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THYROID DISEASE

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HYPOTHYROIDISM & HYPERTHYROIDISM

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THYROID DISEASE

  1. 1. THYROID DISEASE By: Dr Ismah 1
  2. 2. Contents 1. Physiology and development 2. Epidemiology 3. Hyperthyroidism 4. Hypothyroidism 2
  3. 3. 3 1. Physiology and development
  4. 4.  Thyroid glands descend to ant lower neck by the end of 1st trimester 4
  5. 5. 5  Hypothalamic-pituitary-thyroid axis becomes functional in 2nd trimester
  6. 6. 6  Peripheral metabolism of thyroid hormones matures in 3rd trimester
  7. 7.  T3,T4,TSH do not cross placenta in significant amount 7
  8. 8. Functions of thyroid hormones Target tissue Mechanism Nervous system Promote normal brain development Heart • Increase number, affinity of beta adrenergic receptors • Enhance responses to circulating catecholamine Muscle Increase protein breakdown Bone Promote normal growth and skeletal development Gut Associated with carbohydrate absorption Adipose tissue Stimulate lipolysis Lipoprotein Stimulate formation of LDL receptors Other • Stimulate oxygen consumption by metabolically active tissues • Increase metabolic rates • Promote development of reproductive system • Maturation of fetal lungs 8
  9. 9. Normal level of thyroid hormones Age TSH (mIU/L) FreeT4 (pmol/L) Birth-D3 OL <21 26-65 D4-D30 0.51-10.8 12-30 D31-1yr 0.39-7 9-16.1 ≥ 1 yr 0.4-6 13.2-22.2 9
  10. 10. 2. Epidemiology  Hypothyroidism:  Incidence of congenital hypothyroidism worldwide is 1:2500 - 4000 live births  In Malaysia, it is reported as 1:3666  It is the commonest preventable cause of mental retardation in children 10
  11. 11.  Hyperthyroidism:  Study in US (2008) concluded that the incidence among individuals aged 0-11 years was 0.44 cases per 1000 population  The incidence among individuals aged 12-17 years was 0.59 cases per 1000 population.  Thus, the incidence increases throughout childhood, with a peak incidence in children aged 10-15 years 11
  12. 12. 3. Hypothyroidism  Decreased freeT4, increasedTSH  Primary, secondary or tertiary 12
  13. 13. A. Congenital hypothyroidism  Causes  Maldescent thyroid, athyrosis  Dyshormonogenesis  Iodine deficiency  TSH deficiency 13
  14. 14. Clinical features  FTT  Feeding problem  Prolonged jaundice  Constipation  Pale, cold, mottled skin  Quiet baby  Coarse face  Large tongue  Hoarse cry  Goiter  Umbilical hernia  Delayed development 14 MOSTLY , ASYMPTOMATIC AT BIRTH
  15. 15. 15
  16. 16. 16 CORDTSH
  17. 17. Treatment  Timing  Should begin immediately after diagnosis is established  If features of hypothyroidism are present, treatment is started urgently.  Duration  Treatment is life long  Except in children suspected of having transient hypothyroidism where re-evaluation is done at 3 years of age. 17
  18. 18.  Preparation  L-thyroxine tablets  The L-thyroxine tablet should be crushed, mixed with breast milk, formula, or water and fed to the infant.  Tablets should not be mixed with soy formulas or any preparation containing iron (formulas or vitamins), both of which reduce the absorption ofT4. 18
  19. 19. 19Pediatric Protocol 3rd ed
  20. 20. Goal of therapy  To restore the euthyroid state  Serum FT4 level usually normalise within 1-2 weeks, and thenTSH usually become normal after 1 month of treatment.  Some infants continue to have high serumTSH concentration (10 - 20 mU/L) despite normal serum FT4 values due to resetting of the pituitary-thyroid feedback threshold.  Compliance to medication has to be reassessed and emphasised. 20
  21. 21. 21Pediatric Protocol 3rd ed
  22. 22. Follow up  Monitor growth parameters and developmental assessment.  Imaging studies  If the FT4 is low and theTSH value is elevated, permanent hypothyroidism is confirmed and life- long L-thyroxine therapy is needed. 22
  23. 23. Measurement schedule (FT4, TSH)  The recommended by American Academy of Pediatrics  At 2 and 4 weeks after initiation ofT4 treatment.  Every 1 to 2 months during the first 6 months of life.  Every 3 to 4 months between 6 months and 3 years of age.  Every 6 to 12 months thereafter until growth is completed.  After 4 weeks if medication is adjusted.  At more frequent interval when compliance is questioned or abnormal values are obtained. 23
  24. 24. Re-evaluation of patients likely having transient hypothyroidism  Can be due to factors primarily affecting the thyroid-like iodine deficiency or excess, maternal TSHR antibodies, maternal use of anti thyroid drugs  This is best done at age 3 years when thyroid dependent brain growth is completed at this age.  Stop L-thyroxine for 4 weeks then repeat thyroid function test: FT4,TSH. 24
  25. 25. B. Acquired hypothyroidism  The commonest cause autoimmune thyroiditis i.e. Hashimoto thyroiditis 25
  26. 26. Clinical features  Short stature  Cold intolerance  Dry skin  Cold peripheries  Bradycardia  Thin, dry hair  Goiter  Slow relaxing reflexes  Constipation  Delayed puberty  Obesity  Slipped upper femoral epiphysis  Learning difficulties 26
  27. 27. 27
  28. 28. Hashimoto thyroiditis  In older children, adolescence  +ve family h/o thyroid disease in 25-35% of patient  Autoimmune process targeted the thyroid gland thus resulting in fibrosis and atrophy of thyroid glands 28
  29. 29.  Firm, non tender, diffuse goiter  Onset after 6 years old  Associated with DM type 1, adrenal insufficiency and hypoparathyroidism, down syndrome, turner syndrome 29
  30. 30. Diagnosis  Clinically  Confirmed by serum antithyroid peroxidase and antithyroid globulin antibodies 30
  31. 31. Treatment  L thyroxine  MonitorTSH, FT4 6-12 monthly 31
  32. 32. 32 4. Hyperthyroidism IncreasedT4,T3 & decreasedTSH
  33. 33. Clinical features  Systemic  Anxiety  Restlessness  Sweating  Diarrhea  Weight loss  Rapid growth in ht  Tremor  Tachycardia  Warm peripheries  Learning difficulty  Behavior problems  Psychosis 33
  34. 34.  Eye signs (not common in children)  Exophthalmos  Ophthalmoplegia  Lid retraction  Lid lag 34
  35. 35. 35
  36. 36. 36 Lid retraction Exophthalmos
  37. 37. 37 Opthalmoplegia Lid lag means delay in moving the eyelid as the eye moves downwards
  38. 38. A. Graves’ disease  Autonomous functioning of thyroid caused by thyroid stimulating immunoglobulins (TSIs)  Increased thyroid hormones production and peripheral conversion  Firm, diffuse goiter  Common in girls, in adolescence 38
  39. 39. 39 TREATMENT 1. Drugs 2. Surgery 3. Radioactive iodine
  40. 40. Drugs  Block thyroid hormones synthesis  Carbimazole  PTU - Side effect: rash, fever, arthralgia, agranulocytosis, liver damage, lupus like syndrome  Beta blockers e.g. propranolol - To control cardiac manifestation - Contraindicated in asthmatic pt 40
  41. 41. Surgery 41  Thyroidectomy  Indications: - Failed medical treatment - Large goiters, especially with pressure effects - Severe progressive ophthalmopathy
  42. 42. B. Thyroid storm  Medical emergency.The mortality is 20 - 30 %.  Exacerbation of the hyperthyroid state with evidence of decompensation in one or more organ systems  Precipitated by stress including concurrent infections, surgery  Clinical diagnosis with features of severe thyrotoxicosis, hyperpyrexia and neuro-psychiatric manifestations such as delirium 42
  43. 43. Management 43 Rehydration Treat hyperpyrexia (use fans, tepid sponging and oral paracetamol) Do NOT use aspirin or NSAIDs Beta sympathetic blocking agents Oral propanolol 40 mg qid, or I/V 1-2 mg 4-6hourly
  44. 44. Iodide Oral saturated solution of potassium iodide (SSKI) 5 drops 6-hourly or I/V Sodium Iodide 500 mg 8 hourly or oral Lugol's iodine 5-10 drops, 6-hourly Antithyroid Drugs Carbimazole 15-20 mg 6-hourly or propylthiouracil 150-200 mg 6-hourly Corticosteroids I/V dexamethasone 2 mg 6-hourly or I/V hydrocortisone 200 mg 6-hourly 44
  45. 45. C. Other causes (rare)  McCune-Albright syndrome  Thyroid neoplasm  TSH hypersecretion  Subacute thyroiditis  Excessive iodine or thyroid hormone ingestion 45
  46. 46. D. Neonatal hyperthyroidism  Associated with infant of mother with Graves’ disease  Transient placenta transfers of thyroid stimulating immunoglobulins (TSIs)  Potentially fatal 46
  47. 47. Clinical features  Irritability  Tachycardia  Polycythemia  Craniosynthesis  Poor feeding  FTT 47
  48. 48. Treatment  Minimally affected: observation  Severe:  Oral propranolol  PTU  Spontaneous resolution because ofTSIs usually in 2-3 months of age 48
  49. 49. Take home message  Important to understood the physiology of thyroid hormone  Congenital hypothyroidism – screening, treat to prevent MR  Patient education and compliance to treatment/follow up 49
  50. 50. 50American Association of Clinical Endocrinologists (AACE)
  51. 51. References: 1. Nelson Essential of Pediatrics 6th ed 2. IllustratedTextbook of Pediatrics 3rd ed 3. Pediatric Protocol 3rd ed 4. Practice Guidelines forThyroid DisordersThe Malaysian Consensus 2000 Thank You 51
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HYPOTHYROIDISM & HYPERTHYROIDISM

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