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  1. 1. Goiter
  2. 2.  Any enlargement of the thyroid gland is referred to as a goiter.  Most nontoxic goiters are thought to result from TSH stimulation secondary to inadequate thyroid hormone synthesis and other paracrine growth factors.  The thyroid gland enlarges in order to maintain the patient in a euthyroid state.  Goiters may be diffuse, uninodular, or multinodular.  Familial goiters resulting from inherited deficiencies in enzymes necessary for thyroid hormone synthesis may be complete or partial.  The former leads to cretinism, whereas the latter leads to mild hypothyroidism, elevated TSH, and a goiter, although patients may be euthyroid.
  3. 3. Etiology of Non Toxic Goiter  Endemic: iodine deficiency, dietary goitrogens  Medications: iodide, amiodarone, lithium  Thyroiditis: subacute, cronic  Familial: Hormonal dysgenesis from enzyme defects  Resistance to thyroid hormone  Neoplasm
  4. 4.  Elevated TSH levels induce diffuse thyroid hyperplasia  followed by focal hyperplasia resulting in nodules that may or may not concentrate iodine, colloid nodules, or microfollicular nodules.  The TSH-dependent nodules progress to become autonomous, ◦ possibly related to activation of the TSH receptor gene, and, ◦ less commonly to the gsp proto-oncogene.
  5. 5. Clinical Features  Most patients with nontoxic goiters are asymptomatic,  although patients often complain of a pressure sensation in the neck, particularly with motion.  As the goiters become very large, compressive symptoms, such as dyspnea and dysphagia, ensue.  Patients also describe having to clear their throats frequently (catarrh).  Dysphonia from recurrent laryngeal nerve injury is rare, except when malignancy is present.  Obstruction of venous return at the thoracic inlet from a substernal goiter results in a positive Pemberton's sign— ◦ facial flushing and dilatation of cervical veins upon raising the arms above the head
  6. 6.  Sudden enlargement of nodules or cysts because of hemorrhage may cause acute pain.  Physical examination may reveal ◦ a soft, diffusely enlarged gland (simple goiter) or ◦ nodules of various size and consistency in case of a multinodular goiter.  Deviation of the trachea may be apparent.
  7. 7. Diagnostic Tests  Patients are usually euthyroid with normal TSH and low-normal or normal free T4 levels.  If some nodules develop autonomy, patients have suppressed TSH levels or become hyperthyroid.  RAI uptake often shows patchy uptake with areas of hot and cold nodules.  FNA biopsy is recommended in patients who have a dominant nodule or one that is painful or enlarging, ◦ as carcinomas have been reported in 5 to 10% of multinodular goiters.  CT scans are helpful to evaluate the extent of retrosternal extension and airway compression.
  8. 8. Treatment  Most euthyroid patients with small, diffuse goiters do not require treatment.  Some physicians give patients with large goiters exogenous thyroid hormone to reduce the TSH stimulation of gland growth; ◦ this treatment may result in a decrease and/or stabilization of goiter size.  Endemic goiters are treated by iodine administration.
  9. 9.  Surgical resection is reserved for goiters that ◦ (1) continue to increase despite T4 suppression, ◦ (2) cause obstructive symptoms, ◦ (3) have substernal extension, ◦ (4) are suspected to be malignant or are proven malignant by FNA biopsy, and ◦ (5) are cosmetically unacceptable.  Subtotal thyroidectomy is the treatment of choice and patients require lifelong T4
  10. 10. Hyperthyroidism  The clinical manifestations of hyperthyroidism result from an excess of circulating thyroid hormone.  It is important to distinguish disorders  that result from increased production of thyroid hormone ◦ such as Graves' disease and toxic nodular goiter ◦ lead to an increase RAIU  from those disorders that ◦ lead to release of stored hormone from injury to the thyroid gland (thyroiditis)  characterized by low RAIU ◦ or other non-thyroid gland–related conditions.
  11. 11. Differential diagnosis of Hyperthyroidism  Increased hormone synthesis (increased RAIU) ◦ Graves’ disease (diffuse toxic goiter) ◦ Toxic multinodular goiter ◦ Plummer’s disease (Toxic adenoma) ◦ Drug induced - amiodarone; iodine (Jodebasedow) ◦ Thyroid cancer ◦ Struma ovarii ◦ Hydatidiform mole ◦ TSH – secreting pituitary adenoma  Release of preformed Hormone (decreased RAIU) ◦ Thyroiditis- acute phase of Hashimoto’s thyroiditis; subacute thyroiditis ◦ Factitious iatrogenic thyrotoxicosis
  12. 12. Graves' Disease  Although originally described by the Welsh physician Caleb Parry in 1825  The disease is known as Graves' disease after Robert Graves, an Irish physician who described three patients in 1835.  Graves' disease is by far the most common cause of hyperthyroidism in North America, accounting for 60 to 80% of cases.
  13. 13. Graves disease  It is an autoimmune disease of unknown cause with a strong familial predisposition,  F:M = 5:1  peak incidence between the ages of 40 and 60 yrs  characterized by ◦ thyrotoxicosis, ◦ diffuse goiter, and ◦ extrathyroidal conditions, including ophthalmopathy, dermopathy (pretibial myxedema), thyroid acropachy, gynecomastia, and other manifestations.
  14. 14. Etiology, Pathogenesis, and Pathology  The exact etiology of the initiation of the autoimmune process in Graves' disease is unknown.  Some conditions have been suggested as possible trigger such as ◦ the postpartum state, iodine excess, lithium therapy, and bacterial and viral infections  Genetic factors also play a role  Sensitized T-helper lymphocytes stimulate B lymphocytes, which produce antibodies directed against the thyroid stimulating hormone receptor (TRAbs).
  15. 15. Clinical Features  Can be divided into those occurring in any patient with hyperthyroidism and those specific to Graves' disease.  Symptoms common to most patients with hyperthyroidism include ◦ heat intolerance, increased sweating and thirst, and weight loss despite adequate caloric intake.  Symptoms of increased adrenergic stimulation include ◦ palpitations, nervousness, fatigue, emotional lability, hyperkinesis, and tremors.
  16. 16.  The most common gastrointestinal symptoms include increased frequency of bowel movements and diarrhea.  Female patients - amenorrhea, decreased fertility, and an increased incidence of miscarriages.  Children - rapid growth with early bone maturation  Older patients present with cardiovascular complications ◦ such as atrial fibrillation and congestive heart failure.
  17. 17.  On P/E, weight loss and facial flushing may be evident.  The skin may be warm and moist and some darkening  Tachycardia or atrial fibrillation is present ◦ with cutaneous vasodilation leading to a widening of the pulse pressure and ◦ a rapid falloff in the transmitted pulse wave (collapsing pulse).  A fine tremor, muscle wasting, and proximal muscle group weakness with hyperactive tendon reflexes are often present.
  18. 18.  Clinically evident ophthalmopathy-50%.  Exophthalmos, proptosis, periorbital swelling, congestion, and edema of the conjunctiva  Eye symptoms include ◦ lid lag (von Graefe's sign), ◦ spasm of the upper eyelid revealing the sclera above the corneoscleral limbus (Dalrymple's sign) ◦ a prominent stare as a consequence of catecholamine excess.
  19. 19.  True infiltrative eye disease results in ◦ periorbital edema ◦ conjunctival swelling and congestion (chemosis) ◦ proptosis ◦ limitation of upward and lateral gaze (from involvement of the inferior and medial recti muscles, respectively) ◦ keratitis, and even blindness as a result of optic nerve involvement.
  20. 20.  The etiology of Graves' ophthalmopathy is not completely known; ◦ however, orbital fibroblasts and muscles are thought to share a common antigen with thyrocytes, the TSH receptor.  Ophthalmopathy results from inflammation caused by cytokines released from sensitized killer T lymphocytes and cytotoxic antibodies.  Dermopathy occurs in 1 to 2% of patients ◦ characterized by deposition of glycosaminoglycans leading to thickened skin in the pretibial region and dorsum of the foot.
  21. 21.  Pretibial myxedema may be found in 3 to 5% of patients with Graves' disease  Gynecomastia is common in young men.  Thyroid acropachy-Rare bony involvement ◦ subperiosteal bone formation and swelling in the metacarpals  Onycholysis or separation of fingernails from their beds, is a more
  22. 22.  On physical exam, the thyroid is usually diffusely and symmetrically enlarged, as evidenced by an enlarged pyramidal lobe.  There may be an overlying bruit or thrill and loud venous hum in the supraclavicular space.
  23. 23. Diagnostic Tests  Hyperthyroidism - a suppressed TSH with or without an elevated free T4 or T3 level.  If eye signs are present, other tests are generally not needed.  However, in the absence of eye findings, an 123I uptake and scan should be performed. ◦ An elevated uptake, with a diffusely enlarged gland confirms the diagnosis of Graves' disease and helps to differentiate it from other causes of hyperthyroidism.  If free T4 levels are normal, free T3 levels should be determined as they are often elevated in early Graves' or Plummer's disease (T3 toxicosis).
  24. 24.  Anti-Tg and anti-TPO antibodies are elevated in up to 75% of patients, but are not specific.  Elevated thyroid-stimulating hormone receptor (TSH-R) or TSAb are diagnostic of Graves' disease ◦ are increased in approximately 90% of patients.  MRI scans of the orbits are useful in evaluating Graves' ophthalmopathy.
  25. 25. Treatment  Graves' disease may be treated by any of three treatment modalities: 1. antithyroid drugs  propylthiouracil (PTU, 100 to 300 mg three times daily) and methimazole (10 to 30 mg three times daily).  The catecholamine response of thyrotoxicosis can be alleviated by administering beta- blocking agents-propranolol. 2. thyroid ablation with radioactive 131I 3. thyroidectomy
  26. 26.  The choice of treatment depends upon several factors, including ◦ the age of the patient, ◦ the severity of the disease, ◦ the size of the gland, ◦ any coexistent pathology, ◦ associated ophthalmopathy ◦ patient's preferences, and desire for pregnancy
  27. 27. Thyroid Storm  Thyroid storm is a condition of hyperthyroidism accompanied by fever, CNS agitation or depression, cardiovascular dysfunction that may be precipitated by infection, surgery, or trauma.  Occasionally, thyroid storm may result from amiodarone administration.  This condition was previously associated with high mortality rates, but can be appropriately managed in an ICU setting.  Beta blockers are given to reduce peripheral T4-to-T3 conversion and to decrease the hyperthyroid symptoms.
  28. 28.  Oxygen supplementation and hemodynamic support should be instituted.  Non-aspirin compounds can be used to treat pyrexia,  Lugol's iodine or sodium ipodate (intravenously) should be administered to decrease iodine uptake and thyroid hormone secretion.  PTU therapy blocks the formation of new thyroid hormone and reduces peripheral conversion of T4 to T3,  corticosteroids ◦ help to prevent adrenal exhaustion. ◦ also block hepatic thyroid hormone conversion.