Excretory System MCQ for RRB & SSC and other Competitive exams
61
What is the clinical importance of measuring serum urea (BUN - Blood Urea Nitrogen)?
✓ Answer:
B
It reflects kidney function - elevated BUN indicates reduced GFR, dehydration, or increased protein catabolism
BUN (Blood Urea Nitrogen) measures the nitrogen content of urea in blood - a marker of kidney function. Normal BUN: 7-20 mg/dL. Interpretation: Elevated BUN causes = Pre-renal (dehydration, reduced blood flow), Renal failure (AKI, CKD), High protein diet, GI bleeding (blood digested - excess amino acids - urea), Corticosteroids (increase protein catabolism). Low BUN = Liver disease (reduced urea synthesis), malnutrition, pregnancy. BUN:Creatinine ratio (normal = 10:1 to 20:1): >20:1 = Pre-renal AKI (dehydration, haemorrhage, heart failure) and <10:1 = Intrinsic renal disease or liver failure. Together BUN and creatinine are the standard tests for kidney function assessment.
62
What is the significance of the efferent arteriole in kidney physiology?
✓ Answer:
B
It drains blood from the glomerulus and its resistance regulates GFR - constriction increases GFR; dilation decreases GFR
The Efferent Arteriole is the vessel that drains blood OUT of the glomerulus. Its resistance plays a crucial role in regulating GFR: Efferent arteriole constriction (e.g., by Angiotensin II) - increases pressure in glomerular capillaries - increases GFR (blood dammed up in glomerulus). Efferent arteriole dilation - reduces glomerular pressure - decreases GFR. Clinical importance: ACE inhibitors and ARBs (e.g., ramipril, losartan) block Angiotensin II - dilate efferent arteriole - reduce GFR. This is why ACE inhibitors/ARBs are used to protect kidneys in diabetes (reduce proteinuria) but must be used cautiously in renal artery stenosis (may precipitate AKI).
63
What is meant by the term uraemia?
✓ Answer:
B
Accumulation of urea and other nitrogenous waste products in the blood due to kidney failure
Uraemia (uremia) is a clinical syndrome resulting from accumulation of urea and other nitrogenous waste products (creatinine, uric acid, toxins) in the blood due to severe kidney failure (acute or chronic). Symptoms of uraemia: Neurological (confusion, encephalopathy, seizures, coma - uraemic encephalopathy), Cardiovascular (pericarditis - uraemic pericarditis, hypertension), Gastrointestinal (nausea, vomiting, anorexia, uraemic fetor - ammonia/urine smell on breath), Haematological (anaemia, bleeding tendency), and Dermatological (pruritus/itching, uraemic frost - urea crystals on skin). Treatment: Dialysis or kidney transplant. Uraemia is a medical emergency.
64
What is the histological difference between the PCT and DCT?
✓ Answer:
A
PCT is longer and has microvilli (brush border); DCT is shorter with no brush border
Histological differences between PCT and DCT: PCT = longer, narrow lumen (due to cells), brush border PRESENT (microvilli), tall cuboidal cells, abundant mitochondria (high metabolic activity), and major reabsorption function. DCT = shorter, wider lumen, NO brush border, lower cuboidal cells, fewer mitochondria, and fine-tuning function (aldosterone/ADH). The brush border (microvilli) of the PCT dramatically increases surface area for reabsorption - the key identifying feature. On a kidney histology slide, PCT cells appear larger and pinker (more cytoplasm/mitochondria). This is a commonly tested histology question in anatomy and physiology exams.
65
What is nocturia?
✓ Answer:
B
The need to wake up at night to urinate - more than once per night
Nocturia is the complaint of waking from sleep one or more times to void (urinate). It is normal to urinate once at night (especially in elderly), but waking more than once is considered nocturia. Causes: Urological (BPH - benign prostatic hyperplasia - most common in men, overactive bladder, UTI), Cardiac (heart failure - lying down causes redistribution of oedema fluid - increased urine output at night), Renal (CKD - loss of concentrating ability), Metabolic (diabetes mellitus polyuria, diabetes insipidus), Sleep disorders (sleep apnoea - increased ANP secretion - natriuresis), and Excessive evening fluid intake. Common in elderly due to decline in ADH nocturnal surge. Nocturia significantly affects quality of life and sleep.
66
How does the kidney maintain acid-base balance?
✓ Answer:
B
By excreting H+ ions and reabsorbing bicarbonate (HCO3-) in the tubules, and producing ammonia as a buffer
The kidney is the primary regulator of long-term acid-base balance (lungs regulate short-term via CO2): H+ secretion (tubular cells actively secrete H+ into the tubular lumen in PCT, DCT, collecting duct - excreted in urine), HCO3- reabsorption (~85% reabsorbed in PCT - replenishes blood buffers), HCO3- generation (new bicarbonate generated when H+ is buffered by phosphate or ammonia in tubular fluid), and Ammonia buffer (PCT cells produce NH3 from glutamine - combines with H+ - NH4+ excreted in urine). Acidosis = kidneys excrete more H+ and retain more HCO3-. Alkalosis = kidneys excrete more HCO3- and retain H+.
67
What is nephrolithiasis and what are its risk factors?
✓ Answer:
B
Kidney stone disease - risk factors include dehydration, high-calcium diet, hyperuricaemia, recurrent UTIs, and genetic factors
Nephrolithiasis (kidney stones) risk factors: Dehydration (most important) - concentrated urine - crystallisation, Hypercalciuria (excess calcium in urine) - calcium oxalate stones, Hyperuricaemia (gout) - uric acid stones, Recurrent UTIs with urease-producing bacteria (Proteus) - struvite (infection) stones, Hypocitraturia (low citrate - normally inhibits stone formation), High oxalate diet (spinach, nuts, chocolate), Low fluid intake, Genetic factors (cystinuria, hyperoxaluria), and Obesity, high protein diet, sedentary lifestyle. Prevention: High fluid intake (2-3 L/day), dietary modifications, medications based on stone type. First stone by age 30 - 50% chance of recurrence within 10 years.
68
What is renin and where is it produced?
✓ Answer:
B
A proteolytic enzyme produced by juxtaglomerular cells of the kidney that initiates the RAAS cascade to raise blood pressure
Renin is a proteolytic enzyme (aspartyl protease) produced and secreted by the Juxtaglomerular (JG) cells of the afferent arteriole in the kidney. It is the rate-limiting step of the RAAS cascade. Stimuli for renin release: Reduced renal perfusion pressure (hypotension, dehydration, haemorrhage), Decreased NaCl in tubular fluid (detected by macula densa), Sympathetic nervous system activation (via beta-1 receptors), and Decreased blood volume. Renin cleaves angiotensinogen (produced by liver) to Angiotensin I (inactive). Then ACE (in lungs) converts to Angiotensin II (active). Beta-blockers reduce renin release (treating hypertension). Direct renin inhibitors (aliskiren) - newest antihypertensive class.
69
What is a kidney transplant?
✓ Answer:
B
Surgical implantation of a healthy donor kidney into a patient with end-stage renal disease
Kidney (Renal) Transplant is the best treatment for End Stage Renal Disease (ESRD), offering better quality of life and longer survival than dialysis. Key points: The donor kidney is placed in the iliac fossa (pelvis) - NOT where native kidneys are (they are usually left in place unless causing problems). Donor options: Living donor (related or unrelated) or Deceased (cadaveric) donor. HLA (Human Leukocyte Antigen) matching reduces rejection risk. Patient needs lifelong immunosuppression to prevent rejection (tacrolimus, mycophenolate, steroids). The new ureter is connected to the bladder. Success rate: 1-year graft survival ~95% (living donor).
70
What is the role of parathyroid hormone (PTH) in kidney function?
✓ Answer:
B
PTH increases calcium reabsorption in the DCT and collecting duct, and increases phosphate excretion (phosphaturia)
Parathyroid Hormone (PTH) produced by the parathyroid glands has important effects on the kidney: Increases Ca2+ reabsorption in DCT and collecting duct (reduces calcium in urine - hypocalciuria), Decreases phosphate reabsorption in PCT (increases phosphate in urine - phosphaturia), and Activates Vitamin D (1-alpha hydroxylase in PCT converts 25-OH-D3 to 1,25-(OH)2-D3 = Calcitriol - active form - increases intestinal calcium absorption). Net effect: Raises blood calcium, lowers blood phosphate. Hyperparathyroidism > excess PTH > hypercalciuria > kidney stones, nephrocalcinosis. Hypoparathyroidism > low PTH > hypocalcaemia > tetany, seizures.