Tag Archives: Jaundice

Artemisia capillaries

 

Botanical Name : Artemisia capillaries
Family: Asteraceae
Genus: Artemisia
Species: A. scoparia
Order: Asterales

Common Names : Yin Chen Hao
English Name:Capillary Wormwood Herb
Pin Yin Name:Yin Chen

Other Pin Yin Name:Mian Yin Chen,Bai Hao,Rong Hao,Song Mao Ai,Ma Xian,Po Po Hao,Ye Lan Hao

Habitat :Artemisia capillaries  is native to E. Asia – China, Japan, Korea, Manchuria. It  grows on  the grassy thickets, and along rivers and seashores, C. and S. Japan. Humid slopes, hills, terraces, roadsides and river banks at elevations of 100 – 2700 metres in China.

Description:
Artemisia capillaris is a deciduous perennial herb or subshrub.Stem erect height 0.5 to 1 m,root woody,surface color yellow brown,vertical stripin,branches;seedling covered with brown silk hair,hairless when grow up.Bottom Leaf split wide and short,covered with short silky foliage;middle leaf split long and slim as hair,1mm width;top leaf split into 3 parts or no split,no hair.capitulum small and numerous,flower color yellow,pipe like,outer layer 3 to 5 bud,female,fertible,inner layer bisexual 5 to 7,infertility.Fruit long round shape width 0.8mm,hairless.Flowering during September to October.The flowers are hermaphrodite (have both male and female organs) and are pollinated by Wind.and the seeds ripen from Sep to October.

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The plant prefers light (sandy) and medium (loamy) soils and requires well-drained soil.The plant prefers neutral and basic (alkaline) soils..It can grow in semi-shade (light woodland) or no shade.It requires dry or moist soil and can tolerate drought.The plant can tolerates strong winds but not maritime exposure.

Cultivation:
An easily grown plant, succeeding in a well-drained circumneutral or slightly alkaline loamy soil, preferring a sunny position. Established plants are drought tolerant. Plants are longer lived, more hardy and more aromatic when they are grown in a poor dry soil. This species is probably not hardy in all parts of Britain, it tolerates temperatures down to at least -5°c. Plants in this genus are notably resistant to honey fungus. Members of this genus are rarely if ever troubled by browsing deer.

Propagation :
Seed – surface sow from late winter to early summer in a greenhouse. When large enough to handle, prick the seedlings out into individual pots and plant them out in the summer. Cuttings of half-ripe wood, July/August in a frame. Division in spring or autumn.

Edible Uses :
Edible Parts: Leaves.

Leaves and stems – soaked and boiled

Medicinal Uses:
Antibacterial;  Anticholesterolemic;  Antiviral;  CholagogueDiureticFebrifugeHepatic;  Vasodilator.

Yin Chen Hao has been used in Chinese herbal medicine for over 2,000 years. It is considered to be a bitter and cooling herb, clearing “damp heat” from the liver and gall ducts and relieving fevers. It is an effective remedy for liver problems, being specifically helpful in treating hepatitis with jaundice. Modern research has confirmed that the plant has a tonic and strengthening effect upon the liver, gallbladder and digestive system. The leaves and young shoots are antibacterial, anticholesterolemic, antiviral, cholagogue, diuretic, febrifuge and vasodilator. An infusion is used internally in the treatment of jaundice, hepatitis, gall bladder complaints and feverish illnesses. Externally it has been applied in the form of a plaster for treating headaches. The plant is harvested in late spring and can be dried for later use. Yin Chen Hao is contraindicated for pregnant women

Yin chen hao is an effective remedy for liver problems, being specifically helpful for treating hepatitis with jaundice.  Traditional Chinese medicine holds that it is bitter and cooling, clearing “damp heat” from the liver and gall ducts and relieving fevers.  Yin chen hao is also anti-inflammatory and diuretic.  It was formerly used in a plaster for headaches.  Research indicates that yin chen hao has a tonic and strengthening effect on the liver and gallbladder and digestive system.  It is an effective remedy for liver problems, being specifically helpful in treating hepatitis with jaundice.    An infusion of the young shoots is used internally in the treatment of jaundice, hepatitis, gall bladder complaints and feverish illnesses. Externally it has been applied in the form of a plaster for treating headaches.

Known Hazards : Although no reports of toxicity have been seen for this species, skin contact with some members of this genus can cause dermatitis or other allergic reactions in some people.

Disclaimer:The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider

Resources:
http://www.mdidea.com/products/proper/proper05203.html
http://www.pfaf.org/user/Plant.aspx?LatinName=Artemisia+capillaris
http://www.herbnet.com/Herb%20Uses_UZ.htm

http://library.thinkquest.org/25983/4.%20Capillaris.htm

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Infant jaundice

Definition:
Infant jaundice is a yellow discoloration in a newborn baby’s skin and eyes. Infant jaundice occurs because the baby’s blood contains an excess of bilirubin (bil-ih-ROO-bin), a yellow-colored pigment of red blood cells. Jaundice isn’t a disease itself but the name given to the yellow appearance of skin and the conjunctiva (whites) of the eyes.

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Infant jaundice is a common condition, particularly in babies born before 38 weeks gestation (preterm babies) and breast-fed babies. Infant jaundice usually occurs because a baby’s liver isn’t mature enough to get rid of bilirubin in the bloodstream. In some cases, an underlying disease may cause jaundice.

Infant jaundice can be concerning as although the majority of causes are easily treated, some rarer causes are very serious. Also, high levels of unconjugated bilirubin can cause brain damage. This is virtually never seen now due to treatment with UVB light, but it means that it is very important that the baby receives proper treatment.

Types of Infant jaundice:
The most common types of jaundice are:

Physiological (normal) jaundice: occurring in most newborns, this mild jaundice is due to the immaturity of the baby’s liver, which leads to a slow processing of bilirubin. It generally appears at 2 to 4 days of age and disappears by 1 to 2 weeks of age.

Jaundice of prematurity: occurs frequently in premature babies since they are even less ready to excrete bilirubin effectively. Jaundice in premature babies needs to be treated at a lower bilirubin level than in full term babies in order to avoid complications.

Breastfeeding jaundice: jaundice can occur when a breastfeeding baby is not getting enough breast milk because of difficulty with breastfeeding or because the mother’s milk isn’t in yet. This is not caused by a problem with the breast milk itself, but by the baby not getting enough to drink.

Breast milk jaundice: in 1% to 2% of breastfed babies, jaundice may be caused by substances produced in their mother’s breast milk that can cause the bilirubin level to rise. These can prevent the excretion of bilirubin through the intestines. It starts after the first 3 to 5 days and slowly improves over 3 to 12 weeks.

Symptoms:
The main symptom of jaundice is yellow colouring of the skin and conjunctiva of the eyes. Jaundice can also make babies sleepy which can lead to poor feeding. Poor feeding can make jaundice worse as the baby can become dehydrated.

If a baby has conjugated jaundice, it may have white chalky stool (poo) and urine that is darker than normal. (The bilirubin that normally colours the stool is excreted in the urine.)

Medical advise should be sought urgently if:
•Jaundice is present in the first 24 hours of life
•Jaundice is present when the baby is 10 days old
•The baby has problems feeding or is very sleepy
•The stools are pale or the urine is very dark

Causes:
The main cause of jaundice is:
Excess bilirubin (hyperbilirubinemia). Bilirubin is the substance that causes the yellow color of jaundice. It’s a normal part of the waste produced when “used” red blood cells are broken down. Normally, the liver filters bilirubin from the bloodstream and releases it into the intestinal tract. Before birth, a mother’s liver removes bilirubin from the baby’s blood. The liver of a newborn is immature and often can’t remove bilirubin quickly enough, causing an excess of bilirubin. Jaundice due to these normal newborn conditions is called physiologic jaundice, and it typically appears on the second or third day of life.Other causes

A baby may have an underlying disorder that is causing jaundice. In these cases, jaundice often appears much earlier or much later than physiologic jaundice.

Diseases or conditions that can cause jaundice include:
*Internal bleeding (hemorrhage)
*An infection in your baby’s blood (sepsis)
*Other viral or bacterial infections
*An incompatibility between the mother’s blood and the baby’s blood
*A liver malfunction
*An enzyme deficiency
*An abnormality of your baby’s red blood cells

Risk Factors:
Problems with the blood may lead to a rapid breakdown of cells (haemolysis) – if the mother’s blood type isn’t compatible with her baby’s. For example, she may make antibodies that attack and destroy her baby’s red blood cells.

Hormone deficiencies such as low levels of thyroid hormone (hypothyroidism) or pituitary gland hormones (hypopituitarism) can trigger jaundice.

There may be inherited genetic problems with the enzymes that convert or break down bilirubin – these include rare conditions such as Crigler-Najjar syndrome, Gilbert’s syndrome, galactosaemia and tyrosinaemia.

There may be problems with the liver, such as biliary atresia, in which the tubes that drain bile from the liver are blocked. If spotted early, an operation can prevent long-term damage (which is why it is important to investigate jaundice that is still there at 10 days).

Diagnosis:
Doctors, nurses, and family members will watch for signs of jaundice at the hospital, and after the newborn goes home.

Any infant who appears jaundiced should have bilirubin levels measured right away. This can be done with a blood test.

Many hospitals check total bilirubin levels on all babies at about 24 hours of age. Hospitals use probes that can estimate the bilirubin level just by touching the skin. High readings need to be confirmed with blood tests.

Tests that will likely be done include:
•Complete blood count
•Coomb’s test
•Reticulocyte count
Further testing may be needed for babies who need treatment or whose total bilirubin levels are rising more quickly than expected.

Treatment:
Treatment is usually not needed.

When determining treatment, the doctor must consider:

•The baby’s bilirubin level
•How fast the level has been rising
•Whether the baby was born early (babies born early are more likely to be treated at lower bilirubin levels)
•How old the baby is now
Your child will need treatment if the bilirubin level is too high or is rising too quickly.

Keep the baby well hydrated with breast milk or formula. Frequent feedings (up to 12 times a day) encourage frequent bowel movements, which help remove bilirubin through the stools. Ask your doctor before giving your newborn extra formula.

Some newborns need to be treated before they leave the hospital. Others may need to go back to the hospital when they are a few days old. Treatment in the hospital usually lasts 1 to 2 days.

Sometimes special blue lights are used on infants whose levels are very high. This is called phototherapy. These lights work by helping to break down bilirubin in the skin.

The infant is placed under artificial light in a warm, enclosed bed to maintain constant temperature. The baby will wear only a diaper and special eye shades to protect the eyes. The American Academy of Pediatrics recommends that breastfeeding be continued through phototherapy, if possible. Rarely, the baby may have an intravenous (IV) line to deliver fluids.

If the bilirubin level is not too high or is not rising quickly, you can do phototherapy at home with a fiberoptic blanket, which has tiny bright lights in it. You may also use a bed that shines light up from the mattress.

•You must keep the light therapy on your child’s skin and feed your child every 2 to 3 hours (10 to 12 times a day).
•A nurse will come to your home to teach you how to use the blanket or bed, and to check on your child.
•The nurse will return daily to check your child’s weight, feedings, skin, and bilirubin levels.
•You will be asked to count the number of wet and dirty diapers.
In the most severe cases of jaundice, an exchange transfusion is required. In this procedure, the baby’s blood is replaced with fresh blood. Treating severely jaundiced babies with intravenous immunoglobulin may also be very effective at reducing bilirubin levels.

Prognosis:
Usually newborn jaundice is not harmful. For most babies, jaundice usually gets better without treatment within 1 to 2 weeks.

Very high levels of bilirubin can damage the brain. This is called kernicterus. However, the condition is almost always diagnosed before levels become high enough to cause this damage.

For babies who need treatment, the treatment is usually effective

Possible Complications:
Rare, but serious, complications from high bilirubin levels include:

•Cerebral palsy
•Deafness
•Kernicterus — brain damage from very high bilirubin levels

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:
http://www.nlm.nih.gov/medlineplus/ency/article/001559.htm
http://www.mayoclinic.com/health/infant-jaundice/DS00107
http://www.bbc.co.uk/health/physical_health/conditions/jaundice2.shtml

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Jaundice-A Royal Disease

Jaundice, icterus, hepatitis.” These three terms are interchanged by people to describe what they believe is a single common affliction, a disease that causes the skin and eyes to turn yellow. The word “jaundice” is actually a corrupted anglicised version of the French jaune coined in the 19th century by French physicians to describe what they thought was a single disease entity. Unaware of cause or cure, the discolouration was also called the morbus regius (the regal disease), with the belief that only the touch of a king could cure it.

Times have now changed and medicine has become evidence based. Tests can be done if a person becomes “jaundiced” to evaluate the “when, where and why”. Once the cause is removed, the disease will disappear.

The yellow colour is due to a pigment called bilirubin, normally produced in the spleen and liver when old red blood cells are broken down. The pigment is then metabolised in the liver and excreted. The level of bilirubin is usually 0.3 to 1.9mg/dl (milligrams per decilitre). The human eye can discern the yellow colour imparted by bilirubin when the level is three times or more than the normal 3mg/dl in the blood.

Infectious diseases can interfere with the ability of the liver cells to metabolise bilirubin. The most common infections are viral, commonly caused by the hepatitis group of viruses. There are several of these — some are transmitted through contaminated food or water, others through unprotected sex or unsterile injections.

Jaundice owing to viral hepatitis A is the commonest form of jaundice in young people. It is usually a mild self-limited disease that recovers spontaneously in one or two months. No specific treatment is required. Hepatitis B, C or E can be more severe, relapsing, fatal or chronic.

Out of this group, hepatitis A and B are preventable. Vaccination against hepatitis B is offered in a 3-dose schedule before the age of one year (it can be given later to anyone who missed it). Hepatitis A vaccine is given after the age of two years as a 2-dose schedule. Protection is almost 100 per cent.

Other infections caused by the herpes group of viruses, leptospirosis, cytomegalovirus, malaria or even severe bacterial sepsis can also cause jaundice. These diseases are not preventable by immunisation.

Jaundice is not always due to an infection. If for any reason the number of red blood cells destroyed is greater than normal, the liver is unable to cope with the overload of pigment and the person becomes jaundiced. This occurs in some hereditary blood disorders like thalassaemia, and sickle cell disease, or a hereditary metabolic defect like G6PD deficiency.

Sometimes, the liver cells themselves are defective and unable to cope with even the normal amount of bilirubin produced in the body. This occurs in certain inherited conditions like the Dubin-Johnson or the Gilbert syndrome. Several members of a family are affected, the jaundice is mild and fluctuating and it is not fatal.

Medications can be toxic to the liver and cause jaundice. Common examples are an overdose of paracetamol or even oestrogens. Alcohol is a direct toxin, poisonous to the liver cells. Consumption on a regular basis over many years can damage the liver and can result in jaundice.

Even when the bilirubin is adequately metabolised and produced in normal quantities, jaundice can occur, if the drainage ducts are blocked by stones, strictures and primary or secondary cancer deposits.

Sixty per cent of newborns can develop a “physiological” or normal self-limited jaundice. There is a rapid cell turnover in newborns and they produce bilirubin at a rate of 6 to 8 mg per kg per day, (more than twice the production rate in adults). The immature liver cells are initially unable to cope but the bilirubin production and level typically decline to the adult level within 10 to 14 days. Sometimes the jaundice is due to a mother-baby blood group incompatibility. The mother forms antibodies to the infant’s blood. This too is self limited and treatable.

The sudden appearance of jaundice in any age group should not be self diagnosed, ignored, treated with diet restrictions or herbs without a diagnosis. After consultations with a physician, appropriate blood and urine tests and, if necessary, scans or a laproscopy should be done to arrive at a diagnosis.

Eighty per cent of the jaundice in young adults is due to hepatitis A. As this disease is self-limited, quackery and miracle cures (like the touch of the king, amulets and bracelets) abound and appear successful.

Secondary jaundice recovers once the causative factor is removed. Abstaining from alcohol and discontinuing offending drugs may reverse jaundice. If a correctable obstruction is seen on scanning or a laparoscopy, surgical treatment provides relief.

The tragedy of jaundice is that ignorance and superstition stand in the way. Some treatable and curable forms of jaundice are not diagnosed or tackled till it is too late.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Sources: The Telegraph (Kolkata, India)

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Jaundice

 

Definition:
Jaundice, also known as icterus (attributive adjective: “icteric”), is yellowish discoloration of the skin, sclerae (whites of the eyes) and mucous membranes caused by hyperbilirubinemia (increased levels of bilirubin in the blood). This hyperbilirubinemia subsequently causes increased levels of bilirubin in the extracellular fluids. Typically, the concentration of bilirubin in the plasma must exceed 1.5 mg/dL, three times the usual value of approximately 0.5mg/dL, for the coloration to be easily visible. Jaundice comes from the French word jaune, meaning yellow.

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Jaundice is not a disease but rather a sign that can occur in many different diseases. 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.

Normal Physiology
In order to understand how jaundice results, it is important to understand where the pathological processes that cause jaundice take their effect. It is also important to further recognize that jaundice itself is not a disease, but rather a symptom of an underlying pathological process that occurs at some point along the normal physiological pathway of the metabolism of bilirubin.

Pre-hepatic events
When red blood cells have completed their life span of approximately 120 days, or when they are damaged, their membranes become fragile and prone to rupture. As the cell traverses through the reticuloendothelial system, their cell membranes rupture and the contents of the red blood cell is released into the blood. The component of the red blood cell that is involved in jaundice is hemoglobin. The hemoglobin released into the blood is phagocytosed by macrophages, and split into its heme and globin portions. The globin portion, being protein, is degraded into amino acids and plays no further role in jaundice. Two reactions then take place to the heme molecule. The first reaction is the oxidation of heme to form biliverdin.This reaction is catalyzed by microsomal enzyme heme oxygenase and it results in biliverdin (green color pigment), iron and carbon monoxide. Next step is reduction of biliverdin to yellow color tetrapyrol pigment bilirubin by cytosolic enzyme biliverdin reductase. This bilirubin is known as “unconjugated”, “free” or “indirect” bilirubin. Approximately 4 mg per kg of bilirubin is produced each day. The majority of this bilirubin comes from the breakdown of heme from expired red blood cells in the process just described. However approximately 20 per cent comes from other heme sources, including ineffective erythropoiesis, breakdown of other heme-containing proteins, such as muscle myoglobin and cytochromes.

Hepatic events
The unconjugated bilirubin then travels to the liver through the bloodstream. Because this bilirubin is not soluble, however, it is transported through the blood bound to serum albumin. Once it arrives at the liver, it is conjugated with glucuronic acid (to form bilirubin diglucuronide, or just “conjugated bilirubin”) to become more water soluble. The reaction is catalyzed by the enzyme UDP-glucuronide transferase.

Post-hepatic events
This conjugated bilirubin is excreted from the liver into the biliary and cystic ducts as part of bile. Intestinal bacteria convert the bilirubin into urobilinogen. From here the urobilinogen can take two pathways. It can either be further converted into stercobilinogen, which is then oxidized to stercobilin and passed out in the faeces, or it can be reabsorbed by the intestinal cells, transported in the blood to the kidneys, and passed out in the urine as the oxidised product urobilin. Stercobilin and urobilin are the products responsible for the coloration of faeces and urine, respectively.

Symptoms:-
In jaundice, the skin and whites of the eyes appear yellow. Urine is often dark because excess bilirubin is excreted through the kidneys. People may have itching, light-colored stools, or other symptoms, depending on the cause of jaundice. For example, acute inflammation of the liver (acute hepatitis) may cause loss of appetite, nausea, vomiting, and fever. Blockage of bile may result in abdominal pain and fever.
Causes:

Bilirubin comes from red blood cells. When red blood cells get old, they are destroyed. Hemoglobin, the iron-containing chemical in red blood cells that carries oxygen, is released from the destroyed red blood cells after the iron it contains is removed. The chemical that remains in the blood after the iron is removed becomes bilirubin.

The liver has many functions. One of the liver’s functions is to produce and secrete bile into the intestines to help digest dietary fat. Another is to remove toxic chemicals or waste products from the blood, and bilirubin is a waste product. The liver removes bilirubin from the blood. After the bilirubin has entered the liver cells, the cells conjugate (attaching other chemicals, primarily glucuronic acid) to the bilirubin, and then secrete the bilirubin/glucuronic acid complex into bile. The complex that is secreted in bile is called conjugated bilirubin. The conjugated bilirubin is eliminated in the feces. (Bilirubin is what gives feces its brown color.) Conjugated bilirubin is distinguished from the bilirubin that is released from the red blood cells and not yet removed from the blood which is termed unconjugated bilirubin.

Jaundice occurs when there is 1) too much bilirubin being produced for the liver to remove from the blood. (For example, patients with hemolytic anemia have an abnormally rapid rate of destruction of their red blood cells that releases large amounts of bilirubin into the blood), 2) a defect in the liver that prevents bilirubin from being removed from the blood, converted to bilirubin/glucuronic acid (conjugated) or secreted in bile, or 3) blockage of the bile ducts that decreases the flow of bile and bilirubin from the liver into the intestines. (For example, the bile ducts can be blocked by cancers, gallstones, or inflammation of the bile ducts). 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.
When a pathological process interferes with the normal functioning of the metabolism and excretion of bilirubin just described, jaundice may be the result. Jaundice is classified into three categories, depending on which part of the physiological mechanism the pathology affects.

The three categories are:

*Pre-hepatic: The pathology is occurring prior the liver

*Hepatic: The pathology is located within the liver

*Post-Hepatic: The pathology is located after the conjugation of bilirubin in the liver

Pre-hepatic
Pre-hepatic jaundice is caused by anything which causes an increased rate of hemolysis (breakdown of red blood cells). In tropical countries, malaria can cause jaundice in this manner. Certain genetic diseases, such as sickle cell anemia, spherocytosis and glucose 6-phosphate dehydrogenase deficiency can lead to increased red cell lysis and therefore hemolytic jaundice. Commonly, diseases of the kidney, such as hemolytic uremic syndrome, can also lead to coloration. Defects in bilirubin metabolism also present as jaundice. Jaundice usually comes with high fevers.

Laboratory findings include:
*Urine: no bilirubin present, urobilirubin > 2 units (except in infants where gut flora has not developed).

*Serum: increased unconjugated bilirubin.

Hepatic
Hepatic jaundice causes include acute hepatitis, hepatotoxicity and alcoholic liver disease, whereby cell necrosis reduces the liver’s ability to metabolise and excrete bilirubin leading to a buildup in the blood. Less common causes include primary biliary cirrhosis, Gilbert’s syndrome (a genetic disorder of bilirubin metabolism which can result in mild jaundice, which is found in about 5% of the population), Crigler-Najjar syndrome, metastatic carcinoma and Niemann Pick Type C disease. Jaundice seen in the newborn, known as neonatal jaundice, is common, occurring in almost every newborn as hepatic machinery for the conjugation and excretion of bilirubin does not fully mature until approximately two weeks of age.

Laboratory Findings include:
Urine: Conjugated bilirubin present, Urobilirubin > 2 units but variable (Except in children)

Post-hepatic
Post-hepatic jaundice, also called obstructive jaundice, is caused by an interruption to the drainage of bile in the biliary system. The most common causes are gallstones in the common bile duct, and pancreatic cancer in the head of the pancreas. Also, a group of parasites known as “liver flukes” live in the common bile duct, causing obstructive jaundice. Other causes include strictures of the common bile duct, biliary atresia, ductal carcinoma, pancreatitis and pancreatic pseudocysts. A rare cause of obstructive jaundice is Mirizzi’s syndrome.

The presence of pale stools and dark urine suggests an obstructive or post-hepatic cause as normal feces get their color from bile pigments.

Patients also can present with elevated serum cholesterol, and often complain of severe itching or “pruritus”.

Laboratory Tests
No one test can differentiate between various classifications of jaundice. A combinations of liver function tests is essential to arrive at a diagnosis.

Neonatal jaundice(jaundice in newborn infants)
Neonatal jaundice is usually harmless: this condition is often seen in infants around the second day after birth, lasting until day 8 in normal births, or to around day 14 in premature births. Serum bilirubin normally drops to a low level without any intervention required: the jaundice is presumably a consequence of metabolic and physiological adjustments after birth. In extreme cases, a brain-damaging condition known as kernicterus can occur; there are concerns that this condition has been rising in recent years due to inadequate detection and treatment of neonatal hyperbilirubinemia. Neonatal jaundice is a risk factor for hearing loss.

Click to see as per Ayurveda-> Yellow Jaundice, Newborn Jaundice, Causes & Symptoms

Jaundiced eye
It was once believed persons suffering from the medical condition jaundice saw everything as yellow. By extension, the jaundiced eye came to mean a prejudiced view, usually rather negative or critical. Alexander Pope, in ‘An Essay on Criticism’ (1711), wrote: “All seems infected that the infected spy, As all looks yellow to the jaundiced eye.” Similarly in the mid 19th century the English poet Lord Alfred Tennyson wrote in the poem ‘Locksley Hall’: “So I triumphe’d ere my passion sweeping thro’ me left me dry, left me with the palsied heart, and left me with a jaundiced eye.”

Problems Jaundice Cause :

Jaundice or cholestasis, by themselves, causes few problems (except in the newborn, and jaundice in the newborn is different than most other types of jaundice, as discussed later.) Jaundice can turn the skin and sclerae yellow. In addition, stool can become light in color, even clay-colored because of the absence of bilirubin that normally gives stool its brown color. The urine may turn dark or brownish in color. This occurs when the bilirubin that is building up in the blood begins to be excreted from the body in the urine. Just as in feces, the bilirubin turns the urine brown.

Besides the cosmetic issues of looking yellow and having dark urine and light stools, the symptom that is associated most frequently associated with jaundice or cholestasis is itching, medically known as pruritus. The itching associated with jaundice and cholestasis can sometimes be so severe that it causes patients to scratch their skin “raw,” have trouble sleeping, and, rarely, even to commit suicide.

It is the disease causing the jaundice that causes most problems associated with jaundice. Specifically, if the jaundice is due to liver disease, the patient may have symptoms or signs of liver disease or cirrhosis. (Cirrhosis represents advanced liver disease.) The symptoms and signs of liver disease and cirrhosis include fatigue, swelling of the ankles, muscle wasting, ascites (fluid accumulation in the abdominal cavity), mental confusion or coma, and bleeding into the intestines.

If the jaundice is caused by blockage of the bile ducts, no bile enters the intestine. Bile is necessary for digesting fat in the intestine and releasing vitamins from within it so that the vitamins can be absorbed into the body. Therefore, blockage of the flow of bile can lead to deficiencies of certain vitamins. For example, there may be a deficiency of vitamin K that prevents proteins that are needed for normal clotting of blood to be made by the liver, and, as a result, uncontrolled bleeding may occur.

Diseases cause jaundice:-
Increased production of bilirubin
There are several uncommon conditions that give rise to over-production of bilirubin. The bilirubin in the blood in these conditions usually is only mildly elevated, and the resultant jaundice usually is mild and difficult to detect. These conditions include: 1) rapid destruction of red blood cells (referred to as hemolysis), 2) a defect in the formation of red blood cells that leads to the over-production of hemoglobin in the bone marrow (called ineffective erythropoiesis), or 3) absorption of large amounts of hemoglobin when there has been much bleeding into tissues (e.g., from hematomas, collections of blood in the tissues).

Acute inflammation of the liver
Any condition in which the liver becomes inflamed can reduce the ability of the liver to conjugate (attach glucuronic acid to) and secrete bilirubin. Common examples include acute viral hepatitis, alcoholic hepatitis, and Tylenol-induced liver toxicity.

Chronic liver diseases
Chronic inflammation of the liver can lead to scarring and cirrhosis, and can ultimately result in jaundice. Common examples include chronic hepatitis B and C, alcoholic liver disease with cirrhosis, and autoimmune hepatitis.

Infiltrative diseases of the liver
Infiltrative diseases of the liver refer to diseases in which the liver is filled with cells or substances that don’t belong there. The most common example would be metastatic cancer to the liver, usually from cancers within the abdomen. Uncommon causes include a few diseases in which substances accumulate within the liver cells, for example, iron (hemochromatosis), alpha-one antitrypsin (alpha-one antitrypsin deficiency), and copper (Wilson’s disease).

Inflammation of the bile ducts
Diseases causing inflammation of the bile ducts, for example, primary biliary cirrhosis or sclerosing cholangitis and some drugs, can stop the flow of bile and elimination of bilirubin and lead to jaundice.

Blockage of the bile ducts
The most common causes of blockage of the bile ducts are gallstones and pancreatic cancer. Less common causes include cancers of the liver and bile ducts.

Drugs:-
Many drugs can cause jaundice and/or cholestasis. Some drugs can cause liver inflammation (hepatitis) similar to viral hepatitis. Other drugs can cause inflammation of the bile ducts, resulting in cholestasis and/or jaundice. Drugs also may interfere directly with the chemical processes within the cells of the liver and bile ducts that are responsible for the formation and secretion of bile to the intestine. As a result, the constituents of bile, including bilirubin, are retained in the body. The best example of a drug that causes this latter type of cholestasis and jaundice is estrogen. The primary treatment for jaundice caused by drugs is discontinuation of the drug. Almost always the bilirubin levels will return to normal within a few weeks, though in a few cases it may take several months.

Genetic disorders:-
There are several rare genetic disorders present from birth that give rise to jaundice. Crigler-Najjar syndrome is caused by a defect in the conjugation of bilirubin in the liver due to a reduction or absence of the enzyme responsible for conjugating the glucuronic acid to bilirubin. Dubin-Johnson and Rotor’s syndromes are caused by abnormal secretion of bilirubin into bile.

The only common genetic disorder that may cause jaundice is Gilbert’s syndrome which affects approximately 7% of the population. Gilbert’s syndrome is caused by a mild reduction in the activity of the enzyme responsible for conjugating the glucuronic acid to bilirubin. The increase in bilirubin in the blood usually is mild and infrequently reaches levels that cause jaundice. Gilbert’s syndrome is a benign condition that does not cause health problems.

Developmental abnormalities of bile ducts:-
There are rare instances in which the bile ducts do not develop normally and the flow of bile is interrupted. Jaundice frequently occurs. These diseases usually are present from birth though some of them may first be recognized in childhood or even adulthood. Cysts of the bile duct (choledochal cysts) are an example of such a developmental abnormality. Another example is Caroli’s disease.

Jaundice of pregnancy :-

Most of the diseases discussed previously can affect women during pregnancy, but there are some additional causes of jaundice that are unique to pregnancy.

Cholestasis of pregnancy. Cholestasis of pregnancy is an uncommon condition that occurs in pregnant women during the third trimester. The cholestasis is often accompanied by itching but infrequently causes jaundice. The itching can be severe, but there is treatment (ursodeoxycholic acid or ursodiol). Pregnant women with cholestasis usually do well although they may be at greater risk for developing gallstones. More importantly, there appears to be an increased risk to the fetus for developmental abnormalities. Cholestasis of pregnancy is more common in certain groups, particularly in Scandinavia and Chile, and tends to occur with each additional pregnancy. There also is an association between cholestasis of pregnancy and cholestasis caused by oral estrogens, and it has been hypothesized that it is the increased estrogens during pregnancy that are responsible for the cholestasis of pregnancy.

Pre-eclampsia. Pre-eclampsia, previously called toxemia of pregnancy, is a disease that occurs during the second half of pregnancy and involves several systems within the body, including the liver. It may result in high blood pressure, fluid retention, and damage to the kidneys as well as anemia and reduced numbers of platelets due to destruction of red blood cells and platelets. It often causes problems for the fetus. Although the bilirubin level in the blood is elevated in pre-eclampsia, it usually is mildly elevated, and jaundice is uncommon. Treatment of pre-eclampsia usually involves delivery of the fetus as soon as possible if the fetus is mature.

Acute fatty liver of pregnancy. Acute fatty liver of pregnancy (AFLP) is a very serious complication of pregnancy of unclear cause that often is associated with pre-eclampsia. It occurs late in pregnancy and results in failure of the liver. It can almost always be reversed by immediate delivery of the fetus. There is an increased risk of infant death. Jaundice is common, but not always present in AFLP. Treatment usually involves delivery of the fetus as soon as possible.

Diagnosis:-
Many tests are available for determining the cause of jaundice, but the history and physical examination are important as well.

History
The history can suggest possible reasons for the jaundice. For example, heavy use of alcohol suggests alcoholic liver disease, whereas use of illegal, injectable drugs suggests viral hepatitis. Recent initiation of a new drug suggests drug-induced jaundice. Episodes of abdominal pain associated with jaundice suggests blockage of the bile ducts usually by gallstones.

Physical examination
The most important part of the physical examination in a patient who is jaundiced is examination of the abdomen. Masses (tumors) in the abdomen suggest cancer infiltrating the liver (metastatic cancer) as the cause of the jaundice. An enlarged, firm liver suggests cirrhosis. A rock-hard, nodular liver suggests cancer within the liver.

Blood tests
Measurement of bilirubin can be helpful in determining the causes of jaundice. Markedly greater elevations of unconjugated bilirubin relative to elevations of conjugated bilirubin in the blood suggest hemolysis (destruction of red blood cells). Marked elevations of liver tests (aspartate amino transferase or AST and alanine amino transferase or ALT) suggest inflammation of the liver (such as viral hepatitis). Elevations of other liver tests, e.g., alkaline phosphatase, suggest diseases or obstruction of the bile ducts.

Ultrasonography
Ultrasonography is a simple, safe, and readily-available test that uses sound waves to examine the organs within the abdomen. Ultrasound examination of the abdomen may disclose gallstones, tumors in the liver or the pancreas, and dilated bile ducts due to obstruction (by gallstones or tumor).

Computerized tomography (CT or CAT scans)
Computerized tomography or CT scans are scans that use x-rays to examine the soft tissues of the abdomen. They are particularly good for identifying tumors in the liver and the pancreas and dilated bile ducts, though they are not as good as ultrasonography for identifying gallstones.

Magnetic resonance imaging (MRI)
Magnetic Resonance Imaging scans are scans that utilize magnetization of the body to examine the soft tissues of the abdomen. Like CT scans, they are good for identifying tumors and studying bile ducts. MRI scans can be modified to visualize the bile ducts better than CT scans (a procedure referred to as MR cholangiography), and, therefore, are better than CT for identifying the cause and location of bile duct obstruction.

Endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic ultrasound
Endoscopic retrograde cholangiopancreatography (ERCP) provides the best means for examining the bile duct. For ERCP an endoscope is swallowed by the patient after he or she has been sedated. The endoscope is a flexible, fiberoptic tube approximately four feet in length with a light and camera on its tip. The tip of the endoscope is passed down the esophagus, through the stomach, and into the duodenum where the main bile duct enters the intestine. A thin tube then is passed through the endoscope and into the bile duct, and the duct is filled with x-ray contrast solution. An x-ray is taken that clearly demonstrates the contrast-filled bile ducts. ERCP is particularly good at demonstrating the cause and location of obstruction within the bile ducts. A major advantage of ERCP is that diagnostic and therapeutic procedures can be done at the same time as the x-rays. For example, if gallstones are found in the bile ducts, they can be removed. Stents can be placed in the bile ducts to relieve the obstruction caused by scarring or tumors. Biopsies of tumors can be obtained.

Ultrasonography can be combined with ERCP by using a specialized endoscope capable of doing ultrasound scanning. Endoscopic ultrasound is excellent for diagnosing small gallstones in the gallbladder and bile ducts that can be missed by other diagnostic methods such as ultrasound, CT, and MRI. It also is the best means of examining the pancreas for tumors and can facilitate biopsy through the endoscope of tumors within the pancreas.

Liver biopsy
Biopsy of the liver provides a small piece of tissue from the liver for examination under the microscope. The biopsy most commonly is done with a long needle after local injection of the skin of the abdomen overlying the liver with anesthetic. The needle passes through the skin and into the liver, cutting off a small piece of liver tissue. When the needle is withdrawn, the piece of liver comes with it. Liver biopsy is particularly good for diagnosing inflammation of the liver and bile ducts, cirrhosis, cancer, and fatty liver.

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Treatment:

A doctor uses laboratory tests and imaging studies to determine the cause of the jaundice. If the problem is a disease of the liver, such as acute viral hepatitis, the jaundice usually disappears gradually as the condition of the liver improves. If the problem is blockage of a bile duct, surgery or surgical endoscopy (using a flexible viewing tube with surgical instruments attached: Endoscopy) is usually performed as soon as possible to reopen the affected bile duct. Itching caused by jaundice can be treated with cholestyramine Some Trade Names QUESTRAN taken by mouth. Usually, the itching gradually disappears as the liver’s condition improves.

With the exception of the treatments for specific causes of jaundice mentioned previously, the treatment of jaundice usually requires a diagnosis of the specific cause of the jaundice and treatment directed at the specific cause, e.g., removal of a gallstone blocking the bile duct.

You may click to see:->Natural & Herbal Remedies of Jaundice

Liver Care – Dietary And Ayurvedic Treatment, Home Remedies

Jaundice Treatment With Ayurvedic and Home Remedies

Herbal Supliment of Jaundice

Homeopathic Treatment for LIVER DISEASES Liver Enlargement, Hypertrophy, Jaundice, Hepatitis

HOMEOPATHY FOR JAUNDICE

Homeopathic jaundice remedies

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://en.wikipedia.org/wiki/Jaundice
http://www.medicinenet.com/jaundice/page2.htm
http://merck.com/mmhe/au/sec10/ch135/ch135b.html

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Bhumiamla / Phyllanthus niruri

Botanical Name:Phyllanthus niruri
Family:Phyllanthaceae
Genus:Phyllanthus
Species:P. niruri
Kingdom:    Plantae
Order:Malpighiales

Common names : Chanca Piedra in Spanish, Bhumyamalaki in Ayurveda, and Quebra-Pedra in Portuguese, Keezha Nelli  in Tamil, Nela Nelli  in Kannada,Keezhar Nelli in Malayalam and Nela Usiri in Telugu. It has many other common names in assorted languages, including dukong anak, dukong-dukong anak, amin buah, rami buah, turi hutan, bhuiaonla, and Meniran (in Indonesia).

Habitat : Common in central and southern India extending to Sri Lanka.
Historical aspects:
Charaka mentions the plant. In ayurveda the expressed juice of the fresh plant is given for a sluggish liver and also for chronic liver diseases. It is commonly and widely used for dysentery and intestinal colic. Phyllanthus niruri, also called “stonebreaker” due to its strong roots, is native to South America. The plant is dried into an extract that acts as a diuretic and an astringent.

Description:  The annual herb is 30-60cm high, quite glabrous, stem often branched at the base, angular. Leaves numerous subsessile distichous often imbricating, elliptic oblong obtuse.Stem is angular with numerous distichous, elliptic-oblong leaves. Stipules present, very acute. Flowers yellowish, very numerous, axillary, the male flowers 1-3, female flowers are solitary pistillate flower borne axillary. Fruits capsule, very small, globose, smooth, seeds 3-gonous, longitudinally ribbed on the back. Seed to seed cycle occurs in two or four weeks. The flowering time in Indian conditions is July to August.

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Pharmacognoy:
It is safe lipotropic drug and its primary action is on the liver. Blumberg showed in inhibition of DNA polymerase of Hepatitis b virus and a viral-agglutinating activity. The characteristics have been well studied.

Phytochemistry
:
In the aerial parts, three crystalline lignans including phyllanthine and hypophyllanthine have been found. Five flavonoids have been identified, quercetin, astralgin, quercitrin, and rutin. Four leucodelphinidine alkaloids were separated from the leaves and stems one of then being and enantiomorph of securinine.

Medicinal Uses:
A clinical study with Phyllanthus niruri, indicated that it may reduce the levels of urinary calcium.  A subsequent study of 150 patients over a 6-month period indicated that an extract of this herb reduces the incidence of stone formation, and concluded, “Regular self-administration of P. niruri after extracorporeal shock wave lithotripsy for renal stones results in an increased stone-free rate that appears statistically significant for lower caliceal location. Its efficacy and the absolute lack of side effects make this therapy suitable to improve overall outcomes after extracorporeal shock wave lithotripsy for lower pole stones.”  A more recent rat study found that Phyllanthus niruri has been shown to interfere with many stages of stone formation, reducing crystals aggregation, modifying their structure and composition as well as altering the interaction of the crystals with tubular cells leading to reduced subsequent endocytosis.”

Ayurvedic properties :
Guna: Laghu, Ruksha.
Rasa
: Tikta, kashaya.
Veerya: Sheeta.Vipaka: Katu.
Dosha: Kaphapittaghna
karma: Kasaswasahara, Dahaprashamana, Rochana, Yakrutottejaka, kandughna.

Safety:
With the formulation and dosage used no adverse reactions have been reprted.

Cinical Usage:
The fresh root is used for the treatment of viral hepatitis.the plant is also used as a diuretic in oedema.it is also used to increase appetite and locally to relieve inflammations.

Healing Options:
Phyllanthus has been used in Ayurvedic medicine for over 2,000 years and has a wide number of traditional uses.

This includes employing the whole plant for jaundice, gonorrhea, frequent menstruation, and diabetes and using it topically as a poultice for skin ulcers, sores, swelling, and itchiness

CHANCA PIEDRA (Phyllanthus niruri) is a composite name, “chanca” meaning “to break” in Quechua and “piedra” meaning “stone” in Spanish. It is the popular name given to several small shrub-like plants in the Phyllanthus genus (botanical family Euphorbiaceae), including Phyllanthus niruri, and Phyllanthus stipulatis. These two species have the same medicinal effects and look identical, except for their seeds, by which the botanist can tell them apart. A third species, Phyllanthus amarus, has been considered identical (perhaps not a different species at all) to Phyllanthus niruri. These species of Phyllanthus have been proven in scientific research to have antihepatotoxic, antispasmodic, antiviral, bactericidal, febrifugal, and hypoglycemic activity.*

Liver Disorders/ Jaundice :
The herb stimulates the liver and is useful in liver and spleen disorders. It can be used in jaundice and enlargement of liver. The leaf should be administered with black salt and ginger every morning for 10 days in the treatment of such disorders.

Loss of Appetite:
Its root, leaves, fruits, milky juice is very useful in Loss of appetite . It is a major component of many popular liver tonics which increase Appetite & locally to relieve inflammations.

Oedema:
The plant is also used as a diuretic in oedema. Powdered leaves & roots – pulverized & made into poultice with rice-water useful in oedematous swelling and ulcers.

Formulation and Dosage:
Juice: 10-20 ml b.i.d
Herb powder: 3-6 gms b.i.d

Ayurvedic supplements made from Bhumiamla:
Livgood
Livrol Syrup
Arogyavardhini Bati

Liver Tonic Livogod
Herbal Liver Tonic for cirrhosis,alcholic ilver and jaundice

Disclaimer:The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.
Resources:
http://en.wikipedia.org/wiki/Phyllanthus_niruri
allayurveda.com

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