Hypothyroidism by aina
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Transcript of Hypothyroidism by aina
CONTENTS
Physiology Assessment of Thyroid Function Hypothyroidism Congenital Hypothyroidism Acquired Hypothyroidism Goiter Iodine Deficiency Disorders
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
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
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
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
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