THYROID 3

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THYROID 3

  1. 1. TH effects on brain development <ul><li>Exerted through enhancement of nerve growth factor (NGF) production? </li></ul><ul><li>Lack of TH > cretinism </li></ul><ul><li>Causes of cretinism: </li></ul><ul><ul><li>Hypothyroidism during development </li></ul></ul><ul><ul><li>Maternal iodine deficiency </li></ul></ul><ul><li>Result: </li></ul><ul><ul><li>Decreased myelinogenesis, axonal outgrowth </li></ul></ul><ul><ul><li>Decreased protein synthesis </li></ul></ul>
  2. 2. Thermogenesis <ul><li>Homeotherms require mechanisms for generating heat </li></ul><ul><li>Sodium pump theory of thermogenesis </li></ul><ul><li>Na+/K+ ATPase: </li></ul><ul><ul><li>Extrudes 3 Na+ ions; takes in 2 K+ ions </li></ul></ul><ul><ul><li>Requires ATP to move Na+ against electrical gradient </li></ul></ul><ul><li>Heat is given off as phosphate bond is broken in ATP </li></ul>
  3. 3. Thermogenesis, cont’d. <ul><li>TH indirectly “fuels” this process thru its mitochondrial actions </li></ul><ul><li>Inhibit Na+/K+ ATPase with ouabain > reduce TH effects on heat production </li></ul><ul><li>genomic effects of TH also contribute: </li></ul><ul><ul><li>Increases number of Na+/K+ ATPases in plasma membrane </li></ul></ul><ul><ul><li>Increases expression of mitochondrial enzymes </li></ul></ul>
  4. 4. Hypothyroidism <ul><li>Conditions of insufficient TH production </li></ul><ul><li>2 types: </li></ul><ul><ul><li>Primary origin (thyroid problem) </li></ul></ul><ul><ul><li>Secondary origin (problem elsewhere in thyroid axis) </li></ul></ul><ul><li>Cretinism = deficiency during embryonic development >impaired somatic, intellectual dev. </li></ul><ul><li>Myxedema = deficiency during adulthood </li></ul>
  5. 5. Causes of hypothyroidism <ul><li>Iodine deficient diet </li></ul><ul><li>Failure in thyroid development </li></ul><ul><li>Thyroid dyshormonogenesis (failure to produce appropriate enzymes) </li></ul><ul><li>TSH receptor mutations (inactivating) </li></ul><ul><li>TRH receptor mutations (inactivating) </li></ul><ul><li>Low T3 syndrome (failure of peripheral conversion of T4 to T3) </li></ul>
  6. 6. TH receptor defects <ul><li>Often, physical symptoms resemble hypothyroid state </li></ul><ul><li>Exception: elevated TH levels </li></ul><ul><li>Types: </li></ul><ul><ul><li>Generalized resistance to thyroid hormone (GRTH) </li></ul></ul><ul><ul><li>Selective peripheral resistance to thyroid hormone (PerRTH) </li></ul></ul><ul><ul><li>Selective pituitary resistance to thyroid hormone (PRTH) </li></ul></ul>
  7. 7. Hyperthyroidism <ul><li>Thyrotoxicosis (excess TH production) </li></ul><ul><li>Symptoms: </li></ul><ul><ul><li>Increased metabolic rate </li></ul></ul><ul><ul><li>Rapid pulse, elevated body temperature </li></ul></ul><ul><ul><li>Nervousness, anxiety </li></ul></ul><ul><li>Primary origin: </li></ul><ul><ul><li>Neoplasia </li></ul></ul><ul><ul><li>Activating TSH receptor mutation </li></ul></ul><ul><li>Secondary origin: </li></ul><ul><ul><li>TSH-producing tumors </li></ul></ul><ul><ul><li>Thyroid-stimulating antibodies </li></ul></ul>
  8. 8. Graves Disease <ul><li>Overstimulation of thyroid </li></ul><ul><li>Autoimmune response </li></ul><ul><li>Previously thought to be caused by thyroid stimulating antibodies (TSAb) </li></ul><ul><li>TSAb can activate TSH receptor </li></ul><ul><li>Associated with exophthalmos </li></ul>

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