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wired-in
Patient has 5 yr h/o hep C, so it is chronic. Chronic inflammation is characterized by presence of lymphocytes & plasma cells while neutrophils is more characteristic of acute inflammation (Pathoma Ch. 2). AFP is within reference range so probably not HCC. Choice D, palisading lymphocytes & giant cells suggests granuloma which isn't typical of hep C.
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almondbreeze
Fa2019 pg 215, 217 on acute/chronic inflammation
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popofo
But doesn't AFP has not-so-high sensitivity for hepatocellular carcinoma (HCC)? If so, a negative result shouldn't be able to rule out HCC?
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popofo
But doesn't AFP has not-so-high sensitivity for hepatocellular carcinoma (HCC)? If so, a negative result shouldn't be able to rule out HCC?
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fatboyslim
HCC from hepatitis C usually takes decades to occur. This patient has only had HCV infection for 5 yeats
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portland2020
typically you would have a monocytic inflammatory infiltrate as described. The monocytes are an important component of the innate response. The monocytes can differentiate into macrophages.
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wired-in
Patient has 5 yr h/o hep C, so it is chronic. Chronic inflammation is characterized by presence of lymphocytes & plasma cells while neutrophils is more characteristic of acute inflammation (Pathoma Ch. 2). AFP is within reference range so probably not HCC. Choice D, palisading lymphocytes & giant cells suggests granuloma which isn't typical of hep C.
+51
almondbreeze
Fa2019 pg 215, 217 on acute/chronic inflammation
+2
popofo
But doesn't AFP has not-so-high sensitivity for hepatocellular carcinoma (HCC)? If so, a negative result shouldn't be able to rule out HCC?
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popofo
But doesn't AFP has not-so-high sensitivity for hepatocellular carcinoma (HCC)? If so, a negative result shouldn't be able to rule out HCC?
+1
fatboyslim
HCC from hepatitis C usually takes decades to occur. This patient has only had HCV infection for 5 yeats
+1
portland2020
typically you would have a monocytic inflammatory infiltrate as described. The monocytes are an important component of the innate response. The monocytes can differentiate into macrophages.
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figprincess
did you figure out the the ratio by actually divding out the numbers since the q didn't give it as a ratio? also what resource tells us what prerenal spec gravity should be?
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brolycow
I just usually remember from class that spec grav 1.001-1.010 is considered dilute urine, and anything 1.025 and above is concentrated. For this question specifically, I think I remember there only being one option that even had the ratio >=20, all of the others were like 15 or less, so just have to rule them out.
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benzjonez
Very helpful video for acute kidney injury: https://www.youtube.com/watch?v=bMp6IxDKK2Q
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notadoctor
Another explanation that helped me is that inability to concentrate the urine means something is wrong with the kidneys. If you have dilute urine, or the spec gravity is between 1.001-1.010 in someone with low urine output it suggests something is wrong with the concentration mechanisms of the kidney. Because this person had congestive heart failure we were already looking for something that matched up with prerenal azotemia so we can pretty much get rid of all the answer choices that suggest other azotemias. Then finally to get the precise answer I looked at the BUN/Cr ratio which you would expect to be high(>= 20).
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mikay92
Would fully recommend the OnlineMedEd video on AKI. Goes through the differential, lab results, treatment, etc in a very clear and concise manner.
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popofo
I understand that BUN:Cr > 20 if renal perfusion is repaired, but in heart failure wouldn't there be increased secretion of ANP/BNP from the atria that pushes up the sodium excretion?
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an1
what about ANP/ BNP? if CHF is present won't these down regulate RAAS, leading to less ADH and a more dilute urine? I understand this q says the urine output has decreased so this wouldn't be the case here. But when would we know that they want the ANP/BNP theory?
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Can anyone further explain this?! I could eliminate a few item choices and I guessed correctly, just need more information! Thanks