Thyroid | Anatomy2Medicine
Thyroid,Treatment,Causes

Thyroid

    • Thyroid Hormones
      • The thyroid hormones are iodinated derivatives of tyrosine  
      • Iodide is oxidized to iodine by thyroperoxidase.(MCQ)
      • Formation of the Thyroid Hormones

 

  • Iodine is incorporated into tyrosine residues to form monoiodotyrosine (MIT) or diiodotyrosine (DIT).

 

        • Two DITs are coupled to form Levothyroxine (T4).
        • One MIT and two DITs are coupled to form T3, or reverse T3 (rT3).

 

  • In the thyroid gland, most of the iodine is found in MIT and DIT.
  • Thyroxine (T4) is released in larger amounts than T3, the primary active hormone

 

        • rT3 is released but is inactive. (MCQ)
      • Iodine Metabolism

 

  • Although several tissues take up iodide, only the thyroid gland significantly incorporates iodine into protein.

 

        • The thyroid-to-serum ratio of iodide is normally 30:1. (MCQ)

 

  • Iodide is transported into the thyroid at the basal membrane of follicular
  • cells by an active process that may involve Na/K+-ATPase in the trapping mechanism. (MCQ)

 

        • Iodide is oxidized to iodine in the follicular lumen.
          • Iodine is incorporated into tyrosine residues (organification) to form MIT and DIT.
          • Coupling of MIT and DIT form T4 and T3

 

  • T4 and T3 are stored as parts of thyroglobulin residues(MCQ)

 

        • with TSH stimulation the residues are taken into the follicular cells by endocytosis.

 

  • In the cell, thyroglobulin residues are acted on by lysosomal and protease enzymes to form T4 and T3, and to form MIT and DIT.

 

      • Feedback Regulation of Thyroid Function
        • the primary negative feedback is at the pituitary (MCQ)
        • negative feedback regulation also occurs at the hypothalamus by blocking TRH release.
        • T3 and T4 negatively feed back and inhibit TSH release from the anterior pituitary. (MCQ)
        • Somatostatin and dopamine are inhibitory by blocking TSH secretion. (MCQ)
      • Iodide and Thyroid Hormone Homeostasis
        • Iodide mediates thyroid hormone biosynthesis and release.
        • Decreased iodide in the diet decreases T4 and T3 secretions.
        • This increases TSH due to lack of feedback.
        • Increased TSH levels cause hypertrophy and hyperplasia of the thyroid (goiter).

 

  • With decreased iodine availability, the thyroid compensates, secreting more of the active hormone, T3.
  • High iodide intake will decrease both thyroid hormone biosynthesis (Wolff-Chaikoff effect) and release. (MCQ)

 

      • Thyroid Hormone Transport
        • Thyroid-binding globulin (TBG)
          • a glycoprotein produced by the liver
          • binds approximately 70% of the T4 and approximately 80% of the T3 in plasma. (MCQ)
        • Albumin
          • has a much lower affinity for binding the thyroid hormones than does TGB
          • the high concentration of albumin results in the binding of approximately 20% of T4 and approximately 11% of T3.
        • During pregnancy, increased estrogen causes increased TBG production. (MCQ)
          • Pregnant women do not become hyperthyroid, however, because free thyroid hormone levels remain relatively constant. (MCQ)
        • Androgens and cirrhosis of the liver decrease TBG and decrease total thyroid hormone, but individuals does not become hypothyroid, because the amount of free hormone is adjusted to normal levels. (MCQ)
        • salicylates compete with T4 and T3 for binding sites on TBG, producing low total thyroid hormone levels, but free hormone levels again remain relatively normal. (MCQ)
      • Physiologic Actions of Thyroid Hormones
        • T4 and T3 enter cells by passive diffusion

 

  • the biological effects of T4 are thought to be a result of its intracellular conversion to T3.

 

        • The primary effect of the thyroid hormones is to increase O2 consump- tion (calorigenic action) in all tissues of the body except brain, testes, and spleen.
        • Thyroid hormones increase oxygen consumption and basal metabolic rate (BMR).
        • Both respiration and cardiac output are increased in order to supply tissues with increased O2.
        • In the heart, rate and force of myocardial contractions are increased.
        • If BMR increases, and adequate fuel (increased food intake) is not provided, catabolism results and weight is lost.
          • Hyperthyroid individuals often lose weight(MCQ)
          • hypothyroid individuals often gain weight
        • The generalized muscle wasting in the presence of high concentra- tions of the thyroid hormones is associated with muscle weakness and fatigability.
        • High levels of thyroid hormones also cause increased excretion of Ca2+ and PO43−as well as decreased bone mass, and occasionally pathologic fractures, in elderly women. (MCQ)
        • Thyroid hormones increase the BMR and stimulate heat production.
          • Hyperthyroid individuals exhibit peripheral vasodilation and sweating.

 

  • Hypothyroid individuals exhibit peripheral vasoconstriction and intolerance to cold.
  • Thyroid hormones are necessary for normal growth and development.

 

          • Individuals who are hypothyroid from birth are dwarfed and mentally retarded. This condition is known as cretinism.
          • If thyroid hormone replacement is not begun by the end of the first month after birth, the neurologic defects causing mental retardation cannot be reversed.
        • Many thyroid hormone actions are due to a synergistic interaction with the sympathetic nervous system (MCQ)

 

  • Thermogenesis
  • Lipolysis
  • Glycogenolysis

 

        • gluconeogenesis).
      • Adrenergic blockade attenuates many of the cardiovascular and nervous system manifestations (eg, tremor) of hyperthyroidism.