Myorelaxants Flashcards
1
Q
Why do we use Central Muscle Relaxants?
A
- They have a relative specific depressant action on CNS causing decreased motor activity or paralysis of voluntary muscles without loss of consciousness
- using them at therpeutic dose they do not inhibit other functions of CNS
- many of CNS inhibitory drugs demonstrates weaker or stronger muscle relaxants effect, Eg: Phenotiazines < Opioids < Alpha2-agonist < Anaesthetics
- central myorelaxants can potentiate the effect of anaesthetics drugs and combinations
- they are also used to contro certain spasmodic and painful disorders of skeletal (spinal) muscles.
2
Q
Name the different Central Muscle Relaxants drugs:
A
- Guaiphensesin
- Baclophen
- Carisoprodol
- Methocarbamol
3
Q
Guaiphenesin:
- Indications, pharmacokinetics
A
Indications:
- horses, cattle, sheep: to adjunct anaesthesia
- dogs: strichnine poisoning (in pass)
Pharmacokinetics:
- onset and elimination of action is fast, 2-4 and 60-80 min
- large distribution, crosses placenta barrier
- metabolism: conjugation with glucuronide -> excration with urine
4
Q
Guaiphenesin:
- Effect
A
- it is a spinal interneuronal blocking agent: it blocks polysunaptic but not monosynaptic reflexes
- exact mechanism is unknown
- it is effective against convulsion caused by strychnine, tetanus, but inactive in picrotoxin and leptazol induced colvulsions
- it paralyses limb muscles, whils respiratory muscles are generelly unaffected
- the consciousness is retained: sedatives must be applied (alpha2-agonist, opioids, ketamine)
Secondary effect:
- expectorant
5
Q
Guaiphenesin:
- side-effects
A
- mild, at therapeutic dose slight decrease of arterial blood pressure
- only large doses causes respiratory depression
- ut causes haemolysis (concentration dependent), preferred 5% solution with 5% dectrose
6
Q
Baclopen:
- effect, safety and indications
A
Effect:
- acts as agonist at GABAb receptors in the brain and spinal cord, resulting in hyperplarization of neurons due to increased K+ ion conductance
- also inhibitos neural funcion presynaptically, by reducing Ca2+ ion influx, and thereby reducing the release of excitatory neurotransmitters in both the brain and spinal cord.
- it may also reduce pain in patients by inhibiting the release of Substance P in the spinal cord
Safety: Large therapeutic index
- Clinical signs of toxicosis are vomitting, ataxia, and vocalization or disorientation
- life-threatening signs are respiratory arrest, and seizures
Indications: 1-2 mg/kg Orally TID
- spasms of skeletal muscles, rigidity, spinal cord injury and pain caused by injuries
- Baclophen has also been used extralabel in dogs to treat urinary retention by reducing urethral resistance.
-
7
Q
Carisoprodol:
A
(scutamin C tabl)
- usefull against various types of pain (wheter or not related to muscle spasm) because of its analgesic-sparing (potentiating) effect of opioid analgesics)
- inactive in convulsion caused by strychnine
- is available by itself or mixed with Aspirine and in one preparation along with Codeine and Caffeine as well
8
Q
Methocarbamol:
A
(Frexolan tabl)
- acts on the internuncial neurons of the spinal cord
- reduces skeletal muscle hyperactivity alteration in muscle tone
9
Q
Peripheral muscle relaxant drugs:
- classes of neuromuscular blocking agents
A
- Depolarizing neuromuscular blocking agents (succinylcholine)
- Competitive (non-depolarizing) neuromuscular blocking agents (prototype: d-tubocurarine/curare)
10
Q
Uses of neuromuscular blocking agents:
A
By intravenous or systemic administration:
- adjuvant in surgical anaesthesia t obtain relaxation of skeletal muscle
- “balanced” anesthesia, TIVA - to minimize anaesthetic use without compromising analgesia
- to assist in intubation (esp. succinylcholine)
- corneal or retinal surgeries to obtain relaxation of extraocular muscles (cisatracurium)
- therapy of spastic disorders
By topical administration:
- mydriasis in birds (eg. vecuronium)
11
Q
Depolarizing neuromuscular blocking agents and its mechanism:
A
Succinylcholine (suxamethodnium) - twp ACh molecules
Mechanism:
- stimulate opening of nicotinic ACh receptor channel and produce depolarization of the cell membrane
- Succinylcholine persist at the neuroeffector junction and activates the nicotinic receptor channels continouusly, which results in inactivation of voltage-gated sodium channels so that they cannot reopen to support further action potenitals (= “depolarizing blockade”)
12
Q
Succinylcholine (Sucamethonium) chloride:
A
- IV rapid (onset within 1min) and short-lasting block (app. 10min) –> Phase 1 block
- used to facilitate intubation (humans); used illegally in bow hunting or “euthanasia”
- In an emergency can be given IM, but slower and less predictable action
- can cause bradycardia (atropine can prevent!), hyperkalaemia, increased intra-ocular and intragstric pressure, anaphylaxis or malignant hyperhermia in geneticaaly predisposed subjects
- dogs, cattle, sheep sensitive
- horses and pigs less sensitive
13
Q
Depolarizing angents termination of action:
A
metabolised by plasma pseudocholinesterase and liver
14
Q
Depolarizing agents effect on skeletal muscle:
A
- fasciculation - “muscle twitch”
- weakness
- paralysis
15
Q
Depolarizing agents effect on cardiovascular system:
A
- increased blood pressure, increased or decreased heart rate (due to stimulation of parasymp. and/or sympathetic ganglia)
- bradycardia occurs after repeated use more frequently (atropine)
