Liver 2


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Liver 2

  1. 1. Title : LiverObjectives : to1. Describe liver cirrhosis.2. Outline liver abscess.3. Identify alcoholic liver diseases.4. Study metabolic liver diseases.
  2. 2. Liver cirrhosis: End stage of many chronic liver diseases. Refers to diffuse hepatic fibrosis with replacementof normal lobular architecture by parenchymal nodulesseparated by fibrous tissue. suspected on clinical, laboratory, and imaging parameters,but final diagnosis requires liver biopsy. Architectural changes best appreciated on reticulin stain.
  3. 3.  The morphologic classification of cirrhosisis based on size of nodules:o Micronodular : if nodules are less than 3 mm.o Macronodular : if nodules are greater than 3 mm. The size of nodules can define etiology of cirrhosis ,but this is relative since micronodular cirrhosis mayconvert into macronodular type .
  4. 4.  Features indicating etiology of cirrhosis :-• Biliary cirrhosis: garland-shaped nodules, andclear halo in nodular periphery due to edema.• Post hepatitic cirrhosis: necro inflammation.• HBV : ground glass hepatocytes.• HCV: lymphoid aggregates and lymphoid follicles.
  5. 5. • Autoimmune hepatitis: numerous plasma cells.• Genetic hemochromatosis: severe parenchymal siderosis.• a1-Antitrypsin deficiency: hepatocellular inclusionswhich are eosinophilic, PAS positive. Hepatocellular carcinoma commonly arises in cirrhotic liver.Its precancerous stages ( dysplastic foci , large and smallliver cell dysplasia) should be looked for.
  6. 6. Liver abscess : In developing countries: most liver abscessesrepresent parasitic infections (amebic, echinococcal). In developed countries: most are pyogenic, the organismreach liver by:(1) portal vein.(2) arterial supply.(3) ascending cholangitis.(4) direct invasion of liver from nearby source.(5) penetrating injury.
  7. 7. Morphology : Liver abscesses can be solitary or multiple:o Bacteremic spread: multiple small abscesses.o Direct extension and trauma: solitary large abscesses.o Biliary abscesses are usually multiple. Gross and microscopic features are those of any abscess. The causative organism can be identified in fungal orparasitic abscesses .
  8. 8. The liver shows a small abscess filled withmany neutrophils.Amoebic Liver abscessamoebic Liver abscess- trophozoites
  9. 9. Alcoholic liver diseases:Hepatic Steatosis (Fatty Liver): Fatty liver is large , soft , yellow and greasy. Small microvesicular lipid droplets in hepatocytes. With chronic intake of alcohol: large, clear macrovesicular. Initially is centrilobular, in severe cases involve entire lobule. Fatty change is completely reversible if there is abstentionfrom alcohol intake.
  10. 10. Alcoholic Steato Hepatitis- ASH: Grossly :o liver is mottled red with bile-stained areas.o it often contains visible nodules and fibrosis. Microscopically:o Hepatocyte swelling and necrosis.o Mallory bodies: cytokeratin intermediate filamentsvisible as eosinophilic cytoplasmic inclusions.o Neutrophilic reaction: around degenerating hepatocytesparticularly those with Mallory bodies.o Fibrosis.
  11. 11. Common pathological findings in alcoholic steatohepatitis. A. Ballooning and Mallorybodies in damaged hepatocytes . B. Steatosis and polymorphonuclear infiltration (arrow).C. Centrilobular fibrosis. D. Bridging fibrosis in cases of advanced disease.
  12. 12. Alcoholic liver cirrhosis: Final and irreversible form of alcoholic liver disease,usually evolves slowly. Initially cirrhotic liver is yellow-tan, fatty, and enlarged;later on brown ,shrunken, non fatty organ. Uniformly sized micronodules , but with time scatteredlarger nodules create a "hobnail" appearance. Mallory bodies rarely evident ,thus it resembles cirrhosisdeveloping from viral hepatitis and other causes.
  13. 13. Metabolic liver diseases:Nonalcoholic fatty liver (NAFL) : Patients are not heavy drinkers. Men and women are equally affected. Strong association with obesity, dyslipidemia, andinsulin resistance (type 2) diabetes. Patients are largely asymptomatic, with abnormalitiesonly in lab. tests (elevated serum aminotransferasesand/or Ɣ- glutamyl transpeptidase ).
  14. 14.  Liver biopsy shows :• Steatosis (Large and small vesicles of fat)• No hepatic inflammation,No hepatocyte death, No fibrosis.Nonalcoholic steatohepatitis, or NASH: Liver biopsy shows:• Steatosis.• multifocal parenchymal inflammation, Mallory body ,hepatocyte death and sinusoidal fibrosis.• Cirrhosis : may occur.
  15. 15. HEMOCHROMATOSIS : Excessive accumulation of body iron, depositedin parenchymal organs such as liver and pancreas. Tow major types :o Hereditary ( primary ) hemochromatosis :• autosomal-recessive inherited disorder.• gene located on chromosome 6 called HFE gene.o Acquired ( secondary ) hemochromatosis: include:-
  16. 16. • Parenteral iron overload: Transfusions. Iron-dextran injections.• Ineffective erythropoiesis: β-Thalassemia. Sideroblastic anemia.• Increased oral intake of iron.• Congenital atransferrinemia.• Chronic liver disease: Chronic alcoholic liver disease. Porphyria cutanea tarda.
  17. 17.  Fully developed cases exhibit:(1) micronodular cirrhosis in all patients.(2) diabetes mellitus in 75% to 80% of patients.(3) skin pigmentation in 75% to 80% of patients. Symptoms first appear in fifth to sixth decades of life. Males predominate (5 - 7:1).
  18. 18.  Death may result from cirrhosis or cardiac disease. Risk for hepatocellular carcinoma is 200-fold increased. Screening involves :• very high levels of serum iron and serum ferritin.• liver biopsy if indicated.• identification of HFE gene for genetic screening. Treatment: regular phlebotomy.
  19. 19. Morphology: Liver is slightly larger than normal, dense,and chocolate brown. Iron evident as golden-yellow hemosiderin granuleswhich stain blue with Prussian blue stain. Inflammation is absent. Fibrous septa develop slowly, leading ultimatelyto micronodular type of cirrhosis .
  20. 20. The dark brown colorof liver, pancreas(bottom center) andlymph nodes(bottom right) inmiddle-aged manwith hereditaryhemochromatosis .liver cells bear within them Hemosideringranules .Iron(Prussian Blue ) staining: blue granules of hemosiderin
  21. 21. WILSON DISEASE : Autosomal-recessive disorder marked byaccumulation of toxic levels of copper inmany tissues and organs. The gene is ATP7B, located on chromosome 13. Morphology:• Fatty change in hepatocyte.• acute hepatitis.• chronic hepatitis.• with progression cirrhosis will develop.
  22. 22. • Excess copper deposition demonstrated by special stain:rhodanine stain for copper.Liver histology - rhodamine staining for copper
  23. 23.  Clinical Features:• rarely manifests before 6 years of age.• most common presentation is: acute or chronic liver disease. Neuropsychiatric manifestations (mild behavioral changes,frank psychosis, or Parkinson disease-like syndrome). Eye lesions called Kayser-Fleischer rings:green to brown deposits of copper in cornea.
  24. 24.  Diagnosis:• decrease in serum ceruloplasmin.• increase in hepatic copper content.• increased urinary excretion of copper.• Serum copper levels are of no diagnostic value,since tmay be low, normal, or elevated, dependingon stage of evolution of disease. Treatment: copper chelation therapy (D-penicillamine).
  25. 25. Summary:1. Liver cirrhosis is the end stage of many chronicliver diseases.2. Liver abscesses are either due to parasitic infectionor pyogenic.3. Alcoholic liver diseases include steatosis , ASH ,and alcoholic liver cirrhosis.4. Metabolic liver diseases include NAFL , NASH,hemochromatosis, and wilson disease.
  26. 26. Questions:1. Enumerate alcoholic liver diseases, and writeshort assay on one of them?2. How you diagnose wilson disease?THANK YOU