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Pharmacology > SKELETAL MUSCLE RELAXANTS > Flashcards

SKELETAL MUSCLE RELAXANTS Flashcards

1
Q

Define 2 types of skeletal muscle relaxants?

A

• Neuromuscular blockers. Used during surgical procedures and in ICUs to cause paralysis.
• Spasmolytics.
Used to reduce spasticity
in a variety of neurologic conditions.

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2
Q

Division of skeletal muscle relaxants and types?

A

Neuromuscular blockers
Antagonists (Non depolarizing blockers)
Agonists (Depolarizing blockers)

Spasmolytics
For chronic spasm
For acute spasm

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3
Q

CHEMISTRY: NON-DEPOLARIZING BLOCKERS

CHEMISTRY: DEPOLARIZING BLOCKERS?

A

• Non-depolarizing blocking drugs are classified
according to their chemical structure into
benzylisoquinolines and ammonio steroids.

• The depolarizing blocker succinylcholine is two
acetylcholine molecules linked end-to-end.

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4
Q

List 4 Benzylisoquinolones and 3 Ammoni steroids

A 
Benzylisoquinolines Ammonio steroids
Tubocurarine 
Atracurium 
Cisatracurium 
Mivacurium

Ammonio Steroids
Pancuronium
Rocuronium
Vecuronium

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5
Q

MOA NONDEPOLARIZING BLOCKERS

A

• They are competitive antagonists.
• Tubocurarine is the prototype.
• Their action can be overcome by increasing the concentration of acetylcholine in the synapse.
• This can be achieved with neostigmine or
edrophonium.
• During anesthesia, nondepolarizing blockers first cause motor weakness
• Ultimately, skeletal muscles become totally
flaccid and inexcitable to stimulation.

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6
Q

MOA: DEPOLARIZING BLOCKERS?

A

• Succinylcholine activates the nicotinic receptor and depolarizes the junction.
• This causes fasciculations.
• Succinylcholine is not metabolized effectively by
acetylcholinesterase.
• The membrane remains depolarized and unresponsive to additional impulses.
• Flaccid paralysis results.
• The onset of neuromuscular blockade is very
rapid, usually <1 minute.
• Because of its rapid hydrolysis by plasma
pseudocholinesterase, duration of block is 5-10
minutes.

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7
Q

PHARMACOKINETICS OF

NEUROMUSCULAR BLOCKERS?

A

• Neuromuscular blockers contain quaternary
ammonium groups.
• They are highly polar and poorly soluble in lipid.
• Inactive if given by mouth.
• Penetrate membranes very poorly.
• Do not enter cells or cross the BBB.
• Always given IV or IM.

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8
Q

Non depolarizing duration of action

A

SHORT ACTING
Mivacurium

INTERMEDIATE ACTING
Atracurium 
Cisatracurium 
Rocuronium
Vecuronium

LONG-ACTING
Tubocurarine
Pancuronium

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9
Q

Metabolism of Non-depolarizing blockers?

A

• Drugs that are excreted by the kidney typically
have longer half-lives, leading to longer
durations of action.
• Drugs eliminated by the liver tend to have
shorter half-lives and durations of action.

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10
Q

BENZYLISOQUINOLINES Drug, elimination mechanism and duration of action?

A

Atracurium
Enzymatic & nonenzymatic
ester hydrolysis
45 min

Cisatracurium
Spontaneous (80%) and renal
45min

Mivacurium
Plasma pseudocholinesterase
15 min

Tubocurarine
Renal and hepatic
80 min

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11
Q

AMMONIO STEROIDS Drug, elimination mechanism and duration of action?

A

Pancuronium
Renal (80%) and hepatic 90

Rocuronium
Hepatic (80%) and renal 30

Vecuronium Hepatic (80%) and renal 45

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12
Q

Metabolism of Atracurium?

A

ATRACURIUM
• Atracurium is inactivated by hydrolysis by nonspecific plasma esterases and by a
spontaneous reaction.
• No increase in half-life in patients with renal failure.
• One of atracurium metabolites is laudanosine.
• Laudanosine, may cause hypotension and seizures.

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13
Q

Metabolism of Cisatracurium?

A

CISATRACURIUM
• Cisatracurium, a stereoisomer of atracurium
forms much less laudanosine.
• Cisatracurium also causes less histamine release.
• Cisatracurium has largely replaced atracurium in clinical practice.

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14
Q

Metabolism of Mivacurium?

A

MIVACURIUM
• Mivacurium is the only nondepolarizing blocker classified as short acting.
• Hydrolysis by plasma butyrylcholinesterase is the primary mechanism for inactivation.
• Not dependent on liver or kidney.

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15
Q

Metabolism of Rocuronium?

A

ROCURONIUM
• Rocuronium has the most rapid onset among nondepolarizing blockers.
• Can be used as alternative to succinylcholine for
rapid sequence intubation.

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16
Q

Metabolism of Succinylcholine?

A

SUCCINYLCHOLINE
• Succinylcholine has extremely short duration of
action (5–10 minutes).
• Due to hydrolysis by butyrylcholinesterase.

17
Q

Consequence of POLYMORPHISMS OF

BUTYRYLCHOLINESTERASE?

A

• Neuromuscular blockade by succinylcholine and
mivacurium may be prolonged in patients with an abnormal variant of butyrylcholinesterase.
• Treated with mechanical ventilation until muscle function returns to normal.

18
Q

ADVERSE EFFECTS:

NON-DEPOLARIZING BLOCKERS?

A

• Some benzylisoquinolines may cause hypotension due to histamine release and
ganglionic blockade.
• Some ammonio steroids may produce tachycardia due to blockade of muscarinic receptors, which may lead to arrhythmias.

19
Q

ADVERSE EFFECTS:

NON-DEPOLARIZING BLOCKERS in regards to histamine release?

A

HISTAMINE RELEASE
• Tubocurarine, and to a lesser extent, mivacurium and atracurium may release
histamine.
• Antihistamines are useful particularly if given before the neuromuscular blocker.

20
Q

ADVERSE EFFECTS:

NON-DEPOLARIZING BLOCKERS in regards to ganglionic blockade?

A

GANGLION BLOCKADE
• Tubocurarine may block nicotinic receptors of
the autonomic ganglia and the adrenal medulla.
• This causes hypotension and tachycardia.

21
Q

ADVERSE EFFECTS: NON-DEPOLARIZING BLOCKERS

in regards to BLOCKADE OF CARDIAC M2 RECEPTORS

A

BLOCKADE OF CARDIAC M2 RECEPTORS
• The ammonio steroid pancuronium causes
moderate tachycardia due to blockade of cardiac
M2 receptors.
• The cardiovascular effects of pancuronium are
usually not a problem.

22
Q

AE of depolarizing blockers? List 7

A

• Succinylcholine activates all autonomic cholinoceptors:
• Nicotinic receptors in both sympathetic and
parasympathetic ganglia
• Muscarinic receptors in the heart.

  • Bradycardia
  • Histamine Release
  • Muscle Pain
  • Hyperkalemia
  • Increased Intraocular Pressure
  • Increased Intragastric Pressure
  • Malignant Hyperthermia

• No CNS effects due to their inability to penetrate the blood-brain barrier.

23
Q

• Drugs that enhance neuromuscular blockade:?

A
  • Inhaled Anesthetics
  • Aminoglycosides
  • Tetracyclines
24
Q

EFFECTS OF DISEASE AND AGEING ON DRUG RESPONSE?

A

• Several diseases can decrease or increase the
neuromuscular blockade caused by nondepolarizing muscle relaxants.
• Myasthenia gravis increases neuromuscular blockade.
• Advanced age prolongs blockade, probably due
to decreased drug clearance.
• Patients with severe burns and those with upper motor neuron disease are resistant to nondepolarizing muscle relaxants. Due to proliferation of extrajunctional receptors.

25
Q

DEPOLARIZING BLOCKERS:

CONTRAINDICATIONS? List 6

A
  • History of malignant hyperthermia
  • History of skeletal muscle myopathies.
  • Major burns.
  • Multiple trauma
  • Denervation of skeletal muscle
  • Upper motor neuron injury.
26
Q

USES OF NEUROMUSCULAR BLOCKERS

A

• Main clinical use: adjuvants in surgical
anesthesia to obtain relaxation of skeletal muscle.
• Succinylcholine is used to facilitate endotracheal intubation during induction of anesthesia. Also used during ECT.

27
Q

REVERSAL OF NONDEPOLARIZING

NEUROMUSCULAR BLOCKADE?

A

• Upon completion of a surgical procedure neostigmine or edrophonium can be given to reverse competitive blockade.
• Atropine or glycopyrrolate are
used concomitantly to prevent bradycardia.

28
Q

DRUGS FOR CHRONIC SPASM two divisions?

A

• DRUGS THAT ACT IN THE CNS
• DRUGS THAT ACT ON THE SKELETAL
MUSCLE

29
Q

3 drugs that act on cns and moa?

A

DIAZEPAM
• Facilitates action of GABA at GABAa receptors.

BACLOFEN
• GABA agonist at GABAb
receptors.

TIZANIDINE
• Agonist at alpha2-adrenoceptors in the CNS.

30
Q

DRUGS THAT ACT ON THE

SKELETAL MUSCLE and moa?

A

DANTROLENE
• Interferes with the release of Ca2+ by binding to the ryanodine receptor in the
SR of skeletal muscle.
• Also used in malignant hyperthermia.

BOTULINUM TOXIN
• Botulinum toxin is now finding increased application in the treatment of more
generalized spastic disorders, e.g. cerebral palsy.

31
Q

DRUGS FOR ACUTE SPASM?

A 
• Centrally acting drugs.
• Used for relief of acute muscle spasm caused by
local trauma or strain.
• It has been suggested that these drugs act
primarily at the level of the brainstem.
• Cyclobenzaprine is the prototype.
• Structurally related to the TCAs.
• Strong antimuscarinic side effects.

Pharmacology (49 decks)

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