Graves' disease
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Question: 1
Choose a thyroid disorder (e.g., hypothyroidism, hyperthyroidism, Hashimoto’s thyroiditis,
or Graves' disease) and explain the key aspects of its pathophysiology. What are the
primary mechanisms that lead to the disorder? How does the dysfunction in thyroid
hormone production or regulation affect the body at the cellular level? How do laboratory
values (e.g., TSH, free T4, and free T3) correlate with the pathophysiological changes?
My choice of thyroid disorder is Graves' disease. It is the most frequent cause of
hyperthyroidism and an autoimmune disorder. It is a disease caused by the body's immune
system producing thyroid-stimulating immunoglobulins (TSIs), which resemble thyroid-
stimulating hormone (TSH) and attach to thyroid gland TSH receptors. The unregulated thyroid
stimulation occurs due to this binding, culminating in excess production of thyroid hormones (T3
and T4) (Phagoora et al, 2025).
At the cellular level, thyroid oversecretion enhances metabolism by stimulating
mitochondrial metabolism, protein synthesis, and glucose catabolism. This increased metabolic
condition impacts various organ systems and leads to the appearance of such symptoms as
tachycardia, heat intolerance, weight loss, nervousness, and muscle weakness (Chakera et al.,
2012). Graves' disease can also cause thyroid eye disease because of inflammation and fibroblast
activity in orbital tissues caused by the autoimmune response (Lanzolla & Menconi, 2024). In
this case, the laboratory values are usually low TSH due to negative feedback caused by high
levels of thyroid hormones. There is an increase in Free T3 and Free T4 levels and TSI
antibodies, which prove the autoimmune etiology (Burch et al., 2022).
Question: 2
Provide an example of a clinical presentation of a patient with this thyroid disorder. How
do the pathophysiological changes you described relate to the symptoms and physical
findings in the patient?
The classic clinical presentation may include a 35-year-old female with the complaint of
palpitations, inadvertent weight loss, anxiety, heat intolerance, and periodontal anomalies.
Investigations could reveal that she has a diffusely enlarged, painless goiter, exophthalmos,
warm skin, and tachycardia. These are symptoms that are the direct response to the
pathophysiology. The surplus thyroid hormone stimulates hyperactivity in metabolism and the
sympathetic nervous system, whereas orbital inflammation is the cause of the findings of the
eyes.
In summation, the disease Graves is a consequence of an autoimmune reaction that
causes an excess of the thyroid hormone and is accompanied by quite clear metabolic and
clinical effects.
References
Burch, H. B., Perros, P., Bednarczuk, T., Cooper, D. S., Dolman, P. J., Leung, A. M., ... & Stan,
M. N. (2022). Management of thyroid eye disease: a consensus statement by the
American Thyroid Association and the European Thyroid Association. European thyroid
journal, 11(6). Retrieved on 12th September 2025 rom
https://etj.bioscientifica.com/view/journals/etj/11/6/ETJ-22-0189.xml
Lanzolla, G., Marinò, M., & Menconi, F. (2024). Graves disease: latest understanding of
pathogenesis and treatment options. Nature Reviews Endocrinology, 20(11), 647-660.
Retrieved on 12th September 2025 from https://www.nature.com/articles/s41574-024-
01016-5
Phagoora, J., Bakilwal, S., Hamzehpour, A., Kabariti, M., Munarov, J., Cho, H. Y., & Saini, S.
(2024). Graves Disease-A Comprehensive Review. Physician's Journal of
Medicine, 3(1). Retrieved on September 12, 2025, from
https://www.researchgate.net/profile/Jaskomal-Phagoora/publication/
385045804_Graves_Disease_-_A_Comprehensive_Review/links/
6712ac7668ac3041499f124e/Graves-Disease-A-Comprehensive-Review.pdf