Pseudocholinesterase deficiency increasing the action of succinylcholine.
Phase 2 blockade produced by succinylcholine.
Undiagnosed muscular dystrophy and muscular weakness.
|D.||Muscular weakness due to fasciculation produced by succinylcholine.|
Ans: B.)Phase 2 blockade produced by succinylcholine.
It is a depolarizing relaxant, acting in about 30 seconds and with a duration of effect averaging three to five minutes
Mechanism of Action
Phase I Block:
- Succinylcholine acts as a depolarizing neuromuscular blocker by binding acetylcholine receptors at the post-synaptic neuromuscular junction end plate.
- The resultant endplate depolarization initially stimulates muscle contraction; however, because succinylcholine is not degraded by acetylcholinesterase, it remains in the neuromuscular junction to cause continuous endplate depolarization and subsequent muscle relaxation. This is termed a phase I block.
Phase II Block:
- With increasing doses of succinylcholine, a phase II block may occur.
- Continuous activation of acetylcholine receptors leads to ongoing shifts of sodium into the cell and potassium out of the cell.
- Despite this, the post-junctional membrane potential eventually moves in the direction of normal even in the continued presence of succinylcholine.
- This is due to increased activity of the sodium-potassium ATPase pump, which brings potassium into the cell in exchange for sodium.
- The receptor does not respond appropriately to acetylcholine, and the neuromuscular blockade is prolonged.
- Phase II block may be seen clinically with doses of succinylcholine >4mg/kg, but some characteristics of this blockade have been reported at 0.3mg/kg.