Liver Pathology Wednesday objectives Flashcards
Describe the pathologic findings on liver biopsy of alcoholic steatosis and alcoholic hepatitis. What are mallory bodies?
alcoholic steatosis - macrovesicular, lipid accumulation. It is reversible
alcoholic hepatitis - steatosis and inflammation. swelling and necrosis. mallory bodies, which are aggregates of cytokeritin.
some fibrosis can be seen, which is a precursor to sirrhosis
Describe the typical gross appearance of alcoholic cirrhosis.
Early stages - micronodular and fatty
Late stages - liver is shrunken, non-fatty, different nodule sizes, cholestasis. fibrosis
List the major causes of death in alcoholic cirrhosis.
hepatic encephalopathy gi hemorrhage (varices) infection hepatorennal syndrome hepatocellular carcinoma
Define non-alcoholic fatty liver disease. What patient population can get this disease?
Insulin resistance -> fat buildup -> looks like alcoholic liver
Metabolic syndrome, obesity, diabetes, dyslipidemia
Define PBC, and state what type of patient typically gets this disease. What symptoms may be exhibited by a patient with PBC? State a key diagnostic lab test and describe the findings on liver biopsy.
Primary Biliary cirrhosis
middle aged females, northern european.
intrahepatic bile dict destruction –> fatigue and itching, steatorrhea, xanthoma. low vit D
Antimitochonrial antibodies.also high Alk Phos
Biopsy - lymphocytes by the portal tracts. leads to fibrosis then cirrhosis
Define secondary biliary cirrhosis. List some possible causes.
from prolonged obstruction
(stones, tumor Cystic fibrosis)
can lead to fibrosis
Define PSC, and state a key patient population that this disease can occur in. State how you would diagnosis PSC, and describe key pathologic finding on liver biopsy.
Primary sclerosing cholagnitis - autoimmune (p-anca) fibroinflammation of intra and extrahepatic ducts
most are middle ages males
elevated Alk Phos and GGT
diagnose w/ cholangiography - strictures and dilations (beaded). liver biopsy show focal fibrosing cholagitis. used to stage the disease.
Define hereditary hemochromatosis, and describe underlying pathogenesis. State some of the clinical manifestations of the disease. Describe the findings on liver biopsy, and describe how it is diagnosed. What test would you use to screen for this disease? How is it treated?
excessive iron absorption -> organ injury. decreased hepcidin made by liver. HFE gene.
clinically - more males. age 40-60. low penetrance.
biopsy - hemosiderin deposits, micronodular chirrhosis, fibrosis.
screening - cirrhosis, skin pigmentation and diabetes, can present in any organ. over 45% iron saturation
treatment - phelbotomy
Define secondary hemochromatosis, and list some causes. How does the liver biopsy of secondary hemochromatosis differ from hereditary hemochromatosis?
From getting blood transfusions
thallasemia
too many vitamins
deposits are in the kupffer cells
Define Wilson’s disease, and state the abnormalities present on key diagnostic tests. What can be seen on eye exam? When should you consider Wilson’s disease as a diagnostic possibility, and what is typically increased in the liver biopsy?
toxic amounts of copper
chromosome 13
AP7B protein
low ceruloplasmin, so low levels of copper in blood. can’t leave the liver. Increase urine copper.
Present early, child. copper ring on eye called kayser-fleischer ring), cirrhosis.
Define alpha-1-antitrypsin deficiency. describe and contrast the pathogenesis of the lung injury and the liver injury. What test would you order to screen for this disease, and what key finding can be seen on liver biopsy?
codominant disorder
usually inhibits neutrophil elastase.
amount of antitrypsin doesn’t correlate with liver disease.
if you’re making no antitrypsin, it doesn’t accumulate in the liver = no liver presentation.
test with A1AT level
biopsy - globs on PAS stain
Describe the two main categories of drug induced liver injury. Remember to always consider drug or toxin effect as a cause of liver injury.
direct - toxic to liver in dose dependent way. effects everyone exposed
idiosyncratic - not everyone, no particular dose
Describe, using just a few sentences for each, chronic passive congestion, centrilobular hemorrhagic necrosis, cardiac sclerosis, hepatic infarct, Budd-Chiari syndrome, and sinusoidal obstruction syndrome. Make sure that you can describe the pathologic findings and causes of these entities.
Hepatic vein thrombosis (Budd-Chiari syndrome): defined as thrombosis of two or more
hepatic vein branches, with the classic clinical triad of hepatomegaly, ascites, and
abdominal pain.
Sinusoidal obstruction syndrome (hepatic veno-occlusive disease): defined by the presence of obstructive, nonthrombotic lesions of the small (central) hepatic veins in patients exposed to radiation and/or hepatoxins. Pathology demonstrates marked narrowing and obliteration of central vein lumens by subendothelial swelling and fibrosis.
Usually occurs in allogeneic bone marrow (hematopoietic stem cell) transplant patients
Sx: painful hepatomegaly, sudden weight gain, increased serum bilirubin
Define neonatal cholestasis, biliary atresia, and neonatal hepatitis.
.Biliary atresia: defined as complete or partial obstruction of the lumen of the extrahepatic biliary tree within the first 3 months of life. The etiology may be inflammatory (viral infection or autoimmune injury) or due to anomalous embryologic development affecting the biliary tree. Untreated, most cases will progress to destruction of the intrahepatic bile ducts, resulting in neonatal hepatitis and possibly secondary biliary cirrhosis. Biliary atresia accounts for 50% of pediatric liver transplant cases.
neonatal hepatitis is hepatitis in a neonate, go figure
List some causes of granulomatous hepatitis.
. Idiopathic (50%) Sarcoidosis (22%) Drug related (6%) Tuberculosis (3%) Other (19%) (PBC, Histoplasmosis, Lymphoma)
