Mehlman masterfully distills the lethal irony of maternal immunology into a high-yield lesson on physiological trade-offs. It is a sharp reminder that the same mechanisms protecting the fetus can leave the mother tragically defenseless against viral onslaught.
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HY USMLE Q #1576 – Gastro / ImmunoHinzugefügt:
How's it going guys? We have a difficult question for gastro-immuno. 34-year-old woman, G1P0, 34 weeks gestation, comes to physician for a 1-week history progressive yellowing of her eyes, fatigue, fever, right upper quadrant pain. She recently returned from visiting her family in Tibet. 4 days later, transaminases markedly elevated, partial thromboplastin time elevated, serum bile acids normal, does not report itchy skin. She undergoes a C-section and a liver transplantation. And we want to know the most likely explanation for patient's findings. So, there's a lot to unpack here. So, she obviously has progressive jaundice and the right upper quadrant pain, classic for hepatitis with the fever. When we talk about Tibet, Asia is a very buzzy location for hepatitis E in addition to hepatitis A.
A is worldwide. You guys probably can give you Mexico as an example. Tibet, Asia, hepatitis E.
Now, we tell you her transaminases markedly elevated and her PTT is elevated. Now, this is a little bit back to any but it's high yield for your Simile that you know that the greatest, most accurate marker of liver failure is elevated PTT /PT.
Okay, both of them. They can tell you prothrombin time, partial thromboplastin time.
Both of those can be elevated in liver failure.
That's more important than just simply ALT AST elevation. ALT AST elevation can occur with liver damage.
But when you actually have your PT and PTT elevated, then that tells you you have overt liver failure.
Serum bile acids normal, does not report itchy skin. We'll talk about it as we move through. So, acute hepatitis A infection's [ __ ] wrong, okay? So, she has hepatitis E infection. You say, "Well, how do we know that? Why couldn't this be hepatitis A?" It's not that it's impossible for it it's hepatitis A, but you need to know that hepatitis E in pregnant women is notably fatal. 15 to 25% mortality rate. Causes fulminant hepatitis, especially if contracted during third trimester. Okay? And it's because we have more virulence of the hepatitis E envelope proteins in the setting of the immunology in pregnancy, which I'll explain as we move through. Wrong [ __ ] answer.
Choice B intrahepatic cholestasis pregnancy, wrong [ __ ] answer. So more of a 2CK3 diagnosis. This is the answer on USMLE when you have itchy palms and soles in a woman who's in third trimester of pregnancy and she has high serum bile acids and there's increased risk of fetal demise.
Very important, okay? That this is diagnosed in pregnancy and she's given ursodiol, ursodeoxycholic acid decreases secretion of cholesterol in bile, but also decreases bile acids.
Okay? So you can undergo a C-section if a woman has a history of this and she has a third trimester miscarriage in a subsequent pregnancy, she can undergo an early C-section. So we tally bile acids are normal, she doesn't report itchy skin. So ICP, wrong [ __ ] answer.
Choice C intravenous drug use, wrong [ __ ] answer. Me being an [ __ ] because obviously hepatitis B and C are parenteral and you say, "Well, she could have contracted hep B or hep C abroad. That might be the diagnosis here." You're right. But as I already harped on, hep E is notably what causes fulminant hepatitis in pregnancy.
So you want to get emotional and say, "What about hepatitis B and D at the same time? Can't that cause fulminant hepatitis?" You're right. But regardless, wrong [ __ ] answer.
Choice D shift from TH1 to TH2 immunity, correct answer. So, this is what's going to go down. I'll keep this hyper clean and simple. So, I'll ask you watching this, is it normally CD4 CD8 plus T cells that kill virus-infected cells?
It's going to be CD8 plus T cells, right? So, in pregnancy, we have CD4 T cells, TH1 and TH2 are the different types. TH1 tends to stimulate macrophages and CD8 plus T cells.
TH2 CD4 plus T cells tend to stimulate B cells for antibody production.
Now, in pregnancy, we get down regulation of TH1 and up regulation of TH2. What does this mean? It means we have decreased stimulation of macrophages and CD8 plus T cells, which means that we have decreased ability to contain viral-infected cells. And this process, notably, can result in hep E fulminant hepatitis because the hep E virulent envelope proteins need robust CD8 plus immunity to be suppressed.
So, the reason this occurs during pregnancy physiologically is because the maternal immune system is not going to want to reject the fetus.
So, if we have increased TH1, there's an increased risk of rejection of the fetus because we'd have more CD8 activation.
Okay, so, that's also why viral virus infections viral infections in general can get worse during pregnancy. HPV, tangentially, gets worse during pregnancy. Condylomata acuminata, high-grade lesions, okay, they're observed during pregnancy and then after pregnancy, they're they often regress.
Try C stimulation of CD8 immunity is [ __ ] wrong because as we just said, CD8 immunity is going to be suppressed in pregnancy because we have less TH1.
So, CD4 plus TH1 T cells stimulate macrophages and CD8 because we have less TH1, we have less CD8 immunity in pregnancy, which is why hep E becomes very virulent and can cause fulminant hepatitis rather than stimulation of CD8 immunity.
Wrong [ __ ] answer.
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