Jaundice is the result of elevated levels of bilirubin in the blood termed hyperbilirubinaemia. Normal serum bilirubin concentration ranges from 0.3-1.3 mg/dl, about 80% of which is unconjugated. Jaundice becomes clinically evident when the total serum bilirubin exceeds 2 mg/dl. A rise of serum bilirubin between the normal and 2 mg/dl is generally not accompanied by visible jaundice and is called latent jaundice

1. PATHOLOGY AND
TREATMENT OF JAUNDICE
Dr. S P Srinivas Nayak, PharmD, (MSc).
Assistant Professor, Sultan-ul-Uloom
college of Pharmacy, Hyderabad,
Telangana, India.

2. INTRODUCTION
• Jaundice is the result of elevated levels of bilirubin
in the blood termed hyperbilirubinaemia.
• Normal serum bilirubin concentration ranges from
0.3-1.3 mg/dl, about 80% of which is
unconjugated.
• Jaundice becomes clinically evident when the total
serum bilirubin exceeds 2 mg/dl.
• A rise of serum bilirubin between the normal and 2
mg/dl is generally not accompanied by visible
jaundice and is called latent jaundice.

5. Metabolism of bilirubin
• About 80-85% of the bilirubin is derived from the catabolism
of haemoglobin, and 15-20% of the bilirubin comes partly
from non-haemo globin haem-containing pigments such as
myoglobin, catalase and cytochromes, and partly from
ineffective erythropoiesis
• Haeme converts to biliverdin by oxygen and NADPH
• Unconjugated Bilirubin is formed from biliverdin by biliverdin
reductase.

6. • Bilirubin from plasma in the form of Albumin-bound
unconjugated bilirubin enters into the hepatocyte, is
dissociated into bilirubin and albumin. The bilirubin gets
bound to cytoplasmic protein glutathione-S-transferase
(GST)
• Bilirubin UDP-glucuronosyl transferase conjugates bilirubin.
• Conjugated (water-soluble) bilirubin is rapidly transported
directly into bile canaliculi by energydependent process
and then excreted into the bile
• From gall bladder transports to intestines through bile, in
the intestines again converts to urobilinogen and further to
stercobilinogen
• Small portion of Urobilinogen reabsorbs through EHC,
oxidized to urobilin and finally excretes in urine

7. FACTORS THAT CAUSE HYPERBILIRUBINAEMIA
Based on pathophysiology, jaundice may result from
one or more of the following mechanisms:
• 1. Increased bilirubin production
• 2. Decreased hepatic uptake
• 3. Decreased hepatic conjugation
• 4. Decreased excretion of bilirubin into bile.
age-old classification of jaundice
pre-hepatic (haemolytic), hepatic, and post-hepatic
cholestatic.
However, hyperbilirubinaemia due to first three
mechanisms is mainly unconjugated while the last variety
yields mainly conjugated hyperbilirubinaemia.

9. DRUGS THAT CAUSE HAEMOLYSIS
• Cephalosporins (a class of antibiotics), most
common cause.
• Dapsone.
• Levodopa.
• Levofloxacin.
• Methyldopa.
• Nitrofurantoin.
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Penicillin and its derivatives.

11. NEONATAL JAUNDICE
• Jaundice appears in neonates when the total
serum bilirubin is more than 3 mg/dl. It may
be the result of unconjugated or conjugated
hyperbilirubinaemia

12. TREATMENT
• TREAT THE SPECIFIC CAUSE
• In Neonates, Phototherapy
• Restrict fat diet
• Maintain better liver function
• Blood transfusion
• Removal of gall stones
• Symptomatic supportive therapy

13. CASE STUDY
• A 68-year-old woman with a long-standing history of alcoholic liver
disease is admitted to hospital with a 2-week history of vomiting,
confusion, increased abdominal distension and worsening jaundice
On admission laboratory data are as follows:
• Na 116 (133–143mmol/L)
• K 3.8 (3.5–5mmol/L)
• Urea 8.5 (3.3–7.7mmol/L)
• Bilirubin 40 (1-2mg/dl)
• Albumin 23 (35–50g/L)
• ALT 23 (0–35 iu/L)
• Alk P 524 (70–300 iu/L)
• PT 18.6 (13s)
• Drugs on admission are as follows: Spironolactone: 300mg each
morning. Temazepam: 10mg at night. Lactulose: 10mL twice daily

14. Questions
Discuss the initial treatment plan for the
management of:
1. Ascites
2. Nausea and vomiting
3. Confusion

15. ANSWERS
Answer.1
• The patient should be sodium restricted and confined to
bed. Spironolactone therapy should be stopped in view of
the low sodium and confusion, as overuse of diuretics can
precipitate encephalopathy. Fluid restriction is necessary to
reduce the ascites, but sufficient fluid is required to
rehydrate the patient following vomiting.
• Paracentesis should be used to manage the ascites. Every
litre of ascitic fluid removed should be replaced with 6–8g
of albumin.
• A diagnostic ascitic tap should be taken to ensure there is
no infection in the ascites.

16. Answer 2
• Nausea/vomiting management.
• Urea is slightly raised, indicating possible
dehydration as a result of vomiting. The
patient should be rehydrated with dextrose
5%, not saline, as this will worsen the ascites.
• The patient's nausea can be managed with a
suitable antiemetic such as domperidone
10mg four times a day initially and then
titrated according to the response.

17. Answer 3
• Confusion.
• Confusion may be an early sign of encephalopathy in
this patient.
• Temazepam should be stopped. The patient is on an
inadequate dose of lactulose for the management of
encephalopathy, so this should be increased to
produce 2–3 loose motions per day.
• A typical dose would be 20mL three or four times daily.
In view of the patient's confusion, it may be worth
considering other agents in the management of the
encephalopathy, such as metronidazole 400mg twice
daily.