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 +4  (nbme22#2)

So this patient is essentially in hypovolemic shock because he's hemorrhaging blood from the aorta.

A) You'd have increased ADH to conserve volume B) You'd have increased BUN:Cr ratio b/c due to a decrease in blood flow C) Increased TPR naturally due to less pressure on barorecptors D) Decreased Capillary hydrostatic pressure b/c they have decreased volume E) Decreased Carotid sinus firing rate b/c less pressure F) The Answer: RAAS is activated -

drzed  (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.

 +1  (nbme22#31)

2/6 systolic murmur over the left sternal border,an S3 (increased LV filling), low 02 sat, figured this patient had hypertrophic cardiomyopathy and early signs of CHF, so the answer was crackles from the pulmonary edema from fluid back up from the HF as brise pointed out below the 1st comment.





Subcomments ...

Not 100% sure on this one, but here’s how I approached it: histamine causes arterial dilation (=decreased arteriolar resistance), but all of that blood has to go somewhere since you now have more blood flowing through the arteries and that somewhere is the capillaries (increased capillary hydrostatic pressure). Histamine causes increased permeability of the post-capillary venules (one of Dr. Sattar’s favorite facts) so you’d have increased capillary filtration rate.

taediggity  Totally agree, arterial dilation--> increases blood flow into capillaries/increases capillary hydrostatic pressure + increasing permeability of the post-capillary venules= Increased Capillary Filtration Rate +1  
makinallkindzofgainz  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). +2  


submitted by drdoom(354),

You have to think about this using the concept of CONDITIONAL PROBABILITY. Another way to ask this type of question is like this: “I show you a patient with spontaneous pneumothorax. Which other thing is most likely to be true about that person?” Or you can phrase it these ways:

  • Given a CONDITION (spontaneous pneumo), what other finding is most likely to be the case?
  • Given a pool of people with spontaneous pneumothorax, what other thing is most likely to be true about them?

In other words, of all people who end up with spontaneous pneumo, the most common other thing about them is that they are MALE & THIN.

If I gave you a bucket of spontaneous pneumo patients -- and you reached your hand in there and pulled one out -- what scenario would be more common: In your hand you have a smoker or in your hand you have a thin male? It’s the latter.

someduck3  Is this the best approach to all of the "strongest predisposing risk factor" type questions? +  
drdoom  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." +3  
drdoom  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].) +4  
impostersyndromel1000  this is WILD! thanks guy +3  
belleng  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. +  
drdoom  @impostersyndrome I love me some probability and statistics. Glad my rant was useful :P +  
hyperfukus  @drdoom i hate it which is why your rant was extremely useful lol i learned a ton thanks dr.doom! +1  
dubywow  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. +1  
taediggity  It isn't just that this person has Ehlers Danlos and they're more prone to spontaneous pneumo??? +  


Although there are no specific herpes indicators, a CSF panel with mostly leukocytes indicates a viral infection (as well as the normal glucose). So you can rule out TB, neurosarcoidosis and bacterial. Brudzinski/kernig sign are related to meningitis, but even if you don't know what those are, the question says that there is an abnormality in the TEMPORAL lobe (meningitis = meninges). Encephalitis would be the best answer, especially because Herpes Encephalitis affects the temporal lobe.

taediggity  Also look for Kluver-Bucy like symptoms in the stem +  


submitted by seagull(714),

out of curiosity, how may people knew this? (dont be shy to say you did or didnt?)

My poverty education didn't ingrain this in me.

johnthurtjr  I did not +  
nlkrueger  i did not lol +  
ht3  you're definitely not alone lol +  
yotsubato  no idea +  
yotsubato  And its not in FA, so fuck it IMO +1  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +8  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +11  
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle. +  
jaxx  Not a clue. This was so random. +  
wolvarien  I did not +  
ls3076  no way +  
hyperfukus  no clue +  
mkreamy  this made me feel a lot better. also, no fucking clue +1  
amirmullick3  My immediate thought after reading this was "why would i know this and how does this make me a better doctor?" +4  
mrglass  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. +2  
djtallahassee  yea, I mature 30k anki cards to see this bs +3  
taediggity  I literally shouted wtf in quiet library at this question. +1  
bend_nbme_over  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 +1  
drschmoctor  Is it biochemistry? Then I do not know it. +1  
snoochi95  hell no brother +  
roro17  I didn’t +  
bodanese  I did not +  
hatethisshit  nope +  
jesusisking  I Ctrl+F'd glucosamine in FA and it's not even there lol +  
batmane  i definitely guessed, for some reason got it down to arginine and glutamine +  


submitted by nwinkelmann(185),

I found this when trying to understand why increased NO caused headaches: Nitrates/nitrites are a very common headache and migraine food triggers (WebMD) and raise nitric oxide levels. High levels of nitric oxide are associated with migraine (Study). Headaches and migraines are also very common in medications that boost nitric oxide, such a viagra (study), but it is unclear why this happens. The original hypothesis was that nitric oxide increases blood vessel size and triggers a migraine, but the viagra study and others disproved this. Newer studies on nitric oxide shows that it increases the peptide (CGRP) that is considered responsible for triggering migraines (Study) after increases in inflammation. Because nitric oxide is associated neurogenic inflammation diseases, it's likely that headaches and migraines from nitric oxide are a warning sign of this inflammation (Study).

The research is basically stating that nitrates raise nitric oxide levels and high nitric oxide levels increase inflammation and headaches and migraines. However, the exact reason why this happens is unknown.

https://www.quora.com/Why-do-nitrates-cause-headaches

taediggity  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 +1  


submitted by welpdedelp(137),

It was a Ferruginous bodies--> asbestosis. Ferruginous bodies are believed to be formed by macrophages that have phagocytosed and attempted to digest the fibers.

almondbreeze  info about ferruginous bodies being mf can't be found on FA/UW :'( they just say it's 'material' +  
taediggity  FA 2020 677, FA 2019 659... mf?? mofos?? +  
69_nbme_420  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 +1  


submitted by mattnatomy(31),

Severe hypertension often leads to hyperplastic arteriolosclerosis (onion-skin appearance). Also see proliferation of smooth muscle cells.

meningitis  and explains the flame hemorrhages (Goljan) caused by malignant HTN +4  
taediggity  FA 2020 pg. 537 +  
dentist  FA 2020 pg 301* +  


This one was a little tricky. For this one the key is the low radioiodine uptake. This patient has high T4 and low TSH which makes sense in a hyperthyroid patient, perhaps your first thought is that this patient has Grave’s disease. However, in Grave’s your thyroid is being stimulated to make more thyroid hormone from scratch and as such would have an increased radioiodine uptake because the thyroid is bringing in the required (now radiolabeled) iodine. This is why it is not Graves (“release of thyroid hormone from a thyroid stimulated by antibodies”).

So if its not Grave’s what could it be? For this you’d have to know that Hashimoto’s Thyroiditis (also known as Chronic Lymphocytic Thyroiditis and is often referred to as such on board exams to throw you off) has three phases - first they are hyperthyroid, then euthyroid, then the classic hypothyroid that you would expect with low T4 and high TSH. This was the key to this question. The reason for this is that antithyroid peroxidase antibodies in Hashimoto’s cause the thyroid to release all of its stored thyroid hormone making the patient hyperthyroid for a short period of time. After this massive release of thyroid hormone, the antibodies make them unable to make new TH and therefore they become euthyroid for a short period and then hypothyroid which you would expect! Since they can’t make new TH, the thyroid will not take up the radioiodine and therefore there will be low radioiodine uptake. Hence, “release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes.” aka “Lymphocytic (hashimotos) thyroiditis”.

I think “release of thyroid hormone from a lymphomatous thyroid gland” is referring to some kind of thyroid cancer in which case you would expect them to be describing a nodule on radioiodine uptake.

​Summary video here and also a great site in general: https://onlinemeded.org/spa/endocrine/thyroid/acquire

aesalmon  pg 338 of FA lists it under hypothyroidism but it does present as transient hyperthyroidism first +4  
hyperfukus  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 +2  
hello  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). +  
taediggity  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 +3  
pg32  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. +  
vulcania  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 :) +  


submitted by dr.xx(92),

As part of embryonic development, the pancreas forms as two buds from the foregut, an embryonic tube that is a precursor to the gastrointestinal tract. It is therefore of endodermal origin.

https://en.wikipedia.org/wiki/Pancreas#Development

gh889  nice! I reasoned it as that most of the GI system is of endodermal origin +5  
taediggity  FA 2020 pg 613 +  


submitted by bubbles(45),

Basement membrane integrity is the determinant of full lung recovery following pulmonary insult.

Summary:

(1) loss of basement membrane integrity is critical in determining the “point of no return,” and contributes to the inability to reestablish normal lung architecture with promotion of fibrosis;

(2) loss of epithelial cells, endothelial cells, and basement membrane integrity in usual interstitial pneumonia associated with idiopathic pulmonary fibrosis leads to destroyed lung architecture and perpetual fibrosis;

(3) transforming growth factor-β is necessary, but not entirely sufficient, to promote permanent fibrosis;

(4) persistent injury/antigen/irritant is critical for the propagation of fibrosis;

(5) idiopathic pulmonary fibrosis is an example of a process related to the persistence of an “antigen(s),” chronic inflammation, and fibrosis; and

(6) unique cells are critical cellular players in the regulation of fibrosis.

citation: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/

kernicterusthefrog  Lovely +  
endochondral1  any FA or pathoma or uworld correlation? +  
endochondral1  or was this a random? +  
taediggity  Type II pneumocytes serve as the stem cell precursors, w/out those you're more or less fucked: FA 2020 pg 661 +1