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Agreed - I think I got this by thinking about tabes dorsalis (syphillis) and why it has hyporeflexia is due to dorsal root damage
I'm confused about why it wouldn't cause muscle atrophy. Isn't that a fever of LMN damage?
Muscle atrophy wont occur because alpha motor neuron is intact. Motor control of Corticospinal tract on this is intact. so no atrophy. u can move shiti/
But remeber muscle spindle that is responsible for INITIATING stretach reflex send Ia fibre to DRG from where it synapse with Alpha motor neuron. if DRG is damage ur muscle is fine but u cant initiate strech reflex. areflexia
DRG you lose DTR
This is why I was looking for some answer indicating keratinocytes in the stratum spinosum...instead they just gave a bunch of bs choices.
I'm confused because I also know that S. aureus cleaves desmoglein in the stratum granulosum, so why is it specifically this answer?
desomosomes connects cells to cells.
hemidesmosome connects cells to basement membrane.
I think what this is really asking is can you tell Pemphigus Vulgaris from Bullous Pemphigoid
Vulgaris (question)- Attack on DESMOSOMES- this separates some keratinocytes from others (ie some in basal layer from ones above).
Pemphigoid- attack on HEMIDESMOSOMES- this means separation of the keratinocytes from the basement membrane.
It looks like it was a type II RTA. The difference is incredibly subtle from the info given in this question.
He has Fanconi syndrome which is generalized reabsorption defect in PCT which leads to metabolic acidosis and hypophosphatemia → can lead to rickets
Also, does lead to type II RTA
Also the proximal tubule is the place with the highest phosphate absorption rate. That's why PTH works here mostly and a little bit in the distal tubule.
Another easy way to go about this one is the question tells you he has metabolic acidosis, the only that can happen with is Fanconi/Type2 RTA. The rest will cause hypokalemia and metabolic ALKALOSIS. (pg 586 FA)
Personally thought if they were going for Fanconi syndrome they would describe a lot more symptoms for the kid like growth failure or hypophosphatemic rickets but its NBME so.
You're a good man.
Could the pneumothorax also cause less ventilation due to decreased lung surface, retaining more CO2 causing respiratory acidosis? That's how I got to the answer at least.
I think pneumothorax would increase RR because you're probably hypoxic. Also I'm sure when you have a lung collapse on you you'd be scared and that would trigger your sympathetic so your RR will go up either way.
there is no bilateral lung opacities as you would see in ARDS
Was thinking some sort of infection b/c of the atelectasis so picked empyema but this makes sense!
does it need to be ARDS to cause "diffuse alveolar damage"?
Not only that, does having a collapsed lung affect the alveoli?
You just have to know that POMC is a pro-protein that must be cleaved; not sure if there’s anything in the stem that would really have given it away.
Dunno if this helps, but it says "this protein" (singular) is the precursor of two different protein products. This must mean that the modification occurs after the protein is made, which means after transcription and splicing has already happened.
Also I believe mRNA refers to after the splicing already occurs. If the protein products are from the same mRNA then it can't be alternate splicing.
They're cleaved by tissue-specific proteases
Alternative splicing occurs with hnRNA not mRNA. You get mRNA from alternatively splicing the hnRNA. an mRNA can only make 1 type of protein.
Since the question says the 2 proteins comes from the same mRNA it cannot be alternative splice or post transcriptional mod. FA 2018 page 43 has a good illustration.
Just general testing taking strategy i guess, but for this question i was torn between post-transcriptional and post-translational, but then i saw that alternative splicing was also a choice...because alternative splicing IS a post-transcriptional modification you know it has to be post-translational because you can't select two answer choices.