Chapter 14: Liver Failure and viral hepatitis Flashcards
A neurologic symptom of hepatic encephalopathy where the patient has a flapping tremor of the hands.
Asterixis.
An alcoholic man presents with gynecomastia, spider angiomas, and palmar erythema.
Cirrhosis -> feminization in men.
Gonadal failure in women.
What defines portal hypertension?
Absolute increase in portal venous pressure above 8mm Hg
An increase in the pressure gradient betweeen the portal vein and hepatic vein of 5mm Hg or more.
^ meausr ebaove with wedged hepatic vein pressure - free hepatic vein pressure.
What are the three locations at which increased resistance to blood outflow in the portal circuit can lead to portal hypertension?
Sinusoidal: Generally caused by fibrosis (cirrhosis). The hepatic venous pressure gradient is typically increased.
Presinusoidal: Inside extrahepatic portal vein or intrahepatic portal veins or venules (thrombotic occlusion). HVPG can be elevated or normal.
Postsinusoidal: Hepatic veins, venules, or cardiac circulation. HVPG is usually normal.
What organism can cause intrahepatic portal hypertension?
Schistosoma mansoni and Schistosoma japonicum.
Ova released from intestinal veins traverse portal system and lodge in intrahepatic portal venules, induce granulomatous reaction that heals by scarring. Prehepatic portal hypertension - liver function remains intact.
What is a common vascular cause of presinusoidal portal hypertension?
Portal vein thrombosis.
Cirrhosis, tumors, infections, hypercoagulable states, pancreatitis, surgical trauma.
Cavernous transformation: Thrombosed portal or splenic vein replaced by a fibrous cord or interlacing vascular channel.
Arteriovenous fistulas: Osler-Weber-Rendu syndrome, trauma.
A patient with a past medical history of polycythemia vera presents with portal hypertension. Thrombosis of the hepatic veins is discovered.
Upon examination of the liver, there is thrombosis of hepatic veins and diffuse congestion.
Upper right: Needle biopsy - centrilobular necrosis and hemorrhage and expanded sinusoids.
Lower left: Cirrhosis developed with bridging fibrosis emanating from central veins rather than portal tracts. Dilated isnusoids, intact portal tract.
Budd-Chiari syndrome.
A variant is called hepatic veno-occlusive disease: Occlusion of the central venules and small branches of hepatic veins. Ingestion of toxic pyrrolizidine alkaloids in Crotalaria and Senecio genera (bush teas). Antineoplastic chemotherapeutic agents, irridation, bone-marrow transplant.
Collateral veins radiating around the umbilicus produces this pattern.
Caput medusae.
Focal hemorrhages with fibrotic, iron-laden nodules seen in splenomegaly secondary to portal hypertension.
Gamna-Gandy bodies.
What serum-to-ascites albumin gradient is associated with ascites due to portal hypertension from cirrhosis?
SAAG > 1.1.
This is because less protein and albumin spill into ascites fluid as sinusoids become less premeable with fibrosis.
Patient presents with ascites, abdominal pain, and fever.
Paracentesis finds 300 neutrophils/uL.
Spontaneous bacterial peritonitis.
Gram negative bacteria from digestive tract? E. coli, Klebsiella, strep pneumonia.
A patient presents with oliguria, azotemia, and increased plasma creatinine. He has a past medical history of cirrhosis.
Hepatorenal syndrome - renal hypoperfusion.
Liver transplant can restore renal function.
Type I HRS: Rapidly and inexorably progressive. Liver transplant only therapy
Type II HRS: More slowly progressive, seen in setting of severe ascites that is unresponsive to conventional therapies with salt restriction and diuretics.
Patient presents with a pleural effusion with a history of cirrhosis.
Hepatic hydrothorax - pleural effusion attributed to portal hypertension.
Hepatopulmonary syndrome (HPS): Creation of shunts of various size in the pulmonary vascular bed in setting of portal hypertension.
Portopulmonary hypertension: Increased pulmonary vascular resistance in the setting of portal hypertension.
A patient presents with fever, malaise, and anorexia. An aminotransferase is high. A month later, the patient’s values are back to normal.
Hepatitis A virus. No carrier state - no chronic infection. RNA containing enterovirus of picoronavirus group.
Infection provides lifelong immunity.
IgM anti-HAV initially appears. IgG appears during recovery and persists for life.
Transmitted fecal-oral route, contaminated food and water.
A patient with jaundice and elevated liver function tests undergoes serum antibody tests. The results:
HbsAg +
HbsAb -
HbeAg +
HbeAb -
HbcAb -
Acute Hepatitis B virus: Hepatotropic DNA virus.
Core antigen, e antigen (from C gene).
Surface antigen
Vaccine available. Integrates into host genome, allowing chronic infection.
Spread by blood, saliva, semen. Injury caused by cytotoxic T lymphocytes.
A patient tests posive for very high HBV DNA levels, but has normal serum aminotransferase levels and is asymptomatic.
Immune tolerant phase of chronic hepatitis B.
Increased risk of hepatocellular cancer.
A patient presents with elevated LFTs. The following biopsy is obtained.
Acute viral hepatitis.
Apoptotic liver cells appear as small, deeply eosinophilic bodies (Councilman or acidophilic bodies). Disarray of liver cell plates, swollen (ballooned) hepatocytes, and an infiltrate of lymphocytes and scattered mononuclear inflammatory cells.
Central Phlebitis: Lymphocytes infiltrate between wall of central vein and the liver cell plates
Endophlebitis: Swelling and proliferation of endothelial cells of the celtral vein.
A patient presents with severe acute hepatitis B infection. A liver biopsy is taken.
Bridging necrosis: Milder end, bands of necrosis that stretch between adjacent portal triads, adjacent central veins, and between portal tracts and central veins. Best visualized with a reticulin stain.
OTHER FORMS OF CONFLUENT HEPATIC NECROSIS, NOT THIS PICTURE:
Submassive hepatic nerosis: Even more severe, necrosis of entire lobule or groups of adjacent lobules.
A patient presents with severe acute hepatitis B and dies. At autopsy, the following specimens are obtained.
Massive hepatic necrosis (acute yellow atrophy): Uncommon, invariably fatal. Shrunken liver, wrinkled, mottled
A patient presents with mildly elevated LFTs. A liver biopsy is taken.
Mild chronic hepatitis. Portal tract infiltrated by mononuclear inflammatory cells. Lobular parenchyma is intact. Mild fatty change often accompanies hepatitis C.
A patient presents with jaundice and elevated LFTs. He hasn’t visited a doctor in 20 years.
Severe chronic hepatitis.
A. Mononuclear inflammatory infiltrate in an expanded portal tract.
B. Chronic hepatitis with cirrhosis - bridging fibrosis and nodular transformation.
A patient with chronic hepatitis B presents with worsening symptoms. A biopsy is taken.
Hepatocytes are shown with cytoplasm containing hepatitis B surface antigen. Stain with immunoperoxidase is to the left.
Ground-glas hepatocytes. An intralobular lesion - focal necrosis and inflammation.
