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 +2  (nbme21#11)

My thought process was that post-partum bleeding is usually related to the uterus, and much of the pelvic viscera is supplied by branches of the internal iliac artery.

neonem  This sounds like a case of acute endometritis. In any case, uterus is supplied by uterine artery (branch of internal iliac artery) with collateral flow from ovarian artery (comes right off aorta). I don't think there are any branches of external iliac artery into the pelvis; it becomes femoral artery once it passes under inguinal ligament.
tsl19  Here's a picture that I found helpful [Female Reproductive Tract arterial supply] (https://teachmeanatomy.info/wp-content/uploads/Blood-Supply-to-Female-Reproductive-Tract.jpg)
sympathetikey  @tsl - Thank you!
step1soon  uworld Qid:11908

 +9  (nbme23#46)

Skin provides insulation and prevents heat loss. This patient's body will compensate for increased rate of heat loss by increasing metabolic rate.

davidw  This is directly from Goljan I) Hypovolemic shock may occur due to loss of plasma from the burn surface (refer to Chapter 5). • Loss of protein from the plasma loss may result in generalized pitting edema. II) Infection of the wound site and sepsis may occur. (a) Sepsis due to Pseudomonas aeruginosa is the most common cause of infection in burn patients. (b) Other pathogens include methicillin-resistant S. aureus and Candida species. (3) Curling ulcers may occur in the proximal duodenum (refer to Chapter 18). (4) Hypermetabolic syndrome may occur if >40% of the body surface is burned.
yex  Can someone explain why is it not increased ECF?
charcot_bouchard  i picked same. Increased ECF but cant remember why. Can you explain WHY it is increased ECF? what was ur reasoning
isotopes  Burns would lead to a decrease in ECF because the protection from fluid loss is absent; it can lead to shock. :)
tinydoc  My reasoning behind picking ↑ ECV was that your losing fluid but not electrolytes with the burn ⇒ the ecv would have increased osmolarity, so the fluid from the ICV would be pushed the the ECV. It made sense to me at the time. I guess technically its wrong because the loss of fluids and the gain of fluids would amount to pretty much the same thing. But the insulation and heat loss thing makes sense I guess.
yex  Increased ECF, bc I was thinking about the edema formation.... :-/
atbangura  I picked increased ECF because burns increase the capillary permeability coefficient, but now that I am going over it I realized that increasing the permeability would only transfer plasma volume to the interstitial volume, which are both a part of the ECF so therefore ECF would not change. SMH
aisel1787  thanks

 +6  (nbme23#24)

The patient has ATN secondary to renal ischemia. Due to tubular necorsis, the patient will have an elevated FeNa. The patient's urine will also be dilute, but this will be reflected by the low urine osmolality, not the FeNa

mousie  Hypotension can also cause pre renal azotemia with a FENa <1%.... How do you know this is ischemic ATN and not hypotension induced Prerenal Azotemia?
sympathetikey  I had the same thought as you @mousie, but I think "azotemia" and low urine output push it more towards ATN (looking back; I got it wrong too). Plus, the initially MVC / muscle damage probably caused some tubule injury by itself.
ajo  This might help clarify why the pt. has ATN rather than pre renal azotemia. The question did mention, though subtly, that the bleeding was controlled. That most likely indicates that his hypovolemia has been corrected. Developing azotemia 24 hrs after correction of hypovolemia is more suggestive of ATN (since he doesn't have hypovolemia anymore). I hope that helps and feel free to correct me, if I am wrong.
ajo  In addition to my earlier comment, I just noticed the question also explicitly mentioned that he was fully volume restored. Which is consistent with my earlier assumption!
gh889  Although initially, hypotension causes prerenal azotemia, the volume correction pushes you away from prerenal azotemia. but they want you to remember that in hypovolemia, the kidneys are also becoming ischemic, and so development of azotemia 24 hours later is more indicative of intrarenal azotemia due to ATN
sugaplum  for anyone who wants to see it: FA 2019 pg591
divya  i'm confused about one thing. if the tubules aren't working like they should, the bun:cr ratio falls right? doesn't that essentially mean azotemia reduces too?
osler_weber_rendu  Lets all take a moment to admire how shit this question is "Bp 90/60.""Repeated episodes of hypotension in the OR" and still the answer is ATN
donttrustmyanswers  @osler_wever_rendu ATN can be caused by ischemia.

 +16  (nbme23#4)

Malaria can impair hepatic gluconeogenesis and can also consume glucose for its own metabolic demands.

yotsubato  Truly a bull shit question... Its not in FA, Sketchy or Pathoma
meningitis  I will try to remember this by associating it with P. vivax, that stay in the liver (liver=gluconeogenesis). Thank you @thomasalterman.

 +3  (nbme23#30)

Complement is important for removing immune complexes, so patients with complement deficiencies *(c1-c4) are more likely to develop SLE. C1q is a better answer than than MBL (D) b/c the MBL pathway is triggered by bacteria.

myoclonictonicbionic  Thats the reason I put MBL, because the question mentioned that it got worse when she went to the beach so I was thinking some sort of contact with bacteria may have exacerbated her immune system.
thotcandy  @myoclonictonicbionic i think that's just the typical SLE photosensitive malar/butterfly rash

 +8  (nbme23#16)

Methylase methylates DNA, making the DNA resistant to restriction endonucleases


 +14  (nbme23#21)

She just completed the course of rituximab, which targets CD20 receptors. B-cell deficiency can predispose to bacterial infections.

b) BM failure is not associated with rituximab c) wrong d) wrong e) this occurs w/in 7-10 days of starting treatment, and would not occur after completing a 4-month course of rituximab.

meningitis  Forgot the time frame for Serum sickness and got it wrong.. thanks @thomasalterman
stinkysulfaeggs  Same. Crap.

 +4  (nbme23#23)

Trihexphenidyl and Benztropine are antimuscarinics that can treat the resting tremor and rigidity of parkinsonism.

mousie  haloperidol induced Parkinson's... ? adding a anticholinergic can counter these adverse effects of the antipsychotic .. ?
fulminant_life  @mousie yeah it balances the dopamine-cholinergic imbalance caused by the antipsychotics
kai  +So antipsychotics induce Extrapyramidal side effects which is drug induced Parkinson = low Dopamine High Ach, and you would treat this with anticholinergic (Benztropine).This is neurologic. +Antipsychotics also produce non-neurologic, systemic anti-cholinergic effects like dry mouth, sedation, hypotension etc

 +9  (nbme23#17)

The most important hints to the question are as follows, with #2 being the most specific:

1) patient reports pain with overhead motion and reports recurrent overhead motion during work. Overhead motion can damage the supraspinatus muscle due to impingement by the acromion.

2) Pain is worst with internal rotation of the shoulder - this is consistent with the findings of the empty-can test, which indicates a supraspinatus injury.

mousie  I was thinking along the lines of overhead motion - damage to the subacromial bursa which is between the acromion and the supraspinatus ... also its the most commonly injured rotator cuff m. so could have guessed this one right
sympathetikey  Thanks for the explanation. I was scratching my head as to why this is correct, since supraspinatus only does 15 degrees of abduction, but you make a lot of sense.
charcot_bouchard  IDK WTF i picked Trapezius
ls3076  why would injury to supraspinatus cause weakness with internal rotation though?
targetusmle  yeah coz of that i picked subscapularis
maddy1994  ya the whole question pointed to supraspinatus ...but last line internal rotation made me pick subscapularis
darthskywalker306  I went for Trapezius. That shoulder flexion thing was a big distraction. Silly me.

 +13  (nbme23#29)

Patient is current breast-fed, so we can eliminate fructose (fructose is found in honey and fruits and some formula, but not in breast milk). Patient has reducing substances but no glucose in the urine, so he must some non-glucose sugar. My differential for reducing non-glucose sugars in the urine is disorders fructose metabolism or galactose metabolism. We have eliminated fructose, so that leaves us with galactokinase deficiency or classic galactosemia.

sympathetikey  & Galactokinase deficiency would be much milder.
smc213  Big was soybean formula not giving any issues. Soy-milk can be used as a substitute formula in patients with Classic Galactosemia since it contains sucrose (->fructose and glucose).
oslerweberenu  Why can't this be glucose 6 phosphatase deficiency Confused me
almondbreeze  @oslerweberenu G6PD - increased RBC susceptibility to oxidant stress (eg, sulfa drugs, antimalarials, infections, fava beans) -> hemolysis; has nothing to do with presence of reducing sugar
makinallkindzofgainz  @almondbreeze; Glucose-6-phosphatase deficiency is Von Gierke disease, they are not referring to G6PD deficiency (an entirely seperate disease)

 +2  (nbme23#44)

Patient has a fracture to the inferior orbit. This can dmg V2 or entrap the IR muscle. Only IR entrapment would impair vision.

nlkrueger  if this isn't a globe rupture than idk what is tbh
mousie  the air in the center of the globe made me think rupture too .....
sajaqua1  There may be some global rupture, but impairment of one of the ocular muscles causing diplopia would still be the best explanation for this patient's double vision.
catch-22  Globe rupture leads to entrapment of the IR muscle which causes diplopia. The question is asking what is causing his visual complaints, which is diplopia, not loss of vision.

 +11  (nbme23#32)

Patient has a ganglion cyst, which can spontaneously regress.

medschul  Mine would beg to differ >:O
usmleuser007  Where would I have come across something like this (FA, Pathoma, or out of my S)?
motherfucker2  I thought this bitch was a lipoma. Mother fucker
divya  mf2 lipomas is fat. although fat may exist in liquid form, its still opaque, therefore negative transillumination. unlike ganglion cyst.
beanie368  Only knew this because I have one that comes and goes...

 +7  (nbme23#31)

A normoblast is an immature RBC, so it's elevated in states of increased hematopoiesis.

sympathetikey  Don't mind me. Just sippin my dumb ass soda over here.
someduck3  The term "Normoblast" isn't even in first aid.
link981  NBME testing your knowledge of synonyms. Have to know 15 descriptive words of the same thing I guess.
tinydoc  I wish they would stop making it so every other question I know the answer and I can't find it among the answer choices because they decided to use some medical thesaurus on us.
qball  Metamyelocytes = Precursor to neutrophils Siderophages = hemosiderin-containing macrophage aka heart failure cells
llamastep1  Theres a UWorld question about Parvovirus B19 that mentions "giant pronormoblasts" that helped me make the connection

 -4  (nbme23#27)

Mast cell degranulation can be triggered by foreign antigens and trauma

thepromise  I believe what you're speaking about occurs more during hypersensitivity reaction. In this case, there is damage to the endothelial cells, which they also release histamine for vasodilation. which creates permeability for the neutrophills and erythema from the increased blood volume.

 +5  (nbme23#18)

Envelopes benefit the virus in that the virus will look like the host, facilitating fusion. However, an enveloped virus is generally less stable than a naked icosahedral virus (naked viruses are generally icosahedral).

docred123  So do these patients have h.Flu? What was the giveaway? Thanks
mousie  I chose Enveloped simply bc it said dies when heated, not sure if there where any other clues to narrow this down or make me feel more confident in my choice but I went with it anyway
eclipse  I don't think they expected us to narrow down the answer to a specific virus. Enveloped viruses tend to be less stable (?) than the non-enveloped ones and don't survive as well under harsher environments (outside human's body, heat, etc.)

 +6  (nbme23#49)

Androgens cause acne. Testosterone is a better answer than Androstanediol b/c the Testosterone is associated with puberty, Androstanediol is more associated with the adrenal glands.

meningitis  I chose Testosterone but I almost chose GnRH because it is surged when starting puberty and therefore increases everything downstream.
temmy  When answering the question, i thought to myself that if GnRH is correct, LH will be too cos GnRH stimulates the Leydig cells via LH to release testosterone. That left testosterone as the best answer because it had the most direct effect.
goaiable  GnRH and LH are increased in a pulsatile fashion at the onset of puberty, so idk if that constitutes as the "rapid increase" that this question is asking for. Tripped me up also.
tallerthanmymom  I originally eliminated testosterone and chose androstanediol because women can have Acne Vulgaris too, and Testosterone should not be rising to the same degree. Do I not understand how puberty works?
drzed  Women can still make testosterone though; and androstAnediOL is not the same as androstEnediONE

 -12  (nbme23#39)

Niacin can cause hyperglycemia, flushing, and gout. NSAID's can treat gout. Aspirin at high concentrations also inhibits renal reabsorption, but it inhibits secretion at low levels. I went with aspirin over acetaminophen b/c although acetaminophen is an analgesic it lacks anti-inflammatory activity.

redvelvet  this is not that question :)

 +2  (nbme23#40)

According to FA, the splenorenal ligament contains the tail of the pancreas and the splenic artery & vein

littletreetrunk  The pancreas is supplied by the pancreatic branches of the splenic artery. The head is additionally supplied by the superior and inferior pancreaticoduodenal arteries which are branches of the gastroduodenal (from coeliac trunk) and superior mesenteric arteries, respectively.
andersen  FA 2019 page 355 / /

 +14  (nbme23#24)

Patient has polycythemia vera, as evidenced by erythrocytosis, granulocytosis, and headaches & diziness. EPO is decreased due to erythrocytosis. Decreased LAP would indicate CML, not PV.

btl_nyc  I thought this was CML. What am I missing that would say CML over PV?
btl_nyc  Nvm, RBCs go down in CML, but everything goes up in PV.
arcanumm  Tricked me. I knew right away that it was PV, but I thought PV would crowd out normal cell creation (e.g. decrease platelets). So apparently crowding out normal cells is just a quality of AML/CML?
drzed  More AML. Remember Sattar always stresses that all the myeloproliferative disorders are expansions of ALL lineages, ESPECIALLY "xx" (depends on which one, for CML it'll be granulocytes, for PV it'll be RBCs etc). They're called MYELOproliferative because all the myeloid linages go up, but one will be increased more than the rest. In this case, it is the RBCs.

Subcomments ...

submitted by haliburton(139),

my notes from UWORLD: andes aegypti mosquito = dengue south, southeast asia, pacific islands, carribean, americas HA, retro=orbital pain, joint pain, muscle ache. petechiae, purpura, epistaxis, melena, throbocytopenia leukpoenia, hemoconcentration

thomasalterman  Dengue is an arbovirus. The important hints are that she was traveling in endemic (tropical) and that she has **excruciating pain in the joints and muscles**. This is why dengue is aka "break-bone fever" +  
sam  Same vector +  
sam  Same vector +