Hypothyroidism

-Chris Sneha.S
 Contents

• Physiology
• Epideomology
• Etiology
• Congenital hypothyroidism
• Acquired hypothyroidism
• Goitre
• Iodine deficiency disorders
Slide player thyroid disorder Ahmed Shaman
 Function of thyroid hormones

• Somatic & intellectual growth

• Metabolism
• Thermoregulation

TSH levels increase immediately after birth, peaks at 24 hrs .So neonatal screening
is done after 48hrs of birth.
 Epidemiology

• Studies from Mumbai have suggested that congenital hypothyroidism is common in India, the
disease occurring in 1 out of 2640 neonates.

• In a clinic-based study from Mumbai, out of 800 children with thyroid disease, 79% had
hypothyroidism.

• There is often a delay in the diagnosis of congenital hypothyroidism in the country. This delay is
attributable to the lack of awareness about the illness, as well as the lack of facilities available or
screening program.

Ambika et al thyroid disorders in India, Indian J Endocrinol Metab. 2011 Jul; 15(Suppl2): S73–S75
 Hypothyroidism

Hypothyroidism

Hypothalamic pituitary
primary
axis
(central)

High TSH & low

Low FT4 & TSH
FT4
 Etiology

Primary:
1)Dysgenesis:hypothyroidism Peripheral resistance to thyroxine
2)Enzyme
defects &
iodine
deficiency.
Secondary or
3)Autoimmune
tertiary
,thyroid
injury,goitroge Malformati
ns. ons
4) Transient Genetic
causes. defects
CNS
tumors
CNS
insults
 Congenital hypothyroidism

Etiology
• Thyroid dysgenesis (75%) – downs syndrome
• Enzyme defects –pendred syndrome
• Transient causes

Clinical features
• Hoarse cry
• Facial puffiness
• Umblical hernia
• Hypotonia
• Mottling of skin , lethargy
• Prolonged jaundice ,constipation.
• Hypothermia , open posterior fontanel.

Google images
 History to ask:
• Family history of hypothyroidism (dyshormogenesis)
• Anti-thyroid medications
• Iodine deficient area
• Goitre

Evaluation
 Management:
• Thyroid replacement : thyroxine (T4) , 10-15µg/kg/day.
• Central hypothyroidism : cortisol given to prevent adrenal insufficiency.
• TSH levels normalise by 1 week & 1 month.
• FT4 levels upper limit.
• Lifelong for most cases.
• Stop for 1 month at 3 years in transient congenital hypothyroidism , discontinue if
normal.

Screening :
• Dried blood sample postnatal 2-4 days.
• Screen for TSH first .
 Acquired hypothyroidism

Etiology
Primary hypothyroidism
• Autoimmune thyroiditis Secondary hypothyroidism
• Iodine deficiency & goitrogens.
•Neurological insults or tumors

Clinical features:
• Growth retardation
• Delayed skeletal & dental development
• Cold intolerance
• Delayed puberty
• Goitre
• Downs syndrome, turners , celiac type 1 DM .
Evaluation

Finding or sign Etiology

Firm nodular goitre Autoimmune thyroiditis

Round nodular goitre Iodine deficiency or disorder of
synthesis

Pituitary function test & MRI Central hypothyroidism

Antibodies to TPO Primary hypothyroidism

 Management:
100µg /m²/day of thyroxine.

Age Thyroxine dose, µ/kg/day

Neonatal period 10-15

1-6 mon 6-10
1-5 yr 4-6
5-12 yr 3-5
12-18 yr 2-3
> 18 yr 1-2

• Long standing : 25-50% of doses started initially , builded in 3-4 weeks .

• Follow up every 3 month for 2 years , then 6 months.
• Dose modified to maintain normal TSH levels .
 Goitre

Enlargement of thyroid gland .Clinically when lateral lobe is larger than terminal
phalanx of thumb of child.

Causes of goitre
Inflammatory Acute suppurative
thyroiditis ,subacute thyroiditis
Infiltration Autoimmune
thyroiditis,neoplasm,
hemochromatosis
Increased TSH Dyshormogenesis , iodine
deficiency, unilateral agenesis
TSH stimulating antibody Graves disease
 Evaluation
• Clinical:
Nodular goitre- Autoimmune thyroiditis , colloid goitre , chronic lymphocytic
goitre, iodine deficiency.
Diffuse – graves disease ,dyshormonogenesis , Goitrogenic drugs.

• Investigation:
Anti-TPO; autoimmune thyroiditis.
USG & fine needle aspiration: no clue of etiology

Management:
Thyroxine replacement : 100-200 ug.( regression by 2 years in 30%)
Graves : antithyroid medication
Surgery : avoided unless the goitre is large causing difficulty in respiration.
 Iodine deficiency disorder

• Endemic goitre
• Endemic cretinism
• Impaired mental function
• Still birth, perinatal & infant mortality.

Endemic goitre:
Prevalence of goitre in a defined population exceeds 5%.
 Grading endemic goitre
Stage 0 No goitre
Stage 1A Detectable only on palpation &
not visible
Stage 1B Palpable , visible on full extension
of neck
Stage 2 Visible on normal position of
neck, no need for palpation
Stage 3 Very large goitre, seen from
distance

• 24 hr urine iodine excretion.

•Urinary iodine concentration expressed in creatinine concentration.
 Endemic cretinism

Associated with endemic goitre & severe iodine deficiency.

Endemic cretinism

neurological
Deaf mutism,squint, rigity,proximal
spasticity& rigiy in lower
limbs,cerebellar occulomotor
disturbance

myxedematous
Retarded psychomotor
development,severe short stature,
coarse facies,myxedma
Classification of severity of iodine deficiency
Iodine None Mild Moderate Severe
deficiency

Median urine >100 50-99 20-49 <20

iodine , µg/L

Neonatal <3% 3-20% 20-40% >40%

TSH,>5 IU/ml
whole blood
Cretinism none none present present

Prevention & control:

National control programme of ministry of health of India : iodised salt.
Recommended salt intake : 40-20 µg for children upto 10,150µg for older children &
adults, 25&50µg additional in pregnancy and lactation respectively.
Mean intake : 5g/day
Reference :OP Ghai

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