A. Hypothalamus and Pituitary Gland

The hypothalamus is the neuroendocrine interface, producing releasing hormones (GnRH, CRH, TRH, GHRH) and inhibiting hormones (somatostatin, dopamine/PIF). The anterior pituitary (adenohypophysis) under its control produces FLAT PG: FSH, LH, ACTH, TSH, Prolactin, GH. Prolactin is unique in being primarily under inhibitory (dopamine) control. The posterior pituitary (neurohypophysis) stores and releases ADH and oxytocin, both synthesised in hypothalamic nuclei. Regulation throughout is by negative feedback — rising end-hormones suppress their upstream drivers.

B. Thyroid and Parathyroid Glands

The thyroid gland produces T3 and T4 (iodine-dependent; regulate BMR, growth, development) and calcitonin (from C-cells; lowers blood calcium). Iodine deficiency → low T4 → compensatory TSH elevation → thyroid enlargement (simple goitre). Graves' disease (autoimmune TSI-driven hyperthyroidism) presents with exophthalmos, weight loss, and elevated BMR. Hypothyroidism in childhood = cretinism; in adults = myxoedema. The parathyroid glands secrete PTH, which raises blood calcium (bone resorption, renal reabsorption, vitamin D activation). PTH and calcitonin are antagonistic. PTH deficiency → hypocalcaemia → tetany.

C. Adrenal Gland

The adrenal cortex (GFR zones): zona glomerulosa → aldosterone (Na+ retention, blood pressure regulation via RAAS); zona fasciculata → cortisol (gluconeogenesis, anti-inflammatory, stress response); zona reticularis → androgens. The adrenal medulla (neural crest origin) → adrenaline and noradrenaline (fight-or-flight catecholamines). Addison's disease = adrenal cortex hyposecretion (dark skin, hypoglycaemia, weakness). Cushing's syndrome = cortisol excess (moon face, buffalo hump, hyperglycaemia).

D. Pancreas — Endocrine Function

Islets of Langerhans: α-cells → glucagon (raises glucose); β-cells → insulin (lowers glucose — the only hypoglycaemic hormone); δ-cells → somatostatin (inhibits both). Insulin and glucagon are antagonistic regulators of blood glucose. Type 1 DM = autoimmune β-cell destruction (absolute insulin deficiency). Type 2 DM = insulin resistance (relative insufficiency). Diabetes insipidus (ADH-related) must be distinguished from diabetes mellitus — normal blood glucose in DI.

E. Pineal Gland and Thymus

Pineal gland (dorsal forebrain) → melatonin (indole amine): regulates circadian rhythm by responding to light-dark cycles (increases in darkness). Secondary roles: skin lightening, puberty timing. Thymus → thymosins: drive T-lymphocyte differentiation and maturation (cell-mediated immunity). The thymus is maximally active in childhood and involutes (replaced by fat) with age.

F. Hormone Mechanisms

Peptide hormones (water-soluble) → surface receptors → cAMP second messenger → rapid effects. Steroid and thyroid hormones (lipid-soluble) → intracellular receptors → gene transcription → delayed but sustained effects. Chemical nature dictates receptor location, mechanism, and pharmacological route of administration.