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1. Enumerate other sources of interferences or errors that affect the total bilirubin assay.

Unstandardized instruments
Loss of bilirubin after exposure to fluorescent and indirect or direct sunlight.
Hemolysis
Lipemia
Improper storage

2. Describe fully the total bilirubin metabolism. Illustrate the pathway of metabolism.
Iron

RBC
Destruction

Protein

Urine
Bilirubin
Albumin

1-4 mg urobilinogen
excreted in urine/day

Unconjugat

Systematic Circulation
Liver

Unconjugated
bilirubin UDPglucoronyl
transferase
Conjugated Bilirubin

Intestine

Feces

Conjugated
Bilirubin
GI bacteria
Urobilinogen

Small portion of
urobilinogen enters
circulation and is
excreted in urine

Extra hepatic Circulation


20% of urobilinogen
absorbed and
recirculated to the liver
and re exreted in the

50-250 mg pf
urobilinogen
excreted/day

3. Give and briefly describe other methods of total bilirubin assay.

Jendrassik- Grof Procedure


- Uses caffeine benzoate as solubilizer
- Maintains optical sensitivity even at low bilirubin concentration
- Minimal turbidity and relatively constant serum blank
Malloy- Evelyn Procedure
-Method performed at pH 1.2 where azobilirubin produced is red purple in color with a
maximal absorption of 560 nm.

4. What is the clinical significance of abnormal total bilirubin values. Correlate with pre hepatic,
hepatic and post hepatic jaundice.

Pre hepatic jaundice


Occurs when the problem causing the jaundice prior to liver metabolism. It is most
commonly caused by an increased amount of bilirubin being presented to the liver such
as that seen in acute and chronic hemolytic anemias. Hemolytic anemia causes an
increased amount of red blood cell destruction and the subsequent release of increased
amounts of bilirubin presented to the liver for processing.

Hepatic jaundice
Primary problem causing jaundice resides in the liver (intrinsic liver defect or disease).
The intrinsic liver defect or disease can be due to disorder of bilirubin metabolism and
transport defects (Crigler-Najjar syndrome, Dubin Johnson syndrome, Gilberts disease
and neonatal physiologic jaundice of the newborn) or due to diseases resulting in
hepatocellular injury or destruction. Gilberts disease, Crigler-Najjar syndrome and
neonatal physiologic jaundice of the newborn are hepatic causes of jaundice that results
in elevation in unconjugated bilirubin. Conditions such as Dubin-Johnson and Rotor
syndrome are hepatic causes of jaundice that result in elevations in conjugated bilirubin.

Post hepatic jaundice


Result from biliary obstructive disease that prevents the flow of conjugated bilirubin into
the bile canaliculi. Since the liver itself is functioning, bilirubin is effectively conjugated;
however it is unable to be properly excreted from the liver.

5. In tabular form differentiate conjugated bilirubin from unconjugated type


Unconjugated
Non polar
Water insoluble
Found in plasma bound albumin
Only react with diazotized sulfanilic acid
solution in the presence of accelerator

Conjugated
Polar
Water soluble
Found in plasma in free state
React with diazo directly

6. What is delta bilirubin? Describe its characteristics and clinical significance.


Delta bilirubin is conjugated bilirubin covalently bound to albumin. This fraction is seen only
when there is significant hepatic obstruction. This will react in lab method as conjugated
bilirubin.