XVI - The Liver, Gallbladder and Biliary Tree Flashcards
Marked cell enlargement with irregularly clumped cytoplasm showing large, clear spaces.
Ballooning degeneration (TOPNOTCH) Robbins Basic Pathology, 8th ed, p633
Multiple tiny fat droplets that do not displace the nucleus which appear in such conditions as alcoholic liver disease, Reye syndrome, and acute fatty liver of pregnancy.
Microvesicular steatosis Robbins Basic Pathology, 8th ed, p633
A single large fat droplet that displaces the nucleus seen in alcoholic liver disease or in the livers of obese or diabetic individuals.
Macrovesicular steatosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p633
Diffuse, foamy, swollen appearance to the hepatocyte caused by retained biliary material.
Feathery degeneration(TOPNOTCH)Robbins Basic Pathology, 8th ed, p633
Poorly stained mummified hepatocytes.
Coagulative necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p633
Isolated hepatocytes become shrunken, pyknotic, and intensely eosinophilic.
Apoptosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p633
Hepatocyte necrosis is distributed immediately around the central vein, extending into the midzonal area in the setting of ischemia and several drug and toxic reactions.
Centrilobular necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p633
A pattern of nonrhythmic, rapid extension-flexion movements of the head and extremities, best seen when the arms are held in extension with dorsiflexed wrists, seen in patients with hepatic encephalopathy.
Asterixis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p635
A diffuse process characterized by bridging fibrous septa, in the form of delicate bands or broad scars around multiple adjacent lobes, and the conversion of normal liver architecture into structurally abnormal nodules, encircled by fibrotic bands. Liver architecture is disrupted.
Liver Cirrhosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p635
Presence of “ground-glass” hepatocytes, a finely granular, eosinophilic cytoplasm and “sanded” nuclei, shown by electron microscopy
Hepatitis B infection(TOPNOTCH)Robbins Basic Pathology, 8th ed, p645
Necrotic cells appear to have “dropped out,” with collapse of the sinusoidal collagen reticulin framework where the cells have disappeared; scavenger macrophage aggregates mark sites of dropout.
Hepatocyte cytolysis (in viral hepatitis)(TOPNOTCH)Robbins Basic Pathology, 8th ed, p647
Hepatocytes shrink, become intensely eosinophilic, and have fragmented nuclei; effector T cells may be present in the immediate vicinity.
Hepatocyte apoptosis (in viral hepatitis)(TOPNOTCH)Robbins Basic Pathology, 8th ed, p647
The hallmark of serious liver damage.
Fibrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p647
May occur as solitary or multiple lesions, ranging from millimeters to massive lesions, many centimeters in diameter. They are generally produced by gram-negative bacteria such as Escherichia coli and Klebsiella sp.
Pyogenic (bacterial) hepatic abscesses (TOPNOTCH)Robbins Basic Pathology, 8th ed, p648
Liver is enlarged (4-6kg), soft, yellow and greasy.
Hepatic Steatosis (Fatty Liver)(TOPNOTCH)Robbins Basic Pathology, 8th ed, p649
Lipid accumulates to the point of creating large clear macrovesicular globules, compressing and displacing the nucleus to the periphery of the hepatocyte.
Hepatic Steatosis (Fatty Liver)(TOPNOTCH)Robbins Basic Pathology, 8th ed, p649
Eosinophilic, cytoplasmic inclusions characteristic of alcoholic hepatitis.
Mallory bodies(TOPNOTCH)Robbins Basic Pathology, 8th ed, p650
Almost always accompanied by a brisk sinusoidal and perivenular fibrosis; occasionally periportal fibrosis may predominate.
Alcoholic hepatitis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p650
Liver is yellow-tan, fatty, and enlarged, usually weighing over 2 kg. Over the span of years it is transformed into a brown, shrunken, nonfatty organ, sometimes weighing less than 1 kg.
Alcoholic Cirrhosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p650
Pattern of cirrhosis in viral hepatitis.
Macronodular(TOPNOTCH)Robbins Basic Pathology, 8th ed, p650
Pattern of cirrhosis in alcoholic hepatitis.
Micronodular(TOPNOTCH)Robbins Basic Pathology, 8th ed, p650
The liver may shrink to 500 to 700 gm and become transformed into a limp, red organ covered by a wrinkled, overly large capsule. Necrotic areas have a muddy red, mushy appearance with blotchy bile staining. Complete destruction of hepatocytes in contiguous lobules leaves only a collapsed reticulin framework and preserved portal tracts.
Massive hepatic necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p653
Characterized by deposition of hemosiderin in the following organs: liver, pancreas, myocardium, pituitary, adrenal, thyroid and parathyroid glands, joints, and skin; cirrhosis; and pancreatic fibrosis
Hereditary hemochromatosis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p655
Golden-yellow granules in the cytoplasm of periportal hepatocytes, which stain blue with the Prussian blue stain.
Hemosiderin(TOPNOTCH)Robbins Basic Pathology, 8th ed, p655
Green to brown deposits of copper in Descemet membrane in the limbus of the cornea.
Kayser-Fleischer rings (TOPNOTCH)Robbins Basic Pathology, 8th ed, p656
Excessive copper deposition in the liver causing hepatic changes ranging from mild fatty change to massive liver necrosis. In the brain, injury affects the basal ganglia, demonstrating atrophy and cavitation. Kayser-Fleischer rings are characteristic.
Wilson disease(TOPNOTCH)Robbins Basic Pathology, 8th ed, p655
Hepatocytes with round to oval cytoplasmic globular inclusions which are strongly positive in a periodic acid-Schiff stain. By electron microscopy they lie within smooth, and sometimes rough, endoplasmic reticulum.
Alpha-1 antitrypsin Deficiency(TOPNOTCH)Robbins Basic Pathology, 8th ed, p657
A rare disease characterized by microvesicular fatty change in the liver and encephalopathy. Microscopy of hepatocellular mitochondria reveals pleomorphic enlargement and electron lucency of the matrices, with disruption of cristae and loss of dense bodies.
Reye syndrome / “mitochondrial hepatopathies” (TOPNOTCH)Robbins Basic Pathology, 8th ed, p658
A chronic, progressive, and often fatal cholestatic liver disease, characterized by a nonsuppurative destruction of small and medium-sized intrahepatic bile ducts (“florid duct lesion”). On cut surface, the liver is hard, with a finely granular appearance, with extraordinary yellow-green pigmentation.
Primary biliary cirrhosis (TOPNOTCH)Robbins Basic Pathology, 8th ed, p659
A chronic cholestatic disorder, characterized by progressive fibrosis and destruction of extrahepatic and large intrahepatic bile ducts. Affected portal tracts show concentric periductal “onion-skin” fibrosis and a modest lymphocytic infiltrate. Progressive atrophy of the bile duct epithelium leads to obliteration of the lumen, leaving behind a solid, cordlike fibrous scar.
Primary sclerosing cholangitis (TOPNOTCH)Robbins Basic Pathology, 8th ed, p660
Liver is slightly enlarged, tense, and cyanotic, with rounded edges. Microscopically, there is congestion of centrilobular sinusoids. With time, centrilobular hepatocytes become atrophic, resulting in markedly attenuated liver cell cords. Liver fibrosis mostly “centrilobular”.
Passive congestion of the liver secondary to right-sided heart failure.(TOPNOTCH)Robbins Basic Pathology, 8th ed, p660
Hepatocytes in the central region of the lobule undergo ischemic necrosis. The liver takes on a variegated mottled appearance, reflecting hemorrhage and necrosis in the centrilobular regions, alternating with pale midzonal areas, known traditionally as the “nutmeg” liver.
Passive congestion of the liver secondary to left-sided heart failure.(TOPNOTCH)Robbins Basic Pathology, 8th ed, p661
A rare condition wherein there is primary dilation of sinusoids, impeding hepatic blood efflux. Associated with exposure to anabolic steroids, OCP’s and danazol.
Peliosis hepatis(TOPNOTCH)Robbins Basic Pathology, 8th ed, p661
Results from the thrombosis of two or more major hepatic veins and is characterized by hepatomegaly, weight gain, ascites, and abdominal pain. The liver is swollen, is red-purple, and has a tense capsule. The affected hepatic parenchyma reveals severe centrilobular congestion and necrosis.
Budd-Chiari syndrome (TOPNOTCH)Robbins Basic Pathology, 8th ed, p662
Caused by toxic injury to sinusoidal endothelium. Damaged endothelial cells slough off and create emboli that block blood flow. Accompanied by passage of red blood cell into the space of Disse, proliferation of stellate cells, and fibrosis of terminal branches of the hepatic vein.
Sinusoidal Obstruction Syndrome (TOPNOTCH)Robbins Basic Pathology, 8th ed, p662
Well-demarcated but poorly encapsulated lesion, consisting of hyperplastic hepatocyte nodules with a central fibrous scar. Appears in noncirrhotic livers and may reach up to many centimeters in diameter. It occurs in response to local vascular injury.
Focal nodular hyperplasia (TOPNOTCH)Robbins Basic Pathology, 8th ed, p664
These appear in cirrhotic livers, are larger than surrounding cirrhotic nodules but do not display atypical features. Contains more than one portal tract, have an intact reticulin framework, and do not seem to be precursors of malignant lesions.
Macroregenerative nodules (TOPNOTCH)Robbins Basic Pathology, 8th ed, p664
These are lesions larger than 1 mm in diameter that appear in cirrhotic livers. Considered to be precursors of hepatocelluar cancers, are often monoclonal, and may contain chromosome aberrations similar to those present in liver cancers.
Dysplastic nodules (TOPNOTCH)Robbins Basic Pathology, 8th ed, p664
May appear grossly as (1) a unifocal, usually massive tumor, (2) a multifocal tumor made of nodules of variable size or (3) a diffusely infiltrative cancer, permeating widely and sometimes involving the entire liver, blending imperceptibly into the cirrhotic liver background.
Primary Hepatocellular Carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th ed, p665
A distinctive variant of HCC, which occurs in young male and female adults (20-40 years of age) of equal incidence, no association with cirrhosis or other risk factors. usually consists of a single large, hard “scirrhous” tumor with fibrous bands coursing through it. Composed of well-differentiated polygonal cells growing in nests or cords and separated by parallel lamellae of dense collagen bundles.
Fibrolamellar carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th ed, p665