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 +0  (nbme22#7)

Is decreased nocturnal erections not possible due to the incongruity between onset of symptoms and stroke (2 mos versus 3)? Agree that these questions are very vague and frustrating. Not sure where to get a good grasp on this material.


 +0  (nbme22#47)

can anyone explain why (D) metaplasia is incorrect?

angelaq11  because metaplasia would be a transformation of the normal architecture of the respiratory epithelium to one that does not belong there, in response to chronic irritation. This woman had pneumococcal pneumonia that was correctly (and I dare say promptly) treated, so she suffered an acute rather than a chronic insult.




Subcomments ...

After everything its jjust an epidem ques. Below 55 vs Above 55 years

ls3076  can you elaborate please? +  


The most important hints to the question are as follows, with #2 being the most specific:

1) patient reports pain with overhead motion and reports recurrent overhead motion during work. Overhead motion can damage the supraspinatus muscle due to impingement by the acromion.

2) Pain is worst with internal rotation of the shoulder - this is consistent with the findings of the empty-can test, which indicates a supraspinatus injury.

mousie  I was thinking along the lines of overhead motion - damage to the subacromial bursa which is between the acromion and the supraspinatus ... also its the most commonly injured rotator cuff m. so could have guessed this one right +  
sympathetikey  Thanks for the explanation. I was scratching my head as to why this is correct, since supraspinatus only does 15 degrees of abduction, but you make a lot of sense. +1  
charcot_bouchard  IDK WTF i picked Trapezius +7  
ls3076  why would injury to supraspinatus cause weakness with internal rotation though? +5  
targetusmle  yeah coz of that i picked subscapularis +1  
maddy1994  ya the whole question pointed to supraspinatus ...but last line internal rotation made me pick subscapularis +2  
darthskywalker306  I went for Trapezius. That shoulder flexion thing was a big distraction. Silly me. +  


submitted by keycompany(127),

This question is disguised. What they are really asking is "what is the sole determinant of species survival"? The only answer is the ability to procreate. Because DNA Polymerase has proof-reading activity, progeny will be unaffected by RNA Polymerases lack of proof-reading activity.

ls3076  the phrasing of this explanation doesnt make sense to me. +2  
ls3076  oh wait sorry i just read it again. So instead of proofreading how are errors handled with RNA? +  
thomasburton  Think the point is basically although errors with RNA polymerase make make the bacterium not very good at infecting or killing or whatever it does not affect replication as it is not used during replication! +2  


submitted by keycompany(127),

This question is disguised. What they are really asking is "what is the sole determinant of species survival"? The only answer is the ability to procreate. Because DNA Polymerase has proof-reading activity, progeny will be unaffected by RNA Polymerases lack of proof-reading activity.

ls3076  the phrasing of this explanation doesnt make sense to me. +2  
ls3076  oh wait sorry i just read it again. So instead of proofreading how are errors handled with RNA? +  
thomasburton  Think the point is basically although errors with RNA polymerase make make the bacterium not very good at infecting or killing or whatever it does not affect replication as it is not used during replication! +2  


submitted by colonelred_(50),

Attributable risk = incidence in exposed – incidence in unexposed

= 30/1,000 (smokers) - 30/3,000 (nonsmokers)
= 0.03 - 0.01
= 0.02 (so the attributable risk is about 2%)

Applying it to a population of 10,000:

= 0.02 * 10,000
= 200

charcot_bouchard  What if i tell you this is a ques of Attributable risk % in exposed? AR= 0.02 / IR in exposed (30/1000) = 0.6667 30 case in 1000. So 300 case in 10,000 0.6667 x 300 = 200 or in another word 66% cases of 100 lung cancer cases in smokers is actually due to smoking. so in 300 cases of smokers 200 is actually due to smoking +1  
charcot_bouchard  This is a mind fuck. Lemme tell u guys if any consolation while doing the ques during test i did it with AR = 0.02; NNH = 1/0.02 = 50. 50 persons smoke to cause 1 cancer. 10K smoke to cause 200 cancer. +  
ls3076  Sorry if this is a stupid question. Why is it incorrect to simply apply the same proportion (30 cancer per 1000 smokers) to 10,000 smokers? +1  
krewfoo99  @is3076 Thats exactly what is did. I still dont understand how that is wrong. But i guess they want us to think about it in terms of AR +  
hhsuperhigh  @Is3076 and @Krewfoo99, If a person doesn't smoke, the natural risk of getting lung cancer is 30/3000=1%. The smoker's risk is 30/1000=3%. This 3% is not purely contributed by smoking, but mixed with the natural risk. So for calculating the pure contribution made by smoking, you should use 3%-1% which is 2%. And this 2% is the pure contribution of smoking. Not all smokers get lung cancer, the same thing, not all lung cancer among smokers are attributed by smoking. They may get lung cancer anyway despite smoking or not. +  


Disorders common in east Asia according to Goljan: Hepatitis B EBV infection - mostly leading to nasopharyngeal CA Alpha Thalassemia Nitrosamine linked Intestinal type gastric CA

In this question, since the patient is asymptomatic and EBV isnt exactly "screened for", went with HepB as the answer

ls3076  i think asymptomatic is really the key here -- good catch +1  


submitted by sympathetikey(353),

Lucky deduction, but looking back, I believe what they were going for is what she should have been vaccinated for at 6 months of age (since there are no apparent symptoms).

Hep B vaccine is usually given at birth, 1 month, and 6 months of age, so it's pretty important that she be vaccinated against it, unless she already has it, in which case she should be treated to avoid cirrhosis.

ls3076  how can we actually be expected to know vaccination schedules... there must be some other reason the answer is correct +  


submitted by welpdedelp(77),

The pt had asthma (SOB, wakes up at night out of breath, has allergies). It asked for the precursor of leukotrienes, which is arachidonic acid. The prob gave him Montelukast or inhaled glucocorticoids.

ls3076  wtf is up with the phrasing of this question +2  


submitted by seagull(461),

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 +  
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 +  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +5  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +3  
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?" +  


submitted by niboonsh(90),

This is a case of acute transplant rejection. weeks to months after the transplant, recipient cd8 and/or cd4 t cells are activated against the donor (a type 4 HSR) and the donor starts making antibodies against the transplant. This presents as a vasculitis with dense interstitial lymphocytic infiltrates. (FA2018 pg 119)

ls3076  Actually was confused about this due to a UW explanation. UW said acute txp rejection has two types - humoral and humoral and cellular. Humoral has Neutrophilic infiltrate + necrotizing vasculitis while cellular has lymphocytosis. Can anyone simplify/explain this please? +1  


submitted by nwinkelmann(109),

So, I thought this question was super vague and not great... that being said, having gotten it wrong and not really having a good explanation for the answer, I did a little research and found this article: https://www.ahajournals.org/doi/pdf/10.1161/01.STR.30.4.715

This was the main conclusion: "The results of the present study, aimed at assessing the effects of stroke on sexual functioning, reveal a significant decline in libido, coital frequency, sexual arousal, and satisfaction with sexual life in both stroke patients and their spouses. The present results also demonstrate that disorders of sexual functions are most significantly associated with various psychosocial factors, such as patients’ general attitude toward sexuality, fear of impotence, and ability to discuss sexuality, as well as with the degree of poststroke functional disability. Moreover, sexual dysfunction was related to the presence and degree of depression, diabetes mellitus, and cardiovascular medication. The etiology or location of the stroke and the gender or marital status of the patients were not associated with changes in poststroke sexuality in patients in the present study."

Looking at the question again, I'm guessing the "fatigue and difficulting sleeping and concentrating" statement was supposed to be a clue for depression, especially since it started after his stroke. Also, no physical abnormalities suggest functioning is intact and thus nocturnal erections would be preserved normally. This is just stupid.

ls3076  appreciate this kind of effort to look up journal articles but honestly this is not really what nbme answers is for... we should be able to get the answer from process of elimination/basic science concepts and not from looking up studies as we obviously can't do this on the test +  


submitted by alexb(15),

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

ls3076  Really good observation +  


Increased sweat and Na+ concentration should point to cystic fibrosis (CF). The problem with CF is not that the gene is being transcribed less, but that the protein that the gene codes for is altered, which leads to the CF channel being degraded due to mis-folding --> less CF receptors on cell surface --> phenotypic CF.

ls3076  why not membrane receptor? +2  
a1913  delF508 is a 3 base pair deletion of phenylalanine at amino acid position 508. Mutation causes impaired post-translational processing of CFTR (improper folding) which rough ER detects. Sends mutant misfolded CFTR to the proteasome for degradation, preventing it from reaching cell surface. So problem is not malfunctioning CFTR channels in the surface; problem is complete absence of CFTR on cell surface (since they keep getting misfolded and sent to proteasome to be trashed). Source of primary problem: error in protein structure +  
angelaq11  @Is3076 because the CFTR is a channel not a receptor. +  


Our little friend has a Parvovirus infection, which infects erythroid precursors, causing interruption of erythrocyte production. This is the same way it causes hydrops fetalis in unborn babies and aplastic anemia in sickle cell, etc.

gainsgutsglory  I get Parvo has tropism for RBC precursors, but wouldn’t it take 120 days to manifest? +  
keycompany  RBCs don’t just spill out of the bone marrow every 4 months on the dot. Erythropoesis is a constant process. If you get a parvo virus on “Day 1” then the RBCs that were synthesized 120 days before “Day 1” will need to be replaced. They can’t be because of parvovirus. This leads to symptomatic anemia within 5 days because the RBCs that were synthesized 125-120 days before the infection are not being replaced. +2  
drdoom  @gainsgutsglory @keycompany It seems unlikely that “1 week” of illness can explain such a large drop in Hb. It seems more likely that parvo begins to destroy erythroid precursors LONG BEFORE it manifests clinically as “red cheeks, rash, fever,” etc. Might be overkill to do the math, but back-of-the-envelope: 7 days of 120 day lifespan -> represents ~6 percent of RBC mass. Seems unlikely that failure to replenish 6 percent of total RBC mass would result in the Hb drop observed. +  
yotsubato  He can drop from 11 to 10 hgb easily +1  
ls3076  Apologies if this is completely left-field, but I didn't think this was Parvovirus. Parvo would affect face. Notably, patient has fever and THEN rash, which is more indicative of Roseola. Thoughts?? +2  
hyperfukus  @is2076 check my comment to @hello I thought the same thing for a sec too :) +  
hyperfukus  also i think you guys are thinking of hb in adults in this q it says hb is 10g/dL(N=11-15) so it's not relatively insanely low +  
angelaq11  @Is3076 I completely agree with @hyperfukus and I think that thinking of Roseola isn't crazy, but remember that usually with Roseola you get from 3-5 days of high fever, THEN fever is completely gone accompanied by a rash. This question says that the patient has a history of 4 days of rash and 7 days of fever, but never mentioned that the fever subsided before the appearance of the rash. And Roseola is not supposed to present with anemia. +1  


submitted by seagull(461),

If you don't know what Dicumarol does like any normal human. The focus on what aspirin doesn't do, namely it's doesn't affect PT time and most pills don't increase clotting (especially with aspirin). This is how I logic to the right answer.

usmleuser007  If that's then thinking, then how would you differentiate between PT & PTT? +2  
ls3076  Why isn't "Decreased platelet count" correct? Aspirin does not decrease the platelet count, only inactivates platelets. +  
drmohandes  Because dicumarol does not decrease platelet count either. +  
krewfoo99  @usmleuser007 Because the answer choice says decrease in PTT. If you take a heparin like drug then the PTT will increase. Drugs wont increase PTT (that would be procoagulant) +