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Faculty of allied medical sciences. Histopathology and cytology (MLHC-201). Liver Pathology. Supervision: Prof.Dr.Noha Ragab. Outcomes. By the end of this lecture, the student will be able to know: 1-The meaning and causes of jaundice 2-Bilary tract obstruction 3-Cirrhosis - PowerPoint PPT Presentation

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Histopathology and cytologyHistopathology and cytology

((MLHC-201MLHC-201))

Faculty of allied medical Faculty of allied medical sciencessciences

SupervisionSupervision::

Prof.Dr.Noha RagabProf.Dr.Noha Ragab

Liver PathologyLiver Pathology

By the end of this lecture, the student By the end of this lecture, the student will be able to knowwill be able to know::

1-The meaning and causes of jaundice1-The meaning and causes of jaundice

2-Bilary tract obstruction2-Bilary tract obstruction

3-Cirrhosis3-Cirrhosis

4-Viral hepatitis and its types4-Viral hepatitis and its types

OutcomesOutcomes

The liver is the largest The liver is the largest parenchymal organ, parenchymal organ, lying just below the lying just below the diaphragm. diaphragm.

The right lobe is larger The right lobe is larger than the left lobe. than the left lobe.

The falciform ligament The falciform ligament is the rough dividing is the rough dividing line between the two line between the two lobeslobes. .

This is the external This is the external surface of a normal surface of a normal liver. liver.

The color is brown The color is brown and the surface is and the surface is smooth.smooth.

A normal liver A normal liver weighs about 1200 weighs about 1200 to 1600 grams. to 1600 grams.

JaundiceJaundice

JaundiceJaundice

Clinically jaundice occurs with Clinically jaundice occurs with bilirubin levels >2-3 mg/dlbilirubin levels >2-3 mg/dl

Clinical presentation:Clinical presentation: Yellow skin (jaundice) and sclera Yellow skin (jaundice) and sclera

(icterus)(icterus)

Yellow skin (jaundice)Yellow skin (jaundice)

Yellow sclera (icterus)Yellow sclera (icterus)

Causes of jaundiceCauses of jaundice::

1.1. Overproduction of bilirubinOverproduction of bilirubin

2.2. Defective hepatic bilirubin uptakeDefective hepatic bilirubin uptake

3.3. Defective conjugationDefective conjugation

4.4. Defective execretion Defective execretion

Increased RBC’s turnoverIncreased RBC’s turnover:: RBCs are a major source of bilirubinRBCs are a major source of bilirubin

Eitiology:Eitiology:1.1. Hemolytic anemiaHemolytic anemia2.2. Ineffective erythropoiesis (Thalassaemia, Ineffective erythropoiesis (Thalassaemia,

megaloblastic aneamia, etc.)megaloblastic aneamia, etc.)3.3. Chronic hemolytic anemia patients often Chronic hemolytic anemia patients often

develop pigmented bilirubinated gallstones develop pigmented bilirubinated gallstones

Laboratory:Laboratory: increased unconjugated bilirubinincreased unconjugated bilirubin

Physiological jaundice of the Physiological jaundice of the new bornnew born

Definition:Definition: transient unconjugated transient unconjugated hyperbilirubinaemia due to the hyperbilirubinaemia due to the immaturity of the liverimmaturity of the liver

Risk factors:Risk factors: PrematurityPrematurity Hemolytic disease of new born Hemolytic disease of new born

(erythroblastosis fetalis)(erythroblastosis fetalis)

Complication:Complication: kernicteruskernicterus

Biliary tract Biliary tract obstructionobstruction

Biliary tract obstructionBiliary tract obstruction

Eitiology:Eitiology:1.1. GallstonesGallstones

2.2. Tumors (pancreatic, gallbladder and Tumors (pancreatic, gallbladder and bile duct)bile duct)

3.3. StricturesStrictures

4.4. Parasites (liver flukes or fasciola)Parasites (liver flukes or fasciola)

Clinical presentationClinical presentation::1.1. JaundiceJaundice

2.2. Pruritus due to increased plasma levels Pruritus due to increased plasma levels of bile acidsof bile acids

3.3. Abdominal pain, fever and chillsAbdominal pain, fever and chills

4.4. Dark urine (bilirubinuria)Dark urine (bilirubinuria)

5.5. Pale clay colored stoolsPale clay colored stools

Laboratory investigation:Laboratory investigation: Elevated conjugated bilirubinElevated conjugated bilirubin Elevated alkaline phosphataseElevated alkaline phosphatase

CIRRHOSISCIRRHOSIS

CIRRHOSISCIRRHOSIS

Definition:Definition:

End stage liver disease characterized End stage liver disease characterized by distruption of the liver by distruption of the liver architecture by bands of fibrosis that architecture by bands of fibrosis that divide the liver into nodules of divide the liver into nodules of regenerating liver parenchymaregenerating liver parenchyma

Etiology (Causes of Cirrhosis):Etiology (Causes of Cirrhosis):1.1. AlcoholAlcohol

2.2. Viral hepatitisViral hepatitis

3.3. Biliary tract diseaseBiliary tract disease

4.4. HemochromatosisHemochromatosis

5.5. IdiopathicIdiopathic

Grossly:Grossly:1.1. Micronodular nodulesMicronodular nodules

2.2. Macronodular nodulesMacronodular nodules

3.3. Mixed micronodular and macronodularMixed micronodular and macronodular

4.4. At the end stage , the disease results At the end stage , the disease results in mixed pattern, and the etiology may in mixed pattern, and the etiology may not be distinguished based on the not be distinguished based on the appearanceappearance

“Macronodular" cirrhosis

Micronodular cirrhosis

CIRRHOSISCIRRHOSIS

ComplicationsComplications::

A- Portal hypertension:A- Portal hypertension:1.1. AscitisAscitis

2.2. SplenomegalySplenomegaly

3.3. Esophageal varicesEsophageal varices

4.4. HaemorrhoidsHaemorrhoids

5.5. Caput MedusaCaput Medusa

SplenomegalySplenomegaly

Esophageal Varices Esophageal Varices are seen here in the are seen here in the lower esophagus as lower esophagus as linear blue dilated linear blue dilated veins. veins.

There is hemorrhage There is hemorrhage around one of them. around one of them.

Such varices are Such varices are easily eroded, leading easily eroded, leading to massive to massive gastrointestinal gastrointestinal hemorrhagehemorrhage. .

“Caput medusae" which consists of dilated veins seen on the abdomen of a patient with cirrhosis of the liver

B- Decreased detoxification:B- Decreased detoxification:1.1. Hepatic encephalopathyHepatic encephalopathy

2.2. Spider angiomataSpider angiomata

3.3. Palmar erythemaPalmar erythema

4.4. GynecomastiaGynecomastia

C- Decreased synthesisC- Decreased synthesis1.1. HypoalbuminemiaHypoalbuminemia

2.2. Decreased clotting factorsDecreased clotting factors

D- Hepato-renal syndromeD- Hepato-renal syndrome

VIRAL HEPATITISVIRAL HEPATITIS

Clinical presentationClinical presentation::

1.1. AsymptomaticAsymptomatic

2.2. Malaise and weaknessMalaise and weakness

3.3. Nausea and anorexiaNausea and anorexia

4.4. JaundiceJaundice

5.5. Urine may be darkUrine may be dark

Laboratory investigations:Laboratory investigations: Markedly elevated alanine Markedly elevated alanine

aminotransferase (ALT) and aminotransferase (ALT) and aspartate aminotransferase (AST) aspartate aminotransferase (AST)

Acute viral hepatitisAcute viral hepatitis

Definition:Definition:

Signs and symptoms less than six Signs and symptoms less than six monthsmonths

Eitiology:Eitiology:

Any hepatitis virusesAny hepatitis viruses

MicroscopicallyMicroscopically::

1.1. Lobar disarrayLobar disarray

2.2. Hepatocytes swelling (balloon cells)Hepatocytes swelling (balloon cells)

3.3. Apoptotic hepatocytes Apoptotic hepatocytes (councilman(councilman’’s bodies)s bodies)

4.4. Lymphocytes in portal tract and in Lymphocytes in portal tract and in the lobulesthe lobules

5.5. Hepatocytes regenerationHepatocytes regeneration

6.6. cholestasischolestasis

Chronic viral hepatitisChronic viral hepatitis

Definition:Definition:

Signs and symptoms more than six Signs and symptoms more than six monthsmonths

Eitiology:Eitiology:

Caused by hepatitis virus B, C and DCaused by hepatitis virus B, C and D

Microscopically:Microscopically: Chronic persistant hepatitis Chronic persistant hepatitis

inflammation confined to the portal inflammation confined to the portal tractstracts

Chronic active hepatitis inflammation Chronic active hepatitis inflammation spills into the parenchyma causing spills into the parenchyma causing interface hepatitis (piecemeal interface hepatitis (piecemeal necrosis)necrosis)

Hepatitis B often has a ground glass Hepatitis B often has a ground glass hepatocyteshepatocytes

• A large pink cell undergoing "ballooning degeneration" is seen below the right arrow. • At a later stage, a dying hepatocyte is seen shrinking down to form an eosinophilic "councilman body" below the arrow on the left.

ballooning degeneration

councilman body

CompleteComplete::

1-1-Causes of jaundice are…………………….Causes of jaundice are…………………….

2-2-Causes of cirrhosis are……………………Causes of cirrhosis are……………………

3-3-…………. Transient unconjugated …………. Transient unconjugated hyperbilirubinaemia due to the immaturity of the hyperbilirubinaemia due to the immaturity of the liverliver

4-4-Chronic active hepatitis inflammation spills into Chronic active hepatitis inflammation spills into the parenchyma causing …………….the parenchyma causing …………….

5-5-Biliary tract obstruction is caused by…………Biliary tract obstruction is caused by…………

Questions:Questions:

THANK YOUTHANK YOUANDAND

GOOD LUCKGOOD LUCK

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