Posts Tagged ‘Symptoms’

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Hashimoto’s Disease – Causes, Symptoms and Treatment Methods

Friday, November 20th, 2009

Hashimoto’s disease is a disease characterized by the immune system attacking the thyroid gland. . A family history of thyroid disorders is common, with the HLADR5 gene most strongly implicated conferring a relative risk of 3 in the UK. The person may experience symptoms of hyperthyroidism at first when the thyroid may really produce too much thyroid hormones. It is caused by a reaction of the immune system hostile to the thyroid gland. Hashimoto’s disease is the most common cause of hypothyroidism in the United States. Hashimoto’s disease, also known as chronic lymphocytic thyroiditis, causes inflammation of your thyroid gland that often leads to underactive thyroid (hypothyroidism). Lymphocytic thyroiditis may also occur as a self-limited condition which lasts 2-6 months, resolving spontaneously, and leaving most patients with normal thyroid gathering. Chronic thyroiditis or Hashimoto’s disease is a common thyroid gland disorder that can occur at any age, but it is most often seen in middle aged women. It is more prevalent in women than in men (8:1), and its incidence increases with age Blood tests of thyroid gathering are used to detect Hashimoto’s disease. Patients with this form of thyroiditis sometimes exhibit so few symptoms that the disease may go unnoticed for many years, but eventually it may ruin so much thyroid tissue that hypothyroidism develops.

Many people with this disease have no symptoms. Hashimoto’s Disease is often referred to as Hashimoto’s thyroiditis, autoimmune thyroiditis, lymphadenoid goiter, struma lymphomatosa, and chronic lymphocytic thyroiditis. Hashimoto’s Thyroiditis is not uncommon. Many people with Hashimoto’s thyroiditis have other endocrine disorders, such as diabetes, an underactive adrenal gland, or underactive parathyroid glands, and other autoimmune diseases, such as pernicious anemia, rheumatoid arthritis, Sjögren’s syndrome, or universal lupus erythematosus (lupus). In many cases, Hashimoto’s thyroiditis usually results in hypothyroidism, although in its acute phase, it can cause a transient thyrotoxic state. Hashimoto’s disease progresses slowly over a number of years and causes chronic thyroid hurt, leading to a drop in thyroid hormone levels in your blood. Less commonly, Hashimoto’s disease occurs with hypoparathyroidism, adrenal lack, and fungal infections of the mouth and nails in a condition called type 1 polyglandular autoimmune syndrome. The thyroid gland typically becomes and the antibodies the body naturally produces to care for the body and fight foreign substances such as bacteria, are found to ‘hit’ their own thyroid tissue. Behavior with synthetic thyroid hormone replacement tablets usually is simple and effective. Natural behavior options also exist.

Causes of Hashimoto’s disease

The common causes and risk factor’s of Hashimoto’s disease include the subsequent:

The exact cause of Hashimoto’s disease is unknown.

A reaction of the immune system hostile to the thyroid gland.

If a name in your family has had thyroid disease, you may have an increased risk for Hashimoto’s disease.

Hashimoto’s thyroiditis is most common among women, particularly older women, and tends to run in families.

It may rarely be associated with other endocrine disorders caused by the immune system.

A combination of factors including heredity, and age may determine your likelihood of developing the disorder.

Hashimoto’s Thyroiditis is seen more frequently in people taking extra iodine in their diets.

Symptoms of Hashimoto’s disease

Some sign and symptoms related to Hashimoto’s disease are as follows:

Fatigue.

Enlarged neck or presence of goiter.

Small or atrophic thyroid gland.

Dry skin.

Joint stiffness.

Excessive tiredness.

Dry, coarse hair.

Facial swelling.

Hair loss.

Heavy and irregular menses.

Hoarse voice.

An elevated blood cholesterol level.

Intolerance to cold.

Most often, people with Hashimoto’s Thyroiditis suffer from symptoms of Hypothyroidism (fatigue, lethargy, decreased metabolic rate).

Behavior of Hashimoto’s disease

Here is list of the methods for treating Hashimoto’s disease:

Iron supplements.

If Hashimoto’s disease causes thyroid hormone deficiency, you may need replacement therapy with thyroid hormone.

Antibiotics to fight infection.

Hormones to suppress or replace thyroid gathering.

Sucralfate, an ulcer tablets.

Long-term prognosis is very excellent. Most people with the disease can be easily treated.

Cholestyramine (Questran), a tablets used to lower blood cholesterol levels.

Replacement therapy with thyroid hormone is given if the hormone is deficient or may be given if there is evidence of mild thyroid failure.

Kawasaki Disease – Causes, Symptoms and Treatment Methods

Thursday, November 12th, 2009

Kawasaki Disease is an illness that involves the skin, mouth, and lymph nodes. The disease usually starts with a fever unresponsive to tylenol or aspirin which continues for at least 7 – 10 days. Many but not all children develop a swollen area on the neck which looks like an infection. Some researchers believe it is an infection, others an autoimmune disorder stimulated by an infection or exposure to an environmental toxin. The disease is seen more often in the winter and spring seasons. Kawasaki disease, or mucocutaneous lymph node syndrome, is a disease of unknown etiology that most frequently (80% of the time) affects infants and children under five years of age. Some doctors reckon it may be caused by a virus or a bacteria. The illness can last from 2 weeks to a few months. Originally, KD was believed to be an acute, self-limiting febrile disease with an brilliant prognosis; but, subsequent reports indicated that nearly 2% of patients with KD died from the illness, usually as a upshot of secondary cardiac sequelae. It was first noticed in Japanese children subsequent World War II. No blood test for Kawasaki disease is available. The diagnosis is based on symptoms.

Kawasaki disease is a poorly understood illness. The male-to-female ratio among patients with Kawasaki disease is 1.5:1. Children of nearly all racial backgrounds are affected. Recurrences and cases in siblings are seen only occasionally. The most vital part of Kawasaki disease is its tendency to cause inflammation of the coronary arteries which supply blood to the heart. Changes can be found on echocardiogram in about 15% of patients. The inflammation is uncomfortable, but resolves with time. But, the main threat from Kawasaki disease comes from its effect on the heart and blood vessels. Affected children develop red eyes, red mucous membranes in the mouth, red cracked lips, a “strawberry tongue” and swollen lymph nodes. Skin rashes occur early in the disease and peeling of the skin in the genital area, hands, and feet (especially around the nails and on the palms and soles) may occur in later phases. Kawasaki disease is a universal vasculitis of unknown etiology that affects the small- and medium-sized blood vessels of the body, in particular, the coronary arteries. Early behavior is effective in preventing this, but first Kawasaki disease must be recognized.

Causes of Kawasaki disease

The common causes and risk factor’s of Kawasaki disease include the subsequent:

The exect cause of Kawasaki Disease is unknown.

Abnormality of the immune system.

Some doctors reckon it may be caused by a virus or a bacteria. The illness can last from 2 weeks to a few months.

Other researchers believe that KD is caused by a unique bacterial toxin.

Several organisms have been investigated as the possible etiologic agents, as follows: mite-associated bacteria, tick-borne diseases, Rickettsia species, Propionibacterium acnes, and several viruses such as Epstein-Barr virus and retroviruses.

Additional risk factors in the United States include Asian race and male.

A small possible link with carpet shampoo or living near a body of stagnant water, but neither of these theories have yet been established.

Symptoms of Kawasaki disease

Some sign and symptoms related to Kawasaki disease are as follows:

Fever.

Swollen hands and feet.

Diarrhea.

Vomiting.

Eye irritation (conjunctivitis) lacking pus.

Fretfulness.

Abdominal pain.

Palms of hands and soles of feet are red; skin starts to peel off fingers and toes about 2 weeks after illness starts.

A swollen lymph node (“gland”) in the neck area.

A red rash.

Red eyes, lacking pus-like discharge.

Behavior of Kawasaki disease

Here is list of the methods for treating Kawasaki disease:

Kawasaki disease is treated with medications. Long-term care may be needed and might include continued tablets, limited physical activity, and repeated testing.

Intravenous gamma globulin (IVIG) is the standard behavior for Kawasaki disease and is administered in high doses with manifest improvement usually noted within 24 hours.

The child may also be given a high-dose of aspirin to reduce the risk of heart problems.

Corticosteroids have also been used with some success, especially when other treatments fail or symptoms recur, but have not usually been considered a first-line therapy.

Plasma Exchange ( Plasmapheresis ) has been reported as effective in patients who were not responding to aspirin and gamma globulin.

Black Lung Disease ? Causes, Symptoms and Treatment

Wednesday, October 7th, 2009

Black lung disease is an occupational lung disease caused by prolonged lungful of air of coal mine dust. Black lung disease is also called silicosis, coal workers’ pneumoconiosis, or black lung. Learn the signs, symptoms, behavior & prevention of black lung disease. Black lung disease is a type of pneumoconiosis, a condition caused by inhaling certain forms of dust into the lungs. Specifically, black lung disease is caused by the lungful of air of coal dust, which tends to turn the lungs black instead of their normal pink color. It occurs only among workers in coal mines, or those in other work situations that cause high exposure to coal dust.

A chronic occupational lung disease contracted by the prolonged breathing of coal mine dust. The silica and carbon in the coal dust cause black lung disease. About one of every 20 miners studied in the US has X-ray evidence of black lung disease, a form of pneumoconiosis. In its early stages, called simple pneumoconiosis, the disease does not prevent the miner from working or carrying on most normal activities. In some miners, the disease never becomes more severe. In other miners, the disease progresses from simple to complicated pneumoconiosis, a condition also called progressive massive fibrosis. Pneumoconiosis is not reversible. There is no specific behavior.

Causes

Some patients develop emphysema (a disease in which the tiny air sacs in the lungs become hurt, leading to shortness of breath, and respiratory and heart failure) as a complication of black lung disease. Others develop a severe type of black lung disease called progressive massive fibrosis, in which hurt continues in the upper parts of the lungs even after exposure to the dust has finished.

Disease of the lungs caused by an accumulation of dust, especially from coal, asbestos, or silica. Inhaled particles make the lungs gradually rubbery and the victim has difficulty breathing. Over many years the condition causes severe disability.

After the emphysema strikes silently in black lung disease, there comes scarring of the lungs and nodule formation in the lung tissues. The symptoms and breathing gathering test results in patients with black lung disease are often much worse than the chest X-ray picture would suggest. There is, unfortinately, no specific behavior for black lung disease.

Symptoms

The primary symptom of the disease is shortness of breath, which gradually gets worse as the disease progresses. In severe cases, the patient may develop cor pulmonale, an enlargement and strain of the right side of the heart caused by chronic lung disease. This may eventually cause right-sided heart failure.

Simple black lung usually does not cause symptoms. But, many people with this disease cough and easily become small of breath because they also have an airway disease, such as bronchitis or emphysema, and these are more likely to occur in smokers. The severe stages of progressive massive fibrosis, on the other hand, cause coughing and often disabling shortness of breath.

Behavior

Unfortunately, there’s no specific behavior for black lung disease. People whose lung impairment has reached the point that they would benefit from supplemental oxygen, or extra oxygen at home, would certainly receive oxygen. Other than that, there’s unfortunately no specific medicine that reverses the hurt that’s been done to the lungs. The hurt that’s done could be thought of as a scar, and just as you might have a scar on your arm that doesn’t go away or doesn’t heal, scars, or fibrosis inside the lungs don’t go away any.

Paget’s Disease – Definition, Causes, Symptoms and Treatment

Friday, September 25th, 2009

Paget’s disease is the following most common bone disease. Paget’s disease is a chronic bone disorder that is due to irregular breakdown and formation of bone tissue.The disease occurs worldwide, but is more common in Europe, Australia, and New Zealand — where it is seen in up to 5% of the elderly population. Paget’s disease can cause bones to expand and weaken and may upshot in bone pain, arthritis, bone deformity and breaks. Men and women are approximately equally affected. The prevalence of Paget’s disease ranges from 1.5 to 8% depending on age and country of residence. The prevalence of family Paget’s disease (where more than one family member has the disease) ranges from 10 to 40% in different parts of the world. It is usually localized to one bone, but can involve many bones. The actual cause of Paget’s disease is not known. Paget’s disease is also known as osteitis deformans. The disease may localize to one or two areas within the skeleton, or become widespread. Frequently, bones of the pelvis, leg, spine, arm, or the collar bone are involved. The effect on the skull may enlarge head size and cause hearing loss, if the cranial nerves are hurt by the bone growth.

Paget’s disease may affect only one or two areas of your body, or may be widespread. Paget’s disease tends to appear in families. It can be present in as many as 25 percent to 40 percent of the relatives of a name with the disease. It is also more common in people of Anglo-Saxon descent. Many patients do not know they have Paget’s disease because they have a mild case with no symptoms. Sometimes, symptoms may be confused with those of arthritis or other disorders. Symptoms can arise from the effect on calcium levels in the blood stream. When Paget’s disease is active in several bones, the overactive osteoclasts can release enough calcium from the bone as they break it down to cause an elevated calcium level in the blood. This rare complication might cause fatigue, weakness, loss of appetite, abdominal pain, or constipation. A doctor can also detect Paget’s disease from its effect on the heart if excess blood supply is shunted to overactive bones in severe cases. When pain is severe and unrelenting in an area affected by Paget’s disease, the disease may have degenerated into a bone cancer. Paget’s sarcoma (Figure 6) occurs in only about 1 percent of patients with Paget’s disease. These patients are usually older than 70 years of age. This type of malignant bone tumor is very aggressive and carries a poor prognosis.

Paget’s disease occurs most frequently in the spine, skull, pelvis, thighs, and lower legs. Paget’s disease may be caused by a slow virus infection (i.e., paramyxoviruses such as measles and respiratory syncytial virus). Paget’s disease of bone, though they have exposed several genes that appear to be linked to the disorder. Hereditary factors seem to influence whether you’re susceptible to the disease. Environmental factors may also play a role. Several studies have postulated that viruses, particularly paramyxoviruses such as canine distemper or measles virus, play a role in pathogenesis, but definitive evidence for this is missing. Presumably, the declining incidence of Paget’s disease reflects a decline in one or more as yet unidentified environmental influences. The SQSTM1/p62 protein is a selective activator of the transcription factor NFB, which plays an vital role in osteoclast differentiation and activation in response to the cytokines RANK-ligand and interleukin-1.Mutations in the SQSTM1/p62 gene are consequently a plausible cause of Paget’s disease. Germline DNA mutations (present in every osteoclast) cause bone disease that is focal in nature.

Medical are commonly treating Paget’s disease. Behavior include is aspirin, other anti-inflammatory medications, pain medications, and medications that slow the rate of bone turnover, such as calcitonin (Calcimar, Miacalcin), etidronate (Didronel), alendronate (Fosamax), and pamidronate (Aredia). Surgery is used primarily to treat the complications of Paget’s disease. A newer drug, risedronate (Actonel), appears to have a powerful effect hostile to severe Paget’s disease. Miacalcin is administered by injection; 50 to 100 units daily or 3 times per week for 6-18 months. Didronel (etidronate disodium) — Tablet; approved regimen is 200-400 mg once daily for 6 months; the higher dose (400 mg) is more commonly used; no food, beverages, or medications for 2 hours before and after taking. Fosamax (alendronate sodium) — Tablet; 40 mg once daily for 6 months; patients should wait at least 30 minutes after taking before eating any food, drinking anything other than tap water, taking any tablets, or lying down (patient may sit). Eating a healthy diet with sufficient calcium and vitamin D and getting exercise are vital components in maintaining skeletal shape and joint mobility.

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