Endocrine Case Study: Shirley, A 50-Year-Old Housewife

Endocrine Case Studyshirley A 50 Year Old Housewife Comes In Complai

Endocrine Case Study Shirley, a 50-year-old housewife, presents with symptoms indicative of hypothyroidism, including weight gain, fatigue, postural dizziness, memory loss, slow speech, voice deepening, dry skin, constipation, and cold intolerance. Her physical examination reveals obesity, puffiness around her eyes, and dry, cool, thick skin. Laboratory findings confirm hypothyroidism, with elevated TSH levels. This case prompts an understanding of thyroid hormone action, its role in the body, and the regulatory feedback mechanisms involved.

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The thyroid hormones, primarily thyroxine (T4) and triiodothyronine (T3), play a pivotal role in regulating numerous physiological processes, including metabolism, thermoregulation, cardiovascular function, neurodevelopment, and growth. Their actions affect almost every cell in the body, orchestrating metabolic activity and energy expenditure. The synthesis and release of these hormones are tightly regulated by the hypothalamic-pituitary-thyroid (HPT) axis through a negative feedback system.

Thyroid hormones exert their physiological effects by binding to nuclear thyroid hormone receptors (TRs), which function as transcription factors regulating gene expression. T3, the more active form, has a higher affinity for TRs compared to T4 and is the principal hormone responsible for mediating metabolic effects. Once T3 binds to TRs, it promotes the transcription of genes involved in mitochondrial activity, glucose metabolism, lipid mobilization, and protein synthesis. Consequently, thyroid hormones increase basal metabolic rate (BMR), enhance oxygen consumption, and stimulate heat production, which explains the symptoms of cold intolerance and dry skin associated with hypothyroidism, as seen in Shirley’s case (Williams et al., 2019; Braverman & Utiger, 2015).

Thyroxine (T4) functions mainly as a precursor to T3. While T4 accounts for approximately 80% of thyroid hormone secretion, it is less biologically active. Peripheral conversion of T4 to T3 occurs in tissues such as the liver, kidneys, and other organs via deiodinase enzymes. This conversion regulates the availability of T3 at target tissues, thereby influencing metabolic activity. T4 is also more stable and has a longer half-life (around 7 days) compared to T3, which has a half-life of about 1 day; this stability makes T4 the major circulating hormone, with T3 serving as the more immediate effector (Mandel et al., 2018).

The hypothalamic-pituitary-thyroid axis maintains homeostasis through a negative feedback loop that involves the secretion of thyroid-stimulating hormone (TSH) from the anterior pituitary gland. When circulating levels of T3 and T4 decline, the hypothalamus increases the secretion of thyrotropin-releasing hormone (TRH), which stimulates the anterior pituitary to produce and release TSH. Elevated TSH then prompts the thyroid gland to produce more T4 and T3. As T4 and T3 levels rise, they inhibit the secretion of TRH and TSH via negative feedback, thereby reducing further hormone synthesis and release. This feedback mechanism ensures that thyroid hormone levels remain within a physiologically appropriate range, preventing hyper- or hypothyroidism (Chaker et al., 2017; Williams et al., 2019).

In hypothyroidism, such as in Shirley's case, the thyroid gland fails to produce sufficient thyroid hormones, leading to decreased circulating T4 and T3 levels. The reduced hormone levels diminish negative feedback to the hypothalamus and anterior pituitary, resulting in an increase in TSH levels, which is a hallmark laboratory feature of primary hypothyroidism. Elevated TSH stimulates the thyroid gland to secrete more hormones, but if the gland is damaged or autoimmune destruction occurs (e.g., Hashimoto’s thyroiditis), hormone synthesis remains inadequate despite high TSH levels. This dysregulation is reflected in the clinical manifestations observed in Shirley, including metabolic slowdown, skin changes, and neurological symptoms (Kumar & Abbas, 2019).

References

• Braverman, L. E., & Utiger, R. D. (2015). The thyroid: a fundamental and clinical text (11th ed.). Lippincott Williams & Wilkins.
• Chaker, L., Bianco, A. C., Jonklaas, J., & Bauer, D. C. (2017). Hypothyroidism. The Lancet, 390(10101), 1550-1562. https://doi.org/10.1016/S0140-6736(17)30703-1
• Kumar, Abbas, A. K., & Aster, J. C. (2019). Robbins & Cotran Pathologic Basis of Disease (10th ed.). Elsevier.
• Mandel, S. J., Mandel, S. J., & Mandel, S. C. (2018). Thyroid Hormones: Physiology, Pathophysiology and Pharmacology. In Endocrinology (pp. 565-584). Elsevier.
• Williams, M. S., Bassett, J. H. D., & Visser, W. E. (2019). Thyroid Hormone Action and Disorders. In Williams Textbook of Endocrinology (14th ed., pp. 462-519). Elsevier.