Renal – 2016

✅ Metabolic acidosis
The primary acid-base disturbance is a severe metabolic acidosis (low pH, low HCO₃⁻), which is appropriately compensated by respiratory alkalosis (low PCO₂).

Step-by-Step ABG Analysis:

1. Assess the pH (7.1): This is acidemia (pH < 7.35). This tells us the primary process is an acidosis.
2. Determine the Primary Process:
   • HCO₃⁻ (10 mmol/L): This is low (normal range 22-26), indicating a metabolic acidosis.
   • PCO₂ (16 mmHg): This is low (normal range 35-45), which would normally indicate a respiratory alkalosis. However, in the context of acidemia, this low PCO₂ is a compensatory response.
3. Check for Compensation:
   • For a metabolic acidosis, the expected respiratory compensation is PCO₂ = (1.5 × HCO₃⁻) + 8 ± 2 (Winter’s formula).
   • Expected PCO₂ = (1.5 × 10) + 8 = 15 + 8 = 23 ± 2 mmHg (range 21-25 mmHg).
   • The measured PCO₂ is 16 mmHg, which is lower than the expected range. This indicates that in addition to the full metabolic compensation, there is also a primary respiratory alkalosis contributing to the picture. This is a common finding in mixed acid-base disorders, often seen in conditions like sepsis or salicylate poisoning.
4. Evaluate the pO₂ (65 mmHg): This is hypoxemia (pO₂ < 80 mmHg), which is a significant clinical finding. Hypoxemia can be a potent stimulator of respiratory drive, explaining the “over-compensation” with a very low PCO₂.

Clinical Correlation: The patient is a young male with altered consciousness and hypoxemia. This ABG is classic for a severe metabolic acidosis with appropriate respiratory compensation and a superimposed primary respiratory alkalosis likely driven by hypoxemia. A common scenario causing this mixed picture could be:

• Salicylate (Aspirin) Poisoning: Aspirin directly stimulates the respiratory center (causing primary respiratory alkalosis) and also causes an anion gap metabolic acidosis. Altered consciousness is a key feature of toxicity.
• Sepsis/Severe Infection: Can lead to lactic acidosis (metabolic acidosis) and hypoxemia-driven hyperventilation.
• Diabetic Ketoacidosis (DKA) with Pneumonia: DKA causes the metabolic acidosis, and pneumonia could cause the hypoxemia and further hyperventilation.

Explanation of the Incorrect Options

❌ Uncompensated respiratory acidosis
This would present with a low pH and a high PCO₂, with a normal or only slightly elevated HCO₃⁻. Our ABG shows a low PCO₂ and a very low HCO₃⁻, which is the opposite pattern.

❌ Compensated respiratory alkalosis
*A compensated respiratory alkalosis would have a normal or near-normal pH. The primary disturbance would be a low PCO₂, and the compensation would be a low HCO₃⁻. However, in this case, the pH is 7.1, which is severely acidemic. This means the low bicarbonate is the primary problem, not the compensation.*

❌ Respiratory alkalosis
This would be the primary diagnosis if the pH were alkalemic (high) with a low PCO₂. Here, the pH is acidemic, so the low PCO₂ must be a compensatory mechanism for a primary metabolic acidosis.

❌ Renal failure
*While renal failure is a common cause of metabolic acidosis (due to the inability to excrete acid), it is not the best answer. This ABG shows a specific mixed disorder (metabolic acidosis + respiratory alkalosis) that points to an extra-renal cause like salicylate poisoning or sepsis. Renal failure alone would typically cause a simple metabolic acidosis with appropriate respiratory compensation (PCO₂ would be ~24 mmHg, not 16 mmHg).*

✅ Acidosis
Renal glutaminase activity increases in metabolic acidosis to generate ammonia for H⁺ excretion.

Explanation:

• Glutaminase in the proximal tubular cells converts glutamine → glutamate + NH₃ (ammonia).

• Ammonia binds to H⁺ in the tubular fluid → NH₄⁺ (ammonium), which is excreted in urine.

• This process allows the kidney to excrete excess acid while regenerating bicarbonate (HCO₃⁻) for the blood.

• Therefore, renal glutaminase activity rises significantly during acidosis, not in alkalosis or shock.

Explanation of the Incorrect Options

❌ Hemorrhage
Leads to RAAS activation and sodium/water retention, not increased glutaminase activity.

❌ Alkalosis
Glutaminase activity decreases in alkalosis because less H⁺ needs to be excreted.

❌ Shock
Involves hypoperfusion and lactic acidosis, but the direct renal enzyme response is tied specifically to acidosis, not shock itself.

❌ All of these
Incorrect, because glutaminase specifically increases in acidosis only.

✅ Aldosterone
Aldosterone increases sodium reabsorption in the distal nephron, especially important after hemorrhage to restore volume.

Explanation:

• After hemorrhage, blood volume and blood pressure drop.

• This activates the renin–angiotensin–aldosterone system (RAAS).

• Aldosterone, secreted by the zona glomerulosa of the adrenal cortex, enhances sodium reabsorption (and K⁺ secretion) in the distal tubule and collecting duct.

• Sodium reabsorption draws water osmotically, helping restore blood volume.

Explanation of the Incorrect Options

❌ Atrial natriuretic peptide (ANP)
Does the opposite — promotes sodium excretion; it would worsen hypovolemia.

❌ None of these
Incorrect, because aldosterone clearly mediates sodium reabsorption here.

❌ Vasopressin (ADH)
Mainly increases water reabsorption, not sodium reabsorption.

❌ Epinephrine
Causes vasoconstriction and increased cardiac output; not the primary hormone for sodium reabsorption.

✅ Potassium
Hyperkalemia directly stimulates aldosterone secretion from the adrenal cortex.

Explanation:

• Aldosterone, secreted by the zona glomerulosa of the adrenal cortex, regulates sodium and potassium balance.

• Major stimuli for aldosterone release:

  • ↑ Serum potassium (direct stimulus).

  • ↓ Sodium levels (minor effect).

  • Activation of the renin–angiotensin–aldosterone system (RAAS) via angiotensin II.

• Increased potassium strongly stimulates aldosterone secretion to enhance potassium excretion and sodium reabsorption in the distal nephron.

Explanation of the Incorrect Options

❌ Chloride
Does not play a significant role in aldosterone regulation.

❌ Hydrogen
Aldosterone promotes H⁺ secretion, but H⁺ levels themselves do not directly regulate its release.

❌ Sodium
A fall in sodium can stimulate aldosterone indirectly via RAAS, but an increase in sodium does not trigger secretion.

❌ Water
Volume changes (via RAAS/ADH) may influence aldosterone indirectly, but increased water intake does not directly stimulate it.

✅ 70%
*Lean body mass (LBM), which includes muscles, organs, and bones, has a very consistent and high water content of approximately 70-75%.*

The human body’s total water content varies based on body composition. The key distinction is between:

• Lean Body Mass (LBM): This encompasses all non-fat tissues in the body—skeletal muscle, organs, blood, and bone. These tissues are metabolically active and have a high water content. The water within cells (intracellular fluid) makes up a large portion of this.
• Fat Mass (Adipose Tissue): Fat tissue is relatively metabolically inert and contains very little water (approximately 10-20%).

Because muscle and organs are rich in water, the more lean mass a person has, the higher their total body water percentage will be. The figure 70-75% is a well-established physiological constant for the water content of lean body mass. This is why a muscular, lean individual will have a higher total body water percentage (~60-65%) than an obese individual (~45-50%), whose body composition includes a larger proportion of low-water fat tissue.

The commonly cited average total body water of ~60% for a reference adult male is a generalization that assumes an average ratio of lean to fat mass.

Explanation of the Incorrect Options

❌ None of these
*This is incorrect because one of the provided options (70%) is the correct and well-accepted value.*

❌ 90%
*This value is too high. While some individual organs like the brain (~75%) or blood plasma (~92%) have very high water content, the average across all lean tissues (which also include denser tissues like bone) is closer to 70-75%, not 90%.*

❌ 60%
This is a common figure, but it refers to the average total body water as a percentage of total body weight for a standard adult male, not the specific percentage within lean mass itself. It accounts for the presence of fat.

❌ 50%
This value is too low and is closer to the total body water percentage often seen in older adults or females, who typically have a higher body fat percentage and thus a lower overall water content. It does not reflect the hydration of lean tissue.

✅ Benzidine test
The benzidine test is a classical chemical test used to detect blood (hemoglobin) in urine or stool.

Explanation:

• The benzidine test detects the presence of hemoglobin in urine (hematuria or hemoglobinuria) by a peroxidase-like reaction of hemoglobin.

• Modern urinalysis often uses dipstick reagent strips, but the benzidine test is historically well-known.

• A positive result indicates blood in urine, which can be due to infection, stones, tumors, or glomerular disease.

Explanation of the Incorrect Options

❌ Chromatography
Used for separation and analysis of compounds, not specifically for detecting blood in urine.

❌ None of these
Incorrect, because benzidine test does detect blood.

❌ Benedict test
Detects reducing sugars (like glucose), not blood.

❌ Emulsion test
Detects lipids, not blood.

✅ Hypoxanthine-guanine phosphoribosyltransferase (HGPRT) enzyme
Lesch-Nyhan syndrome is caused by a deficiency of HGPRT, leading to impaired purine salvage.

Explanation:

• HGPRT normally salvages hypoxanthine and guanine by converting them back into IMP and GMP using PRPP.

• In Lesch-Nyhan syndrome, absence of HGPRT → purine salvage is defective → excess PRPP and de novo purine synthesis.

• This leads to hyperuricemia, gout, kidney stones, and neurological/behavioral symptoms (self-mutilation, choreoathetosis).

Explanation of the Incorrect Options

❌ Inosine monophosphate dehydrogenase
Catalyzes IMP → XMP in purine synthesis; not defective in Lesch-Nyhan.

❌ Guanine monophosphate synthase
Converts XMP → GMP; not affected in this disease.

❌ Xanthine oxidase
Converts hypoxanthine → xanthine → uric acid; inhibited by allopurinol, but deficiency is not linked to Lesch-Nyhan.

❌ None of these
Incorrect, because HGPRT is the enzyme involved.

✅ Urinary tract infection
Nitrites in urine indicate bacterial conversion of nitrates to nitrites, suggesting a UTI.

Explanation:

• Certain Gram-negative bacteria (e.g., E. coli, Klebsiella, Proteus) contain nitrate reductase, which reduces dietary nitrates in urine to nitrites.

• A positive nitrite test on urinalysis is therefore a strong indicator of a bacterial urinary tract infection (UTI).

• Viral infections, kidney stones, or hydronephrosis do not produce nitrites.

Explanation of the Incorrect Options

❌ Viral infection
Viruses do not convert nitrates to nitrites; urinalysis nitrite test will remain negative.

❌ Hydronephrosis
Represents obstruction/dilation of renal pelvis; not associated with nitrite production.

❌ None of these
Incorrect, because nitrites clearly indicate UTI.

❌ Kidney stones
May cause hematuria or obstruction but not nitrite production.

✅ Aspartate
Aspartate donates an amino group in the reaction converting IMP to AMP.

Explanation:

• In purine nucleotide biosynthesis, IMP (inosine monophosphate) is the branch point for AMP and GMP synthesis.

• To form AMP, IMP is first converted to adenylosuccinate by adenylosuccinate synthetase, using aspartate as the nitrogen donor.

• Adenylosuccinate is then cleaved by adenylosuccinate lyase to yield AMP and fumarate.

This step ensures that AMP synthesis requires GTP as an energy source and aspartate as the amino group donor.

Explanation of the Incorrect Options

❌ Carbon dioxide
Used earlier in purine synthesis (e.g., in carboxylation steps), not in the conversion of IMP to AMP.

❌ Glutamate
Glutamine (not glutamate) donates nitrogen at other steps, but not here.

❌ Glycine
Incorporated into the purine ring during the early steps of de novo synthesis, not at the IMP → AMP branch.

❌ Water
Not a nitrogen donor in this reaction.

✅ Xanthine oxidase
Xanthine oxidase catalyzes the oxidation of hypoxanthine to xanthine, and further to uric acid.

Explanation:
In purine catabolism, hypoxanthine is first oxidized to xanthine, and then xanthine is oxidized to uric acid.

• Both steps are catalyzed by xanthine oxidase, a molybdenum-containing enzyme.

• This pathway is clinically relevant because excess uric acid leads to gout.

• Drugs like allopurinol inhibit xanthine oxidase, reducing uric acid formation.

Explanation of the Incorrect Options

❌ Xanthine dehydrogenase
A related enzyme form, but in humans, the main conversion is through xanthine oxidase.

❌ Xanthine hydrogenase
Not an enzyme recognized in purine metabolism.

❌ Xanthine synthase
Not involved in this pathway; no such enzyme in standard purine degradation.

❌ None of these
Incorrect, because xanthine oxidase is the correct answer.

✅ Mid-stream urine
Mid-stream collection avoids contamination from the external genitalia and urethra, providing the most reliable sample.

Explanation:
For urine analysis (especially culture and sensitivity), a mid-stream clean-catch sample is preferred.

• The initial stream flushes out contaminants from the urethra.

• The mid-stream portion represents bladder urine, least likely to be contaminated.

• The end stream may include epithelial cells and debris.

This method reduces false positives in microbiological tests and improves diagnostic accuracy.

Explanation of the Incorrect Options

❌ From the start till the end
Would include contaminants from urethra and external genitalia → less reliable.

❌ Start urine
Contains urethral flora, increasing contamination risk.

❌ End urine
May contain sediment, epithelial cells, and contaminants.

❌ None of these
Incorrect, because mid-stream is indeed the correct answer.

✅ Bicarbonate buffer
The bicarbonate–carbonic acid buffer system is the most important extracellular buffer that maintains blood pH around 7.4.

Explanation:
The bicarbonate buffer system (H₂CO₃ / HCO₃⁻) is the primary regulator of blood pH because:

• Its pKa (6.1) is close enough to physiological pH (7.4) to be effective.

• It is an open system: CO₂ (acid component) can be exhaled by the lungs and bicarbonate (base component) can be regulated by the kidneys.

• This dual regulation makes it highly adaptable to maintain homeostasis.

Explanation of the Incorrect Options

❌ Phosphate buffer
Important in the intracellular fluid and renal tubules, but not the main buffer in plasma.

❌ Chloride buffer
Chloride shift (Hamburger phenomenon) helps in RBCs, but it is not the dominant systemic buffer.

❌ Hydrogen buffer
Not a recognized physiological buffer system.

❌ Protein buffer
Proteins (especially hemoglobin) play an important role inside RBCs, but systemically, bicarbonate is the strongest.

✅ Hypertension
Hypertension is a feature of nephritic syndrome, not classically of nephrotic syndrome.

Nephrotic syndrome is characterized by:

• Massive proteinuria (>3.5 g/day)

• Hypoalbuminemia (due to protein loss)

• Generalized edema (due to low oncotic pressure)

• Hyperlipidemia and lipiduria (compensatory hepatic lipoprotein synthesis)

Hypertension is a hallmark of nephritic syndrome (due to salt and water retention from reduced GFR and inflammatory damage).

Explanation of the Incorrect Options

❌ Hypoalbuminuria
Correct phenomenon, though better phrased as hypoalbuminemia; results from proteinuria.

❌ Hyperlipidemia
Present in nephrotic syndrome due to increased hepatic lipoprotein synthesis.

❌ Proteinuria
A defining feature of nephrotic syndrome (>3.5 g/day).

❌ Edema
Generalized and severe, due to low plasma oncotic pressure.

❌ Hypertension
Correct — this belongs more to nephritic syndrome, not nephrotic.

✅ 250–750 mg
Normal daily urinary uric acid excretion is about 250–750 mg.

Uric acid is the end product of purine metabolism in humans. Normally, the body produces around 600–1000 mg of uric acid per day, of which ~2/3 is excreted by the kidneys (in urine) and ~1/3 through the gut.
Thus, urinary excretion falls within the range of 250–750 mg/day. Excretion above this level may indicate hyperuricosuria, a risk factor for uric acid stones or gout.

Explanation of the Incorrect Options

❌ 1000–1200 mg
Too high for normal; this would suggest overproduction or reduced gut clearance.

❌ 800–1000 mg
Also above the normal range; could occur in disorders of purine metabolism.

❌ 100–200 mg
Too low for normal; may suggest reduced production or impaired renal handling.

❌ 1–100 mg
Far below normal; not physiologically typical.

✅ Seminal vesicle
Seminal vesicles develop from the mesonephric (Wolffian) ducts, not the urogenital sinus.

The urogenital sinus gives rise to:

• Urinary bladder

• Prostatic urethra and prostate gland

• Membranous and penile urethra in males

• Bulbourethral (Cowper’s) glands

In females, it contributes to the lower vagina and vestibular glands.

The seminal vesicle, however, is derived from an outgrowth of the mesonephric duct, which is distinct from the urogenital sinus.

Explanation of the Incorrect Options

❌ Bulbourethral gland
Derived from the urogenital sinus (outgrowth of spongy urethra).

❌ Urinary bladder
Formed from the upper part of the urogenital sinus (except the trigone, which comes from mesonephric ducts).

❌ Prostate gland
Formed from endodermal outgrowths of the prostatic urethra (urogenital sinus derivative).

❌ Penile urethra
Derived from the phallic part of the urogenital sinus.

❌ Seminal vesicle
Correct — comes from the mesonephric duct, not the urogenital sinus.

✅ Oversecretion of antidiuretic hormone
Excess ADH increases water reabsorption in the collecting ducts, leading to highly concentrated urine with high osmolality.

Antidiuretic hormone (ADH/vasopressin) acts on collecting ducts via V₂ receptors to insert aquaporin-2 water channels. With oversecretion, water is reabsorbed excessively, reducing urine volume and concentrating the solutes left behind. This results in urine osmolality reaching up to 1200 mOsm/L in humans.

Explanation of the Incorrect Options

❌ Non-functioning adrenal gland
May cause electrolyte imbalances (e.g., low aldosterone → salt wasting, hyperkalemia), but not directly high urine osmolality.

❌ Diabetes insipidus
Characterized by lack of ADH effect, leading to dilute urine with low osmolality.

❌ High water intake
Leads to dilute urine (low osmolality), not concentrated urine.

❌ Low sodium
Affects plasma osmolality and fluid balance, but does not directly explain high urine osmolality.

✅ Spironolactone
It is a potassium-sparing diuretic that can lead to hyperkalemia.

Spironolactone is an aldosterone antagonist that works in the collecting ducts. By inhibiting aldosterone, it reduces sodium reabsorption and potassium excretion. This potassium retention can lead to hyperkalemia, especially in patients with renal impairment or when combined with ACE inhibitors/ARBs.

Explanation of the Incorrect Options

❌ Trichlormethiazide
A thiazide diuretic that causes potassium loss → hypokalemia, not hyperkalemia.

❌ Chlorothiazide
Also a thiazide, increases potassium excretion → hypokalemia.

❌ Furosemide
A loop diuretic that increases potassium excretion, leading to hypokalemia.

❌ Bumetanide
Another loop diuretic with the same effect as furosemide → hypokalemia.

✅ Uric acid stone
Uric acid stones are the most common radiolucent urinary stones.

Most urinary stones (e.g., calcium oxalate, calcium phosphate, struvite) are radiopaque, appearing clearly on plain X-ray.

• Uric acid stones are radiolucent (not visible on X-ray) but can be detected by ultrasound or CT scan.

• They are associated with conditions such as gout, myeloproliferative disorders, high cell turnover, and acidic urine.

Explanation of the Incorrect Options

❌ Ammonium magnesium phosphate (struvite)
Radiopaque; typically associated with infection by urease-producing bacteria (e.g., Proteus).

❌ Calcium phosphate
Radiopaque; visible on X-ray.

❌ Calcium oxalate
Most common type overall, but radiopaque, not radiolucent.

❌ Cystine stone
Faintly radiopaque, but not purely radiolucent; detectable on imaging.

Step-by-Step Reasoning

1. Where do stones form?

• Renal calculi typically form from supersaturation of salts in the urine.

• Common sites include:

  • Renal calyces → stones often lodge here.

  • Renal pelvis → stones may form or accumulate here.

  • Ureter → stones pass and may get stuck in narrow segments.

  • Bladder → can form secondary stones, often from stasis or catheters.

2. Nephron

• The nephron (PCT, loop of Henle, DCT) is microscopic and part of tubular urine formation.

• Stones cannot form here because there is continuous flow and very small tubular diameter, preventing crystal aggregation.

3. Check other options

• Bladder → can form stones in stasis conditions. ❌

• Calyces → common site for stone formation. ❌

• Pelvis → common site for stones. ❌

• Ureter → common site for stone obstruction. ❌

Correct Answer: Nephron ✅

Step-by-Step Reasoning

1. Adenine phosphoribosyltransferase (APRT) reaction

• APRT is part of the purine salvage pathway.

• It catalyzes:

Adenine+PRPP⟶AMP+PPiAdenine+PRPP⟶AMP+PPi

• Here, PRPP (phosphoribosyl pyrophosphate) donates the ribose-5-phosphate to adenine to form AMP.

2. Check other options

• Hexose monophosphate shunt → produces NADPH and ribose-5-phosphate but is not directly the donor in this reaction. ❌

• Carbon dioxide → unrelated. ❌

• Dihydrofolate → cofactor in thymidylate synthesis, not APRT reaction. ❌

• Adenosine → substrate/product? Adenine is the substrate; adenosine is not a donor. ❌

Correct Answer: Phosphoribosyl diphosphate (PRPP) ✅

✅ Minimal change disease
This is the classic presentation of Minimal Change Disease (MCD) in a child: nephrotic syndrome (edema, proteinuria) with selective proteinuria, absence of hematuria or casts, and a rapid response to steroid therapy.

Minimal Change Disease (MCD) is the most common cause of nephrotic syndrome in children aged 2-6 years. The diagnosis is strongly supported by the classic clinical triad presented in this case:

1. Clinical Presentation: The patient presents with the hallmark signs of nephrotic syndrome: periorbital edema (“swelling around the eyes”), generalized puffiness (anasarca), and lethargy (due to possible hypovolemia or general illness).
2. Urinalysis Findings:
   • Selective Proteinuria: This refers to the loss of predominantly lower molecular weight proteins (like albumin) while larger proteins are retained. This is a classic feature of MCD.
   • No Hematuria or Casts: The absence of red blood cells and casts is a key differentiator from other glomerulonephritides (like IgA nephropathy or PSGN) which typically present with an active urinary sediment (hematuria, casts).
3. Response to Therapy: A dramatic improvement with corticosteroid therapy is a defining characteristic of MCD. Over 90% of children with MCD will respond within 2-4 weeks of starting steroids.

Pathophysiology: The disease is called “minimal change” because the glomeruli appear normal under a light microscope. The defect is only visible under an electron microscope, which reveals effacement of the podocyte foot processes. This disrupts the glomerular filtration barrier, leading to massive proteinuria.

Explanation of the Incorrect Options

❌ Focal segmental glomerulosclerosis (FSGS)
FSGS can also present with nephrotic syndrome but is more common in older children and adults. It often presents with non-selective proteinuria and is frequently steroid-resistant, meaning the patient in this case would not have improved rapidly with steroids. Hypertension and renal impairment are also more common.

❌ Acute tubular necrosis (ATN)
ATN is a cause of acute kidney injury (AKI), not nephrotic syndrome. It is characterized by elevated BUN/Creatinine and often muddy brown granular casts on urinalysis. It does not typically present with significant selective proteinuria or periorbital edema as the primary feature.

❌ Membranous nephropathy
*This is a common cause of nephrotic syndrome in adults, not children. While it presents with proteinuria, it is often associated with a high risk of thrombosis and is less responsive to steroids alone. It would be a very unusual diagnosis for a 6-year-old.*

❌ IgA nephropathy (Berger’s disease)
This is the most common primary glomerulonephritis worldwide. Its hallmark presentation is macroscopic hematuria that often occurs concurrently with an upper respiratory tract infection (“sympharyngitic hematuria”). The urinalysis would almost always show red blood cells and casts, which are explicitly stated to be absent in this case.

✅ Post-streptococcal glomerulonephritis
Classic presentation: child, cola-colored urine, hypertension, recent streptococcal throat infection (2–3 weeks prior), and RBC casts.

Post-streptococcal glomerulonephritis (PSGN) is an immune complex-mediated nephritic syndrome. It typically develops 1–3 weeks after a streptococcal infection (throat or skin). Hallmarks include:

• Cola/tea-colored urine (hematuria).

• Hypertension.

• Oliguria.

• Red blood cell casts in urine.

• Common in children, but can occur in adults.

Explanation of the Incorrect Options

❌ Goodpasture’s syndrome
Presents with hematuria and hemoptysis due to anti-GBM antibodies; not typically post-strep, and involves pulmonary symptoms.

❌ Membranous nephropathy
Causes nephrotic syndrome (heavy proteinuria, edema, hyperlipidemia), not a classic post-strep nephritic picture.

❌ IgA nephropathy (Berger’s disease)
Causes recurrent hematuria that occurs within days of a respiratory or GI infection (synpharyngitic hematuria), not weeks later.

❌ Alport syndrome
Hereditary nephritis with sensorineural hearing loss and ocular defects; not linked to post-infectious cases.

Step-by-Step Reasoning

1. SCID overview

• SCID is a group of genetic disorders causing severe impairment of T-cell development, often affecting B-cells and sometimes NK cells.

• Leads to combined immunodeficiency (cell-mediated + humoral immunity).

2. Common causes of SCID

• X-linked SCID → mutation in common gamma chain (γc) of cytokine receptors; affects T-cell and NK-cell development.

• Autosomal SCID → mutation in adenosine deaminase (ADA) → toxic accumulation of deoxyadenosine → lymphocyte death.

• Other genes: RAG1/RAG2, JAK3.

3. Check each option

• Bruton tyrosine kinase (Btk) → deficient in X-linked agammaglobulinemia (XLA), primarily B-cell defect. ❌

• Lymphocyte receptor → vague; SCID involves signaling defects but this is too general. ❌

• Adenosine deaminase (ADA) → ✅ deficiency causes one common form of SCID.

• WASP gene → defective in Wiskott-Aldrich syndrome, not SCID. ❌

• None of these → incorrect; ADA deficiency is a known cause. ❌

Correct Answer: Adenosine deaminase ✅

Clinical Correlation

• ADA deficiency SCID: accumulation of deoxyadenosine → toxic to lymphocytes → T⁻ B⁻ NK⁻ phenotype.

✅ Pylorus
The pylorus lies anterior to the left side of the midline (mainly in relation to the stomach and duodenum), not directly in front of the right kidney.

The anterior relations of the right kidney are:

• Superiorly: right suprarenal gland & liver.

• Medially: 2nd part of duodenum.

• Inferolaterally: right colic (hepatic) flexure of colon.
  Thus, the liver, duodenum (2nd part), and hepatic flexure are all in front of the right kidney. The pylorus, however, is more midline and associated with the stomach/duodenum transition, so it is not an anterior relation of the right kidney.

Explanation of the Incorrect Options

❌ 2nd part of duodenum
Yes, directly anterior to the medial border of the right kidney.

❌ Right colic flexure / Hepatic flexure
The right (hepatic) colic flexure lies anterior to the lower part of the right kidney.

❌ Liver
Covers the upper anterior part of the right kidney.

❌ Pylorus
Correct — it is not an anterior relation of the right kidney.

✅ Antidiuretic hormone
ADH primarily regulates water reabsorption and plasma osmolarity, with no direct role in controlling potassium (K⁺) secretion or excretion.

Potassium excretion is a tightly regulated process primarily occurring in the distal nephron (distal convoluted tubule and collecting duct). The key mechanism is the secretion of K⁺ into the tubule by principal cells, which is influenced by several hormonal and physiological factors. Let’s analyze the role of each:

• Aldosterone: This is the primary regulator of potassium excretion. It is secreted by the adrenal cortex in response to high plasma K⁺ levels. Aldosterone increases the activity of Na⁺/K⁺ ATPase pumps on the basolateral side of principal cells and opens apical Na⁺ and K⁺ channels. This enhances Na⁺ reabsorption and, critically, drives K⁺ secretion into the tubular lumen for excretion.
• Angiotensin II: This potent vasoconstrictor stimulates the release of aldosterone from the adrenal glands. Therefore, by increasing aldosterone levels, the Renin-Angiotensin-Aldosterone System (RAAS) indirectly promotes potassium excretion.
• Intracellular K⁺ Concentration: The secretion of K⁺ is a direct function of its intracellular concentration within the principal cells. A higher intracellular K⁺ concentration creates a steeper diffusion gradient, facilitating the movement of K⁺ from the cell into the tubular lumen. Dietary K⁺ intake rapidly influences this intracellular pool.
• Insulin: Insulin promotes the shift of potassium from the extracellular fluid into cells (e.g., liver and muscle cells) by stimulating the Na⁺/K⁺ ATPase pump. By lowering plasma K⁺ levels, it indirectly reduces the stimulus for aldosterone release and K⁺ excretion.

Antidiuretic hormone (ADH or vasopressin), in contrast, is secreted by the posterior pituitary in response to high plasma osmolarity or low blood volume. Its main actions are:

1. Inserting aquaporin-2 water channels in the collecting duct to increase water reabsorption.
2. Acting as a vasoconstrictor.
   While some evidence suggests ADH might have a minor stimulatory effect on K⁺ secretion, this is negligible and not physiologically significant. Its primary and overwhelming role is in water balance, not potassium homeostasis.

Explanation of the Incorrect Options

❌ Intracellular concentration of potassium
This directly affects excretion. A higher intracellular K⁺ concentration in principal cells of the distal nephron creates the gradient necessary for K⁺ secretion into the urine.

❌ Aldosterone
This is the most important hormone controlling potassium excretion. It directly upregulates the pumps and channels in the distal nephron to stimulate K⁺ secretion.

❌ Angiotensin
Angiotensin II, a key component of RAAS, stimulates aldosterone release. Therefore, it has a significant indirect effect on increasing potassium excretion.

❌ Insulin
Insulin causes a shift of K⁺ from the blood into cells, lowering plasma K⁺ levels. This reduction directly decreases the drive for K⁺ excretion by reducing the stimulus for aldosterone secretion.

Step-by-Step Reasoning

1. Salvage pathway overview

• The salvage pathway is a metabolic route in which free bases (purines and pyrimidines) are recycled to form nucleotides, instead of being synthesized de novo.

• This pathway is energy-efficient compared to de novo synthesis.

2. Function and benefit

• Ensures a continuous supply of nucleotides for DNA/RNA synthesis even when de novo synthesis is slow or energy-limited.

• Helps conserve energy and resources in the cell.

3. Check each option

• Provides continuous supply of nucleotides → ✅ correct, matches main purpose.

• Provides continuous supply of nucleic acid → incorrect; nucleic acids are polymers, salvage pathway supplies monomeric nucleotides, not polymeric nucleic acids. ❌

• Increases production of nucleic acid → indirect effect; not primary benefit. ❌

• Increases degradation of nucleotides → opposite function. ❌

• Increases synthesis of nucleotides → partially correct but de novo synthesis is separate; salvage recycles existing bases. ❌

Correct Answer: Provides continuous supply of nucleotides ✅

✅ Respiratory acidosis and respiratory alkalosis
You cannot have both hypoventilation (causing respiratory acidosis) and hyperventilation (causing respiratory alkalosis) occurring at the same time.

Mixed acid-base disorders involve two or more primary processes occurring simultaneously, but they must involve different mechanisms.

• A person can have both anion-gap and non-anion gap metabolic acidosis (e.g., diabetic ketoacidosis + diarrhea).

• Respiratory alkalosis and metabolic acidosis can occur together (e.g., salicylate poisoning).

• Metabolic alkalosis and respiratory acidosis can coexist (e.g., COPD with vomiting).
  However, respiratory acidosis and alkalosis cannot coexist, because one requires retention of CO₂ and the other requires excessive loss of CO₂ — two opposite processes in ventilation.

Explanation of the Incorrect Options

❌ Anion-gap acidosis and non-anion gap acidosis
Possible if two different mechanisms of acidosis occur together (e.g., DKA + diarrhea).

❌ Respiratory alkalosis and metabolic acidosis
Possible in salicylate toxicity (early hyperventilation + metabolic acidosis).

❌ Metabolic alkalosis and respiratory acidosis
Possible in COPD with vomiting or diuretic use.

❌ All of these
Incorrect because only one combination (respiratory acidosis + alkalosis) is truly impossible.

Step-by-Step Reasoning

1. Hyperosmolarity of the renal medulla

• The renal medulla has a high osmolarity gradient (up to ~1200 mOsm/L in humans), which is crucial for concentrating urine.

• This gradient is established by the loop of Henle via the countercurrent multiplier system and must be preserved by blood flow that does not wash it out.

2. Role of the vasa recta

• Vasa recta are specialized capillaries running parallel to the loop of Henle.

• Function: countercurrent exchanger

  • They supply blood to medulla without dissipating the osmotic gradient.

  • Water and solutes move in and out, preserving hyperosmolarity.

3. Check other options

• Peritubular capillaries → surround cortical nephrons; minor role in medulla. ❌

• Collecting duct → urine flows through here; it does not maintain medullary osmolarity itself. ❌

• Renal artery → brings blood to kidney; high flow would wash out gradient if not for vasa recta. ❌

• None of these → incorrect.

Correct Answer: Vasa recta ✅

✅ Chronic pyelonephritis
This condition characteristically produces coarse, irregular corticomedullary scars with blunted calyces and flattened papillae.

Chronic pyelonephritis is a long-standing renal infection often due to vesicoureteral reflux or recurrent infections. The kidney develops coarse, asymmetric, corticomedullary scars that overlie blunted and deformed calyces, especially at the upper and lower poles. The papillae become flattened due to repeated inflammation and fibrosis. This contrasts with smooth cortical thinning seen in other chronic kidney diseases.

Explanation of the Incorrect Options

❌ Acute tubular necrosis
Characterized by necrosis of tubular epithelial cells, mainly affecting proximal tubules and thick ascending limb. No scarring or calyceal deformities.

❌ Acute pyelonephritis
Presents with neutrophilic infiltration, abscesses, and suppurative inflammation — no coarse scarring or calyceal blunting in the acute stage.

❌ Hydronephrosis
Leads to dilation of renal pelvis and calyces with thinning of renal cortex, not irregular corticomedullary scars.

❌ Cystitis
An infection of the bladder; does not cause renal scarring or calyceal deformities.

Step-by-Step Reasoning

1. Kidney position

• Kidneys are retroperitoneal organs, situated on the posterior abdominal wall.

• They extend approximately from T12 to L3 vertebral level.

• Right kidney is slightly lower than the left because of the liver.

2. Other vertebral levels

• T4–T12 → thoracic region; mostly thoracic organs (lungs, heart, esophagus). ❌

• L4–L5 → lower lumbar; location of iliac crest, far below kidneys. ❌

• L5–S3 → sacral region; far below kidney. ❌

• S3–S5 → tail end; not relevant. ❌

Correct Answer: T12–L3 ✅

✅ Collecting duct
ADH acts mainly on the collecting ducts by inserting aquaporin-2 channels, increasing water reabsorption.

ADH (vasopressin) binds to V2 receptors on the basolateral membrane of collecting duct cells. This triggers a cAMP–PKA pathway that causes aquaporin-2 water channels to be inserted into the apical membrane. As a result, water moves passively out of the tubule into the hyperosmotic medullary interstitium, concentrating the urine.

Explanation of the Incorrect Options

❌ Proximal convoluted tubule
Reabsorbs ~65–70% of water, but this is obligatory reabsorption (independent of ADH).

❌ Descending limb
Permeable to water but not solutes; water reabsorption here is not under ADH control.

❌ Ascending limb
Impermeable to water, only reabsorbs solutes (Na⁺, K⁺, Cl⁻).

❌ Distal tubule
Some ADH-mediated reabsorption occurs, but the primary site of ADH action is the collecting duct.

Step-by-Step Reasoning

1. Kidney lymphatic drainage

• The kidneys are retroperitoneal and drain lymph primarily to the lateral aortic (para-aortic) lymph nodes along the abdominal aorta.

• From the para-aortic nodes, lymph eventually drains into cisterna chyli and the thoracic duct.

2. Check each option

• External iliac node → drains pelvic organs, not kidneys. ❌

• Common iliac node → drains lower limbs and pelvis, minor role if any. ❌

• Para-aortic node → ✅ main node for kidney lymphatic drainage.

• Celiac node → drains foregut organs (stomach, liver, pancreas, spleen). ❌

• None of these → incorrect.

Correct Answer: Para-aortic node ✅

✅ Ability to dissolve many solutes
Water is called a universal solvent because its polarity allows it to dissolve a wide range of solutes.

Water molecules are polar, with partial positive charges on the hydrogen atoms and a partial negative charge on the oxygen atom. This polarity enables water to interact with and stabilize ions and polar molecules, effectively breaking ionic bonds and surrounding solutes in a hydration shell. This property explains why water dissolves salts, sugars, amino acids, and many other compounds, earning it the title of “universal solvent.”

Explanation of the Incorrect Options

❌ Having strong hydrogen bonds
Hydrogen bonds make water cohesive and give it high boiling and melting points, but they are not the main reason it dissolves solutes.

❌ Ability to split into ions
Water can ionize into H⁺ and OH⁻, but this is not why it is a universal solvent.

❌ Taking any shape
This is a property of liquids in general, not specifically related to solvent capability.

❌ None of these
Incorrect, because water does dissolve many solutes.

Step-by-Step Reasoning

1. Transitional epithelium (urothelium)

• Specialized epithelium found in the renal pelvis, ureters, urinary bladder, and proximal urethra.

• Function: stretchable lining that protects underlying tissue from urine.

2. Mucus glands in submucosa

• Found mainly in the submucosa of urethra and sometimes urinary bladder, providing lubrication and protection against urine’s toxicity.

• These glands are not present in the nephron segments like PCT, DCT, or Loop of Henle.

3. Check each option

• Proximal convoluted tubule → simple cuboidal epithelium, no glands. ❌

• Distal convoluted tubule → simple cuboidal epithelium, no glands. ❌

• Urinary bladder → lined by transitional epithelium; submucosal glands (especially near urethra) present → ✅ correct.

• Loop of Henle → thin segment, simple squamous epithelium, no glands. ❌

• None of these → incorrect.

Correct Answer: Urinary bladder ✅

✅ Uracil
Deamination of cytosine converts it into uracil.

Cytosine can undergo spontaneous deamination, where the amino group (–NH₂) is replaced by a keto group (=O). This converts cytosine into uracil, a base normally found in RNA but abnormal in DNA. If unrepaired, this mutation leads to a G≡C → A=U (or T) transition, which is a common mutational event in DNA.

Explanation of the Incorrect Options

❌ Methyl cytosine
This is a product of DNA methylation, not deamination.

❌ Cytidylic acid
This is a nucleotide (cytidine monophosphate, CMP), not a deamination product.

❌ Tyrosine
An amino acid, unrelated to nucleic acid base deamination.

❌ Adenine
A purine base; cytosine deamination does not yield adenine.

✅ All of these
Hydronephrosis can occur if obstruction happens at any of the classical ureteric narrowing sites.

The ureter has three natural sites of narrowing where obstruction (often by stones) commonly occurs:

1. Pelviureteric junction (PUJ): where the renal pelvis narrows to form the ureter.

2. Pelvic brim: where the ureter crosses over the iliac vessels.

3. Ureterovesical junction (UVJ): where the ureter enters the bladder.

Obstruction at any of these points can lead to urine backup, causing hydronephrosis.

Explanation of the Incorrect Options

❌ Site of attachment with bladder / Ureterovesical junction
Correct site but not the only one; obstruction here is common but answer is broader.

❌ Pelviureteric junction
Yes, this is a major site, but not the only possible obstruction point.

❌ Pelvic brim
Also a classical narrowing, but again not the only site.

❌ All of these (if excluded)
If this option wasn’t present, then the individual sites could be correct, but since it is included, the comprehensive answer is “All of these.”

✅ NK cells, B cells, and T cells
SCID involves profound defects in both humoral (B-cell) and cell-mediated (T-cell) immunity, and in many forms, NK cells are also affected.

Severe combined immunodeficiency (SCID) is a group of genetic disorders characterized by a failure of lymphocyte development. Depending on the genetic mutation (e.g., IL-2 receptor gamma chain defect, adenosine deaminase deficiency, JAK3 mutation), there can be absent or non-functional T cells, B cells, and NK cells.

• T-cell defects → impaired cell-mediated immunity.

• B-cell defects → impaired antibody production (secondary to lack of T-cell help).

• NK-cell defects → due to cytokine signaling pathway mutations (e.g., IL-15 pathway).

Because multiple immune lineages are affected, patients present early with severe recurrent infections, failure to thrive, and require bone marrow transplantation for survival.

Explanation of the Incorrect Options

❌ NK cells and B cells
SCID typically involves T-cell deficiency as a central feature, so excluding T cells is incorrect.

❌ T cells and B cells
Partially correct but incomplete — many SCID variants also include NK-cell loss.

❌ NK cells only
Too limited — SCID is defined by combined deficiencies.

❌ T cells only
Would describe conditions like isolated T-cell immunodeficiency, not SCID.

• T-cell development is always impaired.

• B-cells may or may not be affected depending on the mutation.

• NK-cells may or may not be affected (ADA deficiency affects all three).

✅ 1200 mOsm/L
With maximum ADH action, urine can be concentrated up to about 1200 mOsm/L.

ADH (vasopressin) increases water reabsorption in the collecting ducts by inserting aquaporin-2 channels. When ADH levels are high, water is reabsorbed to the maximum extent, leaving behind highly concentrated urine. The maximal urinary concentration in humans reaches around 1200 mOsm/L, depending on hydration status and medullary gradient.

Explanation of the Incorrect Options

❌ 200 mOsm/L
Represents dilute urine, typical when ADH is absent or low, not when it is high.

❌ 100 mOsm/L
This is the minimum osmolarity of urine (maximally dilute), occurring with very low ADH levels.

❌ 400 mOsm/L
Intermediate concentration — possible with partial ADH activity but not the maximum.

❌ 600 mOsm/L
Also an intermediate value; maximum concentration is much higher under full ADH effect.

Step-by-Step Reasoning

1. ANP overview

• Hormone secreted by atrial myocytes in response to atrial stretch / increased blood volume.

• Main effect: natriuresis (increased Na⁺ excretion) and diuresis (increased water excretion) to reduce blood volume and blood pressure.

2. Mechanism

• Hemodynamic effect:

  • ANP dilates afferent arterioles and constricts efferent arterioles → increases glomerular hydrostatic pressure → increases GFR → more filtrate → more sodium excretion.

• Tubular effect:

  • Inhibits Na⁺ reabsorption in collecting duct by reducing Na⁺ channels (ENaC) → increases Na⁺ excretion.

3. Check options

• Causes vasodilation of afferent arterioles → ✅ partially correct (part of increasing GFR).

• Decreases GFR → ❌ opposite effect; GFR actually rises.

• Increases GFR → ✅ correct, direct effect causing natriuresis.

• Decreases Na⁺ channels in principal cells → ✅ also contributes to sodium loss.

• Constricts efferent arterioles → ✅ contributes to increased GFR.

Best single answer in MCQs: the primary mechanism is increasing GFR, so: Increases glomerular filtration rate (GFR) ✅

Correct Answer: Increases glomerular filtration rate (GFR) ✅

✅ Glutamine
Glutamine donates nitrogen atoms in both purine and pyrimidine nucleotide synthesis.

Glutamine acts as a nitrogen donor in multiple enzymatic reactions.

• In purine synthesis, glutamine donates nitrogen at the N3 and N9 positions.

• In pyrimidine synthesis, glutamine donates nitrogen for the carbamoyl phosphate (via carbamoyl phosphate synthetase II).

This dual role makes glutamine unique compared to other amino acids in nucleotide biosynthesis.

Explanation of the Incorrect Options

❌ None of these
Incorrect, because glutamine indeed contributes nitrogen in both pathways.

❌ Aspartate
Aspartate contributes nitrogen, but only to a limited extent: it provides N1 in purine rings and contributes to pyrimidine rings. However, it is not involved in both pathways as extensively as glutamine.

❌ Glycine
Important for purine synthesis (provides C4, C5, N7) but not for pyrimidine synthesis.

❌ Valine
Not involved in nucleotide base synthesis. It plays a role in protein synthesis and metabolism, not nitrogen donation here.

Step-by-Step Reasoning

1. Kidney support anatomy

• The kidneys are retroperitoneal, lying between T12–L3.

• They are surrounded by several layers that provide support and protection:

  1. Renal capsule → tough fibrous capsule directly around kidney.

  2. Perinephric (perirenal) fat → cushions and supports the kidney.

  3. Perinephric fascia (Gerota’s fascia / renal fascia) → encloses kidney and fat, anchoring it to surrounding structures.

• These layers prevent excessive movement and protect the kidney from trauma.

2. Check other options

• Median arcuate ligament → fibrous arch of diaphragm over aorta; unrelated to kidney support. ❌

• Peritoneal fluid → lubricates peritoneal cavity; kidney is retroperitoneal, not in peritoneal cavity. ❌

• Greater omentum / Lesser omentum → intraperitoneal structures; do not support retroperitoneal kidney. ❌

Correct Answer: Perinephric fascia ✅

✅ Computed tomography
Non-contrast CT scan is the gold standard for detecting urinary tract stones.

Non-contrast CT (CT KUB) is considered the most reliable diagnostic test for urolithiasis because it provides high sensitivity and specificity, detects even radiolucent stones (like uric acid), and also reveals complications such as hydronephrosis or obstruction. Unlike X-rays or IVP, CT does not depend on stone composition to visualize them.

Explanation of the Incorrect Options

❌ Intravenous pyelogram (IVP)
Previously the standard test, but less sensitive than CT and involves contrast use, which can be risky in renal impairment.

❌ Magnetic resonance imaging (MRI)
Not preferred for stone detection because stones are poorly visualized on MRI; better for soft tissue and vascular structures.

❌ Blood test
May reveal complications (e.g., renal function, infection) but cannot diagnose stones directly.

❌ X-ray
Can detect radio-opaque stones (like calcium oxalate) but misses radiolucent stones (e.g., uric acid, cystine). Limited sensitivity compared to CT.

Step-by-Step Reasoning

1. Macula densa overview

• Specialized cells in the distal convoluted tubule, adjacent to the glomerular afferent arteriole.

• Function as sensors of NaCl concentration in tubular fluid.

2. Mechanism (Tubuloglomerular feedback)

• High NaCl at macula densa → signals afferent arteriole constriction → decreases GFR.

• Low NaCl → signals afferent arteriole dilation and renin release from juxtaglomerular cells → increases GFR and renal blood flow.

3. Effect

• Macula densa autoregulates GFR and renal blood flow via tubuloglomerular feedback.

4. Check options

• Sodium chloride delivery → sensed by macula densa, not directly autoregulated. ❌

• GFR and renal blood flow → ✅ correct.

• Amino acid absorption → not regulated by macula densa. ❌

• Water regulation → indirectly via GFR, but primary mechanism is GFR/RBF regulation. ❌

• Renin release → macula densa influences it, but renin release is a secondary effect, not the main autoregulation. ❌

Correct Answer: GFR and renal blood flow ✅

Step-by-Step Reasoning

1. Detrusor muscle function

• Smooth muscle of the bladder wall.

• Responsible for bladder contraction during urination (micturition).

2. Autonomic innervation

• Parasympathetic (pelvic splanchnic nerves, S2–S4) → stimulatory: contracts detrusor, relaxes internal urethral sphincter.

• Sympathetic (hypogastric nerve, T11–L2) → inhibitory: relaxes detrusor, contracts internal urethral sphincter for urine storage.

• Somatic (pudendal nerve, S2–S4) → controls external urethral sphincter (voluntary).

3. Check each option

• Pelvic splanchnic nerve → supplies detrusor, stimulates contraction → ✅ correct.

• Hypogastric nerve → sympathetic, inhibits detrusor → ❌

• Pudendal nerve → somatic, controls external sphincter → ❌

• Lumbar plexus → no direct role in detrusor innervation → ❌

• None of these → incorrect

Correct Answer: Pelvic splanchnic nerve ✅

Clinical Correlation

• Damage to pelvic splanchnic nerves (e.g., pelvic surgery) → flaccid bladder, urinary retention.

• Hypogastric nerve injury → may affect storage reflex, but contraction still possible via parasympathetics.

✅ Moles per liter of solution
Osmolarity is defined as the number of osmoles of solute per liter of solution.

Concept:

• Osmolarity = osmoles/L of solution.

• It accounts for solute concentration relative to volume of solution.

• Example: A 1 M NaCl solution has an osmolarity of 2 Osm/L (because Na⁺ and Cl⁻ dissociate).

Note: Osmolarity differs from osmolality, which is defined as osmoles/kg of solvent and is often used clinically because it is independent of temperature/volume changes.

Explanation of the Incorrect Options

❌ Liter per moles of solution
This is the reciprocal of molarity, not osmolarity.

❌ Grams per liter of solution
This describes concentration in mass/volume, not osmolarity.

❌ Moles per kg of solution
That is molality (and osmolality, when expressed in osmoles/kg).

❌ None of these
Incorrect, since osmolarity clearly matches moles per liter of solution.

Step-by-Step Reasoning

1. Function of proximal convoluted tubule

• Main site of reabsorption: water, electrolytes, glucose, amino acids.

• Requires a large surface area → microvilli form a brush border.

• Cells are metabolically active → many mitochondria.

2. Epithelium type

• Simple cuboidal epithelium with brush border:

  • Single layer of cube-shaped cells.

  • Microvilli increase surface area for absorption.

  • Found throughout proximal convoluted tubule.

3. Check other options

• Pseudostratified columnar → found in respiratory tract. ❌

• Simple columnar → found in small intestine, gallbladder; taller cells, no prominent brush border like PCT. ❌

• Simple squamous → forms glomerular capsule and thin limbs of Henle. ❌

• Transitional epithelium → lines ureters, bladder, renal pelvis; specialized for stretch. ❌

Correct Answer: Simple cuboidal epithelium ✅

✅ Guanine monophosphate and adenine monophosphate
IMP is the common precursor for both AMP and GMP in the purine nucleotide biosynthesis pathway.

Inosine monophosphate (IMP):

• IMP is formed during de novo purine synthesis.

• It acts as the branch point precursor for:

  • Adenosine monophosphate (AMP) via conversion through adenylosuccinate.

  • Guanosine monophosphate (GMP) via conversion through xanthosine monophosphate (XMP).

Thus, IMP → AMP + GMP are the two end products.

Note: Cytosine, thymine, and uracil nucleotides belong to the pyrimidine pathway, not derived from IMP.

Explanation of the Incorrect Options

❌ Adenine monophosphate and cytosine monophosphate
Cytosine monophosphate (CMP) is a pyrimidine, not derived from IMP.

❌ Cytosine monophosphate and thymine monophosphate
Both pyrimidines — not linked to IMP.

❌ Cytosine monophosphate and guanine monophosphate
CMP (pyrimidine) is not derived from IMP; GMP is correct, but the pair is wrong.

❌ Thymine monophosphate and adenine monophosphate
Thymine monophosphate (TMP) is also a pyrimidine product (from dUMP), not from IMP.

❌ Guanine monophosphate and adenine monophosphate
This is correct — both are purine nucleotides derived from IMP.

✅ Nephron
Stones form in the collecting system (calyces, renal pelvis, ureter, bladder), not within the microscopic tubules of the nephron.

Renal/urinary stones (urolithiasis):

• Stones form when urine becomes supersaturated with salts (e.g., calcium oxalate, uric acid, struvite, cystine).

• Sites where stones occur:

  • Renal calyces

  • Renal pelvis

  • Ureter

  • Bladder

The nephron is too small and narrow (microscopic tubules) to allow for macroscopic stone formation. Instead, crystals may precipitate in the urine, but actual calculi are found only in the collecting system or lower tract.

Explanation of the Incorrect Options

❌ Bladder
Yes — bladder stones are common, especially in urinary stasis or obstruction.

❌ Calyces
Yes — renal stones often begin in the minor/major calyces.

❌ Pelvis
Yes — the renal pelvis is a frequent site of stone formation.

❌ Ureter
Yes — stones can lodge in the ureter, often at narrow points (pelvi-ureteric junction, pelvic brim, vesicoureteric junction).

❌ Nephron
Not a site for visible stones — only crystals or casts can be found here.

Step-by-Step Reasoning

1. Aldosterone overview

• Steroid hormone produced by zona glomerulosa of adrenal cortex.

• Acts primarily on distal convoluted tubule (DCT) and collecting duct.

• Mechanism: binds to intracellular receptors → increases synthesis of Na⁺ channels (ENaC) and Na⁺/K⁺ ATPase → increases Na⁺ reabsorption.

2. Effects on electrolytes

• Na⁺: reabsorbed → water follows → increases blood volume and BP.

• K⁺: secreted into urine → increases K⁺ excretion.

• Cl⁻: follows Na⁺ passively → reabsorbed.

3. Check each option

• Decreases Na⁺ and Cl⁻ reabsorption, and K⁺ excretion → opposite effect. ❌

• Increases Na⁺ and Cl⁻ excretion, and K⁺ reabsorption → opposite. ❌

• Increases Na⁺ and Cl⁻ reabsorption, and K⁺ excretion → ✅ correct.

• Increases Na⁺, Cl⁻, and K⁺ excretion → wrong. ❌

• Increases Na⁺ and K⁺ reabsorption → K⁺ is actually excreted, so wrong. ❌

Correct Answer: Increases Na⁺ and Cl⁻ reabsorption, and K⁺ excretion ✅

Clinical Correlation

• Excess aldosterone → hypernatremia, hypokalemia, hypertension (e.g., Conn’s syndrome).

• Deficiency → hyponatremia, hyperkalemia, hypotension (e.g., Addison’s disease)

Step-by-Step Reasoning

1. Nephron permeability characteristics

2. Check options

• Proximal convoluted tubule → permeable to NaCl. ❌

• Distal convoluted tubule → actively reabsorbs NaCl. ❌

• Descending limb → impermeable to NaCl, only water moves out → ✅ correct.

• Collecting duct → mostly water movement under ADH; some Na⁺ reabsorption occurs. ❌

• Ascending limb → actively reabsorbs NaCl; impermeable to water, but not impermeable to NaCl. ❌

Correct Answer: Descending limb ✅

Step-by-Step Reasoning

1. External urethral sphincter anatomy

• It is a skeletal muscle surrounding the urethra.

• Controls voluntary urination.

• Part of the urogenital diaphragm in both males and females.

2. Nerve supply

• Pudendal nerve (S2–S4) provides somatic motor innervation to the external urethral sphincter.

• This allows voluntary control of micturition.

3. Check other options

• Vesicular nerve → not a recognized anatomical term; possibly a distractor. ❌

• Obturator nerve → innervates medial thigh muscles (adductors). ❌

• Femoral nerve → innervates anterior thigh muscles. ❌

• Gonadal nerve → innervates gonads (testes/ovaries), sensory; not sphincter. ❌

Correct Answer: Pudendal nerve ✅

Clinical Correlation

• Injury to the pudendal nerve (e.g., pelvic trauma, childbirth) can cause loss of voluntary urinary control, leading to stress incontinence.

Step-by-Step Reasoning

1. Types of water reabsorption

• Obligatory water reabsorption → occurs automatically, independent of hormones.

  • Mainly in proximal convoluted tubule (PCT) and descending limb of loop of Henle.

• Facultative water reabsorption → regulated by antidiuretic hormone (ADH).

  • Occurs in collecting ducts (cortical and medullary collecting ducts, including duct of Bellini) depending on body water needs.

2. Check each option

• Proximal convoluted tubule → obligatory water reabsorption, not facultative. ❌

• Bowman’s capsule → filtration only, no reabsorption. ❌

• Duct of Bellini → part of the collecting duct system, responsible for ADH-regulated water reabsorption → ✅ correct.

• Loop of Henle → descending limb: obligatory; ascending limb: impermeable to water. ❌

• None of these → incorrect.

Correct Answer: Duct of Bellini ✅

Step-by-Step Reasoning

1. Function of ureter epithelium

   • The ureters carry urine from the renal pelvis to the bladder.

   • Urine is hypertonic and potentially irritating, so the epithelium must stretch and protect underlying tissue.

2. Transitional epithelium (urothelium)

   • Specially adapted for the urinary tract.

   • Features:

     • Stratified appearance, but cells can stretch when the ureter fills with urine.

     • Umbrella cells at the surface resist the toxicity of urine.

   • Found in: renal pelvis, ureters, bladder, proximal urethra.

3. Check other options

• Stratified squamous non-keratinized → lines esophagus, oral cavity; cannot stretch like transitional epithelium. ❌

• Stratified squamous keratinized → epidermis; not in ureter. ❌

• Pseudostratified columnar → respiratory tract. ❌

• Simple squamous → lining of blood vessels or alveoli; too thin for ureter. ❌

Correct Answer: Transitional epithelium ✅

Step-by-Step Reasoning

1. Renal blood flow facts

   • Kidneys are highly perfused organs despite being only ~0.5% of body weight.

   • Normal RBF: ~1,100 mL/min in an adult (both kidneys).

   • Normal cardiac output: ~5,000 mL/min.

2. Calculate fraction:

Fraction of CO=RBFCO×100=11005000×100≈22%Fraction of CO=CORBF​×100=50001100​×100≈22%

3. Therefore, RBF ≈ 20–25% of total cardiac output.

Correct Answer: 20–25% ✅

Why not the others?

• 30–50%, 45–50% → too high.

• 10–15% → underestimates renal perfusion.

• 1–2% → extremely low; only true for organs with minimal blood flow like some endocrine glands.

Step-by-Step Reasoning

1. Loop of Henle segments:

   • Descending limb: highly permeable to water, but not to solutes.

   • Ascending limb (thin + thick):

     • Impermeable to water.

     • Thick ascending limb actively reabsorbs Na⁺, K⁺, Cl⁻ via the Na⁺-K⁺-2Cl⁻ cotransporter.

     • Known as the diluting segment because it removes solutes but leaves water behind.

2. Check each option:

• Permeability to water is affected by ADH → false. ADH mainly acts on the collecting ducts, not the ascending limb.

• Impermeable to potassium → false. Potassium is reabsorbed here via NKCC2 cotransporter.

• Impermeable to sodium → false. It actively reabsorbs sodium.

• Impermeable to water → ✅ true property of ascending limb.

• Permeable to water → false, this describes the descending limb.

Correct Answer: Impermeable to water ✅

Step-by-Step Reasoning

1. Renal plasma flow (RPF) depends on renal blood flow. Anything that vasoconstricts renal vessels decreases RPF; vasodilators increase it.

2. Check each option:

• Renal hypertension → chronic hypertension damages renal vessels, but the question focuses on immediate physiological regulators. Not the best answer.

• Angiotensin I → relatively inactive precursor; does not significantly affect RPF until converted to angiotensin II.

• None of these → not true, because one of the listed options does affect RPF.

• Prostaglandin → causes vasodilation of renal vessels (especially afferent arteriole), thus increases RPF.

• Aldosterone → acts on distal nephron for sodium reabsorption; does not directly change RPF.

3. Best choice: Renal hypertension.

   • In the context of this MCQ, renal hypertension involves vasoconstriction (elevated pressure → autoregulatory vasoconstriction of afferent arteriole), which decreases RPF.

Correct Answer: Renal hypertension ✅

Step-by-Step Reasoning

1. Cortex vs. Medulla – Nephron distribution

   • Cortex:

     • Glomeruli (Bowman’s capsule + glomerulus)

     • Proximal convoluted tubule (PCT)

     • Distal convoluted tubule (DCT)

     • Cortical collecting ducts

   • Medulla:

     • Loop of Henle (thin descending + thin ascending + thick ascending limb)

     • Medullary collecting ducts

2. Check each option

   • Proximal convoluted tubule → lies in the cortex → ✅ correct.

   • Medullary collecting duct → found in the medulla, not cortex.

   • Thin descending limb → part of loop of Henle, in the medulla.

   • Thin ascending limb → also in the medulla.

   • None of these → wrong, because PCT is clearly in the cortex.

Correct Answer: Proximal convoluted tubule ✅

Step-by-Step Reasoning

1. Ureteric blood supply overview

   • The ureter is supplied segmentally, from top to bottom:

     • Upper part → renal artery, gonadal artery, adrenal arteries.

     • Middle part → aorta, common iliac artery, gonadal artery.

     • Lower part → superior vesical artery, inferior vesical artery (in males), uterine artery/vaginal artery (in females).

2. Check each option

   • Renal artery → yes, supplies the upper part of the ureter.

   • Gonadal artery (testicular/ovarian) → yes, supplies the ureter along its course.

   • Common iliac artery → yes, provides branches to the mid-ureter.

   • Superior vesical artery → yes, supplies the lower ureter.

   • Inferior mesenteric artery → ❌ this artery supplies the large intestine (distal transverse colon, descending colon, sigmoid, rectum), but not the ureter.

Correct Answer: Inferior mesenteric artery ✅

Step-by-Step Reasoning

1. What is the urinary space?

   • Also called Bowman’s space.

   • It’s the space between the visceral layer (podocytes) and the parietal layer of Bowman’s capsule.

   • This is where the glomerular filtrate first collects before flowing into the proximal convoluted tubule.

2. Check each option

   • Proximal convoluted tubule → drains filtrate from Bowman’s space but does not itself contain urinary space.

   • Distal convoluted tubule → part of tubular system, no urinary space.

   • Bowman’s capsule → has urinary (Bowman’s) space → ✅ correct.

   • Collecting duct → carries urine toward renal pelvis, no urinary space.

   • Loop of Henle → responsible for concentration/dilution of urine, not urinary space.

Correct Answer: Bowman’s capsule ✅

1. Glomerular filtration barrier layers

   • Fenestrated endothelium (pores ~70–100 nm).

   • Glomerular basement membrane (negatively charged, prevents large proteins).

   • Slit diaphragm between podocyte foot processes, which contains filtration slit pores.

2. Width of slit pores

   • These pores are much smaller than endothelial fenestrations.

   • Standard physiology texts (e.g., Guyton, Ganong) state slit pores are ~25 nm wide.

3. Significance

   • This narrow width, along with negative charge, restricts albumin and other plasma proteins.

   • Allows water, electrolytes, glucose, and small solutes to pass freely.

Correct Answer: 25 nm ✅

Step-by-Step Reasoning

1. Interpret 0.9% NaCl solution

   • By convention, 0.9% w/v means 0.9 g of NaCl in 100 mL solution.

   • Therefore, in 1 liter (1000 mL):

     0.9 g×10=9.0 g NaCl0.9g×10=9.0g NaCl

2. Find molar mass of NaCl

   • Na = 23 g/mol

   • Cl = 35.5 g/mol

   • M(NaCl) = 23 + 35.5 = 58.5 g/mol

3. Calculate moles of NaCl in 1 L

   moles=massmolar mass=9.058.5moles=molar massmass​=58.59.0​

   Divide carefully:

   • 58.5 × 0.15 = 8.775

   • 58.5 × 0.154 = 9.009

   So,

   moles≈0.154 mol/Lmoles≈0.154mol/L

Correct Answer: 0.154 moles/L ✅

Why not the others?

• 0.157 moles/L – close, but slight rounding error.

• 0.678 moles/L – way too high.

• 0.123 moles/L – too low.

• 0.07 moles/L – far too low.

Step-by-Step Reasoning

• Carbonic anhydrase inhibitors (CAIs):

  • Prototype drug: Acetazolamide.

  • Mechanism: Inhibits carbonic anhydrase in the proximal tubule, decreasing reabsorption of bicarbonate → alkaline urine, metabolic acidosis.

  • Clinical uses: glaucoma, altitude sickness, metabolic alkalosis, idiopathic intracranial hypertension.

• Bumetanide, Furosemide, Torsemide:

  • All are loop diuretics, acting by blocking the Na⁺-K⁺-2Cl⁻ symporter in the thick ascending limb of Henle’s loop.

  • They are not carbonic anhydrase inhibitors.

• “None of these” → incorrect, because acetazolamide is indeed a carbonic anhydrase inhibitor.

Correct Answer: Acetazolamide ✅

Step-by-Step Reasoning

• ADH Mechanism:

  • ADH binds to V2 receptors on the basolateral membrane of collecting duct principal cells.

  • This activates cAMP–PKA signaling, leading to insertion of aquaporin-containing vesicles into the apical (luminal) membrane.

  • The specific water channel inserted is Aquaporin-2 (AQP2).

  • Once inserted, water enters the cell from the lumen, then exits through AQP3 and AQP4 (which are constitutively present in the basolateral membrane).

Correct Answer: Aquaporin-2 ✅

Why not the others?

• Aquaporin-1: Found in proximal tubule and descending thin limb; always open, not ADH-regulated.

• Aquaporin-4: Present in brain and basolateral membrane of collecting duct, but not ADH-regulated.

• Aquaporin-5: Found in salivary glands, lungs, and eyes; unrelated to renal water reabsorption.

• Aquaporin-3: Present in basolateral membrane of collecting duct, but constitutive (not directly regulated by ADH).