DurgicalDurgical
EN
Open the app

Actions of thyroid hormones !

  • Mechanism
  • Exam priority: high

Thyroid hormones set the pace of metabolism: with too much everything speeds up, with too little everything slows down.

Updated 2026-11-01

Also called: T3 and T4, Thyroxine and triiodothyronine

See it in 3D: Thyroid gland

What it is

The thyroid secretes mostly T4, a prohormone; tissues convert it to T3, the active form. T3 enters the nucleus and changes the transcription of many genes, so its effects take hours to days and last. It raises oxygen use and heat, sensitizes the heart to catecholamines and is essential for brain and bone development. The synthesis (iodine, peroxidase) is in Biochemistry.

How it works, step by step

  1. TSH drives follicular cells to take up iodide, make thyroglobulin and release T4 (≈90%) and T3 (≈10%).
  2. In blood almost all hormone is bound (TBG, transthyretin, albumin); only the free fraction enters cells.
  3. Inside the cell, type 1 or 2 deiodinase removes one iodine from T4 to make T3.
  4. T3 binds the nuclear receptor TR, which with RXR binds thyroid response elements in DNA.
  5. Genes such as Na⁺/K⁺-ATPase, mitochondrial proteins, β1 receptors and α-myosin heavy chain are transcribed.
  6. Result: more O₂ and fuel use, more heat, stronger and faster heartbeats, and maturation of the nervous system and bone.

Hormone axes and feedback

Hormone axes and feedback: Hypothalamic–pituitary–thyroid axis Cold (mainly in infants) · circadian rhythm−−+++HypothalamusTRHAnterior pituitary (thyrotrophs)TSHThyroid (follicular cells)T4T3Tissues (deiodinases)T4 → T3

Hypothalamic–pituitary–thyroid axisLesion None (normal)

Tap a box to see the hormone, or choose a lesion to see the lab pattern.

  • Stimulates (+)
  • Inhibits / negative feedback (−)
  • Level ↑
  • Level ↓
Illustrative schematic drawn by Durgical: simplified axes and classic lab patterns; not for clinical decisions.

Hyperthyroidism versus hypothyroidism

SystemExcess (hyper)Deficit (hypo)
Metabolism and temperatureWeight loss despite high appetite, heat intolerance, sweatingWeight gain, cold intolerance
HeartTachycardia, atrial fibrillation, wide pulse pressureBradycardia, low cardiac output, pericardial effusion
Nervous systemAnxiety, fine tremor, brisk reflexesSlowness, sleepiness, delayed reflex relaxation
GutFrequent stoolsConstipation
Skin and lipidsWarm, moist skinDry skin, myxedema, high LDL cholesterol

Clinical notes

  • Graves disease: antibodies that stimulate the TSH receptor; hyperthyroidism with suppressed TSH, diffuse goiter and ophthalmopathy.
  • Iodine-deficiency goiter: high TSH enlarges the gland; in Colombia salt iodization made it far less common.
  • Congenital hypothyroidism: newborn TSH screening (cord or heel blood) allows treatment before the brain is harmed.

Test yourself

Think of the answer, then tap the question to see it.

Why do the effects of thyroid hormone take hours or days to appear?

T3 acts on a nuclear receptor and changes gene transcription; new proteins (Na⁺/K⁺-ATPase, enzymes, receptors) must be made before the effect shows.

Why does a thyrotoxic patient have tachycardia and tremor that improve with a beta-blocker?

T3 increases the number and sensitivity of β-adrenergic receptors; the excess sympathetic effect is blocked at the receptor even while the hormone stays high.

Why does hypothyroidism raise LDL cholesterol?

T3 increases hepatic LDL-receptor expression; with little hormone there are fewer receptors, less LDL is cleared and its level rises.

Why does the thyroid secrete mostly T4 if T3 is the active form?

T4 is a stable circulating reserve (half-life ≈1 week); each tissue sets how much T3 it makes with its deiodinases according to its need.

Add to my cards (4)

See it in 3D

The structures of Durgical's 3D anatomy where it happens.

In Biochemistry

In Pharmacology

← All of physiology

Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 17.4 The Thyroid Gland (OpenStax (Rice University), 2022); Hypothyroidism (StatPearls (NCBI Bookshelf), 2024); Graves Disease (StatPearls (NCBI Bookshelf), 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 77). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake

Representative model, for educational purposes only.