Hemolytic Uremic Syndrome (HUS)

Alternative names:  Haemolytic-uraemic syndrome, HUS

Definition:
Hemolytic uremic syndrome, or HUS, is a kidney condition that happens when red blood cells are destroyed and block the kidneys‘ filtering system. Red blood cells contain hemoglobin—an iron-rich protein that gives blood its red color and carries oxygen from the lungs to all parts of the body.

CLICK & SEE THE PICTURES

When the kidneys and glomeruli—the tiny units within the kidneys where blood is filtered—become clogged with the damaged red blood cells, they are unable to do their jobs. If the kidneys stop functioning, a child can develop acute kidney injury—the sudden and temporary loss of kidney function. Hemolytic uremic syndrome is the most common cause of acute kidney injury in children.

It is a disease characterized by hemolytic anemia (anemia caused by destruction of red blood cells), acute kidney failure (uremia), and a low platelet count (thrombocytopenia). It predominantly, but not exclusively, affects children. Most cases are preceded by an episode of infectious, sometimes bloody, diarrhea acquired as a foodborne illness or from a contaminated water supply and caused by E. coli O157:H7, although Shigella, Campylobacter and a variety of viruses have also been implicated. It is now the most common cause of acquired acute renal failure in childhood. It is a medical emergency and carries a 5–10% mortality; of the remainder, the majority recover without major consequences but a small proportion develop chronic kidney disease and become reliant on renal replacement therapy.

The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the two kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra fluid. Children produce less urine than adults and the amount produced depends on their age. The urine flows from the kidneys to the bladder through tubes called ureters. The bladder stores urine. When the bladder empties, urine flows out of the body through a tube called the urethra, located at the bottom of the bladder.

Symptoms:
STEC-HUS occurs after ingestion of a strain of bacteria, usually types of E. coli, that expresses verotoxin (also called Shiga-like toxin). Bloody diarrhea typically follows. HUS develops about 5–10 days after onset of diarrhea, with decreased urine output (oliguria), blood in the urine (hematuria), kidney failure, thrombocytopenia (low levels of platelets) and destruction of red blood cells (microangiopathic hemolytic anemia). Hypertension is common. In some cases, there are prominent neurologic changes.

A child with hemolytic uremic syndrome may develop signs and symptoms similar to those seen with gastroenteritis—an inflammation of the lining of the stomach, small intestine, and large intestine—such as

*vomiting
*bloody diarrhea
*abdominal pain
*fever and chills
*headache

As the infection progresses, the toxins released in the intestine begin to destroy red blood cells. When the red blood cells are destroyed, the child may experience the signs and symptoms of anemia—a condition in which red blood cells are fewer or smaller than normal, which prevents the body’s cells from getting enough oxygen.

Signs and symptoms of anemia may include:-

*fatigue, or feeling tired
*weakness
*fainting
*paleness

As the damaged red blood cells clog the glomeruli, the kidneys may become damaged and make less urine. When damaged, the kidneys work harder to remove wastes and extra fluid from the blood, sometimes leading to acute kidney injury.

Other signs and symptoms of hemolytic uremic syndrome may include bruising and seizures.

When hemolytic uremic syndrome causes acute kidney injury, a child may have the following signs and symptoms:

*edema—swelling, most often in the legs, feet, or ankles and less often in the hands or face
*albuminuria—when a child’s urine has high levels of albumin, the main protein in the blood
*decreased urine output
*hypoalbuminemia—when a child’s blood has low levels of albumin
*blood in the urine

Causes:
A number of things can cause hemolytic uremic syndrome, but the most common cause — particularly in children — is an infection with a specific strain of E. coli, usually the strain known as O157:H7. However, other strains of E. coli have been linked to hemolytic uremic syndrome, too.

Normally, harmless strains, or types, of E. coli are found in the intestines and are an important part of digestion. However, if a child becomes infected with the O157:H7 strain of E. coli, the bacteria will lodge in the digestive tract and produce toxins that can enter the bloodstream. The toxins travel through the bloodstream and can destroy the red blood cells. E. coli O157:H7 can be found in:

*Contaminated meat or produce
*Swimming pools or lakes contaminated with feces
*undercooked meat, most often ground beef
*unpasteurized, or raw, milk
*unwashed, contaminated raw fruits and vegetables
*contaminated juice

Less common causes, sometimes called atypical hemolytic uremic syndrome, can include:-

*taking certain medications, such as chemotherapy
*having other viral or bacterial infections
*inheriting a certain type of hemolytic uremicsyndrome that runs in families

Children who are more likely to develop hemolytic uremic syndrome include those who
are younger than age 5 and have been diagnosedwith an E. coli O157:H7 infection

*have a weakened immune system
*have a family history of inherited hemolyticuremic syndrome
*Hemolytic uremic syndrome occurs in about two out of every 100,000 children.

Most people who are infected with E. coli, even the more dangerous strains, won’t develop hemolytic uremic syndrome. It’s also possible for hemolytic uremic syndrome to follow infection with other types of bacteria.

In adults, hemolytic uremic syndrome is more commonly caused by other factors, including:

*The use of certain medications, such as quinine (an over-the-counter muscle cramp remedy), some chemotherapy drugs, the immunosuppressant medication cyclosporine (Neoral, Sandimmune) and anti-platelet medications

*Pregnancy

*Certain infections, such as HIV/AIDS or an infection with the pneumococcal bacteria

*Genes, which can be a factor because a certain type of HUS — atypical hemolytic uremic syndrome — may be passed down from your parents

The cause of hemolytic uremic syndrome in adults is often unknown

Diagnosis:
The Doctor diagnoses hemolytic uremic syndrome with

*a medical and family history
*a physical exam
*urine tests
*a blood test
*a stool test
*kidney biopsy

The similarities between HUS, aHUS, and TTP make differential diagnosis essential. All three of these systemic TMA-causing diseases are characterized by thrombocytopenia and microangiopathic hemolysis, plus one or more of the following: neurological symptoms (e.g., confusion, cerebral convulsions, seizures); renal impairment (e.g., elevated creatinine, decreased estimated glomerular filtration rate [eGFR], abnormal urinalysis ); and gastrointestinal (GI) symptoms (e.g., diarrhea, nausea/vomiting, abdominal pain, gastroenteritis).The presence of diarrhea does not exclude aHUS as the etiology of TMA, as 28% of patients with aHUS present with diarrhea and/or gastroenteritis. First diagnosis of aHUS is often made in the context of an initial, complement-triggering infection, and Shiga-toxin has also been implicated as a trigger that identifies patients with aHUS. Additionally, in one study, mutations of genes encoding several complement regulatory proteins were detected in 8 of 36 (22%) patients diagnosed with STEC-HUS. However, the absence of an identified complement regulatory gene mutation does not preclude aHUS as the etiology of the TMA, as approximately 50% of patients with aHUS lack an identifiable mutation in complement regulatory genes.

Diagnostic work-up supports the differential diagnosis of TMA-causing diseases. A positive Shiga-toxin/EHEC test confirms an etiological cause for STEC-HUS, and severe ADAMTS13 deficiency (i.e., ?5% of normal ADAMTS13 levels) confirms a diagnosis of TTP

Complications:
Most children who develop hemolytic uremic syndrome and its complications recover without permanent damage to their health.1
However, children with hemolytic uremic syndrome may have serious and sometimes life-threatening complications, including

*acute kidney injury
*high blood pressure
*blood-clotting problems that can lead to bleeding
*seizures
*heart problems
*chronic, or long lasting, kidney disease
*stroke
*coma

Treatment:
The Doctor will treat a child’s urgent symptoms and try to prevent complications by

*observing the child closely in the hospital
*replacing minerals, such as potassium and salt, and fluids through an intravenous (IV) tube
*giving the child red blood cells and platelets—cells in the blood that help with clotting—through an IV
*giving the child IV nutrition
*treating high blood pressure with medications

Treating Acute Kidney Injury:
If necessary,the Doctor will treat acute kidney injury with dialysis—the process of filtering wastes and extra fluid from the body with an artificial kidney. The two forms of dialysis are hemodialysis and peritoneal dialysis. Most children with acute kidney injury need dialysis for a short time only.

Treating Chronic Kidney Disease:
Some children may sustain significant kidney damage that slowly develops into CKD. Children who develop CKD must receive treatment to replace the work the kidneys do. The two types of treatment are dialysis and transplantation.

In most cases, The Doctor treat CKD with a kidney transplant. A kidney transplant is surgery to place a healthy kidney from someone who has just died or a living donor, most often a family member, into a person’s body to take over the job of the failing kidney. Though some children receive a kidney transplant before their kidneys fail completely, many children begin with dialysis to stay healthy until they can have a transplant. click to know more

Prevention:

Hemolytic uremic syndrome, or HUS, is a kidney condition that happens when red blood cells are destroyed and block the kidneys’ filtering system.
The most common cause of hemolytic uremic syndrome in children is an Escherichia coli (E. coli) infection of the digestive system.
Normally, harmless strains, or types, of E. coli are found in the intestines and are an important part of digestion. However, if a child becomes infected with the O157:H7 strain of E. coli, the bacteria will lodge in the digestive tract and produce toxins that can enter the bloodstream.
A child with hemolytic uremic syndrome may develop signs and symptoms similar to those seen with gastroenteritis, an inflammation of the lining of the stomach, small intestine, and large intestine.

Most children who develop hemolytic uremic syndrome and its complications recover without permanent damage to their health.
Some children may sustain significant kidney damage that slowly develops into chronic kidney disease (CKD).

Parents and caregivers can help prevent childhood hemolytic uremic syndrome due to E. coli O157:H7 by

*avoiding unclean swimming areas
*avoiding unpasteurized milk, juice, and cider
*cleaning utensils and food surfaces often
*cooking meat to an internal temperature of at least 160° F
*defrosting meat in the microwave or refrigerator
*keeping children out of pools if they have had diarrhea
*keeping raw foods separate
*washing hands before eating
*washing hands well after using the restroom and after changing diapers

When a child is taking medications that may cause hemolytic uremic syndrome, it is important that the parent or caretaker watch for symptoms and report any changes in the child’s condition to the Doctor as soon as possible.

Prognosis:
Acute renal failure occurs in 55-70% of patients with STEC-HUS, although up to 70-85% recover renal function. Patients with aHUS generally have poor outcomes, with up to 50% progressing to ESRD or irreversible brain damage; as many as 25% die during the acute phase. However, with aggressive treatment, more than 90% of patients survive the acute phase of HUS, and only about 9% may develop ESRD. Roughly one-third of persons with HUS have abnormal kidney function many years later, and a few require long-term dialysis. Another 8% of persons with HUS have other lifelong complications, such as high blood pressure, seizures, blindness, paralysis, and the effects of having part of their colon removed. The overall mortality rate from HUS is 5-15%. Children and the elderly have a worse prognosis.

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://kidney.niddk.nih.gov/KUDiseases/pubs/childkidneydiseases/hemolytic_uremic_syndrome/

http://en.wikipedia.org/wiki/Hemolytic-uremic_syndrome

http://www.mayoclinic.org/diseases-conditions/hemolytic-uremic-syndrome/basics/causes/con-20029487

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Sophora Flavescens

Botanical Name : Sophora Flavescens
Family: Fabaceae
Subfamily:Faboideae
Tribe: Sophoreae
Genus: Sophora
Species:S. flavescens
Kingdom:Plantae
Order: Fabales

Common Names:Ku Shen, Shrubby sophora

Habitat:Sophora Flavescens is native to Eastern Asia -(From Russia to China.) It grows on Scrub on mountain slopes, river valleys, especially on sandy soils. Grassy places in lowland and waste ground, Central and South Japan

Description:
An evergreen Shrub growing to 1.5m by 1m at a slow rate. It is hardy to zone 6. It is in leaf all year, in flower from July to August, and the seeds ripen in September. The flowers are hermaphrodite (have both male and female organs) and are pollinated by Insects. It can fix Nitrogen. The plant prefers light (sandy), medium (loamy) and heavy (clay) soils and requires well-drained soil. The plant prefers acid, neutral and basic (alkaline) soils. It cannot grow in the shade. It requires moist soil….CLICK & SEE THE PICTURES

Sophora flavescens is a species of plant in the genus Sophora a genus of the Fabaceae family, that contains about 52 species, nineteen varieties, and seven forms that are widely distributed in Asia, Oceanica, and the Pacific islands.About fifteen species in this genus have a long history of use in traditional Chinese medicines. The root is known as Ku shen. is a typical traditional Chinese medicine
Cultivation:
Succeeds in a well-drained moderately fertile soil in full sun. Requires the protection of a sunny wall if it is to flower, and succeeds only in the mildest areas of the country. It grows best in the warmer areas of the country where the wood will be more readily ripened and better able to withstand winter cold. Although hardy to at least -15°c, this species does not do very well in the relatively cool summers of Britain, the plant gradually weakens and eventually succumbs. It can be grown in the milder areas of the country and be treated like a herbaceous perennial, growing afresh from the base each spring. An important medicinal herb in China. Plants should be container-grown and planted out whilst young, older plants do not transplant well. A polymorphic species. The flowers are produced on the current years growth. Plants in this genus are notably resistant to honey fungus. This species has a symbiotic relationship with certain soil bacteria, these bacteria form nodules on the roots and fix atmospheric nitrogen. Some of this nitrogen is utilized by the growing plant but some can also be used by other plants growing nearby.

Propagation:
Seed – best sown as soon as it is ripe in a greenhouse. Pre-soak stored seed for 12 hours in hot (not boiling) water and sow in late winter in a greenhouse. Prick out the seedlings as soon as they are large enough to handle into individual pots in the greenhouse, and grow them on for 2 years under protected conditions. Plant them out into their permanent positions in early summer of their third year. Cuttings of young shoots with a heel, July/August in a frame. Air-layering
Medicinal Uses:
The Sophora Flavescen’s   root (click & see) is anthelmintic, antibacterial, antifungal, antipruritic, astringent, bitter, carminative, diuretic, febrifuge, parasiticide, pectoral, stomachic and tonic. It is used internally in the treatment of jaundice, dysentery, diarrhea and urinary infections. Sophora root is used both internally and externally in the treatment of vaginitis, eczema, pruritis, ringworm, leprosy, syphilis, scabies and itching allergic reactions. The root is harvested in the autumn and dried for later use. The plant is anthelmintic and diuretic. It also has antibacterial activity, inhibiting the growth of Mycobacterium tuberculosis and Trichomonas vaginitis.
Known Hazards: The plant contains cytosine, which resembles nicotine and is similarly toxic. The plant is poisonous when used in quantity[

Resources:

http://en.wikipedia.org/wiki/Sophora_flavescens

http://www.getwellnatural.com/sophora-flavescens.aspx

http://www.pfaf.org/user/Plant.aspx?LatinName=Sophora+flavescens

Glycyrrhiza Uralensis

Botanical Name : Glycyrrhiza Uralensis
Family:    Fabaceae
Genus:    Glycyrrhiza
Species:G. uralensis
Kingdom:Plantae
Order:    Fabales

Common Name: Licorice, Gan Cao, Iriqsus, Kan T’Sao, Kan Ts’Ao, Liquirita, Madhuka, Meyankoku, Mi Ts’Ao, Regaliz, Sus Maikik,Chinese liquorice.

Common Names in Azerbaijani:Ural biyan
Common Names in Chinese:Gan Zao
Common Names in English:Chinese Licorice, Gan-Cao, Russian Licorice
Common Names in French:Réglisse De L´oural, Réglisse De Sibérie
Common Names in German:Chinesische Lakritze, Chinesisches Sübholz
Common Names in Hinese:Gan Cao
Common Names in Japanese:Gurukiruriza Urarenshisu, Uraru Kanzou,
Common Names in Kazakh:Miya-Tamr
Common Names in Russian:Solodka Ural´skaja, Solodka Uralskaya
Common Names in Thai:Cha Em Kha Kai (Central Thailand)
Common Names in Tibetan:Shing-Mngar
Common Names in Vietnamese:Cam thao

Habitat : Native to Central Asia. Licorice grows in sandy soil usually near a stream for ample water. Glycyrrhiza glabra, which is very similar medicinally, comes from the Mediterranea region.

Description:
Glycyrrhiza uralensis is a perennial  herb  growing to 0.6 m (2ft) by 0.4 m (1ft 4in).
It is hardy to zone (UK) 6. It is in flower from Jun to August, and the seeds ripen from Jul to October. The flowers are hermaphrodite (have both male and female organs)It can fix Nitrogen.....CLICK & SEE THE PICTURES

Species:
Glycyrrhiza has several Species and that include:

Glycyrrhiza acanthocarpa
Glycyrrhiza aspera
Glycyrrhiza astragalina
Glycyrrhiza bucharica
Glycyrrhiza echinata – Russian liquorice
Glycyrrhiza eglandulosa
Glycyrrhiza foetida
Glycyrrhiza foetidissima
Glycyrrhiza glabra – liquorice, licorice
Glycyrrhiza gontscharovii
Glycyrrhiza iconica
Glycyrrhiza inflata
Glycyrrhiza korshinskyi
Glycyrrhiza lepidota – American licorice
Glycyrrhiza pallidiflora
Glycyrrhiza squamulosa
Glycyrrhiza triphylla
Glycyrrhiza uralensis – Chinese liquorice
Glycyrrhiza yunnanensis

Cultivation:  
Requires a deep well cultivated fertile moisture-retentive soil for good root production. Prefers a sandy soil with abundant moisture. Slightly alkaline conditions produce the best plants. Plants are hardy to at least -15°c. This species is widely cultivated in China as a medicinal plant. Unless seed is required, the plant is usually prevented from flowering so that it puts more energy into producing good quality roots. A very deep-rooted plant, it can be difficult to eradicate once it is established. This species has a symbiotic relationship with certain soil bacteria, these bacteria form nodules on the roots and fix atmospheric nitrogen. Some of this nitrogen is utilized by the growing plant but some can also be used by other plants growing nearby.

Propagation:    
Pre-soak the seed for 24 hours in warm water and then sow spring or autumn in a greenhouse. Prick out the seedlings into individual pots when they are large enough to handle, and grow them on for their first winter in a greenhouse. Plant out in late spring or early summer when in active growth. Plants are rather slow to grow from seed. Division of the root in spring or autumn. Each division must have at least one growth bud. Autumn divisions can either be replanted immediately or stored in clamps until the spring and then be planted out. It is best to pt up the smaller divisions and grow them on in a cold frame until they are established before planting them out in the spring or summer.

Edible Uses:    
Edible Parts: Root.
The fibrous root is used as a sweetener for foods. It is boiled in water to extract the sugars etc and used as a liquorice substitute in sweets, medicines, drinks etc. The root contains glycyrrhizin, which is 50 times sweeter than sugar.

Parts Uses: Root & the whole herb

Medicinal Uses:
Anodyne, Antioxidant, Antispasmodic, Anti-inflammatory, Demulcent, Depurative, Diuretic, Emollient, Estrogenic, Expectorant, Pectoral

Glycyrrhiza Uralensis is commonly used in Chinese herbalism, where it is considered to be one of the 50 fundamental herbs. It is considered to be second in importance only to Ginseng (Panax spp). Used in excess, however, it can cause cardiac dysfunction and severe hypertension. The root is a sweet tonic herb that stimulates the corticosteroidal hormones, neutralizes toxins and balances blood sugar levels. It is also antibacterial, anti-inflammatory, antiphlogistic, antispasmodic, antitussive, cholagogue, demulcent, emollient, expectorant and laxative. It is used internally in the treatment of Addison’s disease, asthma, coughs and peptic ulcers. Externally, it is used to treat acne, boils and sore throats. It is included in almost all Chinese herbal formulae, where it is said to harmonize and direct the effects of the various ingredients. It precipitates many compounds and is therefore considered to be unsuitable for use with some herbs such as Daphne genkwa, Euphorbia pekinensis and Corydalis solida. It increases the toxicity of some compounds such as ephedrine, salicylates, adrenaline and cortisone. It should not be prescribed for pregnant women or for people with high blood pressure, kidney disease or anyone taking digoxin-based medications. Excessive doses cause water retention and high blood pressure. It can cause impotence in some people. The roots are harvested in early autumn, preferably from plants 3- 4 years old, and is dried for later use. The flowers are alterative and expectorant.

Other Uses:
Fire retardant;  Insulation.
Liquorice root, after the medicinal and flavouring compounds have been removed, is used in fire extinguishing agents, to insulate fibreboards and as a compost for growing mushrooms.

Known Hazards: Liquorice root contains glycyrrhizin, which can cause high blood pressure, salt and water retention, and low potassium levels; it could also lead to heart problems. Patients who take liquorice with diuretics or medicines that reduce the body’s potassium levels could induce even lower potassium levels. Taking large amounts of liquorice root could also affect cortisol levels as well.[citation needed] People with heart disease or high blood pressure should be cautious about taking liquorice root. Pregnant women also need to avoid liquorice root because it could increase the risk of preterm labor.

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

Resources:

http://www.pfaf.org/user/Plant.aspx?LatinName=Glycyrrhiza+uralensis

http://www.angelicaherbs.com/herbdetail.php?id=339&cat=latin_name&latin_name=Glycyrrhiza%20uralensis

http://zipcodezoo.com/Plants/G/Glycyrrhiza%5Furalensis/

http://www.theplantencyclopedia.org/wiki/Glycyrrhiza

Trichosanthes kirilowii

Botanical Name :Trichosanthes kirilowii
Family: Cucurbitaceae
Genus: Trichosanthes
Species:T. kirilowii
Kingdom:Plantae
Order:Cucurbitales

Common Names:  Chinese cucumber in English. And Chinese snake gourd.

Habitat :Trichosanthes kirilowii found particularly in Henan, Shandong, Hebei, Shanxi, and Shaanxi. It is one of the 50 fundamental herbs used in traditional Chinese medicine.

OIt often grows at an altitude of 200-1800m hillside forest, thickets, meadows and Cunpang Tanabe, or in the natural distribution area of bone, widely cultivated. Most parts of China are distributed, located in North, South, East and Liaoning, Shaanxi, Gansu, Sichuan, Guizhou and Yunnan. Most of the country has produced. The main production Shandong, Anhui, Henan and other places.

Description:
Trichosanthes kirilowii is a flowering plant.A Climber,length up to 10m. Tubers cylindrical , fleshy , rich in starch. Stems thick, much branched , with longitudinal ribs and grooves are white stretch pubescent. Leaves alternate ; petiole length 3-10cm, with vertical stripes, is of pubescent ; tendrils 3-7 differences pubescent ; leaves low-quality , contour nearly round or nearly heart-shaped , length and width are about 5-20cm, often 3-5 ( -7 ) lobed to the crack, split or dilute parted and only ranging from large coarse teeth , diamond-shaped lobes obovate , oblong , apex obtuse, acute, often re- lobed edges , base heart-shaped , curved lack of deep 3-4cm, surface dark green , rough, back of the green, on both sides along the veins villous hairy hirsute , basal palmate veins 5 , veinlets reticulate. Dioecious ; male racemes solitary or with a single flower and students, or those in the upper branches solitary, too inflorescence total length 10-20cm, stout, with longitudinal ridges and grooves , puberulent , the top 5 -8 flower, single flower stalk about 15cm, pedicel about 3mm, small bracts obovate or broadly ovate, 1.5-2.5 (-3) cm, width 1-2cm, the upper coarsely toothed , base with handle , pubescent ; calyx tube cylindrical , long 2-4cm, apex expanded diameter of about 10mm, the lower diameter of about 5mm, pubescent , lobes lanceolate, length 10-15cm, width 3-5mm, entire; Corolla white , lobes obovate , about 20mm, width 18mm, with a central green tip apex sides fringed with filaments , pubescent ; anther connivent , about 2mm, diameter of about 4mm, filaments separated , stout, villous ; female flowers solitary, stalk length 7.5cm, pubescent ; calyx tube oblong, 2.5cm, diameter 1.2cm, with male and corolla lobes ; ovary oval, green , long- 2cm, style long 2cm, stigma 3. Fruit oval, flattened , long 11-16mm, width 7-12mm, light brown, almost at the edge of a ridge . Flowering from May to August , the fruit of August to October……CLICK & SEE THE PICTURES

Cultivation:
Requires a rich well-drained soil and plenty of moisture in the growing season. Sometimes cultivated in China for its edible fruit and medicinal uses. Male plants are favoured for root production. This species is not winter hardy in Britain and usually requires greenhouse cultivation. However, it may be possible to grow it as an annual in a very warm sheltered bed outdoors. A climbing plant, supporting itself by means of tendrils. Dioecious, male and female plants must be grown if seed is required.

Propagation:
Seed – sow March in pots in a warm greenhouse in a rich soil. Sow 2 – 3 seeds per pot and thin to the strongest plant. Grow them on fast and plant out after the last expected frosts. Give some protection, such as a frame or cloche, until the plants are growing away well.

Edible Uses:
Edible Parts: Fruit; Leaves; Oil; Oil; Root…….click & see

Fruit. The young fruits are pickled. The pulp of older fruits is eaten. Mature fruits are about 10cm long. Leaves and young shoots – cooked and used as a vegetable. An edible starch is obtained from the root. It requires leeching, which probably means that it has a bitter flavour. The root is harvested in the autumn, cut into thick slices, soaked for 4 – 5 days in water, changing the water daily until the root disintegrates and can be mashed into a fine pulp. It is then steamed into cakes or used for making dumplings. An edible oil is obtained from the seed.

Chemical components: The plant is a source of the toxic anti-HIV type I ribosome-inactiving lectin trichosanthin

Medicinal Uses:
Trichosanthes kirilowii is commonly used in Chinese herbalism, where it is considered to be one of the 50 fundamental herbs. Recent research has isolated a protein called “trichosanthin” in the roots and this is undergoing trials as a possible remedy for AIDS. Skin, vulnerary. The leaf and the stem are febrifuge. The fruit is antibacterial, anticholesterolemic, antifungal, depurative, emollient, expectorant and laxative. It is used in the treatment of pulmonary infections with yellow and thick sputum, chest pains, stuffy feelings in the chest, constipation and dry stool. It has an antibacterial action against E. coli, Bacillus dysenteriae, B. typhi, B. paratyphi, Pseudomonas, Vibrio cholerae, V. Proteus etc. The fruit is traditionally prepared as a winter soup to ward off colds and influenza. The fruit is harvested in the autumn and dried for later use. The rind of the fruit is used to treat a number of ailments, including cancer, jaundice, retained placenta, bronchial infections with thick phlegm and sore throat. The seed is antitussive, emollient and expectorant. The root is antibiotic, anti-inflammatory, febrifuge, galactogogue, laxative, oxytocic, sialagogue and uterine tonic. The fresh root has been noted for centuries as an abortifacient – a sponge soaked in its juice was placed in the vagina and induced an abortion in the second trimester of pregnancy. The root is taken internally in the treatment of diabetes, dry coughs, and to assist in the second stage of labour. The root is harvested in the autumn and dried for later use. The root and/or the seed is powdered and used in the treatment of mammary cancer.

Other Uses:
Oil; ……..An oil from the seed is used for lighting.
Known Hazards: Root extracts are extremely toxic. Intravenous administration can cause pulmonary oedema, cerebral oedema, cerebral haemorrhage and myocardial damage. Seizures and fever in HIV patients with parenteral administration. Self-medication of root not advised
Resources:

http://en.wikipedia.org/wiki/Trichosanthes_kirilowii

http://www.mdidea.com/products/new/new05602.html

http://www.naturalmedicinalherbs.net/herbs/t/trichosanthes-kirilowii=chinese-cucumber.php

http://www.pfaf.org/user/Plant.aspx?LatinName=Trichosanthes+kirilowii

Cholangitis

Definition:
Cholangitis is an infection of the common bile duct, the tube that carries bile from the liver to the gallbladder and intestines. Bile is a liquid made by the liver that helps digest food.

Cholangitis can be life-threatening, and is regarded as a medical emergency. Characteristic symptoms include yellow discoloration of the skin or whites of the eyes, fever, abdominal pain, and in severe cases, low blood pressure and confusion. Initial treatment is with intravenous fluids and antibiotics, but there is often an underlying problem (such as gallstones or narrowing in the bile duct) for which further tests and treatments may be necessary, usually in the form of endoscopy to relieve obstruction of the bile duct.
Symptoms:
The following symptoms may occur:

*Pain on the upper right side or upper middle part of the abdomen. It may also be felt in the back or below the right shoulder blade. The pain may come and go and feel sharp, cramp-like, or dull.

*Fever and chills

*Dark urine and clay-colored stools

*Nausea and vomiting

*Yellowing of the skin (jaundice), which may come and go
Physical examination findings typically include jaundice and right upper quadrant tenderness.Charcot’s triad is a set of three common findings in cholangitis: abdominal pain, jaundice, and fever. This was assumed in the past to be present in 50–70% of cases, although more recently the frequency has been reported as 15–20%.Reynolds’ pentad includes the findings of Charcot’s triad with the presence of septic shock and mental confusion. This combination of symptoms indicates worsening of the condition and the development of sepsis, and is seen less commonly still.

In the elderly, the presentation may be atypical; they may directly collapse due to septicemia without first showing typical features. Those with an indwelling stent in the bile duct (see below) may not develop jaundice.

Causes:
Cholangitis is most often caused by a bacterial infection. This can occur when the duct is blocked by something, such as a gallstone or tumor. The infection causing this condition may also spread to the liver.

Bile duct obstruction, which is usually present in acute cholangitis, is generally due to gallstones. 10–30% of cases, however, are due to other causes such as benign stricturing (narrowing of the bile duct without an underlying tumor), postoperative damage or an altered structure of the bile ducts such as narrowing at the site of an anastomosis (surgical connection), various tumors (cancer of the bile duct, gallbladder cancer, cancer of the ampulla of Vater, pancreatic cancer, cancer of the duodenum), anaerobic organisms such as Clostridium and Bacteroides (especially in the elderly and those who have undergone previous surgery of the biliary system). Parasites which may infect the liver and bile ducts may cause cholangitis; these include the roundworm Ascaris lumbricoides and the liver flukes Clonorchis sinensis, Opisthorchis viverrini and Opisthorchis felineus. In people with AIDS, a large number of opportunistic organisms has been known to cause AIDS cholangiopathy, but the risk has rapidly diminished since the introduction of effective AIDS treatment. Cholangitis may also complicate medical procedures involving the bile duct, especially ERCP. To prevent this, it is recommended that those undergoing ERCP for any indication receive prophylactic (preventative) antibiotics.

The presence of a permanent biliary stent (e.g. in pancreatic cancer) slightly increases the risk of cholangitis, but stents of this type are often needed to keep the bile duct patent under outside pressure

Diagnosis:
Routine blood tests show features of acute inflammation (raised white blood cell count and elevated C-reactive protein level), and usually abnormal liver function tests (LFTs). In most cases the LFTs will be consistent with obstruction: raised bilirubin, alkaline phosphatase and ?-glutamyl transpeptidase. In the early stages, however, pressure on the liver cells may be the main feature and the tests will resemble those in hepatitis, with elevations in alanine transaminase and aspartate transaminase.

Blood cultures are often performed in people with fever and evidence of acute infection. These yield the bacteria causing the infection in 36% of cases, usually after 24–48 hours of incubation. Bile, too, may be sent for culture during ERCP (see below). The most common bacteria linked to ascending cholangitis are gram-negative bacilli: Escherichia coli (25–50%), Klebsiella (15–20%) and Enterobacter (5–10%). Of the gram-positive cocci, Enterococcus causes 10–20%.

You may have the following tests to look for blockages:

*Abdominal ultrasound

*Endoscopic retrograde cholangiopancreatography (ERCP)

*Magnetic resonance cholangiopancreatography (MRCP)

*Percutaneous transhepatic cholangiogram (PTCA)

*You may also have the following blood tests:

#Bilirubin level
#Liver enzyme levels
#Liver function tests
#White blood count (WBC)
Treatment:
Quick diagnosis and treatment are very important.Antibiotics to cure infection is the first treatment done in most cases. ERCP or other surgical procedure is done when the patient is stable.Patients who are very ill or are quickly getting worse may need surgery right away.

Cholangitis requires admission to hospital. Intravenous fluids are administered, especially if the blood pressure is low, and antibiotics are commenced. Empirical treatment with broad-spectrum antibiotics is usually necessary until it is known for certain which pathogen is causing the infection, and to which antibiotics it is sensitive. Combinations of penicillins and aminoglycosides are widely used, although ciprofloxacin has been shown to be effective in most cases, and may be preferred to aminoglycosides because of fewer side effects. Metronidazole is often added to specifically treat the anaerobic pathogens, especially in those who are very ill or at risk of anaerobic infections. Antibiotics are continued for 7–10 days. Drugs that increase the blood pressure (vasopressors) may also be required to counter the low blood pressure.
Prognosis:
Acute cholangitis carries a significant risk of death, the leading cause being irreversible shock with multiple organ failure (a possible complication of severe infections). Improvements in diagnosis and treatment have led to a reduction in mortality: before 1980, the mortality rate was greater than 50%, but after 1980 it was 10–30%. Patients with signs of multiple organ failure are likely to die unless they undergo early biliary drainage and treatment with systemic antibiotics. Other causes of death following severe cholangitis include heart failure and pneumonia.

Risk Factors:
Risk factors include a previous history of gallstones, sclerosing cholangitis, HIV, narrowing of the common bile duct, and, rarely, travel to countries where you might catch a worm or parasite infection.

Risk factors indicating an increased risk of death include older age, female gender, a history of liver cirrhosis, biliary narrowing due to cancer, acute renal failure and the presence of liver abscesses. Complications following severe cholangitis include renal failure, respiratory failure (inability of the respiratory system to oxygenate blood and/or eliminate carbon dioxide), cardiac arrhythmia, wound infection, pneumonia, gastrointestinal bleeding and myocardial ischemia (lack of blood flow to the heart, leading to heart attacks).

Prevention:
Treatment of gallstones, tumors, and infestations of parasites may reduce the risk for some people. A metal or plastic stent that is placed in the bile system may be needed to prevent the infection from returning.
Resources:

http://www.nlm.nih.gov/medlineplus/ency/article/000290.htm

http://en.wikipedia.org/wiki/Ascending_cholangitis

Gastroparesis

Definition:
Gastroparesis (gastro-, “stomach” + -paresis, “partial paralysis”), also called delayed gastric emptying, is a medical condition consisting of a paresis (partial paralysis) of the stomach, resulting in food remaining in the stomach for an abnormally long time. Normally, the stomach contracts to move food down into the small intestine for additional digestion. The vagus nerve controls these contractions. Gastroparesis may occur when the vagus nerve is damaged and the muscles of the stomach and intestines do not properly function. Food then moves slowly or stops moving through the digestive tract….CLICK & SEE

YOU MAY CLICK & SEEOur Digestive System and How It Works 
Symptoms:
The most common symptoms of gastroparesis are the following:
*Chronic nausea (93%)
*Vomiting (especially of undigested food) (68-84%)
*Abdominal pain (46-90%)
*A feeling of fullness after eating just a few bites (60-86%)

Other symptoms include the following:
*Palpitations
*Heartburn
*Abdominal bloating
*Erratic blood glucose levels
*Lack of appetite
*Gastroesophageal reflux
*Spasms of the stomach wall
*Weight loss and malnutrition

Morning nausea may also indicate gastroparesis. Vomiting may not occur in all cases, as sufferers may adjust their diets to include only small amounts of food.

Symptoms may be aggravated by eating greasy or rich foods, large quantities of foods with fiber—such as raw fruits and vegetables—or drinking beverages high in fat or carbonation. Symptoms may be mild or severe, and they can occur frequently in some people and less often in others. The symptoms of gastroparesis may also vary in intensity over time in the same individual. Sometimes gastroparesis is difficult to diagnose because people experience a range of symptoms similar to those of other diseases.

Causes:
Transient gastroparesis may arise in acute illness of any kind, as a consequence of certain cancer treatments or other drugs which affect digestive action, or due to abnormal eating patterns.

It is frequently caused by autonomic neuropathy. This may occur in people with type 1 or type 2 diabetes. In fact, diabetes mellitus has been named as the most common cause of gastroparesis, as high levels of blood glucose may affect chemical changes in the nerves.The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in gastroparesis. Other possible causes include anorexia nervosa and bulimia nervosa, which may also damage the vagus nerve. Gastroparesis has also been associated with connective tissue diseases such as scleroderma and Ehlers-Danlos syndrome, and neurological conditions such as Parkinson’s disease. It may also occur as part of a mitochondrial disease.

Chronic gastroparesis can be caused by other types of damage to the vagus nerve, such as abdominal surgery.  Heavy cigarette smoking is also a plausible cause since smoking causes damage to the stomach lining.

Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection. “Stomach flu”, mononucleosis, and other ailments have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.

Gastroparesis sufferers are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men.A hormonal link has been suggested, as gastroparesis symptoms tend to worsen the week before menstruation when progesterone levels are highest. Neither theory has been proven definitively.

Gastroparesis can also be connected to hypochlorhydria and be caused by chloride, sodium and/or zinc deficiency, as these minerals are needed for the stomach to produce adequate levels of gastric acid (HCL) in order to properly empty itself of a meal.

Other identifiable causes of gastroparesis include intestinal surgery and nervous system diseases such as Parkinson’s disease or multiple sclerosis. For reasons that are not very clear, gastroparesis is more commonly found in women than in men.

Complications:
The complications of gastroparesis can include

*severe dehydration due to persistent vomiting

*gastroesophageal reflux disease (GERD), which is GER that occurs more than twice a week for a few weeks; GERD can lead to esophagitis— irritation of the esophagus

*bezoars, which can cause nausea, vomiting, obstruction, or interfere with absorption of some medications in pill form

*difficulty managing blood glucose levels in people with diabetes

*malnutrition due to poor absorption of nutrients or a low calorie intake

*decreased quality of life, including work absences due to severe symptoms

Diagnosis:
Gastroparesis is diagnosed through a physical exam, medical history, blood tests, tests to rule out blockage or structural problems in the GI tract, and gastric emptying tests. Tests may also identify a nutritional disorder or underlying disease. To rule out any blockage or other structural problems, the doctor may perform one or more of the following tests:

*Upper gastrointestinal (GI) endoscopy. This procedure involves using an endoscope—a small, flexible tube with a light—to see the upper GI tract, which includes the esophagus, stomach, and duodenum—the first part of the small intestine. The test is performed at a hospital or outpatient center by a gastroenterologist—a doctor who specializes in digestive diseases. The endoscope is carefully fed down the esophagus and into the stomach and duodenum. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining. A person may receive a liquid anesthetic that is gargled or sprayed on the back of the throat. An intravenous (IV) needle is placed in a vein in the arm if general anesthesia is given. The test may show blockage or large bezoars—solid collections of food, mucus, vegetable fiber, hair, or other material that cannot be digested in the stomach—that are sometimes softened, dissolved, or broken up during an upper GI endoscopy.

*Upper GI series. An upper GI series may be done to look at the small intestine. The test is performed at a hospital or outpatient center by an x-ray technician, and the images are interpreted by a radiologist—a doctor who specializes in medical imaging. Anesthesia is not needed. No eating or drinking is allowed for 8 hours before the procedure, if possible. If the person has diabetes, a health care provider may give different instructions about fasting before the test. During the procedure, the person will stand or sit in front of an x-ray machine and drink barium, a chalky liquid. Barium coats the small intestine, making signs of gastroparesis show up more clearly on x rays. Gastroparesis is likely if the x ray shows food in the stomach after fasting. A person may experience bloating and nausea for a short time after the test. For several days afterward, barium liquid in the GI tract causes stools to be white or light colored. A health care provider will give the person specific instructions about eating and drinking after the test.

*Ultrasound. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. The procedure is performed in a health care provider’s office, outpatient center, or hospital by a specially trained technician, and the images are interpreted by a radiologist; anesthesia is not needed. The images can show whether gallbladder disease and pancreatitis could be the cause of a person’s digestive symptoms, rather than gastroparesis.

*Gastric emptying scintigraphy. The test involves eating a bland meal—such as eggs or an egg substitute—that contains a small amount of radioactive material. The test is performed in a radiology center or hospital by a specially trained technician and interpreted by a radiologist; anesthesia is not needed. An external camera scans the abdomen to show where the radioactive material is located. The radiologist is then able to measure the rate of gastric emptying at 1, 2, 3, and 4 hours after the meal. If more than 10 percent of the meal is still in the stomach at 4 hours, the diagnosis of gastroparesis is confirmed.

*SmartPill. The SmartPill is a small electronic device in capsule form. The SmartPill test is available at specialized outpatient centers. The images are interpreted by a radiologist. The device is swallowed and moves through the entire digestive tract, sending information to a cell-phone-sized receiver worn around the person’s waist or neck. The recorded information provides a detailed record of how quickly food travels through each part of the digestive tract.

* Breath test. With this test, the person eats a meal containing a small amount of radioactive material; then breath samples are taken over a period of several hours to measure the amount of radioactive material in the exhaled breath. The results allow the health care provider to calculate how fast the stomach is emptying.
Treatment:
Treatment of gastroparesis depends on the severity of the person’s symptoms. In most cases, treatment does not cure gastroparesis, which is usually a chronic, or long-lasting, condition. Gastroparesis is also a relapsing condition—the symptoms can come and go for periods of time. Treatment helps people manage the condition so they can be as comfortable and active as possible.

Treatment includes dietary changes (low-fiber and low residue diets and, in some cases, restrictions on fat and/or solids); oral prokinetic medications such as metoclopramide (Reglan, Maxolon, Clopra), cisapride (Propulsid) (no longer available in the US or Australia), erythromycin (E-Mycin, Erythrocin, Ery-Tab, EES) and domperidone (Motilium) (not approved in the US; can be prescribed/obtained in Canada); adjustments in insulin dosage for those with diabetes; a jejunostomy tube; parenteral nutrition; implanted gastric neurostimulators (“stomach pacemakers”); or botulinum toxin (botox injected into the pylorus).

Sildenafil citrate, which increases blood flow to the genital area in men, is being used by some practitioners to stimulate the gastrointestinal tract in cases of diabetic gastroparesis.

The antidepressant mirtazapine has proven effective in the treatment of gastroparesis unresponsive to conventional treatment. This is due to its anti-emetic and appetite stimulant properties. Mirtazapine acts on the same serotonin receptor (5-HT3) as does the popular anti-emetic ondansetron.

When a person has severe symptoms, a liquid or puréed diet may be prescribed. As liquids tend to empty more quickly from the stomach, some people may find a puréed diet helps improve symptoms. Puréed fresh or cooked fruits and vegetables can be incorporated into shakes and soups. A health care provider may recommend a dietitian to help a person plan meals that minimize symptoms and ensure all nutritional needs are met.

When the most extreme cases of gastroparesis lead to severe nausea, vomiting, and dehydration, urgent care may be required at a medical facility where IV fluids can be given.

CLICK & SEE.……..Home remidies..1……Home remidies..2

In most of the cases if the patient starts Yoga exercise & meditation and does it regularly under the guidance of an expart with dietary changes he or she will get total recovery.

Hope through Research:
The National Institute of Diabetes and Digestive and Kidney Diseases’ (NIDDK’s) Division of Digestive Diseases and Nutrition supports basic and clinical research into GI motility disorders, including gastroparesis.

Researchers are studying whether new medications or surgery can improve gastric emptying and reduce gastroparesis symptoms. Researchers are evaluating the safety and effectiveness of nortriptyline for treatment of gastroparesis.

Participants in clinical trials can play a more active role in their own health care, gain access to new research treatments before they are widely available, and help others by contributing to medical research.
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/Gastroparesis

http://www.niddk.nih.gov/health-information/health-topics/digestive-diseases/gastroparesis/Pages/facts.aspx

Dumping Syndrome

Other Names: Gastric dumping syndrome, or rapid gastric emptying

Definition:
Gastric dumping syndrome, or rapid gastric emptying is a condition where ingested foods bypass the stomach too rapidly and enter the small intestine largely undigested. It happens when the small intestine expands too quickly due to the presence of hyperosmolar (having increased osmolarity) contents from the stomach. This causes symptoms due to the fluid shift into the gut lumen with plasma volume contraction and acute intestinal distention. “Early” dumping begins concurrently within 15 to 30 minutes from ingestion of a meal. Symptoms of early dumping include nausea, vomiting, bloating, cramping, diarrhea, dizziness, and fatigue. “Late” dumping happens one to three hours after eating. Symptoms of late dumping include weakness, sweating, and dizziness. Many people have both types. The syndrome is most often associated with gastric bypass (Roux-en-Y) surgery.

CLICK & SEE

Rapid loading of the small intestine with hypertonic stomach contents can lead to rapid entry of water into the intestinal lumen. Osmotic diarrhea, distension of the small bowel (leading to crampy abdominal pain), and hypovolemia can result.

In addition, people with this syndrome often suffer from low blood sugar, or hypoglycemia, because the rapid “dumping” of food triggers the pancreas to release excessive amounts of insulin into the bloodstream. This type of hypoglycemia is referred to as “alimentary hypoglycemia.”
Dumping Syndrome occurs when food, especially sugar, moves too fast from the stomach to the duodenum—the first part of the small intestine—in the upper gastrointestinal (GI) tract. This condition is also called rapid gastric emptying. Dumping syndrome has two forms, based on when symptoms occur:

*early dumping syndrome—occurs 10 to 30 minutes after a meal

*late dumping syndrome—occurs 2 to 3 hours after a meal

Symptoms:
Symptoms of dumping syndrome are most common during a meal or within 15 to 30 minutes following a meal. They include:

Gastrointestinal:-

*Nausea
*Vomiting
*Abdominal cramps
*Diarrhea
*Feeling of fullness

Cardiovascular:

*Flushing
*Dizziness, lightheadedness
*Heart palpitations, rapid heart rate
Signs and symptoms also can develop later, usually one to three hours after eating. This is due to the dumping of large amount of sugars into the small intestine (hyperglycemia). In response, the body releases large amounts of insulin to absorb the sugars, leading to low levels of sugar in the body (hypoglycemia).

Symptoms of late dumping can include:-

*Sweating
*Hunger
*Fatigue
*Dizziness, lightheadedness
*Confusion
*Heart palpitations, rapid heart rate
*Fainting

A study of more than 1,100 people who had their stomachs surgically removed found that about two-thirds experienced early symptoms and about a third experienced late symptoms of dumping syndrome. Some people experience both early and late signs and symptoms.

No matter when problems develop, however, they may be worse following a high-sugar meal, especially one that’s rich in table sugar (sucrose) or fruit sugar (fructose).
Causes:
Dumping syndrome is caused by problems with the storage of food particles in the stomach and emptying of particles into the duodenum. Early dumping syndrome results from rapid movement of fluid into the intestine following a sudden addition of a large amount of food from the stomach. Late dumping syndrome results from rapid movement of sugar into the intestine, which raises the body’s blood glucose level and causes the pancreas to increase its release of the hormone insulin. The increased release of insulin causes a rapid drop in blood glucose levels, a condition known as hypoglycemia, or low blood sugar.

In dumping syndrome, food and gastric juices from your stomach move to your small intestine in an uncontrolled, abnormally fast manner. This is most often related to changes in your stomach associated with surgery, such as when the opening (pylorus) between your stomach and the small intestine (duodenum) has been removed during an operation.

The pylorus acts as a brake so that stomach emptying is gradual. When it’s removed, stomach material dumps rapidly into the small intestine. The ill effects of this are thought to be caused by the release of gastrointestinal hormones in the small intestine, as well as insulin secreted to process the sugar (glucose).

Dumping syndrome can occur after any operation on the stomach as well as after removal of the esophagus (esophagectomy). Gastric bypass surgery for weight loss is the most common cause today. It develops most commonly within weeks after surgery, or as soon as you return to your normal diet. The more stomach removed or bypassed, the more likely that the condition will be severe. It sometimes becomes a chronic disorder.
Diagnosis:
The doctor will diagnose dumping syndrome primarily on the basis of symptoms. A scoring system helps differentiate dumping syndrome from other GI problems. The scoring system assigns points to each symptom and the total points result in a score. A person with a score above 7 likely has dumping syndrome.

The following tests may confirm dumping syndrome and exclude other conditions with similar symptoms:-

*A modified oral glucose tolerance test checks how well insulin works with tissues to absorb glucose. A health care provider performs the test during an office visit or in a commercial facility and sends the blood samples to a lab for analysis. The person should fast—eat or drink nothing except water—for at least 8 hours before the test. The health care provider will measure blood glucose concentration, hematocrit—the amount of red blood cells in the blood—pulse rate, and blood pressure before the test begins. After the initial measurements, the person drinks a glucose solution. The health care provider repeats the initial measurements immediately and at 30-minute intervals for up to 180 minutes. A health care provider often confirms dumping syndrome in people with

#low blood sugar between 120 and 180 minutes after drinking the solution

#an increase in hematocrit of more than 3 percent at 30 minutes

#a rise in pulse rate of more than 10 beats per minute after 30 minutes
*A gastric emptying scintigraphy test involves eating a bland meal—such as eggs or an egg substitute—that contains a small amount of radioactive material. A specially trained technician performs this test in a radiology center or hospital, and a radiologist—a doctor who specializes in medical imaging—interprets the results. Anesthesia is not needed. An external camera scans the abdomen to locate the radioactive material. The radiologist measures the rate of gastric emptying at 1, 2, 3, and 4 hours after the meal. The test can help confirm a diagnosis of dumping syndrome.

The doctor may also examine the structure of the esophagus, stomach, and upper small intestine with the following tests:

#An upper GI endoscopy involves using an endoscope—a small, flexible tube with a light—to see the upper GI tract. A gastroenterologist—a doctor who specializes in digestive diseases—performs the test at a hospital or an outpatient center. The gastroenterologist carefully feeds the endoscope down the esophagus and into the stomach and duodenum. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining. A person may receive general anesthesia or a liquid anesthetic that is gargled or sprayed on the back of the throat. If the person receives general anesthesia, a health care provider will place an intravenous (IV) needle in a vein in the arm. The test may show ulcers, swelling of the stomach lining, or cancer.

#An upper GI series examines the small intestine. An x-ray technician performs the test at a hospital or an outpatient center and a radiologist interprets the images. Anesthesia is not needed. No eating or drinking is allowed before the procedure, as directed by the health care staff. During the procedure, the person will stand or sit in front of an x-ray machine and drink barium, a chalky liquid. Barium coats the small intestine, making signs of a blockage or other complications of gastric surgery show up more clearly on x rays.

A person may experience bloating and nausea for a short time after the test. For several days afterward, barium liquid in the GI tract causes white or light-colored stools. A health care provider will give the person specific instructions about eating and drinking after the test.
Treatment:
Dumping syndrome is largely avoidable by avoiding certain foods that are likely to cause it; therefore, having a bigger digestive tract balanced diet is important. Treatment includes changes in eating habits and medication. People who have gastric dumping syndrome need to eat several small meals a day that are low in carbohydrates, avoiding simple sugars, and should drink liquids between meals, not with them. Fiber delays gastric emptying and reduces insulin peaks. People with severe cases take medicine (such as octreotide and cholestyramine) or proton pump inhibitors (such as pantoprazole and omeprazole) to slow their digestion. Doctors may also recommend surgery. Surgical intervention may include conversion of a Billroth I to a Roux-en Y gastrojejunostomy.

Medication:
A doctor may prescribe octreotide acetate (Sandostatin) to treat dumping syndrome symptoms. The medication works by slowing gastric emptying and inhibiting the release of insulin and other GI hormones. Octreotide comes in short- and long-acting formulas. The short-acting formula is injected subcutaneously—under the skin—or intravenously—into a vein—two to four times a day. A health care provider may perform the injections or may train the patient or patient’s friend or relative to perform the injections. He or she may injects the long-acting formula into the buttocks muscles once every 4 weeks. Complications of octreotide treatment include increased or decreased blood glucose levels, pain at the injection site, gallstones, and fatty, foul-smelling stools.

Hope through Research:
The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) conducts and supports basic and clinical research into many digestive disorders, including dumping syndrome.

Clinical trials are research studies involving people. Clinical trials look at safe and effective new ways to prevent, detect, or treat disease. Researchers also use clinical trials to look at other aspects of care, such as improving the quality of life for people with chronic illnesses. To learn more about clinical trials, why they matter, and how to participate, visit the NIH Clinical Research Trials and You website at www.nih.gov/health/clinicaltrialsExternal NIH Link. For information about current studies, visit www.ClinicalTrials.govExternal Link

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/Gastric_dumping_syndrome

http://www.niddk.nih.gov/health-information/health-topics/digestive-diseases/dumping-syndrome/Pages/facts.aspx

http://www.mayoclinic.org/diseases-conditions/dumping-syndrome/basics/symptoms/con-20028034

Bowel control

Other Names: Bowel incontinence,Fecal incontinence

Description:
Bowel incontinence is the loss of bowel control, leading to an involuntary passage of stool. This can range from occasionally leaking a small amount of stool and passing gas, to completely losing control of bowel movements..CLICK & SEE

You have a bowel control problem if you accidentally pass solid or liquid stool or mucus from your rectum.* Bowel control problems include being unable to hold a bowel movement until you reach a toilet and passing stool into your underwear without being aware of it happening. Stool, also called feces, is solid waste that is passed as a bowel movement and includes undigested food, bacteria, mucus, and dead cells. Mucus is a clear liquid that coats and protects tissues in your digestive system.

Among people over age 65, most surveys find that women experience bowel incontinence more often than men. One to three out of every 1,000 women report a loss of bowel control at least once per month.

To hold stool and maintain continence, the rectum, anus, pelvic muscles, and nervous system must function normally. You must also have the physical and mental ability to recognize and respond to the urge to have a bowel movement.

Ringlike muscles called sphincters close tightly around your anus to hold stool in your rectum until you’re ready to release the stool. Pelvic floor muscles support your rectum and a woman’s vagina and also help with bowel control.

Causes:
Bowel control problems are often caused by a medical issue and can be treated.

*Chronic constipation, causing the muscles of the anus and intestines to stretch and weaken, and leading to diarrhea and stool leakage (see: encopresis)

*Chronic laxative use

*Colectomy or bowel surgery

*Decreased awareness of sensation of rectal fullness

*Emotional problems

*Gynecological, prostate, or rectal surgery

*Injury to the anal muscles due to childbirth (in women)

*Nerve or muscle damage (from trauma, tumor, or radiation)

*Severe diarrhea that overwhelms the ability to control passage of stool

*Severe hemorrhoids or rectal prolapse

*Stress of unfamiliar environment

*A disease or injury that damages your nervous system

*Poor overall health from multiple chronic, or long lasting, illnesses

*A difficult childbirth with injuries to your pelvic floor—the muscles, ligaments, and tissues that support your uterus, vagina, bladder, and rectum

Diagnosis:
To diagnose what is causing your bowel control problem, your doctor will take your medical history, including asking the questions listed in “What do I tell my doctor about my bowel control problem?” Your doctor may refer you to a specialist who will perform a physical exam and may suggest one or more of the following tests:

* anal manometry
* anal ultrasound
* magnetic resonance imaging (MRI)
* defecography
* flexible sigmoidoscopy or colonoscopy
* anal electromyography (EMG)

Anal manometry. Anal manometry uses pressure sensors and a balloon that can be inflated in your rectum to check how sensitive your rectum is and how well it works. Anal manometry also checks the tightness of the muscles around your anus. To prepare for this test, you should use an enema and not eat anything 2 hours before the test. An enema involves flushing water or a laxative into your anus using a special squirt bottle. A laxative is medicine that loosens stool and increases bowel movements. For this test, a thin tube with a balloon on its tip and pressure sensors below the balloon is put into your anus. Once the balloon reaches the rectum and the pressure sensors are in the anus, the tube is slowly pulled out to measure muscle tone and contractions. No sedative is needed for this test, which takes about 30 minutes.

Anal ultrasound. Ultrasound uses a tool, called a transducer, that bounces safe, painless sound waves off your organs to create an image of their structure. An anal ultrasound is specific to the anus and rectum. The procedure is performed in a doctor’s office, outpatient center, or hospital by a specially trained technician, and the images are interpreted by a radiologist—a doctor who specializes in medical imaging. A sedative is not needed. The images can show the structure of your anal sphincter muscles.

MRI. MRI machines use radio waves and magnets to produce detailed pictures of your internal organs and soft tissues without using x rays. The procedure is performed in an outpatient center or hospital by a specially trained technician, and the images are interpreted by a radiologist. A sedative is not needed, though you may be given medicine to help you relax if you have a fear of confined spaces. An MRI may include the injection of special dye, called contrast medium. With most MRI machines, you lie on a table that slides into a tunnel-shaped device that may be open ended or closed at one end; some newer machines are designed to allow you to lie in a more open space. MRIs can show problems with your anal sphincter muscles. MRIs can provide more information than anal ultrasound, especially about the external anal sphincter.

Defecography. This x ray of the area around your anus and rectum shows whether you have problems with

* pushing stool out of your body
* the functioning of your anus and rectum
* squeezing and relaxing your rectal muscles

The test can also show changes in the structure of your anus or rectum. To prepare for the test, you perform two enemas. You can’t eat anything for 2 hours before the test. During the test, the doctor fills your rectum with a soft paste that shows up on x rays and feels like stool. You sit on a toilet inside an x-ray machine. The doctor will ask you to first pull in and squeeze your sphincter muscles to prevent leakage and then to strain as if you’re having a bowel movement. The radiologist studies the x rays to look for problems with your rectum, anus, and pelvic floor muscles.

Flexible sigmoidoscopy or colonoscopy. These tests are similar, but a colonoscopy is used to view your rectum and entire colon, while a flexible sigmoidoscopy is used to view just your rectum and lower colon. These tests are performed at a hospital or outpatient center by a gastroenterologist—a doctor who specializes in digestive diseases. For both tests, a doctor will give you written bowel prep instructions to follow at home. You may be asked to follow a clear liquid diet for 1 to 3 days before either test. The night before the test, you may need to take a laxative. One or more enemas may be needed the night before and about 2 hours before the test.

In most cases, you will be given a light sedative, and possibly pain medicine, to help you relax during a flexible sigmoidoscopy. A sedative is used for colonoscopy. For either test, you will lie on a table while the doctor inserts a flexible tube into your anus. A small camera on the tube sends a video image of your bowel lining to a computer screen. The test can show problems in your lower GI tract that may be causing your bowel control problem. The doctor may also perform a biopsy, a procedure that involves taking a piece of tissue from the bowel lining for examination with a microscope. You won’t feel the biopsy. A pathologist—a doctor who specializes in diagnosing diseases—examines the tissue in a lab to confirm the diagnosis.

You may have cramping or bloating during the first hour after these tests. You’re not allowed to drive for 24 hours after a colonoscopy or flexible sigmoidoscopy to allow the sedative time to wear off. Before the test, you should make plans for a ride home. You should recover fully by the next day and be able to go back to your normal diet.

Anal EMG. Anal EMG checks the health of your pelvic floor muscles and the nerves that control your muscles. The doctor inserts a very thin needle wire through your skin into your muscle. The wire on the needle picks up the electrical activity given off by the muscles. The electrical activity is shown as images on a screen or sounds through a speaker. Another type of anal EMG uses stainless steel plates attached to the sides of a plastic plug instead of a needle. The plug is put in your anus to measure the electrical activity of your external anal sphincter and other pelvic floor muscles. The test can show if there is damage to the nerves that control the external sphincter or pelvic floor muscles by measuring the average electrical activity when you

* relax quietly
* squeeze to prevent a bowel movement
* strain to have a bowel movement

Treatment:
Home Care:
Incontinence is not a hopeless situation. Proper treatment can help most people, and can often eliminate the problem.

Treating bowel incontinence should begin by identifying the cause of the incontinence. There are several ways to strengthen the anal and pelvic muscles and promote normal bowel function.

Rutine pelvic floor exercise  may improve the condition.

FECAL IMPACTION:
Fecal impaction is usually caused by chronic constipation. It leads to a mass of stool that partially blocks the large intestine. If constipation or fecal impaction contributes to fecal incontinence, usually laxatives and enemas are of little help. A health care provider may need to insert one or two fingers into the rectum and break the mass into smaller pieces that can pass more easily.

Take measures to prevent further fecal impaction. Add fiber to your diet to help form normal stool. Use other medications your health care provider recommends. In addition, drink enough fluids and get enough exercise to enhance normal stool consistency.

DIET:
Bowel incontinence often occurs because the rectal sphincter is less able to handle large amounts of liquid stool. Often, simply changing the diet may reduce the occurrence of bowel incontinence.

Certain people develop diarrhea after eating dairy foods because they are unable to digest lactose, a sugar found in most dairy products. Some food additives such as nutmeg and sorbitol may cause diarrhea in certain people.

Adding bulk to the diet may thicken loose stool and decrease its amount. Increasing fiber (30 grams daily) from whole-wheat grains and bran adds bulk to the diet. Psyllium-containing products such as Metamucil can also add bulk to the stools.

Formula tube feedings often cause diarrhea and bowel incontinence. For diarrhea or bowel incontinence caused by tube feedings, talk to your health care provider or dietitian. The rate of the feedings may need to be changed, or bulk agents may need to be added to the formula.

Eating, Diet, and Nutrition:
Changes in your diet that may improve your bowel control problem include

*Eating the right amount of fiber. Fiber can help with diarrhea and constipation. Fiber is found in fruits, vegetables, whole grains, and beans. Fiber supplements sold in a pharmacy or health food store are another common source of fiber to treat bowel control problems. The Academy of Nutrition and Dietetics recommends getting 20 to 35 grams of fiber a day for adults and “age plus five” grams for children. A 7-year-old child, for example, should get “7 plus five,” or 12, grams of fiber a day. Fiber should be added to your diet slowly to avoid bloating.

*Getting plenty to drink. Drinking eight 8-ounce glasses of liquid a day may help prevent constipation. Water is a good choice. You should avoid drinks with caffeine, alcohol, milk, or carbonation if they give you diarrhea.

MEDICATIONS:
In people with bowel incontinence due to diarrhea, medications such as loperamide (Imodium) may be used to control the diarrhea and improve bowel incontinence.

Other antidiarrheal medications include anti-cholinergic medications (belladonna or atropine), which reduce intestinal secretions and movement of the bowel. Opium derivatives (paregoric or codeine) or diphenoxylate (lomotil), as well as loperamide (Imodium) increase intestinal tone and decrease movement of the bowel.

Other medications used to control bowel incontinence include drugs that reduce water content in the stools (activated charcoal or Kaopectate) or that absorb fluid and add bulk to the stools (Metamucil).

MEDICATION EVALUATION: With your health care provider, review all the medications you take. Certain medications can cause or increase bowel incontinence, especially in older people. These medications include:

*Antacids
*Laxatives

OTHER THERAPIES:
If you often have bowel incontinence, you can use special fecal collection devices to contain the stool and protect your skin from breakdown. These devices consist of a drainable pouch attached to an adhesive wafer. The wafer has a hole cut through the center, which fits over the opening to the anus.

Most people who have bowel incontinence due to a lack of sphincter control, or decreased awareness of the urge to defecate, may benefit from a bowel retraining program and exercise therapies to help restore normal muscle tone.

Special care must be taken to maintain bowel control in people who have a decreased ability to recognize the urge to defecate, or who have impaired mobility that prevents them from independently and safely using the toilet. Such people should be assisted to use the toilet after meals, and promptly helped to the toilet if they have the urge to defecate.

If toileting needs are often unanswered, a pattern of negative reinforcement may develop. In this case people no longer take the correct actions when they feel the urge to have a bowel movement

You may click & See : Toileting safety

SURGERY
People who have bowel incontinence that continues even with medical treatment may benefit from surgery to correct the problem. Several different options exist. The choice of surgery is based on the cause of the bowel incontinence and the person’s general health.

RECTAL SPHINCTER REPAIR
Sphincter repair is performed on people whose anal muscle ring (sphincter) isn’t working well due to injury or aging. The procedure consists of re-attaching the anal muscles to tighten the sphincter and helping the anus close more completely.

GRACILIS MUSCLE TRANSPLANT
In people who have a loss of nerve function in the anal sphincter, gracilis muscle transplants may be performed to restore bowel control. The gracilis muscle is taken from the inner thigh. It is put around the sphincter to provide sphincter muscle tone.

ARTIFICIAL BOWEL SPHINCTER
Some patients may be treated with an artificial bowel sphincter. The artificial sphincter consists of three parts: a cuff that fits around the anus, a pressure-regulating balloon, and a pump that inflates the cuff.

The artificial sphincter is surgically implanted around the rectal sphincter. The cuff remains inflated to maintain continence. You have a bowel movement by deflating the cuff. The cuff will automatically re-inflate in 10 minutes.

FECAL DIVERSION
Sometimes a fecal diversion is performed for people who are not helped by other therapies. The large intestine is attached to an opening in the abdominal wall called a colostomy. Stool passes through this opening to a special bag. You will need to use a colostomy bag to collect the stool most of the time.

Regular Yoga exercise & Meditation under the supervision of an expart  will defenitely help a lot to get rid of the problem.

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.niddk.nih.gov/health-information/health-topics/digestive-diseases/bowel-control/Pages/ez.aspx

http://www.nlm.nih.gov/medlineplus/ency/article/003135.htm

leukonychia

Description::
Leukonychia (or leuconychia), also known as white nails or milk spots, is a medical term for white discoloration appearing on nails. It is derived from the Greek words leuko (“white”) and onux (“nail”). The most common cause is injury to the base of the nail (the matrix) where the nail is formed…..CLICK & SEE

It is harmless and most commonly caused by minor injuries that occur while the nail is growing. Contrary to popular belief, leukonychia is not a sign of excess or deficiency of calcium and zinc or other vitamins in the diet but rather less commonly a medical sign of hypoalbuminemia or chronic liver disease. It is more commonly found on fingernails than toenails. There is no effective treatment for leukonychia. However, the white marks and spots gradually disappear as the nail grows outward from the matrix with the nail plate.

Leukonychia is a nail condition. It manifests as the nail changing color either partially or fully. This disease can be caused by systemic problems or most commonly, it is a genetic disorder. The nail appears to have the standard shape and appearance, except for the fact that the nail turns white. This is caused by the presence of “parakeatotic cells”. These cells have an undeveloped and bulky nucleus, which contain ‘keratohyalins’. This cell variation causes the nail to reflect light and makes the nail appear opaque white.

Types:
Leukonychia totalis :
This condition is a whitening of the entire nail. This may be a clinical sign of hypoalbuminaemia (low albumin), which can be seen in nephrotic syndrome (a form of kidney failure), liver failure, protein malabsorption and protein-losing enteropathies. A genetic condition, and a side effect of sulphonamides, a family of antibiotics can also cause this appearances.

Leukonychia partialis:
This condition is whitening of parts of the nail plate in form of small white dots. There are several types of this condition. There are three variations of partial leukonychia; punctate, transverse and longitudinal leukonychia. Some more serious variations of leukonychia partialis may lead to Leukonychia totalis.

Leukonychia striata:
Leukonychia striata, transverse leukonychia, or Mees’ lines are a whitening or discoloration of the nail in bands or “stria” that run parallel the lunula (nail base). This is commonly caused by physical injury or disruption of the nail matrix. Common examples include excessive tapping of the nails, slamming a car door or extensive use of manicure. It may also occur in great toenails as a result of trauma from footwear. Alternatively, the condition can be caused by heavy metal poisoning most commonly by lead or arsenic. It can also be caused by cirrhosis or chemotherapy. The tendency toward leukonychia striata is sometimes inherited in an autosomal dominant fashion. In other cases, it can be attributed to vigorous manicuring and trauma aforementioned, or to a wide variety of systemic illnesses. Serious infections known for high fevers, measles, malaria, herpes, and leprosy may also cause this condition. In many patients, there is no obvious cause, and the streaks resolve spontaneously. There is a similar condition called Muehrcke’s lines (apparent leukonychia) which differs from leukonychia in that the lines fade with digital compression and does not migrate with the growth of the nail.

Leukonychia punctata:
Also known as “true” leukonychia, this is the most common form of leukonychia, in which small white spots appear on the nails. Picking and biting of the nails are a prominent cause in young children and nail biters. Besides parakeratosis, air that is trapped between the cells may also cause this appearance. It is also caused by trauma. In most cases, when white spots appear on a single or a couple of fingers or toes, the most common cause is injury to the base (matrix) of the nail. When this is the case, white spots disappear after around eight weeks, which is the amount of time necessary for nails to regrow completely. The pattern and number of spots may change as the nail grows.

Longitudinal leukonychia:
Longitudinal leukonychia is far less common and features smaller 1mm white longitudinal lines visible under the nail plate. It may be associated with Darier’s disease.

Symptoms :
Some of the obvious signs of leukonychia are white spots on the fingernail. It is observed in the form of small white lines on the nails and change in color of the nails which become totally white. The white spots may also occur on toenails. The nails become colorless and brittle losing the original texture. The nail may change its color to fully white (leukonychia totalis) or half white (leukonychia partialis).
Apart from the above signs, the person affected with leukonychia may also have problems like deafness, gingivitis, and hyperkeratosis and hammer toes if they are suffering from systemic disorders.

Causes:
It can be due to nail injury or infection. Sometimes it can be due to nail disorder or bacterial infection on the nail-bed. The white spots and change of nail to full-white color is due to the presence of para-karyotic cells that contains a compound called keratohyalins. On reflection to the light the normal color of the nail looks fully white.

Leukonychia can also occur due to heavy poisoning, heart problem, kidney disease, malnutrition, vitamin deficiency and stress.
Lack of essential nutrients like zinc and protein can also cause discoloration of nails. Ulcer in advance form can affect the fingernails. Further it can be caused due to pneumonia and hepatic cirrhosis and various other skin problems.People with diseases like typhoid, cholera, rheumatic fever, and colitis may also show this symptom of white spots on fingernails.

Individuals with family history of leukonychia have more chance of developing this problem than others. Patients who are undergoing chemotherapy or radiation treatment for cancer may also get this disease. Prolonged use of nail enamels and nail hardeners can be the reason for white spots on the fingernail. Bacterial or fungal infection on the nails can cause this problem.

True Leukonychia:
This type of Leukonychia is broken into two variations, total leukonychia and partial leukonychia. The difference seems to lie in the nail being either fully white, or only two thirds discolored as it takes a while for the maturation of the keratin to occur and change.

Total Leukonychia is an autosomal dominant condition. Other circumstances that may cause total leukonychia to occur are;
*Leprosy
*Typhoid
*Cytotoxic drugs
*Nail Biting
*Partial Leukonychia is viewed as a phase of total leukonychia. The most common causes of partial leukonychia are:

*Metastatic carcinoma
*Tuberculosis
*Leprosy

There are three different variants of partial leukonychia.

1.Transverse leukonychia – This causes the nail plate to be multi colored in its opacity. It is seen mostly in women’s fingernails. Possible causes are:
*Acute respiratory infections
*High fever
*Malaria
*Leprosy

2.Punctuate leukonychia This is the most common form and can happen to anyone. The telltale symptom is that the nail appears to have tiny opaque spots which fade with time.

3.Longitudinal leukonychia – A small white line under the nail plate
Pseudo Leukonychia

*This occurs when a discoloration in the nail appears due to a change in the nail bed. Pseudo leukonychia has three different forms:

*Terry’s nails – This affects the majority of the nail and makes it multi-colored. The majority of the nail is white, the rest, pink or brown.
Muhrecke’s nails – The nail appears to have several white transverse bands

*Half and half nails – This is seen as a larger part of the nail being dull white and the rest being brownish in color.

Diagnoses :
It is easy to identify this disease by physically examining the nails of the person affected. If needed, your doctor will ask you to do blood culture and other test for measuring the nutrients like zinc and vitamins. The doctor will take a thorough medical history, and may take blood tests as well as examining liver and kidney function.

Treatment :
You can get some relief from the symptoms by including lot of nutrition in your daily diet. Proteins, vitamins and zinc are essential elements that are to be added in daily food. You can eat nuts and green leafy veggies that carry lot of zinc.

The white spots on the fingernail will gradually diminish if you start taking zinc in daily food.In case if the problem is due to anemia then you will be given folic acid and iron supplement pills. If the symptoms are due to renal failure, then your doctor will initiate treatment for the condition. Suitable medicines will be given for treating the underlying disease like liver problem or ulcer or anemia.

Do not change your nail polish frequently and always use trusted brands. Limit the usage of nail enamels and polish to certain occasions. Avoid biting your nails since it may worsen the condition.

In case if the white spots or white coloration on the fingernails does not improve for more than 2 months, you can consult your doctor who would help you to find the actual cause.

Almost in many cases, the symptoms of leukonychia are due to deficiency of nutrients and zinc and only in rare cases, it will be due to underlying systemic disorders.

Increasing the quantity of grains, vegetables and nuts and even taking a zinc supplement (as zinc deficiency is a cause of leukonychia) is a good preventative and treatment, as is keeping affected nails out of harms way when using chemicals of any kind as they can further damage the nail.

Resources:

http://en.wikipedia.org/wiki/Leukonychia

http://www.nailsfungus.org/nail-fungus/leukonychia.html

http://diseasespictures.com/leukonychia/

Alagille Syndrome


Description:
Alagille syndrome is a genetic disorder that affects the liver, heart, kidney, and other systems of the body. Problems associated with the disorder generally become evident in infancy or early childhood. The disorder is inherited in an autosomal dominant pattern, and the estimated prevalence of Alagille syndrome is 1 in every 100,000 live births.It is named after Daniel Alagille.

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A person with Alagille syndrome has fewer than the normal number of small bile ducts inside the liver. The liver is the organ in the abdomen—the area between the chest and hips—that makes blood proteins and bile, stores energy and nutrients, fights infection, and removes harmful chemicals from the blood.

Bile ducts are tubes that carry bile from the liver cells to the gallbladder for storage and to the small intestine for use in digestion. Bile is fluid made by the liver that carries toxins and waste products out of the body and helps the body digest fats and the fat-soluble vitamins A, D, E, and K. In people with Alagille syndrome, the decreased number of bile ducts causes bile to build up in the liver, a condition also called cholestasis, leading to liver damage and liver disease.

The digestive system:
The digestive system is made up of the gastrointestinal (GI) tract—also called the digestive tract—and the liver, pancreas, and gallbladder. The GI tract is a series of hollow organs joined in a long, twisting tube from the mouth to the anus. The hollow organs that make up the GI tract are the mouth, esophagus, stomach, small intestine, large intestine—which includes the colon and rectum—and anus. Food enters the mouth and passes to the anus through the hollow organs of the digestive system. The liver, pancreas, and gallbladder are the solid organs of the digestive system. The digestive system helps the body digest food.
Symptoms:
The symptoms of Alagille syndrome and their severity vary, even among people in the same family sharing the same gene mutation.

Liver:  In some people, problems in the liver may be the first signs and symptoms of the disorder. These symptoms can occur in children and adults and in infants as early as the first 3 months of life.
Jaundice. Jaundice—when the skin and whites of the eyes turn yellow—is a result of the liver not removing bilirubin from the blood. Bilirubin is a reddish-yellow substance formed when hemoglobin breaks down. Hemoglobin is an iron-rich protein that gives blood its red color. Bilirubin is absorbed by the liver, processed, and released into bile. Blockage of the bile ducts forces bilirubin and other elements of bile to build up in the blood.
Jaundice may be difficult for parents and even health care providers to detect. Many healthy newborns have mild jaundice during the first 1 to 2 weeks of life due to an immature liver. This normal type of jaundice disappears by the second or third week of life, whereas the jaundice of Alagille syndrome deepens. Newborns with jaundice after 2 weeks of life should be seen by a health care provider to check for a possible liver problem.
Dark urine and gray or white stools. High levels of bilirubin in the blood that pass into the urine can make the urine darker, while stool lightens from a lack of bilirubin reaching the intestines. Gray or white bowel movements after 2 weeks of age are very reliable signs of a liver problem.
Pruritus. The buildup of bilirubin in the blood may cause itching, also called pruritus. Pruritus usually starts after 3 months of age and can be severe.
Xanthomas. Xanthomas are fatty deposits that appear as yellow bumps on the skin. They are caused by abnormally high cholesterol levels in the blood, common in people with liver disease. Xanthomas may appear anywhere on the body. However, xanthomas are usually found on the elbows, joints, tendons, knees, hands, feet, or buttocks.
Other Symptoms of Alagille Syndrome are:
Certain signs of Alagille syndrome are unique to the disorder, including those that affect the vertebrae and facial features.

Face.  Many children with Alagille syndrome have deep-set eyes, a straight nose, a small and pointed chin, large ears, and a prominent, wide forehead. These features are not usually recognized until after infancy. By adulthood, the chin is more prominent.

Eyes. Posterior embryotoxon is a condition in which an opaque ring is present in the cornea, the transparent covering of the eyeball. The abnormality is common in people with Alagille syndrome, though it usually does not affect vision.

Skeleton. The most common skeletal defect in a person with Alagille syndrome is when the shape of the vertebrae—bones of the spine—gives the appearance of flying butterflies. This defect, known as “butterfly” vertebrae, rarely causes medical problems or requires treatment.

Heart and blood vessels. People with Alagille syndrome may have the following signs and symptoms having to do with the heart and blood vessels:

heart murmur—an extra or unusual sound heard during a heartbeat. A heart murmur is the most common sign of Alagille syndrome other than the general symptoms of liver disease.1 Most people with Alagille syndrome have a narrowing of the blood vessels that carry blood from the heart to the lungs.1 This narrowing causes a murmur that can be heard with a stethoscope. Heart murmurs usually do not cause problems.

heart walls and valve problems. A small number of people with Alagille syndrome have serious problems with the walls or valves of the heart. These conditions may need treatment with medications or corrective surgery.

blood vessel problems. People with Alagille syndrome may have abnormalities of the blood vessels in the head and neck. This serious complication can lead to internal bleeding or stroke. Alagille syndrome can also cause narrowing or bulging of other blood vessels in the body.
Kidney disease. A wide range of kidney diseases can occur in Alagille syndrome. The kidneys are two bean-shaped organs, each about the size of a fist, that filter wastes and extra fluid from the blood. Some people have small kidneys or have cysts—fluid-filled sacs—in the kidneys. Kidney function can also decrease.
Causes:
Alagille syndrome is caused by a gene mutation, or defect. Genes provide instructions for making proteins in the body. A gene mutation is a permanent change in the DNA sequence that makes up a gene. DNA, or deoxyribonucleic acid, is the material inside cells that carries genetic information and passes genes from parent to child. Approximately 30 to 50 percent of people with Alagille syndrome have an inherited gene mutation, meaning it has been passed on by a parent. In the remaining cases, the gene mutation develops spontaneously.1 In spontaneous cases, neither parent carries a copy of the mutated gene.

Most cases of Alagille syndrome are caused by a mutation in the JAGGED1 (JAG1) gene. In less than 1 percent of cases, a mutation in the NOTCH2 gene is the cause.2

1Spinner NB, Leonard LD, Krantz ID. Alagille syndrome. GeneReviews website. www.ncbi.nlm.nih.gov/books/NBK1273/External NIH Link. Updated February 28, 2013. Accessed July 16, 2014.

2Kamath BM, Bauer RC, Loomes KM, et al. NOTCH2 mutations in Alagille syndrome. Journal of Medical Genetics. 2012;49(2):138–144.
Genetic Disorders: 
Each cell contains thousands of genes that provide the instructions for making proteins for growth and repair of the body. If a gene has a mutation, the protein made by that gene may not function properly, which sometimes creates a genetic disorder. Not all gene mutations cause a disorder.

People have two copies of most genes; one copy is inherited from each parent. A genetic disorder occurs when one or both parents pass a mutated gene to a child at conception. A genetic disorder can also occur through a spontaneous gene mutation, meaning neither parent carries a copy of the mutated gene. Once a spontaneous gene mutation has occurred in a person, it can be passed to the person’s children.
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Complications:
The complications of Alagille syndrome include liver failure, portal hypertension, and growth problems. People with Alagille syndrome usually have a combination of complications, and may not have every complication listed below.:-

Liver failure. Over time, the decreased number of bile ducts may lead to chronic liver failure, also called end-stage liver disease. This condition progresses over months, years, or even decades. The liver can no longer perform important functions or effectively replace damaged cells. A person may need a liver transplant. A liver transplant is surgery to remove a diseased or an injured liver and replace it with a healthy whole liver or a segment of a liver from another person, called a donor.

Portal hypertension. The spleen is the organ that cleans blood and makes white blood cells. White blood cells attack bacteria and other foreign cells. Blood flow from the spleen drains directly into the liver. When a person with Alagille syndrome has advanced liver disease, the blood flow backs up into the spleen and other blood vessels. This condition is called portal hypertension. The spleen may become larger in the later stages of liver disease. A person with an enlarged spleen should avoid contact sports to protect the organ from injury. Advanced portal hypertension can lead to serious bleeding problems.

Growth problems. Alagille syndrome can lead to poor growth in infants and children, as well as delayed puberty in older children. Liver disease can cause malabsorption, which can result in growth problems. Malabsorption is the inability of the small intestine to absorb nutrients from foods, which results in protein, calorie, and vitamin deficiencies. Serious heart problems, if present in Alagille syndrome, can also affect growth.

Malabsorption. People with Alagille syndrome may have diarrhea—loose, watery stools—due to malabsorption. The condition occurs because bile is necessary for the digestion of food. Malabsorption can lead to bone fractures, eye problems, blood-clotting problems, and learning delays.

Long-term Outlook:
The long-term outlook for people with Alagille syndrome depends on several factors, including the severity of liver damage and heart problems. Predicting who will experience improved bile flow and who will progress to chronic liver failure is difficult. Ten to 30 percent of people with Alagille syndrome will eventually need a liver transplant.

Many adults with Alagille syndrome whose symptoms improve with treatment lead normal, productive lives. Deaths in people with Alagille syndrome are most often caused by chronic liver failure, heart problems, and blood vessel problems.

Diagnosis:
The Doctor diagnoses Alagille syndrome by performing a thorough physical examination of the patient and ordering one or more of the following tests and exams:

Blood test. A blood test involves drawing blood at a health care provider’s office or a commercial facility and sending the sample to a lab for analysis. The blood test can show nutritional status and the presence of liver disease and kidney function.

Urinalysis. Urinalysis is the testing of a urine sample. The urine sample is collected in a special container in a health care provider’s office or a commercial facility and can be tested in the same location or sent to a lab for analysis. Urinalysis can show many problems of the urinary tract and other body systems. The sample may be observed for color, cloudiness, or concentration; signs of drug use; chemical composition, including glucose; the presence of protein, blood cells, or bacteria; or other signs of disease.

X ray. An x ray is a picture created by using radiation and recorded on film or on a computer. The amount of radiation used is small. An x-ray technician performs the x ray at a hospital or an outpatient center, and a radiologist—a doctor who specializes in medical imaging—interprets the images. Anesthesia is not needed. The patient will lie on a table or stand during the x ray. The technician positions the x-ray machine over the spine area to look for “butterfly” vertebrae. The patient will hold his or her breath as the picture is taken so that the picture will not be blurry. The patient may be asked to change position for additional pictures.

Abdominal ultrasound. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. The transducer can be moved to different angles to make it possible to examine different organs. In abdominal ultrasound, the health care provider applies a gel to the patient’s abdomen and moves a handheld transducer over the skin. The gel allows the transducer to glide easily, and it improves the transmission of the signals. A specially trained technician performs the procedure in a health care provider’s office, an outpatient center, or a hospital, and a radiologist interprets the images; anesthesia is not needed. The images can show an enlarged liver or rule out other conditions.

Cardiology exam. A cardiologist—a doctor who treats people who have heart problems—performs a cardiology exam in a health care provider’s office, an outpatient center, or a hospital. During a full exam, a cardiologist may inspect the patient’s physical appearance, measure pulse rate and blood pressure, observe the jugular vein, check for rapid or skipped heartbeats, listen for variations in heart sounds, and listen to the lungs.

Slit-lamp exam. An ophthalmologist—a doctor who diagnoses and treats all eye diseases and eye disorders—performs a slit-lamp exam to diagnose posterior embryotoxon. The ophthalmologist examines the eye with a slit lamp, a microscope combined with a high-intensity light that shines a thin beam on the eye. While sitting in a chair, the patient will rest his or her head on the slit lamp. A yellow dye may be used to examine the cornea and tear layer. The dye is applied as a drop, or the specialist may touch a strip of paper stained with the dye to the white of the patient’s eye. The specialist will also use drops in the patient’s eye to dilate the pupil.

Liver biopsy. A liver biopsy is a procedure that involves taking a piece of liver tissue for examination with a microscope for signs of damage or disease. The health care provider may ask the patient to stop taking certain medications temporarily before the liver biopsy. The patient may be asked to fast for 8 hours before the procedure.

During the procedure, the patient lies on a table, right hand resting above the head. A local anesthetic is applied to the area where the biopsy needle will be inserted. If needed, sedatives and pain medication are also given. The health care provider uses a needle to take a small piece of liver tissue. The health care provider may use ultrasound, computerized tomography scans, or other imaging techniques to guide the needle. After the biopsy, the patient should lie on the right side for up to 2 hours and is monitored an additional 2 to 4 hours before being sent home.

Genetic testing. The health care provider may refer a person suspected of having Alagille syndrome to a geneticist—a doctor who specializes in genetic disorders. For a genetic test, the geneticist takes a blood or saliva sample and analyzes the DNA for the JAG1 gene mutation. The geneticist tests for the JAG1 gene mutation first, since it is more common in Alagille syndrome than NOTCH2. Genetic testing is often done only by specialized labs. The results may not be available for several months because of the complexity of the testing.

The usefulness of genetic testing for Alagille syndrome is limited by two factors:

*Detection of a mutated gene cannot predict the onset of symptoms or how serious the disorder will be.

*Even if a mutated gene is found, no specific cure for the disorder exists.

When to Consider Genetic Counseling:
People who are considering genetic testing may want to consult a genetics counselor. Genetic counseling can help family members understand how test results may affect them individually and as a family. Genetic counseling is provided by genetics professionals—health care professionals with specialized degrees and experience in medical genetics and counseling. Genetics professionals include geneticists, genetics counselors, and genetics nurses.

Genetics professionals work as members of health care teams, providing information and support to individuals or families who have genetic disorders or a higher chance of having an inherited condition. Genetics professionals

*assess the likelihood of a genetic disorder by researching a family’s history, evaluating medical records, and conducting a physical exam of the patient and
*other family members

*weigh the medical, social, and ethical decisions surrounding genetic testing

*provide support and information to help a person make a decision about testing

*interpret the results of genetic tests and medical data

*provide counseling or refer individuals and families to support services

*serve as patient advocates

*explain possible treatments or preventive measures

*discuss reproductive options

Genetic counseling may be useful when a family member is deciding whether to have genetic testing and again later when test results are available.

Treatment:
Treatment for Alagille syndrome includes medications and therapies that increase the flow of bile from the liver, promote growth and development in infants’ and children’s bodies, correct nutritional deficiencies, and reduce the person’s discomfort. Ursodiol (Actigall, Urso) is a medication that increases bile flow. Other treatments address specific symptoms of the disorder.

Liver failure. People with Alagille syndrome who develop end-stage liver failure need a liver transplant with a whole liver from a deceased donor or a segment of a liver from a living donor. People with Alagille syndrome who also have heart problems may not be candidates for a transplant because they could be more likely to have complications during and after the procedure. A liver transplant surgical team performs the transplant in a hospital.

Pruritus. Itching may decrease when the flow of bile from the liver is increased. Medications such as cholestyramine (Prevalite), rifampin (Rifadin, Rimactane), naltrexone (Vivitrol), or antihistamines may be prescribed to relieve pruritus. People should hydrate their skin with moisturizers and keep their fingernails trimmed to prevent skin damage from scratching. People with Alagille syndrome should avoid baths and take short showers to prevent the skin from drying out.

If severe pruritus does not improve with medication, a procedure called partial external biliary diversion may provide relief from itching. The procedure involves surgery to connect one end of the small intestine to the gallbladder and the other end to an opening in the abdomen—called a stoma—through which bile leaves the body and is collected in a pouch. A surgeon performs partial external biliary diversion in a hospital. The patient will need general anesthesia.

Malabsorption and growth problems. Infants with Alagille syndrome are given a special formula that helps the small intestine absorb much-needed fat. Infants, children, and adults can benefit from a high-calorie diet, calcium, and vitamins A, D, E, and K. They may also need additional zinc. If someone with Alagille syndrome does not tolerate oral doses of vitamins, a health care provider may give the person injections for a period of time. A child may receive additional calories through a tiny tube that is passed through the nose into the stomach. If extra calories are needed for a long time, a health care provider may place a tube, called a gastrostomy tube, directly into the stomach through a small opening made in the abdomen. A child’s growth may improve with increased nutrition and flow of bile from the liver.

Xanthomas. For someone who has Alagille syndrome, these fatty deposits typically worsen over the first few years of life and then improve over time. They may eventually disappear in response to partial external biliary diversion or the medications used to increase bile fl

Prevention:
Scientists have not yet found a way to prevent Alagille syndrome. However, complications of the disorder can be managed with the help of Doctors. Routine visits with Doctor are needed to prevent complications from becoming worse.

Hope through Research:The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and other Institutes of the National Institutes of Health (NIH) conduct and support research in digestive disorders, including Alagille syndrome. For example, the NIDDK is sponsoring a study called Evaluating the Genetic Causes and Progression of Cholestatic Liver Diseases (LOGIC). Funded under NIH clinical trial number NCT00571272, LOGIC will investigate the progression of cholestatic liver diseases, which can sometimes be caused by Alagille syndrome. The study will work to provide a better understanding of the causes and effects of these liver diseases, which will promote the development of prevention tactics and treatment strategies.

Clinical trials are research studies involving people. Clinical trials look at safe and effective new ways to prevent, detect, or treat disease. Researchers also use clinical trials to look at other aspects of care, such as improving the quality of life for people with chronic illnesses. To learn more about clinical trials, why they matter, and how to participate, visit the NIH Clinical Research Trials and You website at www.nih.gov/health/clinicaltrialsExternal NIH Link. For information about current studies,…click & see

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/Alagille_syndrome

http://www.niddk.nih.gov/health-information/health-topics/liver-disease/Alagille-Syndrome/Pages/facts.aspx