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 +0  (nbme22#26)
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oN ngehca in teyp 1 error adn serceaed in ptey 2 ro?rre anC nmoseeo ealpes ainpxel yh?w

bhangradoc  The P-value is basically the type 1 error, and they keep the p-value the same (at <.05) in both versions of the experiments. By increasing number of patients in the group, they increase power of the study, which reduces type II error. +2

 +1  (nbme22#17)
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woH anc yuo ellt ttha teh enkla ertacfru si ro?iesnev

lnsetick  Because there is avulsion fracture on medial side from deltoid ligament and fibular fracture on oppostie side, this is classic for an eversion. +3
alimd  Its more a CK-type question +

 -2  (nbme21#8)
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I nitkh isth noe is elyrltila tjsu igksan whta rtpa of het neiydk wlil be the msot orpoyl pfeseu.dr That rpta loduw have eht otsm ern.in oA,sl teh amleuld ’ondste have GJ lscle os I eussg sah’tt teanhro rsaneo yhw it culd’tno vahe hte smto neirn.

sklawpirt  Exactly, it has to do with where in the kidney renin is released and requires a bit of knowledge of the artery branches that give rise to the afferent arteriole in the first place and where this branch point is located. http://anatomyforme.blogspot.com/2008/05/histology-of-kidney-lot-to-process.html Where renin production occurs in JGA cells, EPO production occurs in the renal peritubular interstitium (especially the proximal renal tubule, corext and some of the outer medulla.) Thus with the same questions stem it might ask where is concentration of EPO the highest? [And it would still be the cortex, with lower concentrations in the outer medulla, lowest concentration in the inner medulla, and none found in the papilla or renal pelvis. +14
hayayah  Actually, the renal medulla receives significantly less blood flow than renal cortex. So the medulla is the one that's very sensitive to hypoxia and vulnerable to ischemic damage. I don't think this question is related to "what area is the most poorly perfused." It's just knowing that renal artery stenosis is going to decrease blood flow to the kidney. JG cells sense the decrease in perfusion pressure and secrete renin. Knowing that renin is produced by the JG cells and that JG cells are in the cortex should be enough to answer this question. +6
cry2mucheveryday  I thought all the renin would collect in the pelvis where the arteries whould drain into a common vein and changed my answer to pelvis ._. +2

 +2  (nbme21#7)
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reyet,nativAll all eth otehr psnooti ptondei to ishtgn ttah oluwd aacutlyl iasnreec srntooeteest trunidcopo adn ist eft;fcse coyomirtehc duowl losouviyb ont do htt.a





Subcomments ...

submitted by iviax94(7),
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ereTh aehv bnee a cpuoel fo qsuotines tuabo iths itopc no eht enrew .xsema ev’I eben wgnnriesa by aequitng bidoli to strteenosote veells nad rnlancuot eocnestri ot lhehat fo acuatrlsveu ce(sehsroltairos ro )o.tn sI stih rce?rtoc

liverdietrying  When you’re thinking of libido, don’t just equate it to testosterone -- make sure you’re always considering depression! Depression following stroke is common, especially with residual physical disability, so this would decrease his libido. Nocturnal erections equate to “does it actually work?” not just the vasculature but the neural input as well. For example, during prostatectomy damage to the pelvic plexus (nerves) can lead to impotence. There’s nothing to suggest that he has vascular or neurologic erectile dysfunction here, which is why his nocturnal erections are intact. +28  
_pusheen_  @liverdietrying Was it premature to assume he has trouble with erections because of neural damage from the stroke? I put low libido, low nocturnal erections. Is it because the stroke resulted in hemiparesis and not autonomic dysfunction or something like that? +5  
liverdietrying  @pusheen Correct, you won’t classically get impotence after a hemiplegic stroke. His inability to achieve an erection is much more likely to be 2/2 psychosocial effects than organic disease. If this vignette instead said that this had gotten a prostatectomy with resulting damage to the pelvic nerves that allow for erection, then it’d be a more safe choice to put no nocturnal erections. +4  
fast44  Is there a video or somewhere that explains these sexual dysfunctions? This seems to be a topic that keeps repeating on the new exams. +2  
forerofore  well, i though that because he had a stroke he would be likely to have atherosclerosis, which would keep libido high and reduce nocturnal erections, i kinda ignored the whole "he´s depressed" part of the vignette despite understanding the mechanism well. but from a clinical depression point of view, if his arteries are intact, and he is depressed, then libido would be low, and erections present at night. +4  
pg32  I can't remember exactly but I swear the question on NBME 21 the guy's wife had died as well...? Or they had gotten divorced? Either way, he had some psychological baggage as well, but his libido was still normal, and the explanation was that his testosterone would be fine regardless of his depressed mood. So I went with that logic here and missed this question. I don't understand how I am supposed to gauge someone's libido based on vague hints at their mood, especially when in one exam mood does not decrease libido and in the other it does. +1  
drzed  @pg32 bro spoilers +2