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thyroidgland-120420032852-phpapp01.pptx
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- 2. Thyroid gland • Largestgland in the body • Location : in the neck inferior the larynx and spanning over the ventral surface of trachea • Function: – Secretion of thyroxin and triiodothyronine – Secretion of calcitonin
- 3. Thyroid Gland Anteriorsurface of the trachea just inferior to thyroid cartilage (or Adam’s apple) Two lobes connected by an isthmus Microscopic thyroid follicles produce thyroid hormone CCells - produce calcitonin ( Ca2+)
- 4. Structures and Functionsof Endocrine System Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc. 5 Fig. 48-10. Thyroid and parathyroid glands. Note the surrounding structures.
- 5. Thyroid Gland: Hormonesand Iodine Metabolism
- 7. Synthesis of ThyroidHormone Thyroid hormone synthesis and secretion involves processes that occur within follicular epithelial cells and in colloid. I-: iodide ions; I2: iodine; TG: thyroglobulin; MIT: monoiodotyrosine; DIT: diiodotyrosine. I- Na+ I- I2 I2 Thyroid Peroxidase TG TG MIT + DIT -T3 -T4 -MIT -DIT -T -T3 -M4IT -DIT TG TG + T3 + T4 Follicle Epithelium Colloid Blood Pump Tyrosine MIT+DIT T3 DIT+DIT T4
- 8. Releases of ThyroidHormone
- 9. Synthesis of thyroidhormones 1. Iodide trapping – By sodium iodide symporter – Blocked by: • Thiocyanate SCN- • Perchlorate ClO4- • Pertechnetate TcO4- 2. Oxidation of iodide – By thyroid peroxidase – Inhibited by: 3. large intake of iodide >150mcgday 4. Thioamides(refer to hyperthyroidism therapy)
- 10. Synthesis of thyroidhormones 3. Organification – Tyrosine residues of thyroglobulin is iodinated 1. Inhibited by large intake of iodide >150mcgday 2. Thioamides(refer to hyperthyroidism therapy) – Produce monoiodotyrosine residues MIT and diiodotyrosine residues DIT
- 11. Synthesis of thyroidhormones 4. Coupling – DIT+MIT=T3 – DIT+DIT=T4 5. Storage : – Along with thyroglobulin 6. Exocytosis and proteolysis – Release of T4 & T3 7. Conversion of T4 to T3 in peripheral tissue
- 13. T4 vs T3 T4 •Thyroid gland synthesize 90% • 0.04%free • Not active • Long T12 T3 • Thyroid gland synthesize 9% • 0.4% fr • active
- 14. Mechanism of actionof thyroid hormones
- 15. Thyroid Gland Thyroidhormones target almost every body cell Can enter cells & bind to intracellular receptors on mitochondria & in nucleus Effects include: increased ATP production increased cellular metabolism, energy utilization & oxygen consumption increased body temperature growth & development of skeletal, muscular & nervous system in fetus & children
- 16. Effects Of ThyroidHormones On The Cardiovascular System • Increase heart rate • Increase force of cardiac contractions • Increase stroke volume • Increase Cardiac output • Up-regulate catecholamine receptors
- 17. Effects Of ThyroidHormones On The Respiratory System • Increase resting respiratory rate • Increase minute ventilation • Increase ventilatory response to hypercapnia and hypoxia
- 18. Effects Of TheThyroid Hormones On The Renal System • Increase blood flow • Increase glomerular filtration rate
- 19. Effects Of TheThyroid Hormones On Oxygen Carrying Capacity • Increase RBC mass • Increase oxygen dissociation from hemoglobin
- 20. Thyroid Hormone ActionsWhich Increase Oxygen Consumption • Increase mitochondrial Size,Number and Key Enzymes • Increase Plasma membrane Na-K ATPase Activity • Increase Futile Thermogenic Energy Cycles • Decrease Superoxide Dimutase Activity
- 21. Effects Of TheThyroid Hormones On Intermediary Metabolism • Increase glucose absorption from the GI tract • Increase carbohydrate,lipid and protein turnover • Down-regulate insulin receptors • Increase substrate availability
- 22. Effects Of TheThyroid Hormones In Growth And Tissue Development • Increase growth and maturation of bone • Increase tooth development and eruption • Increase growth and maturation of epidermis,hair follicles and nails • Increase rate and force of skeletal muscle contraction • Inhibits synthesis and increases degradation of mucopolysaccharides in subcutaneous tissue
- 23. Effects Of TheThyroid Hormones On The Nervous System • Critical for normal CNS neuronal development • Enhances wakefulness and alertness • Enhances memory and learning capacity • Required for normal emotional tone • Increase speed and amplitude of peripheral nerve reflexes
- 24. Effects Of TheThyroid Hormones On The Reproductive System • Required for normal follicular development and ovulation in the female • Required for the normal maintenance of pregnancy • Required for normal spermatogenesis in the male
- 25. Regulation of ThyroidHormones
- 26. THYROID DISORDERS MAYBE CLASSIFIED AS:- Hyperthyroidism (Thyrotoxicosis) •Overproduction of Thyroid hormones Hypothyroidism (Gland destruction) Underproduction of Thyroid hormones
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- 29. . SIGNS AND SYMPTOMS For Hyperthyroidism:- • Tachycardia • Palpitations • Nervousness • Tremors • Increased BP • Heat intolerance
- 30. For Hypothyroidism • Weightgain despite poor appetite • Cold intoleration • Constipation • Lethargy • But, these symptoms are often non- specific and makes diagnosis difficult.
- 31. LABORATORY EVALUATION • NormalTSH levels practically excludes abnormalities • If TSH is abnormal, next steps:- • Total and free T4 & T3 levels • TSI( Thyroid Stimulating Ig) • TPO(Thyroid Peroxidase Ab) • Anti mitochondrial Ab • Serum Tg (Thyroglobulin) • Radioactive uptake and Thyroid scanning
- 32. Disease of thyroidgland Hypothyroidism • Hashimoto thyroiditis (autoimmune disorder) • Iodine deficiency • Drugs (amiodarone) • Radiation exposure • Pituitary tumors • Myxedema (life threatening condition of hypothyroidism) Hyperthyroidism • Graves disease (autoimmune disease) • Toxic multinodular goiter • Drugs (amiodarone) • Thyroid storm(life threatening condition of hyperthyroidism)
- 33. GOITER • A goiteris a swelling of the neck or the larynx resulting from the enlargement of the thyroid gland ( Thyromegaly ). • Worldwide over 90 % cases of goiter are caused by iodine deficiency. • It may be associated with both Hypothyroidism and Hyperthyroidism.
- 34. . CLASSIFICATION OF GOITERS GROWTH PATTERN:- • UNINODULAR • MULTINODULAR • DIFFUSE SIZE:- • CLASS I • CLASS II • CLASS III
- 36. CAUSES: • Iodinedeficiency • Congenital hypothyroidism • Pituitary diseases • Thyroid cancer • Thyroid hormone insensitivity TREATMENT: • It is treated according to the cause, if thyroid gland is producing too much T4 and T3, • radioactive iodine is given to the patient to shrink the gland. • If the cause is iodine deficiency, it is supplemented as lugol’s solution or KI
- 37. GRAVE’S DISEASE • Alsoknown as toxic diffuse goiter is an autoimmune disease that affects the thyroid gland. • It is the most common cause of hyperthyroidism. • The exact cause of the disease is unclear. • However, it is believed to involve a combination of genetic and environmental factors.
- 38. SIGNS AND SYMPTOMS: •Almost all of the signs of the disease is believed to be a result of hyperthyroidism. • These include insomnia, hand tremors, hyperactivity, heat intolerance, excessive sweating, weight loss despite increased appetite, etc. • Exceptions are ophthalmopathy, goiter and pretibial myxedema .
- 39. MECHANISM: • Thyroid stimulatingimmunoglobins recognize and bind to Thyrotropin receptor (TSH receptor) which further stimulates the release of T3 & T4 • Thyroxine receptors in the pituitary gets activated by surplus hormone suppressing further release of TSH in a negative feedback loop. • The result is very high levels of circulating thyroid hormone and a low TSH level.
- 41. TREATMENT • Treatment ofgraves’ disease include antithyroid drugs which reduces the production of thyroid hormones. • Radioiodine is also used as a measure. Thyroidectomy(surgical excision of gland) is also used in many cases. • Mild cases of ophthalmopathy could be treated by lubricant eye drops or non-steroidal anti inflammatory drops.
- 42. CRETINISM • Cretinism isa condition of severely stunted physical and mental growth due to untreated congenital deficiency of thyroid hormone, usually due to maternal hypothyroidism. PATHOPHYSIOLOGY • Cretinism can be endemic, genetic or sporadic. • Poor growth is apparent as early as the first year of life. It causes mental deterioration, swelling of skin and loss of hair. Bone maturation and puberty is severely delayed. • Ovulation is impeded and infertility is common
- 43. CAUSE AND TREATMENT •Most common cause is iodine deficiency. • Populations living in areas with low soil iodine concentration are prone to this disease. • Sporadic and genetic cretinism results from abnormal development or function of the fetal thyroid gland. • This type of cretinism has been almost completely eliminated in developed countries by early diagnosis by newborn screening schemes followed by lifelong treatment with T4. • Frequent monitoring (every 2–3 weeks during the first months of life) is recommended to ensure that infants with congenital hypothyroidism remain within the high end of normal range.
- 45. MYXEDEMA • Myxedema isa term used synonymously with severe hypothyroidism • Myxedema develops in the patient with almost total lack of thyroid hormone function • It is generally characterized by bagginess under the eyes and swelling of the face. • In this condition, greatly increased quantities of hyaluronic acid and chondroitin sulfate bound with protein form excessive tissue gel in the interstitial spaces, and this causes the total quantity of interstitial fluid to increase.
- 46. Because of thegel nature of the excess fluid, it is mainly immobile, and the edema is the nonpitting type. CAUSES • Myxedema can occur in: • Hyperthyroidism, associated with pretibial myxedema and exophthalmos. • Pretibial myxedema can occur in 1–4% of patients with Graves' disease, a cause of hyperthyroidism. • Hypothyroidism, including Hashimoto's thyroiditis
- 47. PATHOPHYSIOLOGY • Myxedema causesspecific forms of dermal edema. • The connective fibres is separated by an increased amount of monosaccharides. • This protein-monosaccharide complex binds water, producing non-pitting boggy edema. • In particular around eyes, hands, and feet. • Myxedema is also responsible for thickening of tongue and laryngeal and pharyngeal mucous membranes.
- 48. TREATMENT 1. Airway management 2.Thyroid hormone replacement 3. Gluco-corticoid therapy 4. Supportive measures
- 50. HASHIMOTO'S THYROIDITIS • Itis an auto-immune disease in which the thyroid gland is gradually destroyed. • Over time the thyroid may enlarge and form painless goiter. • Some people eventually develop hypothyroidism. • After many years the thyroid shrinks in size. • It is thought to be caused due to a combination of genetic and environmental factors.
- 51. SIGNS AND SYMPTOMS •Fatigue • Weight gain • Pale or puffy face • Feeling cold • Joint and muscle pain • Constipation • Dry and thinning hair • Irregular menstrual cycles • Depression etc
- 52. PATHOPHYSIOLOGY • Various auto-antibodiesmay be present against thyroid peroxidase, thyroglobulin and TSH receptors. • Gross morphological changes within the thyroid are seen in the general enlargement which is far more locally nodular and irregular than more diffuse patterns
- 53. TREATMENT • Managing hormonelevels: • Hypothyroidism caused by Hashimoto's thyroiditis is treated with thyroid hormone replacement agents. • E.g.: Levothyroxine, triiodothyronine.