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  1. 1. Thyroid disorders haimanot c.(MD)
  2. 2. Disease of the Thyroid content • Fetal development • Thyroid physiology • Thyroid regulation • Thyroid hormone studies • Hypothyroidism • Hyperthyroidism • Thyroid carcinoma
  3. 3. Fetal thyroid development The fetal thyroid arises from an outpoaching of the foregut at the base of tongue. Around 8-10wks of gestation it migrates to its normal location over the thyroid cartilage. Characteristic thyroid follicle cell and colloid formation is seen by wk 10.
  4. 4. T4 and lesser extent of T3 synthesis and secretion occurs starting from wk 12.  Maturation of H-P-T axis occurs over 2nd half of pregnancy, normal feedback mechanism starts after 3mo postnatal.
  5. 5. Thyroid physiology Main function- to synthesize thyroid hormone(T4 and T3) And the only physiologic role of iodine(iodized form) is in the synthesis of these hormones. Recommended dietary intake: -infant 30µg/kg/24hrs -chidren 90-120µg/24hrs -adult 150µg/24hrs
  6. 6. Thyroid tissue has an avidity for iodine to trap, transport and concentrate in the follicular lumen for the synthesis of hormones. Then entry of iodide from the circulation in to the thyroid is carried out by sodium iodide symporter. Then diffuses to the colloid via pedrin.
  7. 7. • Before trapped iodide can react with tyrosine, it must be iodized by the help of thyroidal peroxidase. • Thyroid cells produces thyroglobulin (large molecular weight gp) which contains around 150 units of tyrosine.
  8. 8. Then iodination of tyrosine forms monoiodotyrosine and diiodotyrosine and then coupling takes place to form T4 and T3. Once formed, stored as thyroglobulin in colloid until ready to body cells then liberated by activation of proteases and peptides.
  9. 9. The metabolic potency of T3 is 3-4times that T4. And also T3 is physiologically active hormone. Only 20% of T3 is secreted by the thyroid. The remaining produced by deiodination of T4 in liver , kidney, and other extra thyroidal tissues by type I 5’ deiodinases
  10. 10. Thyroid hormone: - Increases oxygen consumption - Stimulate protien synthesis -Influence growth and differentiation - Affect carbohydrate, lipid, and vit. metabolism
  11. 11. Thyroid Regulation  In states of decreased production of thyroid hormone, TSH and TRH are increased.  Exogenous thyroid hormone or increased thyroid hormone synthesis inhibits TSH and TRH production.  Except in the neonate, levels of TRH in serum are very low.
  12. 12. + + - - Synthesize TRH by 6-8th week Secrete TSH by 12th week Feedback mechanism starts by 3rd month
  13. 13. THYROID HORMONE STUDIES Serum thyroid hormone(T3,T4 both total and free) Serum TSH level(sensitive indicator for p. hypothyroidism) Serum TBG(can be affected by different factors) Age should be considered in hormone determination.
  14. 14. Other studies that contribute for diagnosis: -Radionuclide studies -Ultrasonographic studies
  16. 16. Hypothyroidism Hypothyroidism results from deficient production of thyroid hormone or a defect in thyroid hormone receptor activity .  congenital or acquired .
  17. 17. CONGENITALHYPOTHYROIDISM  Most cases of congenital hypothyroidism are not hereditary and result from thyroid dysgenesis.  Some cases may be familial, usually caused by one of the inborn errors of thyroid hormone synthesis, and may be associated with a goiter.
  18. 18. In many cases, the deficiency of thyroid hormone is severe, and symptoms develop in the early weeks of life. In others, lesser degrees of deficiency occur, and manifestations may be delayed for months.
  19. 19. EPIDEMIOLOGY • The prevalence of congenital hypothyroidism based on neonatal screening is 1/4,000 infants worldwide; • Prevalence is lower in black Americans (1/32,000) and higher in Hispanics and Native Americans (1/2,000). • F:M = 2:1
  20. 20. ETIOLOGY(primary or central) PRIMARY: 1.DYSGENESIS -the most common cause of permanent congenital hypothyroidism around 80%-85 (aplasia 33%, hypoplasia or ectopic(66%)). Most causes are unknown and sporadic 8-10% familial (thyroglossal cyst and hemiagenesis in 1st degree relatives support some genetic defect.
  21. 21. 2.DYSHORMONOGENESIS-The problem is in TH synthesis 15% of cases detected by neonatal screening programs. when the defect is incomplete ,compensation occurs, and the manifestation of is delayed. Goiter is almost always present.
  22. 22. 3.TSH unresponsiveness 4.Defect in thyroid hormone transport 5.Resistance to thyroid hormone 6.Maternal antibodies: thyrotropin receptor– blocking antibody 7.Iodine deficiency (endemic goiter) 8.Maternal medications
  23. 23. CLINICAL MANIFESTATIONS Asymptomatic at birth even in case of agenesis birth wt and length normal but head size may be slightly increased Prolonged physiologic jaundice, delayed passage of stool
  24. 24.  Feeding difficulties, especially sluggishness, lack of interest, somnolence, and choking spells during nursing, are often present during the 1st mo of life.  Respiratory difficulties, due in part to the large tongue, include apneic episodes, noisy respirations, and nasal obstruction.  Affected infants cry little, sleep much, have poor appetites, and are generally sluggish.
  25. 25.  There may be constipation that does not usually respond to treatment.  The abdomen is large, and an umbilical hernia is usually present.  The temperature is subnormal, often less than 35°C (95°F), and the skin, particularly that of the extremities, may be cold and mottled.  Edema of the genitals and extremities may be present.
  26. 26. – Macroglossia – Large fontanelles (anterior and posterior) – Umbilical hernia – Mottled, rough or dry skin – Developmental delay – Pallor, hypothermia – Myxedema – Chocking during feeding.
  27. 27. The pulse is slow, and heart murmurs, cardiomegaly, and asymptomatic pericardial effusion are common. Macrocytic anemia is often present and is refractory to treatment.  Because symptoms appear gradually, the clinical diagnosis is often delayed. Approximately 10% of infants with congenital hypothyroidism have associated congenital anomalies.
  28. 28.  Cardiac anomalies are most common, but anomalies of the nervous system and eye have also been reported.  If congenital hypothyroidism goes undetected and untreated, these manifestations progress.  Retardation of physical and mental development becomes greater during the following months, and by 3–6 mo of age the clinical picture is fully developed .
  29. 29.  partial deficiency of thyroid hormone, the symptoms milder, the syndrome incomplete, and the onset delayed.  Although breast milk contains significant amounts of thyroid hormones, particularly T3, it is inadequate to protect the breast-fed infant with congenital hypothyroidism, and it has no effect on neonatal thyroid screening tests.
  30. 30.  stunted, the extremities are short, and the head size is normal or even increased.  The anterior and posterior fontanels are open wide. Myxedema is manifested, in the eyelids, the back of the hands, and the external genitals. The skin shows general pallor. Thickened scalp, and the hair is coarse, brittle, and scanty and hairline reaches far down on the forehead appears wrinkled.
  31. 31. Development is usually retarded. appear lethargic and are late in learning to sit and stand. The voice is hoarse, and they do not learn to talk. The degree of physical and mental retardation increases with age. Sexual maturation may be delayed or may not take place at all.
  32. 32. The muscles are usually hypotonic, but in rare instances generalized muscular pseudohypertrophy occurs.
  33. 33. LABORATORY  T4 ,when T4 is low do TSH  Scintigraphy can help to pinpoint the underlying causes in infants with congenital hypothyroidism  ECG – low voltage P and T waves with diminished QRS complex due to poor LV function and pericardial effusion.
  34. 34. Primary/Central Hypothyroidism Hallmark of primary hypothyroidism *Serum T4 is LOW and TSH is elevated • Hall mark of central Hypothyroidism (Hypothalamus/pitutary) *Serum T4 and TSH levels are low
  35. 35. TREATMENT  Na L-thyroxine given Po is the Rx of choice. dose - neonates 10-15 µg/kg children 4 µg/kg
  36. 36. PROGNOSIS  Early diagnosis and treatment from the first week of life has good prognosis.  Delay in diagnosis ,inadequate treatment and poor compliance will result in variable brain damage.

Hinweis der Redaktion

  • Defect in iodine transport ,Defect in organification and coupling,Defect in thyroglobulin synthesis,Defect in deiodination
  • resistant to endogeneous and exogeneous T4 and T3 most patients have goiter and levels of T4 , T3 and free T4 and T3 is high and TSH moderately elevated or normal
  • The eyes appear far apart, and the bridge of the broad nose is depressed. The palpebral fissures are narrow and the eyelids swollen.
    The mouth is kept open, and the thick, broad tongue protrudes.
    Dentition will be delayed.
    The neck is short and thick, and there may be deposits of fat above the clavicles and between the neck and shoulders.
    The hands are broad and the fingers short.
    The skin is dry and scaly, and there is little perspiration.
  • ; observation of this sign at birth may serve as an initial clue to the early recognition of congenital hypothyroidism.
    Only 3% of normal newborn infants have a posterior fontanel larger than 0.5 cm.
  • ; observation of this sign at birth may serve as an initial clue to the early recognition of congenital hypothyroidism.
  • Tertiary versus Secondary Hypothyroidism

  • Around 20 % of children will have a neuro sensorial hearing loss and without treatment affected infants become profoundly mentally deficit dwarfs.