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A two-lobed thyroid gland releases a thin green trickle of hormone into a tall measuring vessel that stays nearly empty.

Hypothyroidism

~2 min readReviewed

In this topic8

  1. Causes and classification of hypothyroidism
  2. Subclinical hypothyroidism
  3. Congenital hypothyroidism
  4. Autoimmune hypothyroidism
  5. Pathogenesis of autoimmune hypothyroidism
  6. Clinical manifestations of hypothyroidism
  7. Laboratory evaluation of hypothyroidism
  8. Treatment of hypothyroidism

Hypothyroidism is low production of thyroid hormone by the thyroid gland. The gland may itself fail, which is primary hypothyroidism, or it may be under-driven because the pituitary produces too little TSH (thyroid-stimulating hormone), which is central hypothyroidism. Less commonly, the hormone is made but the tissues respond to it poorly. Whichever route is taken, the result is a shortage of thyroid hormone at the tissues, and that shortage slows the metabolism of nearly every organ system.

Because the causes are so different, hypothyroidism is one subject with several branches, and the tests that are trustworthy and the treatment that is appropriate depend on which branch a patient is on. The notes below take the subject from where it begins to how it is managed.

  • Causes and classification of hypothyroidism — where the failure starts, why the site of the fault decides which test is trustworthy, and the main causes. Start here.
  • Subclinical hypothyroidism — the early phase, in which a compensatory rise in TSH keeps the hormone level apparently normal, and what that compensation means for the heart, the liver and pregnancy.
  • Congenital hypothyroidism — the form present from birth, why screening rather than clinical signs finds it, and how the diagnosis is confirmed.
  • Autoimmune hypothyroidism — Hashimoto’s thyroiditis and atrophic thyroiditis, their subclinical and overt phases, their appearance after pregnancy, and their link with infertility.
  • Pathogenesis of autoimmune hypothyroidism — how lymphocytes and cytokines destroy the gland, why the antibodies against thyroid peroxidase (TPO) and thyroglobulin (Tg) amplify the damage without starting it, and the genetic and environmental factors that raise the risk.
  • Clinical manifestations of hypothyroidism — how the slowing of organ systems presents, from the cardiovascular and musculoskeletal changes to the neurological and reproductive effects.
  • Laboratory evaluation of hypothyroidism — why TSH is the first and most sensitive test, how free T4 and the antibody assays are used, and the other laboratory abnormalities.
  • Treatment of hypothyroidism — levothyroxine replacement, how the dose is set and monitored, and the emergency of myxedema coma.