Categories
Ailmemts & Remedies

Amyloidosis

Alternative Names: Amyloid – primary

Definition:
In medicine, amyloidosis refers to a variety of conditions in which amyloid proteins are abnormally deposited in organs and/or tissues. A protein is described as being amyloid if, due to an alteration in its secondary structure, it takes on a particular aggregated insoluble form similar to the beta-pleated sheet.  Symptoms vary widely depending upon the site of amyloid deposition. Amyloidosis may be inherited or acquired.

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The collection of these abnormal proteins interferes with the normal functioning of the organ affected.

Since there are more than 20 different proteins that may form amyloid, there are also many different types of amyloidosis.

Classification of amyloid:
The modern classification of amyloid disease tends to use an abbreviation of the protein that makes the majority of deposits, prefixed with the letter A. For example amyloidosis caused by transthyretin is termed “ATTR.” Deposition patterns vary between patients but are almost always composed of just one amyloidogenic protein. Deposition can be systemic (affecting many different organ systems) or organ-specific. Many amyloidoses are inherited, due to mutations in the precursor protein. Other forms are due to different diseases causing overabundant or abnormal protein production – such as with over production of immunoglobulin light chains in multiple myeloma (termed AL amyloid), or with continuous overproduction of acute phase proteins in chronic inflammation (which can lead to AA amyloid).

Out of the approximately 60 amyloid proteins that have been identified so far,  at least 36 have been associated in some way with a human disease.

Amyloidosis is rare, being diagnosed in between one and five in every 100,000 people every year. It’s more common in older people and is also slightly more common in men than in women.

Causes:
The cause of primary amyloidosis is unknown, but the condition is related to abnormal production of antibodies by a type of immune cell called plasma cells.

The symptoms depend on the organs affected by the deposits. These organs can include the tongue, intestines, skeletal and smooth muscles, nerves, skin, ligaments, heart, liver, spleen, and kidneys.

Primary amyloidosis can result in conditions that include:

•Carpal tunnel syndrome
•Gastrointestinal reflux (GERD)
•Heart muscle damage (cardiomyopathy)
•Kidney failure
•Malabsorption
The deposits build up in the affected organs, causing them to become stiff, which decreases their ability to function.

Risk factors have not been identified. Primary amyloidosis is rare. It is similar to multiple myeloma, and is treated the same way.

Symptoms:

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•Enlarged tongue
•Fatigue
•Irregular heart rhythm
•Numbness of hands and feet
•Shortness of breath
•Skin changes
•Swallowing difficulties
•Swelling in the arms and legs
•Weak hand grip
•Weight loss

Additional symptoms that may be associated with this disease:
•Clay-colored stools
•Decreased urine output
•Diarrhea
•Hoarseness or changing voice
•Joint pain
•Other tongue problems
•Weakness

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Diagnosis:
Exams and Tests
Your doctor may discover that you have an enlarged liver or spleen.

If specific organ damage is suspected, your doctor may order tests to confirm amyloidosis of that organ. For example:

•Abdominal ultrasound may reveal a swollen liver or spleen.
•An abdominal fat pad biopsy, rectal mucosa biopsy, or a bone marrow biopsy can help confirm the diagnosis.
•A heart evaluation, including an ECG,may reveal arrhythmias, abnormal heart sounds, or signs of congestive heart failure. An echocardiogram shows poor motion of the heart wall, due to a stiff heart muscle.
•A carpal tunnel syndrome evaluation may show that hand grips are weak.Nerve conduction velocity shows abnormalities.
•Kidney function tests may show signs of kidney failure or too much protein in the urine ( nephrotic syndrome).
?BUN level is increased.
?Serum creatinine is increased.
?Urinalysis shows protein, casts, or fat bodies.

This disease may also alter the results of the following tests:
•Bence-Jones protein (quantitative)
•Carpal tunnel biopsy
•Gum biopsy
•Immunoelectrophoresis – serum
•Myocardial biopsy
•Nerve biopsy
•Quantitative immunoglobulins
•Tongue biopsy
•Urine protein

Treatment:
It isn’t always easy to treat amyloidosis, and there is no treatment yet that specifically targets the amyloid depositing in the tissues. In cases where it’s secondary to another problem (AA amyloidosis), such as rheumatoid arthritis, treating that original problem may stop the progress of amyloidosis or may even reverse it.

In cases of primary amyloidosis (AL amyloidosis), chemotherapy drugs may be given to suppress production of new amyloid and cause regression of existing amyloid deposits.

In secondary amyloidosis, aggressive treatment of the underlying disease can improve symptoms and/or slow progression of disease. Complications such as heart failure, kidney failure, and other problems can sometimes be treated as necessary.

Occasionally, transplantation of a damaged organ is necessary. However, even after this has been carried out the new organ may become affected by amyloidosis.

Treatment may also be aimed at supporting the function of damaged tissues and treating complications such as heart or kidney failure.

Overall, many types of amyloidosis follow a steadily progressive course and may prove fatal within a year or two.

Prognosis :
The severity of the disease depends upon the organs affected. Heart and kidney involvement may lead to organ failure and death. Systemic involvement is associated with death within 1 to 3 years.

Possible Complications:
•Congestive heart failure
•Death
•Endocrine failure (hormonal disorder)
•Kidney failure
•Respiratory failure

Prevention : There is no known prevention.

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.bbc.co.uk/health/physical_health/conditions/amyloidosis1.shtml
http://www.nlm.nih.gov/medlineplus/ency/article/000533.htm
http://en.wikipedia.org/wiki/Amyloidosis

http://health.allrefer.com/pictures-images/amyloidosis-on-the-face.html

http://health.allrefer.com/health/cardiac-amyloidosis-dilated-cardiomyopathy.html

http://morningreporttgh.blogspot.com/2010/04/amyloidosis.html

http://gsm.utmck.edu/research/HICP/overview.cfm

http://www.pathologyatlas.ro/amyloidosis-kidney-pathology.php

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Categories
Ailmemts & Remedies

Acrodysostosis

Alternative Names  :Arkless-Graham; Acrodysplasia; Maroteaux-Malamut

Definition:
Acrodysostosis is an extremely rare  genetic disorder that is present at birth. It is a rare congenital malformation syndrome which involves shortening of the interphalangeal joints of the hands and feet, mental deficiency in approximately 90% of affected children, and peculiar facies. Other common abnormalities include short head (as measured front to back i.e. [[ ]]), small broad upturned nose with flat nasal bridge, protruding jaw, increased bone age, Intrauterine growth retardation, juvenile arthritis and short stature. Further abnormalities of the skin, genitals, teeth, and skeleton may occur.

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Most reported cases have been sporadic, but it has been suggested that the condition might be genetically related i.e. in a autosomal dominant mode of transmission. Both males and females are affected. The disorder has been associated with older parental age.

Symptoms:
•Growth problems, short arms and legs
•Frequent middle ear infections
•Hearing problems
•Unusual looking face
•Mental deficiency

People with acrodysostosis have certain bones that mature rapidly, before they’ve had enough time to grow fully. The bones most often affected are those of the nose and jaw, and the long tubular bones of the hands and feet.

This abnormal bone development results in a collection of characteristic features, including a typical facial appearance (short nose, open mouth and prominent jaw), small hands and feet.

Those with acrodysostosis often have some degree of mental retardation and learning difficulties.

Causes:
The gene responsible for acrodysostosis has not yet been identified and the condition may result from different genetic problems rather than one specific condition.

Most patients with acrodysostosis have no family history of the disease. However, sometimes the condition is passed down from parent to child.

It appears to be inherited in an autosomal dominant fashion. This means that if one parent is carrying the gene, they will be normal but there is a one in two chance that any child of theirs will have the condition and seems to be more common among older parents.

There is a slightly greater risk with fathers who are older.

Diagnosis:
Exams and Tests
A physical exam confirms this disorder.

click & see the pictures

Findings may include:

•Advanced bone age
•Bone deformities in hands and feet
•Delays in growth
•Problems with the skin, genitals, teeth, and skeleton
•Short arms and legs with small hands and feet
•Short head, measured front to back (brachycephaly)
•Short height
•Small, upturned broad nose with flat bridge
•Unusual features of the face (short nose, open mouth, jaw that sticks out)
•Unusual head
•Wide-spaced eyes (hypertelorism), sometimes with extra skin fold at corner of eye
In the first months of life, x-rays may show spotty calcium deposits, called stippling, in bones (especially the nose). Infants may also have:

•Abnormally short fingers and toes (brachydactyly)
•Early growth of bones in the hands and feet
•Short bones
•Shortening of the forearm bones near the wrist

Treatment:
There’s no cure for acrodysostosis but appropriate support by orthopaedic surgeons and paediatricians is important.

Treatment depends on the physical and mental problems that occur.

Antenatal diagnosis may be made by ultrasound examination of the bones in babies whose mother has the condition, but routine screening isn’t done.

Possible Complications:
•Arthritis
•Carpal tunnel syndrome
•Worsening range of movement in the spine, elbows, and hands

Prognosis ;
Problems depend on the degree of skeletal involvement and mental retardation. In general, patients do relatively well.

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

Resources:
http://www.nlm.nih.gov/medlineplus/ency/article/001248.htm
http://www.bbc.co.uk/health/physical_health/conditions/acrodysostosis1.shtml
http://en.wikipedia.org/wiki/Acrodysostosis

http://www.gfmer.ch/genetic_diseases_v2/gendis_detail_list.php?cat3=1098

http://health.allrefer.com/health/acrodysostosis-info.html

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Categories
Ailmemts & Remedies

Pellagra

Definition:
Pellagra is a lack of a sufficient amount of vitamin B3 (niacin) in the body.It  is a vitamin deficiency disease most commonly caused by a chronic lack of niacin (vitamin B3) in the diet. Niacin is essential for optimal cellular health. Pellagra is caused by an inability of the body to absorb or process niacin or a lack of niacin and/or tryptophan the diet. Pellagra that results from inadequate intake of niacin and/or tryptophan is most common in developing countries of the world or in places where there is poverty and poor nutrition. People at risk for pellagra include those with a poor diet that is lacking in niacin and/or tryptophan.

It can be caused by decreased intake of niacin or tryptophan, and possibly by excessive intake of leucine. It may also result from alterations in protein metabolism in disorders such as carcinoid syndrome. A deficiency of the amino acid lysine can lead to a deficiency of niacin as well, meaning that another potential cause of pellagra is lysine deficiency

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Pellagra can also result from a disease, disorder or condition that affects the absorption or processing of niacin in the body. This is called secondary pellagra. There are many causes of secondary pellagra, including ulcerative colitis, excessive diarrhea, liver cirrhosis, chronic alcoholism, Hartnup disease and carcinoid tumors. Pellagra can also be a side effect of certain medications. People with these conditions are at risk for developing secondary pellagra Symptoms of pellagra typically affect the skin, gastrointestinal system and the nervous system. Pellagra can be serious, even fatal, if untreated. Complications include coma and death. For more details on symptoms and complications.

History :

The traditional food preparation method of corn (maize), nixtamalization, by native New World cultivators who had domesticated corn required treatment of the grain with lime, an alkali. It has now been shown that the lime treatment makes niacin nutritionally available and reduces the chance of developing pellagra. When corn cultivation was adopted worldwide, this preparation method was not accepted because the benefit was not understood. The original cultivators, often heavily dependent on corn, did not suffer from pellagra. Pellagra became common only when corn became a staple that was eaten without the traditional treatment.

Pellagra was first described in Spain in 1735 by Gaspar Casal, who published a first clinical description in his posthumous “Natural and Medical History of the Asturian Principality” (1762). This led to the disease being known as “Asturian leprosy”, and it is recognized as the first modern pathological description of a syndrome(1). It was an endemic disease in northern Italy, where it was named “pelle agra” (pelle = skin; agra = sour) by Francesco Frapoli of Milan.[3] Because pellagra outbreaks occurred in regions where maize was a dominant food crop, the belief for centuries was that the maize either carried a toxic substance or was a carrier of disease. It was not until later that the lack of pellagra outbreaks in Mesoamerica, where maize is a major food crop (and is processed), was noted and the idea was considered that the causes of pellagra may be due to factors other than toxins.

In the early 1900s, pellagra reached epidemic proportions in the American South. There were 1,306 reported pellagra deaths in South Carolina during the first ten months of 1915; 100,000 Southerners were affected in 1916. At this time, the scientific community held that pellagra was probably caused by a germ or some unknown toxin in corn. The Spartanburg Pellagra Hospital in Spartanburg, South Carolina, was the nation’s first facility dedicated to discovering the cause of pellagra. It was established in 1914 with a special congressional appropriation to the U.S. Public Health Service (PHS) and set up primarily for research. In 1915, Joseph Goldberger, assigned to study pellagra by the Surgeon General of the United States, showed that pellagra was linked to diet by inducing the disease in prisoners, using the Spartanburg Pellagra Hospital as his clinic. By 1926, Goldberger established that a balanced diet or a small amount of brewer’s yeast prevented pellagra. Skepticism nonetheless persisted in the medical community until 1937, when Conrad Elvehjem showed that the vitamin niacin cured pellagra (manifested as black tongue) in dogs. Later studies by Tom Spies, Marion Blankenhorn, and Clark Cooper established that niacin also cured pellagra in humans, for which Time Magazine dubbed them its 1938 Men of the Year in comprehensive science.

In the research conducted between 1900–1950, it was found that the number of cases of women with pellagra was consistently double the number of cases of afflicted men. This is thought to be due to the inhibitory effect of estrogen on the conversion of the amino acid tryptophan to niacin. It is also thought to be due to the differential and unequal access to quality foods within the household. Some researchers of the time gave a few explanations regarding the difference. As primary wage earners, men were given consideration and preference at the dinner table. They also had pocket money to buy food outside the household. Women gave protein quality foods to their children first. Women also would eat after everyone else had a chance to eat. Women also upheld the triad of maize, molasses and fat back pork which combine to contribute to cause pellagra.[citation needed]

Gillman and Gillman related skeletal tissue and pellagra in their research in South African Blacks. They provide some of the best evidence for skeletal manifestations of pellagra and the reaction of bone in malnutrition. They claimed radiological studies of adult pellagrins demonstrated marked osteoporosis. A negative mineral balance in pellagrins was noted which indicated active mobilization and excretion of endogenous mineral substances, and undoubtedly impacted the turnover of bone. Extensive dental caries were present in over half of pellagra patients. In most cases caries were associated with “severe gingival retraction, sepsis, exposure of cementum, and loosening of teeth


Symptoms:

The dermatologic features of this disorder include desquamation, erythema, scaling, and keratosis of sun-exposed areas, all of which this patient had.Pellagra is classically described by “the three D’s”: diarrhea, dermatitis and dementia. A more comprehensive list of symptoms includes:

*High sensitivity to sunlight
*Aggression
*Dermatitis, alopecia, oedema
*Smooth, beefy red glossitis
*Red skin lesions
*Insomnia
*Weakness
*Mental confusion
*Ataxia, paralysis of extremities, peripheral neuritis
*Diarrhea
*Dilated cardiomyopathy
*Eventually dementia

Frostig and Spies (acc. to Cleary and Cleary) described more specific psychological symptoms of pellagra as:

*Psycho-sensory disturbances (impressions as being painful, annoying bright lights, odours intolerance causing nausea and vomiting, dizziness after sudden movements)
*Psycho-motor disturbances (restlessness, tense and a desire to quarrel, increased preparedness for motor action)
*Emotional disturbances.

Causes:
Pellagra is caused by having too little niacin or tryptophan in the diet. It can also occur if the body fails to absorb these nutrients. It may develop after gastrointestinal diseases or with alcoholism.

The disease is common in parts of the world where people have a lot of corn in their diet.

Pellagra can be common in people who obtain most of their food energy from maize (often called “corn”), notably rural South America where maize is a staple food. Maize is a poor source of tryptophan as well as niacin if it is not nixtamalized. Nixtamalization of the corn corrects the niacin deficiency, and is a common practice in Native American cultures that grow corn. Following the corn cycle, the symptoms usually appear during spring, increase in the summer due to greater sun exposure, and return the following spring. Indeed, pellagra was once endemic in the poorer states of the U.S. South, like Mississippi and Alabama, as well as among the inmates of jails and orphanages as studied by Dr. Joseph Goldberger.

Pellagra is common in Africa, Indonesia, and China. In affluent societies, a majority of patients with clinical pellagra are poor, homeless, alcohol dependent, or psychiatric patients who refuse food. It was common amongst prisoners of Soviet labor camps, the Gulag. It can be found in cases of chronic alcoholism. In addition, pellagra is a micronutrient deficiency disease that frequently affects populations of refugees and other displaced people due to their unique, long-term residential circumstances and dependence on food aid. Refugees typically rely on limited sources of niacin provided to them, such as groundnuts; the instability in the nutritional content and distribution of food aid can be the cause of pellagra in displaced populations.

List of causes of Pellagra :  Following is a list of causes or underlying conditions ( Misdiagnosis of underlying causes of Pellagra) that could possibly cause Pellagra includes:

•Dietary deficiency of vitamin B3 (niacin)
•Malnutrition
•Malabsorption

The follow list shows some of the possible medical causes of Pellagra that are listed by the Diseases Database:

•Hartnup’s disease
•Carcinoid tumours and carcinoid syndrome

Pellagra Causes: Book Excerpts
•Causes and incidence – Vitamin B deficiencies
•Causes and incidence – Vitamin C deficiency
•Causes and incidence – Vitamin D deficiency
•Causes and incidence – Vitamin E deficiency
•Causes – Vitamin K deficiency
•Causes and incidence – Vitamin A deficiency

Pellagra Related Medical ConditionsTo research the causes of Pellagra, consider researching the causes of these these diseases that may be similar, or associated with Pellagra:

•Alcoholism
•Dermatitis
•Insomnia
•Dementia
•Diarrhoea
•Ataxia
•Nicotinamide
•Niacin
•Vitamin B3
•Carcinoid syndrome
Pellagra: Causes and TypesCauses of Broader Categories of Pellagra: Review the causal information about the various more general categories of medical conditions:

•Vitamin deficiency
•Vitamin B deficiency
•more types…»


Diagnosis:-

Diagnosis is purely based on the patient’s collection of symptoms, together with information regarding the patient’s diet. When this information points to niacin deficiency, replacement is started, and the diagnosis is then partly made by evaluating the patient’s response to increased amounts of niacin. There are no chemical tests available to definitively diagnose pellagra.

Pellagra Diagnosis: Book Excerpts
•Diagnosis – Vitamin B deficiencies
•Diagnosis – Vitamin C deficiency
•Diagnosis – Vitamin D deficiency
•Diagnosis – Vitamin E deficiency
•Diagnosis – Vitamin K deficiency
•Diagnosis – Vitamin A deficiency


Treatment:

The first step in the treatment of pellagra is prevention. Primary pellagra can be prevented with eating a diet that is rich in foods that contain niacin and tryptophan. Niacin is found in whole grains, meats, and fish and in fortified grains and cereals. Tryptophan is found in milk and eggs.

Taking supplements that contain niacin may also be needed to prevent pellagra in people with poor diets. High doses of niacin can be toxic to some people with gout, diabetes, asthma, liver disease, ulcers, or who are on antihypertensive medication.

If diagnosed and treated promptly, pellagra has a good prognosis and cure rate. Early treatment eliminates the risk of developing serious permanent complications, such as dementia, psychosis, coma and death.

Treatment of pellagra generally includes oral or intravenous niacin supplementation. Regular medical care and monitoring of the condition and treatment of any underlying diseases, such as ulcerative colitis, excessive diarrhea, liver cirrhosis, chronic alcoholism, Hartnup disease and carcinoid tumors, are also necessary to ensure a good prognosis.

Treatment of pellagra usually involves supplementing the individual’s diet with a form of niacin called niacinamide (niacin itself in pure supplementation form causes a number of unpleasant side effects, including sensations of itching, burning, and flushing). The niacinamide can be given by mouth (orally) or by injection (when diarrhea would interfere with its absorption). The usual oral dosage is 300-500 mg each day; the usual dosage of an injection is 100-250 mg, administered two to three times each day. When pellagra has progressed to the point of the encephalopathic syndrome, a patient will require 1,000 mg of niacinamide orally, and 100-250 mg of niacinamide by injection. Once the symptoms of pellagra have subsided, a maintenance dose of niacin can be calculated, along with attempting (where possible) to make appropriate changes in the diet. Because many B-complex vitamin deficiencies occur simultaneously, patients will usually require the administration of other B-complex vitamins as well.

Treatment List for PellagraThe list of treatments mentioned in various sources for Pellagra includes the following list. Always seek professional medical advice about any treatment or change in treatment plans.

•Vitamin B3 – possibly used for related severe vitamin B3 deficiency
•Vitamin B3
•Diet – high protein/high calorie, and including meat, milk, peanuts, green leafy vegetables, whole grains and brewers yeast
•Nicotinamide or niacin supplementation
•B complex vitamin supplementation as patients are often suffer from other vitamin deficiencies

Drugs and Medications used to treat Pellagra:Note:You must always seek professional medical advice about any prescription drug, OTC drug, medication, treatment or change in treatment plans.

Some of the different medications used in the treatment of Pellagra include:

•Niacinamide
•Thiamine
•Betaxin
•Thiamilate
•Benerva
•Nicotinic Acid
•Vitamin B3
•Dynamo
•NoDoz Plus

Prognosis:
Untreated pellagra will continue progressing over the course of several years, and is ultimately fatal. Often, death is due to complications from infections, massive malnutrition brought on by continuous diarrhea, blood loss due to bleeding from the gastrointestinal tract, or severe encephalopathic syndrome.

Considerations :
Individuals with diabetes should take supplementary niacin with caution, as it can raise blood sugar levels. Long-term niacin therapy may also increase the risk of gout. At least one study has pointed out the danger of taking too much niacin, especially for elderly people. The short-term side effects of niacin overdose include:

*Flushing.
*Itching.
*Skin disorders.

Over the long term, high doses of niacin can be dangerous. Taking as little as 500 mg of niacin per day over a period of several months may result in liver damage.


Recomendations:

Eat plenty of foods that are high in B vitamins, such as avocados, bananas, broccoli, collards, figs, legumes, nuts and seeds, peanut butter, potatoes, prunes, tomatoes, and whole grain or enriched bread and cereal.

Include in the diet halibut, salmon, sunflower seeds, swordfish, tuna, and white skinless breast of chicken and turkey. These foods are good sources of the amino acid tryptophan, which is converted into niacin in the body.

Nutritional Suppliments :
Unless otherwise specified, the dosages recommended here are for adults. For a child between the ages of 12 and 17 years, reduce the dose to 3/4 the recommended amount. For a child between the ages of 6 and 12, use 1/2 the recommended dose, and for a child under the age of 6, use 1/4 the recommended amount.

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/Pellagra
http://www.wrongdiagnosis.com/p/pellagra/intro.htm
http://www.myoptumhealth.com/portal/ADAM/item/Pellagra
http://www.moondragon.org/health/disorders/pellagra.html

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Our body extricts

The Poop!

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Stool – Healthy and Unhealthy Stool:-

Click to see the  pictures of ->
Bristol  Stool  Chart

This writing might “stink” a little, but this information might serve as an important revelation to many particularly for elderly and persons with contineus stomac problem!

Human poops or  stools, is the waste product of the human digestive system and varies significantly in appearance, depending on the state of the whole digestive system, influenced and found by diet and health.

Normally stools are semisolid, with a mucus coating. Small pieces of harder, less moist feces can sometimes be seen impacted on the distal (leading) end. This is a normal occurrence when a prior bowel movement is incomplete; and feces are returned from the rectum to the intestine, where water is absorbed.

Meconium (sometimes erroneously spelled merconium) is a newborn baby’s first feces. Human feces are a defining subject of humor.

Some persons have bloody stools on and off, usually accompanied by a sight tinch of discomfort. Many times, this doesn’t appear as a threat or danger to them as they often regard it as constipation though they may be passionate lover of fruits and vegetables. This might go  on for some time until one day, bloody stools became really “bloody” and the pain became increasingly painful. Alarmed and paranoid, they call their dear ones who will  recommend  to see the doctor over at his or her clinic.

Now let us see What Does an Ideal Bowel Movement Look Like?

Click to see the pictures

Click for different pictures

Alternative practitioners often ask clients about their stool as part of their assessment. Find out what normal stool should look like, and learn about the causes of green stool, pale stool, yellow stool, blood in stool, mucus in stool, pencil thin stool, infrequent stool, and more.

What Does an Ideal [amazon_textlink asin=’B001U1UKOO’ text=’Bowel Movement’ template=’ProductLink’ store=’finmeacur-20′ marketplace=’US’ link_id=’5c1f8c56-ee7e-11e6-87a4-8d88514c5f8b’]

Look Like?
An ideal bowel movement is medium brown, the color of plain cardboard. It leaves the body easily with no straining or discomfort. It should have the consistency of toothpaste, and be approximately 4 to 8 inches long. Stool should enter the water smoothly and slowly fall once it reaches the water. There should be little gas or odor.

Stool That Sinks Quickly
Rapidly sinking stool can indicate that a person isn’t eating enough fiber-rich foods, such as vegetables, fruits, and whole grains, or drinking enough water. This stool is often dark because they have been sitting in the intestines for a prolonged time. Click to learn 5 tips to boost your water intake.

Pale Stool
Stool that is pale or grey may be caused by insufficient bile output due to conditions such as cholecystitis, gallstones, giardia parasitic infection, hepatitis, chronic pancreatitis, or cirrhosis. Bile salts from the liver give stool its brownish color. If there is decreased bile output, stool is much lighter in color.

Other causes of pale stool is the use of antacids that contain aluminum hydroxide. Stool may also temporarily become pale after a barium enema test.

Pale stool may also be shiny or greasy, float, and be foul smelling, due to undigested fat in the stool (see soft and smelly stool).

Soft, Smelly Stool
Soft, foul-smelling stool that floats, sticks to the side of the bowl, or is difficult to flush away may mean there is increased fat in the stools, called steatorrhea. Stool is sometimes also pale. Click to Learn more about the causes of soft, foul-smelling stool.

Mucus in Stool
Whitish mucus in stool may indicate there is inflammation in the intestines. Mucus in stool can occur with either constipation or diarrhea. Click to Read more about the causes of mucus in stool.

Green Stool
The liver constantly makes bile, a bright green fluid, that is secreted directly into the small intestine or stored in the gallbladder. Continue reading about the causes of green stool.

Loose Stool
In traditional Chinese medicine, loose stools, abdominal bloating, lack of energy, and poor appetite can be signs of a condition known as spleen qi deficiency. It doesn’t necessarily involve your actual spleen, but it is linked to tiredness and weak digestion brought on by stress and poor diet. Learn more about the causes of loose stool.

Pencil Thin Stool
Like loose stools, stool that is pencil thin can be caused by a condition known in traditional Chinese medicine as spleen qi deficiency.

Other symptoms of spleen qi deficiency are: easy bruising, mental fogginess, bloating, gas, loose stools, fatigue, poor appetite, loose stools with little odor, symptoms that worsen with stress, undigested food in the stools, and difficulty ending the bowel movement. Spleen qi deficiency can be brought on by stress and overwork.

Eating certain foods in excess is thought to worsen spleen qi deficiency. Offending foods include fried or greasy foods, dairy, raw fruits and vegetables, and cold drinks, all believed to cause “cold” and “dampness” in the body. Dietary treatment of spleen qi deficiency involves eating warm, cooked foods. Ginger tea and cinnamon tea are also warming.

Pencil thin stool can also be caused by a bowel obstruction. Benign rectal polyps, prostate enlargement, colon or prostate cancer are some of the conditions that can cause obstruction.

Infrequent Stool
With constipation, infrequent or hard stool is passed with straining. Learn about the causes of infrequent stool.

Pellet Stool

Pellet stool is stool that comes out in small, round balls. In traditional Chinese medicine, pellet stool is caused by a condition known as liver qi stagnation. Liver qi stagnation can be brought on by stress. Lack of exercise can worsen the problem. Find out more about the causes of pellet stool.

Yellow Stool
Yellow stool can indicate that food is passing through the digestive tract relatively quickly. Yellow stool can be found in people with GERD (gastroesophageal reflux disease). Symptoms of GERD include heartburn, chest pain, sore throat, chronic cough, and wheezing. Symptoms are usually worse when lying down or bending. Foods that can worsen GERD symptoms include peppermint, fatty foods, alcohol, coffee, and chocolate.

Yellow stool can also result from insuffient bile output. Bile salts from the liver gives stool its brownish color. When bile output is diminished, it often first appears as yellow stool. If there is a greater reduction in bile output, stool lose almost all of its color, becoming pale or grey.

If the onset is sudden, yellow stool can also be a sign of a bacterial infection in the intestines.

Yellowing of stool can be caused by an infection known as Giardiasis, which derives its name from Giardia, an anaerobic flagellated protozoan parasite that can cause severe and communicable yellow diarrhea. Another cause of yellowing is a condition known as Gilbert’s Syndrome. This condition is characterized by jaundice and hyperbilirubinemia when too much bilirubin is present in the circulating blood.

Dark Stool
Stool that is almost black with a thick consistency may be caused by bleeding in the upper digestive tract. The most common medical conditions that cause dark, tar-like stool includes duodenal or gastric ulcer, esophageal varices, Mallory Weiss tear (which can be linked with alcoholism), and gastritis.

Certain foods, supplements, and medications can temporarily turn stool black. These include:

*Bismuth (e.g. Pepto bismol)

*Iron

*Activated charcoal

*Aspirin and NSAIDS (which can cause bleeding in the stomach)

*Dark foods such as black licorice and blueberries

Stool can be black due to the presence of red blood cells that have been in the intestines long enough to be broken down by digestive enzymes. This is known as melena (or melaena), and is typically due to bleeding in the upper digestive tract, such as from a bleeding peptic ulcer. The same color change (albeit harmless) can be observed after consuming foods that contain substantial proportion of animal bloods, such as Black pudding or Ti?t canh. The black color is caused by oxidation of the iron in the blood’s hemoglobin (haemoglobin). Black feces can also be caused by a number of medications, such as bismuth subsalicylate, and dietary iron supplements, or foods such as black liquorice, or blueberries. Hematochezia (also haemochezia or haematochezia) is similarly the passage of feces that are bright red due to the presence of undigested blood, either from lower in the digestive tract, or from a more active source in the upper digestive tract. Alcoholism can also provoke abnormalities in the path of blood throughout the body, including the passing of red-black stool.

Dark stool can also occur with constipation.

If you experience this type of stool, you should see your doctor as soon as possible.

Blue Stool
Prussian blue, used in the treatment of radiation cesium and thallium poisoning, can turn the feces blue. Also, substantial consumption of products containing blue food dye (things such as blue koolaid or grape soda)

Bright Red Stool
When there is blood in stool, the color depends on where it is in the digestive tract. Blood from the upper part of the digestive tract, such as the stomach, will look dark by the time it reaches exits the body as a bowel movement. Blood that is bright or dark red, on the other hand, is more likely to come from the large intestine or rectum.

Conditions that can cause blood in the stool include hemorrhoids, anal fissures, diverticulitis, colon cancer, and ulcerative colitis, among others.

Eating beets can also temporarily turn stools and urine red.

Blood in stool doesn’t always appear bright red. Blood may be also present in stool but not visible, called “occult” blood. A test called the Fecal Occult Blood Test is used to detect hidden blood in stool.

Silver Stool
A tarnished-silver or aluminum paint-like stool color characteristically results when biliary obstruction of any type (white stool) combines with gastrointestinal bleeding from any source (black stool). It can also suggest a carcinoma of the ampulla of Vater, which will result in gastrointestinal bleeding and biliary obstruction, resulting in silver stool.

 

You may click to see white stool:–>   : Should I be concerned

Note: Speak with your doctor about any change or abnormality concerning bowel movements.

YOU MAY CLICK TO SEE :Doctors explain exactly how often you should be pooping and give tips for regularity

Resources
http://gracemagg.blogspot.com/2008/07/poop.html
http://altmedicine.about.com/od/gettingdiagnosed/a/stools.htm
http://www.healingwatersaz.com/colon.html

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

Categories
Ailmemts & Remedies

Acrocyanosis

Definition
Acrocyanosis is a decrease in the amount of oxygen delivered to the extremities. The hands and feet turn blue because of the lack of oxygen. Decreased blood supply to the affected areas is caused by constriction or spasm of small blood vessels.

Description
Acrocyanosis is a painless disorder caused by constriction or narrowing of small blood vessels in the skin of affected patients. The spasm of the blood vessels decreases the amount of blood that passes through them, resulting in less blood being delivered to the hands and feet. The hands may be the main area affected. The affected areas turn blue and become cold and sweaty. Localized swelling may also occur. Emotion and cold temperatures can worsen the symptoms, while warmth can decrease symptoms. The disease is seen mainly in women and the effect of the disorder is mainly cosmetic. People with the disease tend to be uncomfortable, with sweaty, cold, bluish colored hands and feet.

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Causes and symptoms
The sympathetic nerves cause constriction or spasms in the peripheral blood vessels that supply blood to the extremities. The spasms are a contraction of the muscles in the walls of the blood vessels. The contraction decreases the internal diameter of the blood vessels, thereby decreasing the amount of blood flow through the affected area. The spasms occur on a persistent basis, resulting in long term reduction of blood supply to the hands and feet. Sufficient blood still passes through the blood vessels so that the tissue in the affected areas does not starve for oxygen or die. Mainly, blood vessels near the surface of the skin are affected.

Diagnosis
Diagnosis is made by observation of the main clinical symptoms, including persistently blue and sweaty hands and/or feet and a lack of pain. Cooling the hands increases the blueness, while warming the hands decreases the blue color. The acrocyanosis patient’s pulse is normal, which rules out obstructive diseases. Raynaud’s disease differs from acrocyanosis in that it causes white and red skin coloration phases, not just bluish discoloration.

Treatment

There is no standard medical or surgical treatment for acrocyanosis, and treatment, other than reassurance and avoidance of cold, is usually unnecessary. The patient is reassured that no serious illness is present. A sympathectomy would alleviate the cyanosis by disrupting the fibers of the sympathetic nervous system to the area.owever, such an extreme procedure would rarely be appropriate. The same effect could be accomplished with a-adrenergic blocking agents or caclium channel blockers

Acrocyanosis usually isn’t treated. Drugs that block the uptake of calcium (calcium channel blockers) and alpha-one antagonists reduce the symptoms in most cases. Drugs that dilate blood vessels are only effective some of the time. Sweating from the affected areas can be profuse and require treatment. Surgery to cut the sympathetic nerves is performed rarely.

Incidence, Prevalence, and Epidemiology
Although there is no definitive reporting on its incidence, acrocyanosis shows prevalence in children and young adults than in patients thirty years of age or older. Epidemiological data suggests that cold climate, outdoor occupation, and low body mass index are significant risk factors for developing acrocyanosis. As expected, acrocyanosis would be more prevalent in women than in men due to differences in BMI. However, the incidence rate of acrocyanosis often decreases with increasing age, regardless of regional climate. Case reports have found acrocyanosis to be more prevalent in patients with autistic disorders such as Asperger’s Syndrome.

Prognosis
Acrocyanosis is a benign and persistent disease. The main concern of patients is cosmetic. Left untreated, the disease does not worsen.

Newborn Considerations
Acrocyanosis is common initially after delivery in the preterm and full term newborn Intervention normally is not required, although hospitals opt to provide supplemental oxygen for precautionary measures.

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.healthline.com/galecontent/acrocyanosis
http://en.wikipedia.org/wiki/Acrocyanosis_%28benign%29

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