NBME Answers : vulcania's page

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submitted by sattanki(82), visit this page

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Does anyone have any idea on this question? Thought it was ALS.

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ankistruggles I thought it was ALS too (and I think it still could be?) but my thought process was that a lower motor neuron lesion would be the more specific answer. +2

sattanki Yeah makes sense, just threw me off cause ALS is both lower and upper motor neuron problems. Corticospinal tract would have been a better answer if they described more upper motor neuron symptoms, but as you said, they only describe lower motor neuron symptoms. Thanks! +6

mousie Agree I thought ALS too but eliminated Peripheral nerves and LMN because I guess I thought they were the same thing ....??? Am I way off here or could someone maybe explain how they are different? Thanks! +1

baconpies peripheral nerves would include motor & sensory, whereas LMN would be just motor +16

seagull Also, a LMN damage wouldn't include both hand and LE unless it was somehow diffuse as in Guil-barre syndrome. It would likely be specific to part of a body. right??? +1

charcot_bouchard No. if it was a peri nerve it would be limited to a particular muscle or muscles. but since its lower motor neuron it is affecting more diffusely. Like u need to take down only few Lumbo sacral neuron to get lower extremity weakness. but if it was sciatic or CFN (peri nerve) it would be specific & symptom include Sensory. +1

vulcania I think it's ALS too. The correct answer choice here seems more based on specific wording: the answer choice "Corticospinal tract in the spinal cord" wouldn't explain the tongue symptoms, since tongue motor innervation doesn't involve the corticospinal tract or the spinal cord (it's corticobulbar tract). This is a situation of "BEST answer choice," not "only correct answer choice." +

submitted by beeip(141), visit this page

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You can see the aforementioned structure in this diagram.

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lsmarshall Rectal prolapse through posterior vagina ("rectocele"). https://www.drugs.com/cg/images/en2362586.jpg +8

famylife "When a rectocele becomes large, stool can become trapped within it, making it difficult to have a bowel movement or creating a sensation of incomplete evacuation. Symptoms are usually due to stool trapping, difficulty passing stool, and protrusion of the back of the vagina through the vaginal opening. During bowel movements, women with large, symptomatic rectoceles may describe the need to put their fingers into their vagina and push back toward the rectum to allow the stool to pass (“splinting”). Rectoceles are more common in women who have delivered children vaginally." https://www.fascrs.org/patients/disease-condition/pelvic-floor-dysfunction-expanded-version +19

usmleuser007 really like the pubic hair.... +5

nnp why not spasm of external anal sphincter? +

vulcania After looking it up I think that external anal sphincter spasm would be more associated with rectal pain and maybe fecal incontinence. I chose the same answer because I figured if there was a problem with the rectovaginal septum it would have been noted on physical exam... +1

ajss I did the same, put sphincter spasm because I thought a rectocele would be found on a physical exam. +

thisshouldbefree this is the map ive been looking for +1

mnunez187 I didn't choose spasm because the stem says there the rectal tone is normal +1

drdoom ^ linkify @famylife https://www.fascrs.org/patients/disease-condition/pelvic-floor-dysfunction-expanded-version +

drdoom ^ linkify @lsmarshall https://www.drugs.com/cg/images/en2362586.jpg +

submitted by shaydawn88(8), visit this page

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Is it intra-alveolar transudates because this patient might have HF d/t a. fib and left atrial enlargement-> inc hydrostatic pressure-> transudate pleural effusion?

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sajaqua1 Basically. +7

medschul Why can it not be arterial hypertension? +2

meningitis I think Arterial HTN is referring to Pulmonary Artery HTN which would be present in LT HF in the long run with RT HF and edema. Pulm HTN would cause a backflow, and doesn't really answer the question "explain the patients Dyspnea". At least, that's how I saw it. Hope this helped. +6

sugaplum the question has 2 murmurs, so does she have aortic stenosis too? i guess it is not relevant since it asked for what is causing her SOB +2

nukie404 I guess pulmonary HTN would happen in response to increased pressure after the edema happens, and would cause backflow (to the RV) over pulmonary edema. +

vulcania There's a really great diagram in UWorld (QID 234) that explains what happens as a result of mitral stenosis. Very similar sounding to the patient in this question. +

srdgreen123 @sugaplum, yes rheumatic heart disease can cause mitral and aortic stenosis. Rheumatic aortic stenosis can be distinguished from degenerative aortic stenosis by 1)coexisting mitral stenosis and 2)fusion of the commisures. +1

submitted by axsa19(9), visit this page

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AB is the only blood group that does not have preformed IgM antibodies in the plasma.

Blood group A has anti-B IgM

Blood group B has ani-A IgM

Blood group AB "NADA"

Blood group O has both anti-A & anti-B IgM

FA 2017 page 390

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axsa19 anti* +

noname FA 2018 page 400 +

vulcania FA 2019 p. 397 +1

destinyschild blood group O also has IgG, which is significant bc it can cross the placenta and cause hemolytic anemia in a fetus +4

submitted by seagull(1933), visit this page

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Why is this not HUS? How did you guys approach the question?

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joonam I think if this was HUS (d/t a bacterial infection) the leukocyte count would be abnormal (11k<) +

yotsubato normochromic normocytic RBC thats why. You would see schistocytes +11

vulcania Also for HUS I would expect mention of h/o bloody diarrhea, or at least diarrhea (not URI), and mention of something to do with kidney damage. +

fatboyslim HUS has a triad of microangiopathic hemolytic anemia (schistocytes, high LDH, high indirect bilirubin), thrombocytopenia, acute kidney injury (high creatinine) + history of bloody diarrhea (usually from E.coli O157-H7). Check FA 2020 page 427 :) +

submitted by liverdietrying(111), visit this page

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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

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aesalmon pg 338 of FA lists it under hypothyroidism but it does present as transient hyperthyroidism first +9

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 +3

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). +1

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 +16

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 :) +2

submitted by step420(32), visit this page

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B-HCG and LH,FSH,TSH share same alpha subunit, so HCG can activate those receptors if its in high enough quantity. Activating LH receptor will lead to more Testosterone from the Leydig cells. More testosterone can lead to more estrogen formation via aromatase.

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dickass bHCG directly increases testicular aromatase activity, it's not because of the increased amount of testosterone. +6

vulcania And for those who were wondering (cause I was), Sertoli cells have aromatase (FA 2019 p. 614) +10

godby It's a slightly different question, on the stem, what's the purpose of the hCG to him, for infertility or increased sexual demand ? Just curious. +

submitted by infundibidum6(0), visit this page

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I got it down to bleomycin & chlorambucil and went with chlorambucil (sounded like “bu”sulfan ... lol) because I thought bleomycin was for testicular cancer/Hodgkins lymphoma. I later found out that chlorambucil is actually a preferred treatment for CLL! Is it because chlorambucil causes severe immunosuppression? So you wouldn’t be giving it to a 72 yo man in the first place?

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yotsubato Bleomycin is the big boy of cancer treatment. I've never heard of chlorambucil and its not in FA. +1

vulcania I had never heard of chlorambucil either and after researching it found out that it's also an alkylating agent, specifically a nitrogen mustard - same as busulfan, so you weren't wrong! Based on what FA says re: bleomycin & busulfan (extrapolating this to chlorambucil), they both cause pulmonary fibrosis & skin hyperpigmentation, however, in the Lange Pharmacology flashcards it says that the hyperpigmentation with busulfan is from adrenal insufficiency so I guess you would expect to see symptoms of that as well if the same applies to chlorambucil? +1

vulcania jk ignore my previous comment. just checked uptodate and it doesn't list hyperpigmentation as a side effect of chlorambucil. +

submitted by infundibidum6(0), visit this page

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yotsubato Bleomycin is the big boy of cancer treatment. I've never heard of chlorambucil and its not in FA. +1

vulcania jk ignore my previous comment. just checked uptodate and it doesn't list hyperpigmentation as a side effect of chlorambucil. +