Gi System- Hepatitis I & Ii And Jaundice By Leech

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GI System- Hepatitis I & II And Jaundice by Leech

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GI System- Hepatitis I & II And Jaundice by Leech

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Functions of the liver

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1. Largest gland of body – 1-2 kg
2. Exocrine function -> bile
3. Receives most absorbed nutrients via portal vein
4. Functions in fat, carbohydrate, protein metabolism
5. Stores glycogen
6. Detoxifies

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Injury may result in...

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1. Inflammation – acute, chronic inflammatory cells; granulomas
2. Degeneration – swelling & edema of hepatocytes
3. Necrosis - 2° to almost any insult – may be focal-> massive
4. Regeneration – usually in all but most severe
5. Fibrosis - 2° to inflammation or direct toxic insult

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Jaundice

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-bilirubin levels > 2-3 mg/dl
-yellow skin and sclera

causes:
-overproduction of bilirubin
-defective hepatic bilirubin uptake
-defective conjugation
-defective excretion

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Unconjugated (Indirect) Bilirubinemia

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- inc RBC turnover
- physiologic (newborn babies)
- hereditary (gilbery and crigler-najjar syndromes)

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Conjugated (Direct) Bilirubinemia

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-Biliary tract obstruction
-Biliary tract disease (PSC and PBC)
-Hereditary (Dubin-Johnson and Rotor’s syndromes)
-Liver disease (cirrhosis and hepatitis)

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major source of bilirubin:

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Increased RBC turnover
RBCs are the major source of bilirubin

Etiology:
-Hemolytic anemia
-Ineffective erythropoiesis (thalassemia, megaloblastic anemia, etc.)

Lab: increased unconjugated bilirubin
Chronic hemolytic anemia patients often develop pigmented bilirubinate gallstones

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Physiologic jaundice of the newborn

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Definition: transient unconjugated hyperbilirubinemia due to the immaturity of the liver

Risk factors
Prematurity
Hemolytic disease of the newborn (erythroblastosis fetalis)

Complication: kernicterus
Treatment: phototherapy

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Gilbert’s syndrome

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Hereditary hyperbilirubinemias

Gilbert’s syndrome:
Common benign inherited disorder
Unconjugated hyperbilirubinemia
Jaundice is related to STRESS (fasting, infection, etc.)
Mechanism: bilirubin glucuronosyltransferase (UGT) deficiency
No clinical consequences

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Crigler-Najjar syndrome

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Hereditary hyperbilirubinemias
Crigler-Najjar syndrome
Unconjugated hyperbilirubinemia
Type I: fatal because of kernicterus (**one of the only ones with clinical significance... all others are not harmful)
Type II: jaundice
Mechanism: bilirubin glucuronosyltransferase (UGT) absence or deficiency

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Dubin-Johnson syndrome

what do you see gross

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Hereditary hyperbilirubinemias (con’t.)
Dubin-Johnson syndrome
Benign autosomal recessive disorder
Decreased bilirubin excretion due to a defect in the canalicular transport protein
Conjugated hyperbilirubinemia
Gross: black pigmentation of the liver
No clinical consequences

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Rotor’s syndrome

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Hereditary hyperbilirubinemias (con’t.)
Rotor’s syndrome
Autosomal recessive
Conjugated hyperbilirubinemia
Similar to Dubin-Johnson but WITHOUT liver pigmentation
No clinical consequences

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Biliary Tract obstruction

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Etiology:
Gallstones, Tumors (pancreatic, gallbladder, and bile duct), Stricture
Parasites (liver flukes – Clonorchis [Opisthorchis] sinensis)

Presentation:
Jaundice and icterus
Pruritus due to increased plasma levels of bile acids
Abdominal pain, fever, and chills
Dark urine (bilirubinuria) & Pale clay-colored stools

Lab:
Elevated conjugated bilirubin, alkaline phosphatase and 5’-nucleotidase

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Primary biliary cirrhosis (PBC)

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Definition: chronic liver disease of unknown etiology (autoimmune) characterized by inflammation and granulomatous destruction of intrahepatic bile ducts
Epidemiology: males:females=1:10; age 30 – 65

Presentation:
Middle-age females, Obstructive jaundice, Pruritus, Xanthomas, xanthelasmas, and elevated serum cholesterol, Fatigue, Cirrhosis (late complication

Lab:
Elevated conjugated bilirubin
Elevated alkaline phosphatase and 5’-nucleotidase
Antimitochondrial autoantibodies (AMA) are present in more than 90%

Most patients have another autoimmune disease (scleroderma, RA, or SLE)
Micro: lymphocytic and granulomatous destruction of interlobular bile ducts

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Primary sclerosing cholangitis (PSC)

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Definition: chronic liver disease of unknown etiology characterized by segmental inflammation and fibrosing destruction of intrahepatic bile ducts
Epidemiology: Males:females= 2:1, age 20 – 40
Majority are associated with ulcerative colitis
Presentation: similar to PBC
Micro: Periductal chronic inflammation
-Concentric fibrosis around bile ducts
-Segmental stenosis of bile ducts
Cholangiogram: “beaded appearance” of bile ducts
Complications: biliary cirrhosis and cholangiocarcinoma

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Hepatitis viruses

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Clinical presentation
Asymptomatic
Malaise and weakness
Nausea and anorexia
Jaundice
Urine may be dark

Lab: markedly elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST)

Diagnosis: serology

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Acute viral hepatitis

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Definition: signs and symptoms < 6 months
Caused by any of the hepatitis viruses

Micro:
Lobular disarray
Hepatocyte swelling (balloon cells)
Apoptotic hepatocytes (Councilman’s bodies)
Lymphocytes in portal tracts and in the lobule
Hepatocyte regeneration
cholestasis

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Chronic viral hepatitis

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Definition: signs and symptoms > 6 months
Caused by hepatitis virus B, C, and D

Micro
Chronic persistent hepatitis: inflammation confined to portal tracts
Chronic active hepatitis: Inflammation spills into the parenchyma, causing an interface hepatitis (piecemeal necrosis of limiting plate).
Hepatitis B often has “ground glass” hepatocytes (cytoplasmis HBsAg)