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 +4  (nbme20#20)

You can cross out the top three answer choices, A,B,C. You wont be reabsorbing anything in the PCT in fanconi's syndrome. Looking at hypokalemia, hyponatremia, and hypophosphatemia now. Hypokalemia can't be correct because even though potassium is lost it will be reabsorbed at the later thick ascending loop and if that doesnt make sense, the body will adjust for low serum potassium but activating the H+/K+ pump on cells. It isn't hyponatremia because at the collecting duct principal cells, reabsorption will occur. This leaves hypophosphatemia as the correct and only answer choice.

imgdoc  by*
larascon  Excellent explanation, thank you !

 +0  (nbme20#43)

I know it's tempting to think that this may be Androgen insensitivity syndrome but its not, for it to be AIS there needed to be an increase in testosterone. In this case it was in the normal range for a female. Now that we know the person is definitely female -> Mullerian agenesis becomes the best answer.


 +7  (nbme21#33)

I thought about it like this: Patient is having psychogenic ED - its all in his head, libido is normal and nocturnal erections are normal.

If his Testosterone level was low - Libido decreased. If his nervous system (parasympathetic/sympathetic) was damaged - nocturnal erections decreased.

Hope this helps.


 +1  (nbme21#12)

The clinical presentation is that of lower abdominal pain, fever, and chills. This alone made me think it was an inflammatory process. Also the question says there are 3 separate poorly delimited regions of narrow lumen. As far as ulcerative colitis is concerned, there are no skip lesions, it is continuous wherever it is. This coupled with the history of constipation makes diverticulitis the best answer choice.


 +0  (nbme21#15)

Ileocolic (systemic)/inferior mesenteric (portal), and splenic (portal)/left renal (systemic) are the only two portosystemic shunt options. Of which splenic and left renal is the BEST option of the two just based on their proximity to the esophageal varices.


 +0  (nbme21#33)

Question presents an immunosuppressed patient with rash over the lower back which is pruritic. Vesicles (small fluid filled blisters) are present with ulcerated/crusted lesions also found in that area. This is varicella zoster infection: multiple crops of lesions in various stages from vesicles to crusts.


 +1  (nbme21#4)

This question is asking about the insulin receptor tyrosine kinase pathway. So take it from there,

  1. The phosphorylation of the IRS activates a signal transduction cascade that leads to the activation of other kinases as well as transcription factors that mediate the intracellular effects of insulin. Nuclear/Cytoplasmic shuttling - yes (reversible)

  2. Serine/Threonine kinases are also known to reduce the activity of insulin. - yes (reversible)

  3. Ubiquitin - mediated proteolysis - no (not reversible), and also insulin metabolically increases protein synthesis so it doesn't match what insulin does anyways.

correct me if I'm wrong.

usmle11a  i think youre correct cause ubiquitin mediated proteolyis is an irreversible step.

 +0  (nbme21#48)

I think the answer was consensus because the "surrogates" aka family members havent deliberated yet. If this was after their deliberation and they disagree, then it goes spouse -> adult children -> parents -> siblings etc. The question doesn't mention any disagreements, hence they need to decide cumulatively and make a decision.

That was just my take on this question.


 +2  (nbme21#11)

Basically this question just asks "what is power" and asks you to explain that 80% power. Power is 1 - beta (type 2 error), basically when a difference exists and the null hypothesis is rejected is power. So if the Rx detects a mean difference of 0.4 in asthma in the patients in the treatment group, then that data falls in the 80% power range, and its significance is 95% (p<0.05), P value is just the probability of something happening by chance, so you what this to be less that 5% so whatever you observed isn't bullshit.

I hope this helped, and correct me if I'm wrong.

yssya1992  I have a question : whats the relation then between power and P value ?
privatejoker  This one took me a minute and was during the last block so my brain was already fried. But my reasoning was that, as stated above, since it gave you power, it is basically just a long-winded way of asking what Power is, and how this relates to p-value. P-value is the odds that the finding was due to chance alone. Obviously a p-value set to <0.05 implies a greater than 95% chance that the finding is legit. Since the power is said to be 80%, this means that there is an 80% chance that the study finding is legit, at least insomuch that it met the pre-set criteria of being 95% non-chance related.
sahusema  80% chance (power) the study correctly identifies the existence of an association in reality. If an association is determined to exist, >95% chance the study and reality agree with each other (p<.05)

 +4  (nbme22#37)

I think its the right MLF (area C), not the right abducens nucleus that is lesioned on the cross section. If the abducens nucleus were lesioned she wouldn't have abduction in her left eye. The MLF mediates cross talk between the abducens nucleus on both sides to the MLF on the opposite side (2 abducens nuclei, 2 MLF one on each side). In her case, her right MLF wasn't functioning hence why she was gazing left but her right middle rectus wasn't contacting to mediate leftward gaze.

This picture helps: http://what-when-how.com/wp-content/uploads/2012/04/tmp15F9_thumb.jpg

imgdoc  *medial rectus

 +3  (nbme22#1)

I think alot of people might have over emphasized how important ANP and BNP really are, yes it is important to know these peptides get secreted by the atrial/ventricular myocardium during heart failure. However their overall effectiveness in treating heart failure is zilch, a preceptor told me that if ANP and BNP were so useful in natriuresis then why do we give diuretics? It's because RAAS overpowers this system hence causing negative effects and the endless loop of heart failure. AKA why we give ACE inhibitors.

Knowing that ANP gets neutralized by the RAAS system, we can shift our focus back to heart failure in this patient, where cardiac output is decreased, leading to ADH secretion and finally dilutional hyponatremia.





Subcomments ...

submitted by imgdoc(25),

You can cross out the top three answer choices, A,B,C. You wont be reabsorbing anything in the PCT in fanconi's syndrome. Looking at hypokalemia, hyponatremia, and hypophosphatemia now. Hypokalemia can't be correct because even though potassium is lost it will be reabsorbed at the later thick ascending loop and if that doesnt make sense, the body will adjust for low serum potassium but activating the H+/K+ pump on cells. It isn't hyponatremia because at the collecting duct principal cells, reabsorption will occur. This leaves hypophosphatemia as the correct and only answer choice.

imgdoc  by* +1  
larascon  Excellent explanation, thank you ! +  


submitted by celeste(32),

While the lifetime risk in the general population is just below 1%, it is 6.5% in first-degree relatives of patients and it rises to more than 40% in monozygotic twins of affected people. Analyzing classic studies of the genetics of schizophrenia done as early as in 1930s, Fischer concludes that a concordance rate for psychosis of about 50% in monozygotic twins seems to be a realistic estimate, which is significantly higher than that in dizygotic twins of about 10–19% (ncbi.nlm.nih.gov/pmc/articles/PMC4623659/#ref3)

imnotarobotbut  How is one supposed to know this before having read this article? +3  
imgdoc  This question falls under the either you know it or you dont category. It isnt in FA or Uworld +  
jaxx  So why would these A-holes put it on there as if prepping for this exam isn't stressful enough :-| +  
doodimoodi  Lol just why seriously +  
champagnesupernova3  This was mentioned in the Kaplan behavioral videos +  


It said it was fatal to males in utero, and the question asked about live born offspring. Since the males aren’t being born in the first place, I said 50% females and 0% males.

hungrybox  fuck i got baited +7  
jcrll  "live-born offspring" ← baited +3  
sympathetikey  Same :/ +  
arkmoses  smh +  
niboonsh  why is it 50% females tho? +1  
imgdoc  felt like an idiot after i figured out why i got this wrong. +1  
temmy  oh shit! +  


submitted by cantaloupe5(35),

This one was tricky but I think you could’ve done this one without knowledge of NMDA receptors. Stem told you that glutamate activates both non-NMDA and NMDA receptors but it activated only non-NMDA receptors in the early phase. That means NMDA receptors activate after non-NMDA receptors. That means something was delaying NMDA receptor activating and the only answer that made sense as the Mg inhibiting NMDA at resting potential. Once the cell is depolarized by non-NMDA receptors, NMDA receptors can be activated.

hungrybox  I forgot/didn't know this factoid and narrowed it to the correct answer and a wrong answer. Guess which one I chose? +4  
yotsubato  >That means something was delaying NMDA receptor activating and the only answer that made sense as the Mg inhibiting NMDA at resting potential. What makes the fasting gating kinetics choice incorrect then? +2  
imgdoc  NMDA receptors are both voltage gated and ligand gated channels. Glutamate and aspartate are endogenous ligands for this receptor. Binding of one of the ligands is required to open the channel thus it exhibits characteristics of a ligand channel. If Em (membrane potential) is more negative than -70 mV, binding of the ligand does NOT open the channel (Mg2+ block on the NMDA receptor). IF Em is less negative than -70 mV binding of the ligand opens the channel (even though no Mg2+ block at this Em, channel will not open without ligand binding. Out of the answer choices only NMDA receptors blocked by Mg2+ makes sense. Hope this helps. +1  
divya  sweet explanation imgdoc +  


submitted by imgdoc(25),

I think its the right MLF (area C), not the right abducens nucleus that is lesioned on the cross section. If the abducens nucleus were lesioned she wouldn't have abduction in her left eye. The MLF mediates cross talk between the abducens nucleus on both sides to the MLF on the opposite side (2 abducens nuclei, 2 MLF one on each side). In her case, her right MLF wasn't functioning hence why she was gazing left but her right middle rectus wasn't contacting to mediate leftward gaze.

This picture helps: http://what-when-how.com/wp-content/uploads/2012/04/tmp15F9_thumb.jpg

imgdoc  *medial rectus +