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342        SEcTion iii    EndocrinE  ` endocrine—PAthology                                                                                                                  EndocrinE  ` endocrine—PAthology





               Hyperthyroidism
                Graves disease       Most common cause of hyperthyroidism. Thyroid-stimulating immunoglobulin (IgG, can cause
                                       transient neonatal hyperthyroidism; type II hypersensitivity) stimulates TSH receptors on thyroid
               A
                                       (hyperthyroidism, diffuse goiter), dermal fibroblasts (pretibial myxedema), and orbital fibroblasts
                                       (Graves orbitopathy). Activation of T-cells Ž lymphocytic infiltration of retroorbital space
                                       Ž  cytokines (eg, TNF-α, IFN-γ) Ž  fibroblast secretion of hydrophilic GAGs Ž  osmotic
                                       muscle swelling, muscle inflammation, and adipocyte count Ž exophthalmos  A . Often presents
                                      during stress (eg, pregnancy). Associated with HLA-DR3 and HLA-B8.
                                     Histology: tall, crowded follicular epithelial cells; scalloped colloid.



                Toxic multinodular   Focal patches of hyperfunctioning follicular cells distended with colloid working independently
                 goiter               of TSH (due to TSH receptor mutations in 60% of cases).  release of T 3  and T 4 . Hot nodules are
                                       rarely malignant.
                Thyroid storm        Uncommon but serious complication that occurs when hyperthyroidism is incompletely treated/
                                       untreated and then significantly worsens in the setting of acute stress such as infection, trauma,
                                       surgery. Presents with agitation, delirium, fever, diarrhea, coma, and tachyarrhythmia (cause
                                       of death). May see  LFTs. Treat with the 4 P’s: β-blockers (eg, Propranolol), Propylthiouracil,
                                      corticosteroids (eg, Prednisolone), Potassium iodide (Lugol iodine). Iodide load Ž  T 4  synthesis
                                       Ž Wolff-Chaikoff effect.

                Jod-Basedow         Iodine-induced hyperthyroidism. Occurs when a patient with iodine deficiency and partially
                 phenomenon           autonomous thyroid tissue (eg, autonomous nodule) is made iodine replete. Can happen after iodine
                                      IV contrast or amiodarone use. Opposite to Wolff-Chaikoff effect.
                Causes of goiter    Smooth/diffuse: Graves disease, Hashimoto thyroiditis, iodine deficiency, TSH-secreting pituitary
                                      adenoma.
                                    Nodular: toxic multinodular goiter, thyroid adenoma, thyroid cancer, thyroid cyst.



               Thyroid adenoma       Benign solitary growth of the thyroid. Most are nonfunctional (“cold”), can rarely cause
               A                       hyperthyroidism via autonomous thyroid hormone production (“hot” or “toxic”). Most common
                                       histology is follicular (arrows in  A ); absence of capsular or vascular invasion (unlike follicular
                                       carcinoma).






































          FAS1_2019_08-Endocrine.indd   342                                                                             11/7/19   4:30 PM
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