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Liver Pathology - Chapter 9
Terms in this set (49)
Diffuse Hepatocellular Disease
Affects hepatocytes and interferes with liver function.
Measured through liver function tests.
Types: fatty infiltration, acute and chronic hepatitis, early alcoholic liver disease, and acute and chronic cirrhosis.
Intracellular accumulation of triglycerides within hepatocytes.
Reversible with correction of process, although it is thought to be a precursor for significant chronic disease.
Usually asymptomatic. May present with jaundice, nausea/vomiting, and abdominal pain.
Causes include obesity, alcohol abuse, and diabetes.
Normal to elevated hepatic enzymes. Increased alk phos and bilirubin.
Increased echogenicity and attenuation. Impaired vision of borders of portal/hepatic structures. Hepatomegaly. Focal sparing.
Inflammatory and infection disease of the liver.
Results from infections by a group of viruses that specifically target hepatocytes.
May initially present with flulike and gastrointestinal symptoms.
Found worldwide and is spread primarily by fecal contamination, because the virus lives in the alimentary tract.
An acute infection that leads to either full recovery (4-6 months without complications) or death from acute liver failure.
Virus that exists in the bloodstream and can be spread by bodily fluids, contaminated needles, sexual contact, or mother to newborn.
Greatest risk to healthcare workers.
Often asymptomatic, but once established, chronic infection can progress to scarring of the liver.
Spread by blood-to-blood contact, sexual activity, contaminated needles.
Without complications, clinical recovery occurs within 4 months.
Pathological changes: liver cell injury, swelling of hepatocytes, hepatocyte degeneration (may lead to necrosis), reticuloendothelial and lymphatic response with Kupffer cells enlarging, regeneration.
Portal vein borders may be more echogenic than usual: "starry night" sign.
Elevated echogenicity, hepatosplenomegaly, increased thickness of gallbladder wall; increased AST, ALT, and bilirubin.
Clinical or biochemical evidence of hepatic inflammation that extends beyond 6 months.
Causes are viral, metabolic, autoimmune, or drug induced.
Coarse hepatic parenchyma, increased echogenicity, decreased visualization brightness of portal triad, fibrosis may produce soft shadowing; increased AST, ALT, and bilirubin.
Chronic Persistant Hepatits
Type of chronic hepatitis.
A benign, self-limiting process.
Chronic Active Hepatits
Type of chronic hepatitis.
Usually progresses to cirrhosis and liver failure.
A chronic degenerative disease of the liver in which the hepatic lobes are covered with fibrous tissue, the parenchyma degenerates, and the lobules are infiltrated with fat.
Process is chronic and progressive, with liver cell failure and portal hypertension as the end stage.
Coarse parenchyma with modularity, increased echogenicity and attenuation, decreased vascular markings, hepatosplenomegaly with ascites, shrunken liver, portal hypertension; increased alk phos, direct bilirubin, increased AST and ALT.
Altered flow dynamics in Doppler studies.
Type of cirrhosis caused by chronic alcohol abuse.
Type of cirrhosis caused by chronic viral hepatitis or infection.
Glycogen Storage Disease
An inherited disease characterized by the abnormal storage and accumulation of glycogen in the tissues, especially the liver and kidneys.
Disturbance of acid-base balance.
Hepatomegaly, increased echogenicity and attenuation, von Gierke's adenoma
Type I Glycogen Storage Disease/von Gierke's Disease
A form of glycogen storage disease in which abnormally large amounts of glycogen are deposited in the liver and kidneys.
A rare disease of iron metabolism characterized by by excess iron deposits throughout the body.
May lead to cirrhosis and portal hypertension.
Increased echogenicity throughout the liver, increased iron levels in blood
Caused by increased resistance to venous flow through the liver. Associated with cirrhosis, hepatic vein thrombosis, portal vein thrombosis, and thrombosis of the inferior vena cava.
Ultrasound findings include dilation of the portal, splenic, and mesenteric veins; reversal of portal venous blood flow; and the development of collateral vessels.
Portal Venous Hypertension
Increased portal venous pressure or hepatic venous gradient present.
Exists when the portal venous pressure is above 10 mm Hg, or the hepatic venous gradient more than 5 mm Hg.
Findings: collateral circulation, ascites, hepatosplenomegaly; increased liver enzymes, gastrointestinal bleeding, jaundice.
Develops when the portal venous channels become obstructed.
Diverted blood flow causes embryologic channels to reopen; blood flows hepatofugally.
Portal Hypertension Secondary to Portal Vein Thrombosis
Occurs when portal system is invaded by a tumor or thrombosis, blocking blood flow to the liver.
Primary complaint of ascites.
Develops secondary to trauma, sepsis, cirrhosis, or hepatocellular carcinoma.
Shunt attaching the main portal vein at the superior mesenteric vein-splenic vein confluence to the anterior aspect of the IVC.
Shunt attaching the middistal superior mesenteric vein to the IVC.
Shunt attaching the splenic vein to the left renal vein.
Transjugular Intrahepatic Portosystemic Shunt (TIPS)
Metallic expandable stent used intrahepatically.
Uncommon, dramatic illness caused by thrombosis of the hepatic veins or IVC.
Poor prognosis, massive ascites, abdominal pain, hepatomegaly.
Presentation may be acute or chronic illness lasting from a few weeks to several years.
Elevated caudate lobe, atrophy of the right lobe of the liver.
Primary Budd-Chiari Syndrome
Caused by congenital obstruction of the hepatic veins or IVC by a membranous web across the at the upper vena cava or just above the entrance of the left and middle hepatic veins.
Secondary Budd-Chiari Syndrome
Results from thrombosis in the hepatic veins or IVC.
Biliary Obstruction: Proximal
Caused by gallstones, carcinoma of the common bile duct, or metastatic tumor invasion of the porta hepatis.
Patient may be jaundiced, and have pruritus.
Elevated bilirubin and alk phos.
Dilated intrahepatic ducts, normal gallbladder.
Biliary Obstruction: Distal
Caused by stones in the common duct, an extrahepatic mass in the porta hepatis, or stricture of the common duct.
Common duct stones cause RUQ pain, jaundice, pruritus.
Elevated bilirubin and alk phos.
Dilated intrahepatic ducts, usually a small gallbladder, gallstones often present.
Mass in the area of the porta hepatis casing clinical signs like those seen in biliary obstruction.
May arise from lymph nodes or pancreas.
Irregular, ill-defined, hypoechoic, and inhomogeneous mass lesion may be seen in the area of the porta hepatis.
Intrahepatic duct dilation, with a hydropic gallbladder.
Common Duct Stricture
Patient is jaundiced and has had a previous cholecystectomy.
Elevated bilirubin and alk phos.
Dilated intrahepatic ducts with absence of mass in the porta hepatis.
Passive Hepatic Congestion
Develops secondary to congestive heart failure with signs of hepatomegaly.
Normal to slightly elevated LFT's
Dilation of IVC and superior mesenteric, hepatic, portal, and splenic veins.
IVC size changes with breathing.
May be congenital or acquired, solitary or multiple. Often asymptomatic and require no treatment.
Well demarcated, thin walled, and anechoic with posterior acoustic enhancement.
Simple Hepatic Cyst
Finding is usually incidental because most are asymptomatic.
More common in females than males.
Walls are thin, well-defined borders, and anechoic, with distal posterior enhancement. May contain fine linear internal septa
Congenital Hepatic Cysts
Rare and usually an incidental lesion. Arises from developmental defects in the formation of bile ducts.
Solitary and varies in size.
Tiny cysts found more commonly in patients with severe liver disease.
Located centrally within the porta hepatis at the junction of the right and left hepatic ducts.
Seen as discrete, clustered tubular-appearing cyst with a thin septae that parallel the bile ducts and portal veins in the central area of the liver.
Polycystic Liver Disease
Inherited in an autosomal dominant pattern that affects 1 in 500 individuals.
Associated with polycystic renal disease.
2 to 3 mm cysts, spread throughout parenchyma. May cause biliary obstruction.
Anechoic, well-defined borders, increased acoustic enhancement.
Pus-forming abscess. Bacteria gain entrance to the liver through the biliary tree, portal vein, or hepatic artery.
Arise from trauma, biliary disease, or surgery.
Variable appearance, depending on the internal consistency. May see floating debris with acoustic enhancement. May contain gas and have posterior shadowing. Margins are typically irregular.
Caused by a fungal organism.
Common in patients undergoing chemo, organ transplants, or individuals with HIV.
Invades bloodstream and may infect any organ.
Fever and pain.
Small hypoechoic masses with bull's-eye (target) lesions. Small amount of fluid in Morrison's pouch.
Chronic Granulomatous Disease
Genetic disorder in which phagocytes are unable to kill certain bacteria and fungi.
Occurs mostly in children, specifically boys because it is a recessive trait.
Poorly marginated, hypoechoic mass with posterior enhancement. Calcification may be present.
Aspiration is needed to classify.
Collection of pus formed by disintegrated tissue in a cavity, usually the liver.
Caused by the protozoan parasite Entamoeba histolytica.
Primarily a disease of the colon, but can spread to liver, lungs and brain. Parasites reach the liver through the portal vein.
Contracted by ingesting contaminated food or water.
May be asymptomatic with GI symptoms of abdominal pain, diarrhea, leukocytosis, and low fever.
Appearance is variable and nonspecific. Hypoechoic compared to normal liver tissue.
Echinococcal Cyst (Hydatid Cyst)
Common in sheep herding areas of the world.
Tapeworm: Larvae burrow into the mucosa of the small intestine, enter portal circulation, and travel to the liver.
Has an inner layer and an outer, inflammatory layer. May enlarge and rupture.
Most common organism causing opportunistic infections in patients with AIDS. Life threatening.
Affects immunocompromised patients.
Pattern ranges from diffuse, tiny, nonshadowing echogenic foci to extensive replacement of the liver parenchyma by various echogenic clumps of calcification.
Benign hepatic tumor. Most common neoplasm of the liver.
Sponge-like tumor consisting of large, blood filled cystic spaces. Found more frequently in females. Usually asymptomatic, though a small percentage may bleed, causing RUQ pain.
Hyperechoic with enhancement. Round or oval, well defined. Larger masses may show necrosis, degeneration, and calcification.
Focal Nodular Hyperplasia
Second most common benign liver mass after hemangioma.
Found in women under 40 years old, especially those taking oral contraceptives. Possible hormonal influence of FNH.
Usually and incidental finding, asymptomatic. Multiple, well defined with hyperechoic to to isoechoic patterns. Frequently found in right lobe.
Rare benign tumor that consists of normal or slightly atypical hepatocytes, frequently containing areas of bile stasis and focal hemorrhage or necrosis.
More common in women taking oral contraceptives, men taking anabolic steroids, and patients with type I glycogen storage disease.
May present with RUQ pain secondary to bleeding in the tumor.
Hyperechoic with central echogenic area caused by hemorrhage. Solitary or multiple. Fluid may be present.
Most common primary malignant neoplasm. Strongly associated with chronic liver disease (80%).
More common in men.
Presents with palpable mass. No abnormal LFT's. Cause a rise in AFP.
Most common form of neoplastic involvement of the liver. Primary sites are colon, breast, and lung.
Hypoechoic or echogenic mass. Diffuse distortion of bull's-eye pattern. Solitary or multiple. Well to ill defined.
Abnormal LFT's. Jaundice, hepatomegaly, weight loss, decreased appetite.
Malignant neoplasms involving lymphocyte proliferation in the lymph nodes. No specific cause is known.
Two types, Hodgkins and non-Hodgkins.
Hypoechoic or diffuse patterns. Target or echogenic lesions. Intrahepatic and lucent multiple small, discrete solid lesions without enhancement.
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