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Comments ...

 +0  (nbme23#44)

I guess he's taking B12 supplements, otherwise he would have a symptomatic deficiency, right?

 +2  (nbme23#14)

Since there were "small amounts of meconium" I thought it couldn't be atresia. Turns out atresia isn't always absence of lumen, it can also be abnormal narrowing of lumen, allowing just a small amount to pass through...

adong  I don't think that's true, atresia literally means closure/absence of the lumen. I also got tripped up by the meconium but that could be just GI epithelium that was shed while in utero etc. I wouldn't change your definition of atresia.

 +2  (nbme22#21)

The words "most effectively" confused me. I thought to myself "even if it has the highest specificity, it's not very effective if it's got super low sensitivity -- since it will miss a lot of the true +ve's (failing to rule in cancer for the ones that get missed)." That was a story I told myself about their use of the words "most effectively" lol.

 +1  (nbme22#46)

First Aid 2019 page 622 stimulatory growth effects of testosterone include red blood cells. I think they expect us to know this.

 +1  (nbme22#8)

I think there's a UWorld question describing how cystic fibrosis can cause fat soluble vitamin deficiency and how a Vit E def in that context might manifest similarly to B12 def. (Also in first aid)

 +2  (nbme22#1)

There is a decent UWorld question explaining how this works. Only reason I remembered it.

hyperfukus  i had notes from forever ago but i totally forgot lol
carmustine  UWorld question ID 318

 +2  (nbme22#30)

It seems like a lot of the systemic autoimmune diseases are multifactorial. Is there a general rule for this?

ls3076  Really good observation

 +2  (nbme22#1)

It's also just the only option that's "behind" the liver.

 +0  (nbme22#45)

Is the part with "constant studying" just supposed to support that she has a psych disorder related to perfectionism, which is why she's going to extremes to control her weight?

rrasha2  No, the constant studying is to trick you into thinking shes abusing amphetamines.Amphetamines decrease appetite so a lot of people abuse them for weight loss. That combined with increased concentration to study all day errrday.. #onehellofadrug
rrasha2  forgot to mention, another side effect of amphetamines would be increased BP due to the increased catecholamines..don't forget to keep an eye out for that
dentist  would amphetamines influence electrolytes at all?

 +0  (nbme22#25)

What they mean by filtration...

Fluid comprised of water and electrolytes, with a very small amount of protein and other macromolecules, normally leaves capillaries and small postcapillary venules by a process called filtration. Filtration is primarily driven by the capillary hydrostatic pressure, and the amount filtered per unit time is additionally influenced by the permeability of the vessel wall (endothelium and basement membrane). The fluid that filters into the tissue flows within the intercellular space (the interstitium) and most of it is reabsorbed at the venular end of capillaries where the hydrostatic pressure is lower. Some of the filtered fluid is taken up by lymphatic vessels and returned to the circulation.

 +2  (nbme20#17)

I confused myelodysplastic syndrome with primary myelofibrosis because I thought 2-3 of those RBCs looked like teardrop cells. Just like when they show an image for bullous pemphigoid and there's some weird second rip through the dermal/subdermal layer making me think it's not BP even though I don't know what else it would be. fml

whoissaad  Made the same mistake
targetusmle  i thought exactly the same!! 2 cells looked like tear drop cells :/
ilovemypuppies2295  I thought there were tear drop cells too. Seemed like it should be a metaplasia then. Oh well
lynn  I did the same, but looking at FA19 pg 423 it says "ineffective hematopoiesis --> defects in cell maturation of nonlymphoid lineage." You can get bilobed neutrophils, or if it progressed to AML you'd see auer rods. Nothing about tear drop cells. Then on pg 406 tear drop cells would be seen in myelofibrosis, and possibly thalassemias

 +7  (nbme21#13)

Hypoxic pulmonary vasoconstriction (HPV), also known as the Euler-Liljestrand mechanism, is a physiological phenomenon in which small pulmonary arteries constrict in the presence of alveolar hypoxia (low oxygen levels).

While the maintenance of ventilation/perfusion ratio during regional obstruction of airflow is beneficial, HPV can be detrimental during global alveolar hypoxia which occurs with exposure to high altitude, where HPV causes a significant increase in total pulmonary vascular resistance, and pulmonary arterial pressure, potentially leading to pulmonary hypertension and pulmonary edema.


Subcomments ...

submitted by sajaqua1(275),

Because the baby's mother has Type 1 Diabetes mellitus, it is plausible that they had elevated blood glucose levels during or shortly before birth. Insulin does not cross the placenta, but glucose does, so during birth the neonate would have been hyperglycemic. This would lead to the neonatal pancreas releasing insulin, driving glucose into cells and turning down gluconeogenesis; this is why the baby is hypoglycemic right now.

B) Decreased glycogen concentration- I don't know the glycogen concentration compared to an adult patient, but a decrease in glycogen concentration would indicate glycogen/glucose release, which would not be a hypoglycemic state. C) Decreased glycogen synthase activity- decreased glycogen synthase activity indicates energy catabolism, and would lead to higher serum glucose levels. D) Decreased serum insulin concentration- decreased serum insulin would lead to higher levels of glucose in serum. E) Increased serum insulin-like growth factor- IGF does not bind nearly as well to insulin receptors as insulin does, and so would have to be in extremely high concentrations to have this effect. IGF is associated with somatic growth and muscle development.

yotsubato  His glycogen concentration is high, since he's been hyperglycemic with lots of insulin until birth. +3  
alexb  Also explains why he's 12 pounds. +1  
krewfoo99  Also, think of it like this: Insulin causes hypoglycemia, thus this baby must have increased insulin. It is also an anaobolic hormone which is clear by the babys weight. Insulin increases glycogen synthase activity, and causes an increase in concentrations of glycogen. Decrease in insulin would do exactly the opposite +  

submitted by sajaqua1(275),

In an elderly patient with isolated elevated alkaline phosphatase (normal serum calcium and phosphate) Paget's disease of bone should be at the top of the differential. This disease is due to dysregulation of osteoclastic and osteoblastic activity; first an initial osteoclast hyperactivity phase, then increased osteoblast activity for a mixture, then osteoclasts "burnout" leading to over-mineralization and sclerotic bone plaques. In addition, this can create arteriovenous shunts in the bones which decreases resistance, leading to high output cardiac failure (a similar problem can arise in arteriovenous fistulas from blood dialysis). On histology it will have a "mosaic" pattern.

A)- Aneurysmal bone cyst- largely a product of hyperactivity of osteoclasts, this occurs more often in the limbs, and shows a cystic space with balloon-like dilation. B) Angiosarcoma- angiosarcoma of the bone is n almost purely lytic lesion. They occur more frequently in younger people. C) Niacin deficiency- I can find nothing about vitaminb B3 deficiency involving bones. B3 deficienct results in pellagra, with the classic Three D's- dermatitis (rash necklace on C3/C4 dermatome), dementia, and diarrhea. E) Osteosarcoma- Found almost exclusively in younger people, this bone growth occurs at the growth plate, particularly at the proximal end of the tibia, distal end of the femur, or proximal end of the humerus (in the long bones around your knees or at your shoulders). It shows a large, solid growing mass that may raise the periosteum in a sunburst pattern/Codman's triangle. F) Prostatic carcinoma- rare for being one of, if not the only metastatic bone cancer that is purely osteoblastic.

alexb  Great explanation, except that there was a question in NBME 22 in which the prostatic carcinoma was osteolytic. One of the commenters here looked it up and apparently it's like that 30% of the time or something. So I guess you would have to use the high output HF, normal Ca, high ALP, and mosaic pattern to "play odds" as Goljan would say. +  

submitted by uslme123(11),

This question makes no sense to me. She has an extremely low opening pressure yet has signs of increased intracranial pressure. Did they mean to put 32 cm H20?????????

uslme123  Standard lab values are incorrect, way to go NBME. +2  
wutuwantbruv  I think they mean to put mm Hg. Normal CSF pressure is about 100-180 mm H20 which equates to about 8-15 mm Hg. +2  
alexb  I lost a bit of time wondering about that ugh lol +1  
mjmejora  I thought there must be an obstruction in the ventricles somewhere preventing csf from getting to the spine. so pressure is low in spinal tap but in the head it must be really high. +  

submitted by welpdedelp(113),

It was the only peripheral lung cancer, its also more common in women. Metastasis would have shown multiple lesions

sympathetikey  Also, lung adenocarcinoma is the most common lung cancer overall, most common in women, and most common in non-smokers. I know she smoked in the past, but that's what tipped me off to it. +3  
alexb  Yeah I literally picked SCC bc I knew she'd smoked in the past smh +  
maddy1994  20 years of non smoking history ,she wouldnt be at elevated risk for smoking related carcinoma. +  

submitted by welpdedelp(113),

Hemochromatosis, aka "bronze diabetes". Cannot be Addison due to the hyperglycemia and normal BP

alexb  I missed this bc didn't notice it was a middle-aged guy w/ just 3 year hx of Type 1 DM. +1  
tinydoc  I got it mixed up with primary adrenal insufficiency and the acth ⇒ hyperpigmentation. +4  
maddy1994  testicular atrophy &hepatomegaly helped me out to eliminate the options..when i was left with ferritin and saw pigmentation it clicked that it is hemochromatosis +2  
krewfoo99  Symptoms of Darkening of skin, liver dysfunction, diabetes, with testicular atrophy will always be hemochromatosis +  

submitted by calcium196(7),

Ubiquitin-mediated proteolysis is not reversibly affected by insulin. The question asks for reversible ways that insulin affects it, and ubiquitination would lead to degradation via proteases, which is not reversible. Nuclear/cytoplasmic shunting makes sense because FOXO is a transcription factor, so it can’t do its job if it is in the cytoplasm!

meningitis  Thank you for your explanation! One question: How about the serine phosphorylation? Is it answered by pure memorization that the FOXO TF is serine phosphorylated, or is it a general fact that all TF's are serine-threonine phosphorylated? +  
tsl19  I'm not sure, but it may be as simple as this: ubiquitin-mediated proteolysis is irreversible, but both N/C shuttling and phosphorylation are generally reversible processes. +  
didelphus  I also guessed that FOXO must be a part of the PI3K pathway, since insulin regulates metabolism through PI3K and the question stem specifically mentions that. Phosphorylation is a major part of that pathway, so even indirectly phosphorylation would regulate FOXO. Frustrating question. +5  
niboonsh  yes, FOXO is affected downstream of the activation of PI3K. This is a really good video that explains the whole cascade https://www.youtube.com/watch?v=ewgLd9N3s-4 +  
alexb  According to wikipedia (https://en.wikipedia.org/wiki/FOXO1) phosphorylation of FOXO1 is irreversible. This is referring to phosphorylation of serine residues on FOXO by Akt, which occurs in response to insulin. But the NBME answer suggests it's reversible. What's up? +  
almondbreeze  could wiki be wrong on phosphorylation being irreversible? according to this article, it is a reversible process: regulation of FoxO transcription factors by reversible phosphorylation and acetylation (https://www.sciencedirect.com/science/article/pii/S0167488911000735#s0010) some wiki info, however, is helpful : In its un-phosphorylated state, FOXO1 is localized to the nucleus, where it binds to the insulin response sequence located in the promoter for glucose 6-phosphatase and increases its rate of transcription. FOXO1, through increasing transcription of glucose-6-phosphatase, indirectly increases the rate of hepatic glucose production.[19] However, when FOXO1 is phosphorylated by Akt on Thr-24, Ser-256, and Ser-319, it is excluded from the nucleus, where it is then ubiquitinated and degraded. The phosphorylation of FOXO1 by Akt subsequently decreases the hepatic glucose production through a decrease in transcription of glucose 6-phosphatase. +