Essay on Grave’s Disease: A Lifelong Commitment

Hashimoto’s Disease is a chronic Lymphocytic thyroiditis also known as autoimmune thyroiditis. It is due to chronic inflammation; the disease is a failure of the thyroid gland. Hashimoto’s disease is the most common inflammatory disorder of the thyroid and the leading cause of having hypothyroidism. The name of the disease came from a Japanese surgeon named Hashimoto Hakaru. Hakaru first described the chronic disease as Struma Lymphomatosa in a pathology report in the year 1912. Hashimoto’s Disease is a genetic trait and found to be more common in women then in men; and commonly found in women between the ages of thirty to fifty years of age. Hashimoto’s Disease can be found in children too; in the first-degree relatives that have the disease is found to have an increased incident.

Graves ' disease is an immune system disorder that results in the overproduction of thyroid hormones (hyperthyroidism). The thyroid gland is an important organ of the endocrine system. The gland is located at the front of the neck above where the collarbones meet. This gland releases the hormones thyroxine (T4) and triiodothyronine (T3), which control body metabolism. Controlling metabolism is important for regulating mood, weight, and mental and physical energy levels. When the body makes too much thyroid hormone, the condition is called hyperthyroidism. Graves disease is the most common cause of hyperthyroidism and is most common in women over age 20. But the disorder can occur at any age and can affect men as well. Some of the symptoms of Graves diseases are

Experts aren’t sure the exact cause of Graves’ disease because it is an autoimmune disease. There are certain risk factors associated with Graves’ disease which include genetics, gender, age, pregnancy, mental stress, and smoking. People who have family history of this disease are more likely to develop it. Also females are more likely than males to acquire Graves’ disease and onset of the disease usually occurs after the age of 20. Anatomy affected by this disease is the thyroid gland which is part of the endocrine system. It is located at the back of the neck, below the Adam’s apple. This disease doesn’t destroy the thyroid gland, instead an antibody called thyrotropin receptor antibody makes the thyroid produce large amounts of hormone. The thyroid produces two hormones, thyroxine and triiodothyronine. These hormones affect many body systems and play a key role in regulating the body’s metabolic rate. Excessive secretion of these hormones is what causes the signs and symptoms that have already been described.

Hashimoto’s Thyroiditis, also called Hashimoto’s disease is an autoimmune disease in which the body’s immune system attacks the thyroid gland. It was named for the Japanese surgeon who discovered it in 1912 The thyroid is a small butterfly shaped gland in the front of the neck. The thyroid makes hormones called T3 and T4. These hormones regulate metabolism. The thyroid is controlled by hormones of the pituitary gland, which is also called the “master gland.” It is a pea-sized gland located in the base of the brain which, among others, makes thyroid stimulating hormone, or TSH. TSH stimulates the thyroid to make thyroid hormone. With Hashimoto’s disease, the thyroid cells are damaged resulting in the inability to make enough thyroid

Hashimoto thyroiditis is a common disease caused by hypothyroidism. The immune system cells attack the thyroid gland, causing inflammation and eventually destruction of the gland. This reduces the thyroids ability to make hormones. These hormones are known as thyroxine (T4) and tri-iodothyronine (T3) (Better health channel 2015).

Hashimoto’s Thyroiditis can also come as an attack on the thyroid via an autoimmune disorder. The immune system can attack the thyroid; however, no one knows exactly why this

Although the disease often occurs in adolescent or young women, it more commonly appears between 30 and 50 years of age.

However Graves' disease is named after the Irish physician who described several cases in London Medical Journal in 1835. Graves' disease is also known as Parry's disease. In Europe, the disease is known as Basedow's disease. It is the most common cause of thyrotoxicosis (the morbid condition due to over activity of the thyroid gland).

Graves’ disease is autoimmune that effects the thyroid in front of the neck. This thyroid creates T3 and T4 which helps regulate how the body uses energy. We have a small gland called pituitary in the brain that helps the thyroid regulate the hormone level properly. With grave’s disease the immune system creates antibodies that act like TSH (thyroid stimulating hormone) which than makes the thyroid to create more hormones than what the body needs to have. This is called hyperthyroidism. Graves’ disease causes the body to speed up such as the heart and the metabolism. The symptoms for graves’ disease are goiter (enlarged gland) Anxiety and irritability, A fine tremor of your hands or fingers, Heat sensitivity and an increase in perspiration

Grave’s Disease is an autoimmune disease that affects the thyroid and its hormone production. Normally, a healthy immune system releases antibodies that are designed to attack bacteria and viruses. In addition to antibodies, the thyroid creates hormones that regulate overall hormone production. With Grave’s Disease, the immune system releases antibodies that imitate these thyroid hormones; this leads to overproduction of hormones, or hyperthyroidism. Doctors are not sure as to what exactly causes Grave’s disease, but it is speculated that factors such as age play a role; as in, younger people are typically more prone to this illness. Its symptoms include anxiety; sweating; heart

Hyperthyroidism (too much hormone) may result Grave's disease. Symptoms include anxiety, rapid heart rate, diarrhea and weight loss, nervousness, anxiety, and irritability.

The main cause of hyperthyroidism Graves’ disease which affects quite a few people in the general population. This disease is characterized as an autoimmune disorder. This means that the body makes antibodies known as thyroid stimulating immunoglobulin that bind and over activate the production of thyroid hormones [3]. So in essence the antibody mimics the thyroid stimulating hormone and when the negative feedback loop is in affect the antibody still binds to the thyroid and T3 and T4 are over produced [2].

The first disease I’m going to mention is Glaucoma, according to Web MD last updated in 2015, Glaucoma is a condition that causes damage to your eye's optic nerve and gets worse over time. It's often associated with a buildup of pressure inside the eye. Glaucoma tends to be inherited and may not show up until later in life.

The central effects of hyperthyroidism are most pronounced in development. Cerebral circulation and oxygen consumption elevate. "In hyperthyroidism, Beta-adrenergic binding sites in the cerebral cortex increases and gamma-aminobutyric acid (GABA) binding sites are decreases." (Bucurescu,2014). Brain levels of serotonin, 5-hydroxyindoleacetic acid, and substance P are altered. Native pain sensitivity and number of opiate receptors are increases. Thyroid hormones affect myelination, therefore increased levels lead to oxidative damage to the myelin membrane and/or the oligodendroglial cells. The neurological manifestation is primarily due to the effect of thyroid hormones on other neurotransmitters, hormones, and generalized increased basal metabolic rate. Some of the neurological symptoms are:

Grave’s disease (GD) is rare in childhood (1); however, it is the most common cause of hyperthyroidism in children and adolescents (2). Graves’s orbitopathy (GO) is the most common extrathyroid manifestation of GD but it can be present in 5 to 10% of euthyroid patients (3). Usually, both eyes are equally affected, although 9% of patients may present an asymmetric form (4). It can develop before, during or after the onset of hyperthyroidism (5), but presents a wide range of atypical presentations that reveal a pathogenesis still enigmatic. The evidence indicates that anti-TSHR antibodies are probably responsible for the genesis of the GO, and there are some polymorphisms that show a high enough risk of GO suggesting a complex genetic basis (6).