Disease Treatment And Quality Of Life

Graves’ disease was named after Robert J. Graves, MD, around the 1830’s. It is an autoimmune disease indicated by hyperthyroidism due to circulating autoantibodies, which is an antibody that attacks the person’s own body. The immune system attacks the thyroid gland, which causes it to produce too much thyroxine. Thyroxine is a hormone that helps control growth and also regulates metabolism in the body. While the thyroxine levels are high the patient’s metabolic rate increases, which can have an effect on their physical appearance as well as their frame of mind. Graves’ disease is the number one cause of hyperthyroidism in the U.S.

Hashimoto’s thyroiditis has a higher prevalence in women, frequency increases with age, and it is hereditary, commonly occurring in people and their family members with other autoimmune diseases, specifically Graves’ disease (Garber et al., 2012). It is caused by autoimmune-mediated destruction of the thyroid gland, and is characterized by gradual thyroid failure, goiter development, or both (Davies, 2012). The following presentation is a case study for Hashimoto’s

Whereas Hashimoto’s is an under active or under developed thyroid gland, Graves’ disease is the opposite. Graves' disease is an immune system disorder that results in the overproduction of thyroid hormones, better known as hyperthyroidism. Although a number of disorders may result in hyperthyroidism, Graves' disease is a common cause. (http://www.mayoclinic.org/diseases-conditions/graves-disease/basics/definition/con-20025811)

Diagnosis of a thyroid disorder is based on the levels of thyroid-stimulating hormone, thyroxine T4) and triiodothyronine (T3) in the blood (McCance & Huether, 2014). When these levels are not within range, either hypothyroidism or hyperthyroidism can occur. With Graves disease the dysfunction is directly linked to a hypersensitivity type II, which targets auto antibodies to a specific tissue (McCance & Huether, 2014). These antibodies are known as thyroid-stimulating immunoglobins (McCance & Huether, 2014).

Karen Holt describes in her 2010 article Graves’ Disease: Clinical Pathophysiology, Presentation and Treatment Options of certain genetic markers that cause the blood vessels surrounding the thyroid gland to dilate, most often occurring in the second to third decade of life. The dilation of these vessels causes an increase in blood flow and thyroid-stimulating antibodies excite thyrotropin receptors on the gland itself in the same manner that TSH usually works. These antibodies, known as TSAb, bypass the negative feedback loop that TSH works under causing the follicles to produce thyroid hormones in copious amounts without the ability to turn themselves “off”. This in turn causes the thyroid gland to hypertrophy and grow as much as 2 to 3 times its normal size (p. 13-14). In an effort to stop the overproduction of thyroid hormones the pituitary gland will stop making TSH and this becomes part of the diagnosing for Graves’ disease when assessing hyperthyroidism. Increased levels of free T3 and T4 along with an almost non-detectable level of TSH in a blood screen are very indicative of Graves’ disease (Holt, 2010, p. 14). There is no cure for Graves’ disease, but it is treatable with lifestyle adjustments as well as drug therapy it can be managed to a point (p 46).

In the late 1900s graves’ disease was referred to the newspapers as exophthalmic goiter. The earliest it has ever been known was 1879, the Chester Pennsylvania’s Daily Times reported that a Dr. Pepper had 70 patients he had been working on. In 1902 Florence Beckel traveled to New York to see a specialist. As reported from Berlin by The New York Times in 1913, “It was not so many years ago when a diagnosis of exophthalmic goiter was equivalent to a death sentence.” The poor survival rate motivated doctors to seek new treatments, and many doctors thought they found it in X-rays’ 50 percent higher success rate (Gleason, T. (n.d.). A Short History of Graves' Disease Reporting in North American Newspapers. Retrieved August 20, 2014.) The pharmacology for this disease is radioactive iodine therapy and anti-thyroid medications such as propylthiouracil and methimazole (Tapazole). Beta blockers such as propranolol (Inderal), atenolol (Tenormin), Metoprolol (Lopressor, Toprol-XL), and Nadolol (Corgard). For non-pharmacology Surgery is the best way to help remove that thyroid. What I found most interesting is the history part of it. What I learned is that if affects women and it can be fatal if left untreated. Staff, M. (2014,

In November, 2010 my father was diagnosed with Graves disease. He presented symptoms of vertigo, double vision, fatigue, abnormal protrusion of the eyes, insomnia, and irritability. Due to his kidney donation in 2005 doctors were worried about possible complications, and did not think about thyroid conditions. After multiple wrong diagnoses, thyroid tests were conducted. These tests including thyroid function tests, radioactive iodine uptake, and antibody tests, finally a diagnosis of Graves was made (Cooper, 2012). After the diagnosis his anxiety increased dramatically, knowing that he was going to have to deal with a chronic illness the rest of his life. He underwent 2 surgeries to loosen and reposition the muscles that allow your eyes to move. A year later he was still having dangerous swelling and

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].

In this study, the authors set out to examine patients’ perspectives, experiences and opinions on the major forms of MAT: methadone and buprenorphine. This study was actually the qualitative portion of a larger study conducted on MAT treatment options that was called the Treatment Options Study (TOP). This particular study specifically targeted the qualitative data gathered from TOP through semi-structured interviews. The study itself focused on clients’ previous experiences with MAT, either methadone or buprenorphine. It also explored three fundamental questions regarding MAT: “client comparisons between methadone and buprenorphine, interactions with clinicians about treatment options, choices participants made about [MAT],” (Yarborough et al., 2016, p. 113). The overall outcomes of the study showed that increased access to treatment options, such as MAT, promotes the chances of client participation in substance abuse treatment. More relevant to this study

On Thursday, May 3, 2018, my general practitioner, Dr. Marcus Martinez during a routine physical, made me aware, that I more than likely have Graves Disease. This is a disease of the thyroid gland. I have multiple nodules/goiters that have grown over time, which will more than likely require surgery, and radioactive iodine treatments to mention a few options before me. At this time, it has yet to be determined if they are cancerous or malignant, that is the next step. It will be some time before a substitute daily drug for the balance of my life will function and produce the necessary hormones to function properly as a replacement for my thyroid gland hormones. These hormones or replacement drugs are a life’s necessity, and stimulate so much of the natural body functions. With this before me, I have been referred to an Endocrinologist, Dr. Gorson. Should confirmation be

When the Thyroid begins to produce too much of the Thyroid Hormones it can cause a condition called Hyperthyroidism. Hyperthyroidism has been found to have three main causes; Graves Disease (which Ava is currently suffering from), Toxic Multinodular Goiter and Toxic Adenoma (Felicilda-Reynaldo, Kenneally, 2016). Laboratory tests conducted on Ava have shown that her TSH (Thyroid Stimulating Hormone) is low whilst the Triidothyronine (T3) and Thyroxine (T4) levels are much higher. A diagnosis of graves disease is commonly confirmed by low levels of TSH and higher levels of T3 and T4 (Streetman, Khanderia, 2003). The cause behind low TSH (Thyroid Stimulating Hormone) is due to the decline in production based on a negative feedback response stemming from Antibodies binding to TSH receptors, causing the thyroid gland to release it own ‘Thyroid Hormone’ and in turn the haematological levels of ‘Thyroid Hormone’ increases. (Understanding Pathophysiology, 2012, p.258). This particular negative feedback then causes the TSH (Thyroid Stimulating Hormone) production to decrease. Whilst this is occurring those very same increased ‘Thyroid Hormone” levels in the blood begin to activate receptors located at the thyroid gland causing increasing levels

Pregnant women are putting their unborn baby at risk and themselves, studies have concluded that low levels of iodine

The thionamide drugs, propylthiouracil, carbimazole, and its active metabolite methimazole, have been in use to treat thyrotoxicosis for more than 60 years. A meta-analysis of randomised controlled trials showed long term remission of hyperthyroid Graves’ disease in about 50% of those treated with thionamide drugs for a prolonged period. Carbimazole or methimazole are preferred in most situations, as a small risk of serious liver injury (about 1 in 10 000 adults) has recently been highlighted during propylthiouracil use. In addition, carbimazole or methimazole can be taken once daily rather than every eight or 12 hours as is the case for propylthiouracil, and the longer half-life leads to more rapid control. All inhibit the function of TPO, reducing oxidation and organification of iodide. These drugs also reduce thyroid antibody levels by mechanisms that remain unclear, and they appear to enhance rates of remission

As the patient is pregnant, if the condition is not treated, pregnancy complications can occur as a result of the hyperthyroidism, this adverse effect include spontaneous abortion, premature delivery (PD),

Patients should be taught to take heart rates accurately and reminded to check their heart rates daily (Felicilda & Kenneally, 2016). Medications should be taken around the clock, and time between doses should be spaced evenly (Felicilda & Kenneally, 2016). Patients should be informed to avoid over-the counter medications for asthma or cough treatment without checking with the provider. These medications may contain iodide, which would decrease the effects of antithyroid medication. Signs of inadequate therapy or thyrotoxicosis include diarrhea, fever, irritability, listlessness, vomiting, and weakness (Felicilda