jaundice biochemical profile-

Information about jaundice biochemical profile-

Published on May 23, 2014

Author: drmustansar

Source: authorstream.com

Content

HEME DEGRADATION AND JAUNDICE DR MUHAMMAD MUSTANSAR: HEME DEGRADATION AND JAUNDICE DR MUHAMMAD MUSTANSAR PowerPoint Presentation: Largest internal organ Weighs about 1400-1800 gram Located on right side under ribcage Ability to regenerate Has over 500 vital functions Involved in many digestive, vascular and metabolic activities Liver PowerPoint Presentation: FATE OF RED BLOOD CELLS  Life span in blood stream is 60-120 days  Senescent RBCs are phagocytosed and/or lysed Normally, lysis occurs extravascularly in the reticuloendothelial system subsequent to RBC phagocytosis Lysis can also occur intravascularly (in blood stream) PowerPoint Presentation: (Liver, Bone marrow, & Spleen) Hemoglobin Globin Amino acids Amino acid pool Heme Bilirubin Fe 2+ Excreted Phagocytosis & Lysis Extravascular Pathway for RBC Destruction PowerPoint Presentation: Sickled Red Blood Cells Introduction: I ntroduction Bilirubin is the orange-yellow pigment derived from senescent red blood cells. It is a toxic waste product in the body. It is extracted and biotransformed mainly in the liver, and excreted in bile and urine. PowerPoint Presentation: It is a bile pigment Elevations in serum and urine bilirubin levels are normally associated with Jaundice.   PowerPoint Presentation: Erythrocytes become “old” as they lose their flexibility and become pikilocytes (spherical), increasingly rigid and fragile. Once the cell become fragile, they easily destruct during passage through tight circulation spots, especially in spleen, where the intra-capillary space is about 3 micron as compared to 8 micron of cell size PowerPoint Presentation: Races useful life span is 100 to 120 days,After which they become trapped and fragment in smaller circulatory channels, particularly in those of the spleen. For this reason, the spleen is sometimes called the “red blood cell graveyard.” Dying erythrocytes are engulfed and destroyed by macrophages. PowerPoint Presentation:  Primary site of synthesis:- SPLEEN : The Graveyard of Red Blood Cells Secondary site of synthesis:- LIVER & BONE MARROW Formation of Bilirubin PowerPoint Presentation: An average person produces about 4 mg/kg of bilirubin per day. The daily bilirubin production from all sources in man averages from 250 to 300 mg. PowerPoint Presentation: (Liver, Bone marrow, & Spleen) Hemoglobin Globin Amino acids Amino acid pool Heme Bilirubin Fe 2+ Excreted Phagocytosis & Lysis Recycled Extravascular Pathway for RBC Destruction PowerPoint Presentation: DEGRADATION OF HEME TO BILIRUBIN P 450 cytochrome  75% is derived from RBCs In normal adults this results in a daily load of 250-300 mg of bilirubin Normal plasma concentrations are less then 1 mg/dL Hydrophobic – transported by albumin to the liver for further metabolism prior to its excretion “unconjugated” bilirubin PowerPoint Presentation: Hemoglobin – 80% Myoglobin Cytochrome P450s Hemoproteins Macrophage of the reticuloendothelial system Heme Heme Oxygenase Biliverdin Biliverdin Reductase Bilirubin Blood O 2 Fe 3+ + CO NADPH + H + NADP+ Heme Metabolism PowerPoint Presentation: RBCs Breakdown Hemoglobin Produces & Breakdown Heme Biliverdin Bilirubin Heme Oxygenase Biliverdin Reductase Pathophysiology PowerPoint Presentation: The globin is recycled or converted into amino acids , which in turn are recycled or catabolized as required. Heme is oxidized, with the heme porphyrin ring being opened by the endoplasmic reticulum enzyme, heme oxygenase. PowerPoint Presentation: The oxidation occurs on a specific carbon producing equimolar amounts of the biliverdin , iron , and carbon monoxide (CO) . This is the only reaction in the body that is known to produce CO. PowerPoint Presentation: Most of the CO is excreted through the lungs, with the result that the CO content of expired air is a direct measure of the activity of heme oxygenase in an individual. PowerPoint Presentation: III IV I II Oxidation Heme Oxygenase In the first reaction, a bridging methylene group is cleaved by heme oxygenase to form Linear Biliverdin from Cyclic Heme molecule. Fe 2 + is released from the ring in this process. PowerPoint Presentation: I II III IV Fe 2+ NADP H C O 2 O O 2 Heme Oxygenase O PowerPoint Presentation: I II III IV Biliverdin PowerPoint Presentation: NADP H H Bilirubin PowerPoint Presentation: In the next reaction, a second bridging methylene (between rings III and IV) is reduced by biliverdin reductase, producing bilirubin . I I III III IV IV II II Reduction Biliverdin Reductase PowerPoint Presentation: biliverdin causing a change in the color of the molecule from blue-green (biliverdin) to yellow-red (bilirubin). PowerPoint Presentation: The latter catabolic changes in the structure of tetrapyrroles are responsible for the progressive changes in color of a hematoma, or bruise, in which the damaged tissue changes its color from an initial dark blue to a red-yellow and finally to a yellow color before all the pigment is transported out of the affected tissue. PowerPoint Presentation: Peripherally arising bilirubin is transported to the liver in association with albumin, where the remaining catabolic reactions take place. PowerPoint Presentation: Bilirubin is not very water-soluble, so most of it is carried to the liver bound to albumin. PowerPoint Presentation: In cells of the liver, bilirubin undergoes modification to increase its water solubility so that it can be excreted more easily. Bilirubin is conjugated to two molecules of glucuronic acid, creating bilirubin diglucuronide. b. Bilirubin diglucuronide is transported out of the hepatocytes into the bile canaliculi and is thus excreted in bile. PowerPoint Presentation: In Blood The bilirubin synthesized in spleen, liver & bone marrow is unconjugated bilirubin. It is hydrophobic in nature so it is transported to the liver as a complex with the plasma protein, albumin . PowerPoint Presentation: Unconjugated bilirubin Lipid soluble : limits excretion 1 gm albumin binds 8.5 mg bilirubin Fatty acids & drugs can displace bilirubin Indirect positive reaction in van den Bergh test Role of Blood Proteins in the Metabolism of Bilirubin: Role of Blood Proteins in the Metabolism of Bilirubin 1. Albumin Albumin Dissolved in Blood Bilirubin PowerPoint Presentation: Blood Liver Albumin Ligandin (-) charge Bilirubin Albumin Ligandin (-) charge Bilirubin Ligandin Prevents bilirubin from going back to plasma PowerPoint Presentation: In Endoplasmic Reticulum In the microsomes of the endoplasmic reticulum, unconjugated bilirubin is converted to water soluble mono- or di- conjugates by sequential covalent coupling with glucuronic acid. PowerPoint Presentation:  Bilirubin is conjugated in a two step process to form bilirubin mono- & di- glucuronide Conjugation with Glucoronates: Conjugation with Glucoronates COOH COOH Propionate Propionate Methyl Vinyl Vinyl Methyl Glucoronyl transferase BILIRUBIN DIGLUCORONIDE PowerPoint Presentation: Heme Biliverdin Heme oxygenase Bilirubin Biliverdin reductase BILIRUBIN PHYSIOLOGY PowerPoint Presentation: N O FIBROUS TISSUE PowerPoint Presentation: Role of Liver in Metabolism PowerPoint Presentation: Organ Interactions Roll over organs and tissues to see that they all require different fuels and produce different metabolites. PowerPoint Presentation: Excretion of Bilirubin PowerPoint Presentation: In the Intestine In the small intestine, conjugated bilirubins are poorly reabsorbed, but are partly hydrolyzed back to unconjugated bilirubin by catalytic action of bacterial ß-glucuronidases. In the distal ileum and colon, anaerobic flora mediate further catabolism of bile pigments: PowerPoint Presentation: hydrolysis of conjugated bilirubin to unconjugated bilirubin by bacterial β -glucuronidases; multistep hydrogenation (reduction) of unconjugated bilirubin to form colorless urobilinogens; and oxidation of unconjugated bilirubin to brown colored mesobilifuscins. PowerPoint Presentation: Urobilinogens is a collective term for a group of 3 tetrapyrroles; Stercobilinogen (6H) Mesobilinogen (8H)&, Urobilinogen (12H) Upto 20 % of urobilinogen produced daily is reabsorbed from the intestine & enters the entero-hepatic circulation. PowerPoint Presentation: Urobilinogen Structure PowerPoint Presentation: Most of the reabsorbed urobilinogen is taken up by the liver & is re-excreted in the bile. A small fraction (2 % - 5 %) enters the general circulation & appears in the urine. PowerPoint Presentation: In the lower intestinal tract, the 3 urobilinogens spontaneously oxidize to produce the corresponding bile pigments; Stercobilin Mesobilin & Urobilin; which are orange-brown in color and are the major pigments of stool. :  PowerPoint Presentation: Bilirubin Metabolism PowerPoint Presentation: JAUNDICE PowerPoint Presentation: Yellowing of the skin, scleras (white of the eye), and mucous membranes (jaundice) Detectable when total plasma bilirubin levels exceed 2mg/100mL AHHH!!! I have symptoms of hyperbilirubinemia!!! SYMPTOMS PowerPoint Presentation: Hyperbilirubinemia & Types of Jaundice Hyperbilirubinemia : Increased plasma concentrations of bilirubin (> 3 mg/dl) occurs when there is an imbalance between its production and excretion. Recognized clinically as jaundice. Also known as icterus, a yellow discoloration of the skin, sclerae and mucous membrane. Clinical Significance PowerPoint Presentation: Jaundice becomes clinically evident when the serum bilirubin level exceeds 2.5mg/dL. Several types of Jaundice: Hemolytic Hepatocellular Obstructive PowerPoint Presentation: Symptoms: Yellow discoloration of the skin, sclerae and mucous membranes Itching (pruritus) due to deposits of bile salts on the skin Stool becomes light in color Urine becomes deep orange and foamy PowerPoint Presentation: Excessive Production of Bilirubin Reduced Hepatocyte Uptake Impaired Bilirubin conjugation Impaired Bile Flow Different Causes of Jaundice PowerPoint Presentation: Pre-hepatic Hepatic Post-Hepatic Jaundice Classification PowerPoint Presentation: Causes of jaundice PowerPoint Presentation: The causes of jaundice Type Cause Clinical example Frequency Prehepatic Hemolysis Autoimmune Abnormal haemoglobin Uncommon Depends on region Intrahepatic Infection Hepatitis A, B, C Common/ very common Chemical/ drug Acetaminophen Alcohol Common Common Genetic errors: bilirubin metabolism Gilbert ’ s syndrome Crigler-Najjar syndrome Dubin-Johnson syndrome Rotor ’ s syndrome 1 in 20 Very rare Very rare Very rare Genetic errors: specific proteins Wilson ’ s disease  1 antitrypsin 1 in 200,000 1 in 1000 with genotype Autoimmune Chronic active hepatitis Uncommon/rare Neonatal Physiologic Very common PowerPoint Presentation: The causes of jaundice Type Cause Clinical example Frequency Posthepatic Intrahepatic bile ducts Drugs Primary bilary cirrhosis Cholangitis Common Uncommon Common Extrahepatic bile ducts Gall stones Pancreatic tumor Cholangiocarcinoma Very common Uncommon Rare PowerPoint Presentation: Prehepatic (hemolytic) jaundice Results from excess production of bilirubin (beyond the livers ability to conjugate it) following hemolysis Excess RBC lysis is commonly the result of autoimmune disease; hemolytic disease of the newborn (Rh- or ABO- incompatibility); structurally abnormal RBCs (Sickle cell disease); or breakdown of extravasated blood PowerPoint Presentation: High plasma concentrations of unconjugated bilirubin (normal concentration ~0.5 mg/dL) PowerPoint Presentation: Hepatic jaundice Impaired uptake, conjugation, or secretion of bilirubin Reflects a generalized liver (hepatocyte) dysfunction In this case, hyperbilirubinemia is usually accompanied by other abnormalities in biochemical markers of liver function PowerPoint Presentation: Intrahepatic jaundice PowerPoint Presentation: Inflammation of the liver Caused by viruses, alcohol, medications, and other toxins This training will focus on viral hepatitis What is Hepatitis? PowerPoint Presentation: Hepatitis A Virus (HAV) Hepatitis B Virus (HBV) Hepatitis C Virus (HCV) Hepatitis D Virus (HDV) Hepatitis E Virus (HEV) Hepatitis F Hepatitis G (not confirmed yet). These viruses all affect the liver but otherwise are unique PowerPoint Presentation: Virus is the most common cause of hepatitis . Only occasionally can bacterial infections like syphilis or TB be considered Acute Hepatitis PowerPoint Presentation: Hepatitis A (HAV) PowerPoint Presentation: jaundice fatigue abdominal pain loss of appetite nausea diarrhea fever Adults have signs and symptoms more often than children Incubation Period : 15-50 days (average 28 days) Signs and Symptoms of HAV PowerPoint Presentation: Hepatitis B (HBV) PowerPoint Presentation: HBsAg = surface (coat) protein ( 4 phenotypes : adw, adr, ayw and ayr) HBcAg = inner core protein ( a single serotype) HBeAg = secreted protein; function unknown HBV Structure & Antigens Dane particle PowerPoint Presentation: Hepatitis C (HCV) PowerPoint Presentation: jaundice fatigue dark urine abdominal pain  loss of appetite nausea 80% of persons have no signs or symptoms Symptoms of HCV PowerPoint Presentation: Types D, E, F, and G Hepatitis PowerPoint Presentation: Most patients are symptomatic. The most common complaints are: Anorexia, nausea, vomiting Abdominal pain (RUQ) Fever (due to infection or inflammation of liver) Alcoholic Hepatitis Symptoms PowerPoint Presentation: Weight loss due to anorexia Jaundice is usually mild Diarrhea which is due to portal hypertension PowerPoint Presentation: Hemolytic jaundice arises as a consequence of excessive destruction of RBCs. – This overloads the capacity of the RE system to metabolize heme. – Failure to conjugate bilirubin to glucuronic acid causes accumulation of bilirubin in the unconjugated form in the blood. PowerPoint Presentation: Hepatocellular jaundice arises from liver disease, either inherited or acquired. – Liver dysfunction impairs conjugation of bilirubin. – Consequently, unconjugated bilirubin spills over into the blood. –In addition, urobilinogen is elevated in the urine. PowerPoint Presentation: Ongoing liver damage with liver cell necrosis followed by fibrosis and hepatocyte regeneration results in cirrhosis. This produces a nodular, firm liver. The nodules seen here are larger than 3 mm and, hence, this is an example of "macronodular" cirrhosis. PowerPoint Presentation: Mechanism of fibrosis and cirrhosis of the liver PowerPoint Presentation:  Definition : Is a condition characterized by Yellow discoloration of the skin , sclera & mucous membrane as a result of an elevated Sr. Bilirubin conc. due to an obstructive cause. Obstructive jaundice PowerPoint Presentation: Caused by an obstruction of the biliary tree. Plasma bilirubin is conjugated, and other biliary metabolites, such as bile acids accumulate in the plasma. Posthepatic(Obstructive) jaundice PowerPoint Presentation: Characterized by pale colored stools (absence of fecal bilirubin or urobilin), and dark urine (increased conjugated bilirubin). In a complete obstruction, urobilin is absent from the urine. PowerPoint Presentation: Posthepatic jaundice PowerPoint Presentation: • Obstructive jaundice, as the name implies, is caused by blockage of the bile duct by a gallstone or a tumor (usually of the head of the pancreas). – This prevents passage of bile into the intestine and consequently conjugated bilirubin builds up in the blood. PowerPoint Presentation: – Patients with this condition suffer severe abdominal pain associated with the obstruction (if due to gallstone) and their feces are gray in color due to lack of stercobilin. PowerPoint Presentation:   Pre-hepatic Hepatic Post hepatic cause Excessive break down Of RBC ’ s Malaria,HS Gilbert Syndrome Infective Liver Damage Bile Duct Obstruction Serum Bilirubin unconjugated Both conj+unconj . conjugated Urine bilirubin Absent Achloric jaundice Bilirubinemia + Deep yellow urine As in hepatic jaundice ++ Urine urobilinogen Increases Because of increased stercobilinogen Decreases Because of decreased stercobilinogen Absent(-) PowerPoint Presentation:   Pre-hepatic Hepatic Post hepatic Fecal stercobilinogen 20-250mg/day Markedly increased Dark brown stool Reduced Pale coloured stool Absent clay colored stool Fecal fat 5-6% normal Increased 40-50% Bulky,pale greasy foul smelling faeces As hepatic jaundice Liver functions normal Impaired SGOT/SGPT Normal Alkaline phosphatase++ Vonden burg test Indirect+ biphasic Direct+ PowerPoint Presentation: Differential diagnosis of jaundice Prehepatic Intrahepatic Posthepatic Conjugated bilirubin Absent ↑ ↑ AST or ALT Normal ↑ Normal ALP Normal Normal ↑ Urine bilirubin Absent Present Present Urine urobilinogen Present Present Absent PowerPoint Presentation: Common, particularly in premature infants. Transient (resolves in the first 10 days). Due to immaturity of the enzymes involved in bilirubin conjugation. Neonatal Jaundice PowerPoint Presentation: High levels of unconjugated bilirubin are toxic to the newborn – due to its hydrophobicity it can cross the blood-brain barrier and cause a type of mental retardation known as kernicterus If bilirubin levels are judged to be too high, then phototherapy with UV light is used to convert it to a water soluble, non-toxic form. PowerPoint Presentation: If necessary, exchange blood transfusion is used to remove excess bilirubin Phenobarbital is oftentimes administered to Mom prior to an induced labor of a premature infant – crosses the placenta and induces the synthesis of UDP glucuronyl transferase PowerPoint Presentation: Jaundice within the first 24 hrs of life or which takes longer then 10 days to resolve is usually pathological and needs to be further investigated PowerPoint Presentation: CLINICAL FEATURES Severe unconjugated hyperbilirubinemia at birth Prior to phototherapy: Kernicterus Death in infancy Phototherapy: Phototherapy Phototherapy is usually not needed unless the bilirubin levels rise very quickly or go above 16-20 mg/dl in healthy, full term babies. During phototherapy, the treatment of choice for jaundice, babies are placed under blue lights that convert the bilirubin into compounds that can be eliminated from the body. PowerPoint Presentation: Phototherpy for infants PowerPoint Presentation: Kernicterus or brain encephalopathy refers to the yellow staining of the deep nuclei (i.e., the kernel) of the brain namely, the basal ganglia. It is a form of permanent brain damage caused by excessive jaundice. Bilirubin Toxicity - Kernicterus PowerPoint Presentation: The concentration of bilirubin in serum is so high that it can move out of the blood into brain tissue by crossing the fetal blood-brain barrier. This condition develops in newborns with prolonged jaundice due to: Polycythemia Rh incompatibility between mother & fetus Inherited Disorders of Bilirubin Metabolism: Inherited Disorders of Bilirubin Metabolism Gilbert’s Syndrome Crigler-Najjar (Type I) Crigler-Najjar (Type II) Lucey-Driscoll Dubin-Johnson Rotor’s Syndrome Isolated increased serum bilirubin: Isolated increased serum bilirubin Ruling out of hemolysis, subsequent fractionation of the bilirubin Possibility of the following syndromes: Dublin-Johnson Rotor Possibility of following syndromes based on the bilirubin concentration: Gilbert’s - <3 mg/dl Crigler-Najjar (Type I) - >25 mg/dl Crigler-Najjar (Type II) - 5 to 20 mg/dl Lucey-Driscoll - Transiently ~ 5 mg/dl Algorithm for differentiating the familial causes of Hyperbilirubinemia Conjugated Unconjugated PowerPoint Presentation: Crigler-Najjar Syndrome (Type I) is a rare genetic disorder caused by complete absence of UDP-glucuronyltransferase and manifested by very high levels of unconjugated bilirubin. It is inherited as an autosomal recessive trait. Crigler-Najjar Syndrome (Type I) PowerPoint Presentation: Most patients die of severe brain damage caused by kernicterus within the first year of life. Early liver transplantation is the only effective therapy. PowerPoint Presentation: This is a rare autosomal dominant disorder. It is characterized by partial deficiency of UDP-glucuronyltransferase. Unconjugated bilirubin is usually 5 – 20 mg/dl. Unlike Crigler-Najjar Type I, Type II responds dramatically to Phenobarbital & a normal life can be expected. Crigler-Najjar Syndrome (Type II) PowerPoint Presentation: Gilbert’s syndrome is also called as familial non-hemolytic non-obstructive jaundice. mild unconjugated Hyperbilirubinemia. It affects 3% – 5% of the population. It is often misdiagnosed as chronic Hepatitis. Gilbert’s Syndrome PowerPoint Presentation: The concentration of Bilirubin in serum fluctuates between 1.5 & 3 mg/dl. In this condition the activity of hepatic glucuronyltransferase is low as a result of mutation in the bilirubin-UDP-glucuronyltransferase gene(UGT1A1). PowerPoint Presentation: It is a benign, autosomal recessive condition characterized by jaundice with predominantly elevated conjugated bilirubin and a minor elevation of unconjugated bilirubin. Excretion of various conjugated anions and bilirubin into bile is impaired, reflecting the underlying defect in canalicular excretion. Dubin-Johnson Syndrome PowerPoint Presentation: The Liver has a characteristic greenish black appearance and liver biopsy reveals a dark brown melanin-like pigment in hepatocytes and kupffer cells. PowerPoint Presentation: It is another form of conjugated hyperbilirubinemia. It is similar to dubin-johnson syndrome but without pigmentation in liver. Rotor’s Syndrome PowerPoint Presentation: Thank You

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