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Friday 8 March 2013
Saturday 7 April 2012
THYROID DISORDERS: Sujok Accupuncher Accupressure
THYROID DISORDERS
Introduction to thyroid disease
The thyroid gland or simply, the thyroid in vertebrate anatomy, is one of the largest endocrine glands. The thyroid gland is found in the neck, below the thyroid cartilage (which forms the laryngeal prominence, or "Adam's apple"). The isthmus (the bridge between the two lobes of the thyroid) is located inferior to the cricoid cartilage.
The thyroid gland controls how quickly the body uses energy, makes proteins, and controls how sensitive the body is to other hormones. It participates in these processes by producing thyroid hormones, the principal ones being triiodothyronine (T3) and thyroxine which can sometimes be referred to as tetraiodothyronine (T4). These hormones regulate the rate of metabolism and affect the growth and rate of function of many other systems in the body. T3and T4 are synthesized from both iodine and tyrosine. The thyroid also produces calcitonin, which plays a role in calcium homeostasis.
The thyroid gets its name from the Greek word for "shield", due to the shape of the related thyroid cartilage. The most common problems of the thyroid gland consist of an overactive thyroid gland, referred to as hyperthyroidism, and an underactive thyroid gland, referred to ashypothyroidism.
Thyroid and parathyroid |
When I was asked to write an article on "thyroid disease", I took a very deep breath. The task seemed daunting. As any Endocrinologist (hormonespecialist) knows, there are many subtopics within this giant topic, and an article like this could go on for a hundred pages! So, once I caught my breath, I decided to simply design this article to present a "rough guide" to the thyroid. This article will be an outline or introduction to many conditions that involve the thyroid gland. As you read through this, you will find a number of links that will take you to more in-depth articles dealing with the specific topic in question.
Thyroid 101: What is the thyroid and what does it do?
The thyroid is a butterfly-shaped gland located in the front of the neck just below the Adams apple. The gland wraps around thewindpipe (trachea) and has a shape that is similar to a butterfly formed by two wings (lobes) and attached by a middle part (isthmus). The thyroid gland works like a tiny factory that usesiodine (mostly from the diet in foods such as seafood and salt) to produce thyroid hormones. These hormones help to regulate the body's metabolism and effects processes, such as growth and other important functions of the body.
The two most important thyroid hormones are thyroxine (T4) andtriiodothyronine (T3), representing 99.9% and 0.1% of thyroid hormones respectively. The hormone with the most biological power is actually T3. Once released from the thyroid gland into the blood, a large amount of T4 is converted to T3 - the active hormone that affects the metabolism of cells throughout our body.
What is the Thyroid?
The thyroid is a small gland, shaped like a butterfly, located in the lower part of your neck. The function of a gland is to secrete hormones. The main hormones released by the thyroid are triiodothyronine, abbreviated as T3, and thyroxine, abbreviated as T4. These thyroid hormones deliver energy to cells of the body.
Your thyroid gland is a small, butterfly-shaped gland located just below your Adam's apple. The thyroid produces hormones that affect your body's metabolism and energy level. Thyroid problems are among the most common medical conditions but, because their symptoms often appear gradually, they are commonly misdiagnosed.
The three most common thyroid problems are the underactive thyroid, the overactive thyroid , and thyroid nodules.
HYPOTHYROIDISM (Underactive thyroid)
The most common cause of hypothyroidism is Hashimoto's thyroiditis. In this condition, the body's immune system mistakenly attacks the thyroid gland.
Common symptoms of hypothyroidism are:
Common symptoms of hypothyroidism are:
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Hypothyroidism
When the thyroid gland is underactive, improperly formed at birth, surgically removed all or in part, or becomes incapable of producing enough thyroid hormone, a person is said to be hypothyroid. One of the most common causes of hypothyroidism is the autoimmune disease called Hashimoto's disease, in which antibodies gradually target the thyroid and destroy its ability to produce thyroid hormone.
Symptoms of hypothyroidism usually go along with a slowdown in metabolism, and can include fatigue, weight gain, and depression, among others.
Symptoms of hypothyroidism usually go along with a slowdown in metabolism, and can include fatigue, weight gain, and depression, among others.
The symptoms of hypothyroidism -- an underactive thyroid -- tend to mirror the slowing down of physical processes that results from insufficient thyroid hormone. Common symptoms include fatigue, weight gain, constipation, fuzzy thinking, low blood pressure, fluid retention, depression, body pain, slow reflexes, and much more.
HYPERTHYROIDISM (Overactive Thyroid)
The most common cause of hyperthyroidism is Graves' disease. This occurs when the body's immune system overstimulates the thyroid.
Common symptoms of hyperthyroidism are:
Common symptoms of hyperthyroidism are:
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When the thyroid gland becomes overactive and produces too much thyroid hormone, a person is said to be hyperthyroid. The most common cause of hyperthyroidism is the autoimmune condition known as Graves' disease, where antibodies target the gland and cause it to speed up hormone production.
Most thyroid dysfunction such as hypothyroidism or hyperthyroidism is due to autoimmune thyroid disease. Autoimmune disease refers to a condition where the body's natural ability to differentiate between its tissues, organs and glands, vs. outside bacteria, viruses or pathogens, becomes disrupted. This causes the immune system to wrongly mount an attack on the affected area, by producing antibodies. In the case of autoimmune thyroid disease, antibodies either gradually destroy the thyroid, or make it overactive.
The two autoimmune diseases that directly affect the thyroid are Hashimoto's disease and Graves' disease. The symptoms of Hashimoto's disease usually parallel the hypothyroidism that is a result of the disease. Occasionally, however, while the thyroid is failing, it can have periods where it sputters into life and even becomes temporarily overactive. This is known as Hashitoxicosis. Symptoms then can be confusing, with cycling over a period of days or weeks between hypothyroidism and hyperthyroidism symptoms. To understand the difference between hypothyroidism and Hashimoto's disease,
Goiter/Thyroid Nodules
Sometimes the thyroid becomes enlarged -- due to Hashimoto's disease, Graves' disease, nutritional deficiencies, or other thyroid imbalances. When the thyroid become enlarged, this is known as a goiter.
Some people develop solid or liquid filled cysts, lumps, bumps and tumors -- both benign and cancerous -- in the thyroid gland. These are known as thyroid nodules.
Some people develop solid or liquid filled cysts, lumps, bumps and tumors -- both benign and cancerous -- in the thyroid gland. These are known as thyroid nodules.
Symptoms of goiter -- an enlarged thyroid -- include a swollen, tender or tight feeling in the neck or throat, hoarseness or coughing, and difficulty swallowing or breathing. Sometimes, the goiter is visbible to yourself or others.
Symptoms of nodules depend on what action they are having. Some cause no symptoms, while others may cause difficulty swallowing, a feeling of fullness, pain or pressure in the neck, a hoarse voice, or neck tenderness. Some nodules trigger hyperthyroid-like symptoms such as palpitations, insomnia, weight loss, anxiety, and tremors. Nodules can also trigger hypothyroidism, and symptoms might include weight gain, fatigue, depression. Nodules can sometimes cause cycling back and forth between hyperthyroid and hypothyroid symptoms.
What types of thyroid disease can occur when the function of the thyroid is affected??
If the thyroid itself is under-active, or if the regulators of the thyroid gland are not functioning properly, hypothyroidism can result. There are many causes ofhypothyroidism such as the following:
- Hashimoto's thyroiditis (autoimmune thyroiditis)
- Postpartum thyroiditis (inflammation of the thyroid gland after pregnancy)
- Acute thyroiditis
- Silent thyroiditis
- Thyroid hormone resistance
What types of thyroid disease can occur when the structure of the thyroid is affected??
Structural problems with the thyroid gland can occasionally result in altered function, such as toxic multinodular goiter and toxic nodules (adenomas) leading to hyperthyroidism. However, in most cases, structural problems occur in glands that have normal function. These conditions range from simple and benign cysts to more serious problems such as thyroid cancers (papillary, follicular, medullary and anaplastic are the different types of thyroid cancer that may arise). Enlargement of the thyroid gland is referred to as a goiter. Goiters can form and can range in size from hardly noticeable to large enough to require surgical removal. Additionally, the actual location of the thyroid in an individual can be in an abnormal area of the body due to developmental abnormalities.
Risk Factors for Thyroid Disease
Some of the key risk factors for thyroid disease include...- Female: Women are at greater risk than men.
- Age - being 50 and above poses the highest risk of thyroid disease, though it can strike at any age.
- A personal or family history of thyroid and/or autoimmune disease increases risk.
- Surgical removal of all or part of the thyroid, or radioactive iodine treatment to the thyroid -- both which typically result in an underactive thyroid.
- Being left-handed, ambidextrous or prematurely gray mean greater risk of autoimmune disease, including thyroid problems
- Being pregnant or within the first year after childbirth
- Current or former smoker
- Recent exposure to iodine via contrast dye or surgical antiseptic
- Iodine or herbal supplements containing iodine, in pill or liquid form
- Living in an iodine-deficient area
- Various medical treatments, including Interferon Beta-1b, Interleukin-4, immunosuppressants, antiretrovirals, monoclonal antibody (Campath-1H), bone marrow transplant, Lithium, amiodarone (Cordarone), and other medications
- Overconsumption of raw goitrogenic foods, i.e., Brussel sprouts, turnips, cauliflower, soy products and others
- Overconsumption of soy foods
- Recent neck trauma, biopsy, injection or surgery
- Radiation exposure, through radiation to neck area, or exposure to nuclear facility or accident, i.e., Chernobyl
- High stress life events
Thyroid hormone regulation - the chain of command
The thyroid itself is regulated by another gland located in the brain, called the pituitary. In turn, the pituitary is regulated in part by the thyroid (via a "feedback" effect of thyroid hormone on the pituitary gland) and by another gland called the hypothalamus.
The hypothalamus releases a hormone called thyrotropin releasing hormone (TRH), which sends a signal to the pituitary to release thyroid stimulating hormone (TSH). In turn, TSH sends a signal to the thyroid to release thyroid hormones. If overactivity of any of these three glands occurs, an excessive amount of thyroid hormones can be produced, thereby resulting inhyperthyroidism. Similarly, if underactivity of any of these glands occurs, a deficiency of thyroid hormones can result, causing hypothyroidism.
Hypothalamus - TRH
Pituitary- TSH
Thyroid - T4 and T3
The rate of thyroid hormone production is controlled by the pituitary gland. If there is an insufficient amount of thyroid hormone circulating in the body to allow for normal functioning, the release of TSH is increased by the pituitary in an attempt to stimulate more thyroid hormone production. In contrast, when there is an excessive amount of circulating thyroid hormone, TSH levels fall as the pituitary attempts to decrease the production of thyroid hormone.
There is another hormone that is produced by the thyroid called calcitonin. Calcitonin is produced by specific cells in the thyroid gland, and unlike T3 and T4, it is not involved in this regulation of metabolism. Calcitonin is a hormone that contributes to the regulation of calcium and helps to lower calcium levels in the blood. Excess calcium in the blood is referred to ashypercalcemia.
Thyroid Cancers
Main article: Thyroid cancer
Cancers do occur in the thyroid gland and are more common in females In most cases, the thyroid cancer presents as a painless mass in the neck. It is very unusual for the thyroid cancers to present with symptoms, unless it has been neglected. One may be able to feel a hard nodule in the neck.
[edit]Non-cancerous nodules
Further information: Thyroid nodule
Many individuals may find the presence of thyroid nodules in the neck. The majority of these thyroid nodules are benign (non cancerous). The presence of a thyroid nodule does not mean that one has thyroid disease. Most thyroid nodules do not cause any symptoms, and most are discovered on an incidental examination. Doctors usually perform a needle aspiration biopsy of the thyroid to determine the status of the nodules. If the nodule is found to be non-cancerous, no other treatment is required. If the nodule is suspicious then surgery is recommended.
[edit]Congenital anomalies
A persistent thyroglossal duct or cyst is the most common clinically significant congenital anomaly of the thyroid gland. A persistent sinus tract may remain as a vestigial remnant of the tubular development of the thyroid gland. Parts of this tube may be obliterated, leaving small segments to form cysts. These occur at any age and might not become evident until adult life. Mucinous, clear secretions may collect within these cysts to form either spherical masses or fusiform swellings, rarely larger than 2 to 3 cm in diameter. These are present in the midline of the neck anterior to the trachea. Segments of the duct and cysts that occur high in the neck are lined by stratified squamous epithelium, which is essentially identical to that covering the posterior portion of the tongue in the region of the foreamen cecum. The anomalies that occur in the lower neck more proximal to the thyroid gland are lined by epithelium resembling the thyroidal acinar epithelium. Characteristically, next to the lining epithelium, there is an intense lymphocytic inflitrate. Superimposed infection may convert these lesions into abscess cavities, and rarely, give rise to cancers.
==================================
For best treatment
Sujok Accupuncher Accupressure
Contact :
Sanjay Verma
Sai Accupuncher / Acupressure
1 Vynktesh Nagar, Airport Road Indore 452005 India
E : sanjayverma0289@yahoo.com
M : 0091 99811 25993 / 91 8269318533
B : www.sujok-accupressure.blogspot.com
B : www.Sujok-Accupuncher-Accupressure.blogspot.com
http://sujok-accupuncher.blogspot.in/
Tuesday 27 March 2012
Gout:Sujok Accupuncher Accupessure
Gout
INTRODUCTION:
Gout (also known as podagra when it involves the big toe)[1] is a medical condition usually characterized by recurrent attacks of acute inflammatory arthritis—a red, tender, hot, swollen joint. The metatarsal-phalangeal joint at the base of the big toe is the most commonly affected (approximately 50% of cases). However, it may also present as tophi, kidney stones, or urate nephropathy. It is caused by elevated levels of uric acid in the blood which crystallizes and the crystals are deposited in joints, tendons, and surrounding tissues.
History
The word gout was initially used by Randolphus of Bocking, around 1200 AD. It is derived from theLatin word gutta, meaning "a drop" (of liquid).[48] According to the Oxford English Dictionary, this is derived from humorism and "the notion of the 'dropping' of a morbid material from the blood in and around the joints".[49]
Gout has, however, been known since antiquity. Historically, it has been referred to as "the king of diseases and the disease of kings"[6][50] or "rich man's disease".[51] The first documentation of the disease is from Egypt in 2,600 BC in a description of arthritis of the big toe. The Greek physicianHippocrates around 400 BC commented on it in his Aphorisms, noting its absence in eunuchs andpremenopausal women.[48][52] Aulus Cornelius Celsus (30 AD) described the linkage with alcohol, later onset in women, and associated kidney problems:
Again thick urine, the sediment from which is white, indicates that pain and disease are to be apprehended in the region of joints or viscera... Joint troubles in the hands and feet are very frequent and persistent, such as occur in cases of podagra and cheiragra. These seldom attack eunuchs or boys before coition with a woman, or women except those in whom the menses have become suppressed... some have obtained lifelong security by refraining from wine, mead and venery.[53]
While in 1683, Thomas Sydenham, an English physician, described its occurrence in the early hours of the morning, and its predilection for older males:
Gouty patients are, generally, either old men, or men who have so worn themselves out in youth as to have brought on a premature old age - of such dissolute habits none being more common than the premature and excessive indulgence in venery, and the like exhausting passions. The victim goes to bed and sleeps in good health. About two o'clock in the morning he is awakened by a severe pain in the great toe; more rarely in the heel, ankle or instep. The pain is like that of a dislocation, and yet parts feel as if cold water were poured over them. Then follows chills and shivers, and a little fever... The night is passed in torture, sleeplessness, turning the part affected, and perpetual change of posture; the tossing about of body being as incessant as the pain of the tortured joint, and being worse as the fit comes on.
INTRODUCTION:
Gout (also known as podagra when it involves the big toe)[1] is a medical condition usually characterized by recurrent attacks of acute inflammatory arthritis—a red, tender, hot, swollen joint. The metatarsal-phalangeal joint at the base of the big toe is the most commonly affected (approximately 50% of cases). However, it may also present as tophi, kidney stones, or urate nephropathy. It is caused by elevated levels of uric acid in the blood which crystallizes and the crystals are deposited in joints, tendons, and surrounding tissues.
Gout has increased in frequency in recent decades affecting approximately one to two percent of the Western population at some point in their lives. The increase is believed to be due to increasing risk factors in the population, such as metabolic syndrome, longer life expectancyand changes in diet. Gout was historically known as "the disease of kings" or "rich man's disease".
Frequently Asked Questions about Gouty Arthritis
What is gouty arthritis?
Gout is a painful form of inflammatory arthritis caused by an accumulation of uric acid crystals in the joints. Crystals form when there are supraphysiologic levels of serum uric acid.
How common is gout?
Gout affects more than 8.3 million people in the United States today; a sharp increase from only 5 million suffers just a few years ago.
What symptoms would my patient suffer?
Gout is characterized by sudden, severe pain in the affected joint. Half of all first-time gout attacks occur in the large joint of the patient’s great toe, but many other joints can be affected as well, particularly the forefoot, ankle, knee and wrist. Tenderness, redness, stiffness and/or swelling of the joint occur.
The first gout attack can seem like an isolated incident, but will recur within a year in at least 20 percent of individuals.
What are the key risk factors for gout?
- Hyperuricemia
- Metabolic syndrome
- Binge drinking, particularly beer
- Family history of gout
- Persons who have received transplants and are on cyclosporin
Signs and symptoms
Gout can present in a number of ways, although the most usual is a recurrent attack of acuteinflammatory arthritis (a red, tender, hot, swollen joint).[2] The metatarsal-phalangeal joint at the base of the big toe is affected most often, accounting for half of cases.[3] Other joints, such as the heels, knees, wrists and fingers, may also be affected.[3] Joint pain usually begins over 2–4 hours and during the night.[3] The reason for onset at night is due to the lower body temperature then.[1]Other symptoms that may occur along with the joint pain include fatigue and a high fever.[1][3]
Long-standing elevated uric acid levels (hyperuricemia) may result in other symptomatology, including hard, painless deposits of uric acid crystals known as tophi. Extensive tophi may lead to chronic arthritis due to bone erosion.[4] Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stone formation and subsequent urate nephropathy.[5]
Cause
Hyperuricemia is the underlying cause of gout. This can occur for a number of reasons, including diet, genetic predisposition, or underexcretion of urate, the salts of uric acid.[2] Renal underexcretion of uric acid is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%.[6] About 10% of people with hyperuricemia develop gout at some point in their lifetimes.[7] The risk, however, varies depending on the degree of hyperuricemia. When levels are between 415 and 530 μmol/L (7 and 8.9 mg/dL), the risk is 0.5% per year, while in those with a level greater than 535 μmol/L (9 mg/dL), the risk is 4.5% per year.[1]
Lifestyle
Dietary causes account for about 12% of gout,[2] and include a strong association with the consumption of alcohol, fructose-sweetened drinks, meat, and seafood.[4][8] Other triggers include physical trauma and surgery.[6] Recent studies have found dietary factors once believed to be associated are, in fact, not; including the intake of purine-rich vegetables (e.g., beans, peas, lentils, and spinach) and total protein.[9][10]The consumption of coffee, vitamin C and dairy products as well as physical fitness appear to decrease the risk.[11][12][13] This is believed to be partly due to their effect in reducing insulin resistance.[13]
Genetics
The occurrence of gout is partly genetic, contributing to about 60% of variability in uric acid level.[6] Two genes called SLC2A9 and ABCG2have been found to commonly be associated with gout and variations in them can approximately double the risk.[14] A few rare genetic disorders, including familial juvenile hyperuricemic nephropathy, medullary cystic kidney disease, phosphoribosylpyrophosphate synthetasesuperactivity, and hypoxanthine-guanine phosphoribosyltransferase deficiency as seen in Lesch-Nyhan syndrome, are complicated by gout.[6]
Medical conditions
Gout frequently occurs in combination with other medical problems. Metabolic syndrome, a combination of abdominal obesity, hypertension,insulin resistance and abnormal lipid levels occurs in nearly 75% of cases.[3] Other conditions that are commonly complicated by gout include: polycythemia, lead poisoning, renal failure, hemolytic anemia, psoriasis, and solid organ transplants.[6][15] A body mass indexgreater than or equal to 35 increases a male's risk of gout threefold.[10] Chronic lead exposure and lead-contaminated alcohol are risk factors for gout due to the harmful effect of lead on kidney function.[16] Lesch-Nyhan syndrome is often associated with gouty arthritis.
Medication
Diuretics have been associated with attacks of gout. However, a low dose of hydrochlorothiazide does not seem to increase the risk.[17]Other medicines that have been associated include niacin and aspirin (acetylsalicylic acid).[4] The immunosuppressive drugs ciclosporin andtacrolimus are also associated with gout,[6] the former particularly when used in combination with hydrochlorothiazide.[18]
Pathophysiology
Gout is a disorder of purine metabolism,[6] and occurs when its final metabolite, uric acid, crystallizes in the form of monosodium urate, precipitating in joints, on tendons, and in the surrounding tissues.[4] These crystals then trigger a local immune-mediated inflammatoryreaction[4] with one of the key proteins in the inflammatory cascade being interleukin 1β.[6] An evolutionary loss of uricase, which breaks down uric acid, in humans and higher primates is what has made this condition so common.[6]
The triggers for precipitation of uric acid are not well understood. While it may crystallize at normal levels, it is more likely to do so as levels increase.[4][19] Other factors believed to be important in triggering an acute episode of arthritis include cool temperatures, rapid changes in uric acid levels,acidosis,[20][21] articular hydration, and extracellular matrix proteins, such as proteoglycans,collagens, and chondroitin sulfate.[6] The increased precipitation at low temperatures partly explains why the joints in the feet are most commonly affected.[2] Rapid changes in uric acid may occur due to a number of factors, including trauma, surgery, chemotherapy, diuretics, and stopping or starting allopurinol.[1] Calcium channel blockers and losartan are associated with a lower risk of gout as compared to other medications for hypertension. [22]
Prevention
Both lifestyle changes and medications can decrease uric acid levels. Dietary and lifestyle choices that are effective include reducing intake of food such as meat and seafood, consuming adequate vitamin C, limiting alcohol and fructose consumption, and avoiding obesity.[2] A low-calorie diet in obese men decreased uric acid levels by 100 µmol/L (1.7 mg/dL).[17] Vitamin C intake of 1,500 mg per day decreases the risk of gout by 45%.[30] Coffee, but not tea, consumption is associated with a lower risk of gout.[31] Gout may be secondary to sleep apnea via the release of purines from oxygen-starved cells. Treatment of apnea can lessen the occurrence of attacks.[32]
Prognosis
Without treatment, an acute attack of gout will usually resolve in 5 to 7 days. However, 60% of people will have a second attack within one year.[1] Those with gout are at increased risk of hypertension, diabetes mellitus, metabolic syndrome, and renal and cardiovascular diseaseand thus at increased risk of death.[6][44] This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be independent.[44]
Without treatment, episodes of acute gout may develop into chronic gout with destruction of joint surfaces, joint deformity, and painless tophi.[6] These tophi occur in 30% of those who are untreated for five years, often in the helix of the ear, over the olecranon processes, or on the Achilles tendons.[6] With aggressive treatment, they may dissolve. Kidney stones also frequently complicate gout, affecting between 10 and 40% of people, and occur due to low urine pH promoting the precipitation of uric acid.[6] Other forms of chronic renal dysfunction may occur.[6]
- Nodules of the finger and helix of the ear representing gouty tophi
- Gout complicated by ruptured tophi (exudate tested positive for uric acid crystals)==================================For best treatmentSujok AccupuncherAccupessureContact :Sanjay VermaSai Accupuncher / Acupressure1 Vynktesh Nagar, Airport Road Indore 452005 IndiaE : sanjayverma0289@yahoo.comM : 0091 99811 25993 /91 8269318533B : www.sujok-accupressure.blogspot.comB : www.Sujok-Accupuncher-Accupressure.blogspot.comhttp://sujok-accupuncher.blogspot.in/---------------------------
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