HYPOTHYROIDISM

NUR AINA BINTI AB KADIR

CONTENTS

Physiology Assessment of Thyroid Function Hypothyroidism Congenital Hypothyroidism Acquired Hypothyroidism Goiter Iodine Deficiency Disorders

PHYSIOLOGY

PHYSIOLOGY

FUNCTION Regulation of

somatic and intellectual growth

Intermediary metabolism

Thermoregulation

Assessment of thyroid gland

Estimation of serum TSH and free and/or total T3 & T4.

TSH: primary hypothyroidism T4 is a better indicator than T3 Estimation of free(F) thyroid hormone Low FT4 and TSH : central hypothyroidism High TSH : primary hypothyroidism Persistent elevation of TSH + normal FT4 :

subclinical hypothyroidism High FT4 + undetectable TSH : hyperthyroid state

HYPOTHYROIDISM-ETIOLOGY

PRIMARY (thyroid>95%)

SECONDARY/TERTIARY (hypthalamus / pituitary,<5%)

PERIPHERAL (extremely rare)

ETIOLOGY-PRIMARY

Autoimmune thyroiditis

• Trapping, organificationEnzyme defect

• Endemic goiterIodine deficiency

• Aplasia, dysplasia, ectopicDysgenesis

• Surgery, radiation, infectionThyroid injury

• Thiocyanates, thionamidesGoitrogens • Maternal TSH receptor

blocking ABTrasnsient

causes

ETIOLOGY

PERIPHERAL Resistance to

thyroxineMALFORMATIONS• Septo-optic defect

dysplasia, holoprosencephaly

CNS insults• Trauma,surgery,

radiation, infection

CNS tumors• Craniopharyngioma,

germinoma

SECONDARY/TERTIARY

CONGENITAL HYPOTHROIDISM Most common preventable cause of mental

retardation Commonest cause: iodine deficiency(certain

parts in India) Thyroid dysgenesis : non endemic area, more in

Down syndrome Encompasses a spectrum ranging from complete

agenesis,partial agenesis to ectopic thyroid. Biosynthetic defects include disorders affecting

iodine transport, peroxidation, thyroglobulin synthesis and deiodination.

CONGENITAL HYPOTHROIDISM

Pendred syndrome associated with decreased

intracellular transport of iodine and deafness

Transient congenital hypothyroidism may occur

following transplacental passage of TSH

receptor blocking antibodies, iodine

exposure and treatment with drugs like

amiodarone.

CLINICAL FEATURES

Hoarse cry Facial puffiness Umbilical hernia Hypotonia Mottling of the skin Lethargy Prolonged jaundice, constipation, unexplained

hypothermia Open posterior fontanelle Pallor

APPROACH

H/O maternal thyroid disease/ingestion of antithyroid medications

Family H/O hypothyroidism : dyshormogenesis Recurrent transient hypothyroidism :maternal

TSH receptor antibody Residence in iodine deficient area Goiter : transplacental passage of antithyroid

drugs/ disorders of thyroid hormone biosynthesis

Hypoglycemia, mircropenis & midline facial defects :hypothalamic cause

EVALUATION

MANAGEMENT

Should be started immediately after diagnosis Central hypothyroidism: cortisol replacement should

precede thyroid replacemet Thyroxine(T4) : 10-15µg/kg/day Normalize: T4(1 week) & TSH (1 month)- should

measured every visit Lifelong treatment Stopped for 1 month at the age 3y/o : transient

congenital hypothyroidism Discontinued: absence of persistent abnormality & normal

thyroid hormones

OUTCOME

Early diagnosis & treatment normal intellectual

Congenital hypothyroidism who have been diagnosed beyond the neonatal period mental retardation and short stature

SCREENING Dried blood sample collected at postnatal

age 2-4 days Screen first for TSH

ACQUIRED HYPOTHYROIDISM

ETIOLOGY

Autoimmune thyroiditis Thyroid peroxidase antibodies present Other autoimmune endocrinopathies: adrenal

insufficiency, type 1 DM, hypoparathyroidism Congenital abnormalities: thyroid

dysgenesis/inborn error of thyroid hormone synthesis (older children and adolescent)

Other: iodine deficiency,goitrogens Combined hypothalamic-pituitary defects

could be a manifestation of neurological injury insults/tumors

CLINICAL FEATURES

Short stature Cold intolerance Lethargy Constipation Delay in dentition Poor school performances Delayed puberty-but uncontrolled long-

standing hypothyroidismprecocious puberty Goiter: iodine deficiency, chronic lymphocytic

thyroiditis, dyshormogenesis

EVALUATION

Severe short stature & mental retardation: congenital hypothyroidism

Round uniform smooth goiter : iodine deficiency/ disorder of thyroid hormone synthesis

Firm nodular goiter &Family H/O acquired hypothyroidism : autoimmune thyroiditis

Children with central hypothyroidism: pituitary function tests, MRI of the hypothalamic-pituitary region

Antibodies to thyroid peroxidase enzyme(anti-TPO)- acquired primary hypothyroidism

MANAGEMENT

Treatment should be gradual 100µg/m2/day Long standing cases, initial treatment

should be started at 25-50% of these dose with gradual build up every 3-4weeks

Given empty stomach in the morning Follow up: every 3months during the 1st 2

yr of therapy and 6 monthly thereafter Lifelong

AGE THYROXINE DOSE,µg/kg/day

Neonatal period 10-15

1-6 mo 6-10

1-5yr 4-6

5-12yr 3-5

12-18yr 2-3

>18yr 1-2

GOITER

Def: enlargement of the thyroid gland Thyromegaly: lateral lobe of the thyroid is larger

than the terminal phalanx of the thumb of the child

ETILOGY: INFLAMMATORY : acute suppurative thyroiditis,

subacute thyroiditis INFILTRATION: autoimmune thyroiditis,

neoplasm, hemochromatosis INCREASED TSH LEVEL: dyshormogenesis, iodine

deficiency, unilateral agenesis TSH STIMULATING ANTIBODY: Graves’ disease COLLOID GOITER

EVALUATION

Classified as diffuse/nodular goiter

INVESTIGATIONS Thyroid function

test Anti-TPO

antibodies Ultrasound Fine needle

aspiration

MANAGEMENT Directed to the

causes Autoimmune

thyroiditis: followed with annual TFT

‘physiological goiter’: thyroxine 100-200µg daily

Surgery: avoided

IODINE DEFICIENCY DISORDERS Refers to the wide spectrum of effects of

iodine deficiency on growth and development

Endemic goiter Endemic cretinism Impaired mental function in children Goiter in adults Increased rate of stillbirth and perinatal

and infant mortality

ENDEMIC GOITER

Prevalence of goiter in a defined population >5%

ENDEMIC GOITER

Does not differ from non toxic diffuse sporadic goiter

Diagnosis by epidemiologic criteria High TSH with low T4 and T3 Screening : 24-hr urinary iodine

excretion values/ urinary iodine concentration expressed in relation to creatinine concentration

ENDEMIC CRETINISM

Disorders associated with endemic goiter and severe iodine deficiency

Features: Deaf-mutism Squint Mental retardation Spastic/rigid neuromotor disorder 2types : neurological & myxedematous

ENDEMIC CRETINISM

NEUROLOGICAL Deaf-mutism Squint Proximal spasticity Rigidity more in the

lower extremities Disorders of stance &

gait with preservation of vegetative function

Occasional signs of cerebellar/ oculomotor disturbance

Severe mental deficiency

MYXEDEMATOUS Retarded

psychomotor development

Severe short stature

Coarse facial features

Myedema without deaf-mutism

PREVENTION AND CONTROL

Iodinated salt/iodized oil Surgical removal: relieve airway

obstruction/ cosmetic purposes Recommended daily intake of iodine Children upto age 10: 40-120 µg Older children & adults: 150µg Pregnancy: additional 25 µg Lactation: additional 50 µg

Ghai Essential Pediatrics, 8th edition, pg 516-520

THANK YOU

REFERENCES