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Yes smoking is a risk factor but not the best option among the choices given. Check FA, it says that it occurs more in tall thin young males. Smoking isn’t even mentioned. Tall & thin males are more at risk because they have more negative intrapleural pressure. Check Uworld for this.
You have to think about this using the concept of CONDITIONAL PROBABILITY. Another way to ask this type of question is like this: “I show you a patient with spontaneous pneumothorax. Which other thing is most likely to be true about this patient?” Said a different way: Given a CONDITION [spontaneous pneumo], what other finding is most likely to be the case? Still other words: Given a pool of people with spontaneous pneumothorax, what other thing is most likely to be true about them?
In other words, of all people who end up with spontaneous pneumo, the most common other thing about them is that they are MALE & THIN. If I gave you a bucket of spontaneous pneumo patients -- and you reached your hand in there and pulled one out -- what scenario would be more common: In your hand you have a smoker or in your hand you have a thin male? The latter.
Rupture of pulmonary blebs are a common cause of spontaneous pneumothorax in young adult males that are tall and thin. I know it's also associated with smoking, but gender and body habitus seemed like the more likely answer here since the patient is a young male.
Totally agree, arterial dilation--> increases blood flow into capillaries/increases capillary hydrostatic pressure + increasing permeability of the post-capillary venules= Increased Capillary Filtration Rate
I love you explanation, but I don't think filtration rate is dependent upon permeability of the post-capillary venules. I think the filtration rate is increased simply due to the increased blood flow; this is similar to how increased renal blood flow will increase Glomerular Filtration Rate (GFR).
I get Parvo has tropism for RBC precursors, but wouldn’t it take 120 days to manifest?
RBCs don’t just spill out of the bone marrow every 4 months on the dot. Erythropoesis is a constant process. If you get a parvo virus on “Day 1” then the RBCs that were synthesized 120 days before “Day 1” will need to be replaced. They can’t be because of parvovirus. This leads to symptomatic anemia within 5 days because the RBCs that were synthesized 125-120 days before the infection are not being replaced.
@gainsgutsglory @keycompany It seems unlikely that “1 week” of illness can explain such a large drop in Hb. It seems more likely that parvo begins to destroy erythroid precursors LONG BEFORE it manifests clinically as “red cheeks, rash, fever,” etc. Might be overkill to do the math, but back-of-the-envelope: 7 days of 120 day lifespan -> represents ~6 percent of RBC mass. Seems unlikely that failure to replenish 6 percent of total RBC mass would result in the Hb drop observed.
He can drop from 11 to 10 hgb easily
Apologies if this is completely left-field, but I didn't think this was Parvovirus. Parvo would affect face. Notably, patient has fever and THEN rash, which is more indicative of Roseola. Thoughts??
@is2076 check my comment to @hello I thought the same thing for a sec too :)
also i think you guys are thinking of hb in adults in this q it says hb is 10g/dL(N=11-15) so it's not relatively insanely low
@Is3076 I completely agree with @hyperfukus and I think that thinking of Roseola isn't crazy, but remember that usually with Roseola you get from 3-5 days of high fever, THEN fever is completely gone accompanied by a rash. This question says that the patient has a history of 4 days of rash and 7 days of fever, but never mentioned that the fever subsided before the appearance of the rash. And Roseola is not supposed to present with anemia.
@Is3076 another point is that malar rash refers to the butterfly rash on the cheeks that is commonly seen in lupus, so the face is NOT spared.
How do we know the parents are not homozygous
Chances are they are not unless they had or are incestuous
So I chose that one because set point is controlled by the hypothalamus (PGE2 and IL-1 mediate fever in the hypothalamus) and the rest of the answer choices involved something below the level that has been transected. Not 100% sure if that’s accurate though.
Agreed with @its_raining_jimbos -- Fever is mediated by altering set point in hypothalamus. All the other choices, as far as I can tell, involve sympathetic nerves and their effects at target organs.
Not 100% sure on this one, but here’s how I approached it: histamine causes arterial dilation (decreased arteriolar resistance), but all of that blood has to go somewhere since you now have more blood flowing through the arteries and that somewhere is the capillaries (increased capillary hydrostatic pressure). Histamine causes increased permeability of the post-capillary venules (one of Dr. Sattar’s favorite facts) so you’d have increased capillary filtration rate.