Final answer:
The inborn errors in liver bilirubin uptake and glucuronyl transferase activity leading to hyperbilirubinemia are represented by Crigler-Najjar syndrome and Gilbert's disease, resulting in unconjugated hyperbilirubinemia and potential neurological damage.
Step-by-step explanation:
Crigler-Najjar syndrome and Gilbert's disease are two conditions that represent inborn errors in liver bilirubin uptake and glucuronyl transferase activity resulting in hyperbilirubinemia. Crigler-Najjar syndrome is caused by the absence of UDP glucuronyl transferase activity, leading to high serum bilirubin levels. In Gilbert's disease, there is a defect in the liver's uptake of bilirubin due to reduced UDP-glucuronyl transferase activity.
Unconjugated hyperbilirubinemia occurs when UDP glucuronyl transferase activity is not fully developed in infants, causing accumulation of unconjugated bilirubin in the blood and potential neurological damage if levels become too high.
Infective or hepatic jaundice results from liver damage, which can be due to alcoholism, toxic substances, or infections, leading to the failure to conjugate and excrete normally produced bilirubin.
Haemolytic or prehepatic jaundice is caused by excessive hemolysis, resulting in an overproduction of bile pigments that exceed the liver's excretory capacity, leading to accumulation of unconjugated bilirubin.