 The thyroid (Greek thyreos, shield, plus eidos, form) consists of two lobes connected by isthmus  Anterior to the trachea between the cricoid cartilage and the suprasternal notch  Normal thyroid is 12–20 g, vascular, soft  Four parathyroid glands,producing parathyroid hormone, are located posterior to each pole of the thyroid

 The thyroid gland consists of numerous spherical follicles composed of thyroid follicular cells that surround secreted colloid, a proteinaceous fluid containing large amounts of thyroglobulin, the protein precursor of thyroid hormones

 TSH, secreted by the thyrotrope cells of the anterior pituitary, pivotal role in controling thyroid axis  The most useful physiologic marker of thyroid hormone action  The thyroid axis is a classic example of an endocrine feedback loop. Hypothalamic TRH stimulates pituitary production of TSH, which, in turn, stimulates thyroid hormone synthesis and secretion. Thyroid hormones feed back to inhibit TRH and TSH production

 Iodide uptake is a critical first step in thyroid hormone synthesis. Ingested iodine is bound to serum proteins, particularly albumin. Unbound iodine is excreted in the urine. The thyroid gland extracts iodine from the circulation in a highly efficient manner

 Cretinism : mental & growth retardation  Children in iodine-deficient regions who not treated with iodine or thyroid hormone (early life). These children are often born to mothers with iodine deficiency  ∼M aternal T3,T4 deficiency worsens the condition  Concomitant selenium def. ⤳ neurologic manifestations of Cretinism  Iodine supplement of salt, bread etc. ⇨⬇C retinism.  Iodine deficiency the most common cause of preventable mental deficiency  Mild iodine deficiency ⟾ subtle reduction of IQ  Oversupply of iodine ⤳ ⬆A utoimmune thyroid disease

 Iodine deficiency remains the most common cause of hypothyroidism worldwide. In areas of iodine sufficiency, autoimmune disease (Hashimoto's thyroiditis) and iatrogenic causes (treatment of hyperthyroidism) are most common

 Congenital Hypothyroidism  Iatrogenic hypothyroidism  Autoimmune Hypothyroidism ⥥ Hashimoto's ( Goitrous thyroiditis ) ⬇ Atrophic thyroiditis

 Insidious onset : may become aware of symptoms only after euthyroidism  Hashimoto's thyroiditis ⤳ irregular firm goiter rather than symptoms of HypoT  Dry skin, decreased sweating  Puffy face, edematous eyelids  Nonpitting pretibial edema  Constipation & weight gain (despite poor appetite)  Due to fluid retention in the myxedematous tissues

 There is pallor, & often yellow tinge to the skin due to carotene accumulation  Nail growth is retarded  Hair is dry, brittle, difficult to manage, and falls out easily ( diffuse alopecia )  Thinning of the outer third of the eyebrows (Also in Leprosy)  Cool extremities  Impaired Memory & concentration

 Vitiligo  Pernicious anemia  Addison's disease  Alopecia areata  Type 1 diabetes mellitus

 Daily replacement dose of levothyroxine Radiation Early studies of the pathogenesis of thyroid cancer focused on the role of external radiation, which predisposes to chromosomal breaks, leading to genetic rearrangements and loss of tumor-suppressor genes.

Thyroid hormone excess ⤷ Hyperthyroidism Causes of Thyrotoxicosis:  Primary hyperthyroidism  Graves' disease(Genetic + Iodine intake)  Toxic multinodular goiter  Toxic adenoma  Drugs: iodine excess (Jod-Basedow phenomenon)

 Hyperactivity, irritability, dysphoria  Heat intolerance and sweating  Palpitations  Fatigue and weakness  Weight loss with increased appetite  Diarrhea  Polyuria  Oligomenorrhea, loss of libido

Tachycardia; atrial fibrillation in the elderly Tremor Goiter Warm, moist skin Muscle weakness, proximal myopathy Lid retraction or lag Gynecomastia

 By reducing thyroid hormone synthesis  Using antithyroid drugs  Reducing the amount of thyroid tissue with radioiodine ( 131 I) treatment  Thyroidectomy