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Comments ...

 +0  (nbme24#15)

So number of cases with positive serology during "intake" represents prevalence and should not be accounted for when calculating population at risk. Population at risk = Total population - prevalence. Doing that, sum up the annual incidences left = 400 + 250 + 250 + 300 + 300 = 1500.

Applying incidence formula = 1500/(10,000-4000) = 0.25 over a total of 5 years.

Annual = 0.25/5 = 0.05%


 +0  (nbme24#22)

I mean why would a testicle turn around itself when someone's sleeping. This typically occurs after sports/ bicycle riding etc..


 +1  (nbme24#30)

Initially milk drinking was associated with E.coli outbreak with OR=3.9 and P<0.001 (Significant)... After stratification into ate cookies and did not eat cookies OR became 1 instead of 3.9 meaning the association disappeared. Therefore, eating cookies was a confounder and there is no real association between drinking milk and E.coli....instead, milk's (the confounder) contribution was responsible for the OR of 3.9 in the first place. This was furthered demonstrated with OR of 6 in the cookies alone group.


 +0  (nbme23#2)

Pathoma: - Lymphocytes are the most sensitive cells to whole body radiation - Granulocytes (Mainly neutrophils) are particularly very sensitive to chemotherapeutic alkylating agents (requiring G-CSF shortly after)


 +0  (nbme23#30)

So cutting through the intestine will damage the crypts of Lieberkühn which contain stem cells that replace enterocytes/goblet cells (Faid). This lack of regenerative ability will have platelets and inflammatory cells to be recruited in order to mediate healing (which end result is fibrosis) The intestinal wall lacking crypts of Lieberkühn acts pretty much like stable cells (e.g: cardiomyocytes) which cannot be regenerated and so fibrosis ensues (e.g: Scar is always end product after MI).

youssefa  Correction: I meant Permanent cells instead of Stable cells. The hepatocytes in this case will act as a stable cells which will exit G0 phase and proliferate in response to injury.

 +0  (nbme21#24)

Wouldn't acute alcohol consumption even in moderate amount cause reversible hepatic cellular injury characterized by cellular ballooning? It should be the right answer unless the question stem means "Weekends"

hello  No. The order of liver damage due to alcohol is: fatty changes --> cellular swelling (cellular balooning) --> necrosis. This Q stem states to the patient consumed large amount of alcohol on a weekend -- he has acutely drank a large amount of alcohol on one weekend --> this corresponds with fatty changes
et-tu-bromocriptine  It's not in pathoma, but I have it written in (so he or Dr. Ryan may have mentioned it) - Alcoholic hepatitis is generally seen in binge drinkers WITH A LONG HISTORY OF CONSUMPTION.

 +0  (nbme20#30)

From Faid 2019 new figure: IGF-1 mainly functions as an anabolic hormone on muscles and bones (pretty much like insulin-> decreases serum glucose). GH acts separately by promoting insulin resistance (increasing serum glucose). Therefore, IGF-1 is not the answer. If GH was among the answers it would have got really confusing.

charcot_bouchard  Can anyone take a little time to curse on that daughter?
dbg  Sure, charcot. Just wished on her to get a couple of charcots (the triad, your aneuryms, marie tooth, etc).




Subcomments ...

submitted by fahmed14(9),

Histamine plays a major role in the cardinal signs of inflammation. It helps mediate vasodilation and vascular permeability (via endothelial cell contraction). These two functions are already contrary to A, B, C, and D. By increasing fluid in the interstitial space, you can reason that there will be increased lymph flow.

youssefa  If more transudates are leaking into the interstitium wont this dilute the interstitial proteins and cause a decrease in oncotic pressure and increase in interstitial hydrostatic pressure? +1  


Can someone explain why does this patient have hypokalemia?

colonelred_  Catecholamines activate the Na/K pump, which will drive K inside. +5  
trazabone  Read online that catachelamines are released following tonic clonic seizures. Besides that, BP of 180/100 could indicate that catecholamines are circulating. +  
fulminant_life  This mechanism is why giving albuterol for hyperkalemia works +3  
nbmehelp  Why does this guy have increased catecholamines tho +  
johnson  His SNS activity is seriously increased --> increased catecholamines. +  
nbmehelp  Why is his SNS activity increased? Is the BP literally the only hint? +  
youssefa  Alcohol withdrawal creates a hyper- catecholaminergic state + Seizures do that as well. +1  
water  My best guess is that withdrawal puts the body in a state of stress (same for seizures) and with stress you have release of catecholamine which we'll see in the BP and the hypokalemia. +  


Why is it not ovarian follicle cells? I thought the female analog of Sertoli and Leydig is theca/granulosa cells.

colonelred_  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +2  
brethren_md  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
sympathetikey  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
s1q3t3  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
masonkingcobra  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
mcl  Wait, but did anyone mention that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen??? +8  
mcl  But seriously though, pathology outlines says sertoli-leydig tumor "may be suspected clinically in a young patient presenting with a combination of virilization, elevated testosterone levels and ovarian / pelvic mass on imaging studies." As for follicle cell tumors, granulosa cell tumors usually occur in adults and would cause elevated levels of estrogens. Theca cell tumor would also primarily produce estrogens. Putting the links at the end since idk if they're gonna turn out right lol Link pathology outlines for sertoli leydig granulosa cell tumor theca cell tumor +5  
bigjimbo  LOL +  
fallenistand  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +2  
medpsychosis  So after doing some intense research, UPtoDate, PubMed, an intense literature review on the topic I have come to the final conclusion that...... ...... ...... ...... Wait for it.... ..... ..... Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +2  
charcot_bouchard  Hello, i just want to add that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
giggidy  Hold up, so I'm confused - I read all the posts above but I still am unsure - are sertoli-leydig cells notorious for producing androgen? +  
subclaviansteele  Hold the phone.....Females can get sertoli leydig cell tumors which are notorious for producing androgen? TIL TL;DR - Females can get sertoli leydig cell tumors = high androgens +  
cinnapie  I just found a recent study on PubMed saying "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" +  
youssefa  Hahahahaha ya'll just bored +  
water  Bored? you wouldn't think so if you knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
nbmehelp  I dont get it +  
redvelvet  how don't you get it that females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen? +  


submitted by cinnapie(2),

Why does every NBME have one or two erection related questions??

youssefa  Cause we all know what bout to happen to us in this exam :D +1  


submitted by youssefa(6),

So cutting through the intestine will damage the crypts of Lieberkühn which contain stem cells that replace enterocytes/goblet cells (Faid). This lack of regenerative ability will have platelets and inflammatory cells to be recruited in order to mediate healing (which end result is fibrosis) The intestinal wall lacking crypts of Lieberkühn acts pretty much like stable cells (e.g: cardiomyocytes) which cannot be regenerated and so fibrosis ensues (e.g: Scar is always end product after MI).

youssefa  Correction: I meant Permanent cells instead of Stable cells. The hepatocytes in this case will act as a stable cells which will exit G0 phase and proliferate in response to injury. +  


Anyone know how to rule out small intestine on this one? I thought the omentum played a role in healing in the abdomen, but clearly I'm missing something here.

what  Small intestine has smooth muscle in the walls which will fibrose on injury +  
youssefa  So cutting through the intestine will damage the crypts of Lieberkühn which contain stem cells that replace enterocytes/goblet cells (Faid). This lack of regenerative ability will have platelets and inflammatory cells to be recruited in order to mediate healing (which end result is fibrosis) The intestinal wall lacking crypts of Lieberkühn acts pretty much like stable cells (e.g: cardiomyocytes) which cannot be regenerated and so fibrosis ensues (e.g: Scar is always end product after MI) +  


submitted by sajaqua1(169),

Serum sickness is a Type 3 hypersensitivity reaction, in which the body responds to antigenic medical substances and produces antibodies. These antibodies in circulation then bind to the antigenic drugs and set off the complement cascade. Rheumatoid arthritis is also a Type 3 hypersensitivity reaction.

A) Apoptosis of macrophages- apoptosis is generally not a type of hypersensitivity reaction. B) Mast cel degranulation- this is part of a Type 1 hypersensitivity reaction/anaphylaxis, in which mast cells bind IgE on their surface, and IgE binding to the target antigen induces a conformational change in the IgE that sets off mast cell degranulation. C) Natural Killer Cell killing- plays a variety of roles, including cancer suppression and destruction of virally infected cells. If they play a role in hypersensitivity, it is part of Type 2 HSR in which they would respond to Ig on the cell surface. E) Wheel and flare reactions- This is also a Type 1 HSR.

meningitis  I didn't pick this one because I thought Serum sickness was too systemic and RA was a more localized Type 3. Again, im overthinking things. +  
youssefa  Goljan: RA is a mixed type III and type IV immune reaction +  
dinagohe23  I though NK cell killing was similar to T cell so and RA is also Type IV +  
nephcard  ,blll sdouof +  


submitted by sne(10),

Acute asthma exacerbation 1. Albuterol 2. Corticosteroids 3. Ipratropium

youssefa  I guess they described a COPD exacerbation here since she's a smoker and Xray showed a wide AP diameter. Either ways Ipratropium would make the best answer since its used in both cases. +  


submitted by jrod77(12),

I think they might be describing angina...not sure. TXA2 is responsible for platelet aggregation,so it may be contributing to thrombosis, thus ischemia to the cardiac tissue.

sympathetikey  Agreed. I'm pissed though because PGE2 mediates pain, which is why I picked it. +7  
he.sanchez14  If im not mistaken, the question describes unstable angina. Unstable angina is due to thrombosis with incomplete occlusion. So, yes TXA2 is responsible for the thrombus that is causing the symptoms in this patient. I'm also pissed because I also went straight for the PGE2 +  
vik  hahah, seems like all in same boat like me +  
yb_26  thromboxane A2 is also vasoconstrictor, so my thoughts were about vasospastic angina +  
shriya goyal  same I went for pgE2 ... I M PISSED +  
shriya goyal  same I went for pgE2 ... I M PISSED +  
youssefa  Went for PGE2 ... shit +  
need_answers  I went for leukotriene B4, what the hell was I doing....SHIT +1  
hopsalong  I picked Leukotrine B4 thinking that the neutrophil infiltration was the source of the pain, seems wrong lol. +  
bballhandler11  Sometimes it helps me to think of it in a general, non med school textbook kind of way. When answering, I narrowed it down to PGE2 and TXA2 as well. Then I asked myself, if someone is experiencing chest pain, would I recommend Aspirin or Advil? That's helped on a few over the counter pharm questions. +1  
ususmle  same here I M PISSED PGE2 +  


submitted by mcl(167),

Patient may have hereditary angioedema, which is associated with "recurrent attacks of intense, massive, localized subcutaneous edema involving the extremities, genitalia, face, or trunk, or submucosal edema of upper airway or bowels". The article goes on to say "C1-esterase inhibitor works directly on the complement and contact plasma cascades to reduce bradykinin release" which is also probably good to know.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3666183/

notadoctor  Thought this was a trick question as C1 esterase deficiency also results in a decrease in C4. However, the second answer choice was not referring to C4 but to C4 binding protein, which I now know is different. I also didn't realize C1 esterase was technically a complement protein. +3  
youssefa  Based on many sources hereditary angioedema does NOT cause a rash (urticaria) which is a main differentiating point between angioedema and allergy. This mislead me in this question. Any clarification? +2  
ergogenic22  +1 on the above because uptodate states that c1 esterase inhibitor deficiency, both acquired and nonhereditary, are both non-urticarial, non-pruritic, and that is confirmed by the above linked article +1  
sahusema  Question writer probably didn't know the difference between cutaneous urticaria and subcutaneous edema. +  


submitted by jejunumjedi(12),

I think this is describing a signal peptide (hydrophobic at N-terminus). Without signal peptide => can’t be transported into endoplasmic reticulum.

youssefa  Is this even in FA? Biochem chapter only mentions SRPs. +