Neuromuscular Blocking Agents Flashcards by Lethibe Mokgwadi

Under which category does the neuromuscular blockers fall under?

Somatic Nervous System under the Peripheral Nervous System

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Somatic Fiber ?

-Has no ganglia, indirectly innervates muscle
-Has nicotonic receptor
-Has Ach as a neurotransmitter

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Neuromuscular Junction?

Synapse between presynaptic motor neuron and postsynapatic muscle membrane

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General anethesia?

Includes analgesia, amnesia, loss of consciousness, inhibition of sensory and automatic reflexes and skeletal muscle relaxtion.

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Where are neuromuscular blockers used?

Used in anaesthesia and artificial ventilation

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Somatic Nervous System innervation?

Skin, sensory, organs and skeletal muscle-transmits information from CNS to the rest of the body

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Two major neuron types?

*Sensory neurons (afferent
neurons): body -CNS

*Motor neurons (efferent
neurons): brain and
spinal cord muscle
fibers throughout the body

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Normal neuromuscular transmission?

Action potential (AP) conducted along the motor neuron
Depolarization
Ca2+ influx
ACh release from storage vesicles into a synaptic cleft
ACh binds on nicotinic receptors on the motor end plate
Na+ channels on motor end plate open
Na+ influx and depolarization (end plate potential (EPP))
AP produced
Muscle contraction occurs
ACh hydrolyzed by AChE from motor end plate and process starts again

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Which step of neuromuscular transmission do neuromuscular blockers ?

Step 5
5. ACh binds on nicotinic receptors on the motor end plate

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Skeletal Muscle Relaxtants types?

Peripherally-acting agents
-Depolarising NMBD’S
-Nondepolarising NMBDs
Centrally-acting agents
-act on the CNS
Directly-acting agents
-act on the muscle

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Structure of NMBD’S?

Structurally polar-do not cross blood brain barrier

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NMD administration?

All administered parenterally

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NMD action?

Relax voluntary skeletal muscles, diaphragm and laryngeal muscles

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General MOA of NMB?

structurally similar to ACh
act at the post-junction nicotinic receptors

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NMB agonists or antagonists?

*agonists = depolarizing NMBDs
mimic ACh
persisting state of depolarization

*antagonists = non-depolarizing NMBDs
competitive inhibitors of ACh
prevent depolarization

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Types of Peripherally acting NMB?

Depolarizing NMBDs
Non-depolarizing NMBDs
Can be identified by “cur”

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NMB Depolarising drugs?

*Succinylcholine (suxamethonium)

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NMB non-depolarising drugs types?

a) Isoquinoline derivatives

b) Steroid derivatives

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NMB Isoquinoline derivative drugs?

MAD

*Mivacurium
*Atracurium
*d-tubocurarine

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NMB Steroid derivatives drugs?

Very Running People

Vecuronium
Rocuronium
Pancuronium

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Succinylcholine MOA?

only depolarizing NMBD in clinical use
causes ↑ EPP rapid muscle contraction,
clinically observed as muscle fasciculation
this is followed by flaccid paralysis within 30-
60 sec and lasts for 3-5 min
with repeated dose, receptors reach
tolerance rapid and complete muscle
relaxation

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Succinylcholine (SCh) phases?

Phase I

ACh agonist
triggers EPP via the ACh cascade
Voltage-gated Na+ channels open depolarization
increase Ca2+ release from sarcoplasmic reticulum
rapid muscle contraction (muscle fasciculations/twitches)
followed by muscle relaxation (flaccid paralysis)

Phase II

continued SCh exposure (repeated doses)
Na+ channels non-responsive to the stimulus repolarization
rapid and complete muscle relaxation

How long does the phase one of Succinylcholine ?

lasts for 3-5 min

Succinylcholine hyrolysed by?

not hydrolyzed by AChE)

Hydrolysed by plasma pseudocholinesterase

Succinylcholine duration?

resolves spontaneously within 10 minutes

Succinylcholine P/K? M & E

Metabolism: liver (CYP450), plasma (pseudocholinesterases) *Excretion: renal, only 10% excreted unchanged

Succinylcholine DI?

*Cholinesterase inhibitors *Digoxin

Succinylcholine A/E?

*Malignant hyperthermia *myalgia *Bradycardia *Hypotension *Increased IOP *Increased intragastric pressure *Increased salivation

Succinylcholine stimulate which othe receptors and what is their effects?

Stimulation of autonomic muscarinic receptors bradycardia Hypotension Increased salivation

What is the solution to succinylcholine to avoid muscuranic effects?

Atropine prior to repeated doses or continuous infusion of SCh to counteract these effects competitively antagonize muscarinic activity prevent bradycardia and hypotension

Nondepolarizing NMBDs MOA?

competitively antagonize ACh prevent EPP prevent Ca2+ release from sarcoplasmic reticulum muscle relaxation

Nondepolarizing Irr/reversible?

Reversible

Nondepolarizing Administeration?

All administered IV They do not cross the placenta and BBB

Tubocuraine?

Tubocurarine is a toxic alkaloid from curare historically known for its use as an arrow poison. a prototype from which many synthetic nondepolarizing NMBDs were synthesized rarely used in clinical medicine

What do non-depolarising drugs release and what is the exception?

Most nondepolarizing NMBDs (except rocuronium) release histamine and exhibit histamine-related side effects

What are histamine S/E?

Hypotension Bronchospasm

Non-depolarising duration?

Short acting: Mivacurium("Move Mivacurium) Intermediate-acting: Really Very Aware Rocuronium Vecuronium Atracurium Long-acting: Paced DRugs Pancuronium d-tubocurarine

Which non-depolarising NMB is the most rapid onset of action?

Rocuronium

Which non-depolarising NMB is the most slowest but has the longest duration?

Pancuronium

Which non-depolarising NMB is the most potent in releasing histamine?

Mivacuronium

Mivacuronium metabolism?

Plasma cholinesterase

Mivacuronium S/E?

Bronchospasm, Hypotension, prolonged neuromuscular blocker

Atracurium P/K? M, E & DI

M: spontaneous (Hoffman) degradation at body temp. and pH  Drug of choice in liver failure E: renal mainly DI: incompatible with thiopental sodium (used in GA induction phase)

Vecuronium P/K? M& E

M: liver E: bile mainly

Vecuronium S/E?

Bronchospasm, Anaphylaxis

Rocuronium P/K? M, E & DI

M: liver E: bile DI: Phenytoin, carbamazepine may cause recovery

Rocuronium S/E?

Anaphylaxis

Tubocurarine P/K? M & E

M: Hoffman degradation and hepatic E: renal mainly

Tubocurarine S/E?

Hypotension, bronchospasm

Pancuronium P/K? M&E

M: liver (small amount) E: renally mainly unchanged

Pancuronium S/E?

Tachycardia, elevation in BP

NMJ Blockade reversal?

Acetycholinesterase iNhibitors Eg:Neostigmine

NMJ Blockade reversal action?

1. block ACh hydrolysis 2. accumulation of ACh 3. NMJ blocker displacement

What antimuscuranic agent may need to be used to block musarinic effects?

Antimuscarinic agent, atropine, may need to be concurrently used to block the muscarinic effects of ACh i.e. bradycardia