Ppp Shukla

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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 Jaundic e

Transcript of Ppp Shukla

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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.

Jaundice

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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.

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Right lobe Left lobe

Gall bladder

Falciform ligament

InferiorVena cava

Kidney

Abdominal aorta

POSITION Of LIVER

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ANATOMY OF LIVER 

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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 Bilirubinchemistry:-Bilirubin consists of an open chain of four pyrroles (tetrapyrrole); by contrast, the heme molecule is a ring of four pyrroles, called porphyrin

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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

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Metabolism of bilirubin:

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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.

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Jaundice infant

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

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YELLOW SKIN $ EYE

Yellowing of the skin and sclera caused by Hepatitis A. 

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Patient with jaundice, bruising, and weight loss due to pancreatic carcinoma

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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

.

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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) 

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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 uptakeDecreased bilirubin conjugation

2.Predominatly Conjugated Hyperbilirubinaemia (cholestasis)Intrahepatic cholestasis Extrahepatic cholestasis

Morphology Of Liver In Intra And Extrahepatic Cholastasis

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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.

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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)

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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. 

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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.

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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.

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VIRAL HEPATITISThe 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; andHepatitis G virus (HGV), has recently been discovered .All these human hepatitis viruses are RNA viruses except HBV which is a DNA virus .

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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 .

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No. FEATURE HEPATITIS A

HEPATITIS B

HEPATITISC

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 non-enveloped

Double-Shelled, Enveloped

Enveloped Enveloped replication defective

Icosahedral non-enveloped

?

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

?

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 8 

Antigen HAV HBsAg HBsAg HBeAg

HCVC100-3C33cNs5

HBsAgHDV

HEV ?

9 Antibodies Anti-HAV anti-HBsanti-HBcanti-HBe

anti-HCV anti-HBsanti-HDV

anti-HEV ?

10 Severity Mild OccasionallySevere

Moderate OccasionallySevere

Mild ?

11 Chronichepatitis

None Occasional Common Comman None ?

12 CarrierState

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

13 HepatocellularCarcinoma

No. + + 

+ None ?

14 Prognosis Excellent Worse with age

Moderate Acute good;Chronic

Good ?

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 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 8 Indian childhood cirrhosis (ICC) 9 Miscellaneous forms of cirrhosis 10 Cryptogenic cirrhosis

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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

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   Drug treatment:- 1)     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 )2)     Calamine lotion to skin , if itching.3)     Syrup. SORBILIN (sorbitol +tricholin)4)     Dosage:- 1 tsp. t.d.s.5)     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)6)     Dosage :- 1 tab. t.d.s.7)     Inj. Neurobion 2cc I.M.(vit.B1, B6, B12)8)     Inj.Neo-Hepatex :- it is proteolysed liver extract derived from 62.5g of fresh liver having vit-B12. 

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L-OrnithineTRADE NAMESL-Ornithine is available from numerous manufacturers generically; branded products include Hepamerz.

DESCRIPTIONL-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:

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ACTIONSL-Ornithine has putative anabolic, immunomodulatory and wound-healing activities.INDICATIONS AND USAGEIt is claimed that ornithine has anabolic effects and improves athletic performance, that it has wound-healing effects and is immuno-enhancing. CONTRAINDICATIONSL-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.PRECAUTIONSPregnant women and nursing mothers should avoid L-ornithine supplementation.

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ADVERSE REACTIONSDoses higher than 10 grams daily may cause such gastrointestinal symptoms as nausea, abdominal cramps and diarrhea.

DOSAGE AND ADMINISTRATIONThose 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 SUPPLIEDCapsules — 500 mg, 650 mg, 750 mg, 1000 mgPowder

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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

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   Ayurvedic or herbelINTRODUCTIONVirechan 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.

PREPROCEDUREInternal 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

PROCEDUREPatient 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.

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DIETThe patient is advised to take specific diet regime for four days following this treatment. Light food is allowed to consume on the previous day.CAUTIONVirechan is not advisable for infants, the old and pregnant women. This should be taken under specialized medical attention.

Virechan Process

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Herbal Product Used In The Treatment Of Jaundice:-

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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.      

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What patients should do?:-

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

2)    DietFat 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

 

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 How to prevent spread of infective Hepatitis?

 1)     Boiled water for all at home ( and for all locality if it is an epidemic) 2)     Personal hygiene and cleanliness (as faeces are ionfectious) 3)     Use disposable needles and syringes(to be destroyed after use) 4)     Inj. Human Immunoglobulin 10% 2 ml. I.M single dose to contacts  

INVESTIGATIONS 

       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.        Ultra sound for gall bladder if obstructive jaundice is suspected.        Routine Hb % , WBC

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INVESTIGATIONS       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.

• •Ultra sound for gall bladder if obstructive jaundice is suspected.•   Routine Hb % , WBC• 

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HEPATITIS –B PATIENT 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 after 5yrs. Take universal precautions to protect yourself from needlepricks and destroy all used needles, syringes etc.  Continue T.Essentiale (Phospholipids) and T. Hepatinic (Ayurvedic) for 6 months , as a supportive treatement.

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CONCLUSION 

1)     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.2)     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.3)     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 .4)     Jaundice can be fatal ,hence keen observation is required for these patients . Thus for maintaining their food intake plenty of water, fibre, drug like Tab. Liv-52 as herbal medicine and I.V. administration of L-ORNITHINE Etc. is required.

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