The endocrine system is the body’s slow-but-long-lasting control network, using hormones delivered through the blood. CBSE Class 11 and NEET test this heavily — expect two questions a year on specific hormones, their glands and their disorders.
If the nervous system is a phone call (fast, specific, brief), the endocrine system is a mass email (slower, reaches many recipients, lasts longer). Both are needed. The nervous system tells your hand to pull away from a hot stove in milliseconds. The endocrine system tells your bones to grow over months and years. Understanding which gland makes which hormone, what that hormone does, and what goes wrong when it fails — that is the entire framework for this chapter.
Core Concepts
Hypothalamus and pituitary axis
The hypothalamus is the master controller — a small region at the base of the brain that links the nervous system to the endocrine system. It produces releasing hormones (like GnRH, CRH, TRH) and inhibiting hormones that travel through the hypophyseal portal system to the anterior pituitary.
The anterior pituitary responds by secreting six major hormones:
| Hormone | Full name | Target | Action |
|---|---|---|---|
| GH | Growth Hormone | Bones, muscles | Stimulates growth |
| ACTH | Adrenocorticotropic | Adrenal cortex | Stimulates cortisol release |
| TSH | Thyroid Stimulating | Thyroid | Stimulates T3/T4 release |
| FSH | Follicle Stimulating | Gonads | Follicle growth / spermatogenesis |
| LH | Luteinising | Gonads | Ovulation / testosterone |
| PRL | Prolactin | Mammary glands | Milk production |
The posterior pituitary does not synthesise hormones — it stores and releases two hormones made in the hypothalamus:
- ADH (Antidiuretic Hormone / Vasopressin) — acts on kidney collecting ducts, increases water reabsorption
- Oxytocin — stimulates uterine contractions during labour and milk ejection during breastfeeding
The hypothalamus-pituitary axis is the most tested endocrine concept in NEET. Remember: the hypothalamus controls the pituitary, not the other way around. The anterior pituitary makes its own hormones; the posterior pituitary only stores hormones made by the hypothalamus.
Thyroid and parathyroid
Thyroid gland — butterfly-shaped, in the neck, has follicular cells and parafollicular (C) cells.
- T3 (triiodothyronine) and T4 (thyroxine) — iodinated amino acid derivatives. Increase basal metabolic rate, heat production, growth and development. T3 is more active; T4 is more abundant and converted to T3 in tissues.
- Calcitonin (from C cells) — lowers blood calcium by inhibiting osteoclasts and promoting calcium deposition in bone.
Parathyroid glands — four small glands embedded in the back of the thyroid.
- PTH (Parathyroid Hormone) — raises blood calcium by stimulating osteoclasts (bone resorption), increasing Ca reabsorption in kidneys, and promoting Vitamin D activation (which increases intestinal Ca absorption).
Calcitonin and PTH are antagonistic. Together they maintain blood calcium at about 9-11 mg/dL. This is a classic example of hormonal homeostasis.
Adrenal glands
Sit on top of the kidneys. Two distinct regions:
Adrenal cortex (outer, three zones):
- Zona glomerulosa → Aldosterone (mineralocorticoid) — retains Na, excretes K in kidney, raises blood pressure
- Zona fasciculata → Cortisol (glucocorticoid) — raises blood glucose, anti-inflammatory, stress response
- Zona reticularis → Androgens (sex steroids) — minor role in both sexes
Adrenal medulla (inner):
- Adrenaline (epinephrine) and Noradrenaline (norepinephrine) — fight or flight response. Heart rate up, blood pressure up, bronchioles dilate, pupils dilate, blood glucose up, digestive activity down. These are catecholamines, modified amino acids.
Pancreas — dual function
The pancreas is both exocrine (acinar cells produce digestive enzymes) and endocrine (Islets of Langerhans produce hormones).
| Cell type | Hormone | Action |
|---|---|---|
| Alpha () | Glucagon | Raises blood glucose (glycogenolysis, gluconeogenesis) |
| Beta () | Insulin | Lowers blood glucose (promotes glucose uptake, glycogenesis) |
| Delta () | Somatostatin | Inhibits both insulin and glucagon release |
Diabetes mellitus — the most clinically important endocrine disorder:
- Type 1 — autoimmune destruction of beta cells. No insulin produced. Requires insulin injections. Onset usually in childhood.
- Type 2 — insulin resistance. Cells do not respond normally to insulin. Associated with obesity. Managed with diet, exercise and oral drugs.
Normal fasting blood glucose: 70-110 mg/dL. Insulin and glucagon maintain this range through negative feedback.
Gonads
Testes (in males): Leydig cells produce testosterone — drives spermatogenesis, development of male secondary sexual characters (deep voice, facial hair, muscle mass), maintains libido.
Ovaries (in females): Follicular cells produce oestrogen — drives development of female secondary sexual characters, regulates the menstrual cycle. Corpus luteum produces progesterone — maintains the uterine lining for pregnancy, inhibits further ovulation.
Other endocrine tissues
- Pineal gland — produces melatonin, regulates circadian rhythm and sleep-wake cycle. Secretion increases in darkness.
- Thymus — produces thymosin, important for T-cell maturation. Active in childhood, involutes (shrinks) after puberty.
- Heart — produces ANF (Atrial Natriuretic Factor) in response to high blood pressure. Promotes Na and water excretion, lowering BP.
- Kidney — produces erythropoietin (EPO), stimulates RBC production in bone marrow.
- GI tract — produces gastrin, secretin, CCK (covered in the digestion chapter).
Feedback mechanisms
Most hormone systems use negative feedback: the hormone’s effect inhibits further hormone release. Example — high T3/T4 inhibits TSH from the pituitary and TRH from the hypothalamus. When T3/T4 drops, TSH rises again.
Positive feedback is rare but dramatic: oxytocin during labour. Each contraction stimulates more oxytocin, which causes stronger contractions, which stimulate even more oxytocin — until delivery.
Disorders summary table
| Disorder | Cause | Key feature |
|---|---|---|
| Diabetes mellitus | Insulin deficiency or resistance | High blood glucose, glucose in urine |
| Diabetes insipidus | ADH deficiency | Massive dilute urine (15-20 L/day) |
| Goitre | Iodine deficiency | Enlarged thyroid |
| Cretinism | Thyroid deficiency in children | Stunted growth, mental retardation |
| Myxoedema | Thyroid deficiency in adults | Puffy face, low metabolic rate |
| Graves’ disease | Autoimmune hyperthyroidism | Exophthalmos (bulging eyes), weight loss |
| Addison’s disease | Low cortisol | Low BP, darkened skin, fatigue |
| Cushing’s syndrome | Excess cortisol | Moon face, central obesity, high BP |
| Acromegaly | Excess GH in adults | Enlarged hands, feet, jaw |
| Gigantism | Excess GH in children | Abnormally tall stature |
| Dwarfism | GH deficiency in children | Short stature, normal proportions |
Worked Examples
Both cause excessive urination (polyuria) and thirst (polydipsia). Mellitus is Latin for ‘honey-sweet’ — urine contains glucose because of insulin failure. Insipidus means ‘tasteless’ — urine is dilute (no glucose) because of ADH failure. The name dates from when diagnosis involved tasting urine. Different hormones, different mechanisms, similar symptoms.
Low T3/T4 triggers the hypothalamus to release more TRH, which stimulates the anterior pituitary to release more TSH, which stimulates the thyroid to produce more T3/T4. Once T3/T4 levels rise, they feed back negatively to suppress both TRH and TSH. In Hashimoto’s thyroiditis, autoimmune destruction of the thyroid means T3/T4 stays low despite high TSH — the feedback loop is broken on the gland side.
When you face a sudden threat, the adrenal medulla releases adrenaline within seconds. Effects: heart rate increases (more blood to muscles), bronchioles dilate (more oxygen intake), liver breaks down glycogen to glucose (quick energy), blood flow diverts from gut to skeletal muscles, pupils dilate (better vision). All these prepare the body for ‘fight or flight’. The effects last minutes, not hours — just long enough to respond to the threat.
Assertion: Insulin is a protein hormone. Reason: Insulin cannot be taken orally. Both are true and the reason correctly explains the assertion. As a protein, insulin would be digested by proteases in the stomach and small intestine, losing its structure and function. This is why Type 1 diabetics must inject insulin rather than swallow it.
Without iodine, the thyroid cannot make T3/T4. Low T3/T4 means no negative feedback on the pituitary, so TSH keeps rising. Chronically elevated TSH stimulates the thyroid to enlarge (hypertrophy) in a futile attempt to produce more hormone. The enlarged thyroid is visible as a swelling in the neck — goitre. Adding iodine to table salt prevents this.
Common Mistakes
Calling insulin a steroid. It is a protein hormone (51 amino acids, two chains linked by disulfide bonds). Steroids include cortisol, aldosterone, testosterone, oestrogen and progesterone — all derived from cholesterol.
Confusing ADH and aldosterone. ADH (from posterior pituitary) conserves water by making collecting ducts permeable. Aldosterone (from adrenal cortex) conserves sodium in the distal tubule. Both reduce urine volume, but by different mechanisms.
Saying the pituitary controls the hypothalamus. It is the other way around — the hypothalamus controls the pituitary via releasing and inhibiting hormones. The pituitary is sometimes called the ‘master gland’, but the hypothalamus is the true master.
Writing that Type 1 diabetes is caused by insulin resistance. That is Type 2. Type 1 is autoimmune destruction of beta cells — there is no insulin production at all. Type 2 has insulin production but the cells do not respond to it.
Forgetting that the posterior pituitary does not make hormones. ADH and oxytocin are synthesised in hypothalamic neurons (supraoptic and paraventricular nuclei) and transported down axons to the posterior pituitary for storage and release.
Exam Weightage and Strategy
Chemical Coordination and Integration (endocrine chapter) carries 5-6 marks in CBSE Class 11 boards. NEET asks 2-3 questions per year, making it one of the highest-yield physiology chapters. Questions cover hormone-gland matching, disorder identification, and feedback mechanisms.
Make a 4-column table — gland, hormone, action, disorder. About 25 rows covers the entire chapter. Flash-card this table. That is your complete revision tool. For NEET, also learn the chemical nature of each hormone (protein, steroid, amine) since assertion-reason questions test this.
Practice Questions
Q1. A patient has high TSH but low T3/T4. What is the most likely diagnosis?
Primary hypothyroidism (e.g., Hashimoto’s thyroiditis or iodine deficiency). The thyroid is unable to produce adequate T3/T4, so there is no negative feedback on the pituitary. TSH rises in a futile attempt to stimulate the thyroid. If the problem were in the pituitary, TSH would be low.
Q2. Why does a person with Addison’s disease have darkened skin?
In Addison’s disease, the adrenal cortex is destroyed, so cortisol is very low. Low cortisol means no negative feedback on the hypothalamus and pituitary, so ACTH rises dramatically. ACTH is derived from the same precursor (POMC) as MSH (melanocyte-stimulating hormone). Excess ACTH stimulates melanocytes, causing skin darkening, especially in creases and sun-exposed areas.
Q3. Explain why exophthalmos occurs in Graves’ disease.
Graves’ disease is caused by autoimmune antibodies that mimic TSH and stimulate the thyroid (hyperthyroidism). These antibodies also act on tissues behind the eyes, causing inflammation and swelling of the extraocular muscles and fat. This pushes the eyeballs forward (exophthalmos/proptosis). It is not caused by high T3/T4 directly but by the autoimmune antibodies.
Q4. What is the role of melatonin?
Melatonin is produced by the pineal gland. Its secretion increases in darkness and decreases in light. It regulates the circadian rhythm (sleep-wake cycle), seasonal reproduction in some animals, and has antioxidant properties. In humans, melatonin supplements are used to treat jet lag and sleep disorders.
FAQs
What is the difference between endocrine and exocrine glands?
Endocrine glands are ductless — they secrete hormones directly into the blood (e.g., thyroid, adrenal, pituitary). Exocrine glands have ducts and secrete onto surfaces (e.g., salivary glands secrete into the mouth, sweat glands onto the skin). The pancreas is unique — it is both endocrine (islets secrete insulin/glucagon into blood) and exocrine (acini secrete digestive enzymes into the duodenum).
Why are steroid hormones able to cross the cell membrane but protein hormones cannot?
Steroid hormones (cortisol, oestrogen, testosterone) are lipid-soluble, so they pass through the phospholipid bilayer easily and bind to intracellular receptors (usually in the nucleus). Protein and amine hormones (insulin, adrenaline) are water-soluble and cannot cross the membrane, so they bind to surface receptors and trigger second messenger cascades (like cAMP) inside the cell.
What is a second messenger?
A molecule inside the cell that relays the signal from a hormone bound to a surface receptor. The most common is cyclic AMP (cAMP). When adrenaline binds its receptor, it activates adenylyl cyclase, which converts ATP to cAMP. cAMP then activates protein kinases that carry out the hormone’s effect. This amplifies the signal — one hormone molecule can trigger the production of many cAMP molecules.
The endocrine system rewards memorisation with structure. Group hormones by gland, always pair each with its action and its disorder, and the PYQs become predictable.