Physiology
Medical physiology for MBBS: cell and body fluids, blood, nerve and muscle, and the cardiovascular, respiratory, gastrointestinal, renal, endocrine, reproductive and nervous systems, special senses and integrative physiology.
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Definition
The pituitary gland (‘master gland’) lies below the hypothalamus and has two lobes; the hypothalamo–pituitary axis links the brain to the endocrine system.
Anterior Pituitary Hormones
- GH — growth
- TSH — thyroid
- ACTH — adrenal cortex
- FSH / LH — gonads
- Prolactin — milk production
Posterior Pituitary Hormones
- ADH (vasopressin) — water reabsorption
- Oxytocin — uterine contraction, milk ejection
- (both made in hypothalamus, stored here)
Control
- Hypothalamic releasing/inhibiting hormones → anterior pituitary (portal system)
- Posterior lobe — direct neural connection
- Negative feedback by target-gland hormones
The hypothalamus drives the pituitary, which drives target glands — with feedback control. Hormone Target GH Body tissues TSH Thyroid ACTH Adrenal cortex FSH/LH Gonads Prolactin Breast Applied
- Acromegaly / gigantism (↑ GH)
- Panhypopituitarism
- Diabetes insipidus (↓ ADH)
🔑KEY POINTS TO REMEMBER- Pituitary = master gland; anterior (6 hormones) + posterior (ADH, oxytocin).
- Hypothalamus controls it via releasing hormones + portal system.
- Negative feedback by target hormones.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
The thyroid gland secretes thyroxine (T4) and triiodothyronine (T3) (iodine-dependent) and calcitonin; these control metabolism.
Hormones
- T3, T4 — follicular cells (iodine + thyroglobulin)
- Calcitonin — parafollicular (C) cells (↓ Ca²⁺)
Functions of T3/T4
- ↑ Basal metabolic rate and heat production
- Growth and brain development
- ↑ Heart rate and cardiac output
- Metabolism of carbohydrate, fat, protein
Regulation
- Hypothalamus (TRH) → pituitary (TSH) → thyroid
- Negative feedback by T3/T4
TRH → TSH → T3/T4, with negative feedback keeping levels steady. Disorder Cause Features Hypothyroidism ↓ T3/T4 Weight gain, cold, slow Hyperthyroidism ↑ T3/T4 Weight loss, heat, tachycardia Goitre Iodine deficiency Enlarged thyroid Applied
- Cretinism — congenital hypothyroidism
- Myxoedema; Graves’ disease (hyperthyroid)
🔑KEY POINTS TO REMEMBER- Thyroid: T3/T4 (metabolism, iodine-dependent) + calcitonin (↓ Ca²⁺).
- Axis: TRH → TSH → T3/T4 (negative feedback).
- Hypo (weight gain, cold) vs hyper (weight loss, heat).
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
The adrenal gland has a cortex (steroid hormones) and a medulla (catecholamines).
Adrenal Cortex (3 zones)
- Zona glomerulosa — aldosterone (mineralocorticoid)
- Zona fasciculata — cortisol (glucocorticoid)
- Zona reticularis — androgens
Actions
- Aldosterone — Na⁺ retention, K⁺ loss
- Cortisol — ↑ glucose, anti-inflammatory, stress
- Androgens — sexual characteristics
Adrenal Medulla
- Secretes adrenaline & noradrenaline
- Mediates the ‘fight or flight’ response
Cortex makes steroids; medulla makes catecholamines. Zone / part Hormone Main action Glomerulosa Aldosterone Na⁺ retention Fasciculata Cortisol ↑ glucose, anti-inflammatory Reticularis Androgens Sex characters Medulla Adrenaline Fight or flight Applied
- Cushing’s (↑ cortisol); Addison’s (↓ cortisol)
- Conn’s (↑ aldosterone)
- Phaeochromocytoma (medulla tumour)
🔑KEY POINTS TO REMEMBER- Cortex: glomerulosa (aldosterone), fasciculata (cortisol), reticularis (androgens).
- Medulla: adrenaline/noradrenaline (fight or flight).
- Cushing’s, Addison’s, Conn’s, phaeochromocytoma.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
The endocrine pancreas (islets of Langerhans) secretes insulin and glucagon, which regulate blood glucose.
Islet Cells
- Beta cells → insulin (lowers glucose)
- Alpha cells → glucagon (raises glucose)
- Delta cells → somatostatin
Insulin (lowers glucose)
- ↑ Glucose uptake (muscle, fat)
- ↑ Glycogen, protein and fat synthesis
- Released when glucose is high
Glucagon (raises glucose)
- ↑ Glycogenolysis and gluconeogenesis
- Released when glucose is low
Insulin and glucagon act in opposition to hold blood glucose steady. Hormone Cell Effect on glucose Insulin Beta ↓ (lowers) Glucagon Alpha ↑ (raises) Applied
- Diabetes mellitus — insulin deficiency/resistance
- Hypoglycaemia — glucagon rescue
🔑KEY POINTS TO REMEMBER- Islets: beta (insulin ↓ glucose), alpha (glucagon ↑ glucose).
- Insulin → uptake & storage; glucagon → breakdown & release.
- Balance keeps glucose 70–110 mg/dL.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Calcium homeostasis keeps plasma Ca²⁺ in a narrow range (9–11 mg/dL) via PTH, vitamin D (calcitriol) and calcitonin.
PTH (raises Ca²⁺)
- ↑ Bone resorption
- ↑ Renal Ca²⁺ reabsorption, ↓ phosphate
- ↑ Calcitriol → ↑ gut absorption
Vitamin D / Calcitriol
- ↑ Ca²⁺ and phosphate absorption (gut)
- Needed for bone mineralisation
Calcitonin (lowers Ca²⁺)
- From thyroid C cells
- ↓ Bone resorption
Low calcium triggers PTH, which raises calcium from bone, kidney and gut. Hormone Effect on Ca²⁺ PTH ↑ (raises) Calcitriol ↑ (gut absorption) Calcitonin ↓ (lowers) Applied
- Hyperparathyroidism → bone loss, stones
- Rickets / osteomalacia — vitamin D deficiency
- Tetany — low Ca²⁺
🔑KEY POINTS TO REMEMBER- Ca²⁺ 9–11 mg/dL, held by PTH, calcitriol, calcitonin.
- PTH & calcitriol raise Ca²⁺; calcitonin lowers it.
- Deficiency → rickets/tetany; excess PTH → stones/bone loss.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Insulin is a hormone from pancreatic beta cells that lowers blood glucose — the body’s only hypoglycaemic hormone.
Actions
- ↑ Glucose uptake (GLUT4 — muscle, fat)
- ↑ Glycogen synthesis (liver, muscle)
- ↑ Protein and fat synthesis
- ↓ Gluconeogenesis
Regulation
- ↑ Blood glucose → ↑ insulin
- Also stimulated by amino acids, GIP, vagus
Rising glucose triggers insulin, which stores it and lowers blood glucose. Process Effect Glucose uptake ↑ Glycogen ↑ Fat/protein ↑ synthesis Blood glucose ↓ Applied
- Deficiency/resistance → diabetes mellitus
- Insulin therapy in diabetes
🔑KEY POINTS TO REMEMBER- Insulin (beta cells) = only hormone that lowers glucose.
- ↑ uptake (GLUT4), ↑ storage, ↓ gluconeogenesis.
- Deficiency/resistance → diabetes.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Growth hormone (GH, somatotropin) from the anterior pituitary promotes growth and metabolism, acting largely via IGF-1 from the liver.
Actions
- ↑ Linear growth (bones, cartilage)
- ↑ Protein synthesis
- ↑ Lipolysis; ↑ blood glucose (anti-insulin)
- Acts via IGF-1
Regulation
- GHRH (↑), somatostatin (↓)
- ↑ in deep sleep, exercise, hypoglycaemia
GH acts mostly through liver-derived IGF-1 to drive growth. Disorder Cause Gigantism ↑ GH (child) Acromegaly ↑ GH (adult) Dwarfism ↓ GH (child) Applied
- Excess → gigantism / acromegaly
- Deficiency → pituitary dwarfism
🔑KEY POINTS TO REMEMBER- GH acts via IGF-1 → growth + protein synthesis.
- GHRH ↑, somatostatin ↓; ↑ in sleep/exercise.
- Excess → gigantism/acromegaly; lack → dwarfism.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Parathyroid hormone (PTH) from the parathyroid glands is the main hormone that raises plasma calcium.
Actions (raise Ca²⁺)
- Bone — ↑ resorption (releases Ca²⁺)
- Kidney — ↑ Ca²⁺ reabsorption, ↓ phosphate
- ↑ Activation of vitamin D → ↑ gut absorption
Regulation
- ↓ Plasma Ca²⁺ → ↑ PTH
- ↑ Ca²⁺ → ↓ PTH
PTH raises calcium by acting on bone, kidney and gut. Site PTH effect Bone ↑ resorption Kidney ↑ Ca²⁺, ↓ phosphate Gut (via vit D) ↑ absorption Applied
- Hyperparathyroidism → ↑ Ca²⁺, stones, bone loss
- Hypoparathyroidism → tetany
🔑KEY POINTS TO REMEMBER- PTH raises Ca²⁺ (bone, kidney, gut via vit D).
- ↓ Ca²⁺ stimulates PTH.
- Excess → stones/bone loss; deficiency → tetany.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Diabetes mellitus is a metabolic disorder of chronic hyperglycaemia due to insulin deficiency (Type 1) or resistance (Type 2).
Types
- Type 1 — autoimmune β-cell loss (insulin deficiency)
- Type 2 — insulin resistance (commonest)
- Gestational diabetes
Features (the 3 P’s)
- Polyuria, polydipsia, polyphagia
- Weight loss, fatigue
- Glycosuria, ↑ blood glucose
Lack or resistance to insulin raises glucose, spilling into urine and causing symptoms. Feature Type 1 Type 2 Onset Young Adult Insulin Deficient Resistance Treatment Insulin Diet, oral drugs Complications
- Acute — ketoacidosis (T1), hyperosmolar state (T2)
- Chronic — retinopathy, nephropathy, neuropathy, CVD
🔑KEY POINTS TO REMEMBER- Diabetes = chronic hyperglycaemia (T1 deficiency, T2 resistance).
- Features: 3 P’s + glycosuria.
- Complications: retino-, nephro-, neuropathy, CVD.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Oxytocin is a posterior pituitary hormone (made in the hypothalamus) that causes uterine contraction and milk ejection.
Actions
- Uterine contraction (labour)
- Milk ejection (let-down) from the breast
- Bonding behaviour
Regulation (positive feedback)
- Cervical stretch → oxytocin → more contraction (labour)
- Suckling → oxytocin → milk ejection
Oxytocin acts by positive feedback in both labour and breastfeeding. Stimulus Effect Labour (cervix stretch) Uterine contraction Suckling Milk ejection Applied
- Used to induce or augment labour
- Classic example of positive feedback
🔑KEY POINTS TO REMEMBER- Oxytocin → uterine contraction + milk ejection.
- Works by positive feedback (labour, suckling).
- Made in hypothalamus, released from posterior pituitary.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
The adrenal medulla secretes the catecholamines adrenaline (~80%) and noradrenaline, mediating the fight-or-flight response.
Actions
- ↑ Heart rate and force, ↑ BP
- Bronchodilation
- ↑ Blood glucose (glycogenolysis)
- Pupil dilation, ↓ gut activity
Control
- Sympathetic stimulation (a modified sympathetic ganglion)
- Stress, exercise, fear
Stress drives the sympathetic system to release catecholamines for fight-or-flight. Target Response Heart ↑ rate/force Lungs Bronchodilation Glucose ↑ Gut ↓ Applied
- Phaeochromocytoma — tumour → hypertension
- Adrenaline used in anaphylaxis and cardiac arrest
🔑KEY POINTS TO REMEMBER- Adrenal medulla → adrenaline (80%) + noradrenaline.
- Fight-or-flight: ↑ HR/BP, bronchodilation, ↑ glucose.
- Phaeochromocytoma → hypertension.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Melatonin is a hormone from the pineal gland that regulates the sleep–wake cycle (circadian rhythm).
Functions
- Induces sleep (secreted in darkness)
- Regulates the circadian rhythm
- Antioxidant; may modulate puberty
Regulation
- Light ↓ melatonin; darkness ↑ melatonin
- Pathway: retina → suprachiasmatic nucleus → pineal
Darkness triggers pineal melatonin, promoting sleep and setting the body clock. Condition Melatonin Darkness / night ↑ (sleep) Light / day ↓ Applied
- Used for jet lag and insomnia
- Linked to seasonal affective disorder
🔑KEY POINTS TO REMEMBER- Melatonin (pineal) sets the circadian rhythm; ↑ in darkness.
- Promotes sleep; regulated via retina → SCN → pineal.
- Used for jet lag/insomnia.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).