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Comments ...

 +5  (nbme24#15)

I don't know if there is an equation for this, but I basically pumped out every division across the table to get ~5% on average.

Here they are: 400 / 6,000 = 0.067 250 / 5,600 = 0.045 300 / 5,350 = 0.056 300 / 5,050 = 0.059 250 / 4,800 = 0.052

The average of these %s for all the years = 5.58%. So that's close enough to 5%.

seagull  good work. I found this question annoying and gave up doing those considering the amount of time we are given.
vshummy  Well just don’t include the intake year... because that messed me up..
_yeetmasterflex  How would we have known not to include the intake year? From average **annual** incidence?
lamhtu  Do not include intake year because the question stem is asking average annual incidence. The 4000 positives at intake could have acquired HIV whenever, not just in the last year.
neels11  literally didn't think there was an actual way to figure this out. but my thought process was: okay incidence means NEW cases. so the annual average at the end of 5 years would be: (# of NEW people that tested positive at the end of year 5) / (# of people at that were at risk at the beginning of year 5) <--- aka at the end of year 4 250/5050 = 4.95% also if you look at year 5: you'll see that the at risk population is 4800 when 300 new cases were found the year before. 5050 at the end of year 4 MINUS the 300 new cases at the end of year 4 should give you 4750 as the new population at risk. but notice that end of year 5 we have 4800. idk if that means 50 people were false positives before or 50 people were added but in incidence births/death/etc don't matter it's kind of like UWORLD ID 1270. assuming average annual incidence is the same as cumulative incidence this was just a bunch of word vomit. sorry if it was unbearable to follow

 +5  (nbme24#23)

A man with a Hx of EtOH dependence and chronic abd pain as well as X-ray findings of "calcifications in the mid-upper abdomen" is most likely referring to a chronic pancreatitis.

This leads to a lack of lipase secretion hence, pale, foul-smelling stools with oil droplets per pt Hx. This pt's pancreas also doesn't secrete other enzymes, such as amylases, proteases, nor trypsinogen (to activate other enzymes), so the answer is "generalized malabsorption".

karljeon  p. 367 (FA 2018)
usmlecrasherss  pancreatic insufficiency FA 2019 p375 ,
almondbreeze  FA 2019 p391 on chronic pancreatitis
almondbreeze  UW: in chronic alcoholic pancreatitis, alcohol induced secretion of protein rich fluid precipitates in pancreatic duct--> forms ductal plugs that calcify

 +6  (nbme20#2)

This one was a somewhat simple question since chemotherapy --> tumor lysis --> need xanthine oxidase inhibitor (eg, febuxostat).

BUT WHY IS NBME GRAMMAR SO CRAP? PUT YOUR COMMAS IN THE RIGHT PLACE!

malou  I swear I registered just to upvote your comment. #SoFrustratedToo
xoxofossagirl  ,omg, me, too, ,

 +3  (nbme24#23)

Vitamin E deficiency causes hemolytic anemia, acanthocytosis, muscle weakness, posterior column and spinocerebellar tract demyelination.

karljeon  Can anyone explain why the serum lactate dehydrogenase (LDH) level was elevated?
asapdoc  Vitamin E is an antioxidant. Thus a deficiency can cause hemolytic anemia.
sympathetikey  @karljeon Intravascular hemolysis = LDH release from RBCs




Subcomments ...

submitted by karljeon(49),

A man with a Hx of EtOH dependence and chronic abd pain as well as X-ray findings of "calcifications in the mid-upper abdomen" is most likely referring to a chronic pancreatitis.

This leads to a lack of lipase secretion hence, pale, foul-smelling stools with oil droplets per pt Hx. This pt's pancreas also doesn't secrete other enzymes, such as amylases, proteases, nor trypsinogen (to activate other enzymes), so the answer is "generalized malabsorption".

karljeon  p. 367 (FA 2018) +1  
usmlecrasherss  pancreatic insufficiency FA 2019 p375 , +1  
almondbreeze  FA 2019 p391 on chronic pancreatitis +  
almondbreeze  UW: in chronic alcoholic pancreatitis, alcohol induced secretion of protein rich fluid precipitates in pancreatic duct--> forms ductal plugs that calcify +  


submitted by strugglebus(96),

I chose this solely because it was so damn specific

sympathetikey  Same. Learn something new every day: See more: https://www.fda.gov/safety/medwatch-fda-safety-information-and-adverse-event-reporting-program +4  
karljeon  I didn't choose it because it was so damn specific. :( +16  


submitted by strugglebus(96),

As an edit: 108,001 people reported to have side effects when taking Hydrochlorothiazide. Among them, 25 people (0.02%) have Breast discharge

neonem  I think the best way to answer this question was by process of elimination. +  
sympathetikey  That's some bullshit lol +2  
karljeon  Haha I eliminated the answer by process of elimination. +10  
medschul  I eliminated thiazides by process of elimination :( +  
medstudent65  Shit I eliminated thiazides because of elimination went with HTN thinking intercranial bleed effecting the pituitary +1  


submitted by hayayah(603),

Notice, the stem says "precorsors in the skin"

D3 (cholecalciferol) from exposure of skin (stratum basale) to sun, ingestion of fish, milk, plants.

D2 (ergocalciferol) from ingestion of plants, fungi, yeasts.

Both converted to 25-OH D3 (storage form) in liver and to the active form 1,25-(OH)2 D3 (calcitriol) in kidney.

sympathetikey  C is the 3rd letter in the alphabet. Hence, D3 = Cholecalciferol +2  
karljeon  Thanks for the explanation. The question stem made it sound like "what future step will be decreased?" Actual question: "Decreased production of which... is most LIKELY TO OCCUR in this patient?" Maybe NBME needs a grammar Nazi working for them. +3  
bharatpillai  question says "decreased production of which of the following precursors in skin is most likely to occur in this patient? the answer has to be 7-dehydrocholecalciferol! +2  
bharatpillai  7 dehydrocholesterol +2  
brbwhat  Yeah i did the same, but then realised acc to uw flowchart 7dehydrochole.. is converted to cholecalciferol in presence of uv rays. So the decreased precursor would be cholecalciferol since we already have 7 dehydrocholecalciferol not being converted by uvrays Tho the uw chart sites both ergo and chole as dietary sources. +1  
drzed  Wouldn't 7-dehydrocholesterol build up in the skin? Since UV rays convert 7-dehydrocholesterol into cholecalciferol, if you are lacking the conversion, the reactant (7-dehydrocholesterol) should accumulate. +  
brbwhat  They’re asking decreased production of which of the following precursor would occur? 7 dehydrocholestrol builds up, but decreased production of cholecalciferol takes place, which is a precursor in the pathway for vitamin d formation +  


submitted by karljeon(49),

Vitamin E deficiency causes hemolytic anemia, acanthocytosis, muscle weakness, posterior column and spinocerebellar tract demyelination.

karljeon  Can anyone explain why the serum lactate dehydrogenase (LDH) level was elevated? +  
asapdoc  Vitamin E is an antioxidant. Thus a deficiency can cause hemolytic anemia. +4  
sympathetikey  @karljeon Intravascular hemolysis = LDH release from RBCs +1