The endocrine system is a complex structure in the human body consisting of organs and glands. The network utilizes hormones to regulate different functions, including response to injury, mood, metabolism, and growth and development (Gulseren et al., 2006). According to Duyff et al. (2000), thyroid gland is among the most noticeable parts of this system. It plays a significant role in the growth, development, and metabolism of a person’s body. It assists in controlling different body functions by continuously releasing a steady amount of thyroid hormone into the bloodstream. Together with the anterior pituitary gland and hypothalamus, they form a circuit named the hypothalamic-pituitary-thyroid axis. There are various illnesses that affect or impact the thyroid gland, including hypothyroidism, hyperthyroidism, Hashimoto thyroiditis, and Graves disease.
Hypothyroidism refers to a condition caused by a functional or structural derangement that disrupts the thyroid hormone’s production. The illness affects the gland in that it no longer produces the hormone sufficiently. The signs and symptoms vary depending on how serious the deficiency appears. Issues tend to develop slowly, usually over numerous years. Initially, one may seldom detect the indicators such as weight gain and fatigue. The majority of the time, individuals dismiss this by claiming that the situation is caused by ageing. However, as their metabolism continues to slow, they may show clearer problems, including increased sensitivity to cold, dry skin, puffy face, and constipation.
It is easy for someone to confuse this condition with another named hyperthyroidism. In the latter, a hyperactive thyroid gland is responsible for excessively unnecessary quantities of thyroid hormone (Davies & Schwartz, 2003). In order to understand the differences between this illness and hypothyroidism, it is essential that someone checks the indicators. Patients suffering from this disease experience excessive appetite or hunger, hyperactivity, abnormal heart rhythm, rare protrusion of the eyes, and weight loss. Apart from varying clinical manifestations, the two illnesses have different methods of diagnosis.
On the one hand, a diagnosis of hypothyroidism includes a measurement of serum TSH concentration, measurement of free T4, and thyroid autoimmunity Auto-antibodies test. On the other hand, despite physicians utilizing the first two steps mentioned above, in hyperthyroidism, there is the determination of radioactive iodine uptake by the thyroid gland. According to Selmer et al. (2012), attempting to comprehend the specific disease that is responsible for the symptoms is the foundation for treatment. A correct diagnosis is crucial to prevent wasting time on the wrong treatment course. It is true that there exists a difference in how they are both treated (Silva & Bianco, 2008). A hormone replacement therapy such as Levothyroxine is adopted for the purpose of treating hypothyroidism (Singh & Hershman, 2017). With regard to hyperthyroidism, the therapeutic options comprise a β-blocker to control symptoms induced by the increased β-adrenergic ton, radioiodine ablation, thionamide to block new hormone synthesis, and thyroidectomy.
Lastly, it is essential to consider other conditions named earlier affecting the thyroid gland. On the one hand, Hashimoto thyroiditis refers to an autoimmune illness in which thyroid cells are damaged via cell and antibody-mediated immune processes. Medical professionals regard it as the most common cause of hypothyroidism. It results from genetic, hormonal, and environmental factors, consisting of excessive radiation exposure and iodine. On the other hand, Graves’ disease is among the most common etiologies of hyperthyroidism. Understanding all these conditions allows individuals to seek treatment early, increasing their chances of a better quality of life.
References
Duyff, R. F., Van Den Bosch, J., Laman, D. M., Potter Van Loon, B. J., & Linssen, W. H. J. P. (2000). Neuromuscular findings in thyroid dysfunction: A prospective clinical and electrodiagnostic study. Journal of Neurology Neurosurgery and Psychiatry, 68(6), 750–755. Web.
Gulseren, S., Gulseren, L., Hekimsoy, Z., Cetinay, P., Ozen, C., & Tokatlioglu, B. (2006). Depression, anxiety, health-related quality of life, and disability in patients with overt and subclinical thyroid dysfunction. Archives of Medical Research, 37(1), 133–139. Web.
Davies, T. F., & Schwartz, A. E. (2003). Hyperthyroidism. In Endocrine Surgery (pp. 101–114). CRC Press. Web.
Selmer, C., Olesen, J. B., Hansen, M. L., Lindhardsen, J., Olsen, A. M. S., Madsen, J. C., Faber, J., Hansen, P. R., Pedersen, O. D., Torp-Pedersen, C., & Gislason, G. H. (2012). The spectrum of thyroid disease and risk of new onset atrial fibrillation: A large population cohort study. BMJ (Online), 345(7885). Web.
Silva, J. E., & Bianco, S. D. C. (2008). Thyroid-adrenergic interactions: Physiological and clinical implications. Thyroid, 18(2), 157–165. Web.
Singh, I., & Hershman, J. M. (2017). Pathogenesis of hyperthyroidism. Comprehensive Physiology, 7(1), 67–79. Web.