This document discusses skeletal muscle relaxants and neuromuscular blockers. It describes the neuromuscular junction and how depolarizing blockers like succinylcholine and non-depolarizing blockers like d-tubocurarine and pancuronium work. Depolarizing blockers activate nicotinic receptors, causing depolarization and paralysis. Non-depolarizing blockers are competitive antagonists that block acetylcholine receptors. The document also covers pharmacological actions, adverse effects, drug interactions, and factors affecting these drugs, and discusses myasthenia gravis.

1. SUBMITTED TO ASST PROF:SANJEEV KARALE
SUBMITTED BY THEERTHA T
M PHARM DEPARTMENT OF PHARMACOLOGY

2. • Introduction
• Classification of drugs
• Mechanism of action of depolarizing
blockers and nondepolarizing
blockers
• Pharmacological actions of
depolarizing and non depolarizing
blockers
• Adverse affects of depolarizing and
non depolarizing blockers
• Myasthenia gravis

3. NEUROMUSCULAR JUNCTION
The neuromuscular junction
connects the nervous system to the
muscular system via synapses
between efferent nerve fibers and
muscle fibers.
The neuromuscular junction
comprised of a motor neuron and
motor endplate with a synaptic cleft
or junctional gap dividing them

5. Skeletal muscle relaxants
 They are the drugs that act peripherally at
neuromuscular junction or muscle fibre
itself or in cerebrospinal axis to reduce
muscle tone and/ cause paralysis
 Neuromuscular blocking drugs are agents
that act peripherally at nmj /muscle fibre
itself to block neuromuscular transmission
 It is used in conjuction with general
anaesthetics to provide muscle relaxation
for surgery

6. Skeletal muscle relaxants decrese
skeletal muscle tone by peripheral
or central action
neuromuscular blockers include
non depolarizing and depolarizing
blockers
The site of action of both
competitive and depolarizing
blockers is the end plate of skeletal
muscle fibre

8. MOA OF DEPOLARIZING BLOCKERS
Decamethonium and SCh have affinity at Nm receptors
depolarize muscle end plate by opening Na channels
initially
Twitching and fasciculations
prolonged partial depolarization of the region
around muscle end palte
Na channel inactive
Flaccid paralysis

9. PHASES OF BLOCK
PHASE 1 BLOCK:
 Rapid in onset
 Result from persistent depolarization of muscle end
plate
PHASE 2 BLOCK:
 Slow in onset
 Result from desensitization of receptor to Ach

10. SUCCINYLCHOLINE
Most commonly used as muscle relaxants for
passing tracheal tube
Induce rapid, complete and predictable
paralysis with spontaneous recovery with in 5
min
Occasionally SCh is used by continuous i.v
infusion for producing controlled muscle
relaxation

11. PHARAMACOLOGICAL ACTIONS
OF DEPOLARIZING BLOCKERS
 Action on skeletal muscle: typically produce
fasciculations lasting few sec before inducing flaccid
paralysis
 Action on autonomic ganglia :cause ganglionic
stimulation by its agonistic action on nicotinic receptors
 Action on CNS : 1)bradycardia followed by tachycardia
and rise in bp
2) prolonged adminstartion cardiac arrhythmias and
even arrest in patients with burns

12. ADVERSE EFFECTS
muscle pain
Increased IOP
Aspiration of gastric content
Hyperkalaemia
Sinus bradycardia
Malignant hyperthermia

13. MOA NON DEPOLARISING BLOCKERS
Ach Nm receptors (NMJ) d-TC
(agonist) (antagonist)

14. • Ach is the agonist,whereas d-TC is the antagonist
at Nm receptors
curariform drugs competitively anatagonise the
action of Ach at Nm receptors of the NMJ
anticholinesterases are used to reverse the effect
of competitive blockers by incresing the con of
Ach

15. PHARMACOLOGICAL ACTION OF NON
DEPOLARIZING BLOCKERS
Skeletal muscles: iv inj rapidly produces muscle
weekness followed by flacid paralysis
Autonomic ganglia: it produce some degree of
ganglionic blockade
CVS :significant fall in bp due to 1) ganglionic
blockade 2) histamine release 3) reduced venous
return

16. Pancuronium
Steroidal compound, more potent and
longer acting than d-TC
Good cardiovascular stability
Eliminated by renal excreation
Cardiac arrhythmia because of lower
histamine releasing potential

17. pipecuronium
muscle relaxant with slower onset and long
duration of action
Steroidal in nature, recommended for
prolonged surgeries
Little cardiovascular action,chance of
occurance of hypotension and bradycardia

18. ADVERSE EFFECTS :
Hypotension
Respiratory paralysis
Bronchospasm
Aspiration of gastric contents

19. DRUG INTERACTIONS OF SMR
Nondepolarizing blockers * antibiotic
Thiazides /loop diuretics * non DB
Succinylcholine*thiopentone
General anaesthetics*non
depolarizing blockers

20. FACTORS EFFECTING ACTION OF
NEUROMUSCULAR BLOCKERS
Ph changes
Hypothermia
Myasthenia gravis
Aminoglycoside antibiotics
Inhalational anaesthetics

21. MYASTHENIA GRAVIS
Autoimmune disorder due to the development of
antibodies directed to nicotinic receptors at muscle
end plate
Result in weekeness and easy fatigability on repeted
activity with recovery after rest
Neostigmine and its congeners improve muscle
contraction by allowing Ach relesed from prejunctioanl
endings to accumulate and act on the receptors over
large area as well as by directly depolarizing the
endplate

22. REFERENCE:
ESSENTIALS OF MEDICAL
PHARMACOLOGY BY K.D TRIPATHI
PHARAMACOLOGY FOR MEDICAL
GRADUATES BY TARA V SHANBHAG
AND SMITHA SHENOY
RESERCHGATE.NET/PUBLICATION