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Comments ...

 +1  (nbme22#44)

There is a high indirect bilirubin concentration (8 mg/dl out of the total 10 mg/dl) so there must be a problem with conjugation. the enzyme needed for conjugation is UDP-gluronosyltransferase.

In this case, this is physiological neonatal jaundice. due to immature enzyme that resolves without treatment in 1-2 weeks. pg 387 FA 2019


 +4  (nbme22#14)

If you want to think of this simply, the ribs are connected posteriorly to the vertebral column. and the intercostal veins run between them, so they are the closest to the vertebral column.


 +1  (nbme22#13)

corticosteroids - steroid bind to receptor located in nucleus or cytoplasm --> transformation of receptor to expose DNA-binding protein etc pg 332 FA 2019


 +0  (nbme20#41)

High X is bound when low Y is added, and low X is bound when Y is added. So MAYBE they are competing for the same binding spot/epitope due to this relationship (epitope= antibody binding site) ??????????





Subcomments ...

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 yotsubato(214),

"MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is a prodrug to the neurotoxin MPP+, which causes permanent symptoms of Parkinson's disease by destroying dopaminergic neurons in the substantia nigra of the brain. It has been used to study disease models in various animal studies." Wiki

ilikecheese  pg 508 FA 2019 +1  
sbryant6  I thought this was testing "lead pipe rigidity" aka Neuroleptic Malignant Syndrome and its connection to dopamine. Had no clue what MPTP was and got it right still. Probably wrong train of thought though. +