Exercises
Q1. Define the following
(a) Exocrine gland
(b) Endocrine gland
(c) Hormone
Ans.
(a) Exocrine gland:
An exocrine gland is a type of gland that secretes its products into ducts (tubes) that lead to specific body surfaces or body cavities (not directly into the blood). Examples: salivary glands (secrete saliva into the oral cavity), sweat glands (secrete sweat onto skin surface), gastric glands (secrete gastric juice into the stomach), liver (secretes bile into the bile duct leading to the small intestine), pancreas (exocrine part secretes digestive enzymes into the duodenum via pancreatic duct).
(b) Endocrine gland:
An endocrine gland is a ductless gland that secretes its products (hormones) directly into the bloodstream (or lymph). These hormones are then transported through the blood to target organs/tissues located elsewhere in the body. Endocrine glands are also called ductless glands. Examples: thyroid gland, adrenal gland, pituitary gland, pineal gland, gonads (testes, ovaries), parathyroid glands. The pancreas is both exocrine (digestive enzymes) and endocrine (insulin, glucagon — secreted into blood).
(c) Hormone:
A hormone is a chemical messenger secreted by endocrine glands directly into the blood, which is carried to distant target organs/tissues where it produces a specific biological response, even in very small quantities. Hormones regulate various physiological processes including growth, metabolism, reproduction, and homeostasis.
Characteristics of hormones: secreted in small amounts, transported by blood, act on specific target cells (have specific receptors), regulate metabolism and homeostasis, generally non-nutritive in function, may be proteins/peptides (e.g., insulin), steroids (e.g., cortisol, testosterone), or amines (e.g., adrenaline, thyroxine).
Diagrammatically indicate the location of the various endocrine glands in our body.
Answer
The endocrine glands and their locations in the human body:
In the head/neck region
• Hypothalamus: Base of brain (above pituitary gland)
• Pituitary gland (hypophysis): At the base of the brain, in the sella turcica of the sphenoid bone; connected to hypothalamus by the pituitary stalk (infundibulum)
• Pineal gland: In the epithalamus of the brain (between the two cerebral hemispheres)
• Thyroid gland: In the neck, anterior surface of the trachea below the larynx; butterfly-shaped (two lobes + isthmus)
• Parathyroid glands: Four tiny glands embedded in the posterior surface of the thyroid gland
In the thorax
• Thymus: In the upper chest (mediastinum), behind the sternum; prominent in children, regresses with age
• Heart (atria): Atrial walls secrete ANF (Atrial Natriuretic Factor)
In the abdomen
• Adrenal glands: One cap-shaped gland on top of each kidney; adrenal cortex (outer) + adrenal medulla (inner)
• Pancreas (Islets of Langerhans): Behind the stomach; both exocrine and endocrine (α-cells secrete glucagon; β-cells secrete insulin; δ-cells secrete somatostatin)
• Kidneys: Secrete erythropoietin (EPO) and renin
• Gastrointestinal tract: G-cells in stomach secrete gastrin; S-cells in duodenum secrete secretin; I-cells secrete CCK
In the pelvis
• Gonads:
— Testes (in males): In the scrotum; Leydig cells secrete testosterone; Sertoli cells secrete inhibin
— Ovaries (in females): In the pelvic cavity; secrete estrogen, progesterone, relaxin
• Placenta (during pregnancy): Secretes hCG, estrogen, progesterone, and relaxin
Q3. List the hormones secreted by the following
(a) Hypothalamus (b) Pituitary (c) Thyroid (d) Parathyroid
(e) Adrenal (f) Pancreas (g) Testis (h) Ovary (i) Thymus (j) Atrium (k) Kidney (l) G-I Tract
Ans.
(a) Hypothalamus: Gonadotropin-releasing hormone (GnRH), Thyrotropin-releasing hormone (TRH), Corticotropin-releasing hormone (CRH), Growth hormone-releasing hormone (GHRH), Growth hormone-inhibiting hormone/Somatostatin (GHIH), Prolactin-releasing factor (PRF), Prolactin-inhibiting factor (PIF/Dopamine), Melanocyte-stimulating hormone-releasing factor, Oxytocin (stored and released from posterior pituitary), Vasopressin/ADH (stored and released from posterior pituitary).
(b) Pituitary gland:
Anterior pituitary (adenohypophysis): Growth hormone (GH/Somatotropin), Thyroid-stimulating hormone (TSH/Thyrotrophin), Adrenocorticotropic hormone (ACTH/Corticotrophin), Follicle-stimulating hormone (FSH), Luteinizing hormone (LH), Prolactin (PRL), Melanocyte-stimulating hormone (MSH).
Posterior pituitary (neurohypophysis): Stores and releases Antidiuretic hormone (ADH/Vasopressin) and Oxytocin (both produced by hypothalamus).
(c) Thyroid gland: Thyroxine (T₄, tetraiodothyronine), Triiodothyronine (T₃), Calcitonin (thyrocalcitonin — from C cells/parafollicular cells, lowers blood calcium).
(d) Parathyroid glands: Parathyroid hormone (PTH/Parathormone) — raises blood calcium levels.
(e) Adrenal glands
Adrenal cortex: Mineralocorticoids (aldosterone — sodium and water balance), Glucocorticoids (cortisol/cortisone — stress response, anti-inflammatory, gluconeogenesis), Sex corticoids (androgens — DHEA).
Adrenal medulla: Epinephrine (adrenaline) and Norepinephrine (noradrenaline) — catecholamines, fight-or-flight response.
(f) Pancreas (Islets of Langerhans): Insulin (β-cells — lowers blood glucose), Glucagon (α-cells — raises blood glucose), Somatostatin (δ-cells — inhibits insulin and glucagon), Pancreatic polypeptide (PP cells).
(g) Testis: Testosterone (and other androgens — from Leydig cells), Inhibin (from Sertoli cells — inhibits FSH), Estrogen (small amounts).
(h) Ovary: Estrogen (estradiol — follicular cells, corpus luteum), Progesterone (corpus luteum), Relaxin (corpus luteum and placenta), Inhibin (granulosa cells).
(i) Thymus: Thymosins (thymosin α₁, thymosin β₄ — promote T-lymphocyte maturation and immunity), Thymulin, Thymopoietin.
(j) Atrium (heart): Atrial Natriuretic Factor (ANF/ANP — Atrial Natriuretic Peptide) — released when blood pressure is high; promotes Na⁺ and water excretion by kidneys, dilates blood vessels, lowers blood pressure.
(k) Kidney: Erythropoietin (EPO — stimulates RBC production in bone marrow), Renin (enzyme that activates renin-angiotensin-aldosterone system for blood pressure control), 1,25-dihydroxyvitamin D₃ (activates vitamin D).
(l) Gastrointestinal (G-I) Tract: Gastrin (G-cells, stomach — stimulates gastric acid secretion), Secretin (S-cells, duodenum — stimulates pancreatic bicarbonate secretion), Cholecystokinin (CCK, I-cells, duodenum — stimulates bile release, pancreatic enzyme secretion), Gastric inhibitory peptide (GIP — inhibits gastric acid, stimulates insulin), Motilin (stimulates intestinal motility), Ghrelin (stomach — stimulates hunger).
Q4. Fill in the blanks
Hormones → Target gland
(a) Hypothalamic hormones → __________
(b) Thyrotrophin (TSH) → __________
(c) Corticotrophin (ACTH) → __________
(d) Gonadotrophins (LH, FSH) → __________
(e) Melanotrophin (MSH) → __________
Ans.
(a) Hypothalamic hormones → Anterior pituitary gland (adenohypophysis)
(b) Thyrotrophin (TSH) → Thyroid gland
(c) Corticotrophin (ACTH) → Adrenal cortex (of adrenal gland)
(d) Gonadotrophins (LH, FSH) → Gonads (testes in males; ovaries in females)
(e) Melanotrophin (MSH) → Melanocytes (pigment cells in the skin)
Q5. Write short notes on the functions of the following hormones
(a) Parathyroid hormone (PTH)
(b) Thyroid hormones
(c) Thymosins
(d) Androgens
(e) Estrogens
(f) Insulin and Glucagon
Ans.
(a) Parathyroid hormone (PTH):
PTH is secreted by the chief cells of the parathyroid glands when blood Ca²⁺ levels are low. It is the main hormone that raises blood calcium (hypercalcemic agent):
1. Stimulates osteoclasts to resorb bone → releases Ca²⁺ into blood.
2. Increases Ca²⁺ reabsorption in kidney tubules (reduces urinary Ca²⁺ loss).
3. Stimulates conversion of vitamin D to its active form (calcitriol) in kidney → increases Ca²⁺ absorption from gut.
4. Decreases phosphate reabsorption in kidney (increases urinary phosphate loss).
PTH thus maintains calcium homeostasis. Hyperparathyroidism causes hypercalcemia and bone loss; hypoparathyroidism causes hypocalcemia and tetany.
(b) Thyroid hormones (T₃ and T₄):
Thyroxine (T₄) and triiodothyronine (T₃) are iodine-containing hormones secreted by thyroid follicular cells:
1. Regulate basal metabolic rate (BMR): Increase oxygen consumption and heat production in most body cells.
2. Essential for normal growth and development: Especially brain development in infants (deficiency causes cretinism).
3. Protein synthesis: Stimulate protein synthesis for growth.
4. Carbohydrate metabolism: Stimulate glycogenolysis and gluconeogenesis.
5. Fat metabolism: Promote fat mobilization and oxidation.
6. CNS development: Critical for brain maturation in fetus and neonate.
Reproductive function: Necessary for normal gonadal function.
Answer
(c) Thymosins:
Thymosins are peptide hormones secreted by the thymus gland:
1. Promote the differentiation and maturation of T-lymphocytes (T-cells) within the thymus.
2. Promote cell-mediated immunity by stimulating T-cell proliferation and function.
3. Also stimulate the production of cytokines and enhance natural killer (NK) cell activity.
4. Promote humoral immunity by stimulating B-cell differentiation (via T-helper cells).
The thymus is most active in childhood; thymosins decline with age, contributing to reduced immune function in the elderly.
Answer
(d) Androgens:
Androgens are male sex hormones, primarily testosterone, secreted by Leydig cells of the testes (small amounts also from adrenal cortex):
1. Responsible for development of primary sex organs (testes, seminal vesicles, prostate) in the fetus.
2. Produce secondary sexual characteristics in males at puberty: voice deepening, facial/body hair, muscle development, bone density increase, penile growth.
3. Regulate spermatogenesis (sperm production) in seminiferous tubules.
4. Maintain libido (sexual drive).
5. Promote protein anabolism (muscle building) and RBC production.
6. Influence behavior, aggressiveness.
(e) Estrogens
Estrogens (primarily estradiol) are secreted by ovarian follicles (and corpus luteum, placenta, adrenal cortex):
1. Responsible for development of primary sex organs (ovaries, uterus, vagina) in the fetus.
2. Produce secondary sexual characteristics in females at puberty: breast development, widening of hips, distribution of body fat, pubic and axillary hair growth.
3. Regulate the menstrual cycle: stimulate endometrial growth in the follicular phase; trigger LH surge (ovulation).
4. Maintain bone density (loss after menopause leads to osteoporosis).
5. Affect cholesterol levels: raise HDL, lower LDL.
6. Influence mood and cognitive function.
(f) Insulin and Glucagon
These are antagonistic hormones secreted by the Islets of Langerhans of the pancreas, together regulating blood glucose homeostasis.
Insulin (from β-cells, secreted when blood glucose rises):
1. Promotes glucose uptake by cells (especially muscle and adipose tissue via GLUT4 transporters).
2. Promotes glycogenesis: conversion of glucose to glycogen (liver and muscle).
3. Promotes lipogenesis: fat synthesis from glucose.
4. Promotes protein synthesis.
5. Inhibits gluconeogenesis and glycogenolysis.
Net effect: lowers blood glucose (hypoglycemic effect). Deficiency causes diabetes mellitus.
Glucagon (from α-cells, secreted when blood glucose falls):
1. Promotes glycogenolysis: breakdown of glycogen to glucose in liver.
2. Promotes gluconeogenesis: synthesis of glucose from non-carbohydrate sources.
3. Promotes lipolysis: breakdown of fats to release fatty acids.
Net effect: raises blood glucose (hyperglycemic effect).
Q6. Give example(s) of
(a) Hyperglycemic hormone and hypoglycemic hormone
(b) Hypercalcemic hormone
(c) Gonadotrophic hormones
(d) Progestational hormone
(e) Blood pressure lowering hormone
(f) Androgens and estrogens
Ans.
(a) Hyperglycemic hormone (raises blood glucose): Glucagon (pancreatic α-cells), Cortisol (adrenal cortex), Epinephrine/Adrenaline (adrenal medulla), Growth hormone.
Hypoglycemic hormone (lowers blood glucose): Insulin (pancreatic β-cells) — the only clinically significant hypoglycemic hormone.
(b) Hypercalcemic hormone (raises blood calcium): Parathyroid hormone (PTH) — secreted by parathyroid glands. (Note: Calcitonin is hypocalcemic.)
(c) Gonadotrophic hormones (act on gonads): Follicle-stimulating hormone (FSH) and Luteinizing hormone (LH) — both secreted by the anterior pituitary. Also, human chorionic gonadotropin (hCG) secreted by the placenta during pregnancy.
(d) Progestational hormone (prepares uterus for pregnancy): Progesterone — secreted by corpus luteum of the ovary (and later by the placenta). Maintains endometrium, inhibits uterine contractions, prepares mammary glands for lactation.
(e) Blood pressure lowering hormone: Atrial Natriuretic Factor (ANF/ANP) — secreted by atrial cells of the heart in response to high blood pressure; promotes natriuresis (Na⁺ and water excretion), vasodilation, and inhibits renin-angiotensin system.
(f) Androgens: Testosterone, DHEA (dehydroepiandrosterone), androstenedione — secreted by testes (Leydig cells) and adrenal cortex.
Estrogens: Estradiol (E₂), estrone (E₁), estriol (E₃) — secreted by ovarian follicles, corpus luteum, placenta, and in small amounts by adrenal cortex.
Q7. Which hormonal deficiency is responsible for the following
(a) Diabetes mellitus
(b) Goitre
(c) Cretinism
Ans.
(a) Diabetes mellitus:
Caused by deficiency or dysfunction of insulin (secreted by β-cells of pancreatic islets).
• Type I (Insulin-dependent) diabetes mellitus (IDDM): Autoimmune destruction of β-cells → absolute insulin deficiency. Requires insulin injections.
• Type II diabetes mellitus: Insulin resistance (cells fail to respond normally) ± relative insulin deficiency.
Without insulin, cells cannot take up glucose → high blood glucose (hyperglycemia) → glucose in urine (glycosuria), frequent urination (polyuria), excessive thirst (polydipsia), weight loss.
(b) Goitre:
Goitre (enlargement of the thyroid gland) is most commonly caused by deficiency of iodine in the diet, which leads to insufficient synthesis of thyroid hormones (T₃ and T₄). Low T₃/T₄ → increased TSH secretion (negative feedback fails) → TSH stimulates thyroid to grow → goitre.
It can also be caused by deficiency of thyroid hormones (hypothyroidism) due to autoimmune thyroiditis (Hashimoto's disease), or by iodine excess (Wolff-Chaikoff effect).
(c) Cretinism:
Caused by hypothyroidism in infants and young children — deficiency of thyroid hormones (T₃ and T₄) during fetal development and early childhood.
Thyroid hormones are essential for brain development and skeletal growth in the fetus and neonate. Deficiency leads to:
• Stunted physical growth (dwarfism)
• Mental retardation (intellectual disability)
• Delayed bone and sexual maturation
• Abnormal facial features (protruding tongue, flat nose, widely spaced eyes)
• Lethargy, constipation, enlarged abdomen.
Treated with thyroid hormone replacement therapy (started as early as possible to prevent permanent brain damage).
Briefly mention the mechanism of action of FSH.
Answer
FSH (Follicle-Stimulating Hormone) is a glycoprotein hormone secreted by gonadotroph cells of the anterior pituitary, stimulated by GnRH from the hypothalamus.
Chemical nature: FSH is a water-soluble peptide/glycoprotein hormone; it cannot cross the plasma membrane.
Mechanism of action (second messenger mechanism)
1. FSH binds to specific FSH receptors on the surface of target cells (granulosa cells in females; Sertoli cells in males). These receptors are G-protein coupled receptors (GPCRs).
2. Binding activates the receptor, which stimulates Gs protein, activating adenylyl cyclase enzyme.
3. Adenylyl cyclase converts ATP → cyclic AMP (cAMP) — the second messenger.
4. cAMP activates Protein Kinase A (PKA), which phosphorylates specific proteins.
Phosphorylated proteins initiate the cellular response:
Answer
— In females: FSH stimulates growth and maturation of ovarian follicles; promotes estrogen synthesis (by activating aromatase in granulosa cells).
— In males: FSH stimulates Sertoli cells to support spermatogenesis; stimulates production of androgen-binding protein (ABP).
6. FSH also stimulates expression of LH receptors on granulosa cells, making them sensitive to LH for ovulation.
Q9. Match the following
Column I — Column II
(a) T4 — (i) Hypothalamus
(b) PTH — (ii) Thyroid
(c) GnRH — (iii) Pituitary
(d) LH — (iv) Parathyroid
Ans. (a) T₄ (Thyroxine/Tetraiodothyronine) → (ii) Thyroid gland
(b) PTH (Parathyroid hormone) → (iv) Parathyroid gland
(c) GnRH (Gonadotropin-releasing hormone) → (i) Hypothalamus
(d) LH (Luteinizing hormone) → (iii) Pituitary (anterior pituitary)
Important Extra Questions
What is the hypothalamo-hypophyseal axis? Explain its significance.
Answer
The hypothalamo-hypophyseal axis (hypothalamic-pituitary axis) refers to the functional relationship between the hypothalamus and the pituitary gland in controlling hormonal secretion throughout the body.
The hypothalamus produces releasing hormones (e.g., TRH, CRH, GnRH) and inhibiting hormones (e.g., somatostatin, dopamine). These travel via the hypothalamo-hypophyseal portal blood system to the anterior pituitary, where they stimulate or inhibit secretion of tropic hormones (TSH, ACTH, FSH, LH, GH, prolactin).
Significance
1. Hierarchical control: Hypothalamus → anterior pituitary → target endocrine gland → target tissue. This allows integration of neural and hormonal signals.
2. Negative feedback: Hormones from peripheral glands (e.g., cortisol, thyroxine) feed back to inhibit both hypothalamus and pituitary, maintaining homeostasis.
3. Connects the nervous system to the endocrine system, allowing stress, emotions, and environmental signals to influence hormonal responses (e.g., stress → CRH → ACTH → cortisol).
4. Controls growth, reproduction, metabolism, stress response, and lactation.
What are the effects of growth hormone (GH) excess and deficiency?
Answer
Growth hormone (GH/Somatotropin) is secreted by somatotroph cells of the anterior pituitary.
Deficiency of GH
• In children: Pituitary dwarfism — proportionate short stature, normal intelligence (contrast with cretinism). Treated with recombinant human GH.
• In adults: GH deficiency syndrome — increased fat mass, decreased muscle, reduced bone density, fatigue.
Excess of GH
• In children (before epiphyseal plate fusion): Gigantism — abnormally tall stature due to excess long bone growth.
• In adults (after epiphyseal plate fusion): Acromegaly — cannot grow taller, but bones thicken. Enlarged hands, feet, jaw, tongue, internal organs. Often caused by a pituitary adenoma.
GH acts mainly through IGF-1 (Insulin-like Growth Factor-1) produced by the liver, which mediates most of GH's anabolic and growth-promoting effects.
Describe the structure and function of the adrenal gland.
Answer
The adrenal (suprarenal) glands are paired, cap-shaped glands, one on top of each kidney. Each gland has two distinct regions:
Adrenal cortex (outer region, 80–90% of gland)
Three zones:
1. Zona glomerulosa (outermost): Secretes mineralocorticoids (aldosterone). Regulates Na⁺ and K⁺ balance → water retention → blood pressure regulation.
2. Zona fasciculata (middle, largest): Secretes glucocorticoids (cortisol, corticosterone). Regulates stress response, raises blood glucose (gluconeogenesis), anti-inflammatory, immunosuppressive.
3. Zona reticularis (inner): Secretes weak sex steroids (androgens) — DHEA, androstenedione. Contribute to pubic hair development at adrenarche.
Adrenal medulla (inner region, 10–20%)
• Consists of chromaffin cells (modified postganglionic sympathetic neurons).
• Secretes catecholamines: Epinephrine (adrenaline, ~80%) and Norepinephrine (noradrenaline, ~20%).
• Released in response to acute stress (fight-or-flight): increases heart rate, blood pressure, blood glucose, dilates airways, redirects blood to muscles.
What is the role of oxytocin and ADH?
Answer
Both oxytocin and ADH (antidiuretic hormone/vasopressin) are produced by neurons in the hypothalamus and stored in and released from the posterior pituitary (neurohypophysis).
Oxytocin
1. Uterine contraction: Stimulates powerful uterine smooth muscle contractions during labor (parturition). Positive feedback — contractions stimulate more oxytocin release until birth.
2. Milk ejection: Stimulates myoepithelial cells of mammary glands to contract and eject milk (letdown reflex) in response to infant suckling.
3. Bonding and social behavior: Called the "love hormone" — promotes mother-infant bonding, pair bonding, trust, and social interactions.
ADH (Vasopressin)
1. Water retention: Acts on collecting ducts and distal convoluted tubules of kidneys → increases water permeability (via aquaporin channels) → reduces water loss in urine (antidiuretic effect). Maintains blood osmolarity.
2. Vasoconstriction: At high concentrations, constricts blood vessels → raises blood pressure (hence "vasopressin").
3. Released in response to: increased blood osmolarity (detected by hypothalamic osmoreceptors), decreased blood volume/pressure.
Deficiency → diabetes insipidus: inability to concentrate urine → massive water loss (polyuria + polydipsia).
What is the role of the pineal gland? Describe melatonin's functions.
Answer
The pineal gland (epiphysis cerebri) is a small (~8 mm), pinecone-shaped gland located in the epithalamus (between the two cerebral hemispheres, in the posterior part of the third ventricle roof). It is sometimes called the "third eye."
Main secretion: Melatonin — an indoleamine hormone derived from serotonin (5-hydroxytryptamine).
Functions of melatonin
1. Regulation of circadian rhythms: Melatonin is secreted predominantly at night (darkness triggers production; light suppresses it). It signals "biological night" to the body, regulating sleep-wake cycles.
2. Seasonal rhythms (circannual rhythms): Controls seasonal reproduction in photoperiod-sensitive animals (day-length changes melatonin secretion duration, triggering breeding seasons).
3. Sleep induction: Melatonin promotes sleep onset; used as a supplement for jet lag and insomnia.
4. Antioxidant: Scavenges free radicals; protects cells from oxidative damage.
5. Immune modulation: Enhances immune function.
6. Anti-aging: Proposed role in aging (melatonin decreases with age).
7. Inhibits reproductive activity: At high levels (winter nights) inhibits GnRH → suppresses FSH/LH → reduces gonadal function in seasonal breeders.