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Neonatal Jaundice
INTRODUCTION
PATHOPHYSIOLOGY
DIFFERENTIAL DIAGNOSIS
HISTORY
EXAMINATION
INVESTIGATION
INTRODUCTION
Bilirubin is the end product of heme
degradation
Most of the daily production comes from the
breakdown of RBCs in the RES
Heme biliverdin bilirubin
Bilirubin is released & bound to serum
albumin
Bilirubin is uptake & conjugated with
glucuronic acid
Finally conjugated bilirubin is excreted in bile
PATHOPHYSIOLOGY
UNCONJUGATED B. CONJUGATED B.
Tightly compounded Non toxic
to s. albumin Water soluble
Normally very small Loosely bound to
amount is present as albumin. Delta fraction
albumin free
Insoluble in water
can not be excreted
in urine
Toxic
Both conjugated & unconjugated bilirubin
may accumulate systemically & deposit in
tissues
Normally s. bilirubin level vary b/w 0.3 &
1.2mg/dl.
The rate of systemic bilirubin production
is = to the rate of hepatic uptake,
conjugation & biliray excretion .
Jaundice becomes evident when the
s.bilirubin levels rise above 2.0 to
2.5mg/dl
Levels as high as 30 to 40mg/dl can occur
with sever disease
Jaundice occurs when the = b/w bilirubin
production &clearance is disturbed by one
or more of the following mechanisms:
1. Excessive production of bilirubin
2. Reduced hepatic uptake
3. Impaired conjugation
4. Decreased hepatocellular excretion
5. Impaired bile flow
CAUSES OF JAUNDICE
PRDOMINATLY INDIRECT HYPERBILIRUBINEMIA
hemolytic anemia's
resorption of blood from internal hemor.
ineffective erythropoiesis
Reduced hepatic uptake:
drugs
some cases of Gilbert syndrome
Impaired bilirubin conjugation:
physiologic jaundice
breast milk jaundice
genetic deficiency of glcuronosyl transferase
decreased expression of glcuronosyl
transferase
diffuse hepatocellular diseases
PREDOMINATLY DIRECT HYPERBILIRUBINEMIA
inflammatory destruction of
intrahepatic bile ducts
Extra hepatic biliary obstruction: