Chemical Coordination and Integration — NCERT Class 11 Biology

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This page provides complete NCERT Solutions for CBSE Class 11 Biology Chapter 22 — Chemical Coordination and Integration. All intext questions (organised by page number) and chapter-end exercise questions are answered in detail. Use the section headings to jump directly to the question you need help with, or read through the full page for a comprehensive revision of the chapter.

Key Concepts (Quick Recap)

• Hypothalamus: Master control centre; secretes releasing hormones (stimulate anterior pituitary) and inhibiting hormones (suppress anterior pituitary); also produces ADH and oxytocin (stored in posterior pituitary)
• Pituitary — Anterior (Adenohypophysis): GH (growth), PRL (milk production), TSH (thyroid stimulation), ACTH (adrenal cortex stimulation), LH (ovulation, testosterone), FSH (follicle development, spermatogenesis), MSH (skin pigmentation)
• Pituitary — Posterior (Neurohypophysis): Oxytocin (uterine contraction, milk ejection), Vasopressin/ADH (water reabsorption)
• Thyroid: T3 (triiodothyronine) and T4 (thyroxine) — regulate BMR, growth, development; Calcitonin — lowers blood calcium
• Parathyroid: PTH (parathyroid hormone) — increases blood calcium, decreases blood phosphate
• Thymus: Thymosins — T-lymphocyte differentiation and maturation
• Adrenal Cortex: Glucocorticoids (cortisol — gluconeogenesis, anti-inflammatory, stress response), Mineralocorticoids (aldosterone — Na+ reabsorption, K+ excretion), Androgenic steroids (sex hormones, minor role)
• Adrenal Medulla: Adrenaline (epinephrine) and Noradrenaline (norepinephrine) — fight or flight response
• Pancreas (Islets of Langerhans): Alpha cells — Glucagon (increases blood glucose); Beta cells — Insulin (decreases blood glucose)
• Testis: Testosterone — male secondary sex characteristics, spermatogenesis
• Ovary: Estrogen — female secondary sex characteristics, endometrial growth; Progesterone — maintains pregnancy, prepares endometrium for implantation
• Feedback mechanisms: Negative feedback (most common — maintains homeostasis, e.g., TSH–T3/T4, insulin–glucose) and Positive feedback (amplifies response, e.g., oxytocin during childbirth, LH surge during ovulation)

Intext Questions

Page 345

Key characteristics of hormones:

• They are chemical messengers produced by endocrine glands.
• They are secreted directly into the blood (not through ducts — hence endocrine = "ductless" glands).
• They act on specific target cells that have the appropriate receptors.
• They are effective in very low concentrations (nanograms or picograms per mL).
• They regulate physiological processes such as growth, metabolism, reproduction, and homeostasis.
• Their effects are generally slow but long-lasting compared to nervous signals.

(Note: The liver is larger but is not classified as a pure endocrine gland, as it has many other functions. The pituitary gland, often called the "master gland," is much smaller — about the size of a pea.)

The hypothalamus regulates the endocrine system in two ways:

1. Control of anterior pituitary (adenohypophysis): The hypothalamus produces releasing hormones (stimulate secretion) and inhibiting hormones (suppress secretion) that are transported through the hypothalamo-hypophyseal portal system (a network of blood vessels) to the anterior pituitary. These include:

• Releasing hormones: GnRH (stimulates FSH and LH), TRH (stimulates TSH), CRH (stimulates ACTH), GHRH (stimulates GH), PRH (stimulates prolactin)
• Inhibiting hormones: Somatostatin/GHIH (inhibits GH), PIH/Dopamine (inhibits prolactin)

2. Control of posterior pituitary (neurohypophysis): The hypothalamus produces the hormones oxytocin and vasopressin (ADH) in the cell bodies of neurosecretory cells (supraoptic and paraventricular nuclei). These hormones are transported along the axons of these cells to the posterior pituitary, where they are stored and released into the blood upon stimulation.

Since the pituitary gland (the "master gland") itself is controlled by the hypothalamus, the hypothalamus is the ultimate regulator of the endocrine system.

Page 353

(a) Thyroid gland: Triiodothyronine (T3), Thyroxine (T4), and Calcitonin

(b) Adrenal medulla: Adrenaline (Epinephrine) and Noradrenaline (Norepinephrine)

(c) Alpha cells of pancreas (Islets of Langerhans): Glucagon

(d) Posterior pituitary (Neurohypophysis): Oxytocin and Vasopressin (ADH — Antidiuretic Hormone)

(Note: Oxytocin and ADH are produced by the hypothalamus and only stored and released by the posterior pituitary.)

1. Glycogenolysis: Glucagon stimulates the breakdown of glycogen (stored in the liver) into glucose, which is released into the blood.

2. Gluconeogenesis: Glucagon promotes the synthesis of glucose from non-carbohydrate sources (amino acids, lactate, glycerol) in the liver.

3. Lipolysis: Glucagon promotes the breakdown of fats (lipolysis) in adipose tissue, releasing free fatty acids and glycerol. The glycerol can be used for gluconeogenesis.

4. Inhibition of glycogenesis: Glucagon inhibits the synthesis of glycogen from glucose.

5. Inhibition of glycolysis: Glucagon inhibits glycolysis (the breakdown of glucose for energy) in the liver.

Glucagon and insulin work antagonistically to maintain blood glucose homeostasis:

• When blood glucose is high → insulin secretion increases, glucagon secretion decreases → blood glucose decreases.
• When blood glucose is low → glucagon secretion increases, insulin secretion decreases → blood glucose increases.

Role of the thymus in the immune system:

1. Secretion of thymosins: The thymus secretes a group of hormones called thymosins (thymosin, thymopoietin, thymic humoral factor). Thymosins play a crucial role in the differentiation and maturation of T-lymphocytes (T cells), which are essential for cell-mediated immunity.

2. T-cell maturation: Immature T-cell precursors from the bone marrow migrate to the thymus, where they undergo a rigorous selection process:

• Positive selection: T cells that can recognise self-MHC molecules are allowed to survive.
• Negative selection: T cells that strongly react with self-antigens are eliminated (apoptosis).

Only about 2–5% of T cells survive this selection and migrate to peripheral lymphoid organs as mature, functional T cells.

3. Types of T cells produced: The thymus produces helper T cells (Th), cytotoxic T cells (Tc), and regulatory T cells (Treg), which are essential for:

• Cell-mediated immunity (Tc cells kill virus-infected cells and cancer cells)
• Antibody production regulation (Th cells help B cells)
• Immune tolerance (Treg cells prevent autoimmune reactions)

4. Immune competence: The thymus provides the microenvironment for the development of immunocompetent T cells that can distinguish between self and non-self antigens.

Chapter-End Exercise

(a) Hormone: A non-nutrient chemical messenger secreted by an endocrine gland directly into the blood, which transports it to a specific target cell, tissue, or organ where it produces a specific physiological effect. Hormones are produced in minute quantities, act at very low concentrations, and their secretion is regulated by feedback mechanisms. Examples: insulin, thyroxine, adrenaline.

(b) Endocrine gland: A ductless gland that secretes hormones directly into the blood (or lymph) rather than through a duct. Endocrine glands are richly supplied with blood vessels. Examples: pituitary, thyroid, adrenal, pancreas (islets of Langerhans), gonads. (In contrast, exocrine glands like salivary glands and sweat glands secrete their products through ducts.)

(c) Target tissue: A specific tissue or organ that has receptors for a particular hormone and responds to it. Hormones circulate throughout the body via the blood, but they act only on cells that have the appropriate receptor proteins. For example, the target tissues of insulin are liver, muscle, and adipose tissue; the target tissue of TSH is the thyroid gland.

(d) Receptor: A specific protein molecule (either on the cell surface or inside the cell) that binds to a hormone with high affinity and specificity. The binding of a hormone to its receptor triggers a cascade of biochemical reactions that produce the hormone's effect. Peptide hormones bind to cell surface receptors (membrane-bound), while steroid hormones bind to intracellular receptors (in the cytoplasm or nucleus).

1. Hypothalamus: Located at the base of the brain, below the thalamus and above the pituitary gland. It is the master regulator of the endocrine system.

2. Pituitary gland (Hypophysis): Located at the base of the brain, below the hypothalamus, in the sella turcica of the sphenoid bone. Connected to the hypothalamus by the infundibulum.

3. Pineal gland: Located in the dorsal part of the forebrain, near the centre of the brain. Secretes melatonin.

4. Thyroid gland: A bilobed gland located in the neck, on either side of the trachea, connected by a thin isthmus. It is the largest endocrine gland.

5. Parathyroid glands: Four small glands embedded on the posterior surface of the thyroid gland (two on each lobe).

6. Thymus: Located in the upper chest (mediastinum), between the lungs behind the sternum. Large in children, involutes after puberty.

7. Adrenal glands (Suprarenal glands): A pair of glands, one located on top of each kidney. Each has an outer cortex and inner medulla.

8. Pancreas (Islets of Langerhans): Located in the abdominal cavity, behind the stomach, between the duodenum and spleen. The endocrine portion (1–2% of the pancreas) consists of the Islets of Langerhans.

9. Testes (in males): Located in the scrotum, outside the abdominal cavity.

10. Ovaries (in females): Located in the lower abdominal cavity, one on each side of the uterus.

(a) Hypothalamus:

The hypothalamus secretes releasing and inhibiting hormones that regulate the anterior pituitary:

• GnRH (Gonadotropin-Releasing Hormone): Stimulates the anterior pituitary to secrete FSH and LH.
• TRH (Thyrotropin-Releasing Hormone): Stimulates the anterior pituitary to secrete TSH.
• CRH (Corticotropin-Releasing Hormone): Stimulates the anterior pituitary to secrete ACTH.
• GHRH (Growth Hormone-Releasing Hormone): Stimulates the anterior pituitary to secrete GH.
• Somatostatin (GHIH — Growth Hormone-Inhibiting Hormone): Inhibits the secretion of GH (and also TSH and insulin).
• PIH (Prolactin-Inhibiting Hormone / Dopamine): Inhibits the secretion of prolactin.

The hypothalamus also produces oxytocin and vasopressin (ADH), which are transported to and stored in the posterior pituitary.

(b) Anterior Pituitary (Adenohypophysis):

• Growth Hormone (GH / Somatotropin): Stimulates growth of bones, cartilage, and muscles; promotes protein synthesis; stimulates lipolysis and reduces glucose uptake.
• Prolactin (PRL): Stimulates milk production (lactogenesis) in mammary glands after childbirth.
• Thyroid-Stimulating Hormone (TSH / Thyrotropin): Stimulates the thyroid gland to secrete T3 and T4; promotes growth of the thyroid gland.
• Adrenocorticotropic Hormone (ACTH): Stimulates the adrenal cortex to secrete glucocorticoids (mainly cortisol).
• Luteinising Hormone (LH): In females — triggers ovulation, promotes formation of the corpus luteum, stimulates the corpus luteum to secrete progesterone. In males — stimulates the Leydig (interstitial) cells to secrete testosterone.
• Follicle-Stimulating Hormone (FSH): In females — stimulates the growth and maturation of ovarian follicles and the secretion of estrogen by the follicular cells. In males — stimulates spermatogenesis in the seminiferous tubules.
• Melanocyte-Stimulating Hormone (MSH): Regulates skin pigmentation by stimulating melanocytes to produce melanin.

(c) Posterior Pituitary (Neurohypophysis):

The posterior pituitary stores and releases two hormones produced by the hypothalamus:

• Oxytocin: Stimulates uterine contractions during childbirth (labour) and milk ejection from the mammary glands during lactation (let-down reflex). It also plays a role in social bonding and is sometimes called the "love hormone."
• Vasopressin (ADH — Antidiuretic Hormone): Promotes water reabsorption from the collecting ducts in the kidneys, reducing urine volume and concentrating the urine. Also constricts blood vessels (vasoconstriction), increasing blood pressure. Deficiency causes diabetes insipidus (excessive dilute urine).

(d) Thyroid Gland:

• Thyroxine (T4) and Triiodothyronine (T3): Regulate the basal metabolic rate (BMR) — increase the rate of cellular oxidation and heat production; support normal growth and development (especially of the brain during infancy); stimulate protein synthesis; increase heart rate and cardiac output; regulate carbohydrate, fat, and protein metabolism.
• Calcitonin (Thyrocalcitonin): Lowers blood calcium levels by inhibiting osteoclasts (bone-resorbing cells) and stimulating calcium deposition in bones. It acts as an antagonist to parathyroid hormone (PTH).

(e) Adrenal Gland:

Adrenal Cortex (produces steroid hormones):

• Glucocorticoids (mainly Cortisol): Regulate carbohydrate metabolism (stimulate gluconeogenesis, increase blood glucose, promote protein catabolism and lipolysis); anti-inflammatory and immunosuppressive effects; help the body respond to stress.
• Mineralocorticoids (mainly Aldosterone): Regulate mineral and water balance by promoting Na+ reabsorption and K+ excretion in the kidneys, increasing blood volume and blood pressure.
• Androgenic steroids / Sex corticoids (mainly Dehydroepiandrosterone — DHEA): Supplement sex hormones from the gonads, especially before puberty; contribute to the development of secondary sex characteristics; have minimal effect in adult males (testosterone from testes predominates).

Adrenal Medulla (produces catecholamines):

• Adrenaline (Epinephrine): The "fight or flight" hormone — increases heart rate, cardiac output, and blood pressure; dilates bronchioles; stimulates glycogenolysis and lipolysis; increases blood glucose; dilates pupils; redirects blood flow to skeletal muscles.
• Noradrenaline (Norepinephrine): Similar effects to adrenaline but stronger vasoconstriction; increases blood pressure; less effect on heart rate and metabolism.

(f) Pancreas (Islets of Langerhans):

• Insulin (secreted by Beta cells): Lowers blood glucose by promoting glucose uptake by cells (especially muscle and adipose tissue), promoting glycogenesis (conversion of glucose to glycogen), inhibiting gluconeogenesis and glycogenolysis, promoting lipogenesis and protein synthesis.
• Glucagon (secreted by Alpha cells): Raises blood glucose by promoting glycogenolysis (breakdown of glycogen in liver), gluconeogenesis (synthesis of glucose from amino acids), and lipolysis (breakdown of fats).

Insulin and glucagon work antagonistically to maintain blood glucose homeostasis.

Group I: Peptide / Protein / Amino Acid Derivative Hormones (Water-soluble)

These hormones cannot cross the lipid bilayer of the cell membrane. They bind to receptors on the cell surface (membrane-bound receptors).

Mechanism (Second Messenger Model):

1. The hormone (first messenger) binds to a specific receptor on the outer surface of the target cell membrane. 2. The hormone-receptor complex activates a G-protein on the inner surface of the membrane. 3. The activated G-protein activates an enzyme on the inner membrane surface (e.g., adenylate cyclase / adenylyl cyclase). 4. The activated enzyme catalyses the conversion of ATP into cyclic AMP (cAMP) inside the cell. 5. cAMP acts as a second messenger and activates a cascade of protein kinases (kinase cascade) inside the cell. 6. The activated kinases phosphorylate target proteins, altering their activity and producing the hormone's physiological effect. 7. The enzyme phosphodiesterase inactivates cAMP to 5'-AMP, terminating the signal.

Other second messengers include: IP3 (inositol triphosphate), DAG (diacylglycerol), Ca2+ (calcium ions), and cGMP (cyclic GMP).

Examples of hormones using second messengers: Insulin, glucagon, adrenaline, noradrenaline, FSH, LH, TSH, ACTH, ADH, oxytocin.

Group II: Steroid Hormones (Lipid-soluble)

These hormones can diffuse through the lipid bilayer of the cell membrane. They bind to intracellular receptors (in the cytoplasm or nucleus).

Mechanism (Genomic Action / Gene Expression Model):

1. The steroid hormone diffuses through the cell membrane and enters the target cell. 2. In the cytoplasm, the hormone binds to a specific intracellular receptor, forming a hormone-receptor complex. 3. The hormone-receptor complex undergoes a conformational change and translocates to the nucleus (if the receptor was in the cytoplasm) or activates in the nucleus (if the receptor was already nuclear). 4. In the nucleus, the complex binds to specific hormone-responsive elements (HREs) on the DNA. 5. This binding activates or represses the transcription of specific genes. 6. The transcribed mRNA is translated into new proteins (enzymes, structural proteins, etc.). 7. These new proteins carry out the hormone's physiological effect.

Examples of steroid hormones: Cortisol, aldosterone, testosterone, estrogen, progesterone, thyroid hormones (T3, T4 — these are amino acid derivatives but act like steroid hormones through intracellular receptors).

Key differences between the two mechanisms:

(a) Hyperthyroidism vs Hypothyroidism:

(b) Cushing's syndrome vs Addison's disease:

(c) Diabetes mellitus vs Diabetes insipidus:

Role of the hypothalamus:

1. Control of anterior pituitary (adenohypophysis): The hypothalamus secretes releasing and inhibiting hormones that travel through the hypothalamo-hypophyseal portal system (a specialised network of blood vessels connecting the hypothalamus to the anterior pituitary) and regulate the secretion of anterior pituitary hormones:

• GHRH stimulates GH secretion; Somatostatin inhibits GH secretion.
• TRH stimulates TSH secretion.
• CRH stimulates ACTH secretion.
• GnRH stimulates FSH and LH secretion.
• PIH (Dopamine) inhibits prolactin secretion.

2. Control of posterior pituitary (neurohypophysis): The hypothalamus produces oxytocin and ADH in the cell bodies of neurosecretory neurons (supraoptic and paraventricular nuclei). These hormones are transported along the axons of these neurons to the posterior pituitary, where they are stored in nerve endings and released into the blood upon neural stimulation.

3. Autonomic regulation: The hypothalamus controls the sympathetic and parasympathetic divisions of the autonomic nervous system, which in turn regulate the adrenal medulla (sympathetic) and other glands.

4. Biological clock: The hypothalamus contains the suprachiasmatic nucleus (SCN), which acts as the body's biological clock, regulating circadian rhythms and influencing the pineal gland's secretion of melatonin.

5. Feedback regulation: The hypothalamus receives feedback from circulating hormone levels (negative feedback) and adjusts its releasing/inhibiting hormone secretion accordingly. For example:

• High T3/T4 levels → hypothalamus decreases TRH secretion → anterior pituitary decreases TSH secretion → thyroid decreases T3/T4 secretion (negative feedback).
• Low T3/T4 levels → hypothalamus increases TRH → anterior pituitary increases TSH → thyroid increases T3/T4 secretion.

6. Stress response: The hypothalamus activates the HPA axis (Hypothalamic-Pituitary-Adrenal) during stress: CRH from hypothalamus → ACTH from anterior pituitary → cortisol from adrenal cortex.

Structure:

The thyroid gland is the largest endocrine gland in the human body. It is a bilobed (two-lobed) gland located in the neck, on either side of the trachea, just below the larynx. The two lobes are connected by a thin bridge of tissue called the isthmus. The thyroid gland is richly supplied with blood vessels and is composed of numerous spherical follicles.

Thyroid follicles: Each follicle is a spherical structure lined by a single layer of cuboidal epithelial cells (follicular cells) and filled with a colloidal substance called thyroglobulin. The follicular cells synthesise the thyroid hormones T3 and T4, which are stored in the colloid as part of thyroglobulin. When needed, the follicular cells take up thyroglobulin, break it down, and release T3 and T4 into the blood.

Parafollicular cells (C cells): Scattered between the follicles are parafollicular cells (also called C cells or clear cells) that secrete the hormone calcitonin.

Functions (Hormones and their effects):

1. Thyroxine (T4) and Triiodothyronine (T3):

• Regulation of BMR: T3 and T4 increase the basal metabolic rate by stimulating cellular respiration and heat production. They increase oxygen consumption and ATP production in virtually all tissues.
• Growth and development: Essential for normal growth and development, especially of the brain and skeletal system during infancy and childhood. Hypothyroidism in children causes cretinism (stunted growth, mental retardation, low IQ).
• Carbohydrate metabolism: Increase glucose absorption from the intestine, promote glycogenolysis and gluconeogenesis.
• Fat metabolism: Promote lipolysis (breakdown of fats) and increase free fatty acid levels.
• Protein metabolism: In normal amounts, promote protein synthesis. In excess, they promote protein catabolism.
• Cardiovascular system: Increase heart rate, cardiac output, and blood pressure.
• Nervous system: Essential for the development of the CNS and for maintaining normal reflexes and mental alertness.
• RBC production: Stimulate erythropoiesis (red blood cell production).

Note: T3 is the more active form (3–5 times more potent than T4), but T4 is produced in greater quantities. T4 is converted to T3 in target tissues by deiodinase enzymes. Iodine is essential for the synthesis of both T3 and T4 (T4 contains 4 iodine atoms; T3 contains 3).

2. Calcitonin (Thyrocalcitonin):

• Lowers blood calcium levels by inhibiting osteoclasts (bone-resorbing cells) and stimulating calcium deposition in bones.
• Acts as an antagonist to parathyroid hormone (PTH).
• Important for calcium homeostasis, especially after a calcium-rich meal.

Disorders of the thyroid:

• Hypothyroidism: Iodine deficiency → goitre (enlarged thyroid), cretinism (in children), myxoedema (in adults).
• Hyperthyroidism: Graves' disease (autoimmune), thyrotoxicosis — weight loss, rapid heart rate, heat intolerance, exophthalmos.

Structure:

The adrenal glands (suprarenal glands) are a pair of glands, one located on top of each kidney. Each adrenal gland is roughly triangular in shape and consists of two distinct regions that function as separate glands:

1. Adrenal cortex (outer region, ~80% of the gland): Derived from mesoderm. Divided into three zones (from outer to inner):

• Zona glomerulosa: Secretes mineralocorticoids (mainly aldosterone).
• Zona fasciculata: Secretes glucocorticoids (mainly cortisol).
• Zona reticularis: Secretes androgenic steroids (mainly DHEA).

2. Adrenal medulla (inner region, ~20% of the gland): Derived from ectoderm (neural crest cells, same origin as sympathetic ganglia). It is essentially a modified sympathetic ganglion and secretes catecholamines.

Functions:

Adrenal Cortex Hormones:

(a) Glucocorticoids (Cortisol / Hydrocortisone):

• Regulate carbohydrate metabolism: stimulate gluconeogenesis (formation of glucose from amino acids and fats), increase blood glucose, promote glycogen storage in the liver.
• Regulate protein metabolism: promote protein catabolism (breakdown) in muscles and other tissues, releasing amino acids for gluconeogenesis.
• Regulate fat metabolism: promote lipolysis in adipose tissue, redistributing fat from limbs to the trunk and face (giving the "moon face" appearance in Cushing's syndrome).
• Anti-inflammatory and immunosuppressive: suppress the immune response and reduce inflammation by inhibiting prostaglandin and cytokine production. This is why cortisone injections are used for inflammatory conditions.
• Stress response: help the body cope with stress by mobilising energy reserves.

(b) Mineralocorticoids (Aldosterone):

• Regulate mineral and water balance by acting on the renal tubules.
• Promote Na+ reabsorption and K+ excretion in the distal convoluted tubule and collecting duct of the nephron.
• Indirectly promote water reabsorption (as water follows Na+ by osmosis), increasing blood volume and blood pressure.
• Aldosterone secretion is regulated by the renin-angiotensin-aldosterone system (RAAS) and by blood K+ levels.

(c) Androgenic Steroids (DHEA — Dehydroepiandrosterone):

• Precursors to sex hormones (converted to testosterone and estrogen in peripheral tissues).
• In males, contribute minimally compared to testicular testosterone.
• In females, are the primary source of androgens (contribute to libido and body hair).
• Important during puberty for the development of secondary sex characteristics.

Adrenal Medulla Hormones:

(a) Adrenaline (Epinephrine):

• Called the "emergency hormone" or "fight or flight hormone."
• Increases heart rate, cardiac output, and blood pressure.
• Dilates bronchioles (increases airflow to lungs).
• Stimulates glycogenolysis (increases blood glucose).
• Promotes lipolysis (increases free fatty acids).
• Dilates pupils (mydriasis).
• Diverts blood from skin and digestive tract to skeletal muscles.
• Increases sweating.

(b) Noradrenaline (Norepinephrine):

• Similar to adrenaline but with stronger vasoconstrictor effects.
• Increases blood pressure (by causing vasoconstriction).
• Has less effect on heart rate and metabolism compared to adrenaline.
• Also functions as a neurotransmitter in the sympathetic nervous system.

Disorders:

• Cushing's syndrome: Excess cortisol → obesity, moon face, hyperglycaemia, muscle weakness.
• Addison's disease: Deficiency of cortisol and aldosterone → hypoglycaemia, hyponatraemia, hyperkalaemia, low blood pressure, hyperpigmentation.

Types of feedback mechanisms:

1. Negative feedback (most common):

In negative feedback, the product of a pathway inhibits the pathway itself, preventing overproduction. It maintains homeostasis by reversing any deviation from the normal range.

Examples:

• Thyroid hormone regulation: The hypothalamus secretes TRH → anterior pituitary secretes TSH → thyroid secretes T3 and T4. When blood levels of T3 and T4 rise above normal, they inhibit both the hypothalamus (decreased TRH) and the anterior pituitary (decreased TSH), reducing thyroid hormone production. When T3/T4 levels fall, the inhibition is removed, and TRH and TSH secretion increase.

• Insulin–glucose feedback: When blood glucose rises after a meal, the pancreas secretes insulin, which lowers blood glucose. When blood glucose falls, insulin secretion decreases and glucagon secretion increases.

• Cortisol–ACTH–CRH feedback: High cortisol levels inhibit both CRH (hypothalamus) and ACTH (anterior pituitary) secretion, reducing cortisol production.

• Sex hormones and GnRH: High levels of sex hormones (estrogen, progesterone, testosterone) inhibit GnRH, FSH, and LH secretion.

2. Positive feedback (less common):

In positive feedback, the product of a pathway amplifies the pathway, leading to an escalating response that moves the system away from equilibrium. Positive feedback is rare and usually leads to a specific endpoint.

Examples:

• Oxytocin during childbirth: As the baby's head pushes against the cervix, nerve impulses are sent to the hypothalamus, which stimulates the posterior pituitary to release oxytocin. Oxytocin causes stronger uterine contractions, which push the baby further against the cervix, which triggers more oxytocin release. This positive feedback cycle continues until the baby is born.

• LH surge during ovulation: Rising estrogen levels (from the developing follicle) initially suppress LH secretion (negative feedback). But when estrogen reaches a critical high level (threshold), it switches to positive feedback, causing a sudden surge in LH secretion that triggers ovulation.

Significance of feedback mechanisms:

1. Homeostasis: Feedback mechanisms maintain stable internal conditions (blood glucose, calcium, water balance, body temperature) despite external changes. 2. Prevent overproduction: Negative feedback prevents excessive hormone secretion that could be harmful (e.g., preventing hyperthyroidism by inhibiting TSH when T3/T4 levels are high). 3. Prevent underproduction: Negative feedback ensures that hormone production increases when levels fall below the normal range. 4. Precise regulation: Feedback loops allow fine-tuned control of hormone levels, keeping them within narrow physiological ranges. 5. Energy conservation: Without feedback, endocrine glands would continuously produce hormones, wasting energy and potentially causing toxicity.

1. Pituitary Disorders:

• Gigantism: Hypersecretion of GH during childhood/adolescence (before growth plates close). Results in excessive growth of bones, making the person abnormally tall (7+ feet). Caused by pituitary adenoma.
• Acromegaly: Hypersecretion of GH in adults (after growth plates close). Long bones cannot grow further, so only soft tissues and short bones enlarge — protruding jaw, enlarged hands and feet, coarse facial features.
• Dwarfism: Hyposecretion of GH during childhood. Results in stunted growth (height typically < 4 feet) but with normal body proportions and normal intelligence.
• Diabetes insipidus: Hyposecretion of ADH (vasopressin) from the posterior pituitary, or defective ADH receptors in the kidneys. Results in excretion of large volumes of dilute urine (10–20 L/day), excessive thirst, and dehydration.

2. Thyroid Disorders:

• Goitre: Enlargement of the thyroid gland, most commonly caused by iodine deficiency. Without sufficient iodine, the thyroid cannot produce T3 and T4, so TSH secretion increases (loss of negative feedback), causing thyroid hypertrophy. Can also occur in Graves' disease or Hashimoto's thyroiditis.
• Cretinism: Hypothyroidism in children. Caused by severe iodine deficiency or thyroid defects. Symptoms include stunted growth, mental retardation, low IQ, coarse facial features, delayed bone age, and poor motor development. Irreversible if not treated early.
• Myxoedema (Hypothyroidism in adults): Low T3/T4 levels in adults. Symptoms include low BMR, weight gain, cold intolerance, fatigue, dry skin, puffy face, slow heart rate, constipation, and mental sluggishness.
• Graves' disease / Hyperthyroidism: Autoimmune disorder where antibodies stimulate TSH receptors, causing excess T3/T4 production. Symptoms include high BMR, weight loss, rapid heart rate, heat intolerance, tremors, anxiety, and exophthalmos (bulging eyes).

3. Parathyroid Disorders:

• Hyperparathyroidism: Excess PTH causes high blood calcium (hypercalcaemia), bone demineralisation, kidney stones, and muscle weakness.
• Hypoparathyroidism: Deficient PTH causes low blood calcium (hypocalcaemia), leading to tetany (muscle spasms, tingling, cramps), and can be fatal if severe.

4. Adrenal Disorders:

• Cushing's syndrome: Excess glucocorticoids (cortisol). Causes obesity (especially trunk), moon face, buffalo hump, thin skin, purple striae, hyperglycaemia, muscle weakness, osteoporosis, and immunosuppression.
• Addison's disease: Deficiency of both glucocorticoids and mineralocorticoids. Causes low blood glucose, low blood pressure, hyponatraemia (low Na+), hyperkalaemia (high K+), weight loss, fatigue, and skin hyperpigmentation (due to excess ACTH/MSH). Can be life-threatening during stress (adrenal crisis).

5. Pancreatic Disorders:

• Diabetes mellitus: See detailed comparison in Q5 above. Type I (insulin-dependent) and Type II (non-insulin-dependent). Symptoms: hyperglycaemia, glycosuria, polyuria, polydipsia, polyphagia, ketonuria (in Type I).

6. Gonadal Disorders:

• Hypogonadism: Underproduction of sex hormones. In males — low testosterone, reduced facial/body hair, decreased muscle mass, reduced libido. In females — low estrogen, menstrual irregularities, reduced secondary sex characteristics.

Internal Links

• [Chapter 22 Guide — Chemical Coordination and Integration](/school/cbse/class/11/biology/cbse-chemical-coordination)
• [All Class 11 Biology Solutions](/school/cbse/class/11/biology/solutions)
• [Class 11 Biology Subject Guide](/school/cbse/class/11/biology)