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Comments ...

 +3  (nbme22#33)

"she feels happier and more relaxed" after starting kickboxing: this is a MATURE defense mechanism (classic textbook sublimation, as has been said). This question is just plain wrong. It's not displacement, because it's a healthy, socially acceptable outlet that improves her emotional state; punching bags are meant to be punched (thus it is actually NOT neutral). Displacement to an object would be punching a hole in her wall, or breaking her vase (I just like that imagery). Both of those would be better than punching her family, or breaking their car window, which is why it's displacement (unconscious redirection of an emotion to a safer object). However, kickboxing is LITERALLY an example in several psych textbooks for sublimation. Thank you for coming to my TED Talk.

jaxx  Meanwhile, I thought everything was wrong so I went with another Mature defense mechanism.

 +0  (nbme22#9)

Just in case that lovely little equation provided by @keycompany wasn't quite enough for you, here's a link to a more complete explanation by Kahn Academy. Helped me, when I looked at the equation and said, whaaaa?


 +0  (nbme20#8)

This is not an aneurysm, which is what makes this question so weird: "x-rays of the chest do not show widening." My understanding was that dissections usually occur in the picture of aneurysm, especially due to hypertension. However, perhaps that's not the case, particularly in these Stanford Type A dissections? The picture in FA sure makes it look like a widened aorta (aneurysm) with a dissection...


 +1  (nbme20#48)

I also had difficulties with this, especially w/FA being so abbreviated. There is one word in FA that helps, and then I have a link for more info: "grows rapidly and regresses spontaneously by 5-8 years old." Which means it's done with its involution phase by then. This NCBI article helps: The Lessons I Learned from a Hemangioma Clinic TLDR: rapid growth occurs for the first few month, followed by a few months of rest, and then years of involution. Since the question is asking what happens over 5 years, the majority of that time is spent in involution phase. Hope this helps.

whossayin  totally not NBME related, but I think you username is brilliant lol




Subcomments ...

submitted by jooceman739(11),

Retinoblastoma:

The physician said the boy is unlikely to develop any other neoplasms, so he doesn't have the inherited Rb mutation.

In this case, he has the sporadic retinoblastoma. Sporadic retinoblastoma requires two somatic mutations of Rb in the same retinal cell.

Just as a side note: Inherited retinoblastomas tend to be bilateral. Sporadic are unilateral.

carls14  aren't retinal cells a type of somatic cell? Why not is the mutation not considered in the somatic cell of the child? +  
omerta  Although this mutation would be considered somatic, I believe the question is just asking you to be specific as to which cells. If you answered "somatic cells of the child," that's quite broad and could apply to almost anything. +3  
kernicterusthefrog  I had the same struggle and thought process. +  


submitted by bubbles(25),

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? +  


submitted by oznefu(7),

I’m having trouble understanding why this is a better choice than Paget disease, especially with the increased ALP?

zelderonmorningstar  Paget’s would also show some sclerosis. +1  
seagull  ALK is increased in bone breakdown too. Prostate loves spreading to the lumbar Spine. It's like crack-cocaine for cancer. +1  
aesalmon  I think the "Worse at night" lends itself more towards mets, and the pt demographics lean towards prostate cancer, which loves to go to the lumbar spine via the Batson plexus. I picked Paget but i think they would have given something more telling if they wanted pagets, histology or another clue +  
fcambridge  @seagull and aesalmon, I think you're a bit off here. Prostate mets would be osteoblastic, not osteolytic as is described in the vignette. +5  
sup  Yeah I chose Paget's too bcz I figured if it wasn't prostate cancer (which as @fcambridge said would present w/ osteoblastic lesions) they would give us another presenting sx of the metastatic cancer (lung, renal, skin) that might point us in that direction. I got distracted by the increased ALP too and fell for Paget :( +  
kernicterusthefrog  @fcambridge, not exactly. Yes, prostate mets tends to be osteoblastic, but about 30% are found to be lytic, per this study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2768452/ Additionally, the night bone pains point to mets, and Paget's is much more commonly found in the cranial bones and appendicular skeleton, than axial. This could also be RCC mets! +  
sweetmed  I mainly ruled out pagets because they said the physical examination was normal. He would def have other symptoms. +1  


submitted by drdoom(162),

Calculations for dad. The probability of the father being a carrier is 2/3 since it is known that he doesn’t have the disease. Then the probability of him passing it on to his kid is 1/2, thus:

  • Probability of dad being carrier = 2/3
  • Probability of dad passing on disease allele = 1/2

Calculations for mom. With the Hardy-Weinberg Principle, you can figure out the probability of the mother being a carrier:

q = sqrt(1/40,000) = 1/200

So, 2pq = 2 * 1/200 * 199/200, which is approx 1/100.

For the child to get the allele from mom, two things need to happen: (1) mom must be a carrier [“heterozygote”] and (2) mom must pass the allele to child:

  • Probability of mom being carrier = 1/100
  • Probability of mom passing on disease allele = 1/2

Puting it all together. Now, combine all together:

= (probability of dad being carrier) * (probability of dad passing on disease allele) * (probability of mom being carrier) * (probability of mom passing on disease allele)

= 2/3 * 1/2 * 1/100 * 1/2
= 1 in 600

kernicterusthefrog  To quote Thorgy Thor, drag queen: "ew, Jesus, gross" +  
niboonsh  This question makes me want to vomit +  
drdoom  lol +  


submitted by gh889(32),

The answer is due to an exception outlined here where niacin is used in pts w/o diabetes who have refractory hypertriglyceridemia at high risk or has a hx of pancreatitis.

I agree that fibrates are first line (and so does that article) but NBME was honing in on a specific exception that niacin can also be used since VLDL and TGs are high in hypertriglyceridemia.

The "clue" they had was "recurrent pancreatitis" which is supposedly a lead towards niacin.

I also put increase HDL....

wutuwantbruv  Correct, you would not want to give fibrates to someone with recurrent pancreatitis since fibrates increase the risk of cholesterol gallstones due to inhibition of cholesterol 7α-hydroxylase. +  
kernicterusthefrog  FYI @gh889 can't follow your link w/o an NYIT username and password, unless there's a more tech-savvy way around that.. I appreciate the info, though. Niacin rx for familial hypertriglyceridemia w/ recurrent pancreatitis. Now I know.. +1  
impostersyndromel1000  Great points, very in depth knowledge taking place here. Also, familial hypertriglyceridemia (per FA 2019 pg 94) has hepatic overproduction of VLDL so picking this would have been the easiest answer (in retrospect) +1  
hyperfukus  @impostersyndrome1000 literally that's the ONE thing i remembered and i went YOLO lol cuz i was staring for a while +  


submitted by hungrybox(175),

So... theoretically an isolated decrease in HR would increase CO due to inc. preload, right?

But CO decreases in this case b/c the effect of inc. TPR is more powerful?

kernicterusthefrog  @hungrybox: No. Isolating HR, you would look at CO like this: CO=HR*SV so if HR or stroke volume go down, CO goes down. The change in preload wouldn't affect the CO as much as the change in rate of flow. So, the decrease in CO is solely due to the beta1 blocking effect on the AV node to decrease HR. +  


submitted by xxabi(78),

Bronchogenic carcinoma = lung cancer

That being said, lung adenocarcinoma specifically is associated with hypertrophic osteoarthropathy, which is a paraneoplastic syndrome characterized by digital clubbing, arthralgia, joint effusions, and periostosis of tubular bones

luke.10  why not systemic scleroderma since i did this question wrong and i chose systemic sclerosis scleroderma , can someone explain that ? +1  
kernicterusthefrog  My best guess answer to that @luke.10 is that: a) there's no mention of any skin involvement (which there would be in order to be scleroderma) b) Scleroderma shows pitting in the nails, not clubbing c) There would be collagen deposition with fibrosis, not hypertrophy of the bone at joints Saying that, I also got this wrong! (but put RA...) so I'm not claiming to "get this" Hope my thought process helps, though! +1  
yotsubato  This is in FA 2019 page 229 +1  
larascon  I agree with @kernicterusthefrog on this one, Bronchogenic carcinoma = lung cancer. Squamous cell carcinoma gives you hypercalcemia (new bone formation; maybe?), commonly found in SMOKERS ... +  


submitted by thomas(3),

Answer is Astrocyte. Patient has glioblastoma multiforme. Although meningiomas may occur at convexities, meningiomas are benign and often asymptomatic. They may cause h/a seizures, but would be unlikely to cause death w/in 6m of onset of h/a. The size of tumor and course of illness is consistent with the course of GBM

masonkingcobra  Above is obviously incorrect because the answer is Meningeal lol. Here is a link to a good picture: http://neuropathology-web.org/chapter7/chapter7fMiscellaneous.html +1  
kernicterusthefrog  Obviously thomas is disagreeing with the presentation of the question, and I agreed with him! This absolutely sounds like GBM, with rapid onset leading to death, and the symptoms. The question stem leads you to GBM, and the gross image to meningioma (I guess). +1  
kernicterusthefrog  Furthermore, where are the meninges on the gross image form which this (meningioma) grew?! It should at least show the tissue from whence it came! +1  
nala_ula  Had the same problem, got confused since it appeared that the growth was malignant :( +  
sugaplum  FA 2019 pg 514, also agree with everyone. weird presentation. Glios are malignant death within 1 year, meningioma are often asymptomatic or have focal signs. just a gross pathology question at this point +  


submitted by thomas(3),

Answer is Astrocyte. Patient has glioblastoma multiforme. Although meningiomas may occur at convexities, meningiomas are benign and often asymptomatic. They may cause h/a seizures, but would be unlikely to cause death w/in 6m of onset of h/a. The size of tumor and course of illness is consistent with the course of GBM

masonkingcobra  Above is obviously incorrect because the answer is Meningeal lol. Here is a link to a good picture: http://neuropathology-web.org/chapter7/chapter7fMiscellaneous.html +1  
kernicterusthefrog  Obviously thomas is disagreeing with the presentation of the question, and I agreed with him! This absolutely sounds like GBM, with rapid onset leading to death, and the symptoms. The question stem leads you to GBM, and the gross image to meningioma (I guess). +1  
kernicterusthefrog  Furthermore, where are the meninges on the gross image form which this (meningioma) grew?! It should at least show the tissue from whence it came! +1  
nala_ula  Had the same problem, got confused since it appeared that the growth was malignant :( +  
sugaplum  FA 2019 pg 514, also agree with everyone. weird presentation. Glios are malignant death within 1 year, meningioma are often asymptomatic or have focal signs. just a gross pathology question at this point +  


submitted by neonem(227),

Cilostazol is a phosphodiesterase inhibitor; leads to increased cAMP which inhibits platelet degranulation/activation while also causing vasodilation. All of the other options work on either vasculature or platelets but not both.

kernicterusthefrog  Just to add: cAMP activates protein kinase A (PKA), which is the more direct mediator of platelet aggregation inhibition, and of myosin light-chain kinase inhibition (which causes inhibition of smooth muscle contraction and thus vasodilation). Just in case there's a question that gets more specific than this one! +5  


submitted by neonem(227),

Leukotriene B4 is a potent chemotactic molecule for neutrophils. Selective loss of this would have no effect on platelets, mast cells, or endothelium - these are more responsive to changes in TXA2, complement/arachidonic acid, and PGI2, respectively.

kernicterusthefrog  FA says: "Neutrophils arrive B4 others" +  


submitted by xxabi(78),

I think its that the CI contained the number "0" which makes it statistically insignificant

kernicterusthefrog  You're thinking about CI for a **mean difference** b/w 2 variables. This question talks about **relative risk**, for which 'strugglebus' correctly asserts that *a CI including 1 fails to reject the null hypothesis*. #funwithformatting +  
xxabi  Ahhhh you're right, I definitely had them mixed up! Thanks! +1  
xxabi  #biostatsisthebaneofmyexistence +1  


submitted by sympathetikey(252),

As stated below, the Left crus cerebri was damaged (see what it should normally look like below). This contains the corticospinal tract. Since the corticospinal tract decusates at the medulla, below the midbrain section we're looking at, you would see Contralateral (Right) Spastic Hemiparesis

sympathetikey  http://what-when-how.com/wp-content/uploads/2012/04/tmp15F11_thumb.jpg +3  
hello  What identifies that a cross-section is medulla vs midbrain vs pons? +1  
kernicterusthefrog  @hello I like to pay attention to the Cerebral Aqueduct (diamond/spade shape seen mostly in Midbrain, and transitioning to 4th ventricle in rostral Pons), and then the shape and size of the 4th ventricle as you move down Pons to rostral&middle Medulla, and eventual closing and absence of fluid space at caudal Medulla. +4  
hello  @kernicterusthefrog Thank you. +