Ppp Shukla

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

Gall bladder

Falciform ligament Kidney

Inferior Vena cava

Abdominal 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 posttransfusion hepatitis is of hepatitis C type .

No.

FEATURE

HEPATITIS A

HEPATITIS B

HEPATITI S C

HEPATITIS D

HEPATITIS E

HEPATITIS G

1

Agent

HAV

HBV

HCV

HDV

HEV

HGV

2

Year Indentified

1973

1965

1989

1977

1980

1995

3

Viral Particle

27nm

42nm

30-60nm

35-37nm

32-34nm

?

4

Genome

RNA,ss, linear

DNA,ss/ds

RNA,ss/ linear circular

RNA ,ss,

RNA,ss/ linear circular

RNA,ss, linear

5

Morphology

Icosahedral nonenveloped

DoubleShelled, Enveloped

Enveloped

Enveloped replication defective

Icosahedral nonenveloped

?

6

Spread

Faeco-oral

Parenteral, close contact

Parenteral, close contact

Parenteral, close contact

Water-borne

Parenteral

7

Incubation period

15-45 days

30-180 days

20-90 days

30-50 days

15-60 days

?

Antigen

HAV

HBsAg HBsAg HBeAg

HCV C100-3 C33c Ns5

HBsAg HDV

HEV

?

9

Antibodies

Anti-HAV

anti-HBs anti-HBc anti-HBe

anti-HCV

anti-HBs anti-HDV

anti-HEV

?

10

Severity

Mild

Occasionall y Severe

Moderate

Occasionall y Severe

Mild

?

11

Chronic hepatitis

None

Occasional

Common

Comman

None

?

12

Carrier State

None

<1%

<1%

1-10%

Unknwn

1-2%

13

Hepatocellula r Carcinoma

No.

+

+

+

None

?

14

Prognosis

Excellent

Worse with age

Moderate

Acute good; Chronic

Good

?

8

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 Macronodular (nodules less than 3nm)

2 Post –necrotic crisis (10%) 3 Billiary cirrhosis (5-10%) 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. Silybon140mg. 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 2,5diaminopentanoic 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 woundhealing 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 Lornithine 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) 4)

All hepatotocxic drugs should be stopped Eg. Anti tubercular drugs , asprin , methyldopa , alcohol 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 .

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