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Contributor score: 56
Comments ...
pfebo
This is a case of postrenal azotemia. BPH is the only available option tbat causes it
+1
suckitnbme
Question stem also implies that the patient has been driving already. "has not had any collisions while driving his personal motor vehicle".
+19
cbreland
Also 10 years is a really long time. Just didn't seem like a good answer
+1
vetafig692
In the U.S., people with epilepsy can drive if their seizures are controlled with medication or other treatment and they meet the licensing requirements in their state. How long they have to be free of seizures varies in different states, but it is most likely to be between three months and a year.
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extraordinr
correction: GAS erythrogenic toxin causes scarlet fever specifically in this question
there is no reason for this child to have TSS
+6
loaloagubba
SpeA and SpeC toxin is erythrogenic toxin referred to here.
+4
baja_blast
Erythrogenic exotoxin A + Strep Pyogenes is responsible for BOTH Scarlet Fever and Toxic Shock Like Syndrome. It can also cause Necrotizing Fasciitis. It's definitely Scarlet Fever in this question but I just don't want people to get confused. FA2019 pages 133, 136
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baja_blast
Sorry, not A. Just Erythrogenic Exotoxin +.
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cbreland
Lipase (active) and procolipase (inactive) are both secreted by the pancreas. Lipase is inactivated by bile salts in the intestines. Colipase (once activated by trypsin) is able prevent the interaction of bile salts and lipase. End result being that lipase is doesn't have to worry about bile salts if colipase is around
+4
s039p811
To add onto this, I had picked Phospholipase A2, but that's used for phospholipid hydrolysis and not triglyceride hydrolysis specifically.
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nala_ula
I spent so long on this question and same... hahaha
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j44n
also FSH upregs aromatase so you increase test (LH) and increase aromatase (FSH) that then converts that test to estradiol
+1
charcot_bouchard
Update on my prev comment : Yes this is psittacosis. not hypersensitivity pneumonitis. How do u know? Lymphocyte and Presence of Granuloma - response to intracellular chlamydia.
Now HS can also cause loose granuloma too and the clinical picture still more look like HS
You know what ......... fuck this ques
+2
shemle
Here Pt. doesn't have fever!
+9
shakakaka
Noncaseating granuloma, patchy lymphocytic infiltration, and fibrosis are seen in Hypersensitivity pneumonitis , according to Uworld .
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hpsbwz
Why is it regurg instead of stenosis?
+3
minhphuongpnt07
Vague question requires a lot clinical reasoning.
mitral regurgitation: holosystolic murmur( this cv: midsystolic), enlarged LA, LV
Mitral stenosis: diastolic murmur, enlarged LA, normal LV.
only best explanation I can think of: early stage Mitral regur, that's why the murmur is not holosystolic but midsystolic and LV still adequately handle the situation
+4
dickass
@hpsbwz it's regurgitation because the murmur is SYSTOLIC, when the mitral valve is not supposed to make any sound. mitral valve leaks in systole, which causes blood to back up, which causes the left atrium to work harder and eventually hypertrophy.
Mitral stenosis would be a DIASTOLIC sound, which is when the left atrium normally contracts.
+9
themangobandit
I'm still confused as to why mitral regurg has an enlarged left atrium. Are we supposed to think that it was mitral stenosis for a time, the high LA pressure led to hypertrophy, and then became mitral regurg? That's how it works in rheumatic fever, right?
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shapeshifter51
I agree that mitral regurgitation is a holosystolic murmur heard best heard over the apex. However, with the murmur being found in the mitral valve area of auscultation it was the only answer choice that could result in LA enlargement and normal LV. Ruled out mitral valve stenosis since it is a diastolic murmur.
+1
weenathon
@themangobandit I believe mitral regurg could cause an enlarged left atrium from the increased amount of blood flooding back into the left atrium with each systole causing increased pressure on the wall.
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rockodude
why is LV size normal? doesnt cause MR cause increased preload and overload over time leading to enlarged LV?
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Subcomments ...
breis
How is this differentiated from Strep Virdans which is Optochin Resistant? Because Strep Pneumo would also be inhibited by optochin*
+2
mjmejora
its strep viridans. Strep viridans has a "protected chin mask" and strep pneumo is "exposed" in the sketchy.
+8
rthavranek
Once again, another example of me knowing the concept but not knowing the obscure pseudonyms for common knowledge so I get the question wrong
+1
dtransistor
I saw green and immediately thought of pseudomonas and crossed that answer out. Didn't know they were talking about alpha hemolysis!
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breis
Yea i get that, but if the patients CD4 was ~35, how in the world did the CD4 count rise enough to stimulate B cell proliferation...? I don't get it
+10
namira
The only thing i can think of is that:
the cd4 count that is given was taken prior to having started the antiretroviral therapy.
Since the question asks about "improved function", maybe its referring to the therapy actually being effective and its managed to increase cd4 count and function so as to be able to contribute to lymph node enlargement due to myco. avium
+13
kamilia20
I though it transfer to a lymphoma,OMG
+1
bgreen27
This answer explanation implies that dysfunction means scarcity, right? But are the CD4 cells actually dysfunctional in HIV? or just scarce? I don't like this question because clearly both CD4 and B cells are involved in lymph node enlargement AND if improved function = increased number, then both B cells and CD4 cells would meet that criteria.
+1
drdoom
@bgreen27 “depletion” is the more precise term here (although I would not be surprised if CD4s of HIV+ individuals were also somehow dysfunctional).
+1
drdoom
@bgreen27 also, remember that a single CD4 can drive the proliferation of ~many~ B cells. So, yes, lymph node enlargement is driven by CD4s, but virtually all of the mass is attributable to B cell expansion. (That is, if you snipped out an activated lymph node and then weighed all the T cells and than weighed all the B cells, you’d find the lymph node is mostly “B cell weight”.)
+3
bgreen27
so I think I understand, depletion~dysfunction and repletion~"increase in function" but proliferation is neither here nor there because it's really just Bcell "function"
+1
hello
This is great, thank you.
+5
breis
Pathoma ch. 3 pg 23 "Basic Principles"
+9
charcot_bouchard
Shoutout to Imam Satter! Without him this question wasnt possible for me to answer in 10 sec.
+19
fatboyslim
Clonality can also be determined by androgen receptor isoforms, which is also present on the X chromosome (Pathoma Ch. 3 Neoplasia)
+2
lovebug
@fatboyslim thanks for reminding!
+2
makingstrides
Just to make sure I got this right, because this is neoplastic and its monoclonal, you want to look at the isozymes to determine its clonality?
+2
yotsubato
Its not in FA, Sketchy, or Pathoma, or U world.
I knew it wasnt cancer because its bilateral. And Diabetes made no sense to me. So I just threw down Drug effect and walked away.
+10
feliperamirez
The only possible explanation I think is that she was under a K sparing diuretic, such as spironolactone (which would lead to gynecomastia).
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j44n
i thought HTN induced empty sella would cause this because they got type II diabeetus. So if you need a pro zebra hunter holler at me.
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estefanyargueta
Lipoprotein lipase: degradation of TGs circulating in chylomicrons and VLDLs.
+2
lulumomovicky
Hyperchylomicronemia can be due to LPL or Apolipoprotein C-II deficiencies --> leading to high levels of QM, TG, and Cholesterol
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breis
Why would B be incorrect? I realize Broca is "technically lower" but A seems too low to be causing weakness of the lower 2/3 of the face? Am I missing something?
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cienfuegos
@breis, per UW: "a/w r. hemiparesis (face & UE) bc close to primary motor cortex"
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almondbreeze
B is also close to frontal eye field; eyes look toward the lesion
FA pg. 499
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frijoles
I incorrectly picked C. When answering this, Broca's "broken speech" was my first thought, but I figured a lesion causing a facial droop would have to involve the motor strip so I prioritized that and chalked up the speech issue to dysarthria (I understand this is more of a "slurred speech" than broken, abrupt speech, but again, I simply misprioritized concepts.). So for the record, Broca area is part of the motor cortex?
+1
hello
Yep, seems that because the patient has prediabetes, he should avoid eating excessive starchy foods.
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breis
I put nuts thinking of "fats" and that with a bariatric surgery they may have problems with absorption..
+6
teetime
This isn't right because the bariatric surgery will cure the prediabetes. It's dumping.
+2
dr_jan_itor
Why should he avoid eating excessive starchy foods? To avoid gaining weight? It doesn't matter what macronutrients he eats if they are calorie controlled.
+2
dhkahat
yeah but he's prediabetic. you want someone like that to shove a bunch of starch down all the time?
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ergogenic22
Also corticalspinal tract symptoms are not seen, but dorsal column and spinocerebellar tracts are seen
+5
sinforslide
In this case, patient's CF also predisposes fat-soluble vitamin deficiency.
+9
usmleuser007
Correction: Read more on this
Vitamin-E deficiency can in fact cause anemia - hemolytic anemia.
This is b/c VitE work as an anti-oxidant; and therefore with reduced anti-oxidation RBCs are more prone to oxidative injuries.
+4
azharhu786
AMBOSS: Hemolytic anemia; increased fragility of erythrocytes and membrane breakdown are also caused by vitamin E.
+1
kcyanide101
Just to add..... Vitamin E in excess can also be toxic as it inhibits Vitamin K, which increases risk if bleeding etc
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ergogenic22
It is dissection "extra lumen in the media of the proximal aorta" = "a longitudinal intimal (tunica intima) tear with dissection of blood through the media of the aortic wall" ... answer is still hypertension
+2
pg32
First Aid says that aortic dissection causes widening of the mediastinum and is due to an intimal tear, so I thought it wasn't an aortic dissection. Can anyone help me understand why First Aid was wrong in this case? Thanks!
+3
nephroguy
@pg32 The question stems states that there is no widening of the Aorta, not the mediastinum. Widening of the mediastinum is seen in dissection while widening of the aorta is seen in aneurysm. Also the intimal tear creates a false lumen between the intima and media. Hope that helps!
+16
johnthurtjr
I think it may actually be a keloid, not a hypertrophic scar, as it expands beyond the borders of the original incision.
+6
thepacksurvives
I believe this is a keloid; a hypertrophic scar does not extend past the borders of it's original incision, while a keloid does. regardless, the answer to this question is the same :)
+1
breis
First AID pg 219
Scar formation: Hypertrophic vs. Keloid
+1
charcot_bouchard
They give granulation tissue is a option which is type 3 collagen. so if it was hypertrophic scar it would be ap problem since its only excessive growth of Type 3. while keloid is excessive growth of both 1 and 3
+6
bharatpillai
I literally ruled put collagen synthesis defect since this is not a collagen synthesis defect at all ( EDS, Scurvy) :/
hate these kind of questions
+1
kcyanide101
Base off pathoma, this is hypertrophic scaring, as it extends beyond its borders. It will be type 1 collagen. Keloid will be much more excessive and it is a type 3 collagen
+
I put CHF, still not sure why it is wrong over BPH, but my reasoning is that BPH causes obstructive urine flow --> Hydronephrosis and once the urine has been made it can't be redone and is like filling up a damn with water. Straight Stasis. vs CHF there is protective mechanisms in place for a while until frank CKD.