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Welcome to breis’s page.
Contributor score: 56


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 +0  visit this page (nbme18#18)
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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.

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pfebo  This is a case of postrenal azotemia. BPH is the only available option tbat causes it +1

 +2  visit this page (nbme18#26)
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I am not 100% on this being correct, but I briefly remember a Psychiatrist saying that the patient has to be seizure free for 6 months minimum and preferred to have no seizure within the last 3 years to be asymptomatic. Do with that information what you will. but for Boards: 3 years.

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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. +

 -1  visit this page (nbme18#14)
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Streptococcus Pyogens (group A strep) has a superantigen causing shock. This antigen Erythrogenic Exotoxin A causes a Toxic shock-like syndrome: Fever, Rash, Shock, Scarlet Fever.

FA pg 133 (2019)

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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 +
baja_blast  Sorry, not A. Just Erythrogenic Exotoxin +. +

 +6  visit this page (nbme18#48)
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Colipase is a protein that functions as a cofactor for pancreatic lipase, with which it forms a stoichiometric complex. It also binds to the bile-salt covered triacylglycerol interface thus allowing the enzyme to anchor itself to the water-lipid interface.

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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. +

 +0  visit this page (nbme20#41)
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your guess is as good as mine.....................................................................

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nala_ula  I spent so long on this question and same... hahaha +

 +8  visit this page (nbme20#29)
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Doxycycline is a Tetracycline (binds 30s subunit) and is used off label for treatment of Acne. Can cause discoloration of teeth, and is known to be PHOTOSENSITIVE.

This patient had diffuse erythema and mild edema over her face and extremities, most likely from sun exposure while being on the med for Acne.

FA 2019: pg 192

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 +5  visit this page (nbme17#16)
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HCG injections down regulate the pituitary release of GnRH.

however HCG alpha subunit can stimulate cells influenced by LH, FSH, TSH.

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cassdawg  (FA2020 p633) - Basically HCG acts like FSH which stimulates estradiol production by the sertoli cells (see http://www.ansci.wisc.edu/jjp1/equine/male_endo/estrpath.html). There is no feedback inhibition since it is injected so there are elevated levels of estradiol causing gynecomastia. +15
j44n  also FSH upregs aromatase so you increase test (LH) and increase aromatase (FSH) that then converts that test to estradiol +1

 +0  visit this page (nbme20#21)
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Psittacosis (sometimes called ornithosis or parrot disease or parrot fever) is an infection of the lung (pneumonia) caused by the bacterium Chlamydophila (Chlamydia) psittaci.

Signs and symptoms: fever. cough, usually without much phlegm. headache. rash. muscle aches. chest pain. shortness of breath. sore throat.

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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 . +

 +2  visit this page (nbme20#2)
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Dx: Acute Monocytic Leukemia. Proliferation of monoblasts; lack MPO. CD14 + CD13+ MPO -. blasts characteristically infiltrate the gums.

A Xanthine Oxidase inhibitor is given to prevent adverse reactions of Tumor Lysis Syndrome which results from expulsion of cellular debris/material after the cell dies.

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srmtn  FA 2019 p 426 +

 +2  visit this page (nbme20#12)
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Patient has Midsystolic murmur heard at the cardiac apex. there is also a LEFT ATRIAL abnormality. Echo shows LEFT ATRIUM is enlarged.

Mid systolic... enlarged left atrium...

Best choice: Mitral Regurg

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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? +
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. +
rockodude  why is LV size normal? doesnt cause MR cause increased preload and overload over time leading to enlarged LV? +




Subcomments ...

submitted by famylife(110), visit this page
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This is strep pneumo, which has alpha hemolysis (green)

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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! +


submitted by sympathetikey(1600), visit this page
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CD4+ cells activate B-cells which form follicles and cause enlargement of lymph nodes. Therefore, in an AIDS patient, to enlarge the lymph nodes, the CD4+ dysfunction must be resolved.

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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


submitted by hayayah(1212), visit this page
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Neoplasia is new tissue growth that is unregulated, irreversible, and monoclonal.

Clonality can be determined by glucose-6-phosphate dehydrogenase (G6PD) enzyme isoforms. G6PD is X-linked.

*For more information check out Ch. 3 Neoplasia in Pathoma

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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


submitted by strugglebus(189), visit this page
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Nowhere have I been able to find why the hell this is a thing.

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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
breis  same^^^ +
feliperamirez  The only possible explanation I think is that she was under a K sparing diuretic, such as spironolactone (which would lead to gynecomastia). +
chandlerbas  you had me at its not in sketchy ;) +3
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. +


submitted by hayayah(1212), visit this page
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Pt. has Familial dyslipidemias. Type I—Hyperchylomicronemia.

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estefanyargueta  Lipoprotein lipase: degradation of TGs circulating in chylomicrons and VLDLs. +2
breis  FA 2019 pg 94 +4
lulumomovicky  Hyperchylomicronemia can be due to LPL or Apolipoprotein C-II deficiencies --> leading to high levels of QM, TG, and Cholesterol +


submitted by xxabi(293), visit this page
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Broca’s aphasia: expressive (motor aphasia) with agrammatism (pts aware that they don’t make sense) - area A Wernicke’s aphasia: receptive (sensory) aphasia with impaired comprehension (pts lack insight)

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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? +
shaeking  @breis B is incorrect because of the lower 2/3 of the face weakness. B isn't located on the motor cortex but in the premotor cortex, plus it isn't low enough for the lower two thirds of the face. https://thebrain.mcgill.ca/flash/a/a_06/a_06_cr/a_06_cr_mou/a_06_cr_mou.html https://www.sciencenews.org/blog/science-ticker/homunculus-reimagined +1
cienfuegos  @breis, per UW: "a/w r. hemiparesis (face & UE) bc close to primary motor cortex" +
almondbreeze  B is close to premotor cortex which is involved in learned or patterned skills & in planning movements. (i.e. two-hand coordination) slide 25/37 :https://www.slideserve.com/hal/the-motor-system-and-its-disorders +
almondbreeze  B is also close to frontal eye field; eyes look toward the lesion FA pg. 499 +
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


submitted by beeip(141), visit this page
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Thought this would be something regarding "bariatric surgery," but nope, just "no starchy foods, because you're pre-diabetic."

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hello  Yep, seems that because the patient has prediabetes, he should avoid eating excessive starchy foods. +
yotsubato  such a BS question IMO +7
yotsubato  such a BS question IMO +
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? +


submitted by usmleuser007(464), visit this page
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Vitamin E deficiency is known to cause similar spinal defects as Vitamin B12 deficiency. However, anemia is not seen.

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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
breis  FA pg 70 +
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 +


submitted by xxabi(293), visit this page
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I was under the impression that this was an aortic dissection, due to "severe chest pain" as well as the false lumen in the aorta. And HTN is the #1 risk factor for aortic dissection. Someone correct me if i'm wrong, but I think this is aortic dissection rather than aortic aneurysm.

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chefcurry  I believe so, FA 2018 pg 299 +3
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
breis  FA 2019: 301 +
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
j44n  https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.118.312436 pictures worth a 1,000 character limit +


submitted by celeste(96), visit this page
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Sounds like a hypertrophic scar. "Hypertrophic scars contain primarily type III collagen oriented parallel to the epidermal surface with abundant nodules containing myofibroblasts, large extracellular collagen filaments and plentiful acidic mucopolysaccharides." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022978/

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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 +


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