Chapter 58: Glandular Disorders
Loading audio…
ⓘ This audio and summary are simplified educational interpretations and are not a substitute for the original text.
Hyperthyroidism represents excessive thyroid hormone synthesis and secretion, most commonly from Graves' disease, an autoimmune condition accounting for the majority of cases. The distinction between hyperthyroidism and the broader term thyrotoxicosis is clarified, as thyrotoxicosis encompasses exogenous hormone intake and inflammatory conditions that release stored hormones. Diagnostic approaches utilize serum TSH suppression and elevated free T4 and T3 levels, while radioactive iodine uptake testing differentiates between primary overproduction and hormone release. Treatment modalities include antithyroid medications, radioactive iodine ablation, surgical thyroidectomy, and beta-blockade for symptom management, with thyroid storm representing a medical emergency requiring intensive intervention. Hypothyroidism, the opposing disorder of insufficient hormone production, most frequently results from Hashimoto's thyroiditis in developed countries. Diagnosis relies on elevated TSH with low free T4, and management centers on levothyroxine replacement titrated to normalize TSH levels, with special consideration for elderly patients and those with cardiac disease. Thyroid cancer, though the most common endocrine malignancy, carries low lifetime risk and is predominantly papillary in type with favorable prognosis when treated with thyroidectomy and radioactive iodine ablation. Cushing's syndrome develops from chronic inappropriate hypercortisolemia, most often iatrogenic from exogenous glucocorticoid administration but also from pituitary adenomas secreting ACTH. The chapter details characteristic physical findings including central obesity, facial plethora, and skin atrophy, with diagnosis confirmed through 24-hour urinary free cortisol or dexamethasone suppression testing. Adrenal insufficiency, whether primary from autoimmune Addison's disease or secondary from pituitary dysfunction or abrupt steroid withdrawal, requires glucocorticoid and potentially mineralocorticoid replacement with dose adjustment during physiological stress to prevent life-threatening Addisonian crisis.