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 +1  (nbme22#40)

Take a look at that massive platelet count -- over a million per mm3! That should point you towards a myeloproliferative disorder of some sort since this fella isn't bleeding out as far as we can tell from the blood panel (which would put reactive thrombocytosis on the ddx).

Now let's look at those erythrocytes. Normal -- so it's not polycythemia vera, and considering the lack of leukocytosis, probably not CML or myeloid metaplasia.

So our answer must be essential thrombocythemia!


 +3  (nbme22#23)

Can someone explain properly how we know that this trait follows Mendelian genetics and is autosomal recessive and furthermore how the parents were heterozygous?

I guessed a lot on this question and got lucky :(

niboonsh  Autosomal Dominant disorders usually present as defects in structural genes, where as Autosomal Recessive disorders usually present as enzyme deficiencies. P450 is an enzyme, so we are probably dealing with an autosomal recessive disorder. furthermore, the question states there was a "homozygous presence of p450.....". In autosomal recessive problemos, parents are usually heterozygous, meaning that 1/4 of their kiddos will be affected (aka homozygous), 1/2 of the kids will be carriers, and 1/4 of their kids will be unaffected.
nwinkelmann  Is this how we should attack this probelm?: First clue stating endoxifen is active metabolite of Tamoxifen should make us recognize this undering first pass hepatic CYP450 metabolism? Once we know that, the fact that the metabolite is decrease suggests an enzyme defect, which is supported by patient's homozygous enzyme alleles. Then use the general rule that enzyme defects are AR whereas structural protein defects are AD inheritance patters. Once we know the pattern, think that most common transmission of AR comes from two carrier parents. So offspring alleles = 25% homozygous normal, 50% heterozygous carrier, and 25% homozygous affected, thus sister has a 25% of having the same alleles as patient (i.e. homozygous CYP450 2D6*4)?
impostersyndromel1000  we had the exact same thought process, so i too am hoping this is the correct way to approach it get reasoning friend

 +0  (nbme22#2)

Just as clarification, capillary hydrostatic pressure would decrease because of systemic vasoconstriction in response to aortic rupture/systemic hypotension?

lolmedlol  i believe you get peripheral vasoconstriction and central vasodilation in the first stages of shock, which would cause stasis in the capillary beds, which would mean decreased capillary hydrostatic pressure, despite interstital hydrostatic pressure going down as well. https://www.sciencedirect.com/topics/medicine-and-dentistry/vasoconstriction and amboss shock description
trichotillomaniac  ^ this type of question is really hard for me to conceptualize. the link above walks you through it step by step with pictures. Theres not much of an explanation in FA.
trichotillomaniac  Overall is has to do with osmotic vs hydrostatic pressure. osmotic pressure stays the same and hydrostatic decreases. Hydrostatic pressure is the pressure pushing fluid out of the capillary and in the setting of blood loss this would decrease in efforts to keep as much fluid in the intravascular compartment as possible

 +5  (nbme22#42)

Chronic renal insufficiency:

1) poor phosphate clearance --> high serum inorganic phosphorous

2) high serum phosphate --> complexes with divalent cation Ca --> Ca falls

3) Ca falls --> triggers PTH axis

4) kidney failure --> decreased activity of 1-hydroxylase at the kidney --> less calcitriol


 +1  (nbme22#1)

This question confused me a lot because so many questions have drilled me on the importance of the ANP escape mechanism in times of fluid overload (as in CHF).

I thought ANP was a huge player in the loss of Na in circumstances of volume overload as in this patient (which is why you see euvolemic hypOnatremia in patients with SIADH or overactivity of the RAAS as in CHF).

Why is ADH now being named as the responsible agent?

jooceman739  My thinking is that ANP causes natriuresis, so you're losing salt and water at the same time (isoosmotic fluid?). Meanwhile, ADH absorbs only free water, so it would dilute the serum. Correct me if i'm wrong.
bubbles  Ohhh you are right. Thank you for the explanation! I got so fixated on that one mechanism haha.

 +4  (nbme22#47)

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/

endochondral1  any FA or pathoma or uworld correlation?
endochondral1  or was this a random?

 +0  (nbme22#41)

Wouldn't constriction of peripheral vessels also trigger sphlancnic vasoconstriction, which simulates renal ischemia and causes increased RAAS activity?

drdoom  Constriction of peripheral (cutaneous) arterioles/capillaries in response to cold surroundings is an attempt to reduce heat loss & maintain internal body temp; it is not at all coupled with splanchnic vasoconstriction. In fact, the peripheral vasoconstriction is trying to “re-route” blood to more internal/visceral compartments; simultaneous splanchnic vasoconstriction would impede that very process!
bubbles  Ah, okay! I got led off track because I had a bunch of super hard practice questions asking about hepatorenal syndrome and how the constriction of sphlancnic vessels might trigger renal ischemia. Do you know if there would ever be a time when sphlancnic vasoconstriction occur outside of hepatorenal syndrome?
drdoom  @bubbles i would think only in cases of catastrophic shock (when the body is doing everything it can to maintain central tension; pressure to vital organs like heart,kidneys); in those cases, i could see the body sacrificing visceral flow as an "option of last resort"

 +0  (nbme22#50)

Can someone could explain to me how this is unequivocally tuberous sclerosis despite NF-1 and Sturge-Weber also presenting with skin lesions, hypopigmented macules, and seizures?

And considering the negative family history, I would have assumed that a sporadic mutation (like SW) would be more likely...

cocoxaurus  This question was tricky! Tuberous sclerosis= Hypopigmented= Ash leaf spot (The skin lesion in NF is Hyperpigmented- Cafe au lait and in Sturge Weber it's a port wine stain (also not hypopigmented). I'm assuming that the SINGLE raised flesh colored lesion is a Hamartoma (The angiofibromas in NF1 are typically multiple). Although both Tuberous Sclerosis and Sturge Weber are both associated with seizures, I used all the other stuff to narrow it down to the correct answer. Also, don't forget that there is Incomplete penetrance and variable expressivity in Tuberous Sclerosis. So I think the lack of family history of "seizure or major medical illness" was there to throw us off.
bubbles  Thank you! :) I thought I really knew my congenital disorders, so I was a little annoyed when they trotted this question out

 +1  (nbme22#33)

Just to be crystal clear (because I've gotten more thyroid axis questions wrong than I should):

T4 --> T3 is possible but T3 --> T4 isn't?

meningitis  Exactly. I know there are papers saying there is some conversion of T3 to T4 but I try to keep it simple and think of it as once you break it apart (T4->T3), you cant put it back together. Only thyroglobin etc can put another I on it, so any T3 cant become T4 because you need it to be done in thyroid.
angelaq11  I honestly don't know about this, but the way I reasoned this was: she is taking a whole lot of T3, so on top of already having hypothyroidism, she is just making things worse, so TSH is going to be decreased because of feedback inhibition, and hence T4 (Which is the main one produced by the thyroid) is also going to be decreased. I think the high T3 is the exogenous T3.

 +12  (nbme22#13)

For the peeps who got confused on this question bc of UWorld's weird question on HIV viral load:

acute HIV-1 infection: HIGH viral load, low Ab HIV-2 infection: LOW viral load, low Ab (bc standard HIV assays detect p24, which is not present on HIV-2)

Kinda annoyed I missed an easy immunology concept question :/

eacv  I feel you my friend! same stupid mistake over here -.-
step1soon  FA 2019 pg 176

 -2  (nbme22#3)

Sorry if I'm being dense...why does this woman have diarrhea due to statins, diet, and exercise? I didn't really understand what they were asking for here to be honest.

.ooo.   I believe they were asking what the most common effect of statins, which is GI upset (including diarrhea). Rarely you can have hepatotoxicity and myopathy but neither of these are a side effect in the answer choices. Hopefully this helps!
niboonsh  Theyre asking about the most common side effect of Orlistat - which is really fatty diarrhea

 +1  (nbme22#33)

Has anybody found a good explanation for this histology? I genuinely have no idea what I'm looking at.

meningitis  This is common in Klinefelter.. think of the equivalent of Streaked ovaries seen in Turners. White streaks, red/pink material of hyaline, and hyperplasia of Leydig cells. Just remember: It doesn't look like normal structured testicle histology (No organized seminiferous tubules with Sertoli cells around)

 +0  (nbme22#34)

So...case-control studies compare a group of people with the disease and a group of people without the disease. I'm not sure I understand why you can call people randomly and call that a control group. What if among those called randomly, some of them have also had hemorrhagic strokes?

impostersyndromel1000  this is one of those Qs where you just dont over think it and focus on your first point, that they are comparing a group with the disease vs (potentially) one without it. Thats what i took from it at least (sorry fi this is too late)




Subcomments ...

submitted by mcl(231),

To expand on this, pathologyoutlines describes the histology of kapowsi sarcoma as "spindle cells forming slits with extravasated red blood cells"

mcl  lul i don't know why i spell kaposi like that, my b +1  
bubbles  This site is super helpful. Thanks for sharing :) +  
mcl  yesssssss ofc <3 I love path outlines +  
usmleuser007  Just realize that spindle cells are similar to the endothelial cells of blood vessels. Anything that have vessel association might have spindle-shaped cells. a. NF-1 b. NF-2 ~ Schwannoma (Antoni A) = Cutaneous neurofibroma ~ high cellularity (w/ palisading patterns with interspersing nuclear-free zones called Verocay bodies c. Leiomyoma (uterus & esophagus) d. Mesothelioma (cytokeratin positive) e. Anaplastic Thyroid cancer (biphasic & along with giant cells) f. Medullary Thyroid cancer (can also have polygonal cells) g. Primary cardiac angiosarcoma (malignant vascular spindle cells) h. Osteosarcoma (bone cancer) (pleomorphic cells) i. Meningioma j. Kaposi's Sarcoma (HHV-8) = Slit-like vascular spaces with plump spindle-shaped stromal cells +1  


submitted by bubbles(31),

This question confused me a lot because so many questions have drilled me on the importance of the ANP escape mechanism in times of fluid overload (as in CHF).

I thought ANP was a huge player in the loss of Na in circumstances of volume overload as in this patient (which is why you see euvolemic hypOnatremia in patients with SIADH or overactivity of the RAAS as in CHF).

Why is ADH now being named as the responsible agent?

jooceman739  My thinking is that ANP causes natriuresis, so you're losing salt and water at the same time (isoosmotic fluid?). Meanwhile, ADH absorbs only free water, so it would dilute the serum. Correct me if i'm wrong. +7  
bubbles  Ohhh you are right. Thank you for the explanation! I got so fixated on that one mechanism haha. +2  


submitted by bubbles(31),

Wouldn't constriction of peripheral vessels also trigger sphlancnic vasoconstriction, which simulates renal ischemia and causes increased RAAS activity?

drdoom  Constriction of peripheral (cutaneous) arterioles/capillaries in response to cold surroundings is an attempt to reduce heat loss & maintain internal body temp; it is not at all coupled with splanchnic vasoconstriction. In fact, the peripheral vasoconstriction is trying to “re-route” blood to more internal/visceral compartments; simultaneous splanchnic vasoconstriction would impede that very process! +9  
bubbles  Ah, okay! I got led off track because I had a bunch of super hard practice questions asking about hepatorenal syndrome and how the constriction of sphlancnic vessels might trigger renal ischemia. Do you know if there would ever be a time when sphlancnic vasoconstriction occur outside of hepatorenal syndrome? +  
drdoom  @bubbles i would think only in cases of catastrophic shock (when the body is doing everything it can to maintain central tension; pressure to vital organs like heart,kidneys); in those cases, i could see the body sacrificing visceral flow as an "option of last resort" +  


submitted by bubbles(31),

Can someone could explain to me how this is unequivocally tuberous sclerosis despite NF-1 and Sturge-Weber also presenting with skin lesions, hypopigmented macules, and seizures?

And considering the negative family history, I would have assumed that a sporadic mutation (like SW) would be more likely...

cocoxaurus  This question was tricky! Tuberous sclerosis= Hypopigmented= Ash leaf spot (The skin lesion in NF is Hyperpigmented- Cafe au lait and in Sturge Weber it's a port wine stain (also not hypopigmented). I'm assuming that the SINGLE raised flesh colored lesion is a Hamartoma (The angiofibromas in NF1 are typically multiple). Although both Tuberous Sclerosis and Sturge Weber are both associated with seizures, I used all the other stuff to narrow it down to the correct answer. Also, don't forget that there is Incomplete penetrance and variable expressivity in Tuberous Sclerosis. So I think the lack of family history of "seizure or major medical illness" was there to throw us off. +10  
bubbles  Thank you! :) I thought I really knew my congenital disorders, so I was a little annoyed when they trotted this question out +1  


submitted by shaydawn88(5),

I would think resolution involves the stem cells (type II pneumocytes). Is the intact basement membrane the answer because it limits spread?

aesalmon  I would also like to know if anyone can answer this question - I saw it as a Sattar "one day, one week, one month" kind of question. Its probably very simple but I still don't get it +  
bubbles  I posted a new comment explaining: basement membrane integrity is the strongest determinant of full fx recovery following pulmonary insult :) +2  
drdoom  You have to think about it this way: the basement membrane is the “scaffolding” on which [restorative] healing occurs. So, yes, stem cells (type II pneumocytes) would be involved in that healing process but they couldn’t restore the *normal* architecture (“no abnormalities”) without the ‘skeleton’ of the basement membrane telling them where to go, in what direction to grow, which way is “up”, etc. If the basement membrane is destroyed, you can still get healing, but it won’t be organized healing -- it’ll be *disorganized* healing, which does not appear as normal tissue. (Disorganized healing is better than no healing, but without a BM, the regenerating cells don’t have any “direction” and therefore can’t restore the normal architecture.) +4  
nwinkelmann  Yes, this a great summary to the post by @bubbles and the article he posted! Another way to think of the question is not, what causes repair, but what causes irreversible injury/fibrosis. That article explained an experiment that showed TGF-beta was necessary to initiate fibrosis, but if BM was intact and TGF-beta was removed, the fibrosis didn't persist, i.e. intact BM is protective against TGF-beta. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/ +  


submitted by keycompany(127),

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5290806/

Osler Sign is a low-sensitivity, low-specficity finding of Mockenberg Arteriolosclerosis (MA) characterized by "a palpable although pulseless, radial artery while the BP cuff is inflated above systolic pressure".

It is possible that either: a) The low-specificity of this test means it is also applicable to atherosclerosis (not just MA) b) The NBME incorrectly implies that MA is interchangable with atherosclerosis.

bubbles  This was my reasoning, too. I thought this was Mockenberg for sure +  
hello  I don't think think it's a type. According to 2 other comments: "It's atherosclerosis because it said “radial artery is NON-pulsatile BUT REMAINS PALPABLE even as the cuff is inflated”--> normally, you can’t feel the artery when the cuff is overinflated b/c overindlation occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!): "If if something were to not be palpable then it would have to collapse -- atheroclerosis prevents this vessel collapse." +2  
arcanumm  I agree, I just reasoned that atherosclerosis would not be thicker when the lumen is blocked. I don't think they were going for Mockenberg at all. +  
arcanumm  would be thicker +  


submitted by skraniotis(6),

Undialyzed renal failure leads to metabolic acidosis, and as a result bicarb gets depleted as it tries to buffer the accumulation of organic acids.

bubbles  Thanks for the explanation! Do you know why Mg would not be a potential answer? Phosphate also accumulates in those with undialyzed renal failure, so I was thinking that maybe magnesium as a divalent cation would complex with PO3 (in a mechanism similar to Ca). +  
nwinkelmann  From the little bit of research I just did (because I didn't learn anything about dialysis at my medical school), ESRD can be associated with either low or high Mg levels, so the dialysate can cause either increased or decreased Mg levels depending on the patient's serum content, therefore I don't think based on this question, would could determine if removal of dialysis would lead to elevated or decreased magnesium. The end of the first article seems to favor ESRD leading to hypermagnesemia, so if that's the case, then removal of dialysis would cause Mg to increase as well. https://www.karger.com/Article/FullText/452725 and https://www.karger.com/Article/FullText/485212 +1  
hyperfukus  why is it that we aren't learning this stuff and they r just throwing it on step there's barely a blurb in FA about ckd/eskd +  
hyperfukus  does uremia potentially have to do with this? +  
medulla  ESRD and not getting dialysis -> he is uremic -> met acidosis -> dec bic +2  
angelaq11  @medulla this is the best and simplest explanation. I got it wrong and chose Mg, wish I had made that connection. +