muscle relaxants Flashcards
what are central muscle relaxants
they cause decreased motor activity or paralysis of voluntary muscles without loss of consciousness
medical uses of central muscle relaxants
- central myorelaxants can potentiate the effect of anaesthetic drugs and combos
- they are also used to control certain spasmodic and painful disorders of skeletal muscles
guaiphenesin effect
- a spinal interneuronal blocking agent, blocks polysynaptic but not monosynaptic relfexes
- effective against convulsion
- paralyses limb muscles, whilst resp muscles unaffected
- consciousness retained
guaiphenesin is effective against convulsion caused by which agents
strychnine and tetanus but not picrotoxin and leptazol
guaiphenesin secondary effect
expectorant
guaiphenesin indications
- horse, cattle, sheep - to adjunct anaesthesia
- dogs - strychnine poisoning
guaiphenesin onset and elimination
fats, 2-4 and 60-80min
guaiphenesin distribution
large distribution, crosses the placenta barrier
guaiphenesin metabolism
conjugation with glucoronide -> excretion with urine
guaiphenesin side effects
- mild at therapeutic dose slight decrease of blood pressure
- only large doses cause resp depression
- haemolysis
guaiphenesin dosing
due to low potency and conc large volume required
baclophen action
- GABAb receptors agonist in the brain and spinal cord
- hyperpolarisation of neurons due to incr K+ ion conductance
- inhibits neural funct presynaptically, by reducing Ca ion influx-> reduced release of excitatory NTs in brain and spinal cord
baclophen analgesic activity
may reduce pain by inhibiting the release of SP in the spinal cord
baclophen therapeutic index
large
baclophen clinical signs of toxicosis
- vomiting
- ataxia
- vocalisation
baclophen indications
- spasm of skeletal muscles or rigidity
- spinal cord injury and pain caused by injuries
- extralabel use in dogs to treat urinary retention by reducing urethral resistance
baclophen dose
1-2mg/kg orally TID
carisoprodol analgesic abilites
especially useful against various types of pain because of its analgesic-sparing effect on opioid analgesics
carisoprodol effect on convulsions
inactive in convulsions caused by strychnine
carisoprodol avaliability
by itself or mixed with aspirin and in one preparation along with codeine and caffeine as well
methocarbamol features
- acts on internunical neurons of the spinal cord
- reduces skeletal muscle hyperactivity without alteration in muscle tone
classes of neuromuscular blocking agents
- depolarising neuromuscular blocking agents
- competitive neuromuscular blocking agents, prototype curare
whats a nicotinic receptor
a transmembrane ion channel receptor, a pentameric asymmetric molecule
where are the ligand occupation sites on nicotinic receptors
alpha units
do depolarising agents or non depolarising agents act similiarly to Ach
depolarising
uses of neuromuscular blocking agents by IV or systemic administration
- adjuvant in surgical anaesthesia to obtain relaxation of skeletal muscle
- balanced anaesthesia, TIVA
- to assist in intubation -esp succinylcholine
- corneal or retinal surgeries to obtain relaxation of extraocular muscles
- therapy of spastic disorders
uses of neuromuscular blocking agents by topical administration
mydriasis in birds and reptiles - only non depolarising
succinylcholine mechanism
- stimulate opening of nicotinic receptors and produce depolarisation of cell membranes
- persists at neuroeffector junction and activates the nicotinic receptor channels cont. - inactivation of voltag egated sodium channels so they cannot reopen to support other action potentials
succinylcholine uses
- IV rapid and short lasting block -Phase 1 block
- used to facilitate intubation
- used illegally in blow hunting or euthansia
- in an emergency can be given IM, but slower and less predictable action
succinyl choline side effects
- bradycardia
- hyperkalaemia
- incr intra-ocular and intragastric pressure
- anaphylaxis
- malignant hyperthermia
succinylcholine sensitive species
dogs, cattle and sheep are sensitive, horse and pigs less so
depolarising blocking agents phases
- I
- II
phase I block
depolarising block of motor end plate
-block is augmented, not reversed by cholinesterase inhibitors
phase II block
after repolarisation the membrane cannot easily be depolarised again
depolarising agents onset
rapid, 1min
depolarising agents duration
short, however may revert to phase II block
depolarising agents termination of action
metabolised by the plasma, pseudocholinesterase and liver
depolarising agents initial metabolite
succinylmonocholine, weaker, predominantly competitive blocking action
depolarising agents effect on muscle
- fasculation
- weakness
- paralysis
depolarising agents effect on cardiovascular system
- incr blood pressure
- incr/decr heart rate - stim of parasympathetic and or sympathethic ganglia
depolarising agents can be enhanced or potentiated by which
neostigmine, organophosphates and isoflurane
depolarising agents undesirable side effects
- muscle fasciculation, hyperkalamia
- phase II block
- malignant hyperthermia in genetically susceptible animals
- muscarinic actions at high doses
depolarising agents advantages
short duration of action, little histamine release
competitive non depolarising neuromuscular blocking agents mechanism of action
selectively antagonise nicotinic receptors, thus preventing endogenous Ach binding and subsequent muscle cell depolarisation
competitive neuromuscular blocking agents groups
- benzylisoquinoline
- aminosteroid
- gallamine
benzylisoquinoline group examples
- d tubocurarine
- atracurium
- cisatracurium
- mivacurium
aminosteroid group examples
- pancuronium
- vecuronium
- rocuronium
benzylisoquinoline group metabolism
metabolism in blood plasma, histamine release
aminosteroid group metbaolism
metabolism in liver, no histamine release
classifications of agents based on their duration of action
- ultra short
- short
- intermediate
- long duration
intermediate agents examples
- atracurium
- cisatracurium
- rocuronium
- vecuronium
long duration agents examples
- d tubocurare
- dimethyltubocurarine
- pancuronium
- gallamine
effects of competitive blockers on cardiovascular system
- decr blood pressure -due to histamine release
- incr heart rate - baroreceptor reflex
- coagulobility of blood decr - due to release of heparin from mast cells
d tubocurare features
- long acting
- slow onset of action
- slight hypotension and tachycardia
- histamine release
- excretion via urine
- limited use
mivacurium features
- short acting
- succinycholine alternative developed for human use
- HA release, hypotension can occur
- metabolism in plasma
atracurium features
- intermediate acting
- safe in liver and kidney disease
- bradycardia may occur during surgical manipulations
- precipitates in alkaline pH
- can cause HA release at higher doses
- probably most used in veterinary medicine
cisatracurium features
- immediate acting
- R-cis isomer of atracurium
- 3-4x potency
- immediate onset
- metabolism in plasma
- frequently used in opthmologic surgeries
rocuronium
- intermediate acting
- rapid onset of action
- metabolism in liver, excretion with bile
- lack of CV or HA-releasing effects
- quite frequently may cause anaphylactic reaction
vecuronium features
- intermediate acting
- lack of CV or HA releasing effects
- drug of choice when CV stability needed
- metabolism in liver
- excretion with bile and urine
- mydraitic use in birds and reptiles
pancurium features
- slight tachycardia and hypertension
- metabolism in liver, elimination via urine
- liver and kidney disease prolongs its effect
gallamine features
- frequently used in human surgery
- tachycardia and hypertension
- no HA release
- crosses placental barrier
antagonists of competitive blockers
cholinesterase inhibitors or tetanic stimulation
whats used to control the muscarinic side effect of neostigmine
atropine
