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Basilio, Precious

Angel
Jimenez, Dianne
Nicole
Cleofas, Faye
Hansel
MT1041

Graves’ Disease

 TSH receptor antibodies (TRAbs). previously known as thyroid stimulating immunoglobulin or long-acting thyroid stimulators are classified as stimulating or blocking antibodies.  The target of the autoimmune response is the thyrotropin (TSH) receptor found on the follicular cells of the thyroid gland .GRAVES’ DISEASE  An autoimmune condition in which goiter and hyperthyroidism are induced by thyroid stimulating or blocking antibodies (TRAbs) that mimic the action of TSH.

GRAVES’ DISEASE  Most common cause of endogenous hyperthyroidism  Hyperthyroidism caused by excessive hormone production due to thyroid gland’s overall hyperactivity.  Women are affected as much as 10 times more frequently than men.  It has a peak incidence between 20 and 40 years of age .

Infiltrative ophthalmopathy with resultant exophthalmos 3. Localized. Hyperthyroidism due to diffuse. hyperfunctional enlargement of the thyroid. 2. infiltrative dermopathy.GRAVES’ DISEASE It is characterized by a triad of clinical findings: 1. which is present in a minority of the patients . sometimes called pretibial myxedema.

TSH RECEPTOR ANTIBODIES Thyroid growth-stimulating Immunoglobulin Thyroid-binding inhibitor Immunoglobulin TSH TSH recep recep tor tor Thyroid-stimulating Immunoglobulin Follicular Cell of thyroid gland  Mimics action of TSH  Relatively specific for Graves’ disease  Increase T3 and T4  Proliferation of thyroid follicular epithelium  Stimulate (mimic TSH) or inhibit cellular function .

Overstimulation of the thyroid gland Diffuse Goiter due to thyroid hyperplasia Overproduction of T3 and T4 (hyperthyroidism) Increase T3 and T4 in the blood Decease secretion of TSH in the Anterior Pituitary Gland due to negative feedback .

Orbital Preadipocy te Fibroblast Receptors are targeted by the TRAbs TSH TSH recep recep tor tor TSH TSH recep recep tor tor Both express TSH receptor Follicular Cell of thyroid gland  Proliferation and synthesis of ECM proteins  Increase TSH receptor expression  Perpetuating immune response  Progressive infiltration of retro-orbital space and ophthalmopathy Exophthalmos .

EXOPHTHALMOS .

producing an audible “bruit”  Ophthalmopathy    Wide. staring gaze Lid lag Abnormal protrusion of the eyeball (exophthalmos)  Pretibial myxedema  non-pitting edema  Scaly thickening of the skin  Induration .SIGNS AND SYMPTOMS Caused by autoimmune process:  Diffuse Goiter  May be accompanied by increased blood flow.

PRETIBIAL MYXEDEMA .

anxiety) .SIGNS AND SYMPTOMS Caused by hyperthyroidism:  Weight loss despite increased appetite  Palpitations  Hair loss  Excessive sweating  Hand Tremors  Insomnia  Heat intolerance  Muscle weakness  Atrial fibrillation  Hypertension  Behavioral changes (psychosis. mania.

LAB FINDINGS  Measurement of T3 and T4  Elevated free T3 and T4  Measurement of TSH levels  Depressed TSH levels  Measurement of protein bound iodine  Increased radioactive iodine uptake  Radioiodine scans show a diffuse uptake of iodine  CT or Ultrasound (goiter)  Serologic detection of TRAbs .

tachycardia.TREATMENT  Beta-blockers  Address symptoms related to increased beta adrenergic tone  Palpitations. tremulousness  Thionamides  Aimed at decreasing thyroid hormone synthesis  Propylthiouracil  Radioiodine ablation  Surgical intervention .