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Kirstys Flashcards > CPT1: muscle relaxants > Flashcards

CPT1: muscle relaxants Flashcards

1
Q

What do muscle relaxants do?

A

Cause skeletal muscle relaxation

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2
Q

What classes of muscle relaxants are there?

A
  • Centerally acting: acting on the CNS
  • Peripherally acting: act on muscle or neuromuscular junction
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3
Q

What can centerally acting drugs be used for?

A

To treat chronic severe muscle spasms from a variety of causes: (PITA)

  • pain
  • inflammation
  • anxiety
  • trauma

most commonly used for MS

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4
Q

What are the pharmacokinetics of centerally acting muscle relaxants

A

Drug absorebd rapidly from GI tract; distributed widely’ metabolised minimly by liver; excreted in urine

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5
Q

What are examples of centerally acting muscle relaxants?

A

Baclofen

tizanidine

diazepam

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6
Q

What is the mechanism of action of baclofen

A

Baclofen is a GABA agonist. It binds to the GABA receptor and activates it. This causes Cl- influx which leads to membrane polarisation, loss of excitbility and less NT being released. THere is therefore less NT to act on skeletal muscle and cause contraction

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7
Q

How does Diazepam work?

A

Positive allosteric modulator. BInds to BZ binding site on the GABA receptor and facilitates GABA binding. This allows Cl- infulx, membrane hyperpolarisaiton, decrease in excitability and less NT released to act on skelteal muscle

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8
Q

How does Tizanidine work?

A

a2 agonist. Therefore limits NT release which reduces excitability of motor neurone and therefore reducing stimulation of skeletal muscle

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9
Q

What drug interactions occur with centerally acting muscle relaxants?

A
  • CNS depression when taken with other CNS depressants
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10
Q

What are side effects of Centerally acting muscle relaxants?

A
  • Dependance
  • drowsiness
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11
Q

What i the drug of choice to treat spacicty?

A

Dantrolene sodium

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12
Q

What is an example of a peripherally acting drug which acts on the muscle directly?

A

Dantrolene sodium

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13
Q

What is the pharmacokinetics of muscle peripheral drugs?

A
  • absorbed poorly from GI tract; highly protein bound; metabolised by liver; excreteed in urine
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14
Q

what are mucle peripheral drugs mechanism of action?

A

Acts on muscle reducing contractility by interfering with the ability of the sarcoplasmic recticulm to release Ca2+ ions via ryanondine receptors

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15
Q

What are peripharal muscle drugs used for?

A
  • MS
  • cerebral palsy
  • spinal cord injury
  • stroke
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16
Q

What are drug interactions with peripheral muscle muscle relaxants?

A

When taken with CNS depressants can result in sedation, lack of cooridination and resipraotry depression

17
Q

What classes of neuromuscular blocking drugs is there?

A
  • Non depolarising
  • depolarising
18
Q

What classes of non-depolarising muscular blocking drugs is there? what drugs are in these?

A

Aminosteriod

  • pancuronium
  • Rocuronium
  • Vecuronium

Benzylisoquinolinium

  • Atracurium
  • Cisatracurium
  • gallamine
  • micacurium
19
Q

What are depolarising neuromuscular blocking drugs?

A

suxamethonium

20
Q

How do non-depolarising neuromuscular blocking drugs work?

A

They are competivie antagonists of Ach and compete with Ach for the nicotinic acetylcholine receptor and bind to it preventing Ach from binding. There is no conformational change in the receptor leading to influx of Na+ ions in the skeltal muscle so no activation of dihydropyrindine or ryanidine receptors therfore no contraction

21
Q

How do depolarising neuromuscular blocking drugs work?

A

They bind to the NCR receptors and generate an action potential (increase permebability to Na and K). However, because they are not metabolized by acetylcholinesterase, the binding of this drug to the receptor is prolonged resulting in an extended depolarization of the muscle end-plate. As the muscle relaxant continues to bind to the ACh receptor, the end plate cannot repolarize, resulting in a phase I block.

Muslce fibres become insensitive to stimulation

22
Q

What are the major indications for neuromuscular blocking drugs?

A
  • Relax skeletal mucle during surgery
  • reduce intensity of muscle spasms
  • manage patinets fighting the use of a ventilator to help breathing
23
Q

Clinical uses of neuromuscular blocking drugs

A
  • endotracheal intubation
  • dislocated joint
  • in adjunction to anaesthesia
  • eyeball imbolisation prior to eye surgey
  • convulsion control
24
Q

What are cholinesterases in the CNS and periphry called?

where are these found?

A
  • CNS - acetylcholinesterases
  • Peripheral - butyrylcholinesterases
  1. AchE - soluble near nerve terminals and around CSF
  2. BchE - soluble in plasma
25
Q

What effect do AchE have on depolarising anf non-depolarising NBD

Most common AchE

A
  • Reverses the effect of nondepolarising NBD
  • Prolongs the effects of depolarising NBD

Suxamethonium made form 2 Ach molecules so normally hydrolysised and removed by cholinesterases. but AchEs prevent this and prolong its effect

Neostigmine

26
Q

What are the properties required for a NBD

A
  • competitve
  • specific for skeletal muscle NCR
  • consistant response
  • rapid onset of action
    *
27
Q

Where are Non-depolarising NBD dervived from?

A
  • curare alkaloids
  • prototype - tubocurarine
28
Q

What are the pharmacokinetics associated with non-depolarising NBD?

A

administered parentally; distrubuted rapidly throughout the body; mostly excreted unchanged in urine

29
Q

What are drug interactions with non-depolarising NBD

A

aminoglycoside antibiotics and anestheitcs exagerate neuromuscular blockage

30
Q

What are side effects of non-depolarising NBD

A
  • apnea
  • hypotension
  • bronchospasm
31
Q

What are side effects of depolarising NBD

A
  • Stimulates all cholinergic recptors - bradycardia
  • Causes net loss of K+ from muscle (hyperkalmeia) resulting in cardiac dshythmias
  • increased intra ocular pressure
  • muscule pain
  • prolong paralysis when cholinesterase activity reduced
  • malignant hyperthermia
  • suxamethonium produces intense muscle spasms and rise in body temp
32
Q

What is the choice of drug for short term muscle relaxants?

A

Suxamethonium

33
Q

What is the pharmacokinetics of depolarising NBD?

A

Iv or IM; hydroylsed liver and plasma by psedocholonersterases; excreted in kigney

34
Q

What side effect occur with depolarising drugs?

A

apnea, hypotnesion, trachy cardia (1st dose), bradycardia (2nd dose)

35
Q

What are drug interactions with depolarising NBD

A

potientiated by anesthetics and antibiotitcs

36
Q

What are the duration of action and elimation routes for NBD?

A

SAVGTP

  • Suxamethonium (shortest)
  • Atracurium
  • vecuronium
  • Gallamine
  • Tubocurarine
  • Pancuronium (longest)
37
Q

What are the elimination routes of NBD

A
  • Suxamethonium - plasms cholinesterase hydrolysis
  • Gallamine & Pancuronium - renal
  • Tubocurarine & Vecuronium - hepatic
  • Atracurium - spontaneous hydrolysis in plasma

Kirstys Flashcards (116 decks)

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