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Normal structure of liver

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Presentation on theme: "Normal structure of liver"— Presentation transcript:

1 Normal structure of liver

2 Normal function of liver
Metabolic (glucose homeostasis…) Synthetic (albumin, coagulation factors) Storage (glycogen, triglycerides, Fe, Cu, vitamins soluble in fat) Catabolic (endogenous substances – hormones…, exogenous substances – drugs, alcohol…) Excretoric (bile)

3 Histologic examination
Necropsy Excision during laparotomy Fine needle punction Percutaneous punction biopsy unguided laparoscopic guided (Sono, CT) transjugular

4 Liver biopsy Representativeness Quality Clinical data Diagnosis Reproducibility

5 Representativeness Biopsy represents approx. 1/500 000 of organ
Ideal biopsy (Scheuer, MacSween) 2 cm length more than 4 (8) portal tracts Borderline representativeness contact CLINICIAN!! Non-representative

6 Quality Clinical data Clear and sufficient clinical outcome, history
etiology biochemical findings, other markers (oncomarkers, markers of autoimmunity…) treatment previous histology preliminary diagnosis! Unclear contact CLINICIAN!! Insufficient and confusing

7 Quality Diagnosis Diagnosis
recent diagnostic praxis (grading and staging of chronic hepatitis…) recent diagnostic textbooks - contact CLINICIAN!! Methods biopsy - contact CLINICIAN!! immunohistochemistry, ELMI - contact CLINICIAN!! experimental

8 Recently used diagnostic textbooks

9 Histologic examination – special stains and methods
Haematoxylin/eosin Fouchet – bile (green), collagen (red) Fe, Cu – Fe pigment, Cu pigment Gömori – reticulin mesh Orcein – HBsAg PAS, Müller – mucopolysaccharides Immunohistochemistry (HBsAg, HBcAg, a1 fetoprotein, CEA, hepatocytes – OCH1E5) ELMI (metabolic diseases) PCR (HBV DNA, HCV RNA,…)

10 Damage of hepatocytes Type (ischemic-coagulation necrosis, piecemal necrosis, apoptosis) Extent (monocellular, focal, submassive, massive, bridging: C-C; C-P) Localization (centrolobular, periportal, midzonal) Course regeneration, healing ad integrum regeneration + fibrosis: cirrhosis acute liver failure: coma and death

11 Liver failure Jaundice Hypoalbuminemia Coagulopathy Hyperamonemia
Increase of levels of cytosolic enzymes Endocrine complications Hepatoencephalopathy Hepatorenal syndrome Coma

12 Necrosis of liver: damage of hepatocytes

13 Cirrhosis Nodular rearrangement Morphology micronodular macronodular

14 Cirrhosis: etiology Alcohol (60-70%) Chronic hepatitis (10%)
Cryptogenic (10-15%) Biliary (primary, secondary) Haemochromatosis (primary, secondary) Metabolic diseases (tyrosinemia, galactosemia) -very rare

15 Cirrhosis: complications
Portal hypertension Liver failure Hepatocellular carcinoma

16 Portal hypertension Prehepatic (tumor, infection, pancreatitis, pregnancy, peroral contraceptives) Intrahepatic – most frequent (cirrhosis, fibrosis) Posthepatic (congestive cardiac failure, Budd-Chiari syndrome, venoocclusive disease) Signs: portosystemic shunts splenomegaly ascites

17 Cirrhosis

18 Cirrhosis

19 Cirrhosis

20 Cirrhosis + hepatocellular carcinoma

21 Cirrhosis: Masson staining

22 Cirrhosis: Fouchet staining

23 Cirrhosis

24 Cirrhosis: active

25 Cirrhosis: biliary

26 Dysplasia

27 Dysplasia

28 Hepatitis: etiology Infectious (acute, chronic) viruses (most often)
bacteria (TBC, malaria, salmonelosis, leptospirosis,…) parazites (ecchinococcus) protozoal (amebiasis) Non-infectious (acute, chronic) autoimmune metabolic drug induced cryptogenic

29 Viral hepatitis HAV RNA Pikornavirus HBV DNA Hepadnavirus HDV
Defektní virus Non A Non B HCV Flavivirus HEV Kalicivirus HFV Togavirus HGV

30 Viral hepatitis: HBV+HDV

31 Viral hepatitis: HBsAg, ground glass

32 Viral hepatitis: HBsAg, Orcein staining

33 Viral hepatitis: HBcAg, immunohistochemistry

34 Viral hepatitis: HBcAg, electron microscopy

35 Viral hepatitis: course
Acute (HAV, HBV, HCV, HDV, HEV) Chronic (HBV, HBV + HDV, HCV) risk of cirrhosis development risk of hepatocellular carcinoma development Fulminant (HBV, HCV)

36 Acute hepatitis Gross finding – oedematous, red liver
Microscopic finding focal necrosis bridging necrosis panacinar/multiacinar necrosis periportal necrosis Hepatocytes polymorphism balooning degeneration

37 Acute hepatitis Inflammation polynuclear/mononuclear infiltration
activation of Kupfer’s cells Other changes cholestasis damage of bile ducts Regeneration

38 Fulminant hepatitis Gross finding - soft consistency
Microscopic finding – complete necrosis of parenchyma Course liver failure - coma - death regeneration – postnecrotic cirrhosis

39 Acute hepatitis: HBV

40 Acute hepatitis

41 Acute hepatitis

42 Acute hepatitis

43 Acute hepatitis: regeneration

44 Fulminant hepatitis: HBV

45 Fulminant hepatitis: HBsAg, Orcein staining

46 Chronic hepatitis: etiology
HBV, HBV+HDV, HCV Autoimmune Drug induced Wilson’s disease a1 anti-trypsin deficiency Cryptogenic

47 Chronic hepatitis: clinical definition
Clinical symptoms of hepatitis more than: 6 months 12 months in HCV

48 Chronic hepatitis: morphology
Inflammation portal periportal lobular Necrosis/apoptosis piecemal bridging focal Fibrosis Deposits (Cu, PAS globules,…)

49 Chronic hepatitis - portal + steatosis, HCV

50 Chronic hepatitis: portal

51 Chronic hepatitis: periportal

52 Chronic hepatitis: periportal

53 Chronic hepatitis: HCV, transition into the cirrhosis

54 Autoimmune chronic hepatitis
Females, young/middle age Autoantibodies – ANA, AMA Autoimmune „overlap“ syndromes lupus erythematodes arthritis

55 Autoimmune chronic hepatitis - ANA

56 Autoimmune chronic hepatitis - AMA

57 NASH: non-alcoholic steatohepatitis
Hepatomegaly Increase of aminotransferases Histological picture – similar to alcoholic hepatitis without alcohol consumption macrovesicular steatosis lobular hepatitis and necrosis balooning of hepatocytes fibrosis

58 NASH: non-alcoholic steatohepatitis
Epidemiologic signs of NASH Females Obesity DM of II type, hyperglycaemia

59 NASH: non-alcoholic steatohepatitis
Diseases related to NASH Acquired metabolic diseases (obesity, DM, hyperlipidemia, parenteral nutrition) Inherited metabolic diseases (Wilson’s disease, abetalipoproteinaemia, tyrosinaemia) Surgery (jejunoileal bypass, extensive resections of small intestine...) Drugs, toxins (amiodarone, glucocorticoids, tamoxifen, synthetic estrogens…)

60 Toxic and drug induced liver damage
Anorganic substances Organic substances Industrial and plant substances Poisons/venoms Drugs Alcohol

61 Toxic and drug induced liver damage: effect
Expectable Non-expectable (idiosyncratic)

62 Toxic and drug induced liver damage : forms
Necrosis Steatosis macrovesicular (alcohol, corticoids) microvesicular (tetracyklin, aspirine) Cholestasis (steroids-anabolic, contraceptives) Hepatitis mild (aspirin, synthetic penicilines) Hepatitis serious (halotan) Chronic periportal hepatitis (sulphonamides)

63 Toxic and drug induced liver damage : forms
Granulomatous hepatitis (phenylbutazone) Vascular lesions (contraceptives, cytostatics) Hyperplasia, neoplasia (contraceptives)

64 Alcoholic Liver Disease (ALD)
Steatosis (90%) Fibrosis (perivenular, pericellular) Steatofibrosis Alcoholic hepatitis Alcoholic cirrhosis Mallory hyaline Cholestasis Siderosis Hepatocellular carcinoma Dif.dg: NASH

65 Alcoholic Liver Disease (ALD) : steatosis

66 Alcoholic Liver Disease (ALD) : steatosis

67 Alcoholic Liver Disease (ALD) : steatofibrosis

68 Alcoholic Liver Disease (ALD) : cholestasis

69 Alcoholic Liver Disease (ALD) : Mallory hyaline

70 Alcoholic Liver Disease (ALD) : Mallory hyaline

71 Alcoholic Liver Disease (ALD) : steatohepatitis

72 Alcoholic Liver Disease (ALD) : steatohepatitis

73 Alcoholic Liver Disease (ALD) : steatohepatitis, cholestasis, Mallory hyaline

74 Metabolic liver disease
Haemochromatosis Wilson’s disease a1 anti-trypsin deficiency Glycogenoses

75 Haemochromatosis Excessive accumulation of iron in parenchymatous organs Primary (idiopatic), secondary Cirrhosis, diabetes mellitus, pigmentation of skin Dif.dg. of brown pigment within the liver Fe (haemochromatosis) Cu (Wilson’s disease) lipopigment (brown atrophy of liver, lipopigment dystrophy)

76 Haemochromatosis

77 Haemochromatosis

78 Haemochromatosis

79 Brown atrophy of liver: dif.dg.

80 Wilson’s disease Hepatolenticular degeneration
Low levels of ceruloplasmin Increase of Cu in liver and urine Morphology steatosis acute hepatitis chronic hepatitis glycogen nucleus (also typical in DM) increased amount of Cu pigment

81 Wilson’s disease : Cu pigment

82 Wilson’s disease/DM: glycogen nucleus

83 Wilson’s disease/DM: glycogen nucleus

84 a1 anti-trypsin deficiency
Low levels of a1AT (inhibitor of proteases) Emphysema of lungs Liver changes (cholestasis, cirrhosis) PAS positive acidophilic globular inclusions in the cytoplasm ELMI – complementary diagnosis

85 Circulatory disorders of the liver
Disorders of arterial system Disorders of portal system Disorders of venous system Disorders of lobular system

86 Disorders of arterial system
Infarct of the liver Rare Thrombosis, compression, obliteration of a. hepatis branch (polyarteritis nodosa,…) Pale Dif.dg.: Zahn infarct (occlusion of intrahepatic branch of v. portae): no necrosis, local congestion of sinusoids and secondary atrophy

87 Liver infarct

88 Disorders of portal system
Thrombosis and occlusion of v.portae Extrahepatal (phlebitis, pancreatitis, surgery, trauma) Intrahepatal (invasion of tumor)

89 Thrombosis of v.portae

90 Disorders of venous system
Thrombosis of hepatic veins (Budd-Chiari syndrome) causes: polycytemia vera, pregnancy, contraceptives, intraabdominal malignant tumors, hepatocellular carcinoma centrilobular necrosis and congestion, fibrosis Venoocclusive disorder complication of bone marrow transplantation (5-25%) – chemotherapy, radiotherapy Bush-tea (pyrrolizidine alcaloids) obliteration of hepatic veins – subendothelial accumulation of colagen and reticulin, perivenular fibrosis, perivenular hemosiderin

91 Budd-Chiari

92 Disorders of lobular system
Occlusion of sinuses eclampsy Sickle cell anaemia Systemic circulation passive congestion centrilobular necrosis nutmeg liver (venostasis/steatosis)

93 Congestion

94 Pathology of intrahepatal bile ducts
Secondary biliary cirrhosis (SBC) Primary biliary cirrhosis (PBC) Primary sclerosing cholangitis (PSC)

95 SBC Obstruction of extrahepatal bile ducts: atresia, lithiasis, tumor, iatrogenic Striking cholestasis

96 PBC Autoimmune (AMA), Majority of females
Coincidency: Sjögren sy., arthritis, thyreoiditis, vasculitis,.. Hepatomegaly, 4 stages I - granulomatous destruction of ducts II - ductular proliferation and periportal hepatitis III - scarring, necrosis, septal fibrosis IV - cirrhosis

97 PSC Autoimmune (ANA) Inflammation and obliterative fibrosis of bile ducts Coincidency: IBD (Inflammatory Bowel Disease – ulcerative colitis, m.Crohn)

98 PBC: I.stage

99 PBC: I.stage

100 PBC: II.stage

101 PBC: III.stage

102 Patology of liver during pregnancy
Preeclampsy/eclampsy HELLP syndrome: Hemolysis, Elevated Liver enzymes, Low Platelets fibrin within the sinusoids hematomas (fatal rupture of liver) Acute microvesicular steatosis during pregnacy (third trimester) Cholestasis during pregnancy (third trimester)

103 Transplantation Liver disorders related to bone marrow transplantation
Liver disorders related to liver transplantation

104 Liver disorders related to bone marrow transplantation
Time Cause Before transplantation Viral hepatitis Tumor infiltration Day 0-25 Drug related damage Venoocclusive disease Day Acute GVHD (destruction of bile ducts, endothelitis, necrosis of hepatocytes) Opportune infections Day 100- Chronic GVHD (involvement of portal tracts, destruction of bile ducts, endothelitis) Fulminant hepatitis („rebound“ phenomenona)

105 Liver disorders related to liver transplantation
Time Cause 1. week Acute rejection (necrosis, inflammation) Technical complication (vascular anastomoses…) Non-functionality (primary) 2. week-2. month Opportune infections Acute rejection Drug related damage 2. month - Chronic vascular rejection (vasculitis) Vanishing bile ducts syndrome Viral hepatitis

106 Tumors of liver Tumor-like lesion Benign tumors Malignant tumor

107 Tumor-like lesions Focal nodular hyperplasia
Nodular regeneratory hyperplasia (lack of fibrosis) Cysts Hamartoma (von Meyenburg complex) Inflammatory pseudotumor

108 Nodular regeneratory hyperplasia

109 Benign tumors Adenoma hepatocellular (lack of portal tracts!)
cholangiogenic (lack of bile production, less than 1cm, subcapsular) Haemangioma subcapsular cavernous bleeding risk during punction!

110 Cavernous haemangioma

111 Malignant tumors Hepatocellular carcinoma (HCC)
subvariant – fibrolamelar carcinoma Cholangiogenic carcinoma (lack of bile production) peripherial extrahepatal -Klatskin tumor Hepatoblastoma (embryonal, teratoid,…) Angiosarcoma, malignant haemangioendothelioma Metastases (most often) GIT, lung, kidney

112 HCC

113 HCC

114 HCC

115 HCC

116 Cholangiogenic carcinoma

117 Biliary system: cholelithiasis
10-20% of population Cholesterol concrements (females, obesity, steroids, hyperlipidemia) Pigmented/bilirubine concrements (biliary infection, haemolysis) Blockage of bile ducts (acute cholangoitis, sepsis, biliary cirrhosis, pancreatitis) Irritation of gallbladder (cholecystitis, carcinoma) Valve-like blockage (hydrops) Perforation, fistula

118 Cholecystolithiasis

119 Cholecystolithiasis

120 Cholecystitis Acute empyema of gallbladder gangrenous cholecystitis
acalculous cholecystitis (postoperative, trauma, burns, sepsis,…) Chronic fibroproduction (thickening of the wall, adhesion) chronic inflammmation dystrophic calcification (risk of carcinoma development) hydrops

121 Chronic cholecystitis

122 Carcinoma of gallbladder
Adenocarcinoma Infiltrating Exophytic Early invasion into the liver – poor prognosis!

123 Carcinoma of gallbladder

124 Other disorders of biliary system
Atresia of bile ducts (rapid progression, uncelar etiopathogenesis, cirrhosis) Cholesterolosis (strawberry gallbladder) Choledocholithiasis (risk of ascendent cholangoitis, intrahepatic abscess and sepsis, risk of biliary cirrhosis) Tumors of papilla Vateri (ampuloma, periampular carcinoma – difficult diagnosis)

125 Exocrine pancreas: acute pancreatitis
Causes cholelithiasis, alcohol, surgery, trauma, idiopathic Most serious form acute haemorrhagic necrotizing pancreatitis Morphology nekrosis of pancreas nekrosis of fat tissue (steatocytonecrosis, Balzer’s necrosis) haemorrhagy Complication, healing abscesses pseudocysts duodenal obstruction multiorgan failure

126 Pancreatonecrosis

127 Pancreatonecrosis

128 Steatocytonecrosis: omentum

129 Steatocytonecrosis: omentum

130 Exocrine pancreas: chronic pancreatitis
Causes alcohol, hyperlipidemia, hypercalcemia, hereditary Morphology fibrosis reduction of acines obstruction of ducts chronic inflammatory infiltration (lymphocytes, plasmocytes) Complications calcifications, pseudocysts, thrombosis v . lienalis diabetes steatorrhea jaundice

131 Chronic pancreatitis

132 Exocrine pancreas: tumors
Cystic tumors (5%) mucinous cystadenoma mucinous cystadenocarcinoma Carcinoma of pancreas Adenocarcinoma, various degree of differentiation Head (early diagnosis - jaundice), body, tail (difficult diagnosis, late detection) Often - fibroproduction (dif.dg. chron.pancreatitis) Trosseau syndrome – migratory thrombophlebitis in 10%

133 Carcinoma of pancreas

134 Carcinoma of pancreas

135


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