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Diseases of liver

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Clinical features of hepatic failureJaundiceHypoalbuminemiaCoagulopathyDICFetor hepaticusIncreased serum levels of hepatic enzymesGynecomastiaHepatic encephalopathyHepatorenal syndrome

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Слайд 1Diseases of liver

Diseases of liver

Слайд 6Clinical features of hepatic failure
Jaundice
Hypoalbuminemia
Coagulopathy
DIC
Fetor hepaticus
Increased serum levels of hepatic

enzymes
Gynecomastia
Hepatic encephalopathy
Hepatorenal syndrome

Clinical features of hepatic failureJaundiceHypoalbuminemiaCoagulopathyDICFetor hepaticusIncreased serum levels of hepatic enzymesGynecomastiaHepatic encephalopathyHepatorenal syndrome

Слайд 7Diseases of liver
The liver is vulnerable to a wide variety

of metabolic, toxic, microbial, circulatory, and neoplastic insults. In some

instances, the disease is primary to the liver, as in viral hepatitis and hepatocellular carcinoma. More often the hepatic involvement is secondary, often to some of the most often diseases in humans, such as cardiac decompensation, disseminated cancer, alcoholism, and extrahepatic infections.
Diseases of liverThe liver is vulnerable to a wide variety of metabolic, toxic, microbial, circulatory, and neoplastic

Слайд 8MORPHOLOGIC PATTERNS OF HEPATIC INJURY
Regardless of cause, five general reactions

may occur:
Necrosis.
Degeneration.
Inflammation.
Regeneration.
Fibrosis.

MORPHOLOGIC PATTERNS OF HEPATIC INJURYRegardless of cause, five general reactions may occur:Necrosis. Degeneration.Inflammation. Regeneration. Fibrosis.

Слайд 9Types of liver diseases
Hepatosis
Hepatitis
Cirrhosis
Tumors of liver

Types of liver diseasesHepatosisHepatitisCirrhosisTumors of liver

Слайд 10Hepatoses

Hepatoses

Слайд 11Hepatoses – group of diseases characterized by dystrophy and necrosis

of hepatocytes
Chronic
Fatty degeneration
Hepatoses

Acute
Massive progressive necrosis
of the liver
(toxic dystrophy of

the liver)
Hepatoses –  group of diseases characterized by dystrophy and necrosis of hepatocytesChronicFatty degenerationHepatosesAcuteMassive progressive necrosis of

Слайд 12Massive progressive necrosis of liver
Etiology:
exogenous factors-fungi, food toxins, arsenic.
Endogenous-gestosis

of pregnancy, thyrotoxicosis
Pathogenesis-toxic substances affect the hepatocytes direсtly, mainly in

the central part of lobules.

Massive progressive  necrosis of liverEtiology: exogenous factors-fungi, food toxins, arsenic.Endogenous-gestosis of pregnancy, thyrotoxicosisPathogenesis-toxic substances affect the

Слайд 13Massive progressive necrosis of the liver
Morphogenesis:
Stage of yellow degeneration
1-

2 week

Stage of red degeneration –
3 week

Massive progressive necrosis of the liverMorphogenesis:Stage of yellow degeneration 1- 2 weekStage of red degeneration – 3

Слайд 16Massive hepatic necrosis with bleeding diathesis

Massive hepatic necrosis with bleeding diathesis

Слайд 17Massive centrilobular necrosis

Massive centrilobular necrosis

Слайд 18Necrosis

Necrosis

Слайд 19Steatosis (Fatty degeneration)

Steatosis  (Fatty degeneration)

Слайд 20Fatty hepatosis
Etiology: alcohol, medicines, metabolic disorders (diabetes mellitus, defective protein

nutrition, excessive fat consumption), cardiac insufficiency, anemia.
Morphology: in hepatocytes

appear fat droplets, which can be small or big.
Fatty hepatosisEtiology: alcohol, medicines, metabolic disorders (diabetes mellitus, defective protein nutrition, excessive fat consumption), cardiac insufficiency, anemia.

Слайд 21Stages of development
Ordinary (simple) obesity
Obesity in combination with the necroses

of hepatocytes and mesenchymal-cellular reaction
Obesity in combination with the reorganization

of tissue
Outcome: portal cirrhosis of the liver
Stages of developmentOrdinary (simple) obesityObesity in combination with the necroses of hepatocytes and mesenchymal-cellular reactionObesity in combination

Слайд 24Fatty Change And Early Cirrhosis

Fatty Change And Early Cirrhosis

Слайд 25Hepatitis

Hepatitis

Слайд 26Viral hepatitis
Etiology: Viruses hepatitis A,B,C,D…

Viral hepatitis is reserved for infection


of the liver caused by a small (but growing) group

of viruses having a particular affinity for the liver.

Viral hepatitisEtiology: Viruses hepatitis A,B,C,D…Viral hepatitis is reserved for infection of the liver caused by a small

Слайд 27Hepatitis A Virus does not cause chronic hepatitis or a

carrier state and only rarely causes fulminant hepatitis, and so

the fatality rate associated with Hepatitis A Virus is about 0.1 %.
Hepatitis В Virus can produce 1) acute hepatitis, 2) chronic nonprogressive hepatitis, 3) progressive chronic disease ending in cirrhosis, 4) fulminant hepatitis with massive liver necrosis, and 5) an asymptomatic carrier state with or without progressive disease. Furthermore, Hepatitis В Virus plays an important role in the development of hepatocellular carcinoma.
Hepatitis A Virus does not cause chronic hepatitis or a carrier state and only rarely causes fulminant

Слайд 28Transfusion, blood products, dialysis, needle-stick accidents among health care workers,

intravenous drug abuse, and homosexual activity constitute primary risk categories

for Hepatitis В Virus infection.
Hepatitis С Virus has a high rate of progression to chronic disease and eventual cirrhosis, exceeding 50 %.

Transfusion, blood products, dialysis, needle-stick accidents among health care workers, intravenous drug abuse, and homosexual activity constitute

Слайд 29Whatever the agent is, the disease is more or less

the same and can be divided into four phases:
1) an

incubation period,
2) a symptomatic preicteric phase,
3) a symptomatic icteric phase, and
4) convalescence.
Whatever the agent is, the disease is more or less the same and can be divided into

Слайд 30Forms of viral hepatitis
Cyclic icteric
Non-icteric
Cholestatic
Necrotic
Chronic (active and persistent)

Forms of viral hepatitisCyclic ictericNon-ictericCholestaticNecroticChronic (active and persistent)

Слайд 31Morphological signs
Protein degeneration
Proliferation of Kupffer cells
Lymphohistiocytic infiltration
Councilman bodies (

necrotic hepatocytes may be evident as fragmented, eosinophilic bodies оr

may be phagocytosed, leading to the accumulaton of clumps of lymphocytes and macrophages.
Morphological signs Protein degenerationProliferation of Kupffer cellsLymphohistiocytic infiltrationCouncilman bodies ( necrotic hepatocytes may be evident as fragmented,

Слайд 32Signs of acute hepatitis

Signs of acute hepatitis

Слайд 33Cell infiltration

Cell infiltration

Слайд 34Necrotic hepatocytes

Necrotic hepatocytes

Слайд 35Hepatitis (NECROTIC FORM)

Hepatitis (NECROTIC FORM)

Слайд 36Acute hepatitis with secondary submassive necrosis (NECROTIC FORM) Nodule formation reflects regenerative

activity.

Acute hepatitis with secondary submassive necrosis (NECROTIC FORM) Nodule formation reflects regenerative activity.

Слайд 37Hepatitis B virus infection Hepatitis B virus produces intranuclear inclusions.

Hepatitis B virus infection Hepatitis B virus produces intranuclear inclusions.

Слайд 38Cholestatic form

Cholestatic form

Слайд 39CHRONIC HEPATITIS
Symptomatic, biochemical or serologic evidence of continuing or relapsing

hepatic disease for more than 6 months, optimally with histologically

documented inflammation and necrosis, is taken to mean chronic hepatitis.
CHRONIC HEPATITISSymptomatic, biochemical or serologic evidence of continuing or relapsing hepatic disease for more than 6 months,

Слайд 40etiologic forms of hepatitis
Hepatitis A Virus: Extremely rare.
Hepatitis В

Virus: Develops in more than 90% of infected neonates and

5 % of infected adults, of whom one-fourth progresses to cirrhosis.
Hepatitis С Virus: Develops in more than 50 % of infected patients, of whom half progresses to cirrhosis.
Hepatitis D Virus: Rare in acute Hepatitis D Virus/ Hepatitis В Virus coinfection; a more severe chronic hepatitis is the most frequent outcome of Hepatitis D Virus superinfection.
Hepatitis E Virus: Does not produce chronic hepatitis.
etiologic forms of hepatitis Hepatitis A Virus: Extremely rare.Hepatitis В Virus: Develops in more than 90% of

Слайд 41Since 1968, chronic hepatitis has been classified according to the

extent of inflammation:
1. Chronic persistent hepatitis, in which inflammation is

confined to the portal tracts.
2. Chronic active hepatitis, in which portal tract inflammation spills into the parenchyma and surrounding regions of necrotic hepatocytes.
3. Chronic lobular hepatitis, in which persistent inflammation is confined to the lobule.
Since 1968, chronic hepatitis has been classified according to the extent of inflammation:1. Chronic persistent hepatitis, in

Слайд 42Chronic active hepatitis Liver shows significant collapse indicative of progression to

cirrhosis.

Chronic active hepatitis Liver shows significant collapse indicative of progression to cirrhosis.

Слайд 43Chronic hepatitis

Chronic hepatitis

Слайд 44Chronic active hepatitis The limiting plate regions are blurred due to

an inflammatory infiltrate.

Chronic active hepatitis The limiting plate regions are blurred due to an inflammatory infiltrate.

Слайд 45Chronic persistent hepatitis Chronic viral hepatitis manifests as a portal inflammatory

infiltrate.

Chronic persistent hepatitis Chronic viral hepatitis manifests as a portal inflammatory infiltrate.

Слайд 46ALCOHOLIC LIVER DISEASE

ALCOHOLIC LIVER DISEASE

Слайд 48 Alcoholic hepatitis

Alcoholic hepatitis

Слайд 49Markers of AH
Fatty dystrophy and necrosis of hepatocytes
Alcoholic hyaline

( Mallory bodies)
Prevalence of neutrophils in the infiltrate

Markers of AHFatty dystrophy and necrosis of hepatocytes Alcoholic hyaline ( Mallory bodies)Prevalence of neutrophils in the

Слайд 50Alcoholic hepatitis with Mallory's hyaline

Alcoholic hepatitis with Mallory's hyaline

Слайд 51Alcoholism: fatty change and Mallory bodies

Alcoholism: fatty change and Mallory bodies

Слайд 52Alcoholic hyaline

Alcoholic hyaline

Слайд 54Cirrhosis
Is chronic disease of liver which is characterized by hepatic

failure due to structural reorganization of liver.
Cirrhosis is among

the top ten causes of death in the world, largely the result of alcohol abuse, chronic hepatitis and biliary disease.
CirrhosisIs chronic disease of liver which is characterized by hepatic failure due to structural reorganization of liver.

Слайд 55This end stage of liver disease is defined by three

characteristics:
- Fibrosis is present in the form of delicate bands

or broad scars replacing multiple adjacent lobules.
- The parenchymal architecture of the entire liver is disruptured by interconnecting fibrous scars.
- Parenchymal nodules are created by regeneration of hepatocytes, The nodules may vary from micronodules (less than 3 mm in diameter) to macronodules (3 mm to several centimeters in diameter).
This end stage of liver disease is defined by three characteristics:- Fibrosis is present in the form

Слайд 57Congenital biliary atresia

Congenital biliary atresia

Слайд 58Portal (micronodular) cirrhosis

Portal (micronodular) cirrhosis

Слайд 59Postnecrotic (macronodular) cirrhosis

Postnecrotic (macronodular) cirrhosis

Слайд 60Micronodular cirrhosis with portal hypertension and esophageal varices

Micronodular cirrhosis with portal hypertension and esophageal varices

Слайд 61Micronodular Cirrhosis

Micronodular Cirrhosis

Слайд 62Micronodular cirrhosis

Micronodular cirrhosis

Слайд 63Macronodular Cirrhosis

Macronodular Cirrhosis

Слайд 64Cirrhosis

Cirrhosis

Слайд 65Primary biliary cirrhosis Inflamed and destroyed bile ducts are characteristic of

this disorder.

Primary biliary cirrhosis Inflamed and destroyed bile ducts are characteristic of this disorder.

Слайд 66Portal areas contain an extensive scarring process obliterating vascular channels as

well as bile ducts.

Portal areas contain an extensive scarring process obliterating vascular channels as well as bile ducts.

Слайд 67Several features should be understood:
- The parenchymal injury and consequent

fibrosis are diffuse, extending throughout the liver; focal injury with

scarring does not constitute cirrhosis.
- Nodularity is requisite for the diagnosis and reflects the balance between regenerative activity and constrictive scarring.
Several features should be understood:- The parenchymal injury and consequent fibrosis are diffuse, extending throughout the liver;

Слайд 68Several features should be understood:
- Fibrosis, once developed, is generally

irreversible
- Vascular architecture is recognized by parenchymal damage and

scarring, with formation of abnormal interconnections between vascular inflow and hepatic vein outflow.
Several features should be understood:- Fibrosis, once developed, is generally irreversible - Vascular architecture is recognized by

Слайд 69 The ultimate mechanism of most cirrhotic deaths is :
1)

progressive liver failure,
2) a complication related to portal hypertension,
3)

the development of hepatocellular carcinoma.
The ultimate mechanism of most cirrhotic deaths is :1) progressive liver failure, 2) a complication related

Слайд 70The four major clinical consequences are :
1) ascites,
2) the

formation of portosystemic venous shunts,
3) congestive splenomegaly,
4) hepatic

ehcephalopathy.
The four major clinical consequences are :1) ascites, 2) the formation of portosystemic venous shunts, 3) congestive

Слайд 71Caput Medusae

Caput Medusae

Слайд 72Esophageal varices

Esophageal varices

Слайд 73Chronic cholestasis Accumulation of bile salts and their deposition in skin

leads to a strong itching stimulus.

Chronic cholestasis Accumulation of bile salts and their deposition in skin leads to a strong itching stimulus.

Слайд 74Cirrhosis

Cirrhosis

Слайд 75Macronodular Cirrhosis:

Macronodular Cirrhosis:

Слайд 76Liver cancer

Background disease – cirrhosis

Liver cancerBackground disease – cirrhosis

Слайд 77Anatomical forms

Nodular
Massive
Diffuse

Anatomical formsNodularMassiveDiffuse

Слайд 78Histological forms

Hepatocellular carcinoma

Cholangiocellular carcinoma


Histological formsHepatocellular carcinomaCholangiocellular carcinoma

Слайд 86Hepatocellular Carcinoma

Hepatocellular Carcinoma

Слайд 87Hepatocellular carcinoma with invasion of portal vein

Hepatocellular carcinoma with invasion of portal vein

Слайд 88Hepatocellular carcinoma

Hepatocellular carcinoma

Слайд 89Cholangiocarcinoma

Cholangiocarcinoma

Слайд 90Metastatic Carcinoma

Metastatic Carcinoma

Слайд 91The end

The end

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