Page 439 - Concise Pathology for Exam Preparation ( PDFDrive )

424 SECTION II Diseases of Organ Systems

Clinical Features of Jaundice

• Jaundice (excess bilirubin deposited in the skin and mucosae)
• Dark urine (results from excess bilirubin excreted by the kidneys)
• Light-coloured stools (passage of bilirubin into the intestine is blocked)
• Generalized itchiness (retention of bile products in the skin may cause itching, with
subsequent scratching and skin damage)
• Stools may contain too much fat (a condition called steatorrhoea) because bile cannot
enter the intestine to help digest fat in foods
• There is impaired absorption of calcium, vitamin D and K due to decreased entry of bile
in the intestine. The patient has a tendency to bleed due to deficiency of vitamin K.

Classification of Jaundice
The classification of jaundice is based on the pathological mechanisms underlying it
(Table 15.1):
1. Haemolytic jaundice
(a) Increased destruction of red blood cells or their precursors, resulting in a pre-
dominant increase in unconjugated bilirubin
(b) Absence of bilirubin in urine
(c) Urinary urobilinogen is increased (more than 4 mg/24 h).
(d) Other liver function tests are normal.
(e) Evidence of haemolytic anaemia (increased reticulocyte count, or presence of frag-
mented red cells or Schistocytes in the peripheral blood film, decreased haptoglobin,
increased LDH and positive direct Coombs test)
2. Hepatocellular jaundice: In hepatocellular jaundice, concentration of both unconju-
gated and conjugated bilirubin is increased. It has two elements, an ‘obstructive element’,
causing impaired uptake of unconjugated bilirubin into the cell and of conjugated biliru-
bin into biliary canaliculi. Swelling of cells and oedema due to inflammation contribute
to mechanical obstruction of the intrahepatic biliary tree. The ‘hepatocellular element’
results from the liver cell damage.
Indicators of hepatocellular injury:
• Elevated aminotransferase activity
• Acute phase reactant response (iron and ferritin elevation)
• Reduced synthetic function (prolonged PT, low albumin and cholesterol)

TABLE 15.1. Pathophysiological classification of jaundice
Type Mechanism Causes
Prehepatic Increased production of bilirubin Haemolysis (intravascular or extravascular)
Ineffective erythropoiesis
Haemorrhagic infarction
Massive hematomas
Hepatic Reduced uptake Congenital: Gilbert syndrome
Acquired: Drugs (rifampin and contrast dyes), septi-
caemia, fasting
Impaired conjugation Physiological jaundice of newborn
Congenital: Gilbert, Crigler–Najar syndromes
Acquired: Hepatitis, benign and malignant neoplasms
Reduced excretion into the bile Congenital: Dubin–Johnson and Rotor syndromes
Acquired: Drugs (oral contraceptives, methyl testos-
terone, chlorpromazine), hepatitis, biliary cirrhosis
and benign cholestasis of pregnancy
Posthepatic Obstruction of bile ducts Stones, pancreatitis, pancreatic tumour, parasites,
strictures, tumours and biliary atresia (intrahepatic
and extrahepatic)

mebooksfree.com