Excretory System MCQ for RRB & SSC and other Competitive exams
51
What is the medical term for painful urination?
✓ Answer:
C
Dysuria
Dysuria is the medical term for painful, burning, or uncomfortable urination. It is a common symptom of: Urinary Tract Infection (UTI) - most common cause, Cystitis (bladder infection), Urethritis (urethral infection - STIs like gonorrhoea, chlamydia), Pyelonephritis (kidney infection), Kidney stones (as they pass through the ureter/urethra), and Interstitial cystitis (chronic bladder inflammation). Other urinary symptoms: Frequency (urinating often), Urgency (sudden urge), Nocturia (urinating at night), Haematuria (blood in urine), Polyuria (excess urine), Oliguria (reduced urine). Dysuria always warrants urine dipstick and culture.
52
What is the significance of glucosuria in urine?
✓ Answer:
B
Abnormal presence of glucose in urine - most commonly indicates diabetes mellitus when blood glucose exceeds the renal threshold (~180 mg/dL)
Glucosuria (Glycosuria) is the abnormal presence of glucose in urine. Causes: Diabetes Mellitus (most common) - blood glucose > renal threshold (~180 mg/dL) - SGLT2 transporters saturated - glucose in urine - osmotic diuresis - polyuria/polydipsia. Renal Glucosuria - normal blood glucose but low renal threshold - due to SGLT2 genetic defect or PCT dysfunction (Fanconi syndrome) - glucose in urine despite normal blood glucose. Pregnancy - reduced renal threshold - mild glucosuria in normal pregnancy. Glucosuria causes osmotic diuresis - large volumes of dilute, sweet-smelling urine. Historically diagnosed by testing if urine tasted sweet (before modern tests). Now detected by urine dipstick (glucose oxidase reaction).
53
What is SIADH (Syndrome of Inappropriate Antidiuretic Hormone Secretion)?
✓ Answer:
B
Excessive ADH secretion causing water retention, hyponatraemia, and concentrated urine despite low plasma osmolality
SIADH is caused by excessive, unregulated ADH secretion independent of plasma osmolality, leading to water retention and dilutional hyponatraemia (low blood sodium - most common electrolyte disorder in hospitalised patients). Features: Hyponatraemia (Na+ <135 mmol/L), Low plasma osmolality (100, usually >300 mOsm/kg), Urine Na+ >20 mmol/L (kidneys excreting sodium inappropriately), and No oedema (euvolaemic - total body water up, sodium normal). Causes: Malignancy (small cell lung cancer - most common), CNS disease (meningitis, head injury), Drugs (SSRIs, carbamazepine, cyclophosphamide), and Pulmonary disease (pneumonia, TB). Treatment: Fluid restriction, hypertonic saline (severe), Tolvaptan (vasopressin antagonist).
54
What is meant by tubular maximum (Tm)?
✓ Answer:
B
The maximum rate at which a substance can be reabsorbed (or secreted) by the renal tubules - beyond this, excess appears in urine
Tubular Maximum (Tm) is the maximum transport capacity of the renal tubules for a particular substance - determined by the number of carrier proteins available. When plasma concentration of a substance exceeds the Tm: Carrier proteins become saturated (transport maximum reached) and excess substance cannot be reabsorbed - appears in urine. Classic example: Glucose Tm = ~320 mg/min. Normal filtered glucose = ~125 mg/min (all reabsorbed). When blood glucose > 180 mg/dL (renal threshold) - filtered load exceeds Tm - glucosuria. Tm also applies to tubular secretion (e.g., penicillin, PAH - para-aminohippuric acid - used to measure tubular secretion capacity). The Tm concept explains why certain substances appear in urine only when plasma levels are elevated.
55
What is Fanconi syndrome?
✓ Answer:
B
A generalised dysfunction of the PCT causing failure to reabsorb glucose, amino acids, phosphate, uric acid, and bicarbonate - leading to multiple substances in urine
Fanconi Syndrome is a disorder of generalised PCT dysfunction - the PCT fails to reabsorb multiple substances normally: Glucosuria (with normal blood glucose), Aminoaciduria (amino acids in urine), Phosphaturia - hypophosphataemia - rickets/osteomalacia, Uricosuria (uric acid in urine - low serum uric acid), Bicarbonate wasting - proximal RTA (renal tubular acidosis type 2), and Potassium wasting - hypokalaemia. Causes: Wilson's disease (copper accumulation), Cystinosis (most common in children), Lead poisoning, Multiple myeloma, Tenofovir (HIV medication), and Hereditary fructose intolerance. Treatment: treat underlying cause, supplement lost substances.
56
What is the effect of diuretics on kidney function?
✓ Answer:
B
Diuretics increase urine production by reducing tubular reabsorption of sodium and water at various sites in the nephron
Diuretics are drugs that increase urine output by reducing Na+ (and therefore water) reabsorption. Classification by site of action: Loop diuretics (furosemide/frusemide) - block Na+-K+-2Cl- co-transporter in thick ascending Loop of Henle - most potent - used in heart failure/pulmonary oedema. Thiazides (hydrochlorothiazide) - block Na+-Cl- co-transporter in DCT - used in hypertension/calcium stones. K+-sparing diuretics (spironolactone = aldosterone antagonist; amiloride = ENaC blocker) - acting on DCT/collecting duct - prevent potassium loss - used in heart failure/hyperaldosteronism. Carbonic anhydrase inhibitors (acetazolamide) - act on PCT - used in altitude sickness/glaucoma. Osmotic diuretics (mannitol) - act throughout tubule - used in raised ICP/AKI prevention.
57
What is the function of podocytes in the kidney?
✓ Answer:
B
Specialised epithelial cells that form filtration slits in the glomerular filtration barrier, preventing large proteins from entering the filtrate
Podocytes are highly specialised visceral epithelial cells that form the innermost layer of the Bowman's capsule. Key features: Have octopus-like foot processes (pedicels) that wrap around the glomerular capillaries. The gaps between foot processes = Filtration slits (slit diaphragms). Slit diaphragm protein = Nephrin (encoded by NPHS1 gene) - critical for maintaining the filtration barrier. Podocyte injury/damage > filtration slit effacement > proteinuria. Minimal Change Disease (most common nephrotic syndrome in children): Podocyte foot process effacement - only visible on electron microscopy. Podocytes cannot regenerate well - persistent podocyte injury causes permanent scarring (FSGS).
58
What is renal tubular acidosis (RTA)?
✓ Answer:
B
A group of disorders where the kidney tubules fail to acidify urine properly, causing metabolic acidosis with a normal anion gap
Renal Tubular Acidosis (RTA) is a group of disorders where kidney tubules fail to properly acidify the urine, causing metabolic acidosis (normal anion gap). Type 1 (Distal RTA): DCT/collecting duct fails to secrete H+ - urine pH always >5.5 despite acidosis - nephrocalcinosis, kidney stones (calcium phosphate). Causes: Sjogren's syndrome, SLE, amphotericin B toxicity. Type 2 (Proximal RTA): PCT fails to reabsorb HCO3- - bicarbonate lost in urine. Often part of Fanconi syndrome. Type 4 (Hyperkalaemic RTA): Aldosterone deficiency/resistance - reduced H+ and K+ secretion - hyperkalaemia + acidosis. Common in diabetic nephropathy. All types treated with bicarbonate supplementation.
59
What is meant by renal autoregulation?
✓ Answer:
B
The intrinsic ability of the kidney to maintain relatively constant GFR and renal blood flow despite changes in systemic blood pressure (between 80-180 mmHg)
Renal Autoregulation is the ability of the kidney to maintain constant GFR and renal blood flow over a wide range of systemic blood pressures (approximately 80-180 mmHg) through intrinsic mechanisms: 1) Myogenic mechanism = Rise in blood pressure - afferent arteriole smooth muscle stretches - reflexively constricts - reduces blood flow to maintain constant GFR. 2) Tubuloglomerular Feedback (TGF) = Increased GFR - increased NaCl delivery to macula densa - signals afferent arteriole to constrict - GFR returns to normal. These mechanisms operate independently of nerves and hormones. Outside the autoregulatory range (180 mmHg) - GFR changes with BP. In severe hypotension - oliguria/anuria. Neonates and transplanted kidneys have impaired autoregulation.
60
What is the Bowman's capsule filtration pressure?
✓ Answer:
B
Net filtration pressure = Glomerular hydrostatic pressure minus Capsular hydrostatic pressure minus Blood colloid osmotic pressure
Net Filtration Pressure (NFP) determines the rate of glomerular filtration: NFP = GHP - CHP - BCOP. GHP (Glomerular Hydrostatic Pressure) = ~55 mmHg (pushes fluid OUT of capillaries INTO Bowman's capsule - promotes filtration). CHP (Capsular Hydrostatic Pressure) = ~15 mmHg (pushes back AGAINST filtration - opposes). BCOP (Blood Colloid Osmotic Pressure) = ~30 mmHg (proteins in blood pull water back - opposes filtration). NFP = 55 - 15 - 30 = +10 mmHg (net force favouring filtration). Any condition that reduces GHP (shock, dehydration) or increases CHP (obstruction) reduces filtration and reduces urine output.