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Comments ...

 +0  (nbme24#35)

It really looks to me like her sclera have been photoshopped, anyone else notice that? xD


 +0  (nbme22#21)

How many people didn't see that it was 1-specificity and picked E like me :(

jfny21  Here

 +0  (nbme22#47)

Can anyone explain why Fibrous scars with plasma cells is not the correct answer?


 +0  (nbme22#26)

Absolute risk reduction = (Risk in control) - (Risk in experimental). In this case, the risk in the control group is calculated by the number who had an infarction (194) divided by the total (194/2371). Likewise, for the experimental group, (194/2365). This is answer choice B.

adisdiadochokinetic  Whoops, second parenthesis should be 123/2365, sorry!

 +1  (nbme22#48)

The clostridium perfringens alpha toxin is a lecithinase which cleaves lecithin to phosphorylcholine and diglyceride. Essentially, alpha toxin mimics phospholipase C. This means it has a vaguely similar effect of the phospholipases seen in Bacillus Cereus and Listeria Monocytogenes. The end result of the toxin activation is activation of second messenger systems through diglyceride (AKA diacylglycerol), which activates several pathways, most notably in this case Arachidonic acid metabolism and IL-8, with the net effect of increased vascular permeability leading to edema.


 +1  (nbme22#18)

This question is so annoying but this explanation is supported by several papers.





Subcomments ...

submitted by neonem(227),

NRTIs are the main HIV therapy drug that can cause bone marrow suppression (not as common with NNRTIs). This class includes zidovudine, didanosine, emtricitabine, lamivudine, stavudine, abacavir. Zidovudine is most known for this side effect.

Nelfinavir = protease inhibitor azithromycin = aminoglycoside (not really used for HIV) pentamidine = another antimicrobial, mostly used for pneumocystis I think? Lamivudine = another NRTI but less known for bone marrow suppression

adisdiadochokinetic  Azithromycin is a macrolide, not an aminoglycoside FYI, and its use in HIV is primarily as prophylaxis at very low CD4 counts for, among other things, the mycobacterium avium complex. +2  
nbmehelp  How would we have known to choose Zidovudine over Lamivudine tho +1  
mjmejora  @nbmehelp the sketchy with Princess Izolde (Zidovudine) eating bone marrow was my only tip off +1  


submitted by lsmarshall(181),

"Probenecid and high-dose salicylates inhibit reabsorption of uric acid in proximal convoluted tubule (also inhibits secretion of penicillin)." - First Aid 2019

uslme123  so ............... +2  
adisdiadochokinetic  So probenecid is the best answer here because they only specified acetylsalicylic acid, not the dosage, and low-dose acetylsalicylic acid has the opposite effect. +  


submitted by neonem(227),

This patient has major depressive disorder: loss of interest/anhedonia (need to have this or depressed mood),sleep problems, weight changes, decreased energy, thoughts of death. Meets criteria because > 2 weeks timeframe. SSRIs are first-line; paroxetine is in this category. SSRIs also help with weight gain - might be an added benefit if the patient is underweight.

The cardiac stuff might have just been a distractor, except that you probably wouldn't want to give tricyclics (i.e. amitriptyline) since they have pro-arrhythmic side effects. Patient probably has prolonged PR interval due to beta blockers.

adisdiadochokinetic  Another reason not to use TCAs (or alprazolam or haloperidol for that matter) is that the Beers criteria state to avoid the use of all of those drugs in patients over the age of 65. +  


submitted by radshopeful(11),

The classic side effect of anthracyclines is dilated cardiomyopathy. This question could have gotten tricky if you thought the pulmonary symptoms were due to the drug which could have led you to bleomycin (causes pulmonary fibrosis) but these pulmonary symptoms were most likely a result of dilated cardiomyopathy leading to HF and pulmonary edema.

nwinkelmann  What is the clue that this is not pulmonary fibrosis? How do I decide between Doxorubicin and Bleomycin? +  
ilikecheese  Also both bleomycin and methotrexate cause pulmonary fibrosis, so that helped me rule both those out and focus on the HF instead of the pulmonary symptoms +  
adisdiadochokinetic  The S3 gallop and enlarged heart together are very strong evidence for heart failure. It's much more likely for heart failure to cause interstitial edema than for pulmonary fibrosis to directly cause heart failure. +1  


submitted by monkd(3),

Am I crazy or did Uworld not have a question that stated Statins are the most effective drug regardless of baseline lipids. This logic threw my off.

adisdiadochokinetic  You are not crazy. I got this question wrong for the same reason but here's why I think NBME was going with fibrates. You can use the Friedewald equation to calculate LDL cholesterol from the values they give. This equation is LDL= Total Cholesterol-HDL Cholesterol-(Triglycerides/5). The Triglycerides/5 term is an estimate for VLDL. If you calculate it in this case you get an LDL of 120 which is firmly normal and thus the patient would ostensibly not benefit from statin therapy. +2  


Absolute risk reduction = (Risk in control) - (Risk in experimental). In this case, the risk in the control group is calculated by the number who had an infarction (194) divided by the total (194/2371). Likewise, for the experimental group, (194/2365). This is answer choice B.

adisdiadochokinetic  Whoops, second parenthesis should be 123/2365, sorry! +