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submitted by k_tron_3000(24),

Just a random factoid (as far as I know), in patients with pancreatitis the most likely vessel for thrombosis is the splenic vein due to close “anatomic ties” with the pancreas. This would also cause gastro-splenic varices, explaining the vomiting of blood.

meningitis  Also explains the splenomegaly. If you have thrombosed splenic vein, the blood will pool in the spleen, can also cause expansion of red pulp of spleen. +7  
pg32  I picked splenic vein because of this ^^ association. However, why is the patient vomiting blood if there isn't a backup of blood into the left gastric/esophageal veinous system? +1  
savethewhales  The splenic vein drains the fundus of the stomach. So, splenic vein thrombosis can cause gastric fundal varices, which explains his bloody vomit. +3  
medschooler1  how do you rule out arteries? +  
ac3  @medschooler1 Just my guess, but when answering this I assumed that splenomegaly meant splenic congestion with blood which can only happen if its outflow tract (splenic vein) is blocked. +3  


submitted by neonem(451),

The patient has low cortisol, which causes body wasting. The patient is hyperpigmented since low cortisol increases ACTH secretion from the pituitary, but this shares a common precursor protein with melanocyte-stimulating hormone (MSH), so that's often a sign of either adrenal failure or an ACTH-secreting tumor. Put together, the high ACTH but low cortisol happening over a period of 6 months means that the adrenal must be getting hit by something -- only option here was autoimmune adrenalitis. Waterhouse-Friderichsen syndrome also causes adrenal insufficiency but this happens acutely, in the timeframe of hours-days.

sajaqua1  The combination of low blood pressure (from lack of mineralocorticoids) and low glucocorticoids (cortisol) indicate adrenal failure. Hyperpigmented skin is a sign of elevated ACTH, indicating that this is a failure of the adrenal gland and not the pituitary. In the industrialized western world, autoimmune destruction of adrenal glands is the leading cause of primary adrenal failure (disseminated tuberculoid destruction of the adrenal glands is significant outside of industrialized nations). It also fits the time line better than Waterhouse-Friederichsen syndrome, which is sudden in onset and associated with hemorraging. Metastases to the adrenal glands *might* be a possibility, but autoimmune destruction is simply likelier. +16  
mamorumyheart  Chronic Addisons disease. Pretty straightforward here. Decreased gland function -> decreased Cortisol, decreased Aldosterone -> hypotension (with hyponatremic volume contraction) Hyperpigmentation from increased ACTH (from POMC) making MSH. (FA) Due to adrenal atrophy or destruction by disease (autoimmune destruction most common in the Western world; TB most common in the developing world). +1  
ac3  I picked autoimmune adrenalitis but was tempted to pick Waterhouse syndrome because of the low BP (hemorrhaging). But I believe Waterhouse-Fried. syndrome is more likely associated with Neisseria infection +  


option B) (the correct option as per nbme) :the patient has a mini mental state of 23/30, so that should mean that she isn't capable of making her own decisions! so whats the point in talking to her privately without her daughter?

option A) is wrong because you cant just hide the diagnosis from the patient and share it with the family

option C & D)you cannot disregard the test or repeat the test as both the test are positive, RPR is a screening test with less specificity but microhemagglutination is a highly specific test so she definetly has syphillis!

option E) doesnt make sense because why would you do lumbar puncture for syphillis?!

i think they forgot to give an option F) just freakin treat her for syphillis!!!

saturdaynightpalsy  "Patients with suspected neurosyphilis should undergo lumbar puncture and subsequent VDRL, FTA-ABS and/or PCR of cerebrospinal fluid" per my notes and the internet Lumbar puncture is used to diagnose neurosyphilis, so that's what I put. +  
saturdaynightpalsy  To add to that, I didnt choose the other answers you listed for the same reasons you listed. +  
ac3  which of the following is the NEXT BEST STEP meaning you wouldnt want to jump straight to a lumbar puncture especially when there are answer choices that suggest discussing the diagnosis with the patient first. If you went to the doctor and they diagnose you they will discuss this with you before ordering additional testing. +  


submitted by monoloco(113),

If anyone wouldn’t mind: How am I supposed to know that T1DM has a similar pedigree to schizophrenia? Teach me how to think, ples.

ankistruggles  I think they were getting at how developing T1DM and schizophrenia are both multifactorial. I don’t remember what the other choices were off the top of my head, but they had clear inheritance patterns. +7  
pathogen7  Just as a slight tangent, is there a difference between "multifactorial" and "polygenic" inheritance? +  
ac3  polygenic = multiple genes affect phenotype while multifactorial = genes, environmental factors, etc that can affect phenotype +1  


submitted by neonem(451),

Sounds like a case of Li-Fraumeni syndrome - since p53 is a tumor suppressor for a bunch of cell types, mutations in this gene (as in LFS) result in a myriad of familial tumor types.

pparalpha  Li-Fraunemi syndrome = SBLA (sarcoma, breast, leukemia, adrenal gland syndrome) and occurs because of an autosomal dominant inherited mutation of p53 APC: linked to FAP (colorectal cancer) RET: linked to papillary thyroid cancer, MEN 2A, MEN 2B RB1: retinoblastoma +8  
privatejoker  The thing that threw me off was that the only connection in her FH to the above SBLA reference was the mention of a paternal cousin with adrenocortical carcinoma. The other two mentioned had brain cancers, which seem completely outside the scope of the above mnemonic. Then again, as mentioned elsewhere, I suppose the best policy on these is just to rule out the absolute wrong answers. I swear, the NBME is lying when they tell us to choose the "best" answer on some of these. What they actually mean in practice is for us to choose the least shitty. +11  
dbg  ^ this guy cracked the code. nbme ur doomed. +3  
cienfuegos  @privatejoker: I feel the pain. Quick FYI: UW includes brain in the associated tumors. +3  
hyperfukus  we can just make her thing SBBLA and hopefully never get this wrong again +2  
jakeperalta  @privatejoker: according to UW, Li Fraumeni includes SABBB(sarcoma/adrenocortical/breast/brain/blood(leukemia)) +2  
ac3  side note: RB1 = retinoblastoma with an increased risk of osteosarcoma +  
lukin4answer  TP53 associated with SBLA + Brain tumor + Anaplastic Thyroid ca + Transitional cell ca. -UW +  


submitted by aesalmon(65),

Can anyone explain why this is not a pituitary adenoma? Is it just a lack of other symptoms?

benzjonez  I think that they just wanted you to notice the **calcifications**. Per FA, "calcifications are common in craniopharyngiomas," whereas I don't think you'd expect to see calcifications in a prolactinoma. +10  
epr94  also the option is prolactinoma not broad pituitary calcifications and he doesnt show any specific signs of high prolactin +  
madojo  It says hes coming in for constituional delay in growth and puberty, i took this to mean that he had low LH, FSH due to decreased GnRH from the prolactinoma. Why did they have to say low-normal serum gonadotropin, why not just say normal? fck u nbme +  
madojo  It says hes coming in for constituional delay in growth and puberty, i took this to mean that he had low LH, FSH due to decreased GnRH from the prolactinoma. Why did they have to say low-normal serum gonadotropin, why not just say normal? fck u nbme +1  
ac3  @madojo I believe since suprasellar tumors can cause a mass effect on pituitary gland to decrease gonadotropin levels. Where as prolactinoma causes a rise in prolactin which downregulates gonadotropin secretion. Please correct me if I'm wrong +1  
teepot123  fa '19 pg 516 +  


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