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Comments ...

 +1  (nbme24#8)

This probably isn't 100% politically correct but:

Beta 2 agonist is still a beta agonist so it can bind nonspeficially and cause B1 activation which will cause tremor aka activates general sympathetics.

Sweating is generally can be categorized as sympathetic activation but the sweat gland has a muscarinic receptor so it won't be affected by a beta agonist.

the remaining choices are parasympathetic responses.

Subcomments ...

The answer is hyporeflexia because the afferent arc of the muscle stretch reflex has to go through the dorsal rami and dorsal root ganglia. Dumb question, I know, but it’s the only answer that made sense. If you hurt the DRG, you not only lose afferent somatic sensory fibers, you also lose the sensory bodies involved in the various reflexes.

You can also get hyporeflexia from damaging the efferent neurons that innervate the muscle (like a LMN), but as you know these are in the anterior horn and ventral rami.

ankistruggles  Thanks! I agree with you. +  
brethren_md  Great explanation. +  
gonyyong  Agreed - I think I got this by thinking about tabes dorsalis (syphillis) and why it has hyporeflexia is due to dorsal root damage +  
duat98  I'm confused about why it wouldn't cause muscle atrophy. Isn't that a fever of LMN damage? +1  
charcot_bouchard  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 +  

submitted by lsmarshall(228),

"Desmosome (Macula adherens) - A cell-to-cell connection that provides structural support with intermediate filaments, particularly in tissues that undergo mechanical stress (e.g., skin, gastric tissue, bladder). Connects keratinocytes in the stratum spinosum of the epidermis." - AMBOSS

sympathetikey  This is why I was looking for some answer indicating keratinocytes in the stratum spinosum...instead they just gave a bunch of bs choices. +11  
roygbiv  I'm confused because I also know that S. aureus cleaves desmoglein in the stratum granulosum, so why is it specifically this answer? +2  
duat98  desomosomes connects cells to cells. hemidesmosome connects cells to basement membrane. +1  

submitted by seagull(540),

I thought this was a type 1 RTA but I was wrong. Any suggestions?

seagull  It looks like it was a type II RTA. The difference is incredibly subtle from the info given in this question. +1  
gonyyong  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 +7  
duat98  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. +3  

submitted by m-ice(145),

The patient has loss of pain and temperature on the right side of his face. Sensation of the face is ipsilateral, so the issue must be on the patient's right side, which we can confirm by knowing that sensation of the body is contralateral, and he has lost left sided pain and temperature of the body.

Pain and temperature sensation of the body is part of the spinothalamic tract, which always runs laterally through the brainstem. This can be confirmed by remembering that sensation to the face also runs laterally through the brainstem. So, we can confirm this is a right sided lateral brainstem issue.

The loss of gag reflex and paralysis of the vocal cords imply impairment of cranial nerves IX and X, both of which localize to the medulla. Therefore, the answer is right dorsolateral medulla.

duat98  You're a good man. +1  
charcot_bouchard  You must be handsome too +1  

submitted by keycompany(142),

This patient has a pneumothorax. Hyperventillation is not enough to compensate for the overall decrease in lung surface area.

_yeetmasterflex  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. +1  
duat98  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. +1  
kateinwonderland  Arterial blood gas studies may show respiratory alkalosis caused by a decrease in CO2 as a result of tachypnea but later hypoxemia, hypercapnia, and acidosis. The patient's SaO2 levels may decrease at first, but typically return to normal within 24 hours. (https://journals.lww.com/nursing/Fulltext/2002/11000/Understanding_pneumothorax.52.aspx) +1  
linwanrun1357  How about choice C, --ARDS? +  
bullshitusmle  there is no bilateral lung opacities as you would see in ARDS +1  

Why is alternative splicing or post-transcriptional modification incorrect?

tea-cats-biscuits  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. +  
mcl  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. +9  
ngman  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. +  
medschul  They're cleaved by tissue-specific proteases +  
duat98  I think: 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. +4