Jaundice

DEFINITION:-
Jaundice is not a disease but rather a sign that can occur in
many different disease.Jaundice is the yellowish staining of
the skin and sclerae (the whites of the eyes) that is caused by
high levels in blood of the chemical bilirubin. The color of
the skin and sclerae vary depending on the level of
bilirubin. When the bilirubin level is mildly elevated, they
are yellowish. When the bilirubin level is high, they tend to
be brown.
What causes jaundice?

1) too much bilirubin being produced for the liver to

remove from the blood.

2) a defect in the liver that prevents bilirubin from being

removed from the blood, converted to bilirubin/glucuronic
acid or secreted in bile,

3) blockage of the bile ducts that decreases the flow of bile

and bilirubin from the liver into the intestines. The
decreased conjugation, secretion, or flow of bile that can
result in jaundice is referred to as cholestasis: however,
cholestasis does not always result in jaundice.
 Right lobe Left lobe
Falciform
ligament
Gall bladder
Kidney
Inferior
Abdominal
Vena cava
aorta

POSITION Of LIVER
ANATOMY OF LIVER
The structure of bilirubin:-
Bilirubin is a yellow breakdown product of normal heme
catabolism. Its levels are elevated in certain diseases and it is
responsible for the yellow color of bruises and the brown color of
feces structure of Bilirubin
chemistry:-
Bilirubin consists of an open chain of four pyrroles (tetrapyrrole);
by contrast, the heme molecule is a ring of four pyrroles, called
porphyrin
Bilirubin blood tests:-

Bilirubin is broken down by light, and blood collection tubes

(especially serum tubes) should therefore be protected from such
exposure.

 The reference range for total bilirubin is 2 - 14 μmol/L or 0.3 -

1.9 mg/dL. For direct bilirubin, it is 0 - 4 μmol/L or 0 - 0.3 mg/dL.

 Mild rises in bilirubin may be caused by

Hemolysis and Gilbert's syndrome

 Moderate rise in bilirubin may be caused by

Drugs e.g. anti psychotic, sex hormone
Hepatitis

Very high level of bilirubin may be caused by

Crigler-najjar and dubin-johnson syndrome
Metabolism of bilirubin:
NORMAL APPEARANCE:-

YOUNG
Jaundice is a condition produced when excess amounts of
bilirubin circulating in the blood stream dissolve in the
subcutaneous fat causing a yellowish appearance of the skin
and the whites of the eyes.
 Jaundice infant

A natural occurrence in the newborn due to the immature liver.

 YELLOW SKIN $ EYE

Yellowing of the skin and sclera caused by Hepatitis A.

Patient with jaundice, bruising, and weight loss due to pancreatic
carcinoma
CLASSIFICATION AND FEATURES OF JAUNDICE

1.PREDOMINATLY UNCONJUGATED HYPERBILIRU BINAEMIA

a.Increased biliRubin production ( Hemolytic, acholuric or

prehepatic
.
jaundice )
• Intra-and extravascular heterolysis
Ineffective erythropoietin

b. Decreased hepatic uptake

•Drugs
•Prolonged starvation
•Sepsis

c. Decreased billirubin conjugation

•Hereditary disorders (e.g. Gilbert’s and Crigle-Najjar syndrome)
•Acquired defects (e.g. drug, hepatitis, cirrhosis)
•Neonatal jaundice
2.PREDOMINATLY CONJUGATED HYPERBILIRUBI-NAEMIA
CHOLESTASIS
a.
a.a.) Intrahepatic homeostasis (Impaired hepatic excretion.)

•Hereditary disorders or ‘pure cholestasis’ (e.g. Dubin –Johnson

syndromw, Rotor’s syndrome fibrocstic disease of pancreas,,
intrahepatic atresia, Homeostatic jaundice of pregnancy)

•Acquired disorders or ‘ hepatocellurlar cholestasis’ (e.g. viral

hepatitis, drugs, alcohol-induced injury, sepsis , cirrhosis)

b.)Extrahepatic cholestasis (Extrahepatic billiary obstruction)

•Mechanical obstruction (e.g. gallstones, inflammatory strictures,

carcinoma head of pancreas, tumours of bile ducts, sclerosing
cholangitis)
1.Predominantly Unconjugated Hyperbilirubinaemia

This from of jaundice can result from the following three sets of
conditions
Increased Bilirubin Production (Haemolytic, Acholuric or
Prehepatic Jaundice )

Decreased bilirubin uptake

Decreased bilirubin conjugation

2.Predominatly Conjugated Hyperbilirubinaemia (cholestasis)

Intrahepatic cholestasis
Extrahepatic cholestasis

Morphology Of Liver In Intra And Extrahepatic Cholastasis

NEONATAL JAUNDICE

Jaundice appears in neonates when the total serum bilirubin is

more than 3 mg/dl. May be the result of unconjugated or
conjugated hyperbilirubinaemia; the former being more common.
CAUSES OF NEONATAL JAUNDICE
A)UNCONJUGATED HYPERBILIRUBINEMIA

1)Physiologic and prematurity jaundice

2)Haemolytic disease of the newborn and kernicterus
3) Congenital haemolytic
4)Gilbert`s syndroms
5)Crigler-najjar syndromes(type-1 and 2)

B)CONJUGATED HYPERBILIRUBINAEMIA

1)Heriditry(dubin-johnsonsyndromes).
2) Infections (eg.hepatitis B,hepatitis Cor non-A,non-B hepatitis,
syphilis.gram-ve sepsis.
3)Rey`s syndroms
4)Idiophatic (neonatal hepatitis,congenital hepatic fibrosis)
5)Biliary atresia (intra and extrahepatic)
Gilbert`S Syndrome:

This is the commonest of the familial, genetically determined

diseased of the liver affecting 2-5% of the population. Gilbert’s
syndrome is characterized by mild, benign, unconjugated
hyperbilirubinaemia (serum bilirubin 1-5 mg/dl) which is not due to
haemolysis. The condition is inherited as an autosomal dominant
character. The prognsis of patients with Gilbert’s syndrome is
excellent , through chronic jaundice persists throughout life.

Criglar-Najjar Syndrome :
Cirgler-Najjar syndrome is a form of familial nonhaemolytic
jaundice with very high unconjugated hyperbilirubinaemia

There are 2 forms of this condition

Type I and Type II.
Dubin –Johnson Syndrome:

Dubin-Johnson syndrome is autosomal recessive disorder

characterriesed by predominant conjugated hyperbilirubinaemia
(usually less than 5 mg /dl.) with genetic defect in canalicular
excretion of conjugated bilirubin, The condition differs from other
forms of hereditary hyperbilirubinaemias isn producing grossly
greenish blank pigmented liver.

Rotor’s Syndrome :

This is another form of familial conjugated hyperbiliru-binaemia

with mild chronic jaundice but differs from Dubin-Jhnoson
syndrome in having no brown pigment in the liver cells. The
disease is inherited as an autosomal recessive character. Rotor’s
syndrome has an excellent prognosis.
Rey`s syndrome:

It is defined as an acute postviral syndrome of encephalophathy

and fatty change in the vicera. The syndrome may follow almost
any known viral disease but is most common after influenza A or
B and varicella.

 The patient`s are generally children between 6months to

15yrs.of age. within a week after a viral illness,the child develops
intractable vomiting and neurological detarioration due to
encephalopathy, eventually leading to stupor, coma and death.
VIRAL HEPATITIS
The term viral hepatitis is used to describe infection of the liver
caused by hepatotropic viruses. Currently there are 5 main
varieties of these viruses and a sixth poorly –characterized virus,
causing distinct types of viral hepatitis
Hepatitis A virus (HAV), causing a faecally – spred self –
limiting disease ;
Hepatitis B virus (HBV), causing a parenterally transmitted
disease that may become chronic ;
Hepatitis C virus (HCV), previously termed non- A, non- B
(NANB) hepatitis virus involved chiefly in transfusion- related
hepatitis ;
Hepatitis delta virus (HDV) which is sometimes associated as
superinfection with hepatitis B infection ;
Hepatitis E virus (HEV), causing water- borne infection; and
Hepatitis G virus (HGV), has recently been discovered .
All these human hepatitis viruses are RNA viruses except HBV
which is a DNA virus .
Hepatitis C infection is acquired by blood trans-fusions, blood
products, haemodialysis, parenteral drug abuse and accidental
cuts and needle-pricks in health workers. About 90% of post-
transfusion hepatitis is of hepatitis C type .
No. FEATURE HEPATITIS HEPATITIS HEPATITI HEPATITIS HEPATITIS HEPATITIS
A B S D E G
C

1 Agent HAV HBV HCV HDV HEV HGV

2 Year 1973 1965 1989 1977 1980 1995

Indentified

3 Viral Particle 27nm 42nm 30-60nm 35-37nm 32-34nm ?

4 Genome RNA,ss, DNA,ss/ds RNA,ss/ RNA ,ss, RNA,ss/ RNA,ss, linear

linear linear linear
circular circular

5 Morphology Icosahedral Double- Enveloped Enveloped Icosahedral ?

non- Shelled, replication non-
enveloped Enveloped defective enveloped

6 Spread Faeco-oral Parenteral, Parenteral, Parenteral, Water-borne Parenteral

close close close
contact contact contact

7 Incubation 15-45 days 30-180 20-90 days 30-50 days 15-60 ?

period days days
 Antigen HAV HBsAg HCV HBsAg HEV ?
8 HBsAg C100-3 HDV
HBeAg C33c
Ns5

9 Antibodies Anti-HAV anti-HBs anti-HCV anti-HBs anti-HEV ?

anti-HBc anti-HDV
anti-HBe

10 Severity Mild Occasionall Moderate Occasionall Mild ?

y y
Severe Severe

11 Chronic None Occasional Common Comman None ?

hepatitis

12 Carrier None <1% <1% 1-10% Unknwn 1-2%

State

13 Hepatocellula No. + + + None ?

r
Carcinoma

14 Prognosis Excellent Worse with Moderate Acute good; Good ?

age Chronic
CIRRHOSIS

Cirrhosis of the liver is a diffuse having the following 3 features :

 It involves the entire liver.
 There is formation of nodules separated from one another by irregular band
of fibrosis.
 It occurs following hepatocellular necrosis of varying etiology so that there
are alternate nodules.
In the western world, cirrhosis of the liver is one of the ten leading causes of
death.
A MORPHOLOGIC B ETIOLOGIC

1 Micronodular 1 Alcoholic cirrhosis (the mostcommon 60- 70%)

(nodules less than 3nm) 2 Post –necrotic crisis (10%)

2 Macronodular 3 Billiary cirrhosis (5-10%)
(nodules less than 3nm) 4 Pigment cirrhosis in haemochromatosis (5%)

3 Mixed 5 Cirrhosis in Wilson’s disease

6 Cirrhosis in a-1 antitypic deficiency

7 Cardiac Carrhosis
 TREATMENT OF JAUNDICE:

JAUNDICE COME UNDER SCHEDULE-J:-that means diseases and ailments

(by whatever name described) ,which a drug may not purport to prevent or cure
or make claims to prevent or cure.
Eg: AIDS, GENATIC DISORDERS, VERICOSE VEIN,FAIRNESS OF THE
SKIN, MAINTENANACE OR IMPROVEMENT OF THE CAPACITY OF THE
HUMAN BEING FOR SEXUAL PLEASURE,CHANGE OF FOETAL SEX BY
DRUGS,AND JAUNDICE/HEPATITIS/LIVER DISORDERS.(rule no.106 by
G.O.I. in 1930)

Jaundice can be treated by -

 Ayurvadic or herbel
Drug treatment
 Drug treatment:-

) GLUCOSE :- Glucon- D (50g), orally daily. During acute phase and

when nausea $ vomiting are severe, give I.V. glucose. (5%dextrose + 1
amp. M.V.I. in one bottle i.e. multi vitamin )

) Calamine lotion to skin , if itching.

) Syrup. SORBILIN (sorbitol +tricholin)

) Dosage:- 1 tsp. t.d.s.

) Silymarin:- activ principle from the fruit of Silybum Marianum, a mixture

of flavonolignans. silymarin reduces the turnover of membrane
phospholipids and stabilizes cell membrane of hepatocyte. Has potent
antioxidant action and prevents lipid peroxidation. E.g. tab. Silybon-
140mg. t.i.d. (phospholipid to regenerate liver cells)
L-Ornithine
TRADE NAMES
L-Ornithine is available from numerous manufacturers generically;
branded products include Hepamerz.

DESCRIPTION
L-Ornithine is a nonprotein amino acid. It is used in the body in the
biosynthesis of L-arginine, L-proline and polyamines. L-Ornithine
is a basic amino acid, positively charged at physiological pH. It is
also known as alpha,delta-diaminovaleric acid and 2,5-
diaminopentanoic acid. The molecular formula of L-ornithine is
C5H12N2O2, and its molecular weight is 132.16 daltons. The
structural formula is:
ACTIONS
L-Ornithine has putative anabolic, immunomodulatory and wound-
healing activities.
INDICATIONS AND USAGE
It is claimed that ornithine has anabolic effects and improves
athletic performance, that it has wound-healing effects and is
immuno-enhancing.

CONTRAINDICATIONS
L-Ornithine is contraindicated in those with a deficiency of
ornithine-delta-aminotransferase. This is a genetic disorder
resulting in gyrate atrophy of the choroid and retina and
progressive blinding chorioretinal degeneration. It is rare.
L-Ornithine is also contraindicated in those hypersensitive to
any component of an ornithine-containing supplement.
PRECAUTIONS
Pregnant women and nursing mothers should avoid L-
ornithine supplementation.
ADVERSE REACTIONS
Doses higher than 10 grams daily may cause such
gastrointestinal symptoms as nausea, abdominal cramps and
diarrhea.

DOSAGE AND ADMINISTRATION

Those who use L-ornithine take doses of 500 milligrams to 2
grams, usually before bedtime and on an empty stomach. Some
combine L-ornithine with similar doses of L-arginine.

HOW SUPPLIED
Capsules — 500 mg, 650 mg, 750 mg, 1000 mg
Powder
Using bili lights is a therapeutic procedure performed on newborn or premature
infants to reduce elevated levels of bilirubin. If blood levels of bilirubin become
too high, the bilirubin begins to dissolve in the body tissues, producing the
characteristic yellow eyes and skin of jaundice. Bilirubin also has an affinity for
brain tissue, where it can accumulate and cause permanent brain damage
  Ayurvedic or herbel
INTRODUCTION
Virechan is for the elimination of Pitta related disorders and toxins from the
body. This is mainly performed in the Sharad ritu (autumn season). The
process of cleansing is carried out in the intestine and other Pitta zones. Drugs
that stimulate bowel movements are induced for the expulsion of vitiated Pitta
via the rectum.

PREPROCEDURE
Internal oleation with medicated ghee/oil is advised for 3-5 days according to
the patient’s constitutions and dosha followed by external oleation and
therapeutic sudation. It liquefies the aama and bring it to the kostha

PROCEDURE
Patient is told to fast since morning (in the pitta Kaal). Purgatives are given
around 9:00a.m in the morning. They are prepared using roots and fruits of
special herbs, which have properties as laxatives. Some churnas are also
used to make the process highly effective. The doctor based on your
constitution determines the dose. The process will start within 2 hours and is
further aggravated by drinking hot water. The faecal discharge turns fluid after
7 or 8 bowel movements. First the faeces, then the toxic Pitta and finally toxic
kapha are discharged.
DIET
The patient is advised to take specific diet regime for four days
following this treatment. Light food is allowed to consume on the
previous day.
CAUTION
Virechan is not advisable for infants, the old and pregnant women.
This should be taken under specialized medical attention.
Virechan Process
Herbal Product Used In The Treatment Of Jaundice:-
Liv-52:- It Contain Following Herbs.
Himsra (capparis spinosa )………… 34 mg.
Kasani (cichorium intybus)…………34 mg.
Kakamachi( solanum nigrum )………16 mg.
Arjuna (terminalia arjuna )…………..16 mg.
Biranjasipha (achillae millefolium )…..8 mg.
Jhavuka (tamarix galacia )…………….8 mg.
Kasamarda (cassia occidentalis )………8 mg.

Proceed in bhrigaraja (eclipatualba) ,bhumyaamalki (phyllanthus

amarus ), punarnava (boerhaavia diffusa ),chitraka (plumbago
zeylanica ), haritaki (terminalia chebula ).

Preservatives:-
Methyl and Propyl paraben.
Protects the liver against varios hepatotoxins promotes appetite
and growth.

 What patients should do?:-

1) Complete bed rest is very essential till serum bilirubin < 1.5 mg. %

2) Diet
Fat free diet , no oil , ghee and fried foods
•Plenty of sweets , sugar and sugarcane juices
•Boiled water for all at hom
• Strictly no alcohol

3) All hepatotocxic drugs should be stopped

Eg. Anti tubercular drugs , asprin , methyldopa , alcohol

4) No sedatives should be given if jaundice is deep

Steroids should be generally avoided . In acute phase, a short course

may be given eg. Tab Prednisolone 5mg t.d.s for 3-5 days
 ow to prevent spread of infective Hepatitis?

) Boiled water for all at home ( and for all locality if it is an

epidemic)

) Personal hygiene and cleanliness (as faeces are

ionfectious)

) Use disposable needles and syringes(to be destroyed after

use)
 NVESTIGATIONS
Urine for bile salts and bile pigments

Serum Bilirubin every week

Australia Antigen for Hepatitis B if jaundice is recurrent , Chronic

or with weight loss.

ltra sound for gall bladder if obstructive jaundice is suspected.

 EPATITIS –B

ATIENT WITH JAUNDICE IS HEPATITIS –B POSITIVE

Treat the acute phase of jaundice as above.

Treating physician and paramedical staff must be immunised

against hepatitis-B

e.g.INJ. energix-B 1ml. I.M. at 0,1and 6 months.booster afte

5yrs.

Take universal precautions to protect yourself from needleprick

and destroy all used needles, syringes etc.
 ONCLUSION

) According to drugs and cosmetics rule no.106 in 1940,Jaundice comes

under schedule-J that means disease ,to which a drug may not purport to
cure or prevent.

) It is symptom for many disease of bacterial hand viral origin,

there is no drug of choice in alloepathy medicine to cure jaundice .
Hence, a option for ayurvedic and folkolore medicine in Asian
countries than the other Europian countries.

) Jaundice can be cured only by cleaning the body with plenty of

fluid and chelating agent which are able to convert free serum
bilirubin to an inactive metabolite . Hence curing the symptom is
the main objective .
HANK YOU