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(B) You get an increased BUN:Cr ratio because increased urea absorption at the proximal tubule (conservation of water), but you lose the same amount of Cr since none of it is reabsorbed; thus the ratio increases.
I may be wrong but I think more of the urea (BUN) would be absorbed in medullary collecting duct in this situation due to ADH; think I saw a question on this in uworld, could pop up
I believe this patient actually has dilated cardiomyopathy (as opposed to hypertrophic) due to his age, HTN, presence of S3 (hypertrophic usually has S4), and also his murmur. The murmur indicates mitral regurg, the tip-off was "radiating to the axilla". Because the stem states that the PMI is diffuse this can lead us to think that his heart has enlarged in an unpredictable way (ie. making it acceptable that the placement of the murmur is different from where we expect). Lastly, secondary mitral regurg is an indicator of poor prognosis for HF. Once the ventricle has dilated to such a point, the mitral leaflets are unable to properly close and perpetuate the backward flow of blood. Hope this helps!
agreed "granular deposits" rules out MCD (the only other nephrotic syndrome) because MCD is IF (-)
could someone explain why the other choices are ruled out by biopsy?
@cooldudeboy1 PSGN does have a granular immunofluorescence, but there is no previous illness or hematuria mentioned so you can rule that out. Goodpasture is classically linear IF since they're antibodies against the GBM. IgA nephropathy is mesangial IF so it would deposit more in the middle. Minimal change wouldn't show anything on IF
Totally agree w/ you Qball... I thought MPGN too, but I think Penicillamine makes it Membranous Nephropathy
Totally agree, arterial dilation--> increases blood flow into capillaries/increases capillary hydrostatic pressure + increasing permeability of the post-capillary venules= Increased Capillary Filtration Rate
I love you explanation, but I don't think filtration rate is dependent upon permeability of the post-capillary venules. I think the filtration rate is increased simply due to the increased blood flow; this is similar to how increased renal blood flow will increase Glomerular Filtration Rate (GFR).
Is this the best approach to all of the "strongest predisposing risk factor" type questions?
There is a town of 1,000 men. Nine hundred of them work as lawyers. The other 100 are engineers. Tom is from this town. He rides his bike to work. In his free time, he likes solving math puzzles. He built his own computer. What is Tom's occupation most likely to be? Answer: Tom is most likely to be a lawyer! Don't let assumptions distract you from the overwhelming force of sheer probability! "Given that Tom is from this town, his most likely occupation (from the available data) = lawyer."
There is a town of 1,000 spontaneous pneumo patients. Six hundred are tall, thin and male. The other 400 are something else. Two hundred of the 1,000 smoke cigarettes. The other 800 do not. What risk factor is most strongly associated with spontaneous pneumo? (Answer: Not being a smoker! ... because out of 1,000 people, the most common trait is NOT smoking [800 members].)
beautiful! also, i think about odds ratio vs. relative risk...odds ratio is retrospective of case-control studies to find risk factor or exposure that correlates with grater ratio of disease. relative risk is an estimation of incidence in the future when looking at different cohort studies.
@impostersyndrome I love me some probability and statistics. Glad my rant was useful :P
i hate it which is why your rant was extremely useful lol i learned a ton thanks dr.doom!
I caught he was thin. The only reason I didn't pick Gender and body habitus is because he was not overly tall (5'10"). I talked myself out of it because I thought the body habitus was too "normal" because he was not both thin AND tall. Got to keep telling myself to not think too hard on these. Thanks for the explanation.
It isn't just that this person has Ehlers Danlos and they're more prone to spontaneous pneumo???
Also look for Kluver-Bucy like symptoms in the stem
I agree with everything but normal glucose. Glucose here is NOT normal.
to quote wiki
"The glucose level in CSF is proportional to the blood glucose level and corresponds to 60-70% of the concentration in blood. Therefore, normal CSF glucose levels lie between 2.5 and 4.4 mmol/L (45–80 mg/dL)."
NBME reference table gives normal CSF glucose to be 40-70 mg/dL. As far as I'm concerned, for the purposes of the exam the reference table is probably a better source than wiki.
you're definitely not alone lol
And its not in FA, so fuck it IMO
I guessed it because the names sounded similar :D
I also guessed because both words start with "glu")))
same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle.
Not a clue. This was so random.
this made me feel a lot better.
also, no fucking clue
My immediate thought after reading this was "why would i know this and how does this make me a better doctor?"
Generally speaking Glutamine is often used to aminate things. Think brain nitrogen metabolism. You know that F-6-P isn't an amine, and that Glucosamine is, so Glutamine isn't an unrealistic guess.
yea, I mature 30k anki cards to see this bs
I literally shouted wtf in quiet library at this question.
Lol def didn't know it. Looks like I'm not going to be a competent doctor because I don't know the hexosamine pathway lol
Is it biochemistry? Then I do not know it.
I Ctrl+F'd glucosamine in FA and it's not even there lol
i definitely guessed, for some reason got it down to arginine and glutamine
I did not
Narrowed it down to Arginine and Glutamine figuring the Nitrogen would have to come from one of these two but of course I picked the wrong one. Classic.
+1 no idea!
Ahhh yes the classic Glucosamine from fructose 6-phosphate question....Missed this question harder than the Misoprostol missed swing
no idea. i could only safely eliminate carbamoyl phosphate because that's urea cycle
just adding in to say, nope.
Lol I didn't either. I think this is just critical thinking though. The amine has to come from somewhere. Glutamine/glutamate is known to transfer amines at the least
Goljan and FA mentioned this as Monday Disease for people who worked in industries that heavily used nitrates, where they would build tolerance during the week and then get a headache when they went back to work on Monday
Just to add to this- one of the side effect of NG when given to patients with MI is "massive headache"! That's how I the question right!
This is similar in how triptans induce vasoconstriction which is used to treat migraines
info about ferruginous bodies being mf can't be found on FA/UW :'( they just say it's 'material'
FA 2020 677, FA 2019 659... mf?? mofos??
Just to add: The question asks what cell type initiated the Fibrosis → Alveolar macrophages engulf the particles and induce fibrosis (same pathophys for all Pneumoconiosis). Pathoma 2019 Pg 92
and explains the flame hemorrhages (Goljan) caused by malignant HTN
FA 2020 pg 301*
The flame hemmorhages are also a good buzz word for recognizing he has hypertensive retinopathy 2e chronic, uncontrolled HTN. Pt's with hypertensive retinopathy can also present with "cotton wool spots" and "macular star". Pics on FA 2019, p. 299
pg 338 of FA lists it under hypothyroidism but it does present as transient hyperthyroidism first
yep that was the key! Goiter is "HOT" but the remaining answer choices were still kind of bleh D was distracting the hell out of me i spent so long to convince myself to pick C and move on
Pasting nwinkelmann's comment as an addition: Choice "D" is wrong b/c "lymphomatous thyroid gland" = primary thyroid lymphoma (typically NHL, which is very rare) or Hashimoto's thyroid progression. Hashimoto's thyroiditis = lymphocytic infiltrate with germinal B cells and Hurthle cells, which upon continued stimulation, can lead to mutation/malignant transformation to B cell lymphoma. Both of these present with hypothyroidism with low T4 and high TSH (opposite of this patient).
I absolutely love your @liverdietrying, however the pathogenesis of postpartum thyroiditis is similar to Hashimoto's, so I think this person has postpartum thyroiditis and your explanation of transient thyrotoxicosis is spot on, which would also occur in postpartum thyroiditis
I agree with @taediggity. Also note that women eventually recover from postpartum thyroiditis and typically become euthyroid again, which doesn't happen with Hashimoto's.
In FA (2019 p. 338) it says that thyroid is usually normal size in postpartum thyroiditis, but the patient in this question had a thyroid "twice the normal size." I guess at the end of the day it doesn't matter which diagnosis is right for this question cause they both seem to lead to the same correct answer :)
nice! I reasoned it as that most of the GI system is of endodermal origin
any FA or pathoma or uworld correlation?
Type II pneumocytes serve as the stem cell precursors, w/out those you're more or less fucked: FA 2020 pg 661