Classify jaundice according to its aetiology. Make a tabular representation of the blood, urinary and stool findings observed in different types of jaundice.

Classification of Jaundice According to its Aetiology

Jaundice is broadly classified into three main types based on the location of the pathology in the bilirubin metabolic pathway: pre-hepatic, hepatic, and post-hepatic.

1. Pre-Hepatic (Hemolytic) Jaundice

This type of jaundice occurs before bilirubin is processed by the liver. It results from an increased rate of red blood cell breakdown (hemolysis) that overwhelms the liver's capacity to conjugate (process) the excessive unconjugated bilirubin. The liver itself is typically healthy and functional.

• Causes:
  • Hemolytic Anemias: Conditions where red blood cells are destroyed prematurely. Examples include:
    • Sickle cell anemia
    • Thalassemia
    • Hereditary spherocytosis
    • Glucose-6-phosphate dehydrogenase (G6PD) deficiency
    • Autoimmune hemolytic anemia
    • Drug-induced hemolysis
  • Ineffective Erythropoiesis: Conditions where red blood cell production in the bone marrow is abnormal, leading to premature destruction of immature red cells (e.g., pernicious anemia, vitamin B12 or folate deficiency).
  • Large Hematomas: Resorption of large blood clots can release a significant amount of heme, leading to increased bilirubin production.
  • Genetic Disorders:
    • Gilbert's Syndrome: A common, mild genetic disorder affecting the liver's ability to process bilirubin due to reduced activity of the conjugating enzyme.
    • Crigler-Najjar Syndrome (Type I and II): Rare, more severe genetic disorders leading to a significant impairment in bilirubin conjugation.

2. Hepatic (Hepatocellular) Jaundice

This type of jaundice occurs due to intrinsic liver disease, where the liver cells (hepatocytes) are damaged and cannot efficiently uptake, conjugate, or excrete bilirubin. This often leads to a "mixed picture" of both unconjugated and conjugated hyperbilirubinemia, as the liver's ability to perform all these functions is compromised.

• Causes:
  • Viral Hepatitis: Inflammation of the liver caused by viruses such as Hepatitis A, B, C, D, E, Epstein-Barr virus (EBV), and Cytomegalovirus (CMV).
  • Alcoholic Liver Disease: Liver damage ranging from fatty liver (steatosis) to alcoholic hepatitis and cirrhosis due to chronic alcohol consumption.
  • Drug-induced Liver Injury (Hepatotoxicity): Damage to liver cells caused by certain medications (e.g., paracetamol overdose, some antibiotics, anti-tuberculosis drugs).
  • Cirrhosis: Irreversible scarring of the liver, often caused by chronic hepatitis, alcohol abuse, or non-alcoholic fatty liver disease (NAFLD).
  • Autoimmune Hepatitis: The body's immune system attacks its own liver cells.
  • Primary Biliary Cholangitis (PBC): An autoimmune disease causing progressive destruction of small bile ducts within the liver.
  • Primary Sclerosing Cholangitis (PSC): A chronic disease causing inflammation and scarring of the bile ducts inside and outside the liver.
  • Genetic Metabolic Disorders:
    • Wilson's Disease (copper accumulation)
    • Hemochromatosis (iron overload)
    • Alpha-1 antitrypsin deficiency
    • Dubin-Johnson Syndrome and Rotor Syndrome (defects in bilirubin excretion from hepatocytes)
  • Liver Cancer: Primary hepatocellular carcinoma or metastatic liver disease.
  • Sepsis: Severe infection that can cause liver dysfunction.

3. Post-Hepatic (Obstructive/Cholestatic) Jaundice

This type of jaundice occurs after bilirubin has been conjugated by the liver, but its excretion into the digestive tract is blocked. The obstruction can be anywhere along the bile ducts, preventing bile (containing conjugated bilirubin) from reaching the duodenum.

• Causes:
  • Gallstones (Choledocholithiasis): Stones in the common bile duct are the most common cause of obstructive jaundice.
  • Pancreatic Cancer (Head of Pancreas): Tumors in the head of the pancreas can compress the common bile duct.
  • Cholangiocarcinoma: Cancer of the bile ducts.
  • Biliary Strictures: Narrowing of the bile ducts, often due to inflammation, surgery, or chronic pancreatitis.
  • Biliary Atresia: A rare congenital condition in infants where bile ducts are absent or blocked.
  • Pancreatitis (Acute or Chronic): Inflammation of the pancreas can cause swelling and compression of the common bile duct.
  • Parasitic Infections: Certain parasites (e.g., liver flukes, Ascaris lumbricoides) can obstruct bile ducts.
  • Mirizzi's Syndrome: Compression of the common hepatic duct by a gallstone impacted in the cystic duct.

Tabular Representation of Blood, Urinary, and Stool Findings in Different Types of Jaundice

The following table summarizes the key laboratory and clinical findings that help differentiate between the types of jaundice:

Parameter	Pre-Hepatic Jaundice	Hepatic Jaundice	Post-Hepatic Jaundice
Serum Bilirubin	Predominantly Unconjugated (Indirect) bilirubin significantly elevated. Total bilirubin elevated.	Mixed Unconjugated and Conjugated (Direct) bilirubin elevated, with variable proportions depending on the specific liver injury and stage. Total bilirubin elevated.	Predominantly Conjugated (Direct) bilirubin significantly elevated. Total bilirubin elevated.
Urine Bilirubin	Absent or trace (Unconjugated bilirubin is not water-soluble and cannot be filtered by kidneys).	Present (Conjugated bilirubin spills into blood and is water-soluble, thus filtered). Urine is dark brown ("tea-colored" or "coca-cola" colored).	Present (Conjugated bilirubin spills into blood and is water-soluble, thus filtered). Urine is dark brown ("tea-colored").
Urine Urobilinogen	Increased (Excess bilirubin reaches intestines, more urobilinogen formed and reabsorbed).	Normal, decreased, or increased (Highly variable, depends on the extent of liver damage and intrahepatic cholestasis).	Markedly decreased or absent (No bilirubin reaches intestines for urobilinogen formation).
Stool Color	Normal to darker (Increased stercobilin formation due to excess bilirubin).	Normal to pale (Variable, depending on bile excretion impairment).	Pale or Clay-colored (Acholic stools) (Bile pigment is prevented from reaching the intestines, so stercobilin is not formed).
Liver Enzymes (AST/ALT)	Normal or mildly elevated.	Significantly elevated (often >400 IU/L in acute hepatitis). AST/ALT ratio >2:1 often seen in alcoholic liver disease.	Normal or moderately elevated (usually <100-200 IU/L), less than in hepatic jaundice.
Alkaline Phosphatase (ALP) & Gamma-Glutamyl Transferase (GGT)	Normal.	Normal or moderately elevated.	Significantly elevated (often >3 times normal), indicating cholestasis.
Other Findings	Signs of hemolysis (anemia, reticulocytosis, abnormal red cell morphology). No pruritus.	Nausea, vomiting, abdominal pain, fever (in acute hepatitis), fatigue, sometimes pruritus.	Severe pruritus (itching) due to bile salt accumulation, abdominal pain (especially with gallstones or pancreatitis), sometimes fever.