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NBME 23 Answers

nbme23/Block 1/Question#12

A 48-year-old man who is a farmer in a remote area ...

Blockade of postsynaptic inhibition of spinal motor reflexes

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submitted by yb_26(124),
  • binding to the MHC class II receptor and triggering the release of cytokines - superantigens

  • binding to the neuromuscular junction and prevention of ACh release - botulinum toxin

  • blockage of a GTP-binding protein resulting gin the accumulation of cAMP - pertussis toxin

  • blockage of presynaptic inhibition of spinal motor reflexes - tetanus toxin

  • prevention of protein synthesis by blocking elongation of the polypeptide chain - diphtheria toxin, Pseudomonas aeruginosa exotoxin A

thomasburton  Not sure I agree with the second one, M.O.A for botulinum is cleave of SNARE protein preventing pre-synaptic ACH release. Think the second one almost describes something like sux or some other deporalising nicotinic drug. +4  
humble_station  You are right but to get the muscle spasms, trismus & seizures it has to inhibit GABA & Glycine release from Renshaw cells Cleaving the snare proteins will cause paralysis +1  
texaspoontappa  tetanus->postsynaptic inhibition I believe +2  

 +5  upvote downvote
submitted by lfsuarez(114),

Patient present to the clinic with classical symptoms of tetanus. Tetanus toxin work via inhibition of GABA/glycine release from Renshaw inhibitory cells. Without these inhibitory signals on the postsynaptic neuron, they are continuously activated causing muscle tetany.