NBME Answers : impostersyndromel1000's page

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submitted by sup(10),

Somehow I was able to convince myself that increased testosterone --> decreased estrogen --> decreased negative feedback on LH/FSH secretion --> increased FSH. Does anyone care to explain why this logic is wrong? Thanks :)

btl_nyc The increased testosterone is metabolized by granulosa cells to estrogen and by adipose tissue into estrone. Both feed back on the hypothalamus to inhibit FSH & LH secretion, but FSH is much more sensitive to feedback inhibition than LH, causing an increased LH/FSH ratio. +

impostersyndromel1000 @sup, i did the same thing. Had no idea testosterone and androgens can increase epo +

submitted by seagull(840),

So alpha was the answer so my fatigued mind put "A"...well done. You're going to be a doctor. lol

impostersyndromel1000 hope you dont have to write a prescription for me one day lol +2

submitted by cocoxaurus(48),

Almost got tricked by this one because osteosarcoma also causes osteoblastic lesion. Osteosarcoma most commonly metastasizes to lungs though.

impostersyndromel1000 This was in pathoma, he said prostate cancer causes osteoblastic lesions and "the board examiners really want you to know that". also following the potential site of mets helps choose the answer +

snripper Also, osteosarcoma is less common in the elderly, more common in males <20 y/o (per F.A 2020) +

submitted by drdoom(467),

You have to think about this using the concept of CONDITIONAL PROBABILITY. Another way to ask this type of question is like this: “I show you a patient with spontaneous pneumothorax. Which other thing is most likely to be true about that person?” Or you can phrase it these ways:

Given a CONDITION (spontaneous pneumo), what other finding is most likely to be the case?
Given a pool of people with spontaneous pneumothorax, what other thing is most likely to be true about them?

In other words, of all people who end up with spontaneous pneumo, the most common other thing about them is that they are MALE & THIN.

If I gave you a bucket of spontaneous pneumo patients -- and you reached your hand in there and pulled one out -- what scenario would be more common: In your hand you have a smoker or in your hand you have a thin male? It’s the latter.

someduck3 Is this the best approach to all of the "strongest predisposing risk factor" type questions? +

drdoom There is a town of 1,000 men. Nine hundred of them work as lawyers. The other 100 are engineers. Tom is from this town. He rides his bike to work. In his free time, he likes solving math puzzles. He built his own computer. What is Tom's occupation most likely to be? Answer: Tom is most likely to be a lawyer! Don't let assumptions distract you from the overwhelming force of sheer probability! "Given that Tom is from this town, his most likely occupation (from the available data) = lawyer." +4

drdoom There is a town of 1,000 spontaneous pneumo patients. Six hundred are tall, thin and male. The other 400 are something else. Two hundred of the 1,000 smoke cigarettes. The other 800 do not. What risk factor is most strongly associated with spontaneous pneumo? (Answer: Not being a smoker! ... because out of 1,000 people, the most common trait is NOT smoking [800 members].) +4

impostersyndromel1000 this is WILD! thanks guy +3

belleng beautiful! also, i think about odds ratio vs. relative risk...odds ratio is retrospective of case-control studies to find risk factor or exposure that correlates with grater ratio of disease. relative risk is an estimation of incidence in the future when looking at different cohort studies. +

drdoom @impostersyndrome I love me some probability and statistics. Glad my rant was useful :P +

hyperfukus @drdoom i hate it which is why your rant was extremely useful lol i learned a ton thanks dr.doom! +1

dubywow I caught he was thin. The only reason I didn't pick Gender and body habitus is because he was not overly tall (5'10"). I talked myself out of it because I thought the body habitus was too "normal" because he was not both thin AND tall. Got to keep telling myself to not think too hard on these. Thanks for the explanation. +1

taediggity It isn't just that this person has Ehlers Danlos and they're more prone to spontaneous pneumo??? +1

submitted by gh889(66),

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.. +2

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 +

osler_weber_rendu @gh889 I agree niacin is the answer, but even niacin causes increase in HDL. As if getting to the drug wasnt tough enough, NBME puts two of its actions in the options! What a shit question +1

submitted by d_holles(104),

Goljan stresses the Boards giving the leukemia questions away based on the age given in the question stems.

ALL = 0-14

AML = 15-39; 40-59

CLL = 60+

CML = 40-59

https://forums.studentdoctor.net/threads/goljan-on-leukemias.303605/

impostersyndromel1000 thanks for the reminder, often overlooked are the simple demographic hints. helps you make an educated guess +

hyperfukus also a key thing to remember in general is a person who undergoes chemo is a big demographic hint to later developing AML regardless of the clues :) and yes the AGE!!! +1

submitted by atstillisafraud(111),

Alkylating agents (merchlorethamine) (the other drugs listed are microtubule inhibitors) increase the risk of AML.

keycompany Additionally, AML is the only answer choice that has multiple blast forms (myeloblasts, promyelocytes, etc.). ALL is characterized by a single blast form (lymphoblasts). +22

seagull CML has blasts too but they tend to favor mature forms. +4

kash1f You see numerous blast forms == AML, which is characterized by >20% blasts +3

keycompany The answer choices are all of lymphoid origin except for AML and Hodgkin Disease. We know Hodgkin Disease is a lymphoma (not leukemia) and would present with lymphadenoapthy. So the answer must be AML #testtakingstrategies +10

impostersyndromel1000 @atstillisafraud thanks for mentioning the merchlorethamine increasing risk for AML, i was trying to make a connection with the drugs but couldnt. Had to lean on the test taking skills just like key company +

sweetmed Procarbazine is alkylating as well. +

pg32 @keycompany how did you know the phrase "multiple blast forms" meant literally different types of blasts and not just many blast cells were seen? +2

castlblack this link says CLL has 'large lymphocytic variety' under the picture of the peripheral smear. I am not arguing against you, just researching here https://emedicine.medscape.com/article/199313-workup +

submitted by keycompany(214),

Hyperventilation decrease PaCO2. Central chemoreceptors respond to low PaCO2 by vasoconstricting cerebral blood vessels.

A) Arterial Blood Oxygen Concentration: Blood Oxygen Concentration is directly related to Hb concentration and saturation (SaO2) FA2019, p. 653. Via the Bohr Effect, decreased PaCO2 will increase SaO2, thus increasing blood oxygen concentration.

B) Arterial Blood PO2: PaO2 changes in response to decreased PAO2, PIO2, or diffusion. There would be no change in PaO2 during hyperventilation (theoretically).

C) Aterial Pressure: Decreased PaCO2 is associated with vasoconstriction, which would increase blood pressure.

E) Cerebral Tissue pH would increase due to respiratory alkalosis.

keycompany EDIT: Via the **Haldane Effect**, not the Bohr Effect. +

impostersyndromel1000 excellent response +

teepot123 fa 19 pg 489 +

submitted by nwinkelmann(218),

I've never been good at converting units :( lol so had to ask my brother. He told me that:

distance × distance = distance² = area

and,

distance × distance × distance = distance² × distance = distance³ = volume

Gotta love public school for never been taught that ... geesh (obviously I've done the equations and stuff, just never been told it that way/that simple before). Knowing that makes figuring out the equation much easier:

Flow rate = velocity × CSA = 20 cm/sec × 2cm² = 40cm³/sec

To convert to L/min, just multiply:

40cm³/sec × 60 sec/min × 1L/1,000cm³ = 2400 L/1,000 min = 2.4 L/min

Hope this helped!

impostersyndromel1000 to all my public school peeps out there (and not the nice public schools in rich areas, the real public schools)... we made it! +2

angelaq11 Thankfully I was taught how to convert units, but let me tell you that I was SO lost on this one. It's USELESS to know how to do it if you (I, I mean I) don't know the damn formula xD. Obviously got this one wrong, but it's good to know that if it ever comes up again (and I know it won't) I already know it. +1

submitted by endochondral1(10),

is this question asking what we physically pass through or by?

impostersyndromel1000 no, basically the question is testing if you know the branches of the abdominal aorta and which is closest to the renal (in this case, inferior to the renal arteries) +1

impostersyndromel1000 what you are passing by would better answer your question actually +

submitted by endochondral1(10),

is this question asking what we physically pass through or by?

impostersyndromel1000 no, basically the question is testing if you know the branches of the abdominal aorta and which is closest to the renal (in this case, inferior to the renal arteries) +1

impostersyndromel1000 what you are passing by would better answer your question actually +

submitted by link981(105),

Per First Aid 2018 (pg 421) & Merck Manual

a) CML is not the answer because in CML you have HIGH WBCs & Platelets. In the stem there is only high platelets. b) Is the answer because in Essential Thrombocythemia we have normal WBCs and RBCs, just high platelets. c) Myeloid metaplasia refers to well a metaplasia in myeloid cells which are basophils, eosinophils, etc. d) In Polycythemia Vera we have HIGH RBCs, WBCs, and Platelets. e) Reactive thrombocytosis- is a elevated platelet count that occurs secondary to another disorder like:

-Chronic inflammatory disorders (eg, rheumatoid arthritis, inflammatory bowel disease, tuberculosis, sarcoidosis, granulomatosis with polyangiitis) -Acute infection

-Hemorrhage

-Iron deficiency

-Hemolysis

-Cancer

-Splenectomy or hyposplenism

impostersyndromel1000 perfect response right here +

paloma Essential thrombocythemia presents with platelets > 1 million, not reactive thrombocytosis +

submitted by mcl(453),

Beta-2 receptors are coupled to Gs proteins, which activate adenylyl cyclase and increase cAMP. Cyclic AMP then increases activity of protein kinase A, which phosphorylates myosin light chain kinase, ultimately resulting in smooth muscle relaxation. Albuterol, a B2 agonist, is therefore useful in treating bronchospasm.

impostersyndromel1000 are you able to clarify that phosphorylated myosin light chain kinase from cAMP/PKA and dephosphorylated myosin light chain from cGMP both cause smooth muscle relaxation? saw this on another Q with the nitrates causing headache so now im confused +

dubywow @impostersyndromel1000: Here is an image that summarizes cAMP and cGMP actions in smooth muscle cell very will. Hope it helps. link +

iwannabeadoctor2 cGMP is the use of Nitrates for endothelial vasodilation; B2 is a different action, similar end result. See this diagram for the adrenergic receptor actions. https://s3.amazonaws.com/classconnection/769/flashcards/5928769/png/screen_shot_2014-11-04_at_92935_am-1497B7358A4552ACB39.png +

castlblack cAMP INHIBITS myosin light chain kinase causing relaxation according to FA 2020 pg. 317 +

submitted by bubbles(51),

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. +14

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)? +6

impostersyndromel1000 we had the exact same thought process, so i too am hoping this is the correct way to approach it get reasoning friend +

ajss thanks for this explanation, I totally forgot about AR patterns are most likely enzymes deficiencies, this kind of make the question easier if you approach it that way, thanks +

submitted by meningitis(310),

Process of elimination on this one.

I eliminated Carbomyl phosphate, Arginine due to urea cycle.
I eliminated ATP because ATP alone wouldn't change F6P into glucosamine
NAG I got lucky and I eliminated it due to its use in ECM and collagen so I didn't think it was relevant and I kind of remembered it being in urea cycle.

dr.xx you mean, pure luck? :) +12

impostersyndromel1000 lol pretty sound logic here mate +1

nor16 same here, Glutamine is a NH3 (-amin) donor, so guessing made sense +

submitted by seagull(840),

out of curiosity, how may people knew this? (dont be shy to say you did or didnt?)

My poverty education didn't ingrain this in me.

johnthurtjr I did not +1

nlkrueger i did not lol +

ht3 you're definitely not alone lol +

yotsubato no idea +

yotsubato And its not in FA, so fuck it IMO +1

niboonsh i didnt +

imnotarobotbut Nope +

epr94 did not +

link981 I guessed it because the names sounded similar :D +10

d_holles i did not +

yb_26 I also guessed because both words start with "glu"))) +14

impostersyndromel1000 same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle. +

jaxx Not a clue. This was so random. +

wolvarien I did not +

ls3076 no way +

hyperfukus no clue +

mkreamy this made me feel a lot better. also, no fucking clue +1

amirmullick3 My immediate thought after reading this was "why would i know this and how does this make me a better doctor?" +5

mrglass Generally speaking Glutamine is often used to aminate things. Think brain nitrogen metabolism. You know that F-6-P isn't an amine, and that Glucosamine is, so Glutamine isn't an unrealistic guess. +2

djtallahassee yea, I mature 30k anki cards to see this bs +3

taediggity I literally shouted wtf in quiet library at this question. +1

bend_nbme_over Lol def didn't know it. Looks like I'm not going to be a competent doctor because I don't know the hexosamine pathway lol +1

drschmoctor Is it biochemistry? Then I do not know it. +2

snoochi95 hell no brother +

roro17 I didn’t +

bodanese I did not +

hatethisshit nope +

jesusisking I Ctrl+F'd glucosamine in FA and it's not even there lol +

batmane i definitely guessed, for some reason got it down to arginine and glutamine +1

waterloo Nope. +

monique I did not +

issamd1221 didnt +

baja_blast Narrowed it down to Arginine and Glutamine figuring the Nitrogen would have to come from one of these two but of course I picked the wrong one. Classic. +

amy +1 no idea! +

submitted by bubbles(51),

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) +

tiagob Why is not Cohort ? since it compares groups exposed to drug X? +

djinn Cohort studies determines end of disease and CC determines begins +1