simple_goiter1

Simple Goiter
Overview-definition thyroid gland enlargement that does not result from the neoplastic or inflammatory process and is not associated initially with myxedema or thyrotoxicosis Cause-usually unknown sometimes due to ingestion of goitrogens, defect in hormonal biosynthetic pathways or I deficiency Occurrence: when factor or factors prevent the thyroid from secreting sufficient hormones to meet peripheral tissue requirements Pathology Initial effects: uniform hypertrophy/hyperplasia/hypervascularity with progression, the thyroid loses uniform structure involutional/hyperinvolutional structure with colloid accumulation varies of hemorrhage & calcification ultimately functional autonomy with structural heterogeneity Clinical Considerations: Metabolic state: normal; thyroid enlargement Goitrous hypothyroidism (thyromegaly) associated with symptoms/signs of insufficient thyroid hormone Mechanical effects: Compression/displacement of esophagus or trachea Obstructive symptoms euthyroid enlargement is sufficient Superior mediastinal obstruction with large retrosternal goiter with patient's arms above the head: giddiness, suffusion of the face, syncope (Pemberton's sign) Hyperthyroidism may develop in long-standing multinodular goiter (toxic multinodular goiter) Iodide ingestion (excess) can cause thyrotoxicosis development -- i.e.,jodbasedow phenomenon Hypothyroidism may develop in regions with iodine deficiency (severe) and may be associated with goitrous enlargement cretinism (goitrous & non-goitrous) is seen with increased frequency and chiller to goitrous parents not solely dependent on the extent of iodine deficiency-may also involved conditioning factors {dietary/waterborne goitrogens} Diagnosis:simple goiter Euthyroid state with normal serum T₄ & T₃ concentration