Skeletal Muscle Relaxants

Question 1

Peripherally acting SMR types

Answer 1

Directly acting SMR & Neuromuscular blocking agents

Question 2

Directly acting SMR examples

Answer 2

Dantrolene sodium & Quinine

Question 3

Neuromuscular blocking agents divided into

Answer 3

No depolarising and depolarising blockers

Question 4

Depolarising blockers examples

Answer 4

Succinylcholine (suxamethonium) & Decamethonium

Question 5

Long acting competitive nm blockers (hint DPDP)

Answer 5

Delta- tubocurarine, Pancuronium, Doxacurium, Pipecuronium [Pnemonic: DPDP]

Question 6

Intermediate acting NM blockers (VACRR)

Answer 6

Vacuronium, Atracurium, Cisatracurium, Rocuronium, Rapacuronium

Question 7

Mivacurium is

Answer 7

Short acting non depolarising SMR

Question 8

Hoffman’s elimination

Answer 8

Atracurium & cisatracurium

Question 9

Histamine release

Answer 9

Tubocurarine and mivacurium and Atracurium

Question 10

Sch is metabolised

Answer 10

In liver by pseudocholinesterase and butyrylcholinesterase

Question 11

Effect of dTc on Autonomic ganglia

Answer 11

Blockade

Question 12

Effect of Sch on autonomic ganglia

Answer 12

Stimulation

Question 13

Longer acting non depolarising smrs are metabolised by

Answer 13

Kidney

Question 14

Shorter acting drugs like (VACR) are metabolised by

Answer 14

Liver

Question 15

Effect of dtc on CVS

Answer 15

Hypotension & tachycardia

Question 16

Sch effect on CVS

Answer 16

Initially bradycardia(vagal stimulation) then Tachycardia and hypertension(stimulation of sympathetic ganglia) occasionally hypotension(dt muscarinic action)

Question 17

Prolonged administration of Sch causes ? On heart

Answer 17

Arrhythmia and arrest

Question 18

Eliminated in bile

Answer 18

Rocuronium & Vecuronium

Question 19

Laudanosine which causes CNS toxicity of seizures is metabolite of

Answer 19

Atracurium (Liver)

Question 20

Why does atracurium produce seizures but not cisatracurium?

Answer 20

Because seizure caused by laudanosine which is metabolised by liver and cisatracurium undergoes zero hepatic metabolism (100% Hoffman) in contrast to Atracurium which is metabolised partly by both mechanisms

Question 21

Shortest acting competitive blocker

Answer 21

Mivacurium

Question 22

Shortest acting SMR

Answer 22

Sch (<5mins)

Question 23

Sugammadex is selective antagonist of

Answer 23

Rocuronium & atracuronium

Question 24

Most commonly used non depolarising blockers

Answer 24

Vecuronium, cisatracurium, Rocuronium

Question 25

Sch is used for procedures like

Answer 25

Endotracheal intubation, laryngo, broncho, esophagocopies.

Question 26

Ocular surgery proffered SMR

Answer 26

Non depolarising

Question 27

Most cardio toxic local anaesthetic

Answer 27

Bupivacaine

Question 28

LA used as anti arrhythmic drugs

Answer 28

Procainamide & Ludocaine

Question 29

All LAs cause vasodilation except

Answer 29

Cocaine

Question 30

Highest local tissue irritancy among LAs?

Answer 30

Bupivacaine

Question 31

LA used for ophthalmic anaesthesia

Answer 31

Proparacaine

Question 32

LA used for application on eye

Answer 32

Tetracaine

Question 33

Shortest acting LA

Answer 33

Chloroprocaine

Question 34

Longest acting LA

Answer 34

Dibucaine

Question 35

Surface anaesthetics

Answer 35

Lidocaine, Proparacaine, Tetracaine, Cocaine, Benzocaine

Question 36

Methemoglobinemia side effect of

Answer 36

Benzocaine and Prilocaine

Question 37

Allergic reactions more common with

Answer 37

Ester LAs> Amide LAs

Question 38

EMLA is

Answer 38

Eutectic mixture of Local Anaesthetics (lido+prilo)

Question 39

Ester LAs are metabolised by

Answer 39

Pseudocholinesterases

Question 40

DOC for CV toxicity of LA

Answer 40

Lipid emulsion

Question 41

Nerve fibre most susceptible to LA

Answer 41

Autonomic

Question 42

Techniques of LA

Answer 42

1. Spinal 2. Epidural 3. Surface 4. Infiltration 5. Conduction block (Nerve block & field block) 6. Bier block(IV regional anaesthesia