Companion 2nd Year MBBS solutions : Skeletal muscle relaxants

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Q) Classify muscle relaxants.

Q) write a short note on d-Tubocurarine

A) d-Tubocurarine is a long-acting Non-depolarizing or competitive blocker.

 Mechanism of action– d-Tubocurarine competes with the acetylcholine for the binding to post-synaptic Nicotinic cholinergic receptors (Nm) present on the motor end plate. Due to competitive block, Ach. is not able to bind to its receptor resulting in failure of the generation of EPP or end plate potential as a result of non-opening of sodium channels. Further, fall in potential results in failure to trigger propagated muscle action potential(MAP). It has no intrinsic activity. 

At higher concentration – drug enters sodium channels and directly block them.

Reason for the affinity of d-Tubocurarine and Ach. to Nm receptors– Nm receptor is composed of 5 subunits (2α,β,γ,δ,ε). Each α subunits carry negatively charged, Ach. binding sites. Competitive blockers like d-Tubocurarine, have thick bulky molecules, termed pachycurare by Bovet composed of 2 or more quaternary sodium(positively charged) atoms. So, d-Tubocurarine and cationic head of Ach. show affinity for the negatively charged Ach. binding site located on the 2 α subunits. 


(1)Muscle weakness followed by flaccid paralysis in man. Initially,small muscles are affected.Paralysis spread from hands,eyes and feet muscles to that of arm⇒ Leg⇒ neck⇒face⇒ trunk⇒intercostal muscles⇒ Diaphragm. Paralysis of diaphragm results in cessation of respiration. Recovery occurs in reverse sequence . Hence, diaphragm is first to recover and last to become paralyzed.

(2)Cause autonomic ganglia blockade as nicotinic cholinergic receptors are present in ganglia. 

(3)It causes release of histamine form mast cell resulting in flushing, rashes,bronchospasm and increased respiratory secretions.

(4)CVS Effect -Significant fall in blood pressure on administration of d-Tubocurarine due to histamine release,ganglion blockade and reduced venous return from muscle paralysis. 

(4)CNS effect – No C.N.S action as it cannot cross BBB.

 (5) Effect on GIT-Post-operative paralytic ileus i.e. functional blockade of intestine due to paralysis of intestinal muscles which resolves spontaneously withing 2-3 days. 

Uses -1.Used in conjugation with General anesthetics to provide muscle relaxation for surgery.

2. To facilitate tracheal intubation.

3.Skeletal muscle relaxation during surgery. 

4 Preferred for ocular surgeries as low doses of competitive drug provide paralysis of ocular muscles.

 Adverse effects – 1. Hypotension 


3. post-operative ileus 

4. bronchospasm

 5. increased salivation 

6. respiratory depression 

6. Wheezing. 

d-Tubocurarine reversal – reversal by administration of neostigmine. The optimum dose of neostigmine required to establish the complete reversal of severe neuromuscular blockade due to tubocurarine would appear to be in the region of 4 to 5 mg.

Q) Write a short note on succinyl choline

A) Succinyl choline is a long slender and flexible molecule with 2 quaternary sodium atoms, termed Leptocurare by Bovet . It is a depolarizing blocker. 

Mechanism of Action – Sch has affinity to Nm cholinergic receptors. It binds to the post-synaptic receptors and cause depolarization by opening of sodium channels because it possesses sub-maximal intrinsic activity.As Sch. does not dissociate rapidly from the receptor and is not hydrolysed by ACHe ,so,prolonged partial- depolarisation occurs around motor end plate which causes repeated excitation resulting in fasciculations and twitching. Due to prolonged partial-depolarisation the transmembrane potential drops down to -50mV. Owing to this, propagated muscle action potential is not generated by the Ach. which is released from the motor nerve endings. Flaccid paralysis occurs as a result of failure to generate proposed MAP. 

Administration of higher dose of Sch or infused continuously – This produces blockade which can be divided into 2 phases. 

Phase-1 – Phase-1 onset is rapid and occurs due to persistent partial depolarisation Rapid decline due to repolarisation (despite drug at receptor). 

Phase-2 – .Phase-2 onset is slow and occurs due to de-sensitization of the postsynaptic Nm cholinergic receptor to the ACh. Recovery is slow and occurs due to blockade reversal by anticholinesterase. Sch. readily produces block in patients with deficiency of pseudocholinesterase.


(1)flaccid paralysis followed by fasciculations lasting for few seconds. Paralysis spread from the neck, limbs ⇒ face, jaw, eyes, pharynx⇒ trunk⇒intercostal muscles⇒ Diaphragm. Paralysis of diaphragm results in cessation of respiration. Recovery occurs in reverse sequence. Hence, the diaphragm is first to recover and last to become paralyzed. 

(2) May cause ganglionic stimulation by agonistic stimulation on the nicotinic receptors. 

(3) Effect on CVS – Initially, bradycardia occurs due to vagal ganglia stimulation and later, tachycardia occurs due to sympathetic ganglia stimulation. Occasional B.P fall due to its muscarinic actions due to vasodilation of muscles.

(4)It causes release of histamine form mast cell resulting in flushing, rashes,bronchospasm and increased respiratory secretions.

(5)CNS effect – No C.N.S action as it cannot cross BBB.

Uses -1.Used in conjugation with General anesthetics to provide muscle relaxation for surgery. it induces rapid, complete and predictable paralysis with spontaneous recovery within 5 mins.

2.Employed for brief procedures like tracheal intubation

3. Employed for surgical procedures like reduction of fractures, dislocations

4.Skeletal muscle relaxation during surgery.

Adverse effects – 1. Muscle fasciculations and soreness


3. post-operative ileus 

4. bronchospasm

5. increased salivation 

6. respiratory depression 

6. Wheezing 

7.arrythmias (K efflux causing hyperkalemia).

 Q)What is succinyl choline aponea? why it’s duration of action is prolonged in certain individuals?

A)Succinyl choline is a poor substate for more specific ACHe. and it is mainly hydrolyzed by pseudocholinesterase into succinyl monocholine and further to choline and succinic acid. Atypical SCHe (defective gene)or deficiency of pseudocholinesterase causes prolonged phase 2 blockade resulting in muscle paralysis and aponea lasting for about 4-6 hrs which can be overcome by ventilator support.

Q)Write in brief about Pancuronium and atracurium

A)Pancuronium –  

1) synthetic steroidal compound.

2)overcomes the drawbacks seen in d-Tb. 

3) 5 times more potent and longer acting than d-Tb

4)Due to lower histamine release capacity, it rarely induces flushing, bronchospasm and cardia arrhythmia.

5)Due to little ganglion blockade,it causes relatively good cardiovascular stability.


1)bis-quaternary sodium compound.

2)4 times less potent than pancuronium and shorter acting.

3)It is eliminated by spontaneous non-enzymatic degradation(Hoffmann elimination) and cholinesterase.

4)Owning to Hoffmann elimination, its duration of action is not altered in patients with hepatic/renal insufficiency. So, it is indicated as a muscle relaxant in liver/kidney patients, neonates and elderly.

Q)Give therapeutic uses of dantrolene sodium

A)Dantrolene when used orally (25-100mg QID) – reduce spasticity in UMN disorders, hemiplegia, paraplegia, cerebral palsy and multiple sclerosis

B) Dantrolene when given i.v. (1mg/kg repeated as required)– drug of choice for malignant hyperthermia which is due to Calcium-induced calcium exocytosis in the sarcoplasmic reticulum (induced by fluorinated anesthetics used along with Sch. in genetically susceptible individuals with abnormal RyR1 (Ryanodine receptors)calcium channels present in skeletal muscles)


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