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WorksheetsPharmacology Quiz on Muscle Relaxants
Total questions: 20
Worksheet time: 10mins
Succinylcholine apnoea occurs due to
Overdose of anesthetic agents
Deficiency or atypical plasma pseudocholinesterase
Central respiratory depression
Renal failure
Normal termination of action of succinylcholine depends on
Acetylcholinesterase
Plasma pseudocholinesterase
Hepatic metabolism
Renal excretion
Management of succinylcholine apnoea includes
Immediate antidote administration
Mechanical ventilation and supportive care
Neostigmine injection
Atropine only
Dantrolene acts by
Blocking nicotinic receptors
Inhibiting acetylcholinesterase
Reducing Ca2+ release from sarcoplasmic reticulum
Blocking sodium channels
Primary therapeutic use of dantrolene is
Myasthenia gravis
Malignant hyperthermia
Spasticity of spinal origin
Parkinson disease
Botulinum toxin produces paralysis by
Blocking postsynaptic receptors
Inhibiting acetylcholine release at neuromuscular junction
Depolarizing end plate
Blocking calcium channels in muscle
Clinical use of botulinum toxin includes all EXCEPT
Strabismus
Spasticity
Dystonia
Myasthenia gravis
Succinylcholine is a
Non-depolarizing muscle relaxant
Competitive antagonist
Depolarizing muscle relaxant
Central muscle relaxant
d-Tubocurarine (d-TC) is classified as
Depolarizing muscle relaxant
Non-depolarizing muscle relaxant
Central muscle relaxant
Anticholinesterase
Initial effect of succinylcholine at NMJ is
Fasciculations
Flaccid paralysis without twitching
Spastic paralysis
No visible effect
Reversal of non-depolarizing block by neostigmine is due to
Direct receptor activation
Increased acetylcholine at NMJ
Reduced acetylcholine release
Depolarization block
Succinylcholine block cannot be reversed by neostigmine because it
Is irreversible
Produces depolarization block
Is centrally acting
Is rapidly excreted
Example of centrally acting muscle relaxant is
Succinylcholine
Pancuronium
Baclofen
d-Tubocurarine
Centrally acting muscle relaxants act mainly at
Neuromuscular junction
Sarcolemma
Spinal cord or brainstem
Muscle fibers
Rationale for adding adrenaline to lignocaine is to
Increase toxicity
Prolong duration and reduce systemic absorption
Increase onset time
Reduce analgesic effect
Adrenaline with lignocaine is contraindicated in
Minor procedures
Finger and toe blocks
Healthy adults
Dental anesthesia
Addition of adrenaline to lignocaine reduces
Local blood flow
Systemic toxicity
Rate of absorption
All of the above
Botulinum toxin blocks release of which neurotransmitter?
Dopamine
GABA
Acetylcholine
Noradrenaline
Dantrolene is useful in spasticity because it acts on
Sodium channels of nerve
Calcium channels of muscle
GABA receptors
Nicotinic receptors
A major adverse effect of dantrolene is
Hepatotoxicity
Nephrotoxicity
Ototoxicity
Myelosuppression
