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18 Cards in this Set
- Front
- Back
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 |
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) |