ca2+ through sarcoplasmic reticulum –> impairs muscle contraction

36
Q

side effects dantrolene

A

muscle weakness, sedation

37
Q

indications dantrolene

A

treats spasticity associated with upper motor neuron dzs

malignany hyperthermia

38
Q

MOA botulinum toxin

A

cleaves component of SNARE complex involved in exocytosis –> prevents release of ACh

39
Q

clinical uses botulinum toxin

A

strabismus, blepharospasm, chronic migraine, cervical dystonia

40
Q

indications and MOA azathioprine

A

RA and MS

antagonizes purine metabolism and inhibits synthesis of DNA, RNA, and proteins

41
Q

indications and MOA dalfampridine

A

MS

K+ channel blocker –> delays re-polarization and prolongs duration of action potentials

42
Q

indications cyclophosphamide

A

MS

43
Q

indications and MOA glatiramer acetate

A

MS

induces and activates T-lymphocyte suppressor cells specific for a myelin antigen

44
Q

MOA interferons

A

act on BBB by interfering with T cell adhesion to the endothelium by binding to VLA-4 on T cells, or by inhibited T cell expression of MMP

45
Q

indications and MOA mitoxantrone

A

intercalates into DNA resulting in cross-links and strand breaks

MS

46
Q

indications and MOA natalizumab

A

monoclobal antibody against alpha-4 subunit of integrin molecules –> blocks integrin association with vascular receptors, limiting adhesion and transmigration of leukocytes

MS