THYROID PHYSIO-PATHOLOGY

Thyroid hormones: T3 (triiodothyronine)

                                T4 (tetraiodothyronine = thyroxine)

Both have systemic effects. Abnormal thyroid hormone levels lead to hypothyroid and hyperthyroid states. Inadequate thyroid hormone during the development leads to congenital hypothyroidism; also know as cretinism, with associated irreversible brain damage.

Source: Follicles of thyroid. Most T3 formed in blood.

Function: Bone growth (synergism with GH)

                Brain maturation.

                Beta-adrenergic effects: increases stimulation of β1 receptors in heart = ↑ CO, HR, SV, and contractility.

                Basal metabolic rate ↑ via ↑ Na/K-ATPase activity = ↑ 02 consumption, RR, body temperature.

Regulation: TRH (thyrotropin releasing hormone) from the hypothalamus stimulates TSH (thyroid stimulating hormone) in adenohypophysis, which stimulates follicular cells.

Hypothyroidism: Cold intolerance, hypoactivity, weigh gain, fatigue, lethargy, ↓ appetite, constipation, weakness, ↓ reflex, myxedema (facial/periorbital), dry, cool skin, and coarse, brittle hair.

↑ TSH (sensitive test for 1° hypothyroidism), ↓ total T4, ↓ free T4,↓ T3 uptake.

Hyperthyroidism: Heat intolerance, hyperactivity, weigh loss, chest pain/palpitation, arrhythmias, diarrhea, ↑ reflex, warm, moist skin, and fine hair.

 ↓ TSH (if 1°), ↑ total T4, ↑ free T4, ↑ T3 uptake.

Hashimoto’s thyroiditis: Autoimmune disorder resulting in hypothyroidism (can have thyrotoxicosis during follicular rupture). Slow course, moderately enlarged, nontender thyroid. Lymphocyte infiltrate with germinal centers. Antimicrosomal and antithyroglobulin antibodies. Associated with Hürthle cells on histology.

Subacute thyroiditis (de Quervain’s): Self-limited hypothyroidism often following a flulike illness. Elevated ESR, jaw pain, early inflammation, and very tender thyroid gland. Histology shows Granulomatous inflammation.

May be hyperthyroid early in course. Lymphocytes subacute thyroiditis is painless.

Riedel’s thyroiditis: Thyroid replaced by fibrous tissue (hypothyroid). Presents with fixed, hard, and painless.

Cretinism: Due to several fetal hypothyroidism. Endemic cretinism occurs wherever endemic goiter is prevalent (lack of dietary iodine); sporadic cretinism is caused by defect in T4 formation or developmental failure in thyroid formation.

Finding: Pot-bellied, pale, puffy face child protruding umbilicus and protuberant tongue.

Graves’ disease: An autoimmune hyperthyroidism with thyroid-stimulating/TSH receptor antibodies. Ophthalmopathy (proptosis, extraocular muscle swelling), pretibial myxedema, diffuse goiter. Often presents during stress (e.g. childbirth).

Stress-induced catecholamine surge leading to death by arrhythmia. Seen as a serious complication of Graves’ and other hyperthyroidism disorder.

Graves’ is type II hypersensitivity.

Toxic multinodular goiter: Iodine deprivation followed by Iodine restoration. Causes release of T3 and T4. Nodules are not malignant.

Jod-Basedow phenomenon= thyrotoxicosis if a patient with iodine deficiency goiter is made iodine replete.

Thyroid cancer:

1)      Papillary carcinoma- most common, excellent prognosis, ground-glass nuclei (Orphan Annie), psammoma bodies, nuclear grooves. ↑ Risk with childhood irradiation.

2)      Follicular carcinoma-good prognosis, uniform follicles.

3)      Medullary carcinoma-from parafollicular “C cells”; produces calcitonin, sheets of cells in amyloid stroma. Associated with MEN type 2A and 2B.

4)      Undifferenciated/anaplastic- older patients, very poor prognosis.

Lymphoma – associated with Hashimoto’s thyro