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 +4  (nbme24#26)

in the other hand , urine potassium is high enough , so if seizures =>rhabdomyolysis => myoglobinuria => ATN => high potassium excretion , why not?

krewfoo99  True but hypokalemia would occur in the recovery phase. So weeks after the inciting phase.

 +0  (nbme22#4)

why not sarcoidosis? 1.rheumatoid arthritis like symptoms 2.uveitis 3.kidneys ...only serositis is a bit controversial

seracen  I usually look for the hilar manifestation, when considering sarcoidosis, or the skin manifestations. Personally, I thought Sjogren's when I read this.

 +0  (nbme22#4)

why not sarcoidosis? 1.rheumatoid arthritis like symptoms 2.uveitis 3.kidneys ...only serositis is a bit controversial





Subcomments ...

submitted by neonem(265),

this patient has symptomatic aortic stenosis. This can be identified by the ventricular hypertrophy (to compensate for increased functional afterload from non-compliant aortic valve), midsystolic murmur and the location at the normal aortic area.

Per UpToDate on Clinical manifestations of Aortic Stenosis:

"Dizziness and syncope — Syncope occurs as a presenting symptom in approximately 10 percent of patients with symptomatic severe AS (or approximately 3 percent of all patients with severe AS) [3]. There are several proposed explanations for exertional dizziness (presyncope) or syncope in patients with AS, both of which reflect decreased cerebral perfusion. Exercise-induced vasodilation in the presence of an obstruction with fixed cardiac output can result in hypotension."

guillo12  What does "fixed cardiac output" signify? +  
usmleuser007  "fixed cardiac output" might mean that with the stenosis (ie. narrowed aortic valve) there is a limited or rather reduced cardiac output. Exercise would not increase cardiac output because the stenosis is caused by a mechanical (physical) rather than a biochemical process. Therefore, At any given moment the heart can not increase its output no matter how forcefully it contracts. +1  
fallot4logy  why not option A?arterial compression ? +  
sunshinesweetheart  @fallot4logy LVH does not lead to coronary artery compression. only reallyyyy rarely will pulmonary artery dilation cause coronary artery compression. plus that would cause angina but probably wouldnt decrease cerebral bloodflow to syncope. her murmur + LVH point us toward aortic stenosis which does cause those --> fixed CO +  


submitted by colonelred_(48),

The analysis only showed a mutation in one allele. CF is an autosomal recessive disease: the disease only manifests if there are mutations in both alleles of the CFTR gene.

If you still have 1 functional copy of the CFTR gene, you can still make the CFTR protein (the chloride channel/transporter), hence your body won’t have any issues.

This is analogous to tumor suppressor genes like Rb: so long as one of the alleles you have is functional, you can make enough of the protein to “make up” for the defective allele. If both get knocked out (Rb-/-), you lose the protection provided by the gene because now you make no protein at all.

The only thing that made sense for this question was the fact that the other allele was not included in the analysis.

charcot_bouchard  OR another allele has a diff type of mutation because CF is done by like hundreds of diff type of mutation. SO the 70 types that we screened covered one type from one parent but not another that was inherited from other parent. +4  
soph  I put D thinking there was a mutation in another protein that interacts with CFTR....thus u dont have CF but some disease with similar phenotype. Is this wrong bc its simply not the case ?? +  
nbmehelp  @charcot_bouchard I think that makes more sense if I understand what you're saying- Probably had a mutation only in 1 of 2 of the same alleles in the analysis but had another mutation in 2 of 2 alleles at a different location not included in the analysis, right? +  
fallot4logy  CF is a rare disease , and the possibility to have a mutated gene plus a gene that its not belong to 70 most common cf mutations is extremely rare +  


submitted by lilamk(5),

I am so confused! The only logic I could come up w is that NSAIDs decrease dilation of afferent arteriole so this more constricted arteriole is interpreted as decreased blood flow and Renin increases? My issue w this is that when I google it and search UW for this renin affect nothing comes up only article I could find actually contradicts it and says renin would DECREASE from NSAIDs leading to the hyperkalemia we sometimes see ...

Any thoughts would be helpful! Thanks geniuses.

generic_login  I used that reasoning to pick C, but in looking it up now it seems like you are right ... There appear to be a bunch of mistakes on this test, and it’s not giving me a lot of confidence for the real thing. +  
mee48  I think it is because NSAIDs inhibit the local prostaglandin (PGE2) in afferent arteriole —-> less AA dilation —-> stimulation renin release. I think my reasoning came from sketchy pharm nsaid video but I can’t 100% remember +  
keycompany  NSAIDs constrict the afferent arteriole. ​ A. GFR would decrease due to decreased renal blood flow. B. Renal Blood flow would decrease. C. Renin would increase due to renal hypoperfusion. D & E. PGE2 and TXA would decrease (by MOA of NSAIDs). +1  
fallot4logy  UW says that Nsaids is one o +  
fallot4logy  UW says that Nsaids is one of the 5 drug categories that is able to cause hyperkalemia.Specificly ,Nsaids lower PG andrenin secretion .PGE2 stimulates JG cells to secrete renin...(how can i delete my previous unfinished message,lol?) +  


submitted by lilamk(5),

I am so confused! The only logic I could come up w is that NSAIDs decrease dilation of afferent arteriole so this more constricted arteriole is interpreted as decreased blood flow and Renin increases? My issue w this is that when I google it and search UW for this renin affect nothing comes up only article I could find actually contradicts it and says renin would DECREASE from NSAIDs leading to the hyperkalemia we sometimes see ...

Any thoughts would be helpful! Thanks geniuses.

generic_login  I used that reasoning to pick C, but in looking it up now it seems like you are right ... There appear to be a bunch of mistakes on this test, and it’s not giving me a lot of confidence for the real thing. +  
mee48  I think it is because NSAIDs inhibit the local prostaglandin (PGE2) in afferent arteriole —-> less AA dilation —-> stimulation renin release. I think my reasoning came from sketchy pharm nsaid video but I can’t 100% remember +  
keycompany  NSAIDs constrict the afferent arteriole. ​ A. GFR would decrease due to decreased renal blood flow. B. Renal Blood flow would decrease. C. Renin would increase due to renal hypoperfusion. D & E. PGE2 and TXA would decrease (by MOA of NSAIDs). +1  
fallot4logy  UW says that Nsaids is one o +  
fallot4logy  UW says that Nsaids is one of the 5 drug categories that is able to cause hyperkalemia.Specificly ,Nsaids lower PG andrenin secretion .PGE2 stimulates JG cells to secrete renin...(how can i delete my previous unfinished message,lol?) +