HYPOTHYROIDISM & HYPERTHYROIDISM

1. THYROID DISEASE
By: Dr Ismah
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2. Contents
1. Physiology and development
2. Epidemiology
3. Hyperthyroidism
4. Hypothyroidism
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3. 3
1. Physiology and development

4.  Thyroid glands descend to ant lower neck by
the end of 1st trimester
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5. 5
 Hypothalamic-pituitary-thyroid axis becomes
functional in 2nd trimester

6. 6
 Peripheral metabolism of thyroid hormones
matures in 3rd trimester

7.  T3,T4,TSH do not cross placenta
in significant amount
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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
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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
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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
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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
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12. 3. Hypothyroidism
 Decreased freeT4, increasedTSH
 Primary, secondary or tertiary
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13. A. Congenital hypothyroidism
 Causes
 Maldescent thyroid, athyrosis
 Dyshormonogenesis
 Iodine deficiency
 TSH deficiency
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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
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MOSTLY , ASYMPTOMATIC AT BIRTH

15. 15

16. 16
CORDTSH

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.
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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.
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19. 19Pediatric Protocol 3rd ed

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.
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21. 21Pediatric Protocol 3rd ed

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.
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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.
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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.
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25. B. Acquired hypothyroidism
 The commonest cause autoimmune
thyroiditis i.e. Hashimoto thyroiditis
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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
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27. 27

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
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29.  Firm, non tender, diffuse goiter
 Onset after 6 years old
 Associated with DM type 1, adrenal
insufficiency and hypoparathyroidism, down
syndrome, turner syndrome
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30. Diagnosis
 Clinically
 Confirmed by serum antithyroid peroxidase
and antithyroid globulin antibodies
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31. Treatment
 L thyroxine
 MonitorTSH, FT4 6-12 monthly
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32. 32
4. Hyperthyroidism
IncreasedT4,T3 & decreasedTSH

33. Clinical features
 Systemic
 Anxiety
 Restlessness
 Sweating
 Diarrhea
 Weight loss
 Rapid growth in ht
 Tremor
 Tachycardia
 Warm peripheries
 Learning difficulty
 Behavior problems
 Psychosis
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34.  Eye signs (not common in children)
 Exophthalmos
 Ophthalmoplegia
 Lid retraction
 Lid lag
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35. 35

36. 36
Lid retraction
Exophthalmos

37. 37
Opthalmoplegia
Lid lag means delay in moving the
eyelid as the eye moves downwards

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
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39. 39
TREATMENT
1.
Drugs
2.
Surgery
3.
Radioactive
iodine

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
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41. Surgery
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 Thyroidectomy
 Indications:
- Failed medical treatment
- Large goiters, especially with pressure
effects
- Severe progressive ophthalmopathy

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
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43. Management
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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. 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
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45. C. Other causes (rare)
 McCune-Albright syndrome
 Thyroid neoplasm
 TSH hypersecretion
 Subacute thyroiditis
 Excessive iodine or thyroid hormone
ingestion
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46. D. Neonatal hyperthyroidism
 Associated with infant of mother with Graves’
disease
 Transient placenta transfers of thyroid
stimulating immunoglobulins (TSIs)
 Potentially fatal
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47. Clinical features
 Irritability
 Tachycardia
 Polycythemia
 Craniosynthesis
 Poor feeding
 FTT
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48. Treatment
 Minimally affected: observation
 Severe:
 Oral propranolol
 PTU
 Spontaneous resolution because ofTSIs
usually in 2-3 months of age
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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
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50. 50American Association of Clinical Endocrinologists (AACE)

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
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