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Disorders of the Thyroid gland (THYROIDITIS (SUBACUTE THYROIDITIS…

- - - - FIGURE 405-10
      - characteristic patchy inflammatory infiltrate w/ disruption of thyroid follicles and multinucleated giant cells within some follicles. The follicular changes progress to granulomas accompanied by fibrosis. Finally, the thyroid returns to normal, usually several months after onset.
- - - - TABLE 405-3
    - - TABLE 405-2
  - - - TSH levels change dynamically in response to alterations of T4 and T3-->approach to thyroid testing is to first determine whether TSH is suppressed, normal, or elevated.
        
        (With rare exceptions), a normal TSH level excludes a primary abnormality of thyroid function
        
        abnormal TSH level--> measurements of circulating thyroid hormone levels; measure free, or unbound, hormone levels, which correspond to biologically available hormone pool.
        
        direct methods
        
        (1) unbound thyroid hormone competition with radiolabeled T4 (or an analogue) for binding to a solid-phase antibody,
        
        (2) physical separation of the unbound hormone fraction by ultracentrifugation or equilibrium dialysis
        
        indirect method
        
        free T3 or free T4 index= total [T4 or T3] x THBR
        (for most purposes unbound T4 enough)
        thyroid hormone binding ratio (THBR): derived from T3-resin uptake test: binding of labeled T3 to resin incr when there is reduced unoccupied protein binding sites (e.g., TBG deficiency) or incr total thyroid hormone in sample
      - Total thyroid hormone levels
        
        elevated when TBG is incr due to estrogens (pregnancy, oral contraceptives, hormone therapy, tamoxifen, selective estrogen receptor modulators, inflammatory liver disease)
        
        decr when TBG binding is reduced (androgens, nephrotic syndrome); Genetic disorders and acute illness can also cause abnormalities in thyroid hormone binding proteins, and various drugs (phenytoin, carbamazepine, salicylates, and NSAIDs) can interfere with thyroid hormone binding.
      - TSH should not be used as an isolated laboratory test to assess thyroid function in patients with suspected or known pituitary disease
    - - Autoimmune: TPO Abs. About 5–15% of euthyroid women and up to 2% of euthyroid men have thyroid antibodies; such individuals are at increased risk of developing thyroid dysfunction. Almost all patients with autoimmune hypothyroidism, and up to 80% of those with Graves’ disease, have TPO antibodies, usually at high levels.
      - TSIs: antibodies that stimulate the TSH-R in Graves’ disease; measured by TRAb (TSH receptor antibody)
      - Serum Tg levels incr in all types of thyrotoxicosis except thyrotoxicosis factitia caused by self-administration of thyroid hormone; main role for Tg measurement in follow-up of thyroid cancer patients. After total thyroidectomy and radioablation, Tg levels should be undetectable;
- - - - In Hashimoto’s thyroiditis, there is a marked lymphocytic infiltration of thyroid; Thyroid cell destruction is primarily mediated by the CD8+ cytotoxic T cells, which destroy their targets by either perforin-induced cell necrosis or granzyme B–induced apoptosis. In addition, local T cell production of cytokines, such as tumor necrosis factor (TNF), IL-1, and interferon γ (IFN-γ), may render thyroid cells more susceptible to apoptosis mediated by death receptors, such as Fas, which are activated by their respective ligands on T cells; Antibodies to TPO and Tg are clinically useful markers of thyroid autoimmunity, but any pathogenic effect is restricted to a secondary role in amplifying an ongoing autoimmune response
      - the risk of either autoimmune hypothyroidism or Graves’ disease is incr among siblings; Down’s syndrome; female esterogen; Turner’s syndrome; high iodine intake;
    - - uncommon in children and usually presents with slow growth and delayed facial maturation. The appearance of permanent teeth is also delayed. Myopathy, with muscle swelling, is more common in children than in adults. In most cases, puberty is delayed, but precocious puberty sometimes occurs. There may be intellectual impairment if the onset is before 3 years and the hormone deficiency is severe.
    - - FIGURE 405-7
- - - - diffuse enlargement of thyroid + absence of nodules and hyperthyroidism--> diffuse nontoxic/simple/colloid goiter
      - most commonly caused by iodine deficiency and is termed endemic goiter when it affects >5% of the population. In nonendemic regions, sporadic goiter occurs, and the cause is usually unknown. Thyroid enlargement in teenagers is sometimes referred to as juvenile goiter.
      - more common in women than men (bc AI underlying + incr iodine demands associated with pregnancy)
      - TSH: u. normal or only slightly incr
      - environmental goitrogens : thiocyanate
      - relatively rare: inherited defects in thyroid hormone synthesis
    - - most asymptomatic
      - symmetrically enlarged, nontender, generally soft gland without palpable nodules.
      - If thyroid is markedly enlarged--> tracheal or esophageal compression (unusual in absence of nodular disease and fibrosis)
      - Substernal goiter may obstruct thoracic inlet.
        
        Pemberton’s sign refers to symptoms of faintness with evidence of facial congestion and external jugular venous obstruction when the arms are raised above the head, a maneuver that draws the thyroid into the thoracic inlet.
        
        Respiratory flow measurements and CT or MRI should be used to evaluate substernal goiter in patients with obstructive signs or symptoms
  - - - more common in women than men; incr in prevalence with age.
      - more common in iodine-deficient regions (many factors)
      - wide variation in nodule size.
      - spectrum of morphologies: hypercellular regions to cystic areas filled with colloid. Fibrosis often extensive, and areas of hemorrhage or lymphocytic infiltration may be seen.
      - hyperplastic response to locally produced growth factors and cytokines. (since most nodules are polyclonal in origin)
      - TSH, u. not elevated
    - - Most asymptomatic and euthyroid
      - develops over many years
      - compressive symptoms; uncommon.
      - Symptomatic MNGs are u. extraordinarily large and/or develop fibrotic areas that cause compression.
      - Sudden pain in an MNG u. caused by hemorrhage into a nodule but should raise the possibility of invasive malignancy. Hoarseness, reflecting laryngeal nerve involvement, also suggests malignancy
- - - - TABLE 405-8
    - - TABLE 405-9