Post Synaptic Muscle Relaxants

martinezdvm's version from 2015-10-13 18:13


Question Answer
What are the therapeutic goals of muscle relaxants? What type of agents can use to achieve this goal?Muscle relaxation. General anasthetic agents (dissociative anasthe -like ketamine- require combination with muscle relaxants), local anesthetic agents, benzos, guaifenesin, NeuroMuscular blocking agents
What anesthetic agent leads to paralysis?local anesthetics
Name a centrally acting muscle relaxantGuaifenesin
What are the therapeutic targets of muscle relaxants and what part of the NS (nervous system) do they belong to?GABA receptor, alpha receptors and guafenesin (Central nervours syst) & Neuromuscular junction - nicotinic receptors & acetylcholine-esterease- (peripheral NS)
Guaifenesin is added as what in anesthesia? In what animal? An adjunct. In the horse.
What does guaifenesin achieve?Sedation (very little) & muscle relaxation
What are the mechanisms of action of Guaifenesin?Selectively depresses transmission at internuncial neurones in the spinal cord, brainstem and subcortical areas
What are the indication of Guaifenesin when added as an adjunct ? Induction & Maintenance of anesthesia (TIVA "total IV anesthesia ")
What are the indications of Guaif in humans?Used as an expectorant (OTC)
What are the contents of a "triple drip"Ketamine, alpha agonist and guiafenesin
Effects of GuaiFe in the CNS?Selectively depresses impulse neurotransmission at internuncial neurons
Does guaifenesin provide analgesia?No
How does guiafenesin affect respiratory muscles? At low and high doses?It doesn't at LOW/therapeutic doses. @ HIGH doses =relaxation of laryngeal and pharyngeal muscles.
What happens to the musculoskeletal system if GuaiFe is given at EXCESSIVE doses?Paradoxical increase in muscle rigidity
What happens s to the musculoskeletal system if GuaiFe is given at THERAPEUTIC doses?Muscle relaxation
How long does the recumbency effect of Guaifenesin last?~6mins max
How long does sedation last when using Guaifenesin?15-30mins
Are there gender differences when using Guaifenesin?halflife in male ponies is 85 mins and in females 60mins
What is the metabolite produced when hepatic metabolism of Guaifenesin has ended?Glucoronide
What drug should you not use Guaifenesin in combination with?Physostigmine (nor any other parasympathetic drug)
If given in > 5% concentration in cow (Guaifenesin) what would you expect?Hemolysis

NM blockers (non-depolarizing blockers)

Question Answer
Neuromuscular blocking drugs can pre or post synaptically? What is their mechanism?Both: Presynaptically by (1) inhibiting Ach synthesis and (2) inhibiting Ach release & Post-synaptically by interacting with postsynaptic actions of ACh
What are the indications of Neuro-muscular blocking drugs?Used as an adjunct to anesthesia, artificial ventilation is essential because it stops all smooth muscle (therefore not to be used as a therapeutic intervention)
Clinically relevant NM blockers act by? What are they known as?Interfering with the postsynaptic effects of ACh. Known as (1) Non depot & (2) depolarizing blockin agents.
How do non-depolarizing blocking agents act w ACh receptors (mech of action)?blocking ACh receptors (nicotinic receptors)
How do depolarizing bloking agents act w ACh receptors (mech of action)?they act as agonists
name a famous non-depolarizing agent and its synthetic variants.curare, synthetic variants are "gallamine, pancuronium, vecuronium & atracurium"
How are the quaternary ammonium compounds absorbed? (bioavailability)poorly absorbed and rapidly excreted (limited volume of distribution (Vd); poor biovailability)
what non depolarizing blocking agent is the only one that binds irreversibly & what is its affinity (strong vs poor)?alpha-bungarotoxin, binds with high affinity
Non-depol blocking agent's effect when binding to ACh nicotinic receptor:Binding of antagonists results in stabilization of the receptor (no depolarization because no electrostatic forces produced)
What are the side effects attributed to TUBOCURARINE? what is its synthetic derivative?hypotension & bronchoconstriction. its derivative is alcuronium (has fewer side-effects)
What are the side effects attributed to ATRACURIUM? Degradation time?Transient hypotension. Spontaneous degradation.
Name the Neuromuscular blockers that release HISTAMINE?Tubocurarine, Atracurium, Doxacurium & Mivacurium
What are the side effects attributed to DOXACURIUM? Duration?SideEffect similar to Atracurium (transient hypotension) Long lasting due to its stability in plasma
What are the side effects attributed to MIVACURIUM? Transient hypotension (like atracurium and doxacurium)
Which NM blocker is hydrolyzed by plasma choline-estereases?Mivacurium
Long lasting NM blockersTubocurarine, Doxacurium, Pancuronium, Pipecuronium ("Long Tube-like Dauchsund ate Pan in a Pipe")
Short acting NM blockersMivacurium
Intermediate lasting NM blockersAtracurium, Rocuronium, Vecuronium
Vagolytic NM blockers?Pancuronium, Pipecuronium, Rocuronium, Vecuronium
Steroid based NM blocker? (therefore safer than tubocurarine)Pancuronium
Which NM blocker can lead to occasional prolonged paralysis?Rocuronium
Side effects of Pancuronium? and Pipecuronium?Slight Tachycardia, no hypotension
Side effect rocuronium?Produces an active metabolite of vecuronium
Side effect of vecuronium?Very few (insignificant). Therefore it is widely used in human medicine

Depolarizing Blocking Agents

Question Answer
What is the mode of action/mech behind Depol blockers?Interferes w/ ACh-mediated depolarization of POST-Synaptic membrane
What is fasciculation?Initial muscle stimulation
How are depolarizing agents leading to antagonistic effects?Prolonged increase in the permeability to Na & K causes that ACh cannot act as a NT and transmission fails (relaxation of smooth muscle)
Which are the depolarizing blockers?Decamethonium, Suxamethonium ("Deca Sux!")
Which depolarizing blocker has long duration of action?Decamethonium ("deca = 10, ten times more prolonged than Sux")
Which depolarizing blocker is closely related to Ach?Suxamethonium (also closely related to decamethonium)
Which depolarizing blocker has a short duration of action? Why?Suxamethonium (it's so slow it Sux), rapid hydrolysation by plasma cholinesterase's
Which depolarizing blocker causes fasciculations?Decamethonium, they subside after a few seconds (when excitability of motor end plate is lost)
Effects of depolarizing blockers on the end-plate?To slow down diffusion to the endplate and remain there for a prolonged period of time
Effects of depolarizing blockers on acetylcholine?Ach will be released in short burts and will be rapidly hydrolyzed
Side effects of Suxamethonium?Bradycardia, Potassium release --> ventricular dysrythmia, increased intra-ocular pressure, prolonged paralysis
What is the safety margin for Depol Blockers?75% (minimum) of POST-junctional NICOTINIC receptors must be blocked & 90% must be blocked for complete cessation of transmission.