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 +3  (nbme24#42)


Theres multiple allele variants for the CFTR gene in a single locus, so you could get cystic fibrosis from a mutation in any one of those allele variants(theres over 1500 different mutations described) the question stem mentioned they tested for the most common types, so we can assume they probably just missed testing for mutations in other alleles.

 +0  (nbme23#36)

Maybe they went with serum sickness (a type III hypersensitivity rxn) on this question based on the serology used to diagnose RA. Pts with RA have antibodies to immunoglobulin G (IgG), called rheumatoid factors (RFs). It makes some sense that upon these rheumatoid factors reacting with "self" circulating IgG, immune complexes would form that would later deposit in tissues (explaining in part the extraarticular manifestations seen with RA, ex. rheumatoid nodules, pleuritis, pericarditis etc..)


Subcomments ...

submitted by enbeemee(8),

i get why it's hyporeflexia, but why not fibrillations? it's also an LMN sign

et-tu-bromocriptine  Imagine a simple reflex arc: you have an afferent neuron, some interneuron shenanigans, and an efferent neuron (aka LMN neuron). If you damage the LMN, you will get hyporeflexia (due to damaged reflex arc) and fibrillations (because your LMN won't be able to effectively contract muscle on command). However, if you damage the afferent part of the arc, you will still get a damaged reflex arc (hyporeflexia), but your motor neuron will still be able to do its stimulating effectively, so your muscles won't show weak contractions when stimulated by a higher pathway. Kinda confusing but I hope I made it a tad simpler! +5  
eli_medina9  https://imgur.com/1z4OF4l Gonna piggy back off your comment and just post this kaplan image +1