It is inherited as an autosomal recessive trait. Unlike Crigler-Najjar Type I, Type II responds dramatically to Phenobarbital & a normal life can be expected.Gilberts Syndrome: Gilberts Syndrome Gilberts syndrome is also called as familial non-hemolytic non-obstructive jaundice. Go Premium Sign Up Sign In Take a Tour Help Home Browse Browse Presentations Featured Presentations Most Viewed Channels Categories Greeting Cards PowerPoint Templates PowerPoint Templates PowerPoint Diagrams Upload Upload from Desktop Single File Upload Presentations (PPT, KEY, PDF) Presentations (PPT, KEY, PDF) PowerPoint Templates . In addition, urobilinogen is elevated in the urine.PowerPoint Presentation: Posthepatic (Obstructive) jaundice Caused by an obstruction of the biliary tree. logging in or signing up Bilirubin Metabolism drraghu74 Download Post to : URL : Related Presentations : Let's Connect Share Add to Flag Embed Email Add to Channel Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed Use HTTPS URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. I I III III IV IV II II Reduction Biliverdin ReductasePowerPoint Presentation: biliverdin causing a change in the color of the molecule from blue-green ( biliverdin ) to yellow-red ( bilirubin ). In this condition the activity of hepatic glucuronyltransferase is low as a result of mutation in the bilirubin -UDP- glucuronyltransferase gene(UGT1A1).Dubin-Johnson Syndrome: Dubin-Johnson Syndrome It is a benign, autosomal recessive condition characterized by jaundice with predominantly elevated conjugated bilirubin and a minor elevation of unconjugated bilirubin. 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 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 investigatedPhototherapy: 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. Cookies are required to use this site.
The daily bilirubin production from all sources in man averages from 250 to 300 mg .Extravascular Pathway for RBC Destruction: Extravascular Pathway for RBC Destruction (Liver, Bone marrow, & Spleen) Hemoglobin Globin Amino acids Amino acid pool Heme Bilirubin Fe 2+ Excreted Phagocytosis & Lysis RecycledPowerPoint Presentation: Within cells of the RE system, heme degraded to bilirubin in a two-step process . .. This condition develops in newborns with prolonged jaundice due to: Polycythemia Rh incompatibility between mother & fetusInherited Disorders of Bilirubin Metabolism: Inherited Disorders of Bilirubin Metabolism Gilberts Syndrome Crigler-Najjar (Type I) Crigler-Najjar (Type II) Lucey -Driscoll Dubin -Johnson Rotors SyndromeIsolated 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: Gilberts - 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 UnconjugatedCrigler-Najjar Syndrome (Type I): Crigler-Najjar Syndrome (Type I) 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. Unconjugated bilirubin is usually 5 20 mg/dl. It is often misdiagnosed as chronic Hepatitis. Send to Blogs and Networks Processing . Some suggestions: Go back to the last page Go to the home page .. 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. 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: JAUNDICEClinical Significance: Clinical Significance Hyperbilirubinemia & Types of Jaundice Hyperbilirubinemia : Increased plasma concentrations of bilirubin (> 3 mg/dl) occurs when there is an imbalance between its production and excretion. Numeric tags are not allowed.
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