Excretory Products and their Elimination — NCERT Class 11 Biology

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This page provides complete NCERT Solutions for CBSE Class 11 Biology Chapter 19 — Excretory Products and their Elimination. 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)

• Excretory Products: Ammonia (ammonotelic — aquatic animals), urea (ureotelic — mammals, terrestrial amphibians), uric acid (uricotelic — birds, reptiles, insects), creatinine, and other nitrogenous wastes
• Kidneys: Paired organs in the abdominal cavity; each kidney has about 1 million nephrons; cortex contains glomeruli, medulla contains loops of Henle and collecting ducts
• Nephron: Structural and functional unit of the kidney; consists of Bowman's capsule (with glomerulus), proximal convoluted tubule (PCT), loop of Henle (descending and ascending limbs), distal convoluted tubule (DCT), and collecting duct
• Glomerular Filtration Rate (GFR): Approximately 125 mL/min or 180 L/day; only 1–1.5 L is excreted as urine (99% reabsorption)
• Urine Formation: Three steps — glomerular filtration, tubular reabsorption, tubular secretion
• Composition of Urine: Water (95%), urea (2.5%), salts (2%), uric acid (0.3%), other trace substances; pH approximately 6.0
• ADH (Vasopressin): Released from posterior pituitary; increases water reabsorption in collecting ducts; deficiency causes diabetes insipidus
• RAAS (Renin-Angiotensin-Aldosterone System): Regulates blood pressure and glomerular blood flow; renin released from JGA converts angiotensinogen to angiotensin I and then II
• Dialysis: Haemodialysis (artificial kidney) and peritoneal dialysis — used when kidneys fail
• Kidney Transplant: Best long-term solution for kidney failure; donor kidney placed in iliac fossa
• Disorders: Uremia (accumulation of urea in blood), kidney stones (calculi), glomerulonephritis, renal failure

Intext Questions

Page 291

1. Myogenic mechanism: An increase in blood pressure stretches the afferent arteriole wall, causing it to respond by contracting (vasoconstriction). This reduces blood flow into the glomerulus and prevents a rise in GFR. A decrease in blood pressure relaxes the afferent arteriole (vasodilation), increasing blood flow and maintaining GFR.

2. Juxtaglomerular apparatus (JGA) mechanism: When GFR increases, the faster flow of filtrate past the macula densa cells in the ascending limb of the loop of Henle is detected. This triggers the release of locally acting chemicals that cause vasoconstriction of the afferent arteriole, reducing GFR back to normal. Conversely, a fall in GFR triggers the release of renin from JG cells, activating the renin-angiotensin system to increase blood pressure and restore GFR.

Page 297

(a) Ammonotelism — (ii) Water (ammonotelic animals excrete ammonia, which requires large amounts of water, so they are mostly aquatic)

(b) Uricotelism — (i) Birds, (iii) Insects (uricotelic animals excrete uric acid as a semi-solid paste, needing very little water — includes birds, reptiles, and insects)

(c) Ureotelism — (iv) Mammals (ureotelic animals excrete urea, which is less toxic than ammonia and requires moderate amounts of water — includes mammals and terrestrial amphibians)

Page 300

1. Regulating the volume of blood plasma and interstitial fluid through water reabsorption in the collecting ducts (controlled by ADH). 2. Maintaining the concentration of ions (Na+, K+, Cl−, HCO3−) through selective reabsorption and secretion in the nephron tubules. 3. Producing either concentrated urine (when water needs to be conserved) or dilute urine (when excess water needs to be eliminated).

Osmoregulation ensures that the osmotic pressure of body fluids remains around 300 mOsm/L, which is essential for the proper functioning of cells and organs.

Terrestrial animals have limited access to water and cannot afford to lose such large volumes. Therefore, they convert ammonia into less toxic forms:

1. Ureotelic animals (mammals, terrestrial amphibians): Convert ammonia to urea in the liver via the ornithine-urea cycle. Urea is less toxic and requires only about 50 mL of water per gram for excretion. It can be stored at higher concentrations in the body temporarily.

2. Uricotelic animals (birds, reptiles, insects): Convert ammonia to uric acid. Uric acid is the least toxic and is nearly insoluble in water, so it can be excreted as a semi-solid paste with minimal water loss (about 10 mL per gram). This is particularly advantageous for animals like birds that need to conserve water and for egg-laying animals where waste must be stored within the egg.

Chapter-End Exercise

(a) Ammonotelism: The process of excreting nitrogenous wastes primarily in the form of ammonia. Ammonia is the most toxic nitrogenous waste and requires large volumes of water for its elimination. Ammonotelic animals include bony fishes, aquatic invertebrates, and aquatic amphibians. Since ammonia dissolves readily in water, these animals can excrete it directly into the surrounding water through gills or skin.

(b) Ureotelism: The process of excreting nitrogenous wastes primarily in the form of urea. Urea is less toxic than ammonia and requires less water for excretion (about 50 mL per gram). Ureotelic animals include mammals, terrestrial amphibians, and some marine fishes. Ammonia is converted to urea in the liver through the ornithine-urea cycle, and urea is then filtered and excreted by the kidneys.

(c) Uricotelism: The process of excreting nitrogenous wastes primarily in the form of uric acid. Uric acid is the least toxic nitrogenous waste and is nearly insoluble in water, so it can be excreted as a semi-solid paste with minimal water loss. Uricotelic animals include birds, reptiles, insects, and land snails. This mode of excretion is advantageous for animals that need to conserve water or for egg-laying animals where nitrogenous waste must be stored within the egg shell.

1. Juxtaglomerular (JG) cells: Modified smooth muscle cells in the walls of the afferent arteriole that secrete renin. 2. Macula densa cells: Modified epithelial cells in the distal convoluted tubule that sense the NaCl concentration and flow rate of the filtrate. 3. Mesangial cells: Located between the afferent and efferent arterioles.

Role of JGA:

• When blood pressure or blood volume drops, the JG cells detect the reduced stretch of the afferent arteriole and release renin.
• Renin converts angiotensinogen (from the liver) to angiotensin I, which is then converted to angiotensin II by ACE (angiotensin-converting enzyme) in the lungs.
• Angiotensin II: (a) constricts efferent arterioles, raising glomerular blood pressure and GFR; (b) stimulates the adrenal cortex to release aldosterone, which increases Na+ reabsorption in the DCT; (c) increases blood pressure by causing vasoconstriction; (d) stimulates ADH release, increasing water reabsorption.
• The macula densa cells also regulate GFR through tubuloglomerular feedback — they signal the afferent arteriole to constrict or dilate based on the NaCl concentration in the tubular fluid.

Regulation of GFR occurs through three mechanisms:

1. Intrinsic autoregulation: The kidneys maintain a relatively constant GFR despite changes in systemic blood pressure through: (a) Myogenic mechanism — increased blood pressure causes afferent arteriole constriction, reducing blood flow and GFR; decreased pressure causes dilation, increasing flow. (b) Tubuloglomerular feedback — macula densa cells sense NaCl in the distal tubule and signal the afferent arteriole to adjust its diameter accordingly.

2. Renin-angiotensin mechanism (extrinsic): When GFR drops, JG cells release renin, which activates the renin-angiotensin-aldosterone system (RAAS). Angiotensin II constricts efferent arterioles, raising glomerular pressure and GFR. Aldosterone increases Na+ and water reabsorption, restoring blood volume.

3. Atrial Natriuretic Factor (ANF): When blood pressure increases, the atria release ANF, which causes vasodilation of afferent arterioles and constriction of efferent arterioles, increasing GFR. ANF also inhibits renin and aldosterone secretion, promoting Na+ and water excretion, thereby decreasing blood volume and pressure.

1. Ornithine-urea cycle: The liver converts toxic ammonia (produced by deamination of amino acids in the liver) into less toxic urea through the ornithine-urea cycle. This involves a series of reactions using ornithine, citrulline, and arginine, consuming CO2 and releasing urea and water. The urea is then transported via the blood to the kidneys for excretion.

2. Deamination of amino acids: When proteins are broken down, amino acids undergo deamination in the liver, where the amino group (−NH2) is removed and converted to ammonia, which is then quickly converted to urea.

3. Detoxification: The liver detoxifies various harmful substances including drugs, alcohol, and metabolic wastes. These detoxified products are then excreted by the kidneys or through bile.

4. Bile pigment formation: The liver breaks down aged red blood cells and converts the haemoglobin into bilirubin and biliverdin (bile pigments), which are excreted through bile into the intestine and eliminated in faeces.

1. Renal corpuscle (Malpighian body):

• Bowman's capsule: A double-walled, cup-shaped structure. The outer layer (parietal) is made of simple squamous epithelium. The inner layer (visceral) is made of podocytes that wrap around the glomerular capillaries.
• Glomerulus: A tuft of capillaries formed by the afferent arteriole and drained by the efferent arteriole. The glomerulus sits within the Bowman's capsule. The space between the two layers of Bowman's capsule is called the capsular space, where the glomerular filtrate collects.

2. Renal tubule: This is a long, coiled tube consisting of:

• Proximal Convoluted Tubule (PCT): Highly coiled, lined by simple cuboidal brush border epithelium. It is the main site of reabsorption (65–80% of filtrate). Reabsorbs glucose, amino acids, Na+, K+, Ca2+, Cl−, HCO3−, and water.
• Loop of Henle: U-shaped tube with a thin descending limb (permeable to water) and thick ascending limb (impermeable to water, actively transports NaCl). The loop of Henle creates a counter-current multiplier system that concentrates the medullary interstitium.
• Distal Convoluted Tubule (DCT): Shorter than PCT, lined by simple cuboidal epithelium (without brush border). It performs selective reabsorption and secretion under hormonal control (aldosterone and ADH).
• Collecting duct: Receives filtrate from multiple nephrons. Under ADH control, it reabsorbs water and concentrates urine. It empties into the renal pelvis.

Types of nephrons:

• Cortical nephrons (85%): Have a short loop of Henle that extends only slightly into the medulla. Their glomeruli are in the outer cortex.
• Juxtamedullary nephrons (15%): Have a long loop of Henle that extends deep into the medulla. Their glomeruli are near the medulla. They play a major role in concentrating urine.

Mechanism:

The glomerular capillary wall acts as a filter. It has three layers: 1. Endothelium of glomerular blood vessels — fenestrated (has pores) that allows passage of all plasma components except blood cells. 2. Basement membrane — a thin, non-cellular layer of collagen and glycoproteins that blocks the passage of large plasma proteins. 3. Epithelium of Bowman's capsule (podocytes) — has slit pores (filtration slits) between foot processes that further prevent the passage of proteins.

Filtration pressure (net filtration pressure): Net filtration pressure = Glomerular hydrostatic pressure − (Glomerular colloidal osmotic pressure + Capsular hydrostatic pressure) = 60 mmHg − (32 mmHg + 18 mmHg) = 10 mmHg

This net filtration pressure of about 10–15 mmHg forces plasma (minus proteins and cells) from the glomerular capillaries into the Bowman's capsule, producing the glomerular filtrate.

Composition of glomerular filtrate: It is similar to blood plasma minus large proteins and cells. It contains water, glucose, amino acids, urea, uric acid, creatinine, and ions (Na+, K+, Cl−, HCO3−).

The GFR is approximately 125 mL/min (180 L/day). Of this, 99% is reabsorbed, and only about 1.5 L is excreted as urine.

1. Counter-current multiplier (Loop of Henle):

• The descending limb of the loop of Henle is permeable to water but impermeable to NaCl. As filtrate descends, water moves out into the increasingly concentrated medullary interstitium, making the filtrate more concentrated (up to 1200 mOsm/L at the tip).
• The ascending limb is impermeable to water but actively transports NaCl out. This makes the filtrate dilute (about 100 mOsm/L entering the DCT) and creates a concentration gradient in the medullary interstitium (300 mOsm/L at the cortex to 1200 mOsm/L at the inner medulla).
• The opposing flows in the two limbs (counter-current) and the active NaCl transport in the ascending limb together "multiply" the concentration gradient — hence the name counter-current multiplier.

2. Counter-current exchanger (Vasa recta):

• The vasa recta (blood vessels running parallel to the loop of Henle) maintain the medullary concentration gradient by acting as a counter-current exchanger. Blood descending in the vasa recta picks up NaCl and loses water; blood ascending loses NaCl and picks up water. The net effect is that the vasa recta supply blood to the medulla without washing away the concentration gradient.

Significance:

• Creates and maintains a high osmolarity gradient (up to 1200 mOsm/L) in the medullary interstitium.
• This gradient allows the collecting duct to reabsorb water under ADH influence, producing concentrated urine.
• Enables the kidney to produce urine that is 4–5 times more concentrated than blood plasma.
• Essential for water conservation, especially in conditions of dehydration.

Mechanism of action:

1. Stimulus for release: Osmoreceptors in the hypothalamus detect an increase in blood osmolarity (above 300 mOsm/L), which occurs when the body is dehydrated or has excess solutes. This triggers ADH release from the posterior pituitary into the blood.

2. Action on the kidney: ADH binds to receptors on the basolateral membrane of the collecting duct cells and principal cells of the DCT. This activates a cAMP-mediated signalling pathway that causes water channel proteins (aquaporin-2) to be inserted into the apical membrane of these cells.

3. Effect: The insertion of aquaporin-2 channels makes the collecting duct permeable to water. As the filtrate passes through the medullary region (which has a high osmolarity due to the counter-current mechanism), water is reabsorbed from the collecting duct into the medullary interstitium and then into the blood. This produces concentrated (hypertonic) urine and conserves body water.

4. Conditions for decreased ADH: When blood osmolarity decreases (excess water intake), ADH secretion is reduced, aquaporins are removed from the collecting duct membrane, and the duct becomes less permeable to water. This results in dilute (hypotonic) urine and increased water excretion.

Disorders:

• Diabetes insipidus: Caused by deficiency of ADH or defective ADH receptors. The patient produces large volumes of dilute urine (up to 15–20 L/day) and experiences excessive thirst (polydipsia).

(a) Cortical nephrons vs Juxtamedullary nephrons:

(b) Ascending limb vs Descending limb of loop of Henle:

(c) Tubular reabsorption vs Tubular secretion:

Conditions when dialysis is needed:

1. Acute renal failure: Sudden loss of kidney function due to severe injury, infection, drug toxicity, or obstruction. 2. Chronic renal failure (end-stage kidney disease): Progressive and irreversible decline in kidney function over months or years, often due to diabetes mellitus, hypertension, or glomerulonephritis. 3. Uraemia: Accumulation of urea and other nitrogenous wastes in the blood, leading to symptoms like nausea, vomiting, fatigue, and mental confusion. 4. Severe electrolyte imbalance: Dangerous levels of K+ (hyperkalaemia) or acidosis that cannot be managed medically. 5. Drug overdose or poisoning: When certain drugs or toxins need to be rapidly removed from the blood.

Types of dialysis:

1. Haemodialysis: Blood from an artery (usually radial) is passed through a dialysing unit (artificial kidney) containing a cellophane membrane. On the other side of the membrane flows the dialysis fluid, which has the same composition as normal plasma but lacks nitrogenous wastes. Wastes like urea, uric acid, and creatinine diffuse from the blood into the dialysis fluid. The purified blood is returned to the body through a vein. Typically done 2–3 times per week, each session lasting 4–6 hours.

2. Peritoneal dialysis: The peritoneum (the membrane lining the abdominal cavity) acts as the dialysis membrane. Dialysis fluid is introduced into the abdominal cavity through a catheter. Wastes from the blood vessels lining the peritoneum diffuse into the dialysis fluid. After several hours, the fluid is drained out and replaced. Can be done at home.

Process:

1. The urinary bladder is a stretchable muscular sac that stores urine. As urine is produced by the kidneys, it flows down the ureters into the bladder by peristalsis. 2. When the bladder fills to about 300–400 mL of urine, the stretch receptors on the bladder wall are activated. 3. These stretch receptors send signals via sensory neurons to the spinal cord (sacral segments S2–S4). 4. The spinal cord processes this information and sends motor signals that cause:

5. The person becomes aware of the urge to urinate. Voluntary relaxation of the external urethral sphincter (skeletal muscle) allows urine to flow out through the urethra. 6. The process of micturition is primarily a spinal reflex, but it is also under voluntary control through higher brain centres (cerebral cortex and pons). A person can voluntarily delay urination by contracting the external sphincter. 7. Once micturition begins, it is sustained by a positive feedback mechanism — as urine flows through the urethra, it stimulates further contraction of the detrusor muscle until the bladder is empty.

• Contraction of the detrusor muscle (the smooth muscle of the bladder wall).
• Relaxation of the internal urethral sphincter (involuntary, smooth muscle).

1. Uraemia: A condition characterised by the accumulation of urea and other nitrogenous wastes in the blood due to kidney failure. Symptoms include nausea, vomiting, fatigue, loss of appetite, mental confusion, and oedema. Severe uraemia can be fatal and requires dialysis or kidney transplant.

2. Kidney stones (Renal calculi): Hard deposits of salts and minerals (calcium oxalate, uric acid, struvite, cystine) that form inside the kidneys. They can cause severe pain (renal colic) when they block the ureter, blood in urine (haematuria), and urinary tract infections. Small stones may pass spontaneously; larger stones may require lithotripsy (shock wave therapy) or surgical removal.

3. Glomerulonephritis: Inflammation of the glomeruli, often caused by infections (post-streptococcal), autoimmune diseases, or other conditions. Symptoms include haematuria (blood in urine), proteinuria (protein in urine), oedema (swelling, especially around eyes and ankles), and reduced GFR. It can lead to chronic kidney disease if untreated.

4. Renal failure: The inability of the kidneys to filter waste products from the blood adequately.

• Acute renal failure: Sudden onset, often reversible. Caused by severe injury, infection, drug toxicity, or obstruction.
• Chronic renal failure: Gradual, progressive, and irreversible decline in kidney function over months or years. Common causes include diabetes mellitus and hypertension. Requires dialysis or kidney transplant.

5. Diabetes insipidus: Caused by deficiency of ADH (vasopressin) or defective ADH receptors in the kidneys. The kidneys cannot concentrate urine, leading to excretion of large volumes of dilute urine (up to 15–20 L/day) and excessive thirst (polydipsia). Treated with synthetic ADH (desmopressin).

6. Nephrotic syndrome: Damage to the glomerular filtration barrier leading to massive proteinuria (>3.5 g/day), hypoalbuminaemia, severe oedema, and hyperlipidaemia. Common causes include minimal change disease (in children) and membranous nephropathy (in adults).

7. Urinary tract infection (UTI): Bacterial infection of any part of the urinary system — kidneys (pyelonephritis), bladder (cystitis), or urethra (urethritis). Symptoms include burning during urination, frequent urge to urinate, cloudy urine, and pelvic pain. More common in women due to shorter urethra.

Internal Links

• [Chapter 19 Guide — Excretory Products and their Elimination](/school/cbse/class/11/biology/cbse-excretory-products)
• [All Class 11 Biology Solutions](/school/cbse/class/11/biology/solutions)
• [Class 11 Biology Subject Guide](/school/cbse/class/11/biology)