Pathology Pathophysiology And Real Life


Thyrotoxicosis, also known as hyperthyroidism is a hypermetabolic condition that occurs as a consequent of excess levels of free triiodothyronine T3 and thyroxine T4 in the blood plasma. Other commonly known causes include diffused hyperplasia of the thyroid gland, which is often associated with Grave’s Disease, hyperfunctional multinodular goiter, or hyperfunctional adenoma of the thyroid (Kumar,Abbas, Fausto and Aster, 2014). The major function of the thyroid-stimulating hormone is to stimulate energy production, which is used in metabolic process in the body (Ahmed, 2016). In this regard, excessive levels of the hormone in the circulatory system increase the basal metabolic rate thus increased blood flow. Research statistics reveal that about 1.2 percent of citizens in the United States are likely to report cases of hyperthyroidism (Fleming, 2018). Moreover, women having type 1 diabetes and are above 60 years have a higher prevalence of experiencing thyrotoxicosis than men in similar cases although cases of hyperthyroidism are less common (Kumar and Clark, 2012). In this relation, this paper analyses the pathology of thyrotoxicosis, briefly discusses the pathophysiology of Grave’s Disease, and relates an understanding of the diseases to a real life situation, the Sharon’s case study.


Histology of the Thyroid Hormones

Thyroid hormones refer to the two hormones T3 and T4 produced and released by the thyroid gland. These tyrosine-based hormones are primarily responsible for the regulation of metabolic processes or the basal metabolic rate (BMR). The thyroid follicular epithelial cells in the thyroid gland concentrates iodide from iodine components in the body using an iodide pump, which actively pumps the iodide from the blood into the follicles using the sodium/iodine symporter (Fleming 2018). The iodide in the follicles is then activated into a reactive form by enzyme peroxidase and associates with the protein, thyroglobulin. Thyroglobulin hormone then converts into lesser amounts of T3 and more of T4 hormones (iodothyronines). The latter are then released into the blood system where the peptides are reversibly bound to plasma proteins like thyroxine-binding globulin and transthyretin, which are transported to peripheral tissues (Ahmed, 2016).

The binding proteins maintain the serum concentration levels while ensuring the hormones are readily available to the tissues (Kumar,Abbas, Fausto and Aster, 2014). In the periphery, some parts of T4 are deionized to T3 while the remaining composition binds to the thyroid hormone nuclear receptor on the target organ hence result in the formation of a polypeptide hormone receptor complex that interacts with the thyroid hormone response elements thus causing gene transcription (Kumar,Abbas, Fausto and Aster, 2014). High levels of the iodothyronines increase the BMR of all cells in the body, body temperature, and a slight decrease in heat tolerance. T3 and T4 also increase the rate of lipolysis, stimulate protein synthesis and degradation, potentiate the effects of catecholamines in the cardiovascular system, and increase bone turnover (Sarezky et al, 2016).

Nevertheless, elevated levels of T3 and T4 potentiate adverse cellular effects. As earlier noted, the iodothyronines increase the BMR. That is to say, excessive levels of the hormones in the blood initiate an abnormal rise in the BMR hence increased blood flow to supply energy and oxygen for metabolism (Kumar,Abbas, Fausto and Aster, 2014). Notably, an increased blood flow in the system enhances vasodilation of blood vessels to enable heat loss. Moreover, cardiac output significantly increases due to increased contraction and relaxation of the cardiac muscles and increased cellular oxygen requirements. (Kumar and Clark, 2012) Also, the shift in the BMR raises results in higher levels of calorigenesis thus initiating a characteristic weight loss despite an urgent need to eat more food. Plainly, these activities describe earliest clinical manifestations and features of thyrotoxicosis. For instance, the skin of thyrotoxicosis patients tend to be soft and warm, which is a sign associated with blood vessel vasodilation. In addition, these patients have increased appetite despite registering body weight loss (Ahmed, 2016). Heat intolerance and sweating is also common due to increased cardiac contractility and high calorigenesis. Patients with chronic hyperthyroidism, experience an increased risk of bone fractures or osteoporosis since the thyroid hormones also stimulate bone reabsorption (Sarezky et al, 2016). These symptoms are further clarified in a case study and other common causes of thyrotoxicosis.

Case Study

The case study analyses a health incidence of a 32-year-old woman, Shannon, who works at the local Community Mental Health Service Centre. Shannon’s medical history shows she developed type 1 diabetes at the age of 15 years; nonetheless, her sugar levels are within the expected levels. At First, Shannon continuously complains of fatigue and apprehension. Moreover, she finds it challenging to cope with her normal work load. Shannon also says her eyes are increasingly protruding and further opthalmological examinations confirm eyelid lag.

According to Kumar, Abbas, Fausto and Aster (2014) the symptoms of Grave’s Disease in relation to autoantibodies effects include a characteristic thyroid eye disease, which presents itself as a lid retraction or lid lag. In addition, other presentation of other symptoms as a consequent of metabolic processes stimulation are tremor, palpitations, significant weight loss, and higher cardiac output thus instances of fatigue.

Shannon’s physical examination confirms a BMI of 17.5kg/m, which is medically classified as underweight. Additionally, laboratory tests suggest increased cardiac output. For instance, Shannon’s temperature is above normal levels, that is 37.5 while her blood pressure and pulse rate is 130/70 mmHg and 88/min respectively. Also her respiration is high with 20/min. In this regard, Shannon experiences clear symptoms of increased thyroid activity or hyperthyroidism. Regardless, some of her test results out rule a diagnosis of thyrotoxicosis. For example, Shannon’s laboratory studies reveal increased levels of free T4 at 37.8pmol/L (10-20 pmol), and undetectable levels of thyroid stimulating hormone in the blood plasma (0.5-5 mlU/L). Moreover, she assumes significantly elevated levels of TSH receptor antibodies and antithyroglobulin antibodies. The presence of these antibodies in the system concludes her diagnosis to be that of Grave’s Disease.

The Pathology of Grave’s Disease

Grave’s Disease is the most common cause of thyrotoxicosis with an incidence rate of 70 percent. The disease mostly affects young women between the age of 20 and 40 years. Moreover, females have a higher prevalence of the disease as compared to men. (Kumar and Clark, 2012) The mechanism of infection of Grave’s Disease is similar to type 1 diabetes and rheumatoid arthritis, where the body’s defense system initiates antibodies to attack its own organs particularly the thyroid glands. That is to say, the thyroid stimulating antibodies produced from the thyroid gland associate with the TSH receptor to form anti-TSH receptor antibodies (Kierszenbaum and Tres, 2015). These autoantibodies then stimulate the thyroid cell to produce excess thyroid hormone thus causing thyrotoxicosis (Kumar,Abbas, Fausto and Aster, 2014).

Some of the distinct clinical findings in Grave’s Disease include sympathetic over activity, which causes signs of a staring gaze and lid lag. Also, the opthalmopathy of the disease causes exophthalmos, an abnormal protrusion of the eyeball. (Melmed, 2016) In addition, laboratory findings in Grave’s Disease include elevated levels of T4 and T3 and depressed levels of TSH. Notably, the increased stimulation of the thyroid follicles increase iodine uptake, which are confirmed in radioiodine scans (Kumar,Abbas, Fausto and Aster, 2014). Despite this, the Grave’s Disease has other signs commonly associated with early diagnosis of thyrotoxicosis such as diffused hyperplasia of the thyroid and increased blood flow through the hyperactive gland (Kierszenbaum and Tres, 2015).

Treatment for Grave’s Disease and associated complications

The occurrence of Grave’s Disease is likely in patients with a history of recurrent disease in the presence of a large goiter, when TSH-receptor antibody persists or when T3 persists despite controlled levels of T4 with antithyroid drugs. On this note, major reliable treatments for Grave’s Disease are similar to those of thyrotoxicosis since both of them have some common characteristic symptoms (Suzuki et al, 2015).

Drug Treatment

Antithyroid drugs such as thionamides are often prescribed to patients experiencing Grave’s Disease symptoms. These drugs inhibit thyroid follicle reactions that stimulate the excessive synthesis of iodothyronine. Doctors recommend short-term treatments in cases patients given drug treatment for Grave’s Disease before considering long term definitive therapy. Notably, starting doses of 15 – 20 mg daily for mild hyperthyroidism and 30 – 40 mg for critical cases avoids difficulties endured in surgery and radioiodine (Fleming 2018). For instance, Shannon can be prescribed to take 15 – 20 mg of carbimazole daily to reduce hyperactivity of the thyroid hormones and decrease the levels of T4 to normal in her blood plasma. Also, drug treatment for Shannon reduces costs, which are normally endured in cases of surgical preparations or radioactive iodine. Similarly, beta- adrenergic blockers like propranolol may be prescribed to control the sympathetic nerve symptoms such as tremor and decrease her basal metabolic rate (Kumar, Abbas, Fausto and Aster, 2014). However, the risk of the disease relapse rises to more than 50 percent once drug consumption is stopped hence the patient’s recurrence is more severe than in a previously controlled event (Fleming 2018).

Radioiodine therapy

Radioactive iodine is a major preferential choice for most patients experiencing severe symptoms of the Grave’s Disease besides drug treatment (Melmed, 2016). Radioiodine therapy operates on the principles that the thyroid tissue is the only body organ that assimilates iodine; therefore, the radioactive iodine selectively kills the cells that integrate iodine without causing harm to the body (Fleming 2018). Radioactive iodine- 131 is taken orally as a capsule or liquid at a higher dose to destroy the cells of the thyroid gland that produce the iodothyronines (Fleming 2018). Nevertheless, about 50 percent of radioactive iodine treatment patients later experience hypothyroidism since the thyroid hormone-producing cells was destroyed (Suzuki et al, 2015). Furthermore, the therapy does not guarantee a patient’s recovery from the thyroid eye disease since it may worsen the condition in severe cases of the thyroid eye disease (Fleming 2018).

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Thyrotoxicosis is a condition commonly associated with diffused hyperplasia of the thyroid gland. The abnormal hyperactivity of the iodothyronines in the target organs initiates characteristic symptoms of increased BMR due to high energy metabolic processes. The Grave’s Disease is one of the common causes of thyrotoxicosis accounting for 70 percent of thyroid diseases and mostly affects women between 20 and 40 years. Shannon’s case study further highlights associated signs and symptoms of the disease besides its diagnosis.


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  • Sarezky, M. D., Corwin, D. J., Harrison, V. S., & Jacobstein, C. (2016). “Hyperthyroidism presenting with pathologic fractures”. Pediatrics, peds-2015.
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