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Lect 3-thyroid disorders


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thyroid disorders

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Lect 3-thyroid disorders

  1. 1. Thyroid Gland Disorders<br />SMS3023<br />By: Dr. Mohanad<br />
  2. 2. Thyroid Gland: Introduction<br />The largest pure endocrine gland (15-25 gm), located in the anterior neck <br />Consists of two lateral lobes connected by a median tissue mass called the isthmus.<br />2<br />
  3. 3. Thyroid Gland: introduction<br />Blood supply <br />Arterial blood supply<br />Superior thyroid artery from external carotid<br />Inferior thyroid artery from subclavians<br />Blood flow 4-6 ml/min/gm<br />Venous blood supply<br />Three pairs of veins supply blood to the gland <br />
  4. 4. Thyroid Gland: introduction<br />The thyroid gland is made up of closely packed sacs called thyroid follicles.<br />The structural and functional unite of thyroid gland.<br />Cyst-like structure <br />0.2 – 0.9 mm in diameter <br />Simple cuboidal epithelial (follicular cells) surrounding a lumen filled with colloid.<br />T4 and T3 present in colloid bound to a large protein called thyroglobulin.<br />
  5. 5. Thyroid follicles <br />
  6. 6. Thyroid follicles <br />
  7. 7. Thyroid Follicles <br />
  8. 8. Thyroid Gland: Introduction<br />Thyroid gland secret 3 hormones<br />Thyroxin or (T4) <br />Tri-iodotyronine or (T3)<br />Main hormones secreted by thyroid gland<br />Secreted by follicular cells<br />Amino acid derivatives (tyrosine)<br />Calcitonin<br />Produced by parafollicular cells – C cells<br />
  9. 9. Hypothalamus-Pituitary-Thyroid Axis <br />
  10. 10. Thyroid Gland: Introduction<br />Synthesis of T4 and T3 are stimulated by:<br />↑TSH<br />Synthesis of T4 and T3 are reduced by:<br />↓ TSH <br />Glucocorticoid, dopamin and somatostatine.<br />
  11. 11. Actions of Thyroid Hormones<br />Increase the body’s overall basal metabolic rate <br />Increase oxygen consumption<br />Essential for normal growth<br />Mental development<br />Sexual maturation<br />Increase the sensitivity of CVS and CNS to catecholamines (↑COP and HR)<br />
  12. 12. Diseases of the Thyroid Gland<br />Congenital diseases<br />Inflammation<br />Functional abnormality<br />Diffuse and Multinodular goiters<br />Neoplasia<br />
  13. 13. Congenital Thyroid Diseases<br />Agenesis /Aplasia<br />Hypoplasia<br />Accessory or aberrant thyroid glands<br />Thyroglossal duct cyst<br />
  14. 14. Thyroglossal Duct Cyst<br />A thyroglossal duct cyst is a neck mass or lump that develops from cells and tissues remaining after the formation of the thyroid gland during embryonic development. <br />Children<br />Failure of regression<br />Neck, medial<br />Squamous or columnar lining<br />often appears after an upper respiratory infection when it enlarges and becomes painful.<br />Complications: inflammation, <br /> sinus tracts<br />
  15. 15. Inflammation<br />Thyroiditis<br />Acute illness with pain<br />Infectious<br />Acute<br />Chronic<br />Subacute or granulomatous (De Quervain’s)<br />Little inflammation with dysfunction<br />Subacute lymphocytic thyroiditis<br />Fibrous (Riedel) thyroiditis<br />Autoimmune<br />Hashimoto thyroiditis <br />
  16. 16. HASHIMOTO THYROIDITIS<br />Most common cause of hypothyroidism<br />Autoimmune, non-Mendelian inheritance<br />45-65 years, F:M = 10-20:1<br />Painless symmetrical enlargement<br />Risk of developing <br />B-cell non-Hodgkin’s lymphoma<br />Other concomitant autoimmune diseases<br />Endocrine and non-endocrine <br />
  17. 17. Hashimoto ThyroiditisPathogenesis<br />Immune systems reacts against a variety of thyroid antigens<br />Progressive depletion of thyroid epithelial cells which are gradually replaced by mononuclear cells -> fibrosis<br />Immune mechanisms may includes:<br />CD8+ cytotoxic T cell-mediated cell death<br />Cytokine-mediated cell death <br />Binding of antithyroid antibodies -> antibody dependent cell-mediated cytotoxicity <br />
  18. 18. Morphology-Hashimoto Thyroiditis<br />Diffuse enlargement<br />Firm or rubbery<br />Pale, yellow-tan, firm & somewhat nodular cut surface<br />firm consistency: may be confused with carcinoma<br />not stony hard as in Riedel's thyroiditis<br />a distinctly multinodularqualityfascial attachment to the tracheal wall slightly thickened, but no strong fixation<br />
  19. 19. Morphology<br />Necrosis<br />Calcification<br />Resembles a hyperplastic lymph node<br />Resembles a hyperplastic lymph node<br />
  20. 20. Histopathology-Hashimoto Thyroiditis<br />Massivelymphoplasmcyticinfiltration with lymphoid follicles formation <br />Destruction of thyroid follicles<br />Remaining follicles are small and many are lined by Hurthle cells<br />Increased interstitial connective tissue<br />plasma cells, histiocytes<br />scattered intrafollicular multinucleated giant cells<br />Polyclonal lymphoplasmacytic population<br />ashimoto's thyroiditis showing lymphoid follicles with prominent germinal centers and oncocytic follicular epithelium.<br />
  21. 21. Histopathology-Hashimoto Thyroiditis<br />Follicles: small and atrophic<br />most lined by variably sized Hürthle cells<br />Nuclei of Hürthle cells may be: enlarged and hyperchromaticoptically clear and overlapping (reminiscent of papillary carcinoma)<br />Squamous nests: thought to arise from metaplasia of follicular cells<br />Hashimoto's thyroiditis with extensive fibrosis, atrophy of follicular epithelium, and squamous metaplasia.<br />
  22. 22. Follicles: small and atrophic<br />
  23. 23. Hashimoto's thyroiditis<br />This symmetrically small thyroid gland demonstrates atrophy. <br />This is the end result of Hashimoto's thyroiditis.<br />
  24. 24. Hashimoto's thyroiditis<br />A lymphocytic infiltration with prominent follicles with germinal centers<br />
  25. 25. Symptoms<br />Fatigue, Depression<br /> Modest weight gain, Cold intolerance<br /> Excessive sleepiness, Dry, coarse hair, Dry skin<br /> Constipation, Increased cholesterol levels<br />Muscle cramps, Decreased concentration<br /> Vague aches and pains, <br /> Swelling of the legs<br />
  26. 26. Thyroid disorders <br />Hypothyroidism<br />Underactive thyroid<br />Hyperthyroidism <br />Overactive thyroid <br />Goiter <br />Thyroid enlargement <br />
  27. 27. Hypothyroidism <br />Outlines<br />Definition <br />Causes <br />Clinical features <br />Investigation <br />Treatment <br />
  28. 28. Hypothyroidism<br />Definition<br />A clinical and biochemical syndrome that results from a deficiency in thyroid hormone secretion from thyroid gland or in the action<br />The disease ranges from subclinical hypothyroidism to primary and secondary hypothyroidism and the extreme medical emergency, myxoedema coma.<br />28<br />
  29. 29. 29<br />Hypothyroidism <br />Prevalence<br />It is a common disorder with prevalence ranges from 2-15% population<br />♀ > ♂ <br />Female to male ratio = 10:1<br />↑ with age; ♀ = ♂<br />Mean age at diagnosis is 50 years <br />
  30. 30. Primary Hypothyroidism<br />Disease of the thyroid gland <br />Secondary Hypothyroidism <br />Hypothalamic-pituitary diseases (reduced TSH)<br />Hypothyroidism <br />
  31. 31. Causes of Hypothyroidism<br />PRIMARY<br />Congenital<br />Agenesis <br />Ectopic thyroid remnants <br />Defects of hormone synthesis<br />Iodine deficiency <br />Dyshormonogenesis<br />Antithyroid drugs <br />Other drugs (e.g. lithium, amiodarone, interferon)<br />
  32. 32. Causes of Hypothyroidism<br />Autoimmune<br />Atrophic thyroiditis<br />Hashimoto's thyroiditis<br />Postpartum thyroiditis<br />Infective<br />Post-subacutethyroiditis<br />
  33. 33. Causes of Hypothyroidism<br /><ul><li>post-surgery</li></ul>Post-irradiation<br />Radioactive iodine therapy <br />External neck irradiation <br />Infiltration<br />Tumour<br />SECONDARY<br />Hypopituitarism<br />Isolated TSH deficiency <br />
  34. 34. Symptoms and Signs <br />
  35. 35. Investigation of primary hypothyroidism <br />Serum TSH <br />The investigation of choice. <br />A high TSH level confirms primary hypothyroidism. <br />Serum T4<br />low free T4 level confirms the hypothyroid state.<br />Thyroid and other organ-specific antibodies .<br />
  36. 36. Investigations of other abnormalities:<br />Anaemia.<br />Increased serum aspartatetransferaselevels, from muscle and/or liver <br />Increased serum creatinekinaselevels, with associated myopathy<br />Hypercholesterolaemia<br />Hyponatraemia due to an increase in ADH and impaired free water clearance. <br />
  37. 37. Treatment <br />Replacement therapy with levothyroxine(thyroxine, i.e. T4) is given for life. <br />In the young and fit, 100 μg daily is suitable.<br />thyroid function tests after at least 6 weeks on a steady dose<br />the aim is to restore T4 and TSH to well within the normal range<br />An annual thyroid function test is recommended .<br />
  38. 38. Myxoedema coma <br />Severe hypothyroidism, associated with: <br /> - confusion or even coma. <br /> - hypothermia.<br /> - severe cardiac failure. <br /> - Hypoventilation. <br /> - Hypoglycaemia.<br /> - hyponatraemia. <br />patients require full intensive care.<br />
  39. 39. Pathogenesis <br /><ul><li>Myxedema coma/crisis occurs most commonly in older women with long-standing, undiagnosed or undertreated hypothyroidism who experience an additional significant stress, such as infection, a systemic disease, certain medications, and exposure to a cold environment.
  40. 40. When hypothyroidism is long-standing, physiologic adaptations occur.
  41. 41. Reduced metabolic rate and decreased oxygen consumption result in peripheral vasoconstriction, which maintains core temperature.
  42. 42. The number of beta-adrenergic receptors is reduced, usually with preservation of alpha-adrenergic receptors and circulating catecholamines, causing beta/alpha-adrenergic imbalance, diastolic hypertension, and reduced total blood volume.
  43. 43. Myxedema coma/crisis is a form of decompensated hypothyroidism in which adaptations are no longer sufficient.
  44. 44. Essentially, all organ systems are affected. </li></li></ul><li>Metabolic<br />Thyroid hormones are critical for cell metabolism and organ function. <br />With an inadequate supply, organ tissues do not grow or mature, energy production declines, and the action of other hormones is affected. <br />Although weight gain is common, severe obesity is rarely secondary to hypothyroidism alone. <br />However, long-standing, untreated hypothyroidism may result in years of inactivity, eventually with a large increase in weight. <br />Because of decreased drug metabolism, overdoses of medications (eg, morphine, hypnotics, anesthetic agents, sedatives) can occur and can even precipitate myxedema crisis. <br />
  45. 45. Neurologic<br />Although the condition is called myxedema coma, the absence of coma does not exclude the diagnosis of this disorder. <br />The presenting mental status may be lethargy or stupor. The exact mechanisms causing changes in mental status are not known. <br />Brain function is influenced by reductions in cerebral blood flow and oxygen delivery, a lack of thyroxine (T4) and triiodothyronine (T3), and reductions in oxygen and glucose consumption; all of these factors are probably involved. <br />Hyponatremiabrought on by renal dysfunction may be an additional cause of altered mental function.<br />
  46. 46. Myxoedema coma <br />Treatment:<br />T3 orally or intravenously in doses of 2.5-5 μg every 8 hours, then increasing the dose. <br />oxygen (by ventilation if necessary) <br />monitoring of cardiac output and pressures <br />gradual rewarming <br />hydrocortisone 100 mg i.v. 8-hourly <br />glucose infusion to prevent hypoglycaemia. <br />
  47. 47. Hyperthyroidism <br />(Thyroid Overactivity, Thyrotoxicosis)<br />
  48. 48. Hyperthyroidism<br />A common disorder.<br />affecting females more than males <br />sex ratio of 5 : 1.<br /> most often between ages 20 and 40 years. <br />Nearly all cases (> 99%) are caused by intrinsic thyroid disease.<br />A pituitary cause is extremely rare <br />
  49. 49. Causes of hyperthyroidism<br />Common <br />Graves' disease (autoimmune) <br />Toxic multinodulargoitre<br />Solitary toxic nodule/adenoma <br />
  50. 50. Causes of hyperthyroidism<br />Uncommon <br />Acute thyroiditis<br />viral <br />autoimmune <br />post-irradiation <br />Gestational thyrotoxicosis<br />Neonatal thyrotoxicosis (maternal thyroid antibodies) <br />Exogenous iodine <br />Drugs - amiodarone<br />
  51. 51. Graves' disease<br />The most common cause of hyperthyrodism<br />It is an autoimmune disorder. where the thyroid is overactive, producing an excessive amount of thyroid hormones (a serious metabolic imbalance known as hyperthyroidism and thyrotoxicosis)<br />More common in young adults.<br />Can be familial and associated with other autoimmune diseases<br />The resulting is a dramatic constellation of neuropsychological and physical signs and symptoms.<br />Characterized by hyperthyroidism, ophthalmopathy with exophthalmos and dermopathy (pretibialmyxedema)<br />
  52. 52. Graves’ Disease<br />Autoimmune disease with breakdown of helper-T-cell tolerance<br />Excessive production of TWO thyroid autoantibodies: <br />Thyroid-stimulating antibody (TSAb) &<br />Growth-stimulating antibody (GSAb)<br />Antibodies bind to the TSH receptor of the follicular cell<br />Stimulation of the cell resulting in:<br />Increased levels of thyroid hormones &<br />Hyperplasia of the thyroid gland<br />Hyperthyroidism and Thyroid gland enlargement<br />
  53. 53. PATHOGENESIS<br />Type II reaction:- autoimmune antibodies target somatic tissues such as extraocular muscles causing an antigen-antibody reaction.<br />A large number of lymphokines are implicated in the inflammatory process.<br />Inflammation results in production of mucopolysaccharidesby fibroblasts leading to swelling followed by collagen production resulting in restriction.<br />There is a high concentration of macrophages in the inferior rectus muscle as well as CD4+ memory T cells and CD8 T cells. <br />This may account for the clinical observation of maximal disease activity in this muscle.<br />
  54. 54. Graves' disease<br />Morphology:<br />Grossly : the thyroid gland is diffusely enlarged because of the presence of diffuse hypertrophy and hyperplasia of thyroid follicular epithelial cells <br />
  55. 55. Graves' disease<br />note the prominent infoldings of the hyperplastic epithelium<br />
  56. 56. Graves' disease<br />The tall columnar thyroid epithelium lines the hyperplasticinfoldings<br />into the colloid. Note the clear vacuoles in the colloid next to the epithelium.<br />
  57. 57. Hyperthyrodism<br />Clinical features: due to<br />Hypermetabolic state <br />Overactivity of sympathetic nervous system<br />
  58. 58. Symptoms <br />Weight loss<br />Increased appetite<br />Irritability<br />Tremor<br />Goiter <br />Restlessness<br />Stiffness<br />Muscle weakness<br />Breathlessness <br /><ul><li>Palpitation
  59. 59. Heat intolerance
  60. 60. Excessive sweating
  61. 61. Itching
  62. 62. Thirst
  63. 63. Vomiting
  64. 64. Diarrhoea
  65. 65. Oligomenorrhoea
  66. 66. Loss of libido </li></li></ul><li>Signs <br />Tremor<br />Irritability<br />Psychosis<br />Tachycardia or atrial fibrillation<br />Warm vasodilator peripheries<br />Systolic hypertension<br />Cardiac failure<br />
  67. 67. Signs <br />Exophthalamus<br />Lid lag<br />Conjunctivaloedema<br />Ophthalamoplegia<br />Periorbitaloedema<br />Goiter<br />Weight loss<br /><ul><li>Proximal myopathy
  68. 68. Proximal muscle wasting
  69. 69. Onycholysis
  70. 70. Palmarerythema</li></li></ul><li>THYROID EYE DISEASE<br />INFILTRATION<br />1. soft tissue involvement :- chemosis, conjunctival injection over the recti insertions, puffy lids<br />
  71. 71. Eye disease <br />
  72. 72. Investigation <br />Thyroid function test:<br />Serum TSH is suppressed in hyperthyroidism .<br />Diagnosis is confirmed with a raised free T4 or T3.<br />
  73. 73. Treatment <br />Antithyroid drugs:<br /> 1. Carbimazole.<br /> 2. Propylthiouracil. <br />These drugs inhibit the formation of thyroid hormones.<br />Thyroid hormone synthesis is reduced very quickly.<br />T4 has long half-life (7 days) means that clinical benefit is not apparent for 10-20 days.<br />
  74. 74. Treatment <br /><ul><li>Antithyroid drugs:
  75. 75. Relapse
  76. 76. About 50% of patients will relapse after a course of carbimazole or propylthiouracil, mostly within 2 years</li></li></ul><li>Treatment <br />Radioactive iodine <br />RAI accumulates in the thyroid and destroys the gland by local radiation.<br />It takes several months to be fully effective.<br />
  77. 77. Treatment <br />Surgery: <br />subtotal thyroidectomy<br />Only in patient who have previously been rendered euthyroid.<br />Stop the antithyroid drugs 10-14 days <br />Give potassium iodide – reduce vascularity of the gland <br />
  78. 78. Thank you<br />