NCERT grounding
NCERT Class XI Biology, Chapter 19 (§19.2.7 Adrenal Gland) is the syllabus anchor. The chapter states that the body has one pair of adrenal glands, one above each kidney, and that the gland is composed of two types of tissues — a centrally located adrenal medulla and an outer adrenal cortex. The medulla secretes two catecholamines — adrenaline (epinephrine) and noradrenaline (norepinephrine) — that NCERT explicitly labels emergency hormones or hormones of fight or flight. The cortex secretes corticoids, of which cortisol is the principal glucocorticoid and aldosterone is the principal mineralocorticoid; the cortex also secretes small amounts of androgens. NCERT names two disorders directly — Addison's disease (cortex hypofunction) and the cortisol-excess picture later tagged as Cushing's syndrome by the NEET 2024 paper.
Two glands inside one — medulla and cortex
The adrenal is the textbook example of a compound endocrine organ: a single capsule that contains two embryologically and functionally separate glands. The outer cortex is mesodermal in origin and secretes only steroid hormones — all built from cholesterol. The inner medulla is neural-crest derived; its chromaffin cells are effectively modified post-ganglionic sympathetic neurons that have lost their axons and instead dump their transmitter into the bloodstream. That is why medullary hormones act in seconds and cortical hormones act in minutes to hours: one is a short-circuited nerve, the other is a slow-burn metabolic regulator.
The location is fixed: one gland on the upper pole of each kidney, embedded in the perinephric fat. The right gland is pyramidal and the left semilunar, but NEET does not test gross morphology — it tests the tissue layering and the hormone outputs. The standard NCERT diagram (Figure 19.4) shows the medulla as a small central island surrounded by the much thicker cortex, with the kidney slung beneath.
Adrenal medulla (inner)
Catecholamines
Adrenaline + noradrenaline
- Neural-crest derived (modified sympathetic neurons)
- Amino-acid-derived hormones (from tyrosine)
- Water-soluble; cell-membrane receptors; act in seconds
- Fight-or-flight; raise HR, BP, glycogenolysis, alertness
- Not essential for life — removal is survivable
Adrenal cortex (outer)
Corticoids
Glucocorticoids + mineralocorticoids + androgens
- Mesodermal origin; classical steroid-producing tissue
- Steroid hormones (cholesterol-derived)
- Lipid-soluble; intracellular receptors; act in minutes-hours
- Metabolic homeostasis, Na+/water balance, BP support
- Essential for life — total loss is fatal (Addisonian crisis)
Adrenal medulla — catecholamines
The medulla secretes two hormones that NCERT names explicitly — adrenaline (epinephrine) and noradrenaline (norepinephrine). Both are synthesised in the chromaffin cells from the amino acid tyrosine via the sequence tyrosine → DOPA → dopamine → noradrenaline → adrenaline. Because they share a catechol nucleus, the pair is collectively called catecholamines. This puts adrenaline in the same biochemical category as dopamine — and a different category from cortisol and aldosterone. NEET 2018 Q.159 used this distinction directly: of epinephrine, ecdysone, estradiol and estriol, only epinephrine is an amino-acid-derived hormone; the rest are steroids.
NCERT calls catecholamines emergency hormones or hormones of fight or flight because they are rapidly secreted in response to stress of any kind and during emergency situations. The release is triggered by preganglionic sympathetic fibres splanchnic to the adrenal — acetylcholine on the chromaffin cell drives exocytosis of catecholamine-loaded vesicles. The effects, as listed by NCERT §19.2.7, are: increased alertness, pupillary dilation, piloerection (raising of hairs), sweating, increased heart beat, increased strength of heart contraction, increased rate of respiration, and stimulation of glycogenolysis with consequent rise in blood glucose. NCERT also notes that catecholamines stimulate the breakdown of lipids and proteins.
Cardiovascular
Heart rate ↑. Force of contraction ↑.
Blood pressure ↑. Peripheral vasoconstriction in skin and gut, vasodilation in skeletal muscle.
NEET-style factRespiratory & CNS
Rate of respiration ↑. Bronchodilation.
Alertness ↑. Pupillary dilation, piloerection, sweating.
Fight-or-flight signsMetabolic
Glycogenolysis ↑ in liver and muscle → blood glucose ↑.
Lipolysis ↑ in adipose; proteolysis stimulated.
Trap: same direction as cortisol but fasterTiming
Onset: seconds.
Duration: short-lived; rapidly cleared by COMT and MAO.
Why it is an "emergency" hormoneThree cortical zones
NCERT divides the adrenal cortex into three concentric layers. Reading from inside out, the order in the chapter is zona reticularis (inner) → zona fasciculata (middle) → zona glomerulosa (outer). The mnemonic "GFR — salt, sugar, sex" reads from outside in: glomerulosa makes the salt-balancing mineralocorticoids, fasciculata makes the sugar-managing glucocorticoids, and reticularis makes the sex-corticoid androgens.
Figure 1. The adrenal sits on the upper pole of the kidney. Going inwards from the capsule: zona glomerulosa (mineralocorticoids), zona fasciculata (glucocorticoids), zona reticularis (adrenal androgens), and the central medulla (catecholamines).
Zona glomerulosa — salt
The outermost layer is a narrow band of clustered cells just under the connective-tissue capsule. Its product is the mineralocorticoid aldosterone, the hormone NCERT names as the principal mineralocorticoid of the human body. Its release is governed mainly by the renin–angiotensin system from the kidney and by plasma K+, not by pituitary ACTH — a small but exam-relevant distinction.
Zona fasciculata — sugar
The thickest layer, with cells arranged in straight cords (Latin fasciculi) running perpendicular to the surface. It secretes the glucocorticoid cortisol, the principal glucocorticoid in our body. Cortisol release is driven by pituitary ACTH from the pars distalis (anterior pituitary) under hypothalamic CRH — the classical HPA (hypothalamic–pituitary–adrenal) axis.
Zona reticularis — sex
The innermost cortical layer is a network (Latin reticulum) of branching cell cords abutting the medulla. It secretes small amounts of adrenal androgens — sex corticoids — which NCERT credits with a role in the growth of axial, pubic and facial hair during puberty. Their contribution is small in males (testicular testosterone dominates) but physiologically important in females, where the adrenal is a major source of circulating androgens.
Cortex hormones — cortisol and aldosterone
Both are steroid hormones, built from cholesterol through a common pregnenolone intermediate and branching to either an 11-, 17- and 21-hydroxylated glucocorticoid (cortisol) or an 18-aldehyde mineralocorticoid (aldosterone). Both are lipid-soluble, both circulate bound to carrier proteins (corticosteroid-binding globulin and albumin), and both act on intracellular receptors that translocate to the nucleus to alter gene transcription — the mechanism NEET 2019 Q.19 asked about for steroid hormones (binding to DNA and forming a gene–hormone complex).
Cortisol — the principal glucocorticoid
Cortisol is built for sustained metabolic stress. NCERT lists its actions explicitly in §19.2.7: glucocorticoids stimulate gluconeogenesis, lipolysis and proteolysis, and inhibit cellular uptake and utilisation of amino acids. Cortisol is involved in maintaining the cardiovascular system as well as kidney function. Glucocorticoids, particularly cortisol, produce anti-inflammatory reactions and suppress the immune response. Cortisol also stimulates RBC production.
The five NCERT-listed actions
1. Gluconeogenesis (raises blood glucose). 2. Lipolysis. 3. Proteolysis. 4. Anti-inflammatory and immune suppression. 5. Cardiovascular and renal support; stimulates RBC production.
Aldosterone — the principal mineralocorticoid
Aldosterone is the body's master sodium-retainer. NCERT writes: aldosterone acts mainly at the renal tubules and stimulates the reabsorption of Na+ and water and excretion of K+ and phosphate ions. Thus, aldosterone helps in the maintenance of electrolytes, body fluid volume, osmotic pressure and blood pressure. The principal target is the distal convoluted tubule (DCT) and the cortical collecting duct, where aldosterone upregulates ENaC sodium channels and the Na+/K+-ATPase. Where ADH controls free water reabsorption to regulate plasma osmolality, aldosterone controls Na+ reabsorption (with water following passively) to regulate plasma volume and pressure.
Cortisol release on stress — the HPA axis
-
Step 1
Stress signal
Physical or emotional stress, hypoglycaemia or fever activates the hypothalamus.
CRH release -
Step 2
Pituitary
CRH drives the pars distalis to secrete adrenocorticotrophic hormone (ACTH).
ACTH ↑ -
Step 3
Adrenal cortex
ACTH drives the zona fasciculata to synthesise and release cortisol.
Cortisol ↑ -
Step 4
Feedback
Cortisol suppresses hypothalamic CRH and pituitary ACTH — classical negative feedback.
Loop closed
Figure 2. Aldosterone diffuses into the DCT cell, binds the mineralocorticoid receptor (MR) and drives transcription of ENaC and Na+/K+-ATPase. The cell now reabsorbs Na+ and water from filtrate into blood, while K+ and H+ are excreted into urine.
Addison's disease and Cushing's syndrome
Two NEET-favourite disorders bracket the cortex. NCERT names the first explicitly: under-production of hormones by the adrenal cortex alters carbohydrate metabolism, causing acute weakness and fatigue — the clinical picture called Addison's disease. The deficit is mainly of cortisol with variable aldosterone loss; the consequences are hypoglycaemia, hypotension, hyponatraemia, hyperkalaemia and weight loss, with skin hyperpigmentation when the primary cause is at the adrenal itself (compensatory ACTH rise drives melanocyte stimulation).
The mirror image is over-production of cortisol — Cushing's syndrome. NCERT does not name Cushing's in §19.2.7, but NEET 2024 Q.200 lists its cardinal features in matching form: "excess secretion of cortisol, moon face and hyperglycaemia". Other features include central (truncal) obesity, buffalo hump, purple abdominal striae, easy bruising, osteoporosis, hypertension and immune suppression. Cushing's syndrome is the umbrella term; the pituitary-ACTH-driven subtype is specifically called Cushing's disease, but NEET treats the two interchangeably.
Addison's disease
Hypo
↓ cortisol (± aldosterone)
- NCERT-named ("acute weakness and fatigue")
- Hypoglycaemia, hypotension
- Hyponatraemia, hyperkalaemia
- Weight loss, skin pigmentation
- NEET 2019 Q.89 maps corticoids → Addison's
Cushing's syndrome
Hyper
↑ cortisol
- NEET 2024 Q.200 — "moon face, hyperglycaemia"
- Truncal obesity, buffalo hump
- Hypertension, hypokalaemia
- Osteoporosis, immune suppression
- Purple striae, easy bruising
Worked examples
A NEET aspirant is asked: which of the following is not a steroid hormone — (1) cortisol, (2) testosterone, (3) progesterone, (4) glucagon?
Answer: (4) glucagon. Cortisol, testosterone and progesterone are cholesterol-derived steroid hormones. Glucagon is a 29-amino-acid peptide hormone from the alpha cells of the islets of Langerhans. Adrenaline, although also a medullary hormone of the adrenal gland, is an amino-acid-derived catecholamine — not a steroid either. NEET has tested this category split repeatedly (NEET 2024 Q.156).
Match the gland with its disease: (a) Pituitary, (b) Thyroid, (c) Adrenal, (d) Pancreas with (i) Graves' disease, (ii) Diabetes mellitus, (iii) Diabetes insipidus, (iv) Addison's disease.
Answer: a–iii, b–i, c–iv, d–ii. Diabetes insipidus follows ADH (vasopressin) failure from the posterior pituitary. Graves' disease is hyperthyroidism with exophthalmos. Addison's disease is the adrenal cortex disorder — under-production of cortisol. Diabetes mellitus is insulin deficiency from pancreatic beta cells. This is the exact NEET 2020 Q.63 match, and the answer here is option (2) on that paper.
A patient presents with moon-face, central obesity, hyperglycaemia and purple abdominal striae. Plasma cortisol is markedly elevated. Which gland is dysfunctional and in which direction?
Answer: Adrenal cortex — hyperfunction (Cushing's syndrome). The clinical features map directly onto cortisol excess: gluconeogenesis raises blood glucose (hyperglycaemia); proteolysis weakens dermal collagen producing striae; lipid redistribution drives the moon face and central obesity. The cause may sit at the pituitary (excess ACTH → Cushing's disease), at the adrenal itself (cortical adenoma) or be exogenous (long-term glucocorticoid therapy). NEET 2024 Q.200 codifies the picture as "excess secretion of cortisol, moon face and hyperglycaemia".