Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MNI (neuro pharm) > L20- Skeletal Muscle Relaxants > Flashcards

L20- Skeletal Muscle Relaxants Flashcards

1
Q

name the two types of skeletal muscle relaxants and their uses (include subtypes)

A

Neuromuscular Blockers: surgical procedures and in ICUs –> paralysis

  • agonists - depolarizing blocker
  • antagonists - non-depolarizing blocker

Spasmolytics: reduce spasticity in variety of neurological conditions

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

list the non-depolarizing blockers

A 
(antagonists)
Benzylisoquinolines:
-mivacurium
-atracurium, cisatracurium
-tubocurarine (prototype)

Ammonio-steroids:

  • rocuronium, vocuronium
  • pancuronium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

______ is the only depolarizing blocker, include structure

A

succinylcholine: 2 ACh molecules linked end-to-end

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

Non-depolarizing blockers work as (1) agents at NMJ. (2) is the prototype. Their effects can be overcome by (3), as seen with the use of (4) drugs, often used for recovery post-anesthesia.

A

1- competitive antagonists at AChR
2- tubocurarine
3- inc [ACh] in synapse
4- neostigmine, edrophonium (AChE inhibitors)

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

describe the effect of non-depolarizing blockers on muscles during anesthesia

A
  • first cause motor weakness
  • skeletal muscles become totally flaccid
  • inexcitable to stimulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Succinylcholine is an agonist of (1) receptors, initially causing (2) in muscles. Since succinycholine is not readily (3) in the synapse, (4) continues and (5) is the end result.

A 
1- nAChR
2- fasciculations
3- metabolized by AChE
4- membrane remains depolarized --> unresponsive to additional impulses
5- flaccid paralysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

discuss the onset and duration of action of succinylcholine, explain

A

Onset- rapid, <1 min

Duration: rapid, 5-10 mins — rapid hydrolysis via plasma pseudocholinesterases (BChE)

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

Neuromuscular blockers:

  • (1) is an important group that gives the agents strong (polar/non-polar) qualities
  • due to this quality, (3) and (4) are the main drawbacks
  • (5) is the main benefit of this quality (hint- related to (4))
A

1- quaternary ammonium
2- highly polar – poorly soluble in lipids
3- inactive if given by mouth — give IV, IM
4- penetrates cell membranes poorly
5- doesn’t cross BBB

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

list the non-depolarizing blockers by duration of action

A

Short: mevacurium

Intermediate:

  • atracurium, cisatracurium
  • rocuronium, vecuronium

Long:

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

describe the mechanism of elimination of each benzylisoquinoline and relationship to duration of action

A

Mivacurium- plasma pseudocholinesterases, 15min

Atracurium- enzymatic, non-ezymatic ester hydrolysis, 45min
Cisatracurium- spontaneous (80%), renal, 45min

Tubocurarine- renal, hepatic, 80min

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

______ is a non-depolarizing blocker that can degrade spontaneously

A

cisatracurium

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

describe the mechanism of elimination of each ammonio-steroid and relationship to duration of action

A

Recuronium, Vecuronium: hepatic (80%), renal; 30min, 45min respectively

Pancuronium: renal (80%), hepatic, 90min

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

Atracurium may produce (1) as one of its metabolites that can cause (2). (3), a stereoisomer of atracurium forms much less (1) in addition to a decrease in (4) release. Therefore (3) has mostly replaced atracurium.

A

1- laudanosine
2- hypotension, seizures
3- cisatracurium
4- histamine release

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

(1) is the only short-acting non-depolarizing blocker due to its hydrolysis via (2).

A

1- mivacurium

2- plasma BChE // plasma pseudocholinesterases — short b/c metabolism is not dependent on liver, kidney

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

(1) has the most rapid onset among the non-depolarizing blockers, and can be used as an alternative for (2) in (3) situations

A

1- rocuronium
2- succinylcholine
3- rapid sequence intubation

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

what is the key factor to investigate in patients before giving a short-acting neuromuscular blocker (name them) and how would it be treated

A

succinylcholine and mivacurium:

  • BChE polymorphisms / variants => prolonged action of these neuromuscular blockers
  • must check FHx

-treat with mechanical ventilation until muscle function returns

17
Q

(1) is the main AE seen with benzylisoquinolines due to (2) and (3) activity
(4) is the main AE seen with ammonio-steroids due to (5) actions; (4) may possibly develop into (6)

A

1- hypotension
2- histamine release
3- ganglionic blockade

4- tachycardia
5- M2 blockade
6- arrhythmias

18
Q

(1) is often given before the administration of benzylisoquinolines in order to avoid (2). (3) list strength of the effect based on each agent.

A

1- antihistamine
2- hypotension via histamine release
3- tubocurarine&raquo_space; mevacurium, atracurium

19
Q

(1) neuromuscular blocker may block nAChRs in (2) areas in order to cause hypotension and (3)

A

(ganglion blockade)
1- tubocurarine
2- autonomic ganglia, adrenal medulla
3- reflex tachycardia

20
Q

(1) is a neuromuscular blocker that can cause moderate tahycardia due to (2) mechanism, although (3) is usually not an issue with (1) in general

A

1- pancuronium
2- M2 blockade
3- CVS effects usually not an issue

21
Q

Succinylcholine:

  • (1) mechanism of AEs
  • (2) importantly absent group of AEs
A

1- activates nAChR in SNS/PSNS ganglia and mAChR in heart (+ histamine release)

2- CNS effects, doesn’t cross BBB

22
Q

list the many AEs of succinylcholine based on MOA

A

nAChR: muscle pain (irregular contraction –> K+ release), hyperkalemia, inc intraocular P (EOM contractions), inc intragastric P, malignant hyperthermia

mAChR: bradycardia

Histamine release

23
Q

list the drugs that enhance neuromuscular blockade

A
  • inhaled anesthetics
  • aminoglycosides
  • tetracyclines
24
Q

Name the disease or process that has the following effects on non-depolarizing neuromuscular blockers:

  • (1) inc neuromuscular blockade
  • (2) prolongs blockade due to dec drug clearance
  • (3) and (4) patients are resistant to non-depolarizing muscle relaxants due to proliferation of (5)
A

1- myasthenia gravis
2- ageing

3- severe burns
4- UMN injury
5- extrajunctional receptors

25
Q

list the contraindications to non-depolarizing neuromuscular blockers

A
  • h/o malignant hyperthermia
  • h/o skeletal muscle myopathies
  • major burns
  • multiple traumas
  • denervation of skeletal muscle
  • UMN injury
26
Q

list the main uses of neuromuscular blockers

A

1) ALL- adjuvants in surgical anesthesia –> skeletal muscle relaxation
2) Succinylcholine- facilitate endotracheal intubation during anesthesia induction + used in ECT

27
Q

______ is often given after completion of surgical procedure to reverse muscular blockade

A

(AChE inhibitors)
neostigmine
edrophonium

28
Q

______ are often given during anesthesia with neuromuscular blockers in order to prevent bradycardia

A

(ammonio-steroids blockade – need antimuscarinics to prevent M2 blockade)

  • atropine
  • glycopyrrolate
29
Q

list the Spasmolytic drugs: act on CNS for chronic spasms

A
  • diazepam
  • baclofen
  • tizanidine
30
Q

list the Spasmolytic drugs: act on skeletal muscle for chronic spasms

A
  • dantrolene

- botulinum toxin

31
Q

Chronic Spasms, CNS:

______ facilitates action of GABA via GABA(a) receptor modulation

A

diazepam

32
Q

Chronic Spasms, CNS:

______ is a GABA agonist at GABA(b) receptors

A

baclofen

33
Q

Chronic Spasms, CNS:

______ is an agonist at α2-adrenoreceptors

A

tizanidine- inhibits neurotransmitter release

34
Q

Dantrolene:

  • (1) uses
  • (2) MOA
A

1- chronic muscle spasms; malignant hyperthermia

2- binds ryanodine receptor in SR of skeletal muscle –> prevents Ca release from SR

35
Q

(1) has been used increasingly more for generalized spastic disorders like cerebral palsy by working on skeletal muscles with (2) actions

A

1- botulinum toxin

2- prevents ACh release

36
Q

Acute muscle spasms:

  • (1) is the main cause
  • (2) is the location drugs primarily act, (3) is the prototype – structurally related to (4)
  • (3) has strong (5) AEs
A 
1- local trauma, strain
2- brainstem
3- cyclobenzaprine
4- TCAs
5- antimuscarinic AEs

MNI (neuro pharm) (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions