What is the endocrine system? — Electrical Engineering MCQ

B. A system of glands that secrete hormones directly into the bloodstream to regulate body functions — The Endocrine System is a collection of ductless glands that produce and secrete hormones directly into the bloodstream (not through ducts), which then travel to target organs to produce specific effects. Key features: Ductless glands (unlike exocrine glands which have ducts e.g. salivary glands, sweat glands). Effects are slower but longer lasting compared to the nervous system. Regulates: Growth, metabolism, reproduction, mood, homeostasis, stress response. Major endocrine glands: Hypothalamus, Pituitary, Thyroid, Parathyroid, Adrenal, Pancreas, Gonads (testes/ovaries), Pineal, Thymus.

A. A system of ducts that carries secretions to body surfaces

C. A network of nerves controlling involuntary functions

D. A system responsible only for digestion

What is a hormone? — Electrical Engineering MCQ

B. A chemical messenger secreted by endocrine glands into the blood that acts on specific target cells — A Hormone is a chemical messenger produced by endocrine glands, secreted into the bloodstream, and transported to target cells/organs where it produces a specific physiological effect by binding to specific receptors. Classification of hormones: Peptide/Protein hormones (Insulin, glucagon, ADH, GH, TSH - water-soluble - act on surface receptors), Steroid hormones (Cortisol, aldosterone, sex hormones - lipid-soluble - cross cell membrane - act on nuclear receptors), and Amine hormones (Adrenaline, noradrenaline, thyroid hormones - derived from amino acids). The concept of hormones was introduced by Ernest Starling (1905).

A. An enzyme that speeds up chemical reactions in cells

C. A protein that transports oxygen in the blood

D. A substance produced by exocrine glands through ducts

Which gland is known as the master gland of the endocrine system? — Electrical Engineering MCQ

D. Pituitary gland — The Pituitary Gland (Hypophysis) is called the master gland because it controls the activity of most other endocrine glands through its hormones. It is located at the base of the brain in a bony depression called the Sella Turcica (Turkish saddle) of the sphenoid bone. It is connected to the hypothalamus by the pituitary stalk (infundibulum). Two lobes: Anterior pituitary (Adenohypophysis) = Produces GH, TSH, ACTH, FSH, LH, Prolactin. Posterior pituitary (Neurohypophysis) = Stores and releases ADH and Oxytocin (produced by hypothalamus). However, the hypothalamus is considered the true master as it controls the pituitary.

What hormones does the anterior pituitary gland produce? — Electrical Engineering MCQ

C. GH, TSH, ACTH, FSH, LH, and Prolactin — The Anterior Pituitary (Adenohypophysis) produces 6 major hormones - mnemonic FLAT PiG: F = FSH (Follicle Stimulating Hormone) stimulates follicle development in ovaries and sperm production in testes. L = LH (Luteinising Hormone) triggers ovulation and stimulates testosterone production in testes. A = ACTH (Adrenocorticotrophic Hormone) stimulates adrenal cortex to produce cortisol. T = TSH (Thyroid Stimulating Hormone) stimulates thyroid to produce thyroid hormones. Pi = Prolactin stimulates milk production (lactation). G = GH (Growth Hormone) stimulates growth of bones and muscles.

What hormones are released by the posterior pituitary gland? — Electrical Engineering MCQ

C. ADH (Vasopressin) and Oxytocin — The Posterior Pituitary (Neurohypophysis) does NOT produce hormones - it stores and releases two hormones that are produced by the hypothalamus (in the supraoptic and paraventricular nuclei): ADH (Antidiuretic Hormone / Vasopressin) = Increases water reabsorption in kidney collecting ducts causing concentrated urine and raises blood pressure. Released when blood osmolarity rises (dehydration). Deficiency causes Diabetes Insipidus. Oxytocin = Stimulates uterine contractions during labour and milk ejection (let-down reflex) during breastfeeding. Also called the love hormone - promotes bonding, trust, and social behaviour.

B. Prolactin and Growth Hormone

What is Growth Hormone (GH) and what does it do? — Electrical Engineering MCQ

B. Stimulates growth of bones, muscles, and organs - secreted by the anterior pituitary — Growth Hormone (GH / Somatotropin) is secreted by somatotroph cells of the anterior pituitary. It is the most abundant anterior pituitary hormone. Actions: Stimulates bone growth (lengthening at epiphyseal plates) and muscle growth, Promotes protein synthesis and fat breakdown (lipolysis), Raises blood glucose (anti-insulin effect - diabetogenic), Acts via IGF-1 (Insulin-like Growth Factor 1) from the liver (indirect effects). GH excess (before puberty): Gigantism (excessive height). GH excess (after puberty): Acromegaly (enlargement of hands, feet, jaw, tongue - due to closed epiphyses). GH deficiency (children): Dwarfism (short stature). Regulated by: GHRH (stimulates) and Somatostatin (inhibits) from hypothalamus.

A. Controls blood sugar by stimulating insulin release

C. Regulates calcium levels in blood

D. Controls the menstrual cycle

What is the thyroid gland and where is it located? — Electrical Engineering MCQ

B. Located in the neck, produces thyroid hormones (T3 and T4) that regulate metabolism — The Thyroid Gland is a butterfly-shaped gland located in the anterior neck, below the larynx (Adam's apple), wrapping around the trachea. It has two lobes connected by an isthmus. Weight: ~25-30 g. It is the largest purely endocrine gland in the body. Produces: T3 (Triiodothyronine) = More active form. T4 (Thyroxine) = Main form secreted; converted to T3 in tissues. Calcitonin = Produced by parafollicular C-cells - lowers blood calcium (by inhibiting bone resorption). Requires iodine for T3/T4 synthesis. Regulated by TSH from anterior pituitary (controlled by TRH from hypothalamus).

A. Located in the abdomen, produces insulin

C. Located behind the sternum, produces cortisol

D. Located near the kidneys, produces adrenaline

What are the main functions of thyroid hormones (T3 and T4)? — Electrical Engineering MCQ

B. Increase basal metabolic rate, promote growth and development, and regulate body temperature — Thyroid Hormones (T3 and T4) are essential for: Increased Basal Metabolic Rate (BMR) - stimulate O2 consumption and heat production (calorigenic effect), Growth and development - essential for normal brain development in infants and children (deficiency causes cretinism), Protein synthesis - promote growth of muscles and organs, Heart rate - increase heart rate and cardiac output, Gut motility - stimulate peristalsis, Temperature regulation - increase heat production, and Nervous system - maintain alertness, reflexes, and mood. T3 is 3-5 times more potent than T4 but T4 is more abundant. Both are lipid-soluble and travel bound to TBG (Thyroxine Binding Globulin) in blood.

A. Regulate blood sugar and stimulate insulin secretion

C. Control the menstrual cycle and promote lactation

D. Regulate calcium and phosphate levels in blood

What is hypothyroidism? — Electrical Engineering MCQ

B. Deficiency of thyroid hormones causing weight gain, fatigue, cold intolerance, and slow metabolism — Hypothyroidism is a condition of insufficient thyroid hormone production. Features (mnemonic SLOW): Slow metabolism (weight gain, constipation, bradycardia), Low energy (fatigue, lethargy, depression), Oedema (myxoedema - non-pitting oedema - puffy face, periorbital oedema), and Warm clothing needed (cold intolerance, dry skin, hair loss). Most common cause: Hashimoto's thyroiditis (autoimmune - anti-TPO antibodies) in iodine-sufficient countries. Iodine deficiency = most common worldwide cause causing Goitre. In neonates: Cretinism (intellectual disability, short stature, deafness). Treatment: Levothyroxine (T4 replacement). Diagnosis: TSH elevated + Low T4.

A. Excessive production of thyroid hormones causing weight loss and rapid heart rate

C. Inflammation of the thyroid causing sudden hormone release

D. Excess iodine causing thyroid enlargement

What is hyperthyroidism? — Electrical Engineering MCQ

C. Overproduction of thyroid hormones causing weight loss, rapid heart rate, and heat intolerance — Hyperthyroidism is a condition of excess thyroid hormone production. Features (mnemonic FAST): Fast metabolism (weight loss despite increased appetite, frequent bowel movements), Agitated heart (tachycardia, palpitations, atrial fibrillation), Sweating and heat intolerance, tremor, anxiety, insomnia, and Thyroid enlargement (goitre). Most common cause: Graves' Disease (autoimmune - TSI/TRAb antibodies stimulate TSH receptors causing excess T3/T4). Specific signs of Graves': Exophthalmos (bulging eyes - proptosis), pretibial myxoedema, thyroid acropachy. Treatment: Antithyroid drugs (carbimazole, propylthiouracil), Radioactive iodine (131I), Surgery (thyroidectomy). Beta-blockers (propranolol) for symptom control.

A. Underproduction of thyroid hormones

B. Inflammation of the parathyroid gland

D. Calcium imbalance due to thyroid disease

What is a goitre? — Electrical Engineering MCQ

B. Enlarged thyroid gland - can occur in both hypothyroidism and hyperthyroidism — A Goitre is simply an enlargement of the thyroid gland - it can occur with normal, low, or high thyroid hormone levels. Types: Simple/Endemic goitre (due to iodine deficiency - thyroid enlarges trying to compensate for inadequate iodine causing hypothyroidism - most common cause worldwide - iodised salt has dramatically reduced endemic goitre), Toxic goitre (Graves' disease - hyperthyroidism with goitre), Multinodular goitre (multiple nodules - may be toxic or non-toxic), Physiological goitre (during puberty or pregnancy - increased demand), and Hashimoto's thyroiditis (autoimmune hypothyroidism with goitre). A goitre can cause neck swelling, difficulty swallowing (dysphagia), and compressive symptoms.

A. Inflammation of the thyroid causing hypothyroidism only

C. A benign tumour of the parathyroid gland

D. Excess calcium deposition in the thyroid

What are the parathyroid glands and what hormone do they produce? — Electrical Engineering MCQ

B. Four small glands located on the posterior thyroid that produce PTH to regulate calcium — The Parathyroid Glands are 4 small glands (each the size of a grain of rice, ~50 mg each) located on the posterior surface of the thyroid gland. They produce Parathyroid Hormone (PTH) - the primary regulator of blood calcium levels. PTH is released when blood calcium falls. Actions of PTH (raises calcium): Bone (stimulates osteoclasts - bone resorption - releases Ca2+ into blood), Kidney (increases Ca2+ reabsorption in DCT, increases phosphate excretion, activates Vitamin D via 1-alpha hydroxylase), and Gut (indirectly increases calcium absorption via activated Vitamin D). Calcitonin (from thyroid C-cells) has the OPPOSITE effect - lowers calcium.

A. Two glands in the neck that produce calcitonin to raise calcium levels

C. Glands in the adrenal cortex that regulate potassium

D. Glands that produce TSH to stimulate the thyroid

What is hyperparathyroidism? — Electrical Engineering MCQ

B. Excess PTH secretion causing high blood calcium (hypercalcaemia), bone resorption, and kidney stones — Hyperparathyroidism is excess PTH secretion leading to hypercalcaemia. Types: Primary (parathyroid adenoma - most common 85%, hyperplasia, carcinoma rare), Secondary (chronic hypocalcaemia from CKD or Vitamin D deficiency causing parathyroid hyperplasia - appropriate response), and Tertiary (long-standing secondary causing autonomous parathyroid). Features of hypercalcaemia - mnemonic Bones, Stones, Groans, Psychic Moans: Bones (bone pain, fractures, Osteitis Fibrosa Cystica - brown tumours), Stones (kidney stones - calcium oxalate/phosphate, nephrocalcinosis), Groans (nausea, vomiting, constipation, pancreatitis, peptic ulcer), and Psychic Moans (depression, confusion, lethargy, coma).

A. Low PTH causing high calcium levels

C. Excess calcium in the diet causing PTH suppression

D. Inflammation of the parathyroid causing low calcium

What are the adrenal glands? — Electrical Engineering MCQ

B. Two triangular glands located on top of the kidneys - each with a cortex (outer) and medulla (inner) — The Adrenal (Suprarenal) Glands are two small, triangular/pyramidal glands located on the superior pole of each kidney. Each weighs ~4-5 g. Two distinct regions: Adrenal Cortex (outer, 90%) - derived from mesoderm - produces steroid hormones: Zona Glomerulosa (outermost) = Aldosterone (mineralocorticoid - regulates Na+/K+), Zona Fasciculata (middle, largest) = Cortisol (glucocorticoid - stress response), and Zona Reticularis (innermost) = Androgens (DHEA - weak sex hormones). Adrenal Medulla (inner, 10%) - derived from neural crest (modified sympathetic ganglion) - produces Adrenaline (80%) + Noradrenaline (20%) (catecholamines). Mnemonic for cortex zones: GFR = Salt (Glomerulosa), Sugar (Fasciculata), Sex (Reticularis).

A. Glands located in the pelvis that produce sex hormones only

C. Glands located behind the stomach that produce digestive enzymes

D. Glands at the base of the brain that control the pituitary

What is cortisol and what are its functions? — Electrical Engineering MCQ

B. A glucocorticoid produced by the adrenal cortex that regulates stress response, metabolism, and immune function — Cortisol is the primary glucocorticoid produced by the zona fasciculata of the adrenal cortex under control of ACTH (from pituitary) and CRH (from hypothalamus). It is the stress hormone. Functions: Raises blood glucose (gluconeogenesis, glycogenolysis - anti-insulin, protein catabolism), Anti-inflammatory (suppresses immune response - inhibits prostaglandins, cytokines, phospholipase A2 - basis for steroid drugs), Fat redistribution (chronic excess) = central obesity, moon face, buffalo hump, Blood pressure maintenance (permissive effect on catecholamines), and Suppresses immune system. Diurnal variation: Highest in early morning, lowest at night (follows circadian rhythm).

A. A mineralocorticoid that regulates sodium balance

C. A catecholamine released during exercise

D. A hormone produced by the anterior pituitary that stimulates growth

What is Cushing's syndrome? — Electrical Engineering MCQ

B. Excess cortisol causing central obesity, moon face, hypertension, and purple striae — Cushing's Syndrome is caused by chronic excess cortisol. Features: Central (truncal) obesity with thin limbs (protein catabolism), Moon face (rounded face), Buffalo hump (fat pad between shoulder blades), Purple/violet striae (stretch marks - due to collagen breakdown), Hypertension, Diabetes (hyperglycaemia), Osteoporosis, Muscle weakness, thin skin, easy bruising, and Mood changes (depression, psychosis). Causes: Iatrogenic (most common - long-term steroid use), Cushing's Disease (pituitary ACTH-secreting adenoma - most common endogenous cause), Adrenal adenoma/carcinoma, Ectopic ACTH (small cell lung cancer). Diagnosis: 24-hr urine cortisol, low-dose dexamethasone suppression test, midnight salivary cortisol.

A. Deficiency of cortisol causing hypotension and hypoglycaemia

C. Excess aldosterone causing hypokalaemia

D. Deficiency of ACTH causing adrenal insufficiency

What is Addison's disease? — Electrical Engineering MCQ

B. Primary adrenal insufficiency - deficiency of cortisol and aldosterone causing weakness, hyperpigmentation, and hypotension — Addison's Disease (Primary Adrenal Insufficiency) is caused by destruction of the adrenal cortex causing deficiency of cortisol AND aldosterone. Most common cause: Autoimmune (70-80%) - anti-21-hydroxylase antibodies. Other causes: TB (historically most common), metastatic cancer, haemorrhage (Waterhouse-Friderichsen syndrome - meningococcal). Features: Hyperpigmentation (bronze skin) = Excess ACTH stimulates melanocytes (MSH action) - characteristic sign. Hypotension, postural hypotension (lack of aldosterone causing Na+ loss), Weakness, fatigue, weight loss, Hyponatraemia, Hyperkalaemia (lack of aldosterone), and Hypoglycaemia (lack of cortisol). Treatment: Hydrocortisone + Fludrocortisone (mineralocorticoid replacement). Addisonian crisis: Life-threatening - treat with IV hydrocortisone and saline.

A. Overproduction of cortisol by the adrenal cortex

C. Excess aldosterone causing hypertension and low potassium

D. Tumour of the adrenal medulla causing hypertension

What is aldosterone and what does it do? — Electrical Engineering MCQ

B. A mineralocorticoid produced by the zona glomerulosa that increases sodium reabsorption and potassium excretion in the kidney — Aldosterone is a mineralocorticoid produced by the zona glomerulosa of the adrenal cortex. Regulated by: RAAS (Renin-Angiotensin-Aldosterone System), blood potassium levels (high K+ stimulates aldosterone), and ACTH (minor role). Actions on DCT and collecting duct of kidney: Increases Na+ reabsorption (water follows - increases blood volume and pressure), Increases K+ excretion (into urine - hypokalaemia in excess), and Increases H+ excretion (alkalosis in excess). Primary Hyperaldosteronism (Conn's Syndrome): Adrenal adenoma causing excess aldosterone, hypertension + hypokalaemia. Hypoaldosteronism (Addison's disease): Na+ loss, K+ retention, hypotension.

A. A glucocorticoid that raises blood glucose during stress

C. A catecholamine released during fight-or-flight response

D. A steroid hormone that promotes muscle growth

What is adrenaline (epinephrine) and what are its effects? — Electrical Engineering MCQ

B. A catecholamine produced by the adrenal medulla that mediates the acute fight-or-flight response — Adrenaline (Epinephrine) is a catecholamine produced by chromaffin cells of the adrenal medulla (80% adrenaline, 20% noradrenaline). Derived from tyrosine via dopamine. Released in response to stress, hypoglycaemia, exercise. Effects (fight or flight): Heart (increased heart rate - tachycardia, increased force of contraction), Lungs (bronchodilation - opens airways), Blood (increased glucose via glycogenolysis and gluconeogenesis, increased free fatty acids), Blood vessels (vasoconstriction in skin/gut; vasodilation in muscles), and Pupils (dilation - mydriasis). Clinical use: Anaphylaxis treatment (IM adrenaline 1:1000), cardiac arrest (IV adrenaline in ALS protocol), and local anaesthetic additive (reduces bleeding).

A. A steroid hormone produced by the adrenal cortex during stress

C. A pituitary hormone that controls the adrenal cortex

D. A hormone that lowers blood pressure during stress

What is a phaeochromocytoma? — Electrical Engineering MCQ

B. A tumour of the adrenal medulla causing excess catecholamine secretion and hypertensive crises — A Phaeochromocytoma is a catecholamine-secreting tumour arising from chromaffin cells of the adrenal medulla (or extra-adrenal sympathetic ganglia - paraganglioma). Classic presentation: Triad of paroxysmal hypertension (episodic severe high blood pressure) + headache + sweating + palpitations (5 Ps: Pressure, Pain-headache, Perspiration, Palpitations, Pallor). Rule of 10s: 10% bilateral, 10% extra-adrenal, 10% malignant, 10% familial. Associated with MEN 2A and 2B (Multiple Endocrine Neoplasia), VHL syndrome, and Neurofibromatosis type 1. Diagnosis: 24-hr urine/plasma metanephrines. Treatment: Alpha-blockade first (phenoxybenzamine), then beta-blockade, then surgery.

A. A tumour of the adrenal cortex causing excess cortisol

D. A pituitary adenoma causing excess growth hormone

What is the pancreas and what are its endocrine functions? — Electrical Engineering MCQ

B. A mixed gland - exocrine (digestive enzymes) and endocrine - the endocrine portion (islets of Langerhans) produces insulin and glucagon — The Pancreas is a mixed gland with both exocrine and endocrine functions: Exocrine (99%) = Acinar cells produce digestive enzymes (amylase, lipase, proteases) secreted into the duodenum. Endocrine (1%) = Islets of Langerhans - scattered clusters of cells: Alpha cells (~25%) produce Glucagon (raises blood glucose), Beta cells (~65%) produce Insulin (lowers blood glucose - most numerous), Delta cells (~5%) produce Somatostatin (inhibits insulin and glucagon), and PP cells produce Pancreatic Polypeptide (inhibits pancreatic secretion). Discovered by Paul Langerhans (1869). Insulin was isolated by Banting and Best (1921).

A. A purely digestive organ that only produces enzymes

C. An organ that produces cortisol and aldosterone

D. A gland attached to the stomach that secretes acid

What is insulin and what does it do? — Electrical Engineering MCQ

C. A hormone produced by beta cells of the pancreas that lowers blood glucose by promoting cellular glucose uptake — Insulin is a peptide hormone produced by beta cells of the islets of Langerhans in the pancreas. Released when blood glucose rises (after meals). Actions - all ANABOLIC (building) and hypoglycaemic (glucose-lowering): Increases glucose uptake by cells (especially muscle and fat) via GLUT-4 transporters, Promotes glycogen synthesis (glycogenesis) in liver and muscle, Promotes fat synthesis (lipogenesis) and inhibits fat breakdown, Promotes protein synthesis, and Inhibits gluconeogenesis and glycogenolysis in liver. Discovered by Frederick Banting and Charles Best (1921, University of Toronto) - Nobel Prize 1923. Insulin deficiency/resistance causes Diabetes Mellitus.

A. A hormone that raises blood glucose by stimulating glycogenolysis

B. A hormone produced by alpha cells of the pancreas that raises blood glucose

D. A digestive enzyme that breaks down carbohydrates

What is glucagon and what does it do? — Electrical Engineering MCQ

B. Produced by alpha cells of the pancreas - raises blood glucose by stimulating glycogenolysis and gluconeogenesis — Glucagon is a peptide hormone produced by alpha cells of the islets of Langerhans. Released when blood glucose falls (hypoglycaemia, fasting, exercise). Actions - all CATABOLIC (breaking down) and hyperglycaemic (glucose-raising): Glycogenolysis (breaks down liver glycogen - releases glucose into blood), Gluconeogenesis (synthesis of new glucose from amino acids, lactate, glycerol), Lipolysis (breaks down fat - releases fatty acids for energy), and Ketogenesis (promotes ketone body formation from fatty acids). Glucagon and Insulin are antagonistic - they maintain blood glucose homeostasis together. Clinical use: IV/IM glucagon to treat severe hypoglycaemia (unconscious diabetic patient) when IV access not available.

A. Produced by beta cells - lowers blood glucose by promoting glycogen synthesis

C. A digestive hormone produced by the stomach

D. A hormone that promotes fat storage in adipose tissue

What is Type 1 Diabetes Mellitus? — Electrical Engineering MCQ

B. Autoimmune destruction of pancreatic beta cells causing absolute insulin deficiency - requires insulin injections — Type 1 Diabetes Mellitus (T1DM) - previously called Juvenile-onset or Insulin-Dependent Diabetes Mellitus (IDDM). Cause: Autoimmune destruction of pancreatic beta cells by T-lymphocytes causing absolute insulin deficiency (no insulin production). Features: Usually presents in childhood/adolescence (but can occur at any age), Thin patient (loss of fat and muscle due to catabolism), Polyuria (osmotic diuresis), Polydipsia (thirst), Polyphagia (hunger - cells starving), Weight loss, Prone to DKA (Diabetic Ketoacidosis) - life-threatening emergency, Anti-GAD, Anti-islet cell, Anti-insulin antibodies positive, and Genetic association: HLA-DR3, HLA-DR4. Treatment: Lifelong insulin therapy (multiple daily injections or insulin pump).

A. Insulin resistance causing high blood glucose in overweight adults

C. Excess glucagon secretion from alpha cells

D. Gestational diabetes occurring only during pregnancy

What is Type 2 Diabetes Mellitus? — Electrical Engineering MCQ

B. Insulin resistance with relative insulin deficiency - strongly associated with obesity and lifestyle factors — Type 2 Diabetes Mellitus (T2DM) - previously called Adult-onset or Non-Insulin-Dependent Diabetes Mellitus (NIDDM). Most common type (~90-95% of all diabetes). Cause: Insulin resistance (cells don't respond to insulin) + progressive beta cell failure causing relative insulin deficiency. Risk factors: Obesity (especially central/abdominal), physical inactivity, family history, age >45, ethnicity (South Asian, Afro-Caribbean). Features: Often asymptomatic for years (insidious onset), less prone to DKA but can develop HHS (Hyperosmolar Hyperglycaemic State). Complications: Macro (heart disease, stroke, peripheral vascular disease) and Micro (retinopathy, nephropathy, neuropathy). Treatment: Lifestyle changes (diet, exercise, weight loss), Metformin (first-line drug), then additional agents (SGLT2 inhibitors, GLP-1 agonists, etc.).

A. Autoimmune destruction of beta cells requiring insulin therapy from diagnosis

C. Complete absence of insulin from birth

D. Diabetes occurring only during pregnancy

What is diabetic ketoacidosis (DKA)? — Electrical Engineering MCQ

B. A life-threatening complication mainly of Type 1 diabetes characterised by hyperglycaemia, ketosis, and metabolic acidosis — Diabetic Ketoacidosis (DKA) occurs mainly in T1DM (can occur in T2DM). Precipitated by: Missed insulin dose, infection, surgery, stress. Pathophysiology: No insulin causing cells unable to use glucose causing glucose accumulates (hyperglycaemia) causing cells use fat causing fatty acids causing ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) causing metabolic acidosis. Features: Hyperglycaemia (>11 mmol/L), Metabolic acidosis (pH <7.3, HCO3 <15), Ketonaemia/Ketonuria, Osmotic diuresis causing dehydration, Kussmaul breathing (deep, rapid - compensatory respiratory alkalosis), Fruity/acetone breath, and Nausea, vomiting, abdominal pain. Treatment: IV fluids + Insulin infusion + K+ replacement (fixed rate insulin infusion protocol).

A. A complication of Type 2 diabetes caused by excess insulin

C. Low blood glucose causing seizures in diabetics

D. Kidney failure caused by chronic diabetes

What are the male sex hormones called and where are they produced? — Electrical Engineering MCQ

B. Androgens (primarily testosterone) - produced mainly by Leydig cells of the testes under LH stimulation — Male sex hormones (Androgens) - primarily Testosterone - are produced by: Leydig cells (interstitial cells) of the testes (95% of testosterone) stimulated by LH from pituitary, and Adrenal cortex (zona reticularis) which produces weak androgens (DHEA, androstenedione) - 5%. Functions of Testosterone: Spermatogenesis (with FSH acting on Sertoli cells), Development of male secondary sexual characteristics (puberty) - deepened voice, facial/body hair, penile/testicular growth, muscle mass, bone density, Anabolic effects (muscle and bone growth), Libido (sex drive), and in fetal life development of male genitalia. Testosterone is converted to DHT (Dihydrotestosterone) - more potent - by 5-alpha reductase (important in prostate and hair follicles).

A. Oestrogens - produced in the testes

C. Progesterone - produced by the adrenal medulla

D. FSH - produced in the testes

What are the female sex hormones and where are they produced? — Electrical Engineering MCQ

B. Oestrogen and Progesterone - produced mainly by the ovaries (follicles and corpus luteum) — Female sex hormones are primarily: Oestrogen (Oestradiol - E2 most potent) = Produced by ovarian follicles (granulosa cells), corpus luteum, adrenal cortex, and placenta (in pregnancy). Functions: Development of female secondary sex characteristics (puberty), breast development, uterine growth, menstrual cycle regulation, bone maintenance, cardiovascular protection. Progesterone = Produced mainly by the corpus luteum (after ovulation) and placenta (in pregnancy). Functions: Prepares and maintains uterus for pregnancy (thickens endometrium), maintains pregnancy, inhibits uterine contractions, thickens cervical mucus. Both hormones are regulated by FSH and LH from the pituitary and are essential for the menstrual cycle and pregnancy.

A. Testosterone and DHT - produced in the ovaries

C. FSH and LH - produced in the ovaries

D. Prolactin and oxytocin - produced in the uterus

What is oxytocin and what are its functions? — Electrical Engineering MCQ

C. A neuropeptide produced by the hypothalamus (released by posterior pituitary) that stimulates uterine contractions and milk ejection — Oxytocin is a neuropeptide produced in the hypothalamus (paraventricular nucleus) and released by the posterior pituitary. Functions: Uterine contractions during labour - creates positive feedback loop (Ferguson's reflex): Cervical stretching causes oxytocin release causing more contractions causing more cervical stretching. Milk ejection (let-down) reflex during breastfeeding - baby suckling causes oxytocin release causing myoepithelial cells in mammary gland to contract causing milk ejected. Love hormone - promotes bonding (mother-infant, pair bonding), trust, empathy, social behaviour. Clinical use: Syntocinon (synthetic oxytocin) - to induce or augment labour and prevent postpartum haemorrhage.

A. A hormone produced by the anterior pituitary that stimulates ovulation

B. A catecholamine that causes uterine relaxation

D. A steroid hormone produced by the placenta during pregnancy

What is the function of prolactin? — Electrical Engineering MCQ

B. Stimulates milk production (lactogenesis) in the mammary glands - produced by anterior pituitary — Prolactin (PRL) is produced by lactotroph cells of the anterior pituitary. Primary function: Stimulates and maintains milk production (lactogenesis) in breast tissue - acts on mammary gland alveolar cells. Regulation: Dopamine (PIH - Prolactin Inhibiting Hormone) = The main inhibitor of prolactin (tonically suppresses prolactin secretion). TRH (from hypothalamus) = Stimulates prolactin. Suckling = Stimulates prolactin release (neurogenic reflex). Prolactin suppresses ovulation (explains why breastfeeding can reduce fertility - lactational amenorrhoea). Hyperprolactinaemia: Most common cause = Prolactinoma (pituitary adenoma). Also: dopamine antagonists (metoclopramide, antipsychotics), hypothyroidism. Features: Galactorrhoea (nipple discharge), amenorrhoea, infertility, hypogonadism in men. Treatment: Dopamine agonists (cabergoline, bromocriptine).

A. Stimulates ovulation and the menstrual cycle

C. Promotes uterine contractions during childbirth

D. Stimulates testosterone production in the testes

What is the pineal gland and what does it produce? — Electrical Engineering MCQ

B. Located in the epithalamus, produces melatonin to regulate circadian rhythms and sleep — The Pineal Gland is a small (~150 mg), pine cone-shaped gland located in the epithalamus (posterior diencephalon), between the two superior colliculi. Sometimes called the third eye. It produces Melatonin - synthesised from serotonin (which is derived from tryptophan). Regulation: Darkness causes sympathetic stimulation of the pineal causing increased melatonin (promotes sleep). Light (via retino-hypothalamic-pineal pathway) suppresses melatonin (promotes wakefulness). Functions of melatonin: Regulates circadian rhythm (sleep-wake cycle), influences seasonal reproductive cycles (photoperiodism), antioxidant properties. Clinical use: Jet lag, shift work disorder, insomnia treatment.

A. Located in the anterior neck, produces calcitonin

C. Located in the pituitary fossa, produces ACTH

D. Located near the kidneys, produces aldosterone

What is the thymus gland? — Electrical Engineering MCQ

B. Located in the mediastinum - primary lymphoid organ that produces T-lymphocytes and thymosin hormone for immune development — The Thymus Gland is a bilobed lymphoid organ located in the superior mediastinum (behind the sternum, in front of the heart). It is largest in childhood and involutes (atrophies) after puberty - in adults it is replaced largely by fat. Functions: Primary lymphoid organ - site of T-lymphocyte (T-cell) maturation. Immature lymphocytes (thymocytes) from bone marrow migrate to thymus - undergo positive and negative selection - mature T-cells released to blood/lymph. Produces Thymosin, Thymopoietin, Thymulin - hormones that promote T-cell development and maturation. DiGeorge syndrome (22q11 deletion): Thymus hypoplasia/aplasia causing deficient T-cell immunity, recurrent infections, cardiac defects, hypocalcaemia. Thymoma: Tumour of thymus - associated with Myasthenia Gravis.

A. A gland in the neck producing thyroid hormone

C. Located near the kidney producing aldosterone

D. A gland in the brain producing melatonin

What is negative feedback in the endocrine system? — Electrical Engineering MCQ

B. When the output of a system inhibits or reduces its own further production - maintaining hormone levels within a normal range — Negative Feedback is the most common control mechanism in the endocrine system - it maintains hormone levels within a narrow range (homeostasis). How it works: A gland produces a hormone, hormone level rises, this rise feeds back (negatively) to inhibit further production. Classic example - HPT (Hypothalamo-Pituitary-Thyroid) axis: Hypothalamus produces TRH, pituitary produces TSH, thyroid produces T3/T4. Rising T3/T4 inhibits TRH and TSH causing thyroid to reduce production. Other examples: HPA axis (cortisol inhibits CRH and ACTH), HPG axis (sex hormones inhibit FSH and LH). Positive feedback is rare - example: Oxytocin/labour (cervical stretch causes more oxytocin causing more contractions) and LH surge (oestrogen stimulates LH surge causing ovulation).

A. When a hormone stimulates further production of the same hormone

C. When two hormones work together to produce an effect

D. When a hormone is produced in excess causing disease

What is Diabetes Insipidus (DI)? — Electrical Engineering MCQ

C. A disorder of ADH deficiency or resistance causing production of large volumes of dilute urine and excessive thirst — Diabetes Insipidus (DI) is characterised by polyuria (large volumes of very dilute urine - up to 20 L/day) and polydipsia (excessive thirst). Two types: Cranial DI (ADH deficiency - due to hypothalamic/posterior pituitary damage from head trauma, neurosurgery, tumour, infection. Treatment: Desmopressin/DDAVP - synthetic ADH analogue) and Nephrogenic DI (ADH resistance - kidneys fail to respond to ADH. Causes: Lithium toxicity, hypercalcaemia, hypokalaemia, genetic. Treatment: Thiazide diuretics - paradoxically reduce urine volume, and low sodium diet). Distinguished from Diabetes Mellitus by: Normal blood glucose, no glucose in urine, very low urine specific gravity (<1.005), very low urine osmolality. Water deprivation test + Desmopressin test differentiates cranial from nephrogenic DI.

A. Type 2 diabetes causing insulin resistance

B. A condition of excess glucose in urine due to high blood sugar

D. A pituitary tumour causing excess cortisol

What is SIADH (Syndrome of Inappropriate ADH Secretion)? — Electrical Engineering MCQ

B. Excessive unregulated ADH secretion causing water retention, dilutional hyponatraemia, and concentrated urine — SIADH occurs when ADH is secreted inappropriately (despite low plasma osmolality) causing water retention and dilutional hyponatraemia (Na+ <135 mmol/L). Features: Hyponatraemia (low blood sodium), Low plasma osmolality (100 mOsm/kg), Normal blood volume (euvolaemia - no oedema), and Urine Na+ >20 mmol/L. Causes: Malignancy (small cell lung cancer - most common), CNS disorders (meningitis, head injury, stroke), Pulmonary disease (pneumonia, TB), and Drugs (SSRIs, carbamazepine, cyclophosphamide, vincristine). Treatment: Fluid restriction (first-line), hypertonic saline (severe symptomatic hyponatraemia), and Tolvaptan (vasopressin V2 receptor antagonist).

A. ADH deficiency causing dilute urine and dehydration

C. Excess aldosterone causing water retention and hypertension

D. Insulin excess causing hypoglycaemia

What is acromegaly? — Electrical Engineering MCQ

B. Excess growth hormone in adults (after epiphyseal fusion) causing enlargement of hands, feet, jaw, and facial features — Acromegaly results from chronic excess GH in adults (after epiphyseal growth plates have closed). Most common cause: GH-secreting pituitary adenoma (somatotrophinoma). Features: Enlarged hands and feet (increased ring/shoe size - key symptom), Prognathism (protruding jaw), macroglossia (large tongue), coarse facial features, Frontal bossing, widely spaced teeth, Carpal tunnel syndrome (nerve compression), Sweating, oily skin, hypertension, diabetes, Visual field defects (bitemporal hemianopia - tumour compresses optic chiasm), and Arthritis (joint damage from overgrowth). Compare with Gigantism: Same cause (GH excess) but occurs before epiphyseal closure causing excessive height. Diagnosis: IGF-1 level + Oral Glucose Tolerance Test (GH not suppressed by glucose). Treatment: Transsphenoidal surgery, Somatostatin analogues (octreotide, lanreotide), Pegvisomant (GH receptor antagonist).

A. Growth hormone deficiency in adults causing muscle wasting

C. Excess growth hormone in children causing gigantism

D. Deficiency of GH causing dwarfism in adults

What is Graves' disease? — Electrical Engineering MCQ

B. Autoimmune hyperthyroidism caused by TSI antibodies stimulating the TSH receptor - causing excess thyroid hormone production — Graves' Disease is the most common cause of hyperthyroidism (~70-80% of cases). It is an autoimmune disease where Thyroid Stimulating Immunoglobulins (TSI) - also called TRAb (TSH Receptor Antibodies) - bind to and activate the TSH receptor causing continuous stimulation of thyroid and excess T3/T4. Features of hyperthyroidism PLUS unique Graves' features: Exophthalmos (Proptosis) = bulging eyes due to inflammation and GAG deposition in orbital tissues (NOT just thyroid hormone), Pretibial myxoedema = firm, non-pitting swelling over shins (despite the name - it's hyperthyroidism), Thyroid acropachy = periosteal new bone formation + finger clubbing, and Diffuse goitre with bruit. Diagnosis: TFTs (low TSH, high T3/T4), TRAb positive. Treatment: Antithyroid drugs, radioiodine, surgery.

A. Autoimmune hypothyroidism with destruction of thyroid tissue

C. Thyroid cancer associated with radiation exposure

D. Subacute thyroiditis causing temporary hyperthyroidism

What is Hashimoto's thyroiditis? — Electrical Engineering MCQ

C. The most common cause of hypothyroidism in iodine-sufficient countries - autoimmune destruction of the thyroid with anti-TPO and anti-Tg antibodies — Hashimoto's Thyroiditis (Chronic Autoimmune Thyroiditis) is the most common cause of hypothyroidism in developed (iodine-sufficient) countries. Named after Japanese physician Hakaru Hashimoto (1912). It is an autoimmune condition where the immune system attacks the thyroid: Anti-TPO antibodies (Thyroid Peroxidase - most common and sensitive marker) and Anti-Tg antibodies (Anti-Thyroglobulin). Lymphocytic infiltration causes destruction of thyroid follicles causing reduced T3/T4 production. Features: Hypothyroidism (fatigue, weight gain, cold intolerance, dry skin, constipation) and goitre (early - may have small/no goitre later as gland is destroyed). More common in females (7:1 female:male ratio). Associated with other autoimmune diseases (Type 1 DM, coeliac disease, Addison's, rheumatoid arthritis, pernicious anaemia). Treatment: Levothyroxine (T4 replacement).

A. Autoimmune hyperthyroidism with excess T3 and T4 production

B. Bacterial infection of the thyroid gland

D. Thyroid cancer caused by iodine deficiency

What is the role of calcitonin? — Electrical Engineering MCQ

B. Produced by C-cells (parafollicular cells) of the thyroid - lowers blood calcium by inhibiting osteoclast-mediated bone resorption — Calcitonin is produced by parafollicular C-cells (clear cells) of the thyroid gland (not follicular cells - which produce T3/T4). It is released when blood calcium rises. Actions - all calcium-lowering (opposite of PTH): Inhibits osteoclasts causing reduced bone resorption causing reduced calcium release from bone into blood, Increases renal calcium excretion (minor effect), and Inhibits intestinal calcium absorption (minor effect). In humans, calcitonin plays a relatively minor physiological role (PTH is far more important for calcium regulation). However, calcitonin is clinically important as a tumour marker for Medullary Thyroid Carcinoma (MTC) - which arises from C-cells. Salmon calcitonin is used clinically to treat Paget's disease of bone and hypercalcaemia of malignancy.

A. Raises blood calcium by stimulating bone resorption

C. Regulates phosphate excretion in the kidney

D. Stimulates parathyroid hormone release

What is the function of FSH (Follicle Stimulating Hormone)? — Electrical Engineering MCQ

C. Stimulates follicle development in females and sperm production (spermatogenesis) in males — FSH (Follicle Stimulating Hormone) is a gonadotrophin produced by gonadotroph cells of the anterior pituitary, regulated by GnRH (Gonadotrophin Releasing Hormone) from the hypothalamus. Functions: In Females = Stimulates follicular development in the ovary causing follicles to produce oestrogen and prepares for ovulation. In Males = Stimulates Sertoli cells in the testes causing promotion of spermatogenesis (sperm production). FSH and LH work together - FSH sets the stage, LH triggers the event (ovulation). FSH is elevated in primary gonadal failure (ovarian/testicular failure) because negative feedback from sex hormones is lost. Low FSH indicates secondary (pituitary/hypothalamic) cause of hypogonadism. Clinical use: Fertility treatments (IVF - ovarian stimulation uses FSH injections).

A. Stimulates the adrenal cortex to produce cortisol

B. Triggers ovulation in females

D. Promotes milk production in the mammary glands

What is LH (Luteinising Hormone) and what does it do? — Electrical Engineering MCQ

C. Triggers ovulation in females and stimulates testosterone production by Leydig cells in males — LH (Luteinising Hormone) is a gonadotrophin from the anterior pituitary (regulated by GnRH). Functions: In Females = Triggers ovulation (LH surge around day 14 of the menstrual cycle causing follicle rupture and egg release). After ovulation, LH stimulates the ruptured follicle to become the corpus luteum, and corpus luteum produces progesterone (maintains uterine lining for potential pregnancy). In Males = Stimulates Leydig cells in the testes to produce testosterone. LH surge is detected by ovulation predictor kits (OPKs) - used to time intercourse for conception. Polycystic Ovary Syndrome (PCOS): Elevated LH:FSH ratio (>2:1), excess androgens, anovulation, and cystic ovaries.

A. Stimulates follicle growth in females and Sertoli cells in males

B. Suppresses testosterone production in males

D. Stimulates the adrenal cortex to produce androgens

Endocrine System MCQ [ Free PDF Download ] for RRB & SSC and other Competitive exams

Endocrine System MCQ for RRB & SSC and other Competitive exams

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What is the significance of the HPA axis (Hypothalamo-Pituitary-Adrenal axis)?

✓ Answer: C A three-tier hormonal cascade regulating cortisol - CRH (hypothalamus) > ACTH (pituitary) > Cortisol (adrenal) - controls stress response and metabolism

The HPA (Hypothalamo-Pituitary-Adrenal) Axis is the body's major stress response system: 1) Stress/low cortisol causes Hypothalamus to release CRH (Corticotrophin-Releasing Hormone). 2) CRH causes Anterior pituitary to release ACTH (Adrenocorticotrophic Hormone). 3) ACTH causes Adrenal cortex (zona fasciculata) to produce and release Cortisol. 4) Rising cortisol causes Negative feedback suppressing CRH and ACTH. Diurnal rhythm: Cortisol peaks at ~8 AM (highest), lowest at midnight - follows circadian rhythm. Clinical tests: Short Synacthen Test (synthetic ACTH given causing cortisol should rise - tests adrenal reserve), Low-dose dexamethasone suppression test (LDDST) (cortisol should suppress - used to screen for Cushing's), and Insulin tolerance test (gold standard for HPA axis integrity - causes hypoglycaemia causing stress causing HPA activation).

What is the role of androgens in prostate disease?

✓ Answer: B Testosterone and DHT stimulate prostate cell growth - excess leads to BPH and prostate cancer - treatments target androgen signalling

The Prostate gland is highly androgen-dependent. DHT (Dihydrotestosterone) - converted from testosterone by 5-alpha reductase in prostate cells - is the primary androgen stimulating prostate growth. Benign Prostatic Hyperplasia (BPH): Age-related prostate enlargement due to chronic DHT stimulation causing urinary obstruction (frequency, nocturia, weak stream, hesitancy, retention). Treatment: 5-alpha reductase inhibitors (finasteride, dutasteride) block testosterone to DHT conversion causing reduced prostate size; Alpha-1 blockers (tamsulosin) relax prostate smooth muscle. Prostate Cancer: Androgen-sensitive tumour. Advanced prostate cancer treatment: Androgen Deprivation Therapy (ADT) = GnRH analogues (leuprorelin causing castrate testosterone levels), anti-androgens (bicalutamide, enzalutamide), and abiraterone (inhibits androgen synthesis). Eventually causes castration-resistant prostate cancer.

What is the overall importance of the endocrine system in human health?

✓ Answer: C The endocrine system - working alongside the nervous system - regulates virtually every body function including growth, metabolism, reproduction, stress response, homeostasis, and behaviour

The Endocrine System is one of the body's two major control and communication systems (alongside the nervous system). Summary of functions: 1) Growth and Development (GH, thyroid hormones, sex hormones, insulin). 2) Metabolism (Thyroid hormones BMR, insulin/glucagon glucose, cortisol stress metabolism, leptin/ghrelin appetite and energy balance). 3) Reproduction (FSH, LH, sex hormones, oxytocin, prolactin, HCG). 4) Homeostasis (ADH for water, aldosterone/RAAS for Na+/BP, PTH/calcitonin/Vit D for calcium, insulin/glucagon for glucose). 5) Stress Response (Adrenaline acute, cortisol sustained). 6) Behaviour and Mood (Cortisol, serotonin, dopamine, oxytocin, melatonin). 7) Immune Modulation (Cortisol immunosuppressive, thymosin T-cell development, melatonin). The endocrine system acts slowly but produces long-lasting effects compared to the rapid but brief nervous system. The neuroendocrine system (integration of both) is the true master regulator of all body functions.

What is meant by hormone receptor up-regulation and down-regulation?

✓ Answer: B Up-regulation = increased receptor number (increasing sensitivity); down-regulation = decreased receptor number (reducing sensitivity) - important in endocrine homeostasis

Receptor Regulation is an important mechanism of endocrine homeostasis. Down-regulation: Chronic excess hormone causes cells to reduce receptor number/sensitivity causing decreased response despite high hormone levels. Example: T2DM - chronic hyperinsulinaemia causes insulin receptor down-regulation causing insulin resistance. Also: Desensitisation in beta-adrenergic receptors with prolonged adrenaline (explains tachyphylaxis with bronchodilators in asthma). Up-regulation: Chronic hormone deficiency causes cells to increase receptor number causing enhanced sensitivity. Example: Hypothyroidism causes up-regulation of TSH receptors. Addison's disease causes up-regulation of ACTH receptors. Clinical relevance: Drug receptor desensitisation (tachyphylaxis), insulin resistance in T2DM, and steroid withdrawal (HPA suppression from exogenous steroid use causing adrenal atrophy causing down-regulation of ACTH receptors).

What is the role of insulin in carbohydrate metabolism?

✓ Answer: B Insulin promotes glucose uptake, glycogen synthesis, and inhibits glucose production - the main hormone for lowering blood glucose after meals

Insulin's effects on carbohydrate metabolism - all hypoglycaemic (glucose-lowering). In Muscle: Increases GLUT-4 transporter translocation to cell surface causing glucose uptake, Stimulates glycogen synthesis (glycogenesis), and Stimulates glycolysis (glucose breakdown for energy). In Liver: Stimulates glycogenesis (glucose to glycogen storage), Inhibits glycogenolysis (glycogen breakdown), and Inhibits gluconeogenesis (new glucose synthesis). In Adipose tissue: Increases GLUT-4 causing glucose uptake and Stimulates lipogenesis (glucose to triglycerides). After a meal: Blood glucose rises causing insulin secreted causing all above actions causing blood glucose restored to normal (~5 mmol/L or 90 mg/dL). In T1DM/insulin deficiency: Liver produces excess glucose (gluconeogenesis, glycogenolysis unchecked) causing hyperglycaemia even during fasting.

What is the role of testosterone in male puberty?

✓ Answer: B Rising testosterone at puberty drives development of secondary sexual characteristics in males - triggered by the hypothalamic-pituitary-gonadal axis

Male Puberty (typically begins at age 9-14). Trigger: Pulsatile GnRH from hypothalamus causes LH and FSH from pituitary causes testosterone from Leydig cells. Rising testosterone causes: 1) Testicular enlargement (first sign of puberty in boys), 2) Pubic and axillary hair growth, 3) Penile growth, 4) Voice deepening (laryngeal growth), 5) Facial hair (beard, moustache), 6) Muscle mass increase (anabolic effects), 7) Bone density increase and growth spurt (before epiphyseal closure), 8) Spermatogenesis begins, and 9) Acne (sebaceous gland stimulation). DHT (Dihydrotestosterone): Converted from testosterone by 5-alpha reductase - responsible for beard growth, male-pattern baldness, prostate growth, and genital development (testosterone + DHT). Adrenarche (adrenal androgens - DHEA): Pubic hair growth, body odour - precedes gonadal puberty.

What is the significance of the C-peptide test in diabetes?

✓ Answer: B C-peptide is co-secreted with insulin from beta cells - measuring it distinguishes endogenous insulin production from exogenous insulin injection

C-peptide (Connecting peptide) is a byproduct of proinsulin processing in beta cells. Proinsulin is cleaved into Insulin + C-peptide in equal molar amounts and both are secreted together. Clinical significance: Distinguishes T1DM from T2DM = Low/absent C-peptide = T1DM (beta cells destroyed). Normal/high C-peptide = T2DM (beta cells still working). Detects exogenous insulin injection vs endogenous = Exogenous insulin (injected) does NOT contain C-peptide causing Low C-peptide + High insulin = exogenous injection (Used in Munchausen syndrome/factitious hypoglycaemia - injecting insulin covertly). Insulinoma (beta cell tumour) = Spontaneous hypoglycaemia + High insulin + High C-peptide confirms endogenous insulin excess. C-peptide has a longer half-life than insulin (35 min vs 4 min) making it more reliable to measure.

What is female puberty and what hormones drive it?

✓ Answer: B Rising GnRH triggers FSH and LH release - oestrogen causes breast development, uterine growth, menarche, and the adolescent growth spurt

Female Puberty (typically begins at age 8-13). Trigger: Pulsatile GnRH causes FSH and LH causing oestrogen (from ovarian follicles). Rising oestrogen causes (Tanner stages): 1) Breast development (Thelarche) - FIRST sign of puberty in girls (stage 2 Tanner), 2) Pubic hair (Pubarche) - from adrenal androgens (adrenarche), 3) Uterine and vaginal growth, 4) Widening of hips (pelvis prepares for childbearing), 5) Adolescent growth spurt (oestrogen + GH), and 6) Menarche (first menstruation) - usually 2-3 years after thelarche. Adrenarche: DHEA from adrenal glands causes pubic and axillary hair, body odour (before ovarian oestrogen rises). Precocious puberty: Before age 8 in girls, before age 9 in boys. Most commonly idiopathic/central in girls.

What is the effect of stress on the endocrine system?

✓ Answer: B Acute stress activates the sympatho-adrenal axis (adrenaline) and HPA axis (cortisol) - chronic stress can disrupt reproductive, thyroid, and growth hormone axes

Stress and the Endocrine System: Acute stress response (seconds to minutes) = Sympatho-adrenal axis: Hypothalamus causes sympathetic nervous system causes adrenal medulla causes Adrenaline + Noradrenaline causing fight-or-flight. Subacute stress (minutes to hours) = HPA axis: CRH causes ACTH causes Cortisol causing mobilisation of energy (glucose, fatty acids), anti-inflammatory, maintains blood pressure. Chronic stress - maladaptive effects: Reproductive axis (HPG) suppression = CRH inhibits GnRH causing suppression of FSH/LH causing amenorrhoea, low libido, infertility (functional hypothalamic amenorrhoea - common in athletes, anorexia, chronic illness). Thyroid axis suppression = Non-thyroidal illness syndrome (sick euthyroid) - cortisol inhibits TSH. GH suppression = Chronic cortisol reduces GH secretion. Immune suppression = Chronic cortisol increases infection risk. Hippocampal damage = Cortisol reduces neurogenesis causing depression and memory impairment.

What is the role of the thyroid gland in fetal development?

✓ Answer: B Thyroid hormones are essential for normal fetal brain development - deficiency causes cretinism

Thyroid hormones are critical for normal fetal and infant brain development. The fetal thyroid starts functioning at ~10-12 weeks gestation. Before this, maternal T4 crosses the placenta and supports fetal brain development. Thyroid hormones are essential for: Neuronal migration, myelination, synapse formation in the developing brain. Cretinism (Congenital Hypothyroidism): Caused by fetal/neonatal thyroid deficiency (iodine deficiency, thyroid agenesis, dyshormonogenesis). Features: Intellectual disability, short stature, coarse facial features, large tongue, umbilical hernia, hypotonia, deafness. Most common preventable cause of intellectual disability worldwide. Newborn screening (Guthrie test/heel prick test): Measures TSH (and T4) - detects congenital hypothyroidism within 5-7 days of birth. Early treatment with levothyroxine (within 2 weeks of birth) causes normal intellectual development. Iodine deficiency remains the most common worldwide cause - iodised salt is the major preventive strategy.

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