<unk>  may present clinically with one or more of these characteristic signs: *Rapid heartbeat (80%) *Diffuse palpable goiter with audible bruit (70%) *Tremor (40%) *Exophthalmos (protuberance of one or both eyes), periorbital edema (25%) *Fatigue (70%), weight loss (60%) with increased appetite in young people and poor appetite in the elderly, and other symptoms of hyperthyroidism/thyrotoxicosis *Heat intolerance (55%) *Tremulousness (55%) *Palpitations (50%) Two signs are truly 'diagnostic' of<unk>  (i.e., not seen in other hyperthyroid conditions): exophthalmos and nonpitting edema (pretibial myxedema). Goiter is an enlarged thyroid gland and is of the diffuse type (i.e., spread throughout the gland). Diffuse goiter may be seen with other causes of hyperthyroidism, although<unk>  is the most common cause of diffuse goiter. A large goiter will be visible to the naked eye, but a small one (mild enlargement of the gland) may be detectable only by physical examination. Occasionally, goiter is not clinically detectable, but may be seen only with computed tomography or ultrasound examination of the thyroid. Another sign of<unk>  is hyperthyroidism; that is, overproduction of the thyroid hormones T3 and T4. Normal thyroid levels are also seen, and occasionally also hypothyroidism, which may assist in causing goiter (though it is not the cause of the<unk> . Hyperthyroidism in<unk>  is confirmed, as with any other cause of hyperthyroidism, by measuring elevated blood levels of free (unbound) T3 and T4. Other useful laboratory measurements in<unk>  include thyroid-stimulating hormone (TSH, usually undetectable in<unk>  due to negative feedback from the elevated T3 and T4), and protein-bound iodine (elevated). Serologically detected thyroid-stimulating antibodies, radioactive iodine (RAI) uptake, or thyroid ultrasound with Doppler all can independently confirm a diagnosis of<unk> . Biopsy to obtain histiological testing is not normally required, but may be obtained if thyroidectomy is performed. The goiter in<unk>  is often not nodular, but thyroid nodules are also common. Differentiating common forms of hyperthyroidism such as<unk> , single thyroid adenoma, and toxic multinodular goiter is important to determine proper treatment. The differentiation among these entities has advanced, as imaging and biochemical tests have improved. Measuring TSH-receptor antibodies with the h-TBII assay has been proven efficient and was the most practical approach found in one study. Eye disease Thyroid-associated ophthalmopathy (TAO), or thyroid eye disease (TED), is the most common extrathyroidal manifestation of<unk> . It is a form of idiopathic lymphocytic orbital inflammation, and although its pathogenesis is not completely understood, autoimmune activation of orbital fibroblasts, which in TAO express the TSH receptor, is thought to play a central role. Hypertrophy of the extraocular muscles, adipogenesis, and deposition of nonsulfated glycoaminoglycans and hyaluronate, causes expansion of the orbital fat and muscle compartments, which within the confines of the bony orbit may lead to dysthyroid optic neuropathy, increased intraocular pressures, proptosis, venous congestion leading to chemosis and periorbital edema, and progressive remodeling of the orbital walls. Other distinctive features of TAO include lid retraction, restrictive myopathy, superior limbic keratoconjunctivitis, and exposure keratopathy. Severity of eye disease may be classified by the mnemonic: "NO SPECS": *Class 0: No signs or symptoms *Class 1: Only signs (limited to upper lid retraction and stare, with or without lid lag) *Class 2: Soft tissue involvement (oedema of conjunctivae and lids, conjunctival injection, etc.) *Class 3: Proptosis *Class 4: Extraocular muscle involvement (usually with diplopia) *Class 5: Corneal involvement (primarily due to lagophthalmos) *Class 6: Sight loss (due to optic nerve involvement) Typically the natural history of TAO follows Rundle's curve, which describes a rapid worsening during an initial phase, up to a peak of maximum severity, and then improvement to a static plateau without, however, resolving back to a normal condition.
Graves' disease
Hashimoto's thyroiditis
Autoimmune thyroiditis
Riedel's thyroiditis
Ord's thyroiditis
Cushing's disease
Radiation-induced thyroiditis
Behr syndrome