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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.
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)
This is directly from Goljan
I) Hypovolemic shock may occur due to loss of plasma from the burn surface (refer to
• 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.
Can someone explain why is it not increased ECF?
i picked same. Increased ECF but cant remember why. Can you explain WHY it is increased ECF? what was ur reasoning
Burns would lead to a decrease in ECF because the protection from fluid loss is absent; it can lead to shock. :)
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.
Increased ECF, bc I was thinking about the edema formation.... :-/
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
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?
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.
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.
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!
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
for anyone who wants to see it: FA 2019 pg591
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?
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
Truly a bull shit question... Its not in FA, Sketchy or Pathoma
I will try to remember this by associating it with P. vivax, that stay in the liver (liver=gluconeogenesis). Thank you @thomasalterman.
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.
@myoclonictonicbionic i think that's just the typical SLE photosensitive malar/butterfly rash
Forgot the time frame for Serum sickness and got it wrong.. thanks @thomasalterman
haloperidol induced Parkinson's... ? adding a anticholinergic can counter these adverse effects of the antipsychotic .. ?
@mousie yeah it balances the dopamine-cholinergic imbalance caused by the antipsychotics
+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
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
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.
why would injury to supraspinatus cause weakness with internal rotation though?
ya the whole question pointed to supraspinatus ...but last line internal rotation made me pick subscapularis
I went for Trapezius. That shoulder flexion thing was a big distraction. Silly me.
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).
Why can't this be glucose 6 phosphatase deficiency
@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
@almondbreeze; Glucose-6-phosphatase deficiency is Von Gierke disease, they are not referring to G6PD deficiency (an entirely seperate disease)
if this isn't a globe rupture than idk what is tbh
the air in the center of the globe made me think rupture too .....
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.
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.
Where would I have come across something like this (FA, Pathoma, or out of my S)?
mf2 lipomas is fat. although fat may exist in liquid form, its still opaque, therefore negative transillumination. unlike ganglion cyst.
Only knew this because I have one that comes and goes...
Don't mind me. Just sippin my dumb ass soda over here.
The term "Normoblast" isn't even in first aid.
NBME testing your knowledge of synonyms. Have to know 15 descriptive words of the same thing I guess.
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.
Metamyelocytes = Precursor to neutrophils
Siderophages = hemosiderin-containing macrophage aka heart failure cells
Theres a UWorld question about Parvovirus B19 that mentions "giant pronormoblasts" that helped me make the connection
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.
So do these patients have h.Flu? What was the giveaway?
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
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.)
I chose Testosterone but I almost chose GnRH because it is surged when starting puberty and therefore increases everything downstream.
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.
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.
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?
Women can still make testosterone though; and androstAnediOL is not the same as androstEnediONE
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.
I thought this was CML. What am I missing that would say CML over PV?
Nvm, RBCs go down in CML, but everything goes up in PV.
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?
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.
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"