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 +0  (nbme23#32)

so I was stuck on this because his BUN /creatinine ratio led me to think he had an intrinsic renal dysfunction. And a PGI2 inhibition would lead to a pre-renal azotemia, where the BUN/ creatinine ratio would be more than 20. I know that NSAIDs inhibit PGIS. But how are you supposed to cross out induction of distal tubular acidosis?

purdude  You can cross out Distal RTA because the urine pH is 5. In Distal RTA, urine pH becomes greater than 5.5 because a-IC cells can't secrete H+

 +4  (nbme22#21)

The question is asking what point would be the most likely to rule in cancer, and high specificity when positive rules in cancer. The highest specificity value is A, bc the the X axis shows (1-specificity)!

sbryant6  SPin and SNout. Specificity in, sensitivity out.




Subcomments ...

submitted by mcl(167),

Patient with bilateral renal artery bruits and hypertension will for sure have activation of RAS system and therefore increase in angiotensin.

Although pheochromocytoma and consequent elevated catecholamines can increase blood pressure, symptoms are typically episodic and renal bruits are not likely to be heard. Elevated levels of serotonin can also cause hypertension, but we would also expect to see flushing; also, there is nothing in the stem to indicate patient is taking SSRIs or something else that could predispose her to elevated levels of serotonin. Elevated levels of thyroid hormone could also give patient hypertension, but we would also expect other signs of hyperthyroidism (tremors, weight loss, etc.).

I was a little confused if EPO would be elevated -- if there is stenosis of renal arteries (as indicated by the bruits) the kidneys could also detect this as hypoxia and ramp up production of EPO. However, I ended up going with angiotensin since it seemed more "concrete" to me that RAS would be up. Does anyone know why it's not EPO?

brise  Wouldn't that be more long term? +  
sugaplum  I think Epo would indicate Rcc or renal failure, she seems like she has "just" refractory HTN, and no other sx to indicate anemia. +  
davidw  She has Fibromuscular dysplasia which should be in your differential for a young female with hypertension ( along with Conns syndrome and pheochromocytoma). it typically causes stenosis and aneurism formation of the renal arteries leading to elevated renin. +  


submitted by seagull(348),

This is a likelihood ratio. LR+= Sens/1-Specif

Any value greater than 10 (per first aid) indicated "usefulness of diagnostic test" which is comparable to PPV (ruling in a dz). Point "A" is the closest mark to where 10 should be on the Y axis.

brise  The question is asking what point would be the most likely to rule in cancer, and high specificity when positive rules in cancer. The highest specificity value is A, bc the the X axis shows (1-specificity)! +4  
hello  brise is correct. Knowing the LR+ value = 10 does not help in this situation because estimating where "10" should fall on an axis is arbitrary. The way to approach this Q is to know that a high specificity is will mean that a positive result is very very likely to be a true positive. In theory, suppose that the specificity was 0.99. This is 99% specificity. Then, you look at the graph. The X-axis is "1-specificity." So, suppose the best test has a specificity of 99%. Then, calculating 1-specificity = 1 - 0.99 = 0.1. You would then chose the datapoint that corresponds to having an "X-value" that is closest to the origin. In this problem, it corresponds to data point "A." +2  


submitted by mattnatomy(20),

Crackles either indicates chronic bronchitis or consolidation (from pneumonia or pulmonary edema).

Given that there's only a 1 day history of SOB, I'm leaning more towards lobar pneumonia. Maybe that's also what's causing the S3 at the LLSB? If it's Staph Aureus, I guess we could be looking at acute endocarditis + pneumonia? Or Q Fever? But that's just speculation. Could also just be that the lung consolidation is altering blood flow, leading to the back up into the Right Atrium & Ventricle.

brise  Patient has CHF from the S3 heart sound and has MR. You hear fine crackles in early congestive heart failure. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4518345/ +9  
usmleuser007  No Infection - normal temps ; Q-fever presents with A patient with exposure to waste from farm animals who develops: a. nonspecific illness (myalgias, fatigue, fever [>10 days], b. retroorbital headache) c. normal leukocyte count d. Thrombocytopenia e. increased liver enzymes +  


Why is this not increased binding of DNA polymerase?

This mutation should cause cellular division ie DNA replication and cause increased binding to origin replication sequences ie TATA by DNA polymerase.

brise  It's talking about mutations on the transcription of genes that inhibit the cell division. Also RNA polymerase binds to the promoter region. +  
nwinkelmann  Also, the question specifically (though in a very wordy, convoluted way) asked what the effect of the mutation on transcription was. DNA pol is not used in transcription, it is used in replication. RNA pol is used in transcription. In terms of increased or decreased binding, argining is polar/positively charged and proline is neutral/nonpolar, so there are fewer H-bonding sites, and thus decreased binding of the RNA pol. +1  
medn00b  Could this convoluted question also mean.......... that since the gene to make p53 is messed up due to the hydrogen bonds, RNA polymerase will not be able to bind to make the mRNA ... So there will be cancer? Because P53 is a tumor suppressor... lemme know thanks guys +