NBME Answers : raffff's page

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Oral vesicle (hint hint). Blistering vesicular lesion on the hand. No fever, not toxic-appearing. This is Herpes (you may remember dentists getting herpetic whitlow in your studies, which is what this is). Most folks get HSV1 as children, though obviously not all are symptomatic. HSV is a large double-stranded, linear DNA virus.

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jiya why cant this be hand foot and mouth disease cause of coxsache +16

drachenx Also thought it was Hand-foot-mouth an RNA virus but I did consider Herpes. Changed because I thought Hand foot and mouth would be more common. +1

llamastep1 Hand foot mouth usualy involves all 3 places (hands, feet and mouth/perioral area) and the lesions on the hand arent localized to just one finger. +5

aneurysmclip Hand foot mouth disease affects palms and soles. ref: FA 2019 - 150 +6

raffff wouldnt the history also be different for coxsakie +1

focus I think this image is trying to show the "dew drops on a rose petal" sign on Hermes, the god of Herpes on Sketchy Micro +2

drpee Google some images of HF&M disease. The small blisters look very different from herpetic whitlow. +2

drdoom ^ https://www.google.com/search?q=hand+foot+and+mouth+disease&tbm=isch +2

drdoom ^ ... some images of HF&M disease ... +2

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Can someone please explain why it would not be glycogen depletion? I thought the question was talking about the Warburg phenomenon... so why not breakdown of glycogen to glucose?

I guess it would not explain the edema?

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hello Glygocen stores are depleted within 24h. This person has signs and symptoms of longterm nutritional deficiences. +2

raffff it would not explain the edema, yes +

drzed Also the warburg phenomenon has to do with cancers preferentially taking up glucose; there is no indication that he has cancer. +

haydenelise The first sentence says that he has lung cancer. +2

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I think alot of people might have over emphasized how important ANP and BNP really are, yes it is important to know these peptides get secreted by the atrial/ventricular myocardium during heart failure. However their overall effectiveness in treating heart failure is zilch, a preceptor told me that if ANP and BNP were so useful in natriuresis then why do we give diuretics? It's because RAAS overpowers this system hence causing negative effects and the endless loop of heart failure. AKA why we give ACE inhibitors.

Knowing that ANP gets neutralized by the RAAS system, we can shift our focus back to heart failure in this patient, where cardiac output is decreased, leading to ADH secretion and finally dilutional hyponatremia.

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almondbreeze a concept continuously emphasized by uw, but I get always wrong :'( +4

almondbreeze good work done! +1

raffff why does the body make anp at all since its so useless +4

makinallkindzofgainz @raffff - at least BNP gives us a good marker for heart failure exacerbations :) thanks body! +1

mannan Yeah it's important clinically because it has a high sensitivity (if negative, rule out) for Heart failure. +1

alimd At the same time ANP inhibits renin release? +1

freemanpeng If it is High RAAS, Aldo must be High as well(AngII induce Aldo more than ADH). Then that would be SALT-WATER retention rather than PURE WATER retention. NO hyponatremia +

plaguedbyspleen This patient is third-spacing and therefore has low effective circulating volume. I like to think that given his CV history, he is probably on an ACE inhibitor or something similar. So that leaves ADH to do its thing. Also high aldosterone saving salt isn't something we need to consider given the stem and answer choices. +