Coupon Accepted Successfully!

 Thyroid Hormone
  1. Thyroid hormone synthesis occurs in colloid & follicular cells. Thyroxin secretion begins by 20th  week.
  Inactive Active
Colloid Abundant Scalloped/ reabsorption Lacunae
Follicle Large Small
Cells Flat Columnar
  1. The minimum daily iodine intake for normal thyroid function is 150 µg in adults.
  2. About 120 µg/d taken up by thyroid gland.
  3. The thyroid secretes 80 µg/d in the form of T3 and T4 , while 40 µg/d diffuses back into the ECF. 
  4. Net loss of I– in the stool of approximately 20 µg/day & rest is excreted in the urine.
  5.  Iodine uptake occurs in thyroid gland, salivary gland, mammary gland, gastric mucosa, placenta, choroids plexus via Na+ /I- symporter which is a secondary active transport.
  1. Thyroid Hormone Synthesis & Secretion
  2. Organification: iodide is oxidized to iodine, and then incorporated into the carbon 3 position of tyrosine residues of a glycoprotein called thyroglobulin in the colloid.
  3. Thyroglobulin is synthesized and secreted by the thyroid cells.
  4. The oxidation and reaction of iodide with the secreted thyroglobulin is mediated by thyroid peroxidase, a membrane-bound enzyme in apical membrane.
  5. The first product of iodination is monoiodotyrosine (MIT). MIT is next iodinated on the carbon 5 position to form diiodotyrosine (DIT).
  6. Two DIT molecules then undergo an oxidative condensation to form T4, T3 is formed by condensation of MIT with DIT. A small amount of RT3 is also formed, probably by condensation of DIT with MIT. 
  7. Colloid is internalized by the thyrocytes by endocytosis. The peptide bonds of thyroglobulin are hydrolyzed, and free T4(80 µg) ,T3(4 µg)  & RT3(2µg)  are secreted.
2. Transport & Metabolism of Thyroid Hormones
  1. Thyroid hormones in blood are transported combined with plasma proteins.
  2. Normally 99.98% of T4 &99.8%T3 in plasma is protein bound. Plasma protein which bind T4 & T3 are:
    a. Albumin
    b. Thyroxine binding prealbumin (TBPA or transthyretin)
    c. Thyroxine binding globulin (TBG)
Plasma Concentration
T4 binding % T3 binding %
TBG 2 67max 46
Transthyretin (TBPA) 15 20 1min
Albumin 3500 13 min 53 max
  1. Estrogens, methadone, heroin, major tranquilizers, clofibrate increase concentrations of Thyroid Hormone-Binding Proteins but the Free Plasma T4, T3, RT3 remains normal and person is euthyroid.
  2. Glucocorticoids, androgens, danazol, asparaginase decrease conc. of Thyroid Hormone-Binding Proteins but again the Free Plasma T4, T3, RT3 remains normal and person is euthyroid.
  3. T4 and T3 are deiodinated in the liver, the kidneys, and many other tissues. One third of the circulating T4 is normally converted to T3 in adult humans, and 45% is converted to RT3. Only about 13% of the circulating T3 is secreted by the thyroid while 87% is formed by deiodination of T4.
  4. Three different deiodinases: D1, D2, and D3. All contain selenium. D1 is present in in the liver, kidneys, thyroid and pituitary. D2 is present in the brain, pituitary and brown fat. D3 is present in the brain and in reproductive tissues.
  5. T4 and T3 are conjugated in the liver to form sulfates and glucuronides. These conjugates enter the bile and secreted in intestine. The thyroid conjugates are hydrolyzed, some are reabsorbed (enterohepatic circulation) and some are excreted in the stool.
  6. Various drugs inhibit deiodinases, producing a fall in plasma T3 levels and a reciprocal rise in RT3. Selenium deficiency has the same effect. A wide variety of nonthyroidal illnesses also suppress deiodinases. These include burns, trauma, advanced cancer, cirrhosis, renal failure, MI and febrile states. 
  7. In fasting:   T3­RT3 (Which helps in energy conservation) & T4 ( Free & Bound) remains normal
  8. In Over feeding: ­T3 RT3
  T4 T3
% Bound
% Free
0.15 ng/dl
T ½
Longer 6-7 days
Shorter 1-2 days
Maxm binding
TBG (67%)
Albumin (53%)
Much more rapid
In colloid
More (25%)
Less (7%)
In secretion
More (80 µg/d)
Less (4µg/d)
Reverse Form
No RT4
RT3 is present
3-5 times more potent
Binding to nuclear receptors
Thyroid hormone actions:
Thyroid hormones enter cells and binds to thyroid receptors (TR) in the nuclei. The hormone-receptor complex then binds to DNA via zinc fingers and affects transcription of a no. of proteins.
Target Tissue
Chronotropic Inotropic
Increased number of β-adrenergic receptors
Enhanced responses to circulating catecholamines, Increased Cardiac output
Increased proportion of α-myosin heavy chain (with higher ATPase activity)
Adipose tissue
Stimulated lipolysis, lower circulating cholesterol levels
Increased protein breakdown
Promote normal growth and skeletal development (can also accelerate bone resorption)
Nervous system
Promote normal brain development , can cause rapid mentation, irritability, and restlessness, reaction time of reflex decreased
Increased rate of carbohydrate absorption, stimulate motility
Formation of LDL receptors
hepatic conversion of carotene to vitamin A, carotenemia in hypothyroidism
Stimulated oxygen consumption by metabolically active tissues (exceptions: testes, uterus, lymph nodes, spleen, anterior pituitary)
Increases metabolic rate by stimulating Na+K- ATPase
Increased heat production: Peripheral resistance decreases because of cutaneous vasodilation

  1. Human TSH is a glycoprotein encoded by a gene on chromosome 6 and chromosome 1.
  2. The biologic half-life of human TSH is about 60 min. Secretion is pulsatile, and mean output starts to rise at about 9:00 PM, peaks at midnight.
  3. The normal secretion rate is about 110 g/d. The average plasma level is about 2 g/mL
  4. Because the subunit in hCG is the same as that in TSH, large amounts of hCG can activate thyroid receptors nonspecifically.
  5. It increases iodide trapping & binding; synthesis of T3, T4  and iodotyrosines; secretion of thyroglobulin and endocytosis of colloid.
  6. Inhibited by Stress, Dopamine, Somatostatin, Glucocorticoids & T3  T4 
Thyroid Resistance
Type of resistance
Whether TSH is suppressible by external T3/T4
Peripheral tissue + pituitary
Not clinically hypothyroid
Inappropriately high
Pituitary only
Hyper thyroid
Inappropriately normal / high
Peripheral tissue only
a. Wolff–Chaikoff effect: High iodine conc. inhibiting formation of thyroid hormones due to down-regulation of sodium-iodide symporter.

b. Jod-Basedow effect: This phenomenon is an iodine-induced hyperthyroidism, typically presenting in a patient with endemic goiter

Test Your Skills Now!
Take a Quiz now
Reviewer Name