Liver and Biliary Tract Pathology Liver Pathology, Lectures 1, 2, 3
|
|
- Audra Tucker
- 7 years ago
- Views:
Transcription
1 I. GENERAL MORPHOLOGIC & FUNCTIONAL PATTERNS OF HEPATIC INJURY A. ANATOMY 1. Gross Pathology The liver is the largest viscus of the body, usually contributing 1/50 of the entire body weight ( g) in adults and a much larger proportion (about 1/20), in the newborn child. It does not fall into the pelvis because of its firm attachment to the diaphragm by the coronary ligament, left & right triangular ligaments, and attachment to anterior body wall by the falciform ligament. Two-thirds of the blood supply to the liver comes from the portal vein, the other third comes from the hepatic artery. Blood drains into the hepatic veins and enters the inferior vena cava. 2. Microscopic Architecture a. Lobule: Classic hexagonal structure with portal tracts at the periphery and central vein (=terminal hepatic venule) at the center. b. Acinus: (Newer concept based on the hepatic microcirculation). The acini are roughly triangular with the bases being the terminal branches of the portal vein and hepatic artery and apices are the central vein (terminal hepatic venule). The acinus is divided into zones: i. Zone 1: Adjacent to portal venous system, richest in oxygen and nutrient supply. ii. Zone 2: Intermediate between 1 & 3 iii. Zone 3: At the apex, adjacent to the terminal hepatic venules; and affected most by anoxia and most toxins. B. FUNCTION The hepatocyte is unrivaled by any other parenchymal cell type in functional diversity and complexity. 1. Metabolic glucose homeostatis, lipid metabolism 2. Synthetic albumin, coagulation proteins I, II, V, VII-XIII, specific binding proteins 3. Storage glycogen, triglycerides, iron, copper, lipid and soluble vitamins 4. Catabolic ammonia->urea, contain hormones + proteins, detoxification of many foreign compounds, drugs and chemicals 5. Excretory bile excretion 6. Survival agenesis of the liver is incompatible with life - 1 -
2 C. LABORATORY ASSESSMENT OF LIVER FUNCTION 1. Serum Transaminases: Damaged cells leak contents into the circulation AST = Aspartate aminotransferase (SGOT) ALT = Alanine aminotransferase (SGPT) 2. Alkaline Phosphatase: Enzyme that exists as different isoenzymes in the liver, bone and intestine. In cholestatic disorders there is de novo synthesis which leaks into the circulation by undefined mechanisms. 3. Gamma Glutamyl Transpeptidase (GGT): Elevations in levels of this enzyme differentiate whether or not an elevated alkaline phosphatase is of liver or non-liver origin. GGT levels may be elevated in conditions other than liver disease such as in response to some chemicals and drugs, but when both GGT and alkaline phosphatase are elevated, the liver/biliary tree is the likely source of both of these elevated enzymes. 4. Bilirubin: Bilirubin is primarily a product of RBC destruction. Unconjugated bilirubin is roughly equal to "indirect bilirubin" as measured in the laboratory. It is toxic and may cross the blood brain barrier and in newborns result in kernicterus. Conjugated bilirubin is roughly equivalent to "direct bilirubin" as measured in the laboratory. It is non-toxic and can be excreted in the urine
3 D. BILIRUBIN METABOLISM Steps in Bilirubin Metabolism Etiology/Pathogenesis 1. Bilirubin production 1. Unconjugated hyperbilirubinemia Breakdown of senescent Increased destruction of rbcs RBC's - 70% -hemolytic anemia Hemoproteins - 30% -reabsorption of large hematoma -ineffective erythropoesis 2. Uptake/binding 2.Unconjugated hyperbilirubinemia Bilirubin is transported Impaired uptake/binding across the hepatocyte membrane -hepatocellular injury and is taken up by a protein carrier -drugs -newborns -Gilbert s 3. Conjugation 3. Unconjugated hyperbilirubenemia Bilirubin is released from Impaired Conjugation the ligand and its next -newborns conjugated with 2 molecules -Crigler-Najjar syndrome of glucoronic acid, catalyzed by -Gilbert s UDP glucoronosyl transferase 4. Excretion 4. Predominantly conjugated Conjugated bilirubin diffuses hyperbilirirubinemia through the cytosol to the -Dubin Johnson syndrome bile canaliculus where -Rotor s syndrome it is excreted into the bile -hepatocellular injury -toxins -intrahepatic bile duct disease -extrahepatic biliary disease 5. Eventually bile is excreted into the small bowel. Bacterial flora in the GI tract hydrolyses it to free bilirubin that is now unconjugated and reduced to a mixture of pyroles called urobilinogen. Most of the urobilinogen is excreted into feces, however, some returns via the enterohepatic circulation and is reexcreted in bile or in the urine. 6. Pathology: The pathologic features seen in the liver depend on the etiology of the hyperbilirubinemia of the hereditary hyperbilirubinemias, the most characteristic pathologic features are seen in Dubin Johnson syndrome which shows abundant pigmented granules within the hepatocyte cytoplasm and gives the liver a jet black color
4 7. Clinical Pathologic Correlation: The clinical features depend on the etiology of the hyperbilirubinemia, however most can lead to clinical jaundice. a. Jaundice or icterus describes the yellow-green discoloration of the skin, sclera, and other tissues and is clinically manifested when circulating bilirubin concentration reach levels greater than 2.0 to 2.5 mg/dl. b. Uncongugated hyperbilirubinemia can cross the blood brain barrier in the infant resulting in kernicterus. E. CHOLESTASIS Definition: Cholestasis refers to decreased bile flow which is accompanied by the accumulation in the blood of substances normally excreted in bile (bilirubin, bile salts and cholesterol). 1. Pathology: Cholestatic liver changes a. Canalicular bile plugs b. Intracellular bile in hepatocytes c. "Feathery degeneration" d. Bile ductule proliferation e. Bile lakes and bile infarcts 2. Clinical Pathologic Correlation: a. Jaundice due to increased bilirubin b. Pruritus due to increased bile acids in serum c. Steatorrhea due to malabsorption of fats d. Hemorrhagic disorders due to decreased absorption of vitamins A, D, and K e. Xanthomas due to increased serum cholesterol 3. Etiology/Pathogenesis: Intrahepatic cholestasis Extrahepatic obstruction - Drug - Gallstones - Cholestasis of pregnancy - Neoplasms - Benign recurrent cholestasis - Strictures - Hepatocellular injury (hepatitis) - Sclerosing cholangitis - Sepsis - Biliary atresia - PSC, PBC - Bile duct anomalies - Congenital - Metabolic disorders - 4 -
5 F. CIRRHOSIS Definition: A diffuse process characterized by fibrosis and a conversion of normal architecture into structurally abnormal nodules. 1. Pathology: a. Fibrosis; delicate diffuse bands of collagen tissue bridging portal-portal, portal-central or central-central areas to form large diffuse broad scars surrounding nodules of hepatic parenchyma. b. The normal architecture is replaced by interconnecting fibrous scar. c. Regenerative nodules ranging from micronodules (less than 3 mm) to macronodules (greater than 3mm), are created by the regeneration of hepatocytes. 2. Clinical Pathologic Correlation: a. Silent b. Nonspecific symptoms, anorexia, weight loss, weakness 3. Symptoms associate with more advanced liver disease a. progressive liver failure b. complications of portal hypertension i. ascites ii. porto systemic venous shunts iii. congestive splenomegaly c. hepatic encephalopathy 4. Etiology/Pathogenesis: a. Collagen deposition in all portions of the hepatic lobule. b. Major source of excess collagen in cirrhosis is believed to be the hepatic stellate cell (Ito cell) c. Exact stimulus for the fibrosis is uncertain, but etiologies include: Alcoholic liver disease alpha-1-at deficiency Viral hepatitis Cryptogenic (see Non-alcoholic steatohepatitis) Biliary diseases Metabolic disorders Drug reaction Primary hemochromatosis Infection Wilson's disease - 5 -
6 G. HEPATIC FAILURE Definition: A clinical syndrome with appreciable morbidity and mortality (70-95% overall mortality) that results from inadequate liver function when either hepatocytes are sufficiently diminished in number or their function is greatly impaired. 1. Pathology: a. Massive hepatic necrosis b. Non-necrotic liver failure (ultrastructural damage without cell necrosis) c. Chronic liver disease 2. Clinical Pathologic Correlation: a. Jaundice b. Hepatic encephalopathy i. C.C.C.C. (confusion, unconsiousness, conculsions, coma ii. Asterixis c. Coagulopathy i. bleeding due to increased synthesis of coagulation factors ii. Increased PT time due to increased factor VII iii. Thrombocytopenia due to hypersplenism, Bone marrow suppression iv. DIC due to necrosis of hepatocytes Activation of Factor XII d. Hepatorenal syndrome i. Renal failure in favored theory is decreased absence of any anatomic changes renal blood flow and shunting of blood from cortex to medulla resulting in decreased GFR e. Hypoalbuminemia i. edema due to impaired sythesis of albumin f. Pulmonary complications i. decreased arterial several proposed mechanisms O2 saturation g. Endocrine-related problems i. Gynecomastia feminization due to reduced catabolism female body habitus of estrogen and weak androgens - 6 -
7 H. FULMINANT HEPATITIS Liver and Biliary Tract Pathology 1. hepatic insufficiency progressing from onset to death (or liver transplantation) within 2 to 3 weeks 2. sub-fulminant hepatic failure denotes a course of up to 3 months to 65% of cases are viral hepatitis to 30% are from drug or chemical toxicity 5. may present with jaundice, encephalopathy, fetor hepaticus, coagulopathy and bleeding, cardiovascular instability, renal failure, ARDS, electrolyte and acid disturbances, and sepsis 6. mortality is 25 to 90% without transplantation 7. the entire liver or just portions may be involved 8. affected areas are soft, muddy-red or bile stained 9. liver is shrunken 10. entire lobules destroyed, collapsed reticulin network, inflammation minimal 11. regeneration is disorderly, scar may form, coarsely lobulated pattern of necrosis II. INFECTIOUS DISORDERS A. ACUTE HEPATITIS 1. Definition a. Pathologist : Inflammation of the liver b. Clinician: Syndrome by which the patient demonstrates laboratory evidence of liver cell necrosis (elevated AL T &AST) often preceded or accompanied by malaise, fever and jaundice - 7 -
8 2. Pathology a. Liver cell injury and necrosis i. single cell necrosis (councilman body); dead hepatocyte ii. ballooning degeneration; swollen dying hepatocyte iii. spotty necrosis; localized collection of inflammatory cells and Kupffer cells where a hepatocyte should be iv. piecemeal necrosis; inflammatory cells spilling out beyond the limiting plate and associated with hepatocellular necrosis v. bridging necrosis; necrotic hepatocytes and inflammation extending from portal to portal, portal to central or central to central areas. b. Confluent hepatic necrosis: bridging necrosis to necrosis of all hepatic parenchyma c. Portal and lobular inflammation d. Cholestasis - 8 -
9 4. Hepatitis B serology a. Positive: HBsAg, IgM anti HBc = acute infection b. Positive: IgM anti HBc = acute infection c. Positive: HBsAg only = early acute or chronic inflammation d. Positive: HBsAg, HBeAg, HBV DNA by molecular studies = chronic with continuing infection, high infectivity or early acute infection e. Note: Beware HBe is a marker for active viral replication with shedding. of complete virions into blood stream & thus high infectivity 5. Hepatitis F -A double stranded DNA virus, presumably the enteric agent responsible for sporadic non-a, non-b hepatitis in humans, was successfully transmitted to rhesus monkeys by means of a stool extract from a patient -these findings have yet to be confirmed by others before it's existence can be accepted 6. Hepatitis G -In January 1996, a new, blood borne RNA hepatitis virus was identified and designated as Hepatitis G virus -similar to Flaviviridae family (HCV) -related to HCV but does not seem to cause liver disease -has a worldwide distribution -parenteral route of exposure -can be transmitted simultaneously with HCV (co-infection) -progression of HIV (human immunodiffenciency virus) is delayed in persons who are co-infected with GB virus-c (GBV-C) -common in patients with HIV infection (Sept 2001 NEJM) 7. Other Viruses a. EBV b. Adenoviruses c. CMV d. Enterovirus e. HSV f. Rubella g. Yellow fever - 9 -
10 h. Lassa fever i. Marburg + Ebola virus B. CHRONIC HEPATITIS Liver and Biliary Tract Pathology 1. Definition: Symptomatic, biochemical or serologic evidence of continuing or relapsing hepatic disease for more than 6 months. 2. Pathology: Chronic hepatitis with assessment of inflammatory activity [=Grade] (mild to severe) and evaluation of degree of fibrosis and/or cirrhosis [=Stage] 3. Clinical Pathologic Correlation: a. Asymptomatic b. Fatigue, malaise, jaundice, anorexia, fever, nausea c. Extrahepatic manifestations (cryoglobulinemia, glomerulonephritis) d. Chronic liver failure N.B. clinical findings are not specific and correlate poorly with severity of disease 3. Etiology/Pathogenesis: a. Hepatitis B, C, D b. Autoimmune hepatitis c. Drugs d. Wilson's Disease e. ai-at deficiency III. DRUG- & TOXIN-INDUCED LIVER DISEASE A. Definition: Xenobiologies (therapeutic agents or environmental toxins) can produce a broad spectrum of liver disease from clinically trivial transient cholestasis to fatal fulminant hepatitis. Hepatic injury secondary to drugs accounts for approximately 5% of all causes of jaundice and up to 25% of cases of fulminant hepatic necrosis
11 B. Pathology: Basically a drug or toxin can produce any form of liver pathology from hepatocellular injury (acetaminophen-hepatic necrosis) to vascular abnormalities and even neoplasms (anabolic steroids -liver cell adenoma) C. Clinical Pathologic Correlation: In a patient with liver chemistry abnormalities or asymptomatic liver dysfunction - ALWAYS THINK OF POSSIBLE DRUG/TOXIN HEPATOCYTE DAMAGE Etiology /Pathogenesis: (see Table 19-4 page 869 in Robbins for list of drugs and toxins) D. ALCOHOLIC LIVER DISEASE 1. Definition: Long term excessive alcohol consumption resulting in a spectrum of liver pathology. Alcohol and its metabolites are direct hepatotoxic agents. 2. Pathology: a. Hepatic steatosis; grossly, the liver may be enlarged and on cut section is soft and greasy. Microscopically there is first microvesicular steatosis then macrovesicular steatosis. i. Microvesicular steatosis small lipid droplets in cytoplasm ii. Macrovesicular steatosis cytoplasm is replaced by a large lipid vacuole that displaces the nucleus to the side b. Alcoholic Hepatitis i. liver cell necrosis ii. Mallory Bodies - Worm-like perinuclear eosinophilic inclusions composed of cytokeratin intermediate filaments and other proteins. iii. Neutrophilic reaction iv. Fibrosis c. Alcoholic cirrhosis i. Grossly the liver is transformed into a shrunken firm diffusely nodular organ. ii. Histologically, there are parenchymal nodules of varying size surrounded by dense fibrous tissue. 3. Clinical Pathologic Correlation: a. Steatosis i. asymptomatic ii. mild increase of bilirubin and alkaline phosphatase b. Alcoholic hepatitis
12 i. asymptomatic ii. Malaise, anorexia, weight loss, abdominal pain, increase bilirubin and increase alkaline phosphatase iii. fulminant hepatic failure iv % risk of death/episode v. 1/3 will develop cirrhosis with repeated episodes c. Alcoholic cirrhosis i. 10% diagnosed at autopsy ii. may present with complications of portal hypertension iii. malaise, weakness, weight loss, anorexia - jaundice, ascites and peripheral edema iv. increase transaminases, increase bilirubin, decrease protein & anemia v. hepatic failure 4. Etiology/Pathogenesis: a. Steatosis i. increase lipid biosynthesis ii. lipoprotein abnormalities iii. increase peripheral catabolism of fat b. Hepatocyte injury i. induction of cytochrome P450 ii. generation of free radicals iii. direct effects of ETOH & acetaldehyde iv. immune reactions c. Fibrogenesis i. multifactorial
13 E. Non- alcoholic steatohepatitis Liver and Biliary Tract Pathology The term Non-alcoholic steatohepatitis (NASH) was first used in 1980 by Ludwig-in 20 non-etoh patients -a part of the spectrum of Non-alcoholic fatty liver disease -Now better known as Non-alcoholic fatty liver disease (NAFLD) -histopathology ranges from simple fatty liver, fatty change with lobular inflammation, hepatocellular injury, Mallory hyalin, may occur with or without fibrosis, to cirrhosis -NASH is a liver disease that - NASH can also occur in lean, until recently has been an otherwise healthy individuals. unrecognized as a common -even in children cause of elevated liver -generally benign enzymes -may be progressive -liver biopsy findings similar to alcoholic (ETOH) hepatitis - may lead to cirrhosis -no history of significant ETOH consumption -often middle aged and obese -coexisting DM or hyperlipidemia -therapy - poorly defined : weight loss and ursodeoxycholic acid (UDCA) have beneficial effect -has been shown to.be a cause of cryptogenic cirrhosis -liver biopsy: the gold standard IV. INBORN ERRORS OF METABOLISM A. HEMOCHROMATOSIS 1. Definition: Although Robbins still refers to the progressive pathologic accumulation of iron in tissues with the potential for cellular damage and functional derangement as "Hemochromatosis," the newer terminology for these groups of diseases is best referred to as Iron Overload Disorders or Iron Storage Diseases
14 2. Pathology: Accumulation of iron in parenchymal tissues a. Liver: Iron accumulates in periportal hepatocytes and may progress to accumulate in Kupffer cells and biliary epithelium. In some iron overload conditions such as parenteral iron overload, Kupffer cells may be the first to accumulate the iron. Fibrosis develops leading to cirrhosis. i. Prussian-blue stain: (also referred to as "the iron stain") stains hemosiderin granules blue-black and is used to grade the amount of iron visually seen on a liver biopsy. ii. Quantitative biochemical hepatic iron concentration: The amount of hepatic iron is measured on a fresh biopsy tissue by biochemical methods. b. Pancreas: Iron accumulates in both the acinar and islet cells. c. Heart: Iron accumulation in myocytes d. Skin: increased melanin in basal melanocytes and iron accumulation in dermal macrophages and fibroblasts resulting in a bronze or slate grey appearance of skin. d. Other tissues: joint and testis will accumulate iron 3. Clinical Pathologic Correlation: a. Hepatomegaly, abdominal pain b. Skin pigmentation c. Abnormal glucose metabolism - diabetes d. Cardiac dysfunction e. cirrhosis and complications f. Hepatocellular carcinoma N.B. all related to increased iron deposition 4. Etiology/Pathogenesis: a. Direct iron toxicity i. lipid peroxidation ii. iron stimulation of collagen formation iii. Iron-DNA interactions
15 b. Primary/Hereditary iron overload: Autosomal recessive disorder, limited to the short arm of chromosome 6 and characterized by continued absorption of excessive iron. c. Secondary iron overload: iron accumulation in the liver and other tissues due to a variety of disease process. 5. Additional/lmportant Information: Primary iron overload is a treatable disease with a potentially normal life expectancy if diagnosed before irreversible tissue damage has occurred. It is therefore important to identify other family members that may be at risk. Elevated serum iron, total iron binding capacity and ferritin levels are suggestive of iron overload and should be followed by a liver biopsy with quantitative hepatic iron concentration studies. Treatment involves phlebotomy and the use of iron chelating agents. B. WILSON'S DISEASE 1. Definition: An autosomal recessive disorder of copper metabolism associated with chromosome 13, resulting in deposition of copper in many organs; particularly the liver, eye and brain. 2. Pathology: a. Liver: The pathology varies from steatosis (fatty change) to acute hepatitis, chronic hepatitis, cirrhosis and rarely fulminant hepatic necrosis. Although not specific, numerous glycogenated nuclei ("nuclear cleaning") are present in the hepatocytes and increased copper stores can be identified with special stains. Rhodamine or rubeanic acid stain ("the copper stain") stains copper as red granules in hepatocyte cytoplasm. i. quantitative hepatic copper concentration: Because the Rhodamine and rubeanic stains are a bit capricious, the most helpful way to determine t copper is by a biochemical determination of fresh tissue. b. Brain: copper deposits in areas of the brain with toxic injury to the neurons c. Eye: Kayser-Fleischer rings are copper deposits in Descemet membrane appearing as a brown discoloration of the peripheral ring of the cornea. 3. Clinical Pathologic Correlation a. Hepatic symptoms ranging from jaundice to hepatitis and cirrhosis
16 b. Neurologic symptoms include; tremors, spasticity, behavioral abnormalities and dementia c. Ophthalmic: Kayser-Fleischer rings (copper deposits in Descemet membrane in the limbus of the cornea) 4. Etiology/Pathogenesis: The exact pathogenesis remains obscure, but involves the liver inability to export copper effectively. 5. Additional Important Information: A potentially treatable disorder with early recognition and long term use of copper chelating agents (penicillamine) to prevent accumulation of copper and progression of disease. MUST CONSIDER THIS DIAGNOSIS IN ANY YOUNG PERSON WITH HEPATIC DISEASE! Important to screen family members. Laboratory screening studies suspicious of Wilson's disease are a low serum ceruloplasmin and increased urinary excretion of copper. C. ALPHA-1 [ 1] ANTITRYPSIN DEFICIENCY 1. Definition: Autosomal recessive disorder marked by abnormally low levels of α-l antitrypsin. α-1 AT's major function is the inhibition of proteases, particularly the potent elastase found in neutrophils which are released at sites of cell injury and inflammation. A deficiency of α-1 antitrypsin may lead to pulmonary emphysema and hepatic damage. 2. Pathology: a. Hepatic pathology varies from neonatal hepatitis with or without cholestasis in the newborn to features of chronic active hepatitis and cirrhosis. b. Hallmark feature is the presence of α1-at cytoplasmic globules in hepatocytes. The diagnostic globules are not consistently present until about 3 months of age. PAS with diastase stain: α1-at globules stain pink with the PAS stain and remain pink even after treatment with the enzyme diastase. If on liver biopsy these globules are identified, they are confirmed as α1-at globules with an immunohistochemical stain specific for α1-at
17 3. Clinical Pathologic Correlation a. Neonatal hepatitis with cholestatic jaundice in newborn. b. Hepatitis c. Cirrhosis 4. Etiology/Pathogenesis The predominant site of α1-at synthesis is the hepatocyte, under the codominant alleles at a locus on the long arm of chromosome 14. The α1- AT gene locus is termed Pi and over 75 variants have been identified. The most common variant associated with disease is the PiZZ homozygote which have α1-at levels that are only 10% of the normal level. The exact mechanisms for the development of liver disease are not entirely clear. V. INTRAHEPATIC BILIARY TRACT DISEASE A. PRIMARY BILIARY CIRRHOSIS (PBC) 1. Definition: Non-suppurative granulomatous destruction of medium size intrahepatic bile ducts resulting in a chronic progressive and often fatal chollestatic liver disease. 2. Pathology: Traditionally conceptualized as 4 stages with the understanding that PBC is focal, variable and may exhibit different degrees of severity in different portions of the liver. (In other words, not an easy diagnosis to make for a pathologist on a liver biopsy) a. Stage 1. Florid duct lesion (granulomatous inflammation) b. Stage 2. Decreased bile ducts with ductular proliferation and portal inflammation c. Stage 3. Fibrosis d. Stage 4. Cirrhosis 3. Clinical Pathologic Correlation a. asymptomatic b. cholestatic symptoms; pruritus, xanthomas, steatorrhea - related to increase serum bile salts, cholesterol and decrease bile in GI tract c. jaundice and hepatic decompensation - late manifestation
18 4. Etiology/Pathogenesis a. primarily a disease of middle-aged woman b. 90% have antimitochondrial antibodies (+AMA) c. Autoimmune etiology is thought to be the most likely pathogenesis B. SECONDARY BILIARY CIRRHOSIS 1. Definition: Prolonged obstruction to the extrahepatic biliary tree resulting in fibrosis leading to cirrhosis 2. Pathology a. cholestasis - initial injury, described earlier b. periportal fibrosis c. cirrhosis, usually with yellow-green hepatic discoloration grossly 3. Clinical Pathologic Correlation a. cholestatic symptoms of pruritus, jaundice, malaise, dark urine, light stools 4. Etiology/Pathogenesis a. Gall stones b. Neoplasms (carcinoma of the head of the pancreas) c Strictures d. PSC e Biliary atresia f Bile duct anomalies g Flukes C. PRIMARY SCLEROSING CHOLANGITIS (PSC) 1. Definition: A fibro inflammatory process that narrows and eventually obstructs bile ducts. This process can occur anywhere from the ampulla of Vater to the intrahepatic intralobular bile ducts 2. Pathology: a. concentric peri ductal fibrosis followed by fibrous obliteration and disappearance of bile duct b. other ducts may be dilated presumably due to fibrous obstruction of downstream bile ducts 3. Clinical Pathologic Correlation
19 a. asymptomatic with elevated alk phosphatase b. cholestatic symptoms c. chronic liver disease d. increased risk of cholangiocarcinoma 4. Etiology/Pathogenesis a. commonly associated with inflammatory bowel disease ( 70% of pts with PSC have co-existing IBD) b. PSC-like illness is seen in AIDS patients with cryptosporidial and CMV biliary disease c. ERCP (Cholangiogram) shows characteristic "beading" or pruning of intrahepatic and/or extrahepatic biliary tree on imaging studies d. Exact etiology is uncertain VI. CIRCULATORY DISORDERS A. IMPAIRED BLOOD FLOW INTO THE LIVER 1.Hepatic Artery Compromise 2. Portal Vein Obstruction & Thrombosis B. IMPAIRED BLOOD FLOW THROUGH THE LIVER 1. PASSIVE CONGESTION/CENTRILOBULAR NECROSIS a. Definition: hepatic injury pattern resulting from systemic circulatory compromise. 2. Pathology: a. Passive congestion i. enlarged liver with nutmeg appearance on cut section ii. congestion of centrilobular sinusoids iii. atrophy of centrilobular hepatocytes b. Centrilobular necrosis i. coagulative necrosis of centrilobular hepatocytes ii. no inflammation iii. influx of blood
20 C. PELIOSIS HEPATIS Liver and Biliary Tract Pathology 1. Definition: A rare condition characterized by the presence of cystic blood-filled spaces in the liver. 2. Pathology: Macro- or microscopic randomly distributed cystically dilated spaces filled with blood. 3. Clinical Pathologic Correlation Generally asymptomatic, rarely may result in intra-abdominal hemorrhage or hepatic failure 4. Etiology/Pathogenesis a. Associated with drugs; anabolic steroid, rarely oral contraceptives and Danazol. b. AIDS; usually caused by the organism Bartonella henselae c. Reported with a variety of other chronic diseases D. HEPATIC VEIN OUTFLOW OBSTRUCTION 1.BUDD-CHIARI SYNDROME (HEPATIC VEIN THROMBOSIS) Definition: The term Budd-Chiari syndrome is usually applied to the clinical manifestations of hepatic venous outflow obstruction secondary to hepatic vein thrombosis. The term has also been applied to symptoms related to suprahepatic obstruction of the IVC and diseases affecting small hepatic vein branches. a. Pathology: i. Acute: liver is swollen, with centrilobular congestion and necrosis ii. Slow chronic thrombosis: centrilobular fibrosis/sclerosis, +/- webs b. Clinical Pathologic Correlation: hepatomegaly, ascites, abdominal pain, varying degrees of hepatic dysfunction c. Etiology/Pathogenesis: i. polycythemia vera ii. pregnancy iii. paroxysmal nocturnal hemoglobinopathy iv. intraabdominal malignancies
21 2. VENO-OCCLUSIVE DISEASE (VOD) Definition: fibrotic occlusion of small hepatic veins with secondary hepatic congestion. a. Pathology: i.. Subintimal edema and hemorrhage involving small hepatic veins ii Centrilobular congestion and hepatocellular necrosis iii Dense perivenular fibrosis, and fibrous obliteration d. Clinical Pathologic Correlation: acute tender hepatomegaly, ascites, weight gain and jaundice e. Etiology/Pathogenesis: i. ingestion of pyrrolizidine alkaloids (herbal teas and contaminated grains) ii. bone marrow transplants (BMT) - 5 % incidence in autologous BMT -25 % incidence in allogenic BMT -drugs, oral contraceptives d. pathogenesis is thought to be sinusoidal endothelial injury VII. TRANSPLANTATION PATHOLOGY A. Drug toxicity: hepatic damage due to drugs given during BMT. Two specific forms of drug injury include VOD and nodular regenerative hyperplasia. B. Graft versus Host Disease (GVHD): Injury due to immunologically competent transplanted cells with the main targets typically being the GI tract, skin and liver. This usually results after a BMT and the main histologic features of hepatic GVHD are portal inflammation, bile duct damage, cholestasis and endothelialitis. C. Hepatic allograft rejection: Hepatic injury as a result of the recipient's immune system attacking the transplanted donor liver. It may be hyperacute (rare), acute cellular (early in the post-transplant period), or chronic ductopenic (late in the post-transplant period) rejection which result from alloantigensspecific cellular or humoral immune mechanisms. Acute cellular rejection is characterized by portal inflammation, bile duct and endothelialitis. Features of chronic rejection finding include bile duct loss (=ductopenia) and transplant vasculopathy. D. Infections: Due to the immunosuppression, a variety of bacterial, viral, protozoan and fungal infections are common
22 E. Recurrence of primary disease: i.e., recurrence of hepatitis B, hepatitis C or malignant hepatic tumors. VIII. TUMORS & TUMOROUS CONDITIONS A. TUMOROUS CONDITIONS: 1.CYSTS a. multiple intrahepatic cysts i. Polycystic Disease ii. iii. congenital hepatic fibrosis Caroli s disease 2. Parasitic cysts B. FOCAL NODULAR HYPERPLASIA 1. usually solitary, well circumscribed mass 2. usually less than 5 cm. 3. central stellate scar, containing blood vessels, lymphocytes and proliferative bile ducts 4. most commonly seen in year old women 5. association with oral contraceptive use has been a long and hotly debated topic 6. no malignant potential 7. current belief is that it is essentially a vascular malformation with A-V anastomoses and localized overgrowth of all liver constituents
23 C. NODULAR REGENERATIVE HYPERPLASIA 1. partial or diffuse, nonfibrosing transformation of hepatic parenchyma into hyperplastic nodules 2. associated with a bewildering number and variety of diseases 3. may be a cause of "non-cirrhotic portal hypertension" 4. difficult diagnosis to make on biopsy, requiring a reticulin stain to appreciate the "nodularity" of the parenchyma D. BENIGN TUMORS: 1. EPITHELIAL TUMOR a. Liver cell adenoma i.. predominately in women of child bearing age ii.. established association with oral contraceptives iii.. may be seen in men on androgen therapy iv. risk of hemoperitoneum (rupture) v. usually solitary, but may be multiple vi. pale, yellow-tan grossly vii histologically; sheets and cords of normal hepatocytes viii rarely associated with hepatocellular carcinoma. b. Bile duct adenoma i. may represent aggregates of reactive bile ducts ii. usually subcapsular, small iii. composed of uniform benign epithelial-lined ducts iv. surgeons often biopsy at the time of laparotomy to rule out metastatic disease
24 E. BENIGN NON-EPITHELIAL TUMORS 1. Hemangioma a. most common benign tumor b. complications: bleeding, sequestration of platelets c. dilated vascular spaces with connective tissue support 2. Hemangioendothelioma a. seen in children b. may be associated with hepatic failure and congestion c. vessels lined by plump endothelial cells with a supporting fibromyoid stroma F. MALIGNANT PRIMARY HEPATIC TUMORS: 1. HEPATOCELLULAR CARCINOMA (HCC) a. Definition: Primary carcinoma of the liver composed of malignant hepatocytes b. Pathology: i. single, multifocal or diffuse infiltrative, usually bile stained c. Microscopically: i. trabecular, acinar, pseudoglandular patterns ii. bile present iii clear cell and undifferentiated variants d. Clinical Pathologic Correlation: i. vague symptoms of upper abdominal pain, malaise, weight loss ii. serum alpha-fetoprotein (60-70% patients) iii. metastatic disease to lungs, lymph nodes and bones iii. prognosis is poor, but dependent on stage of tumor and clinical status of patient e. Etiology/Pathogenesis i. Hepatitis B/C - World wide incidence of HCC correlates to HBV and HCV infection - HCC most common malignancy in Taiwan and parts of Africa
25 - 200x increased risk in HCC in patients acquiring HBV infection by vertical transmission from mother ii. Aflatoxins - toxic product of Aspergillus flavus and contaminant of food stuff iii. Cirrhosis - important, but not mandatory - associated with Hepatitis B & C, alcohol, iron overload disorders iv. Hereditary Tyrosinemia - Most likely disease to lead to HCC - 40% of patients develop tumor despite adequate control 2. FIBROLAMELLAR VARIANT OF HCC a. Definition: A variant of HCC, usually occurring in younger patients b. Pathology: usually single firm mass; malignant welldifferentiated polygonal cells separated by dense collagen bundles c. Clinical Pathologic Correlation: i. age 5-35 years ii. 90 % arise in noncirrhotic livers iii. non-specific symptoms d. Etiology/Pathogenesis: no clear association with HBV infection 3. INTRAHEPATIC CHOLANGIOCARCINOMA a. Definition: Primary carcinoma of the liver composed of malignant bile duct epithelium which may arise from the large intrahepatic bile ducts at the porta hepatitis to the smallest bile ductules of the periphery of the lobule. b. Pathology: i. single, multiple of diffusely infiltrative c. Microscopically: malignant glandular or tubular structures associated with a dense collagenous stroma, no bile production d. Clinical Pathologic Correlation: i. world wide, cholangiocarcinomas are less common ii. peripheral tumors - usually clinically silent iii. hilar tumors - symptoms of biliary obstruction predominate
26 iv. Klatskin Tumor: Eponym for a cholangiocarcinoma arising at the hepatic hilum, shares many clinicopathologic features with extrahepatic bile duct carcinoma d. Etiology/Pathogenesis. Thorotrast: radio-opaque agent used years ago to study the liver ii. Parasitic infections: Opisthorchis and Clonorchis iii Fibropolycystic liver diseases: i.e., congenital hepatic fibrosis, Caroli's disease, choledochal cysts 4. HEPATOBLASTOMA a. Definition: The most common primary malignant hepatocellular neoplasms of childhood. b. Pathology: - Solitary masses (5-25 cm) - Histologically: immature epithelial cells resembling fetal or embryonic hepatocytes, sometimes with an admixed mesenchymal component c. Clinical-Pathologic Correlation: - usually present within first 3 years of life - hepatomegaly, growing mass - failure to thrive d. Etiology/Pathogenesis: associated with numerous disorders, but no clear etiology 5. ANGIOSARCOMA a. Definition: The most common primary sarcoma of the liver b. Pathology: i. multiple gray hemorrhagic masses (0.1-5 cm) may be a single large mass nonneoplastic liver is usually normal Histologically: proliferation of malignant endothelial cells c. Clinical Pathologic Correlation i. usually occurs in men - 70 years of age ii. nonspecific symptoms; abdominal pain, weight loss iii. may manifest as an acute abdomen due to rupture of the tumor e. Etiology/Pathogenesis: associated with exposure to thorotrast, vinyl chloride and arsenic
27 G. METASTATIC MALIGNANT TUMORS a. Definition: b. Pathology: i. Single or multiple lesions ii.histologically: varies and depends on primary malignancy c. Clinical Pathologic Correlation: Asymptomatic (small lesions) or jaundice and hepatic failure with massive involvement d. Etiology/Pathogenesis: i. Breast, lung and colon for adults: most common ii. Neuroblastoma, Wilms tumor and rhabdomyosarcoma for children
Pathology of the Liver & Biliary Tract I, II, III, and IV
Grace Guzman, M.D. UIC College of Medicine Assistant Professor of Pathology, UIC M2 Pathology Course Phone: 312-996-9288 Lectures #59, 60, 63, 64 e-mail: graceguz@uic.edu Tuesday, February 3, 2004 10:30-11:20,
More informationLiver, Gallbladder and Pancreas diseases. Premed 2 Pathophysiology
Liver, Gallbladder and Pancreas diseases Premed 2 Pathophysiology Pancreas Pancreatitis Acute Pancreatitis Autodigestion of the pancreas due to activation of the enzymes Hemorrhagic fat necrosis, calcium
More informationThe child with abnormal liver function tests
The child with abnormal liver function tests Dr Jane Hartley Consultant Paediatric Hepatologist Birmingham Children s Hospital, UK 1 st Global Congress CIP, Paris 2011 Contents Over view of liver anatomy,
More informationApproach to Abnormal Liver Tests
Approach to Abnormal Liver Tests Naga P. Chalasani, MD, FACG Professor of Medicine and Cellular & Integrative Physiology Director, Division of Gastroenterology and Hepatology Indiana University School
More informationService Definition with all Clinical Terms Service: Laprascopic Cholecystectomy Clinic (No Gallstones in bile duct)
Service Definition with all Clinical Terms Service: Laprascopic Cholecystectomy Clinic (No Gallstones in bile duct) Section 1 Service Details Service ID: 7540540 Service Comments: Referrer Alert: Service
More information190.25 - Alpha-fetoprotein
Other Names/Abbreviations AFP 190.25 - Alpha-fetoprotein Alpha-fetoprotein (AFP) is a polysaccharide found in some carcinomas. It is effective as a biochemical marker for monitoring the response of certain
More informationHOW TO EVALUATE ELEVATED LIVER ENZYMES
HOW TO EVALUATE ELEVATED LIVER ENZYMES Kenneth E. Sherman, MD, PhD Gould Professor of Medicine Director, Division of Digestive Diseases University of Cincinnati College of Medicine LABORATORY TESTS OF
More informationHepatitis C. Laboratory Tests and Hepatitis C
Hepatitis C Laboratory Tests and Hepatitis C If you have hepatitis C, your doctor will use laboratory tests to check your health. This handout will help you understand what the major tests are and what
More informationLIVER FUNCTION TESTS
LIVER FUNCTION TESTS University of PNG School of Medicine and Health Sciences, Division of Basic Medical Sciences, Discipline of Biochemistry & Molecular Biology VJ Temple 1 What are some of the functions
More informationBile Duct Diseases and Problems
Bile Duct Diseases and Problems Introduction A bile duct is a tube that carries bile between the liver and gallbladder and the intestine. Bile is a substance made by the liver that helps with digestion.
More informationGeir Folvik, MD Division of Gastroenterology Department of Medicine, Haukeland University Hospital Bergen, Norway 30.11.2015
Benign liver diseases Geir Folvik, MD Division of Gastroenterology Department of Medicine, Haukeland University Hospital Bergen, Norway 30.11.2015 1 Agenda Benign focal liver lesions Fatty liver disease
More informationEvaluation of Liver Function tests in Primary Care. Abid Suddle Institute of Liver Studies, KCH
Evaluation of Liver Function tests in Primary Care Abid Suddle Institute of Liver Studies, KCH Liver Function tests Markers of hepatocellular damage Cholestasis Liver synthetic function Markers of Hepatocellular
More informationLIVER TUMORS PROFF. S.FLORET
LIVER TUMORS PROFF. S.FLORET NEOPLASM OF LIVER PRIMARY 1)BENIGN 2)MALIGNANT METASTATIC/SECONDARY LIVER Primary Liver Cancer the Second Killer among tumors high morbidity and mortality(20.40/100,000) etiology
More informationIndications in Hepatology and Liver Diseases
exclusively working in Health Care sananet GmbH Tilo Stolzke Breite Str. 6-8 23562 Lübeck Germany Telefon : +49 451 400 8301 Telefax : +49 451 400 8302 E-Mail : stolzke@sananet.com Internet : www.sananet.com
More informationAlbumin. Prothrombin time. Total protein
Hepatitis C Fact Sheet February 2016 www.hepatitis.va.gov Laboratory Tests and Hepatitis If you have hepatitis C, your doctor will use laboratory tests to about learn more about your individual hepatitis
More informationNP/PA Clinical Hepatology Fellowship Summary of Year-Long Curriculum
OVERVIEW OF THE FELLOWSHIP The goal of the AASLD NP/PA Fellowship is to provide a 1-year postgraduate hepatology training program for nurse practitioners and physician assistants in a clinical outpatient
More informationDisclosures. Interpreting Liver Tests: What Do They Mean? Liver Function Tests. Objectives. Common Tests. Case 1
Disclosures Interpreting Liver Tests: What Do They Mean? I have no financial disclosures to make. Roman Perri, MD Vanderbilt University Medical Center Nashville, TN Objectives Discuss tests commonly used
More informationProf. of Tropical Medicine Faculty of Medicine Alexandria University
prof. Dr. Ali El-Kady (MD) Prof. of Tropical Medicine Faculty of Medicine Alexandria University DRUGS THAT MAY CAUSE LIVER DYSFUNCTION DAMAGE The liver is the principal organ that is capable of converting
More informationLIVER FUNCTION TESTS AND LIVER DISEASES. Prof. Fang Zheng Department of Laboratory Medicine School of Medicine, Wuhan University
LIVER FUNCTION TESTS AND LIVER DISEASES Prof. Fang Zheng Department of Laboratory Medicine School of Medicine, Wuhan University Content the Anatomy of Liver the Function of Liver Tests of Liver Function
More informationABNORMAL LIVER ENZYMES: A PRACTICAL CLINICAL APPROACH. David C. Twedt, DVM, Diplomate ACVIM Colorado State University twedt@colostate.
ABNORMAL LIVER ENZYMES: A PRACTICAL CLINICAL APPROACH David C. Twedt, DVM, Diplomate ACVIM Colorado State University twedt@colostate.edu The detection of abnormal liver biochemical tests in the asymptomatic
More informationOMG my LFT s! How to Interpret and Use Them. OMG my LFT s! OMG my LFT s!
How to Interpret and Use Them René Romero, M.D. Clinical Director, Pediatric Hepatology CPG Gastroenterology, Hepatology and Nutrition Emory University School of Medicine Objectives Understand the anatomy
More informationPatterns of abnormal LFTs and their differential diagnosis
Patterns of abnormal LFTs and their differential diagnosis Professor Matthew Cramp South West Liver Unit and Peninsula Schools of Medicine and Dentistry, Plymouth Summary liver function / liver function
More informationEvaluation of a Child with Elevated Transaminases. Linda V. Muir, M.D. April 11, 2008 Northwest Pediatric Liver Disease Symposium
Evaluation of a Child with Elevated Transaminases Linda V. Muir, M.D. April 11, 2008 Northwest Pediatric Liver Disease Symposium Disclosures I do not have a financial interest, arrangement or affiliation
More informationLIVER CANCER AND TUMOURS
LIVER CANCER AND TUMOURS LIVER CANCER AND TUMOURS Healthy Liver Cirrhotic Liver Tumour What causes liver cancer? Many factors may play a role in the development of cancer. Because the liver filters blood
More informationLiver Function Tests. Dr Stephen Butler Paediatric Advance Trainee TDHB
Liver Function Tests Dr Stephen Butler Paediatric Advance Trainee TDHB Introduction Case presentation What is the liver? Overview of tests used to measure liver function RJ 10 month old European girl
More informationEvaluation of abnormal LFT in the asymptomatic patient. Son Do, M.D. Advanced Gastroenterology Vancouver, WA
Evaluation of abnormal LFT in the asymptomatic patient Son Do, M.D. Advanced Gastroenterology Vancouver, WA Definition of chronic, abnormally elevated LFT Elevation of one or more of the following for
More informationLIVER FUNCTION TESTS
MODULE Liver Function Tests 17 LIVER FUNCTION TESTS 17.1 INTRODUCTION Liver function tests are a group of tests done to assess the functional capacity of the liver as well as any cellular damage to the
More informationLCD for Viral Hepatitis Serology Tests
LCD for Viral Hepatitis Serology Tests Applicable CPT Code(s): 86692 Antibody; Hepatitis, Delta Agent 86704 Hepatitis B Core Antibody (HBcAb); Total 86705 Hepatitis B Core Antibody (HBcAb); IgM Antibody
More informationAssessment of some biochemical tests in liver diseases
Assessment of some biochemical tests in liver diseases By Prof. Mohamed Sharaf-Eldin Prof. of Hepatology & Gastroenterology Faculty of Medicine Tanta University, Egypt. Significant liver damage may occur
More informationWhat to do with abnormal LFTs? Andrew M Smith Hepatobiliary Surgeon
What to do with abnormal LFTs? Andrew M Smith Hepatobiliary Surgeon "it looks like there's something wrong.with your television set. Matt Groenig, creator of The Simpsons Probability of an abnormal screening
More informationAsymptomatic Elevated Liver Function Tests: Physiology, Chemistry, and Workup
Asymptomatic Elevated Liver Function Tests: Physiology, Chemistry, and Workup James T. Sing, Jr., D.O., FACG, AGAF Scott & White Clinic Assistant Professor Department of Internal Medicine Division of Gastroenterology
More informationCMS Limitations Guide - Laboratory Services
CMS Limitations Guide - Laboratory Services Starting October 1, 2015, CMS will update their exisiting medical necessity limitations on tests and procedures to correspond to ICD-10 codes. This limitattions
More informationLIVER. Update on Staging of Fibrosis and Cirrhosis. Staging and Liver Fibrosis. Stage is more than liver fibrosis
Linda Ferrell, MD Distinguished Professor Vice Chair Director of Surgical Pathology Dept of Pathology LIVER Update on Staging of Fibrosis and Cirrhosis Staging and Liver Fibrosis Two important concepts
More informationLiver Diseases. An Essential Guide for Nurses and Health Care Professionals
Brochure More information from http://www.researchandmarkets.com/reports/1047385/ Liver Diseases. An Essential Guide for Nurses and Health Care Professionals Description: Liver disease is a rapidly growing
More informationBenign Liver Tumors. Cameron Schlegel PGY-1 3/6/2013
Benign Liver Tumors Cameron Schlegel PGY-1 3/6/2013 Outline Benign Liver Tumors are, in general. Asymptomatic Diagnosed: imaging Treatment: Do no harm Unless Malignant potential Causing symptoms Differential
More informationDrug Induced Liver Disease. Thomas S. Foster, Pharm.D. Integrated Therapeutics PHR 961
Drug Induced Liver Disease Thomas S. Foster, Pharm.D. Integrated Therapeutics PHR 961 Introduction Drug-induced liver disease encompasses a broad spectrum of hepatic lesions, including both acute and chronic
More informationAmylase and Lipase Tests
Amylase and Lipase Tests Also known as: Amy Formal name: Amylase Related tests: Lipase The Test The blood amylase test is ordered, often along with a lipase test, to help diagnose and monitor acute or
More informationManaging LFT s in General Practice
Managing LFT s in General Practice Sulleman Moreea FRCP(Edin Edin) ) FRCS(Glasg Glasg) Consultant Gastroenterologist/Hepatologist Bradford Hospitals Trust The normal liver Managing LFT s History and examination
More informationLiver Function Essay
Liver Function Essay Name: Quindoline Ntui Date: April 20, 2009 Professor: Dr. Danil Hammoudi Class: Anatomy and Physiology 2 Liver function The human body consist of many highly organize part working
More informationchronic leukemia lymphoma myeloma differentiated 14 September 1999 Pre- Transformed Ig Surface Surface Secreted Myeloma Major malignant counterpart
Disease Usual phenotype acute leukemia precursor chronic leukemia lymphoma myeloma differentiated Pre- B-cell B-cell Transformed B-cell Plasma cell Ig Surface Surface Secreted Major malignant counterpart
More informationNCD for Lipids Testing
Applicable CPT Code(s): NCD for Lipids Testing 80061 Lipid panel 82465 Cholesterol, serum or whole blood, total 83700 Lipoprotein, blood; electrophoretic separation and quantitation 83701 Lipoprotein blood;
More informationNUTRITION IN LIVER DISEASES
NUTRITION IN LIVER DISEASES 1. HEPATITIS: Definition: - Viral inflammation of liver cells. Types: a. HAV& HEV, transmitted by fecal-oral route. b. HBV & HCV, transmitted by blood and body fluids. c. HDV
More informationThe State of the Liver in the Adult Patient after Fontan Palliation
The State of the Liver in the Adult Patient after Fontan Palliation Fred Wu, M.D. Boston Adult Congenital Heart Service Boston Children s Hospital/Brigham & Women s Hospital 7 th National Adult Congenital
More information190.33 - Hepatitis Panel/Acute Hepatitis Panel
190.33 - Hepatitis Panel/Acute Hepatitis Panel This panel consists of the following tests: Hepatitis A antibody (HAAb), IgM antibody; Hepatitis B core antibody (HBcAb), IgM antibody; Hepatitis B surface
More informationLiver, Gallbladder, Exocrine Pancreas KNH 406
Liver, Gallbladder, Exocrine Pancreas KNH 406 2007 Thomson - Wadsworth LIVER Anatomy - functions With disease blood flow becomes obstructed Bile All bile drains into common hepatic duct Liver Bile complex
More informationThe most serious symptoms of this stage are:
The Natural Progression of Hepatitis C The natural history of hepatitis C looks at the likely outcomes for people infected with the virus if there is no medical intervention. However, the process of trying
More informationCytomegalovirus (HHV5/CMV) Roseolovirus (HHV6 & 7)
Betaherpesvirinae Cytomegalovirus (HHV5/CMV) Roseolovirus (HHV6 & 7) CYTOMEGALOVIRUS CMV is thought to be amongst the oldest type of herpesvirus in evolutionary terms. CMV is the prototype of beta-herpesviruses
More informationLaboratory Monitoring of Adult Hospital Patients Receiving Parenteral Nutrition
Laboratory Monitoring of Adult Hospital Patients Receiving Parenteral Nutrition Copy 1 Location of copies Web based only The following guideline is for use by medical staff caring for the patient and members
More informationInterpretation of abnormal liver function tests. Dr Rania Bakry, MD
Interpretation of abnormal liver function tests Dr Rania Bakry, MD Liver function tests Noninvasive method of screening for the presence of liver dysfunction Pattern of lab test abnormality allows recognition
More informationLIVER TRANSPLANTATION IN ALAGILLE SYNDROME
LIVER TRANSPLANTATION IN ALAGILLE SYNDROME Ronald J. Sokol, MD Children s Hospital Colorado University of Colorado School of Medicine Treatment of Liver Disease in Improve bile flow ALGS Ursodeoxycholic
More informationAlanine aminotransferase (serum, plasma)
Alanine aminotransferase (serum, plasma) 1 Name and description of analyte 1.1 Name of analyte Alanine aminotransferase (ALT) 1.2 Alternative names Systematic name L alanine:2 oxoglutarate aminotransferase
More informationAdams Memorial Hospital Decatur, Indiana EXPLANATION OF LABORATORY TESTS
Adams Memorial Hospital Decatur, Indiana EXPLANATION OF LABORATORY TESTS Your health is important to us! The test descriptions listed below are for educational purposes only. Laboratory test interpretation
More informationFast Facts. Fast Facts: Liver Disorders. Thomas Mahl and John O Grady. 2006 Health Press Ltd. www.fastfacts.com
Fast Facts Fast Facts: Liver Disorders Thomas Mahl and John O Grady 2006 Health Press Ltd. www.fastfacts.com Fast Facts Fast Facts: Liver Disorders Thomas Mahl MD University at Buffalo School of Medicine
More informationNew Development in Treating Liver Disorders: Approaches to liver function test from mild to fulminant disorders
Research and Reviews New Development in Treating Liver Disorders: Approaches to liver function test from mild to fulminant disorders JMAJ 53(4): 218 223, 2010 Hirohito TSUBOUCHI,* 1 Akio IDO,* 2 Seiichi
More informationBACKGROUND MEDIA INFORMATION Fast facts about liver disease
BACKGROUND MEDIA INFORMATION Fast facts about liver disease Liver, or hepatic, disease comprises a wide range of complex conditions that affect the liver. Liver diseases are extremely costly in terms of
More informationBLOOD GROUP ANTIGENS AND ANTIBODIES
BLOOD GROUP ANTIGENS AND ANTIBODIES Over 20 blood group systems having approximately 400 blood group antigens are currently recognised. The ABO and Rhesus (Rh) blood group systems are of major clinical
More informationIschemia and Infarction
Harvard-MIT Division of Health Sciences and Technology HST.035: Principle and Practice of Human Pathology Dr. Badizadegan Ischemia and Infarction HST.035 Spring 2003 In the US: ~50% of deaths are due to
More informationInterpretation of liver chemistry tests
Interpretation of liver chemistry tests Fuad A.M. Hasan, Salim Owyed Bulletin of KIMS carries some articles specifically designated as CME/CPD. They provide the opportunity for the reader to obtain credit
More informationSouthern Derbyshire. Shared Care Pathology Guidelines. Abnormal Liver Function Tests (LFTs) in Adults
Southern Derbyshire Shared Care Pathology Guidelines Abnormal Liver Function Tests (LFTs) in Adults Purpose of Guideline The management of patients with abnormal liver function test results Scope This
More informationDiseases of peritoneum Lect. Al Qassim University, Faculty of Medicine Phase II Year III, CMD 332 Pathology Department 31-32
Diseases of peritoneum Lect Al Qassim University, Faculty of Medicine Phase II Year III, CMD 332 Pathology Department 31-32 Describe the etiology, pathogenesis and types of peritonitis Define ascites and
More informationAssessment of Liver Function and Diagnostic Studies. Disclosures
Assessment of Liver Function and Diagnostic Studies 2011 Joseph Ahn, M.D., M.S. Assistant Professor of Medicine Medical Director, Liver Transplantation v.3 Disclosures Absolute Autopsy Key Points 1. Review
More informationDifferential Diagnosis of NAFLD- A Short Summary:
Differential Diagnosis of NAFLD- A Short Summary: Almost a fifth of our general pediatric population is now classified as overweight in the United States. When such children present with elevated liver
More information2.1 AST can be measured in heparin plasma or serum. 3 Summary of clinical applications and limitations of measurements
Aspartate aminotransferase (serum, plasma) 1 Name and description of analyte 1.1 Name of analyte Aspartate aminotransferase (AST) 1.2 Alternative names Systematic name L aspartate:2 oxoglutarate aminotransferase
More informationAbnormal Liver Tests. Dr David Scott Gastroenterologist
Abnormal Liver Tests Dr David Scott Gastroenterologist Talk Outline Understanding Liver Tests Examples of Liver Diseases Case Studies Blood Tests for the Liver LFTs = Liver Function tests Hepatocyte damage
More informationLiver Failure. Nora Aziz. www.3bv.org. Bones, Brains & Blood Vessels
Liver Failure Nora Aziz www.3bv.org Bones, Brains & Blood Vessels Severe deterioration in liver function Looses ability to regenerate/repair decompensated Liver extensively damaged before it fails Equal
More informationSpleen. Anatomy. (Effective February 2007) (1%-5%) Normal. Related Anatomy Anterior to spleen. Medial border. Posteriorly
Spleen (Effective February 2007) (1%-5%) Anatomy Normal Intraperitoneal, except hilum Left hypochondrium Left hemidiaphragm superior generally considered to be ovoid, with a convex superior and a concave
More informationBilirubin (serum, plasma)
Bilirubin (serum, plasma) 1 Analyte 1.1 Name of analyte Bilirubin 1.2 Alternative names None 1.3 NLMC code 1.4 Description of analyte Bilirubin is a linear tetrapyrrole (MW 585 Da), the final product of
More informationNORD Guides for Physicians #1. Physician s Guide to. Tyrosinemia. Type 1
NORD Guides for Physicians #1 The National Organization for Rare Disorders Physician s Guide to Tyrosinemia Type 1 The original version of this booklet was made possible by donations in honor of Danielle
More informationInflammation and Healing. Review of Normal Defenses. Review of Normal Capillary Exchange. BIO 375 Pathophysiology
Inflammation and Healing BIO 375 Pathophysiology Review of Normal Defenses Review of Normal Capillary Exchange 1 Inflammation Inflammation is a biochemical and cellular process that occurs in vascularized
More informationApproach to Abnormal Liver Tests
This Morning s Presentation Approach to Abnormal Liver Tests Hal F. Yee, Jr., M.D., Ph.D. Rice Distinguished Professor, UCSF Chief of Gastroenterology, SFGH hyee@medsfgh.ucsf.edu Clinical vignettes representing
More informationPreoperative Laboratory and Diagnostic Studies
Preoperative Laboratory and Diagnostic Studies Preoperative Labratorey and Diagnostic Studies The concept of standardized testing in all presurgical patients regardless of age or medical condition is no
More informationWHAT S WRONG WITH MY GALL BLADDER? GALL BLADDER POLYPS
WHAT S WRONG WITH MY GALL BLADDER? GALL BLADDER POLYPS This is a patient information booklet providing specific practical information about gall bladder polyps in brief. Its aim is to provide the patient
More informationBLOOD-Chp. Chp.. 6 What are the functions of blood? What is the composition of blood? 3 major types of plasma proteins
6.1 Blood: An overview BLOOD-Chp Chp.. 6 What are the functions of blood? Transportation: oxygen, nutrients, wastes, carbon dioxide and hormones Defense: against invasion by pathogens Regulatory functions:
More informationHKCPath Anatomical Pathology Peer Review and Scores : PDF version for download
AP2003R1 http://hkcpath.org. Correspondence: pkhui@ha.org.hk 1of 10 07/08/2003 HKCPath Anatomical Pathology Peer Review and Scores : PDF version for download AP141 Bone Marrow: Metastatic Carcinoma from
More informationCardiovascular diseases. pathology
Cardiovascular diseases pathology Atherosclerosis Vascular diseases A disease that results in arterial wall thickens as a result of build- up of fatty materials such cholesterol, resulting in acute and
More informationInfluenza (Flu) Influenza is a viral infection that may affect both the upper and lower respiratory tracts. There are three types of flu virus:
Respiratory Disorders Bio 375 Pathophysiology General Manifestations of Respiratory Disease Sneezing is a reflex response to irritation in the upper respiratory tract and is associated with inflammation
More informationunderstanding CIRRHOSIS of the liver A patient s guide from your doctor and
understanding CIRRHOSIS of the liver A patient s guide from your doctor and Cirrhosis Basics The liver is one of the most important organs in your body and weighs about 3 pounds. It sits in the upper right
More informationa series of fact sheets written by experts in the field of liver disease HCV DISEASE PROGRESSION
www.hcvadvocate.org HCSP FACT SHEET Symptoms & Complications of Cirrhosis Foreword After many years of infection with hepatitis C the liver can become severely scarred. The process starts with inflammation
More informationCommonly Asked Questions About Chronic Hepatitis C
Commonly Asked Questions About Chronic Hepatitis C From the American College of Gastroenterology 1. How common is the hepatitis C virus? The hepatitis C virus is the most common cause of chronic viral
More information2015 Outpatient Chronic Hepatitis B Management
2015 Outpatient Chronic Hepatitis B Management Hepatitis B Hepatitis B Info 70% of acute infections are subclinical More severe symptoms when in addition to other liver disease Fulminant Hepatitis
More informationLIPID PANEL CHOLESTEROL LIPOPROTEIN, ELECTROPHORETIC SEPARATION LIPOPROTEIN, DIRECT MEASUREMENT (HDL) LDL DIRECT TRIGLYCERIDES
Test Code Test Name CPT CHOL Cholesterol, Serum 82465 HDL HDL, (High Density Lipoprotein) 83718 TRIG Triglycerides, Serum 84478 FTRIG Triglycerides (Fluid) 84478 LIPID Lipid Panel 80061 LDL LDL (Low Density
More informationIRON METABOLISM DISORDERS
IRON METABOLISM DISORDERS ANEMIA Definition Decrease in the number of circulating red blood cells Most common hematologic disorder by Most common hematologic disorder by far 1 Blood loss ANEMIA Causes
More informationKidney Cancer OVERVIEW
Kidney Cancer OVERVIEW Kidney cancer is the third most common genitourinary cancer in adults. There are approximately 54,000 new cancer cases each year in the United States, and the incidence of kidney
More informationCirrhosis and Ascites. Thomas S. Foster, Pharm.D. Integrated Therapeutics PHR 961
Cirrhosis and Ascites Thomas S. Foster, Pharm.D. Integrated Therapeutics PHR 961 Overview Liver weighs about 3 pounds and is the largest organ in the body. It is located in the upper right side of the
More informationINITIATING ORAL AUBAGIO (teriflunomide) THERAPY
FOR YOUR PATIENTS WITH RELAPSING FORMS OF MS INITIATING ORAL AUBAGIO (teriflunomide) THERAPY WARNING: HEPATOTOXICITY AND RISK OF TERATOGENICITY Severe liver injury including fatal liver failure has been
More informationViral Liver Disease. The Liver and Its Functions
Viral Liver Disease The Liver and Its Functions The liver, the body's largest organ weighing about three pounds, is located on the right side of the abdomen, protected by the lower rib cage. It is responsible
More informationA912: Kidney, Renal cell carcinoma
A912: Kidney, Renal cell carcinoma General facts of kidney cancer Renal cell carcinoma, a form of kidney cancer that involves cancerous changes in the cells of the renal tubule, is the most common type
More informationEvaluation and Prognosis of Patients with Cirrhosis
Evaluation and Prognosis of Patients with Cirrhosis Marion G. Peters, MD John V. Carbone, MD, Endowed Chair Professor of Medicine Chief of Hepatology Research University of California San Francisco Recorded
More informationCANCER OF THE LIVER HEPATOCELLULAR CARCINOMA
CANCER OF THE LIVER HEPATOCELLULAR CARCINOMA WHAT IS CANCER OF THE LIVER? Hepatocellular carcinoma is the most common form and it comes from the main type of liver cell, the hepatocyte. About 3 out 4
More informationYour Life Your Health Cariodmetabolic Risk Syndrome Part VII Inflammation chronic, low-grade By James L. Holly, MD The Examiner January 25, 2007
Your Life Your Health Cariodmetabolic Risk Syndrome Part VII Inflammation chronic, low-grade By James L. Holly, MD The Examiner January 25, 2007 The cardiometabolic risk syndrome is increasingly recognized
More informationBlood & Marrow Transplant Glossary. Pediatric Blood and Marrow Transplant Program Patient Guide
Blood & Marrow Transplant Glossary Pediatric Blood and Marrow Transplant Program Patient Guide Glossary Absolute Neutrophil Count (ANC) -- Also called "absolute granulocyte count" amount of white blood
More informationEXECUTIVE BLOOD WORK PANEL
EXECUTIVE BLOOD WORK PANEL Below is a list of all blood and urine testing done on the day of your Executive Medical. MALE Serum Glucose Random Serum Glucose Fasting Creatinine Uric Acid Sodium Potassium
More informationLiver Cancer. What is liver cancer? About the liver
Style Definition: List Bullet,List Bullet 1: Indent: Left: 0.13", Tab stops: 0.12", Left + Not at 2.8" What is liver cancer? Liver Cancer Cancer starts when cells in the body begin to grow out of control.
More informationHemodynamic Disorders Edema, Hyperemia/Congestion, Hemorrhage
Michele D. Raible, M.D., Pharm.D. UIC College of Medicine Deputy Head for Pathology Education M2 Pathology Course Assistant Professor of Clinical Pathology,UIC Lecture #12 Phone: 312-996-7250 Monday, September
More informationUCLA Asian Liver Program
CLA Program Update Program Faculty Myron J. Tong, PhD, MD Professor of Medicine Hepatology Director, Asian Liver Program Surgery Ronald W. Busuttil, MD, PhD Executive Chair Department of Surgery Director,
More informationSession 11: The ABCs of LFTs Learning Objectives
Session 11: The ABCs of LFTs Learning Objectives 1. Define 3 key components of the patient history that should be further evaluated when liver function testing reveals elevated aminotransferases. 2. Identify
More information37 2 Blood and the Lymphatic System Slide 1 of 34
1 of 34 Blood is a connective tissue that contains both dissolved substances and specialized cells. 2 of 34 The functions of blood include: collecting oxygen from the lungs, nutrients from the digestive
More informationWhat to Do with the Patient With Abnormal Liver Enzymes? Nizar N. Zein, M.D. The Cleveland Clinic
What to Do with the Patient With Abnormal Liver Enzymes? Nizar N. Zein, M.D. The Cleveland Clinic Introduction Elevated liver enzymes is often not a clinical problem by itself. However it is a warning
More informationCardiac Masses and Tumors
Cardiac Masses and Tumors Question: What is the diagnosis? A. Aortic valve myxoma B. Papillary fibroelastoma C. Vegetation from Infective endocarditis D. Thrombus in transit E. None of the above Answer:
More informationCystic Fibrosis. Cystic fibrosis affects various systems in children and young adults, including the following:
Cystic Fibrosis What is cystic fibrosis? Cystic fibrosis (CF) is an inherited disease characterized by an abnormality in the glands that produce sweat and mucus. It is chronic, progressive, and is usually
More information