Ch. 14 Liver Part 2 Portal HTN, Hepatitis Flashcards
Most common cause of pre-sinusoidal portal HTN:
Portal vein thrombosis, usually in setting of cirrhosis.
Can also be caused by tumors, septic thrombi, or hypercoaguable states.
Your patient presents to the ER complaining of abdominal pain and jaundice. You notice ascites and hepatosplenomegaly.
If the eventual pathology report showed thrombi in the hepatic veins and dilated sinusoids, what does your patient have?
What type of portal HTN is it?
Budd-Chiari syndrome-congestive disease of liver caused by occlusion of hepatic arteries due to polycythemia vera, hypercoaguability, tumors, or infections.
Post-sinusoidal portal HTN
What is a deadly complication of portal hypertension that presents as hematemesis?
Bleeding esophageal varices
What is the physiological response to portal HTN that leads to ascites?
Peripheral arterial vasodilation occurs in portal HTN, and cardiac output can’t keep up. RAS gets activated leading to sodium and water retention. Fluid leaks from the sinusoids, into the space of Disse and the peritoneal cavity. Decreased albumin contributes to the fluid movement.
What is hepatorenal syndrome?
Renal hypoperfusion in the setting of cirrhosis, but the kidneys are able to restore normal function if the hepatic pathology is reversed.
Micro crossover! What kind of viruses are Hep A, B, C, D, and E? Which have vaccines?
Hep A: RNA picornavirus, vaccine
Hep B: DNA hepadnavirus, vaccine
Hep C: RNA flavivirus, enveloped
No vaccine because frequently mutates
Hep D: RNA
Hep E: RNA, hepeviridae, enteric, vaccine in works, not yet in US
How is Hep A transmitted?
Hep B?
Hep C?
Hep D?
Wait for it….Hep E?
A: Fecal-oral tranmission (shed in bile)
B: Vertical transmission, IV drug use, sexual transmission
C: blood contact, less commonly sexual transmission
D: only infects people who are also infected with Hep B (superinfection, as opposed to coinfection, is more serious)
E: usually in poor countries, fecal-oral, seafood contamination
Describe the clinical course of Hep A
Nonspecific symptoms, can be jaundiced. Never becomes chronic, no carrier state, lifelong immunity from infection
If your patient is not currently sick, but has anti-HBc (antibody to core antigen) in their serum, what does that mean?
They were previously infected with Hep B
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| If your patient has Anti-HBs (antibody to serum antigen) in their serum, what does that mean?</p>
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They have completely recovered from Hep B infection or have been previously vaccinated</p>
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If they have recovered, there will also be Anti-HBc present</p>
Which is the first Hep B antigen to appear, and the last to leave?
HBsAg (surface antigen)
What does the presence of HBeAg (e antigen) mean for your patient?
They are very infectious as the virus is undergoing replication
Which hepatitis infections can lead to hepatocellular cancer, chronic hepatitis and immune complex deposition causing disease?
Hep B and C both increase risk of liver cancer
Hep B can lead to serum sickness syndrome, polyarteritis, and glomerulonephritis
Hep C is strongly associated with mixed cryoglobulinemia (systemic vasculitis), which can also involve the kidneys and nervous system.
Describe the pathology of acute viral hepatitis (hint, they’re all similar)
Scattered necrosis with eosinophilic bodies (Councilman/acidophilic bodies) with hydropic swelling and lobular disarray, with chronic inflammatory cells.
What are three types of confluent hepatic necrosis (acute viral hepatitis with the death of numerous liver cells in a geographical distribution)
Bridging necrosis: mild, bands of necrosis between portal tracts. Collapse of the collagenous stroma
Submassive: Necrosis of entire lobules
Massive: uncommon, fatal. Wrinkled liver capsule, almost all hepatocytes are dead. Macrophages and RBCs fill sinusoids.
