NMJ neuropharm

Question 1

MOA of botulinum toxin

Answer 1

inhibits acetylcholine release (synaptobrevin-synaxin-SNAP25)

Question 2

MOA of black widow spider venom

Answer 2

increases ACh release (neurexin 1 - latrophilin)

Question 3

MOA of curarare (tubuocurarine)

Answer 3

NMJ competitive antagonist of the Nm receptor. So prevents channel opening and depolarization and produces a flaccid paralysis.

Question 4

MOA of atacurium

Answer 4

Isoquinoline derivative of curare. So same MOA (NMJ competitive blocker (non-depolarizing)

Question 5

MOA of succinylcholine

Answer 5

NMJ competitive blocker. Agonist of the Nm receptor with prolonged binding. So it opens the channel causing depolarization, but doesn’t allow a repolarization or subsequent action potential and produces flaccid paralysis. NOT hydrolyzed by AChE, but rapidly hydrolyzed by pseudocholinesterases.

Question 6

MOA of rocuronium?

Answer 6

steroid derivative of curare. so same MOA (NMJ competitive blocker (non-depolarizing).

Question 7

what would you use if someone OD’d on curare or a curare like drug?

Answer 7

Edrophonium/neostigmine. BUT, they can worsen neuromuscular blockade caused by succinylcholine.

Question 8

butyrylcholinesterase?

Answer 8

“pseudo” cholinesterase. preferentially hydrolyzes long chain esters like succinylcholine.

Question 9

Signs of muscarinic receptor OD?

Answer 9

DUMBBELS-Defecation, Urination, Miosis, Bradycardia, bronchospasm/bronchorrhea, emesis, lacrimation, salivation

Question 10

Signs of nicotinic receptor OD?

Answer 10

MATCH - muscle weakness, fasiculations, adrenal medulla activity inrease, tachycardia, cramping of skeletal muscle, hypertension.