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I think this one was pretty easy if you just know the regional anatomy. That was the only answer choice that could remotely have that presentation, so I think it was just testing your knowledge of the structures listed relative to the description.
I also didn't realize the surgeon's hands would so deep in he could touch the IVC on a Lappy....kinda eliminates the point of a Lappy....
"A laparotomy is a surgical procedure involving a large incision through the abdominal wall to gain access into the abdominal cavity." Exploratory laparOTOMY very different than LaparoSCOPY, which is what I think you may be confused about. One is a gaping hole from which you can observe everything, and the other uses tiny incisions and scopes. Even still, a hand port used during laparoscopy can allow for digital manipulation of organs as needed.
I dont think the physician caused the avulsion, I think it was there already and he grazed the area. Causing it to fully avulse and break what ever clotting was going on.
I think they were getting at how developing T1DM and schizophrenia are both multifactorial. I don’t remember what the other choices were off the top of my head, but they had clear inheritance patterns.
Just as a slight tangent, is there a difference between "multifactorial" and "polygenic" inheritance?
polygenic = multiple genes affect phenotype while multifactorial = genes, environmental factors, etc that can affect phenotype
Multifactorial: cleft lip, cleft palate, type 1 diabetes mellitus, sjogren syndrome, pyloric stenosis, congenital heart disease, neural tube defects
why not midsternal thoracotomy?
Agreed -- went with E. Coli like a dingus, just because I didn't associate DIC with S. Pneumo. Thought it was too easy.
Isn't E. Coli also an encapsulated organism? What makes Strep pneumo more likely in this question just because its the more common cause?
Pseudomonas aeruginosa is encapsulated as well. I think the right answer has to do with DIC but why?
The only reason i found was S. pneumo is more common, I went with Pseudomonas because of the "overwhelming sepsis" :(
Everyone is correct about the Encapsulated microbes, but this is one of those of "MOST LIKELY",
and by far the most likely is S.Pneumo>>H.infl>N.Mening. (omitting that patients with history of splenectomy must be vaccinated.
Gram negative are more common in DIC my friends
Correct me if I am wrong, but I am pretty sure that E. coli is NOT a common cause of pneumonia because it must be aspirated to enter the lung. Thus, only patients with aspiration risk (e.g. stroke, neurogenic conditions) would be at a chance of getting E. coli pneumonia.
Meckel diverticulum also occurs distal to the CBD but less likely to be associated with bilious vomiting
Correct. Might cause pain due to ectopic gastic tissue.
Yeah, I was thinking about that while taking the exam. Just got thrown off because I don't see how that matters, now that they've fractured the femur. How do prior increases in bone density allow for better chances of bone healing?
I think that bone density is important here, but think about all of the other things that go in to recovering from a fracture at that age too. How strong are the muscle that will stabilize you while going through the motions of physical therapy? How conditioned are you?
Usually on the left because the liver prevents herniation through the right hemidiaphragm
aka congenital diaphragmatic hernia
What's weird to me is that if you usually see air in the intestines on x-ray when they are in the abdomen, why is there no air in the thorax in CDH? The intestines should still have air in them, right? Also, what is filling the abdomen that causes it to appear grayed-out in CDH?
@pg32 You can actually see a gastric bubble if you squint hard enough. Look at where the NG tube is placed; there is a radiolucency to the patient's right of the NG tube which is most likely the stomach. It probably then is radioopaque distally due to the pyloric sphincter, and air having a tendency to rise.
Any idea what "absence of bowel gas in the abdomen" is referring to?
my interpretation was absence of bowel gas in abdomen --> the bowel is not in the abdomen --> incomplete formation of pleuroperitoneal membrane
bowel gas is a normal finding that you often see on x rays of the abdomen in a normal patient
@rkdang is it also abnormal that you cannot see any air in the lungs? This threw me off when I was trying to read the radiograph.
Crepitus is used to describe bone-on-bone grinding. Subcutaneous crepitus is very specific sound referencing air finding its way into the skin which you can hear but also feel by rubbing your hand over the affected area. The addition of subcutaneous lets you know we are specifically talking about air in the skin.
You may also see the word in regards to gas gangrene (C. perfringens soft tissue infection) FA 2019 pg 138
This is why I picked this one because of the mucoid stools/inflammatory nature :)
But that doesn't make sense. Page 233 of First Aid 2019 edition clearly states that being plasma protein bound creates the lowest volume of distribution, because not being bound to proteins increases the chance it will reach deep into the tissues before it reaches the kidneys. Discrepancy with First Aid?
my reasoning was comparing two drugs, both with Vd of 1, the drug with the lower albumin binding would be cleared faster @kingtime. I don't think you're considering that A and B have equal Vd.
Vasoconstriction of the EFFERENT arteriole actually leads to increased GFR. It selective VASODILATION of the efferent arteriole effect of ACE inhibitors since they undo Angiotensin II actions.
This patient already has rescued renal blood flow due to bilateral renal artery stenosis, the addition of an ACE inhibitor further decrease GFR prompting an increase in renin due to loss of negative feedback.
We should always expect GFR to drop a little after adding an ACE-inhibitor due to efferent arterial vasodilation. For this reason we should also expect Renin levels to rise via tubuloglomerular feedback. So it's not really the reaction to the ACE inhibitor that gives this away as RAS (which is why I got it wrong). I think what we are expected to be looking at it are lab values: Hypokalemia, and secondary hyperaldosteronism. https://www.aafp.org/afp/2017/1001/hi-res/afp20171001p453-t5.gif
ACE inhibitors would actually have the opposite effect of AT-II, and result in efferent dilation. But the actual mechanism of increased renin activity per UWorld is lack of systemic vasoconstriction by AT-II leading to blood shunting away from the kidney.
omg monoloco!! I miss you dude! We used to hang forever ago, hope all is going well in med school!
yeah, i’ve never heard of antiphospholipids increasing PT time ...
Not sure if that little detail was to throw us off. I think the point of the question was to ID antiphospholipid syndrome based on the clinical criteria (spontaneous abortion + thrombosis)
I actually went down a rabbit hole with this one recently - essentially in vitro findings =/= in vivo findings, clot-wise with anti-phospholipid antibodies.
No mention of lupus anticoagulant, anticardiolipin, or anti Beta 2 antibodies. FA mentios prolonged PTT but nothing on PT. What a piece of shit question. But thanks to the dudes above who explained it
UWorld mentioned "prolong aPTT (and sometimes PT)" in APS
@yb_26 Can u please tell the QID because the one I have seen it says, "Although patients often have prolonged ptt (because the antiphospholipid interferes with ptt test), pt is normal."
just to clarify, lupus anticoag is in antiphospholipid and presents with paradoxical increased ptt +/- pt despite increase risk thrombosis