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 +0  (nbme22#26)

No change in type 1 error and decrease in type 2 error? Can someone please explain why?

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.

 +1  (nbme22#17)

How can you tell that the ankle fracture is eversion?

lnsetick  Because there is avulsion fracture on medial side from deltoid ligament and fibular fracture on oppostie side, this is classic for an eversion.

 -2  (nbme21#8)

I think this one is literally just asking what part of the kidney will be the most poorly perfused. That part would have the most renin. Also, the medulla doesn’t have JG cells so I guess that’s another reason why it couldn’t have the most renin.

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.
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.
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  (nbme21#7)

Alternatively, all the other options pointed to things that would actually increase testosterone production and its effects; orchiectomy would obviously not do that.

Subcomments ...

submitted by iviax94(5),

There have been a couple of questions about this topic on the newer exams. I’ve been answering by equating libido to testosterone levels and nocturnal erections to health of vasculature (atherosclerosis or not). Is this correct?

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. +15  
_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? +4  
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. +1  
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. +  
drzed  @pg32 bro spoilers +2  

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