Hypothyroidism is a hypometabolic state caused by a deficiency of thyroid hormones. It can be primary, secondary, or tertiary in nature. Primary hypothyroidism is usually due to autoimmune thyroiditis or iatrogenic causes like radiation or surgery. Symptoms include fatigue, weight gain, dry skin, and constipation. Treatment involves lifelong thyroid hormone replacement therapy with levothyroxine to restore euthyroidism. Monitoring includes clinical evaluation and measurement of TSH and free T4 levels.

1. THYROID DISORDERS: HYPOTHYROIDISM

2. REFERENCES Practice Guidelines for Thyroid Disorders The Malaysian Consensus 2000 Ministry of Health Malaysia Oxford Handbook of Endocrinology & Diabetes Helen E. Turner, and John A.H. Wass 1 st edition, 2003 Update on the management of hyperthyroidism and hypothyroidism, Kenneth A. Woeber,, Arch Fam Med (2000) 9; 743-747

3. INTRODUCTION Hypometabolic state due to deficiency of thyroid hormones Accumulation of GAGs (mucopolysaccharides) in the SC tissue Incidence : mid-50s : male:female ratio -> 1:10

4. ETIOLOGY PRIMARY : THYROID FAILURE ( 95%) SECONDARY : PITUITARY TSH DEFICIT TERTIARY : HYPOTHALAMIC DEFICIENCY OF TSH PERIPHERAL RESISTANCE TO THE ACTIONS OF THYROID HORMONES

5. Autoimmune hypothyroidism: Hashimoto’s thyroiditis Atrophic thyroiditis Iatrogenic: Radio-iodine therapy Thyroidectomy External radiation to the neck (lymphoma/CA) Drugs : Antithyroid drugs , amiodarone, lithium, interferon Congenital hypothyroidism: Thyroid agenesis Dyshormogenesis TSH-R mutation PRIMARY CAUSES Iodine deficiency Infiltrative disorder

6. 2°, 3° AND OTHER CAUSES Hypopituitarism (2°): Tumour Surgery Radiation Postpartum: Sheehan’s syndrome Hypothalamic causes (3°): Tumour Trauma Peripheral resistance (rare)

10. LABORATORY INVX Diagnosis : serum TSH : serum T 4  total or free? : thyroid autoantibodies In outpatient setting -> serum TSH !!! SUBCLINICAL HYPOTHYROIDISM: patient is not overtly hyperthyroid serum free T4 is normal, but TSH is ↑

11. MANAGEMENT Aim: to make patient euthyroid, clinically & biochemically. Treatment with L-thyroxine is life-long -> ensure compliance!! Monitoring: Clinically & biochemically Measure TSH and free T4 2-3 month after initiation of therapy -> determine maintenance dose

12. Continue.. OVERT HYPOTHYROIDISM Starting dose : 50-100 ug/d ->-> 100-200ug/d within 2 weeks IHD / grossly hypothyroid / elderly: Start at 25 ug/d ↑ slowly within 2-4/52 according to pt response Angina: withhold / ↓ dose. Proper mx of IHD Hypopituitarism: Cortisol: to avoid adrenal crisis

13. SUBCLINICAL HYPOTHYROIDISM: L-thyroxine to ↓ risk of CAD 50-100 ug/d ->-> adjust to maintain TSH at normal level PREGNANCY: ↑ dose, especially in 2 nd / 3 rd trimester

14. EMERGENCY: MYXEDEMA COMA

15. Severe, uncompensated form of prolonged hypoTH Precipitated by stress / infection / drug Complication: Hypoventilation Cardiac failure Fluid & electrolyte imbalance coma

16. PLAN OF MANAGEMENT Treat precipitating cause Gradual rewarming -> blanket Accurate core T° -> rectal thermometer Aim for slow ↑ in core T° : 0.5 °C/hr Cardiac monitoring Correction of electrolyte abnormalities Adequate hydration & nutrition (dextrose) L-thyroxine (300-400 ug oral/iv) & tri-iodothyronine 10 ug 8 hrly 8. Hydrocortisone : blood cortisol

17. CONGENITAL HYPOTHYROIDISM

18. Incidence : 1 in 4000-5000 live births Importance of TH hormones: Normal development of nervous system !! Features: Prolonged jaundice Poor feeding Constipation Unusually quite baby

19. Continue.. Signs (if left untreated, appear at 3-6 months): Coarse facies Dry skin Hoarse cry Umbilical hernia macroglossia Delayed developmental milestones

20. MANAGEMENT Newborn screening Diagnosis confirmed -> treat ASAP Dose: start at 10-12 ug/kg/day Aim : maintain TSH at normal level : maintain free T4 at upper limit of normal range Life-long treatment: if transient hypoTH is suspected, re-evaluate at 2 years old. Monitoring: antropometry/milestones/bone age progression

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