Question
Describe the hormones produced by the thyroid gland. How are T3 and T4 regulated by the hypothalamus-pituitary-thyroid axis? Compare the disorders caused by hypothyroidism and hyperthyroidism. What is the role of calcitonin?
(NEET + CBSE Board — mechanism + disorders)
Solution — Step by Step
| Hormone | Full Name | Function |
|---|---|---|
| T4 (Thyroxine) | Tetraiodothyronine | Increases BMR, promotes growth and development, protein synthesis |
| T3 | Triiodothyronine | Same as T4 but 4-5x more active (T4 is converted to T3 in tissues) |
| Calcitonin (TCT) | Thyrocalcitonin | Lowers blood calcium — promotes calcium deposition in bones |
Both T3 and T4 require iodine for their synthesis. This is why iodine deficiency directly affects thyroid function.
- Hypothalamus releases TRH (Thyrotropin Releasing Hormone)
- TRH stimulates the anterior pituitary to release TSH (Thyroid Stimulating Hormone)
- TSH stimulates the thyroid gland to produce T3 and T4
- High levels of T3/T4 in blood inhibit TRH and TSH release (negative feedback)
- Low T3/T4 levels release the brake — TRH and TSH increase again
This negative feedback loop maintains thyroid hormone levels within a narrow range.
| Feature | Hypothyroidism | Hyperthyroidism |
|---|---|---|
| Hormone level | Low T3/T4 | High T3/T4 |
| BMR | Decreased | Increased |
| Body weight | Weight gain | Weight loss |
| Heart rate | Slow (bradycardia) | Fast (tachycardia) |
| Temperature tolerance | Cold intolerance | Heat intolerance |
| In children | Cretinism (stunted growth, mental retardation) | Rare |
| In adults | Myxedema (puffy face, lethargy) | Graves’ disease (exophthalmos — bulging eyes) |
| Iodine-related | Goitre (enlarged thyroid due to iodine deficiency) | Can also cause goitre (due to overstimulation) |
Calcitonin and PTH (Parathyroid Hormone) work as antagonists:
- Calcitonin: Lowers blood calcium (deposits Ca²⁺ into bones)
- PTH: Raises blood calcium (releases Ca²⁺ from bones)
Together, they maintain calcium homeostasis.
graph TD
A["Hypothalamus"] -->|TRH| B["Anterior Pituitary"]
B -->|TSH| C["Thyroid Gland"]
C -->|T3, T4| D["Target Tissues"]
D -->|"Negative Feedback"| A
D -->|"Negative Feedback"| B
C -->|Calcitonin| E["Bones: Ca2+ deposition"]
style A fill:#93c5fd,stroke:#000
style C fill:#fbbf24,stroke:#000,stroke-width:2px
style D fill:#86efac,stroke:#000Why This Works
The thyroid is the body’s metabolic thermostat. T3 and T4 enter nearly every cell and increase the rate of cellular metabolism. The HPT axis ensures precise control — too much hormone triggers the brake (negative feedback), too little releases it. This is why thyroid disorders produce such widespread symptoms — they affect virtually every organ system.
Calcitonin operates independently of the HPT axis. It responds directly to blood calcium levels — high calcium stimulates calcitonin release, which pushes calcium into bones.
Common Mistake
Students often confuse cretinism (hypothyroidism in children — stunted growth, mental retardation) with myxedema (hypothyroidism in adults — puffy face, lethargy). Both are hypothyroid conditions, but the consequences differ based on age. Cretinism is irreversible if not treated early. NEET frequently tests this age-based distinction.
For NEET: iodine deficiency causes goitre (simple/endemic goitre). The thyroid enlarges because TSH keeps stimulating it to produce more hormone, but without iodine, it cannot. The gland swells in a futile attempt to compensate. Iodised salt prevents this — a public health fact NEET loves to test.