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Match List I (Hormones) with List II (Functions):
A. Cortisol → I. Stimulates formation of alveoli in mammary glands
B. Aldosterone → II. Produces anti-inflammatory reactions
C. Cholecystokinin → III. Stimulates reabsorption of Na+ and water
D. Progesterone → IV. Stimulates secretion of pancreatic juice
Options
1
A-II, B-III, C-IV, D-I
2
A-I, B-III, C-II, D-IV
3
A-III, B-IV, C-I, D-II
4
A-II, B-I, C-IV, D-III
Correct Answer
Option 1: A-II, B-III, C-IV, D-I
Solution
1

A. Cortisol → II (Anti-inflammatory): Glucocorticoid. Inhibits inflammation, immune response.

B. Aldosterone → III (Na+ and water reabsorption): Mineralocorticoid. Acts on DCT/collecting duct.

2

C. Cholecystokinin → IV (Pancreatic juice): GI hormone. Stimulates pancreatic enzyme secretion.

D. Progesterone → I (Alveoli in mammary glands): Develops secretory alveoli of breast during pregnancy.

Cortisol→Anti-inflammatory | Aldosterone→Na+/water | CCK→Pancreatic juice | Progesterone→Mammary alveoli
Theory: Human Physiology
1. Adrenal Cortex Hormones

Adrenal cortex has three zones producing different hormones. Zona glomerulosa (outermost): produces mineralocorticoids. Main: aldosterone. Function: Na+ retention, K+ excretion, water retention → blood pressure and volume. Controlled by: angiotensin II, high K+, low Na+. Zona fasciculata (middle, largest zone): produces glucocorticoids. Main: cortisol (hydrocortisone). Functions: glucose metabolism (gluconeogenesis), protein catabolism, fat mobilisation, anti-inflammatory, immunosuppressive, stress response. Controlled by: ACTH from pituitary (which is controlled by CRH from hypothalamus). Zona reticularis (innermost): produces adrenal androgens. Main: DHEA (dehydroepiandrosterone), androstenedione. Weak androgens, important in females (adrenal androgen = main androgen source in post-menopausal women). Controlled by: ACTH.

2. Cortisol — Anti-Inflammatory Mechanism

Cortisol is the primary glucocorticoid in humans. Anti-inflammatory mechanisms: Inhibits phospholipase A2: prevents arachidonic acid release → no prostaglandins, leukotrienes, thromboxanes formed (master anti-inflammatory action). Stabilises lysosomal membranes: prevents release of inflammatory enzymes. Inhibits neutrophil migration: reduces infiltration to inflammation site. Reduces vascular permeability: decreases oedema. Inhibits T cell proliferation: reduces lymphokine secretion. Reduces eosinophils and lymphocytes. Clinical use of glucocorticoids (synthetic: prednisone, prednisolone, dexamethasone, methylprednisolone, betamethasone): most widely used anti-inflammatory/immunosuppressive drugs. Used for: asthma, rheumatoid arthritis, SLE, organ transplantation, IBD, MS, skin disorders. Side effects of chronic use: Cushing syndrome (obesity, hypertension, diabetes, osteoporosis, thin skin, immune suppression, proximal myopathy).

3. Gastrointestinal Hormones

GI hormones coordinate digestion. Cholecystokinin (CCK): secreted by I-cells in duodenum/jejunum in response to fat and protein in duodenum. Functions: (1) Stimulates pancreatic acini to secrete digestive enzymes (pancreatic juice with lipase, proteases, amylase). (2) Stimulates gallbladder contraction → bile released into duodenum. (3) Relaxes sphincter of Oddi → allows bile and pancreatic juice to enter duodenum. (4) Inhibits gastric emptying (slows food leaving stomach). (5) Signals satiety to brain (reduces appetite). Secretin: secreted by S-cells in response to acidic chyme in duodenum. Stimulates: pancreatic duct cells to secrete bicarbonate (HCO3-) rich juice → neutralises stomach acid in duodenum. Gastrin: from G-cells in gastric antrum in response to stomach distension, protein. Stimulates: gastric acid (HCl) secretion by parietal cells. GIP (glucose-dependent insulinotropic peptide): from K-cells. Incretin effect — stimulates insulin secretion in response to glucose in gut.

4. Progesterone — Mammary Gland Development

Mammary gland development requires coordinated hormonal action. Oestrogen: develops the ductal system (ducts that carry milk). Stimulates duct elongation and branching. Progesterone: develops the lobular-alveolar system (secretory units that produce milk). Stimulates alveoli (lobular buds) formation. Both oestrogen and progesterone high during pregnancy → full lobular-alveolar development. Prolactin: stimulated during late pregnancy and after delivery. Promotes milk production (lactogenesis). During pregnancy: high progesterone inhibits prolactin action. After delivery: progesterone drops (placenta delivered) → prolactin can act → lactation begins. Colostrum: first milk (days 1-3 post-partum). Rich in IgA, proteins, growth factors. Important for neonatal immunity and gut development. Oxytocin: milk ejection (let-down) reflex — triggered by suckling → posterior pituitary releases oxytocin → myoepithelial cells contract → milk expulsion from alveoli through ducts.

5. Thyroid Hormones

Thyroid gland produces: T4 (thyroxine, 3,5,3,5-tetraiodothyronine): major secreted product. Prohormone. T3 (3,5,3-triiodothyronine): more active. Most T3 formed by peripheral deiodination of T4 (by deiodinases in liver, kidney). Calcitonin: from parafollicular cells (C cells). Lowers blood calcium (inhibits osteoclasts). Synthesis: iodine + thyroglobulin → MIT + DIT → T3, T4. TSH (thyroid stimulating hormone) from pituitary stimulates synthesis and secretion. Functions of T3/T4: Increase basal metabolic rate (BMR) — thermogenesis. Essential for normal growth and development (especially brain — cretinism if deficient in infancy). Positive chronotropic and inotropic effect on heart. Promotes glucose absorption and glycogenolysis. Enhances sensitivity to catecholamines. Disorders: Hypothyroidism (low T3/T4): myxoedema (adults), cretinism (congenital). Weight gain, fatigue, cold intolerance, constipation, dry skin. Hyperthyroidism (high T3/T4): Graves disease (autoimmune). Weight loss, heat intolerance, palpitations, exophthalmos (bulging eyes in Graves).

6. Pancreatic Hormones

Endocrine pancreas: Islets of Langerhans (1-2% of pancreatic mass). Alpha cells (25%): glucagon. Raises blood glucose: stimulates glycogenolysis and gluconeogenesis in liver. Beta cells (60-70%): insulin. Lowers blood glucose: promotes glucose uptake by cells (muscle, adipose, liver), glycogen synthesis, protein synthesis, lipogenesis. Inhibits glucagon. Delta cells (5-10%): somatostatin. Inhibits both insulin and glucagon. PP cells (1-2%): pancreatic polypeptide. Inhibits pancreatic exocrine secretion. Exocrine pancreas: acinar cells produce digestive enzymes (lipase, amylase, trypsinogen, chymotrypsinogen, elastase). Ductal cells produce bicarbonate. Stimulated by CCK (enzymes) and secretin (bicarbonate). Diabetes mellitus: Type 1 (autoimmune destruction of beta cells → no insulin). Type 2 (insulin resistance → inadequate insulin response). Both result in chronic hyperglycaemia → complications (retinopathy, nephropathy, neuropathy, cardiovascular disease).

7. Hypothalamus-Pituitary Axis

The hypothalamus-pituitary axis is the master regulator of the endocrine system. Hypothalamus: receives inputs from higher brain centres (emotions, circadian rhythm, body temperature). Produces releasing and inhibiting hormones. TRH → TSH → T3/T4. CRH → ACTH → cortisol. GnRH → LH, FSH → testosterone/oestrogen. GHRH → GH; Somatostatin → inhibits GH. Dopamine → inhibits Prolactin. Anterior pituitary (adenohypophysis): Tropic hormones: ACTH, TSH, LH, FSH, GH (growth hormone), Prolactin, MSH. Posterior pituitary (neurohypophysis): stores and releases hormones made in hypothalamus. ADH (vasopressin): water retention, vasoconstriction. Oxytocin: uterine contraction (labour), milk ejection, social bonding. Feedback loops: cortisol inhibits CRH and ACTH. T3/T4 inhibit TRH and TSH. Testosterone/oestrogen inhibit GnRH, LH, FSH. These negative feedback loops maintain homeostasis.

8. Sex Hormones

Oestrogens (oestradiol main form): primarily from ovary (theca cells → androgen → granulosa cells → aromatase → oestradiol). Functions: female secondary sex characteristics (breast development, fat distribution), endometrial growth (proliferative phase of menstrual cycle), bone density maintenance, duct development in mammary gland, cardiovascular protection in pre-menopausal women. Progesterone: from corpus luteum (after ovulation) and placenta (in pregnancy). Functions: secretory transformation of endometrium (luteal phase), maintains pregnancy (inhibits uterine contractions), alveolar development in breast, negative feedback to prevent new ovulation. Testosterone: from testis Leydig cells. Functions: male secondary sex characteristics, spermatogenesis, muscle mass, bone density, libido. Converted to oestradiol (by aromatase) and DHT (by 5-alpha-reductase — more potent, affects prostate and hair follicles).

Frequently Asked Questions
1. What is CCK and how does it differ from secretin? ⌄
CCK (Cholecystokinin): released by I-cells of duodenum/jejunum in response to FATS and PROTEINS in duodenum. Actions: stimulates pancreatic ENZYME secretion (lipase, protease, amylase from acinar cells), stimulates GALLBLADDER contraction (releases bile), inhibits gastric emptying, signals satiety. Secretin: released by S-cells of duodenum in response to ACID (low pH) in duodenum. Actions: stimulates pancreatic BICARBONATE secretion (from ductal cells — neutralises stomach acid), inhibits gastric acid and gastrin. Key distinction: CCK → ENZYMES (from acinar cells) and bile. Secretin → BICARBONATE (from ductal cells). Both work together: CCK provides enzymes for digestion, secretin provides alkaline environment to activate those enzymes (proteases need pH 7-8 to work).
2. What is Cushing syndrome and how does cortisol excess cause it? ⌄
Cushing syndrome: clinical syndrome caused by prolonged excess of cortisol. Causes: Iatrogenic (most common): long-term corticosteroid therapy. Cushing disease: pituitary ACTH-secreting adenoma → excess cortisol. Adrenal adenoma/carcinoma: autonomous cortisol production. Ectopic ACTH: small cell lung cancer producing ACTH. Features (all due to cortisol excess): Central obesity: fat redistributed to abdomen, face (moon face), upper back (buffalo hump). Thin skin, easy bruising: cortisol breaks down collagen. Striae (stretch marks): purple striae on abdomen. Proximal myopathy: muscle weakness in thighs/shoulders. Hypertension: cortisol has mineralocorticoid activity. Diabetes: cortisol promotes gluconeogenesis. Osteoporosis: cortisol inhibits osteoblasts, promotes osteoclasts. Immunosuppression: increased infections. Psychological: depression, anxiety. Diagnosis: 24-hour urinary free cortisol, late-night salivary cortisol, dexamethasone suppression test.
3. What is Conn syndrome? ⌄
Conn syndrome (primary hyperaldosteronism): excess aldosterone production from adrenal cortex (most commonly unilateral aldosterone-producing adenoma). Aldosterone excess → excessive Na+ and water retention → hypertension + K+ excretion → hypokalaemia. Clinical features: hypertension (often severe, resistant to treatment), hypokalaemia (low K+) → muscle weakness, cramps, constipation, cardiac arrhythmias. Metabolic alkalosis (H+ also excreted with K+). Screening: plasma aldosterone to renin ratio (high ratio). Diagnosis: CT scan of adrenals, adrenal vein sampling. Treatment: unilateral adenoma → adrenalectomy. Bilateral hyperplasia → aldosterone antagonist (spironolactone, eplerenone). Conn syndrome accounts for approximately 5-10% of all hypertension (much more common than previously thought).
4. What hormones are produced by adrenal medulla? ⌄
Adrenal medulla (inner adrenal gland): produces catecholamines from chromaffin cells. Main products: Adrenaline (epinephrine): ~80% of secretion. Noradrenaline (norepinephrine): ~20%. Both from tyrosine via: tyrosine → DOPA → dopamine → noradrenaline → adrenaline (PNMT enzyme, only in adrenal medulla). Synthesis stimulated by: sympathetic nervous system (preganglionic fibres directly innervate chromaffin cells), ACTH, stress. Effects (fight-or-flight response): increased heart rate and force, vasodilation in skeletal muscle, vasoconstriction in skin/gut, bronchodilation, pupil dilation, increased glucose (glycogenolysis), decreased digestion, increased alertness. Adrenaline vs noradrenaline: adrenaline acts more on beta receptors (heart, bronchi, vasodilation). Noradrenaline acts more on alpha receptors (vasoconstriction, blood pressure). Both bind adrenergic receptors.
5. What is the role of progesterone in pregnancy maintenance? ⌄
Progesterone is essential for maintaining pregnancy. Functions in early pregnancy: Produced by corpus luteum (stimulated by hCG from trophoblast) for first 10 weeks. Then: placenta takes over progesterone production. Progesterone actions: Maintains uterine lining (endometrium) in secretory state for embryo implantation and nutrition. INHIBITS uterine contractions: prevents premature labour (progesterone = pro-gestational = supports gestation). Thickens cervical mucus: prevents bacteria from entering uterus. Inhibits maternal immune response: prevents rejection of the embryo (immunosuppressive). Suppresses new ovulation (via feedback on GnRH/LH). Stimulates mammary alveoli: prepares breast for lactation. At term: progesterone levels fall → allows oxytocin receptors to increase → labour begins. Luteal phase deficiency: insufficient progesterone → recurrent miscarriage in early pregnancy. Treatment: progesterone supplementation in first trimester.
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