Renal – 2021

The description of diffuse effacement of foot processes on electron microscopy is classic for Minimal Change Disease (MCD), the most common cause of nephrotic syndrome in children. A key clinical feature of MCD is that it shows a dramatic response to corticosteroids, with most children achieving complete remission after treatment. This makes the given option correct.

Why the Other Options Are Incorrect

• Progression to chronic renal failure ❌
  Minimal Change Disease rarely progresses to chronic renal failure. Most children respond well to steroids, and long-term prognosis is excellent. Only steroid-resistant cases or rare relapses may cause complications.

• None of these ❌
  This is incorrect because one option (dramatic steroid response) is indeed true.

• Spike and dome appearance ❌
  This is the hallmark of Membranous nephropathy, not Minimal Change Disease. In membranous nephropathy, subepithelial immune complex deposits cause this characteristic appearance on light microscopy with special stains.

• Presence of immune complex deposits ❌
  Minimal Change Disease is not caused by immune complex deposition. Instead, it is thought to involve T-cell–mediated damage and cytokines affecting podocyte structure. Immune deposits are seen in other nephrotic conditions such as membranous nephropathy or lupus nephritis.

A cadaveric donor refers to an individual who donates an organ after death. In this case, the kidney comes from someone who is about to die (often following brain death or circulatory death, with consent from the patient’s family or prior consent by the donor). Cadaveric donation is one of the primary sources of transplant organs worldwide, especially when a living donor is not available.

Why the Other Options Are Incorrect

• Genetically related donor ❌
  This refers to a living family member (such as a sibling, parent, or child) who is genetically related and donates a kidney. Since the donor in this case is dying and not a family member, this is not correct.

• Non-related donor ❌
  This term usually refers to a living person who is not genetically related but still donates (sometimes a friend or spouse). That is different from a cadaveric donor.

• Living donor ❌
  A living donor is someone alive at the time of donation, willingly donating one of their kidneys. In this scenario, the donor is dying, so it does not qualify.

• Living unrelated donor ❌
  Again, this refers to a living donor with no genetic relation (e.g., a spouse). The donor here is not alive at the time of donation.

In the proximal convoluted tubule (PCT), sodium ions are reabsorbed actively through multiple transporters. One of the key mechanisms is the Na⁺/H⁺ exchanger (NHE3) on the luminal (apical) membrane. In this process, sodium ions move into the tubular cell in exchange for hydrogen ions, which are secreted into the tubular lumen. This exchange is crucial for maintaining acid–base balance and for bicarbonate reabsorption in the kidney.

Why the Other Options Are Incorrect

• Glucose ❌
  Glucose is indeed reabsorbed with sodium in the PCT, but this occurs through a sodium–glucose co-transporter (SGLT), not via exchange. Both sodium and glucose move into the cell together, not one in place of the other.

• Potassium ions ❌
  Potassium is not exchanged with sodium in the PCT. Most potassium handling occurs in the loop of Henle and distal nephron, not by direct exchange with sodium in the PCT.

• Chloride ions ❌
  Chloride reabsorption in the PCT occurs mostly through passive paracellular pathways or later segments where Cl⁻ follows sodium and water. It is not the primary ion exchanged for sodium here.

• Phosphate ions ❌
  Phosphate reabsorption occurs in the PCT, but through sodium–phosphate co-transporters, not an exchange mechanism.

Renal stones (urolithiasis or nephrolithiasis) are not congenital. They are acquired conditions that develop due to metabolic imbalances (such as hypercalciuria, hyperoxaluria, or uric acid excess), dehydration, infections, or dietary factors. They can occur at any age but are not present from birth, distinguishing them from congenital renal diseases.

Why the Other Options Are Incorrect

• Horseshoe kidney ❌
  This is a congenital anomaly in which the lower poles of the two kidneys fuse, forming a U-shaped structure. It results from abnormal migration of the kidneys during embryogenesis.

• Renal agenesis ❌
  A true congenital defect, renal agenesis is the complete absence of one or both kidneys, caused by failure of the ureteric bud to develop. Bilateral renal agenesis is incompatible with life.

• Polycystic kidney disease ❌
  This is a genetic congenital disorder characterized by the development of multiple renal cysts. It can present in infancy (autosomal recessive) or adulthood (autosomal dominant), but the predisposition is congenital.

• Medullary cystic kidney disease ❌
  This is another congenital, inherited disorder. It causes cysts in the medullary collecting ducts, leading to progressive renal dysfunction.

Juxtaglomerular (JG) cells are specialized smooth muscle cells located mainly in the wall of the afferent arteriole (near its entry into the glomerulus). Their main function is to synthesize, store, and secrete renin, an enzyme that plays a central role in the renin–angiotensin–aldosterone system (RAAS). Renin release is triggered by decreased renal perfusion pressure, sympathetic stimulation, or reduced sodium chloride delivery to the macula densa. This makes the statement correct.

Why the Other Options Are Incorrect

• Macula densa is a part of the proximal convoluted tubule ❌
  This is incorrect because the macula densa is actually a group of specialized epithelial cells located in the distal convoluted tubule (DCT), where it comes in contact with the afferent arteriole. It is not part of the proximal convoluted tubule.

• Juxtaglomerular cells are found in both afferent and efferent arterioles ❌
  This is wrong because JG cells are predominantly located in the afferent arteriole. While a few may be seen near the efferent arteriole, their functional concentration is along the afferent arteriole, making this statement misleading.

• Macula densa cells secrete renin ❌
  This is false. Macula densa cells do not secrete renin; instead, they detect sodium chloride levels in the tubular fluid and signal JG cells to release renin when NaCl is low.

• None of these ❌
  This is incorrect because one of the given statements (JG cells secrete renin) is in fact true.

The nephron carries out three fundamental and interrelated processes to form urine:

1. Filtration

   • Occurs in the glomerulus.

   • Plasma (minus proteins and large molecules) is filtered into Bowman’s capsule.

2. Reabsorption

   • Selective movement of substances from the tubular lumen back into the blood (e.g., glucose, amino acids, water, electrolytes).

3. Secretion

   • Active transport of substances from peritubular capillaries into the tubule (e.g., H⁺, K⁺, drugs, creatinine).

These three are ongoing, interconnected processes in the nephron.

Why not the others?

• Filtration, secretion, and excretion ❌

  • Misses reabsorption, which is crucial — without it, we would lose essential solutes and water.

• Filtration and excretion ❌

  • Oversimplified. Excretion is the end result (filtration – reabsorption + secretion), but not a separate nephron process.

• Filtration, reabsorption, and excretion ❌

  • Same issue: excretion is not a nephron process, just the final outcome.

• Reabsorption, secretion, and excretion ❌

  • Leaves out filtration, the starting step.

• The kidney converts 25-hydroxycholecalciferol (from the liver) into 1,25-dihydroxycholecalciferol (calcitriol) via the enzyme 1α-hydroxylase in the proximal tubule.

• Calcitriol is the active form of vitamin D.

• Its major action on the intestine:

  • Increases calcium and phosphate absorption by upregulating calbindin and other transport proteins.

• This role is crucial in maintaining bone health and calcium balance.

Erythropoietin ❌

• Synthesized in the kidney (peritubular interstitial cells).

• Acts on the bone marrow, stimulating red blood cell production.

• Does not act on the intestine.

Albumin ❌

• Synthesized mainly by the liver, not the kidney.

• Maintains plasma oncotic pressure and transports substances.

Parathyroid hormone (PTH) ❌

• Produced by the parathyroid glands, not the kidney.

• Indirectly increases calcium absorption in the intestine by stimulating renal calcitriol production, but itself does not directly act on intestine.

Calcitonin ❌

• Produced by parafollicular C-cells of the thyroid gland.

• Lowers blood calcium by inhibiting bone resorption.

• Does not act on the intestine.

• Nitric oxide (NO) is a vasodilator released by endothelial cells.

• In the kidney, NO causes afferent arteriolar dilation, which increases renal blood flow (RBF) and raises glomerular hydrostatic pressure, thereby increasing GFR.

• It plays a protective role, balancing the vasoconstrictor effects of angiotensin II and sympathetic tone.

Sympathetic nervous system stimulation ❌

• Causes afferent arteriole vasoconstriction via α1 receptors.

• This decreases renal blood flow and lowers GFR (as part of the “fight or flight” shunting blood away from kidneys).

Urinary tract obstruction ❌

• Raises hydrostatic pressure in Bowman’s capsule, which reduces net filtration pressure and decreases GFR.

Epinephrine ❌

• Similar to sympathetic stimulation, it causes afferent vasoconstriction → decreases RBF and GFR.

Angiotensin II ❌

• Preferentially constricts the efferent arteriole, which can initially maintain or slightly increase GFR despite reduced RBF.

• However, at high levels, it reduces renal plasma flow more than it helps GFR, so the net effect is reduced filtration fraction if unchecked.

• In exam settings, Ang II is not considered the main “GFR increasing” mechanism — the safe best answer here is NO.

• In the fetus, most amniotic fluid from the 2nd trimester onward is produced by the kidneys as urine.

• Bilateral renal agenesis → no urine production → markedly reduced amniotic fluid volume (oligohydramnios).

• This leads to the Potter sequence:

  • Flattened facies

  • Pulmonary hypoplasia (due to lack of amniotic fluid expansion)

  • Limb deformities

• It is usually fatal shortly after birth.

Polyhydramnios ❌

• Caused by impaired swallowing (e.g., anencephaly, esophageal/duodenal atresia), not by absent kidney function.

Renal failure later in life ❌

• Bilateral renal agenesis is incompatible with life after birth; the fetus usually dies in utero or shortly after birth.

Hypertension ❌

• May occur in other renal diseases (e.g., chronic kidney disease), but not relevant here since the kidneys never develop.

Hypertrophy of kidneys ❌

• Seen in unilateral renal agenesis, where the single kidney undergoes compensatory hypertrophy.

• In bilateral agenesis, both kidneys are absent.

The de novo synthesis pathways for purines and pyrimidines are distinct but share key common substrates. The compound “glutamine, carbon dioxide, and aspartate” refers to carbamoyl phosphate, a critical intermediate synthesized by carbamoyl phosphate synthetase II (CPS II) in the pyrimidine pathway. However, let’s break down the roles of these molecules in both pathways:

1. Glutamine:
   • Purines: Donates its amide nitrogen at two steps (N3 and N9 positions of the purine ring).
   • Pyrimidines: Donates its amide nitrogen for the synthesis of carbamoyl phosphate (via CPS II) and also for the conversion of UTP to CTP.
2. Carbon Dioxide (CO₂):
   • Purines: Incorporated as the C6 carbon of the purine ring.
   • Pyrimidines: Incorporated as the C2 carbon of the pyrimidine ring during carbamoyl phosphate synthesis.
3. Aspartate:
   • Purines: Provides the N1 atom of the purine ring.
   • Pyrimidines: Provides the entire pyrimidine ring backbone (aspartate + carbamoyl phosphate → orotic acid) and the nitrogen for CTP synthesis.

Thus, all three—glutamine, CO₂, and aspartate—are directly involved in building both purine and pyrimidine rings.

Why the Other Options Are Incorrect:

❌ Tetrahydrofolate (THF):

• • THF is crucial for purine synthesis (donates formyl groups for C2 and C8 positions) and thymidylate (dTMP) synthesis in pyrimidine metabolism. However, it is not involved in the initial ring construction of pyrimidines (uracil, cytosine). Thus, it is not common to both pathways for ring formation.

    ❌ Aspartate (alone):

    • While aspartate is used in both pathways (as explained above), the question asks for the option that best captures the common contributors. “Aspartate alone” is incomplete because glutamine and CO₂ are equally critical for both pathways.

      ❌ Glutamine (alone):

      • Glutamine is a key nitrogen donor in both pathways, but CO₂ and aspartate are also essential. Using glutamine alone ignores the roles of CO₂ (carbon source) and aspartate (carbon/nitrogen source).

        ❌ Glycine:

        • Glycine is incorporated entirely into the purine ring (as C4, C5, and N7). It plays no role in pyrimidine synthesis.

• The pyrimidine ring (cytosine, thymine, uracil) is assembled from carbamoyl phosphate and aspartate.

• The contributions are:

  • Aspartate → contributes three atoms to the ring (N1, C4, C5, C6).

  • Glutamine → donates the nitrogen used by CPS II to form carbamoyl phosphate.

  • Carbon dioxide (CO₂) → contributes one carbon atom to the carbamoyl phosphate, which becomes part of the pyrimidine ring.

• Tetrahydrofolate (THF) is used in purine synthesis (donates C1 units at positions C2 and C8 of the purine ring), not pyrimidines.

• Glycine contributes to purine ring synthesis (providing N7, C4, C5), not pyrimidines.

• Glutamate is a nitrogen donor in other reactions but not directly in the pyrimidine ring skeleton.

Thus, the single carbon atom in the pyrimidine ring comes from carbon dioxide.

• The bladder is lined by transitional epithelium (urothelium).

• This specialized epithelium allows the bladder wall to stretch and recoil as urine volume changes.

• Transitional epithelium has multiple layers of cells, with dome-shaped “umbrella cells” on the surface that flatten when stretched.

Nephron ❌

• The nephron is lined by simple cuboidal epithelium in most parts (e.g., PCT, DCT, collecting tubule) and simple squamous epithelium in thin limbs of the loop of Henle.

• Not transitional.

Prostate gland ❌

• The prostate is lined by pseudostratified columnar epithelium, sometimes with areas of simple columnar or cuboidal.

• Not transitional.

Collecting duct ❌

• Collecting ducts are lined by simple cuboidal to columnar epithelium depending on segment.

• Not transitional.

Urethra ❌

• The urethra varies:

  • Prostatic urethra → transitional epithelium.

  • Membranous/penile urethra → pseudostratified/stratified columnar.

  • Distal urethra → stratified squamous.

• But when asked in a single best-answer format, the bladder is the classical structure associated with transitional epithelium.

• The standard hemodialysis regimen for most end stage renal disease (ESRD) patients is three sessions per week, each lasting about 4 hours.

• This schedule balances clearance of uremic toxins, fluid removal, and practicality for patients.

• Some patients may require longer or more frequent sessions, but “4 hours × 3/week” is the classic exam answer and the most widely practiced schedule.

Can be done at home 4 times per day ❌

• This describes peritoneal dialysis, not hemodialysis.

• Home hemodialysis is possible but rare, and not typically done 4 times per day.

No need for hemodialysis in acute kidney injury ❌

• Incorrect. Dialysis is indicated in acute kidney injury (AKI) when complications arise (e.g., severe hyperkalemia, acidosis, volume overload, uremic symptoms).

No restriction on diet and fluid intake ❌

• Wrong. Patients on hemodialysis must restrict sodium, potassium, phosphate, and fluid intake to prevent complications between sessions.

Screening for hepatitis C is not required ❌

• Wrong. Hemodialysis patients are at increased risk of blood-borne infections (hepatitis B, C, HIV).

• Routine screening and vaccination (where available) are essential.

• The arteriovenous fistula (AVF) is the preferred long-term vascular access for hemodialysis.

• It is created surgically by connecting an artery (usually radial or brachial) to a vein (usually cephalic).

• Benefits:

  • Provides high blood flow for effective dialysis.

  • Has a low risk of infection and thrombosis compared to central venous catheters.

• AVF requires preservation of arm veins (especially cephalic vein) in patients with chronic kidney disease.

Preservation of arm veins is not important ❌

• Wrong. Preservation is very important, as arm veins may be needed later for AVF creation.

Long term dialysis is done by two-way catheter in the central vein ❌

• Central venous catheters (internal jugular, subclavian, femoral) are used for short-term access, not preferred for long-term use due to high infection and thrombosis risk.

Long term catheter is placed in the femoral vein ❌

• The femoral vein is used only for emergency short-term dialysis.

• Long-term femoral catheters are avoided due to high infection rates and difficulty with ambulation.

None of these ❌

• Incorrect, because AVF is clearly the right long-term access method.

• The patient has classic features of pyelonephritis: fever, flank pain, hematuria, and WBC casts (which localize the infection to the kidney).

• While the traditional threshold for “significant bacteriuria” in asymptomatic cases is ≥10⁵ CFU/ml, in symptomatic males, even ≥10³ CFU/ml is considered diagnostic.

• Therefore, 10⁴ CFU/ml in a symptomatic patient with WBC casts is significant and should be treated as UTI/pyelonephritis without delay.

10⁴ CFU/ml is not significant ❌

• Wrong. In symptomatic patients, especially men, lower colony counts are clinically meaningful.

Go for a pyelogram ❌

• An intravenous pyelogram (IVP) is not the first-line test in suspected infection. It carries risks (contrast, radiation) and is unnecessary for diagnosis.

Urine culture should be done again ❌

• Repeating the culture delays treatment. The patient already has strong evidence of infection with supportive symptoms and urine findings.

An ultrasound should be performed ❌

• Ultrasound may be useful to rule out obstruction or abscess in complicated cases, but the priority here is to treat the infection. Imaging is supportive, not the immediate next step.

• In older men, Benign Prostatic Hyperplasia (BPH) is the most common cause of bladder outlet obstruction (BOO). The enlarged prostate compresses the prostatic urethra, leading to incomplete bladder emptying.
  Over time, this causes increased intravesical pressure, which is transmitted backward to the kidneys → resulting in hydronephrosis with distension of the renal pelvis and calyces, even if the ureters and bladder still appear normal in early or moderate stages

❌ Why Other Options Are Incorrect:

• • Ectopic fused kidney:
    Congenital condition (e.g., horseshoe or cross-fused kidney). It may cause altered kidney position or ureteral course, but not isolated hydronephrosis with normal ureters/bladder in old age.

  • Retroperitoneal fibrosis:
    Causes extrinsic compression of the ureters, leading to hydroureteronephrosis (dilated ureters as well). Here, the ureters are reported as normal, which rules this out.

  • Congenital vesicoureteral reflux (VUR):
    Typically a childhood condition causing reflux of urine from bladder → ureters → kidney. It results in dilated ureters (hydroureter) and scarring over time — not seen here, and very rare to present de novo at 65.

  • Horseshoe kidney:
    A congenital fusion anomaly where the kidneys are joined at their lower poles. While it can predispose to obstruction at the ureteropelvic junction (UPJ), it would have been evident earlier in life and visible on ultrasound as a fused renal mass.

Renal plasma flow (Correct) ✅

• PAH is a compound that is freely filtered at the glomerulus and the remaining amount in plasma is actively secreted into the tubule by the proximal tubule cells.

• Nearly all PAH that enters the kidney is excreted in urine in a single pass (at low plasma concentrations).

• Therefore, the clearance of PAH ≈ effective renal plasma flow (ERPF).

• Since about 90% of plasma is cleared of PAH, it provides a reliable estimate of renal plasma flow.

Glomerular filtration rate (GFR) ❌

• Measured using inulin clearance (gold standard) or creatinine clearance (practical estimate).

• PAH clearance reflects total plasma flow, not filtration.

Urine output ❌

• Simply the volume of urine excreted — measured directly, no special marker needed.

Renal blood flow ❌

• Can be calculated from renal plasma flow:

  • RBF = RPF ÷ (1 – hematocrit)

  • But PAH directly measures plasma flow, not total blood flow.

None of these ❌

• Incorrect because PAH clearly measures renal plasma flow.

• Total body water (TBW) = about 60% of body weight.

  • For a 70 kg adult → ~42 L.

• TBW is divided into:

  • Intracellular fluid (ICF): ~2/3 (≈ 28 L)

  • Extracellular fluid (ECF): ~1/3 (≈ 14 L)

• Within the ECF:

  • Interstitial fluid = ~3/4 of ECF (~10–11 L).

  • Plasma = ~1/4 of ECF (~3–4 L).

So:

• Intracellular ❌ → has 2/3, not 1/3.

• Interstitial ❌ → only part of the extracellular fraction, ~25% of TBW.

• Plasma ❌ → ~8% of TBW.

• Intracellular and interstitial ❌ → together >75% of TBW, not 1/3.

• Extracellular ✅ → this is exactly 1/3 of total body water.

✅ Correct Answer: Drug-induced interstitial nephritis

✅ Why this is correct

The patient recently took antibiotics and developed:

• Fever

• Rash

• Eosinophils in urine (eosinophiluria)

These findings strongly indicate a hypersensitivity reaction in the kidney interstitium → classic for drug-induced interstitial nephritis.

❌ Why other options are incorrect

The pelvicalyceal junction (also called the ureteropelvic junction) is the narrowest part of the upper urinary tract, where the renal pelvis tapers to form the ureter. This area is a common site of obstruction by kidney stones, as the lumen sharply narrows.

The three classical constrictions of the ureter are:

1. Pelvi-ureteric junction (PUJ) — at the junction of renal pelvis and ureter (first and narrowest)

2. Pelvic brim — where the ureter crosses the iliac vessels

3. Vesico-ureteric junction (VUJ) — where the ureter pierces the bladder wall (second narrowest overall)

Because the question specifies “well above the urinary bladder”, the correct site is the pelvicalyceal (ureteropelvic) junction.

Why the other options are incorrect:
❌  Major calyx – This is part of the collecting system inside the kidney, not the ureter. Stones here are called cayceal stones, not ureteric stones.
❌  Minor calyx – Even higher within the renal pyramids; not a ureteric narrowing.
❌  Pelvic brim – This is the second constriction, lower than the PUJ, where the ureter crosses the iliac vessels.
❌  Bladder wall – Refers to the vesicoureteric junction, the lowest constriction, near the bladder — not “well above” it.

• This is the most common cause of recurrent UTIs in young children.

• Pathophysiology: The vesicoureteral junction is incompetent, allowing backward flow of urine from bladder into the ureters and kidneys.

• Consequences:

  • Promotes recurrent UTIs.

  • Predisposes to renal scarring (reflux nephropathy).

  • Can ultimately lead to chronic kidney disease if untreated.

Dysplastic kidney ❌

• A congenital malformation with abnormal renal tissue development.

• May cause impaired function but is not a classic cause of recurrent UTIs.

Minimal change disease ❌

• A nephrotic syndrome of childhood with massive proteinuria and edema.

• Does not cause recurrent UTIs.

Horseshoe kidney ❌

• Fusion anomaly of the kidneys at their lower poles.

• May predispose to obstruction or stones, but recurrent UTIs in children are more classically linked to vesicoureteral reflux.

Polycystic kidney disease ❌

• A genetic disorder with multiple cysts.

• Causes hypertension, progressive renal failure, and palpable abdominal masses, but not primarily recurrent UTIs at this age.

• The urachus is a fetal remnant of the allantois, connecting the apex of the urinary bladder to the umbilicus.

• Normally, after birth, it obliterates to form the median umbilical ligament, a fibrous cord running in the midline from the bladder to the umbilicus.

Umbilicus ❌

• This is the navel itself, not a remnant of the urachus. It is where the umbilical cord was attached, not derived from urachal tissue.

Medial umbilical ligament ❌

• These are the remnants of the obliterated umbilical arteries, not the urachus. They run on either side of the bladder.

Lateral umbilical ligament ❌

• These are folds that cover the inferior epigastric vessels. They are not embryological remnants, but peritoneal folds.

Umbilical artery ❌

• In the fetus, the umbilical arteries carry deoxygenated blood to the placenta. After birth, they become the medial umbilical ligaments, not related to the urachus.

• The urachus is a fetal structure connecting the apex of the bladder to the umbilicus (a remnant of the allantois). Normally, it obliterates and forms the median umbilical ligament.

• If the urachus remains completely patent, it results in a urachal fistula: an abnormal connection between the bladder and umbilicus.

• Clinical feature: urine discharge from the umbilicus in infants or children.

Urachal sinus ❌

• Occurs when the urachus obliterates at the bladder end but remains open at the umbilical end.

• Results in a blind pouch opening at the umbilicus, but not communicating with the bladder.

Urachal cyst ❌

• Occurs when a small part of the urachus remains patent in the middle, but both ends are closed.

• Forms a fluid-filled cyst in the midline between bladder and umbilicus.

Urogenital sinus ❌

• A normal embryological cavity that gives rise to parts of the urinary bladder, urethra, and genitalia.

• It is not a pathological remnant of the urachus.

None of these ❌

• Incorrect because the correct anomaly described is clearly a urachal fistula.

• Found in the central part of the glomerulus between capillaries.

• Functions:

  • Matrix-forming → they produce mesangial matrix, which supports the glomerular capillary loops.

  • Contractile → contain actin-like filaments; contraction regulates capillary surface area available for filtration.

  • Phagocytic → they clear immune complexes and trapped residues from the glomerular basement membrane (GBM).

  • Secretion → release cytokines, prostaglandins, and growth factors, contributing to glomerular regulation and pathology.

Podocytes ❌

• Specialized epithelial cells of the visceral layer of Bowman’s capsule.

• Have primary and secondary (foot) processes, forming filtration slits.

• Not phagocytic or matrix-forming.

Distal convoluted tubule cells ❌

• Epithelial cells specialized for reabsorption (e.g., Na⁺, Ca²⁺) under hormonal control (aldosterone, PTH).

• Not located among glomerular capillaries, and not phagocytic.

Juxtaglomerular cells ❌

• Modified smooth muscle cells in the afferent arteriole wall.

• They secrete renin, regulating blood pressure via RAAS.

• Not phagocytic, nor matrix-forming inside the glomerulus.

Basal lamina cells ❌

• Refers to the glomerular basement membrane (GBM) structure itself, not discrete cells.

• Provides filtration barrier but does not actively contract or phagocytose.

• At the end of an information or counseling session, a common patient-centered technique called the “teach-back method” is recommended.

• The patient is asked to briefly summarise:

  • Details of the disease/condition (what they have and why it matters).

  • Details of the drug (name, purpose, dosage, side effects, adherence).

  • Details of the doctor/healthcare provider’s instructions (follow-up, precautions, lifestyle advice).

• This ensures that the patient has understood the key points, strengthens recall, and identifies gaps in communication.

None of these ❌

• Incorrect, because patients are encouraged to summarise what they learned.

Details of the doctor ❌

• While knowing the provider’s name is useful, it’s not the main purpose of summarising an information session.

Details of the drug ❌

• Partial answer. The patient must recall not just medication details but also their illness and medical advice.

Details of the disease ❌

• Again, incomplete — the drug and instructions are equally important.

• The traditional microbiological criterion for a significant UTI is the presence of ≥100,000 colony forming units (CFU)/ml of a single organism in a midstream, clean-catch urine sample.

• This threshold helps distinguish between true infection and contamination.

• Thus, the diagnostic culture result is 100,000 CFU/ml or more.

100–1000 CFU/ml ❌

• Too low to indicate infection. This level is usually considered contamination from urethra or perineum.

50,000–100,000 CFU/ml ❌

• This is a borderline range. In symptomatic women, ≥10⁴ CFU/ml may sometimes be considered significant, but standard textbooks and exam criteria stick with ≥10⁵ CFU/ml.

1000–5000 CFU/ml ❌

• Not considered diagnostic. Again, most likely contamination.

10,000–100,000 CFU/ml ❌

• Same as above — can occasionally suggest infection in children or catheterized patients, but in classic exam settings the cutoff is ≥100,000 CFU/ml.

• The kidney is maintained in position by a combination of structural supports:

• Perinephric fat (perirenal fat) → surrounds the kidney, providing cushioning and support. Loss of this fat (e.g., in extreme weight loss) can lead to nephroptosis (downward displacement).

• Renal fascia (Gerota’s fascia) → fibrous connective tissue layer that encloses the kidney and adrenal gland. It anchors the kidney to surrounding structures, preventing excessive movement.

• Collagen bundles → part of the fibrous capsule and surrounding connective tissue that firmly adheres to the kidney and provides stability.

• Paranephric fat → located outside the renal fascia, also contributes to holding the kidney in place within the retroperitoneum.

• Since all of these structures contribute, the correct choice is “All of these.”

Why not each option alone?

• If only perinephric or paranephric fat were present, the kidney would still be mobile.

• Renal fascia alone provides anchorage but is aided by the fat cushions.

• Collagen alone gives firmness but not positional stability.

• It’s the combination that maintains the kidney in its anatomical position.

• When a renal mass is incidentally found on ultrasound, the gold standard next step is a contrast-enhanced CT scan of the abdomen (CT KUB/CT abdomen with contrast).

• CT allows:

  • Differentiation between solid vs cystic masses.

  • Assessment of vascularity, calcification, fat content, necrosis.

  • Accurate staging if malignancy (e.g., renal cell carcinoma) is suspected.

• This is essential for guiding management decisions.

Plain radiography KUB ❌

• Useful for detecting renal calculi, but not for characterizing renal masses.

• Cannot differentiate solid vs cystic lesions.

MRI pelvis ❌

• MRI is helpful in renal mass characterization, particularly in patients with contraindications to contrast CT (e.g., allergy, poor renal function).

• However, it is not the first-line follow-up after an incidental ultrasound finding.

Ultrasound KUB ❌

• The mass was already found on ultrasound.

• Repeat ultrasound adds little value for further characterization.

X-ray KUB ❌

• Similar to plain radiography, used for stones, not renal mass evaluation.

• No role in staging or characterizing renal tumors.

• Ultrasound of the kidneys, ureters, and bladder (KUB) is often considered the first-line investigation in suspected renal colic.

• It is non-invasive, radiation-free, inexpensive, and readily available — making it especially useful in emergency settings, children, and pregnant women.

• It can detect hydronephrosis, renal stones, and bladder pathology. Although not as sensitive as CT for small ureteric stones, it is generally the initial investigation of choice before proceeding to more advanced imaging if required.

Plain radiography KUB ❌

• Can detect only radiopaque stones (calcium oxalate, phosphate, struvite), but misses radiolucent ones (uric acid, cystine).

• Less sensitive overall compared to ultrasound.

MRI scan ❌

• Rarely used in acute stone disease because it does not detect calcifications well.

• More useful for soft tissue or vascular pathology, not acute renal colic.

CT scan ❌

• Non-contrast CT KUB is the most accurate imaging modality, but due to radiation exposure and cost, it is not always the first investigation.

• It is usually reserved for cases where ultrasound is inconclusive.

X-ray KUB ❌

• Similar to plain radiography; limited use in initial diagnosis.

• Cannot detect radiolucent stones and provides less information compared to ultrasound.

Retroperitoneal fibrosis (Correct) ✅

• Extrinsic causes are those that compress the ureter from outside, rather than originating within the lumen or the ureteral wall.

• Retroperitoneal fibrosis is characterized by dense fibrous tissue in the retroperitoneum, which can entrap and compress the ureters, leading to unilateral or bilateral partial obstruction.

• This is a classic example of an extrinsic cause.

Congenital vesicoureteral reflux ❌

• This is a functional/structural abnormality at the ureterovesical junction that allows backward flow of urine from bladder to ureter.

• It is not an extrinsic compression; it is an intrinsic congenital defect.

Renal calculi ❌

• Kidney/ureteral stones obstruct the ureter from within the lumen → intrinsic cause.

Ectopic fused kidney ❌

• Fusion anomalies (e.g., crossed fused ectopia) may cause ureteral distortion, but the obstruction is considered due to abnormal anatomy rather than a classical extrinsic compressive process.

Horseshoe kidney ❌

• In horseshoe kidney, the isthmus of renal tissue lies low across the midline. While it can alter ureteral course and predispose to obstruction, it is primarily a congenital positional anomaly of the kidney, not a typical acquired extrinsic compressive cause.

Indole positive gram-negative rods (Correct) ✅

• The most common cause of community-acquired urinary tract infections (UTIs) is Escherichia coli.

• E. coli is a gram-negative rod, lactose fermenter, and indole positive.

• The nitrite-positive urine test strongly suggests infection by an enteric gram-negative rod, because these bacteria reduce urinary nitrates to nitrites (a property of E. coli and other Enterobacteriaceae).

• Thus, the correct description of the pathogen is indole positive gram-negative rods.

Catalase negative gram-positive rods ❌

• Most gram-positive rods (e.g., Corynebacterium, Listeria) are not typical causes of UTI. Catalase-negative organisms are usually streptococci, which are cocci, not rods.

Gram-negative spiral rods ❌

• Refers to organisms like Helicobacter pylori or Campylobacter, which cause GI infections, not UTIs.

Urease positive gram-negative rods ❌

• Refers to Proteus species.

• Proteus mirabilis causes UTIs with alkaline urine and struvite stones (due to urease activity), but it is not the most common cause.

• The question asks for the most common causative agent, which is E. coli.

Catalase positive gram-positive rods ❌

• Describes organisms like Corynebacterium diphtheriae — not a urinary pathogen.

125/75 mmHg (Correct) ✅

• In patients with chronic kidney disease (CKD), especially when proteinuria is present, strict blood pressure control is crucial to slow progression of renal damage.

• Guidelines recommend:

  • <130/80 mmHg for CKD patients without significant proteinuria.

  • ~125/75 mmHg for CKD patients with proteinuria (>1 g/day or even 1+), because proteinuria accelerates glomerular injury and stricter control offers renal protection.

• Thus, the best target here is 125/75 mmHg.

140/90 mmHg ❌

• Acceptable for the general population or uncomplicated hypertension, but too high for patients with CKD and proteinuria.

160/100 mmHg ❌

• Much too high — poorly controlled BP at this level will rapidly worsen renal damage and cardiovascular risk.

150/90 mmHg ❌

• Still above the recommended target for CKD with proteinuria.

130/80 mmHg ❌

• Correct for CKD patients without proteinuria, but for those with proteinuria, the goal is stricter (<125/75 mmHg).

Chlamydia trachomatis (Correct) ✅

• Chlamydia is the most common cause of non-gonococcal urethritis (NGU) in young sexually active men.

• Hallmark clue: neutrophils present in urine/urethral discharge, but no bacteria seen on Gram stain or culture, because Chlamydia is an obligate intracellular organism and does not grow on routine media.

• This explains the “sterile pyuria” (WBCs in urine without detectable bacteria).

Escherichia coli ❌

• Common cause of urinary tract infections (UTIs) and prostatitis.

• But E. coli is a Gram-negative bacillus easily seen on culture and Gram stain — so it would not present as WBCs without bacteria.

Treponema pallidum ❌

• Causes syphilis, which typically presents with a painless chancre or systemic signs later (rash, gummas).

• It does not cause acute urethritis with pyuria and negative cultures.

Candida albicans ❌

• Can cause yeast infections of the urinary tract or genitals, especially in immunocompromised or catheterized patients.

• Would typically show budding yeast/pseudohyphae on microscopy, not a sterile pyuria.

Coxiella burnetii ❌

• Causes Q fever, usually presenting with fever, hepatitis, or atypical pneumonia.

• Not a genitourinary pathogen in this context.

Lupus nephritis (Correct) ✅

• The key clue here is the systemic feature: oral ulcers. This strongly suggests systemic lupus erythematosus (SLE), which can involve the kidneys.

• SLE leads to immune complex deposition in the glomeruli → lupus nephritis.

• Renal manifestations include hematuria, proteinuria, and sometimes pyuria (WBCs in urine without infection).

• Proteinuria in this case is mild (+1), which fits early or less severe lupus nephritis.

IgA nephropathy ❌

• Typically presents after a respiratory or GI infection with gross hematuria (synpharyngitic hematuria).

• Oral ulcers are not a feature.

Membranous nephropathy ❌

• Causes nephrotic syndrome (heavy proteinuria, >3.5 g/day, hypoalbuminemia, edema).

• This patient has only mild proteinuria and hematuria, not nephrotic-range findings.

Acid excretion ❌

• Not a diagnosis — more a physiological process. Not relevant here.

Glomerulonephritis ❌

• A general term that could describe the findings, but the question is asking for the specific most probable cause. The systemic clue (oral ulcers) points clearly toward lupus nephritis

Paracellular route (Correct) ✅

• In the proximal convoluted tubule (PCT), about 65% of filtered calcium is reabsorbed.

• Most of this reabsorption occurs passively, via the paracellular route between cells, driven by:

  • Solvent drag (as water follows sodium and other solutes, it carries calcium along).

  • The slight positive transepithelial potential difference in this segment.

• Importantly, this process is not under strong hormonal regulation here (unlike in the distal nephron).

Transcellular route ❌

• Occurs mainly in the distal convoluted tubule (DCT), where calcium enters cells via TRPV5 channels, binds to calbindin, and is extruded basolaterally by Na⁺/Ca²⁺ exchanger (NCX1) and Ca²⁺-ATPase.

• This segment is under tight regulation by parathyroid hormone (PTH).

Facilitated diffusion ❌

• Facilitated diffusion involves carrier proteins, but calcium in the PCT does not primarily use this pathway.

Secondary active transport ❌

• Not the main mechanism for calcium here. Secondary active transport is more relevant for glucose (via SGLT) or phosphate with sodium, not calcium in the PCT.

Active transport ❌

• Calcium is not actively pumped across PCT cells. Active calcium transport does occur in the DCT, but not in the PCT.

Thick ascending limb of loop of Henle (Correct) ✅

• The Na⁺-K⁺-2Cl⁻ symporter (NKCC2) is located here and plays a central role in establishing the medullary concentration gradient through the countercurrent multiplier system.

• This segment is impermeable to water, so reabsorption of solutes without water makes the tubular fluid hypotonic while concentrating the medullary interstitium.

• Clinically, this is the target of loop diuretics (furosemide, bumetanide, torsemide).

Collecting duct ❌

• Sodium transport here occurs mainly via ENaCs (epithelial sodium channels) regulated by aldosterone, not the Na⁺-K⁺-2Cl⁻ symporter.

Proximal convoluted tubule ❌

• Major sodium reabsorption here is via Na⁺-glucose symporter (SGLT), Na⁺-H⁺ exchanger (NHE3), and other cotransporters, not NKCC2.

Thin ascending limb of loop of Henle ❌

• This segment is permeable to solutes but lacks the Na⁺-K⁺-2Cl⁻ transporter in high abundance; instead, solute movement is largely passive.

Thin descending limb of loop of Henle ❌

• This part is highly permeable to water, not solutes. It lacks significant active transporters like NKCC2.

Decreased Na⁺-H⁺ exchange (Correct) ✅

• Normally, in the proximal tubule, sodium is reabsorbed in exchange for hydrogen ions (via the Na⁺/H⁺ exchanger, NHE3).

• The secreted H⁺ combines with filtered HCO₃⁻ to form carbonic acid, which breaks down into CO₂ and H₂O. These are reabsorbed and eventually regenerate bicarbonate inside the cell.

• If Na⁺-H⁺ exchange decreases, less H⁺ is secreted → less HCO₃⁻ is reabsorbed → more bicarbonate stays in the lumen and is excreted.

• To maintain electroneutrality, chloride reabsorption falls, and bicarbonate replaces chloride as the major urinary anion.

Increased Na⁺-H⁺ exchange ❌

• Would do the opposite: increase H⁺ secretion → more HCO₃⁻ reabsorption → less bicarbonate in urine.

Retention of acid metabolites ❌

• This refers to conditions like renal failure, where acids accumulate. It doesn’t directly cause bicarbonate to replace chloride in the urine.

Ketoacidosis ❌

• In ketoacidosis, the urine contains ketone bodies and usually chloride is preserved. The question specifically asks about bicarbonate replacing chloride, which happens in metabolic alkalosis or decreased H⁺ secretion states, not ketoacidosis.

Increased acid secretion ❌

• If more acid is secreted, bicarbonate is conserved, not excreted. This would not lead to HCO₃⁻ replacing Cl⁻ in the urine.

Glutamine, carbon dioxide, and aspartate (Correct) ✅

• Pyrimidine synthesis begins with carbamoyl phosphate, formed by carbamoyl phosphate synthetase II (CPS II) in the cytosol.

• CPS II uses glutamine (as nitrogen donor) and CO₂ (as carbon source).

• Later, aspartate combines with carbamoyl phosphate to form carbamoyl aspartate, the first committed step toward pyrimidines.

• Thus, all three — glutamine, CO₂, and aspartate — are essential.

Glutamine and aspartate ❌

• Partially correct, but incomplete — carbon dioxide is also required.

Aspartate only ❌

• Aspartate is necessary (contributes atoms to the pyrimidine ring), but cannot form pyrimidines on its own.

NADH only ❌

• NADH is important in general metabolism but is not a building block in pyrimidine synthesis.

Glutamine and NADH ❌

• Again, NADH is irrelevant here. Carbon dioxide and aspartate are missing, making this option wrong.

65% of filtered load is reabsorbed (True)

• The PCT reabsorbs about 65–70% of the filtered sodium load, along with water, chloride, bicarbonate, and nutrients like glucose and amino acids.

• This is a standard physiology fact and is correct.

80% of filtered load is reabsorbed (False) ❌ → Correct Answer

• Sodium reabsorption is substantial in the PCT, but it does not reach 80%.

• The extra sodium reabsorption beyond the PCT occurs in the loop of Henle, DCT, and collecting ducts.

• Thus, this statement overestimates PCT contribution and is not true.

None of these ❌

• Incorrect because one of the statements is clearly false (80%).

Reabsorption occurs through Na⁺-H⁺ ATPase pump (True)

• Sodium is reabsorbed in the PCT mainly via Na⁺/K⁺ ATPase pump on the basolateral membrane, which drives sodium out of the cell into blood, maintaining a low intracellular sodium concentration.

• On the apical side, sodium enters via Na⁺/H⁺ exchanger (NHE3), sodium-glucose symporter (SGLT), and other co-transporters.

• So, this mechanism is correctly described.

Sodium shares the same transporter as glucose (True)

• Glucose is reabsorbed in the PCT via sodium-glucose cotransporter (SGLT) on the apical membrane.

• This is a classic example of secondary active transport where sodium gradient drives glucose uptake.

Aldosterone (Correct) ✅

• Principal cells are located in the late distal convoluted tubule and collecting ducts.

• Aldosterone binds to intracellular mineralocorticoid receptors in principal cells, leading to increased expression of:

  • ENaCs (epithelial sodium channels) on the apical side → ↑ Na⁺ reabsorption.

  • Na⁺/K⁺-ATPase on the basolateral membrane → pumps sodium into blood and brings K⁺ into cells.

  • Enhanced K⁺ secretion into the lumen.

• Net effect: Na⁺ and water retention, K⁺ and H⁺ excretion.

Parathyroid hormone ❌

• Acts on the proximal tubule (inhibits phosphate reabsorption) and the distal tubule (stimulates calcium reabsorption).

• It does not act on principal cells.

Anti-diuretic hormone (ADH) ❌

• Acts mainly on principal cells too, but via V2 receptors, inserting aquaporin-2 channels to increase water permeability.

• However, in exam settings, when they ask specifically about the hormone classically associated with principal cells, the answer is aldosterone. ADH’s role is water balance rather than Na⁺/K⁺ exchange.

Angiotensin ❌

• Angiotensin II acts primarily on the proximal tubule to stimulate sodium reabsorption and also constricts efferent arterioles.

• Its main target is not the principal cells.

Cortisol ❌

• Cortisol can bind to mineralocorticoid receptors, but in the kidney, the enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) converts cortisol to inactive cortisone, preventing its action.

• Therefore, cortisol normally does not drive principal cell activity.

UT-2 (Correct) ✅

• Urea transporters (UTs) are specialized proteins that facilitate passive urea movement in different nephron segments.

• UT-2 is expressed in the thin descending limb and thin ascending limb of the loop of Henle, where it allows urea secretion from the medullary interstitium into the tubular lumen.

• This recycling of urea into the loop of Henle is critical for maintaining the medullary osmotic gradient, which drives water reabsorption under ADH influence.

UT-1 ❌

• Located in the inner medullary collecting duct (IMCD).

• Functions mainly in urea reabsorption (from tubular fluid into medullary interstitium), especially under ADH control.

UT-3 ❌

• Found in the vasa recta, facilitating urea exchange between blood and interstitium.

• Helps maintain the countercurrent exchange system but not directly responsible for urea secretion in the loop of Henle.

UT-4 ❌

• Less commonly tested, but generally associated with non-renal tissues.

• Not significant in loop of Henle physiology.

UT-5 ❌

• Rarely referenced in standard nephron physiology.

• Not the transporter responsible for loop of Henle secretion.

Bowman’s capsule (Correct) ✅

• The visceral layer of Bowman’s capsule is formed by specialized epithelial cells called podocytes.

• Podocytes have primary processes that give rise to secondary processes (foot processes or pedicels), which wrap around the glomerular capillaries.

• These processes interdigitate, leaving filtration slits that are spanned by slit diaphragms (containing nephrin protein).

• This structure is essential for selective filtration of plasma into the urinary space.

Distal convoluted tubule ❌

• The DCT contains cuboidal epithelial cells with few microvilli (smooth lumen) but no podocytes and no primary/secondary processes.

Proximal convoluted tubule ❌

• PCT cells are also cuboidal, with a brush border (dense microvilli) to increase surface area for absorption.

• These microvilli are not the same as podocyte processes — they are apical modifications, not specialized interdigitating foot processes.

Macula densa ❌

• This is a specialized region of the DCT near the glomerulus.

• Cells here sense sodium chloride concentration and regulate renin release via juxtaglomerular cells.

• They are tightly packed columnar cells, but they do not have primary or secondary processes.

Collecting duct ❌

• The collecting duct contains principal cells (water and Na⁺ regulation) and intercalated cells (acid–base regulation).

• No podocytes or specialized foot processes are present here.

Proteus mirabilis (Correct) ✅

• Proteus species are Gram-negative rods, non-lactose fermenters, and are famous for their swarming motility on agar plates.

• Among them, Proteus mirabilis is the most common cause of urinary tract infections (UTIs), especially in elderly males, patients with catheters, or those with structural urinary tract abnormalities.

• They produce urease, which alkalinizes urine and predisposes to struvite stone formation.

Pseudomonas aeruginosa ❌

• Also a Gram-negative rod and non-lactose fermenter, but it does not exhibit swarming motility.

• Instead, it produces a characteristic blue-green pigment (pyocyanin) and has a grape-like odor.

• More often associated with catheter-related infections, burns, and hospital-acquired infections.

Proteus vulgaris ❌

• Shares many features with P. mirabilis (swarming, urease positivity).

• However, P. vulgaris is less common in UTIs compared to P. mirabilis.

• In exam settings, when swarming motility and UTI are described, the answer is usually P. mirabilis.

Escherichia coli ❌

• The most common cause of community-acquired UTI, but it is a lactose fermenter (pink colonies on MacConkey agar).

• The question specifically says non-lactose fermenting, which rules it out.

Enterococcus faecalis ❌

• A Gram-positive cocci, not a Gram-negative rod.

• Important cause of hospital-acquired UTIs, especially with catheters, but the Gram stain and motility pattern exclude it.

Cortical columns (Correct) ✅
Also known as columns of Bertin, these are cortical tissue extensions that project inward between adjacent renal pyramids of the medulla. They contain blood vessels and urinary tubules and help structurally separate the renal pyramids. They are part of the cortex, not the medulla.

Minor calyx ❌
This is part of the renal collecting system. A minor calyx collects urine from the papilla (apex) of each renal pyramid. It is not a cortical structure.

Major calyx ❌
Formed by the convergence of several minor calyces, the major calyces drain into the renal pelvis. Like the minor calyx, this belongs to the collecting system, not the cortical/medullary tissue.

Medullary rays ❌
These are vertical striations in the cortex, extending from the base of the pyramids into the cortex. They consist of straight tubules and collecting ducts, not cortical extensions into the medulla.

Cortical rays ❌
This term is sometimes used synonymously with medullary rays, referring to the same structures extending into the cortex. They are not the cortical tissue between pyramids.

T12–L3 (Correct) ✅
Each kidney extends vertically from the level of T12 superiorly to L3 inferiorly. The right kidney is usually slightly lower than the left because of the large right lobe of the liver. This vertebral span is a classic anatomical relationship, important for surface anatomy, imaging interpretation, and surgical approaches.

T12–L1 ❌
This range is too short. The kidneys are larger and extend lower than L1, so this option underestimates their true anatomical span.

T12–L4 ❌
This range is too long. Kidneys don’t usually extend down to L4; that would place the lower pole well into the pelvic cavity, which is not normal (except in cases like nephroptosis).

T12–L2 ❌
This misses the inferior pole — the kidneys extend below L2, down to about L3.

T11–L3 ❌
Too high — the upper pole of the kidney does not usually reach T11 (except sometimes the left kidney slightly). Normally, T12 is the correct upper landmark.

Metabolic alkalosis (Correct) ✅
Aldosterone acts on the principal cells and intercalated cells of the distal nephron.

• In principal cells: it increases sodium reabsorption and potassium secretion.

• In intercalated cells (type A): it promotes H⁺ secretion into the tubular lumen.
  Excess H⁺ secretion → loss of acid → rise in plasma bicarbonate → metabolic alkalosis. This is why conditions like primary hyperaldosteronism (Conn’s syndrome) often present with metabolic alkalosis and hypokalemia.

Hyponatremia ❌
Aldosterone actually causes sodium retention. Hyponatremia would not result unless there was excessive free water retention (e.g., in SIADH).

Hypernatremia ❌
Although aldosterone promotes sodium reabsorption, it is usually accompanied by water reabsorption (due to ADH and thirst mechanisms). Thus, plasma sodium concentration does not usually rise significantly — so hypernatremia is not a direct effect.

Hyperkalemia ❌
Aldosterone increases potassium secretion → hypokalemia, not hyperkalemia. This is why patients with aldosterone excess often present with low serum potassium.

Metabolic acidosis ❌
The opposite occurs. By promoting H⁺ secretion, aldosterone prevents acidosis. Acidosis may occur in aldosterone deficiency (Addison’s disease).

1200 mOsm/L (Correct) ✅
The renal medulla exhibits a high osmolarity gradient, created by the countercurrent multiplier system of the loop of Henle and the urea recycling from the collecting ducts. At the deepest part of the medulla (inner medulla near the papilla), the interstitial fluid can reach a maximum osmolarity of about 1200 mOsm/L in humans (and up to ~1400 in some species). This hyperosmotic environment is crucial for water reabsorption in the collecting ducts under the influence of ADH.

1800 mOsm/L ❌
This is higher than what is physiologically achieved in humans. Some desert animals (e.g., kangaroo rat) can concentrate urine to such high osmolarity, but not humans.

600 mOsm/L ❌
This value is too low. It may correspond to the mid-medullary region (not the maximum osmolarity) or to conditions where concentration is impaired, but it does not represent the peak osmolarity at the papilla.

1000 mOsm/L ❌
Closer to the correct value but still below the established maximum in humans. This might be seen in moderately concentrated states, but not as the highest osmolarity.

800 mOsm/L ❌
Again, lower than the physiological maximum. This value would more likely be observed in species with less concentrating ability or in partial dehydration states, not in the deepest medulla of humans.

Body (Correct) ✅
The body of the bladder is the primary distensible region. As urine accumulates, its walls stretch out while maintaining relatively low internal pressure because of the rugae and the bladder’s compliance. This adaptation allows storage of urine without immediate triggering of the micturition reflex.

Fundus ❌
The fundus, or posterior dome, does not undergo major change during bladder filling. It is more of a fixed anatomical landmark rather than the main site of expansion.

Trigone ❌
The trigone, lying between the two ureteric orifices and the internal urethral orifice, remains stable and non-distensible. Its rigidity ensures that the openings of the ureters and urethra are not distorted, thus preventing backflow of urine (vesicoureteral reflux).

Neck ❌
The neck of the bladder leads into the urethra and is associated with the internal urethral sphincter. It remains firm and fixed in position, designed to regulate urine outflow rather than storage.

Base ❌
The base of the bladder, forming its lower part, also does not undergo much change in filling. Like the trigone and neck, it maintains the orientation of bladder outlets rather than serving as a reservoir.

Metabolic alkalosis occurs when there is a primary increase in plasma bicarbonate (HCO₃⁻), usually due to loss of hydrogen ions (e.g., vomiting, diuretics) or excess alkali intake.

• The rise in HCO₃⁻ leads to a rise in plasma pH (alkalemia).

• As compensation, the respiratory system hypoventilates to retain CO₂, but this is only partial and cannot fully normalize pH.

• Thus, the hallmark of metabolic alkalosis is elevated plasma HCO₃⁻ and elevated pH.

Why Other Options Are Wrong

• HCO₃⁻ only ❌ – Increase in bicarbonate alone is not enough; the pH also rises.

• Plasma pH only ❌ – pH rise happens, but it is directly due to elevated HCO₃⁻, so both increase.

• Plasma pH and pCO₂ ❌ – pCO₂ actually tends to increase compensatorily, but that is not the primary change. The defining features are ↑ pH + ↑ HCO₃⁻.

• Plasma pH and lactic acid ❌ – Lactic acid increases in metabolic acidosis, not alkalosis.

The ureter has a segmental blood supply along its course, and the arterial supply differs for the upper, middle, and lower parts:

• Upper part of the ureter → Supplied mainly by the renal artery.

• Middle part of the ureter → Supplied by branches from the gonadal arteries (testicular/ovarian), as well as the abdominal aorta and common iliac artery.

• Lower part of the ureter → Supplied by branches of the internal iliac artery (e.g., superior vesical artery, uterine artery in females, inferior vesical artery in males).

Thus, the renal artery is the key supplier of the upper ureter.

Why Other Options Are Wrong

• Internal iliac artery ❌ – Supplies the lower part of ureter, not the upper.

• External iliac artery ❌ – Does not significantly supply the ureter.

• Common iliac artery ❌ – Contributes to the middle part, not the upper.

• Gonadal artery ❌ – Supplies the middle portion, not the upper ureter.

This patient presents with nephrotic syndrome (proteinuria, hypoalbuminemia, edema, hyperlipidemia). The biopsy findings are classic:

• Light microscopy (LM): Normal glomeruli → no obvious histological abnormality.

• Electron microscopy (EM): Effacement (fusion) of podocyte foot processes → hallmark feature.

• Immunofluorescence (IF): Negative (no immune deposits).

This triad points directly toward Minimal Change Disease (MCD).

• It is the most common cause of nephrotic syndrome in children and can occur in young adults as well.

• It usually responds dramatically to corticosteroids.

Why Other Options Are Wrong

• Acute pyelonephritis ❌ – A bacterial infection of kidney; presents with fever, flank pain, WBC casts, not nephrotic syndrome.

• Chronic pyelonephritis ❌ – Recurrent infections → scarring and deformities of calyces; not associated with podocyte effacement.

• IgA nephropathy ❌ – Causes recurrent hematuria (nephritic syndrome), not classic nephrotic syndrome.

• Rapidly progressive glomerulonephritis ❌ – Nephritic syndrome with crescents on LM, hematuria, oliguria; very different histology.

The ureter has segmental lymphatic drainage that follows its anatomical course:

• Abdominal part of the ureter → drains into paraaortic (lumbar) lymph nodes, located along the abdominal aorta.

• Pelvic part of the ureter → drains into common iliac, external iliac, and internal iliac nodes, depending on the level.

This makes sense because lymphatics generally follow the blood supply:

• The abdominal ureter is supplied by branches from the renal, gonadal, and abdominal aortic vessels → hence it drains to the paraaortic nodes.

Why Other Options Are Wrong

• Deep inguinal nodes ❌ – Drain superficial structures of lower limb, perineum, lower abdominal wall, not the ureter.

• External iliac nodes ❌ – Drain pelvic viscera like bladder, prostate, cervix; not the abdominal ureter.

• Common iliac nodes ❌ – Important for pelvic ureter drainage, not the abdominal part.

• Internal iliac nodes ❌ – Drain pelvic organs (rectum, prostate, cervix, vagina, bladder base), not abdominal ureter.

• Allopurinol is a structural analog of hypoxanthine, a natural purine base.

• After administration, allopurinol is converted to oxypurinol (alloxanthine), which strongly inhibits xanthine oxidase, the enzyme responsible for converting hypoxanthine → xanthine → uric acid.

• By inhibiting this pathway, allopurinol lowers uric acid production, making it a cornerstone in the management of gout and hyperuricemia.

Why Other Options Are Wrong

• Uric acid ❌ – Allopurinol decreases uric acid production but is not a structural analog of it.

• Xanthine oxidase ❌ – This is the enzyme target, not the structural analog.

• Inosine monophosphate (IMP) ❌ – Intermediate in purine nucleotide metabolism, unrelated structurally.

• Phosphoribosyl pyrophosphate (PRPP) ❌ – A ribose-phosphate donor in nucleotide synthesis, not structurally similar to allopurinol.

• Micturating cystourethrography (MCUG/VCUG) is an X-ray study in which contrast is instilled into the bladder and images are taken during filling and micturition.

• Its primary indication is to diagnose vesicoureteric reflux (VUR) – the abnormal backward flow of urine from the bladder into the ureters and kidneys.

• It can also evaluate bladder anatomy, posterior urethral valves, strictures, or fistulae, but the main and most common reason is suspected VUR, especially in children with recurrent UTIs.

Why Other Options Are Wrong

• Acute urinary tract infection ❌ – Contraindicated during acute infection; risk of worsening the infection.

• Fistula ❌ – Can be demonstrated, but it is not the primary indication.

• Urethral trauma ❌ – Retrograde urethrography (RUG) is preferred for trauma evaluation, not MCUG.

• Urethral malignancy ❌ – CT urography, MRI, or cystoscopy are better for assessing malignancy.

• Clinical clue 1: Age & Presentation – A 10-year-old boy with palpable purpura over lower extremities and buttocks is highly suggestive of HSP, an IgA-mediated small-vessel vasculitis.

• Clinical clue 2: Renal involvement – HSP can present with a nephritic syndrome picture (hematuria, RBC casts, mild proteinuria, ↓GFR).

• Triad of HSP:

  1. Palpable purpura (non-thrombocytopenic, usually lower limbs/buttocks)

  2. Arthralgia/arthritis

  3. Abdominal pain

  4. Renal involvement (similar to IgA nephropathy)

Why Other Options Are Wrong

• Minimal change disease ❌ – Common in children but presents with nephrotic syndrome (massive proteinuria, edema, hypoalbuminemia) without purpura.

• Systemic lupus erythematosus (SLE) ❌ – Can cause nephritis, but SLE is more common in adolescent females; purpura with buttock predominance is not classic.

• Focal segmental glomerulosclerosis (FSGS) ❌ – Causes nephrotic syndrome, not palpable purpura.

• Post-streptococcal glomerulonephritis (PSGN) ❌ – Also nephritic, but follows a recent strep infection; rash is not a feature.

• 0.9% Normal Saline (NS) is called “isotonic saline.”

• It contains 9 g of NaCl per liter of water.

• When dissolved, sodium chloride dissociates completely into Na⁺ and Cl⁻ ions.

• This gives:

  • 154 mmol/L of Sodium (Na⁺)

  • 154 mmol/L of Chloride (Cl⁻)

• The osmolarity is therefore about 308 mOsm/L, which is close to plasma osmolarity (~285–295 mOsm/L), making it “isotonic.”

Why Other Options Are Wrong

• Na 159, Cl 154 ❌ – Sodium is not 159 mmol/L; it’s 154.

• Na 154, Cl 150 ❌ – Chloride is equal to sodium, not slightly less.

• Na 150, Cl 154 ❌ – Sodium is not lower than chloride.

• None of these ❌ – Incorrect because the correct pair Na 154, Cl 154 is present in the options.

Why “Free Water Restriction” is Correct:

This clinical scenario presents a classic case of chronic, asymptomatic, euvolemic hyponatremia. The most likely cause, given the patient’s history of being thin, elderly, and bed-bound for a year, is the Syndrome of Inappropriate Antidiuretic Hormone (SIADH). Common triggers in this setting include chronic illness, pain, and immobilization.

The cornerstone of management for chronic, asymptomatic SIADH is free water restriction. Here’s why:

1. Pathophysiology: SIADH is characterized by inappropriate water retention due to excess ADH. The body holds onto water, diluting the sodium. The problem is not a total lack of sodium, but an excess of water relative to sodium.
2. Asymptomatic Nature: Because the hyponatremia has developed slowly over time, the brain has had time to adapt by extruding osmolytes. This prevents cerebral edema and neurological symptoms. Rapid correction is unnecessary and dangerous.
3. Risk of Rapid Correction: The major danger in this situation is causing osmotic demyelination syndrome (ODS), a catastrophic neurological injury that can occur if chronic hyponatremia is corrected too quickly. The goal rate of correction should be no more than 4-6 mmol/L in 24 hours.
4. Mechanism of Action: Restricting free water intake (e.g., to 800-1000 mL/day) allows the body to excrete the excess water gradually and naturally, raising the sodium concentration slowly and safely.

Why the Other Options Are Incorrect:

Repeat sodium: While it is always prudent to ensure a lab value is accurate, a sodium level of 125 mmol/L is significantly low and likely real. The clinical context (elderly, bed-bound) strongly supports a legitimate chronic hyponatremia. Repeating the lab does not constitute management; it is merely a diagnostic confirmation step. The first management step is free water restriction.

Add sodium chloride tablet: This is incorrect and potentially harmful. Administering salt tablets without addressing the underlying water excess is ineffective. In SIADH, the kidneys will simply excrete the ingested sodium while retaining water, failing to correct the imbalance and potentially worsening the urinary sodium loss. This is not a treatment for euvolemic hyponatremia.

Start hypertonic saline immediately: This is absolutely contraindicated and dangerous. Hypertonic saline (3% NaCl) is reserved for patients with severe symptomatic hyponatremia (e.g., seizures, coma). Using it in an asymptomatic patient with chronic hyponatremia drastically increases the risk of causing osmotic demyelination, leading to permanent brain damage or death.

None of these: This is incorrect because “Free water restriction” is the correct and evidence-based first step.

The most common cause of acute kidney injury (AKI) overall is Acute Tubular Necrosis (ATN).

• ATN is an intrinsic renal cause of AKI.

• It typically follows either:

  • Ischemia (prolonged pre-renal states such as hypovolemia, shock, sepsis)

  • Nephrotoxins (aminoglycosides, radiocontrast, heavy metals, myoglobin in rhabdomyolysis).

• Pathophysiology: Renal tubular epithelial cell injury → tubular necrosis & sloughing → obstruction → ↓ GFR.

• Urine findings: Muddy brown granular casts are classic for ATN.

Why Other Options Are Wrong

Pre-renal failure ❌

• Very common but represents a functional decrease in renal perfusion, not actual renal injury. If untreated, it may progress to ATN.

Acute glomerulonephritis ❌

• Much less common; presents with hematuria, proteinuria, and RBC casts, but not the leading cause of AKI.

Post-renal failure ❌

• Due to obstruction (stones, BPH, tumors); important but far less frequent than ATN.

Tubulo-interstitial nephritis ❌

• Usually drug-induced (e.g., penicillins, NSAIDs); relatively rare compared to ATN.

To differentiate pre-renal from renal (intrinsic) acute renal failure, the urine analysis is most useful because it directly reflects kidney function at the tubular level.

• Pre-renal failure (due to hypoperfusion without tubular damage):

  • Urine osmolality: >500 mOsm/kg (concentrated urine)

  • Urine sodium: <20 mEq/L

  • Fractional excretion of sodium (FENa): <1%

  • Urine sediment: Bland, no casts

• Renal failure (intrinsic, e.g., acute tubular necrosis):

  • Urine osmolality: <350 mOsm/kg (dilute urine)

  • Urine sodium: >40 mEq/L

  • FENa: >2%

  • Urine sediment: Granular (“muddy brown”) casts, tubular epithelial cells

Thus, urine findings help determine whether the problem is functional (pre-renal) or structural (renal).

Why Other Options Are Wrong

Computed tomography (CT) pyelogram ❌

• Used for obstructive uropathy, stones, or masses, not for functional differentiation between pre-renal vs renal ARF.

Serum creatinine ❌

• Elevated in both pre-renal and renal failure, cannot differentiate the cause.

Arterial blood gases (ABGs) ❌

• May show metabolic acidosis in renal failure, but does not help distinguish pre-renal from intrinsic renal causes.

Ultrasound kidneys, ureters, and bladder (KUB) ❌

• Useful to exclude post-renal obstruction, but not for pre-renal vs renal differentiation.

• Effective communication is the foundation of safe and ethical medical practice.

• When a patient does not understand the language, giving treatment without proper counselling or relying on partial understanding can lead to misuse of medicines, non-compliance, or harm.

• The best and most ethical option is to involve a colleague (or interpreter) who speaks the patient’s language, ensuring that the patient directly receives the information. This maintains accuracy, confidentiality, and patient autonomy.

Why Other Options Are Wrong

Admit the patient till you can find a doctor who speaks their language ❌

• Unnecessary, impractical, and a misuse of hospital resources. Admission should only be for medical needs.

Prescribe medication and do not provide informational care ❌

• Unsafe and unethical. Patients must understand their illness, medication use, and lifestyle changes in diabetes.

Provide informational care to her son ❌

• The son is only 14 years old, not a reliable translator. This risks miscommunication, loss of accuracy, and confidentiality issues.

Refer her to a doctor in Balochistan ❌

• Impractical and delays care. Patients should be managed where they present if possible, with available resources.

• In medicine, counselling is the process of educating, guiding, and supporting patients about their illness in a clear, empathetic, and professional way.

• The goal is to ensure the patient understands the nature of the disease, treatment options, risks, prognosis, and lifestyle modifications — all in simple, understandable language.

• It also addresses the emotional, psychological, and social concerns of the patient, helping them make informed decisions about their care.

Why the Other Options Are Wrong

Informational care ❌

• Too vague. Information is a part of counselling, but the structured and interactive process of explanation and support is specifically called counselling.

Crises intervention ❌

• Used in acute psychological emergencies (e.g., suicide attempt, panic attack, trauma). Not the same as routine patient education about cancer.

Psychotherapy ❌

• A form of treatment for mental health disorders (e.g., depression, anxiety). Colorectal cancer education is not psychotherapy.

Research ❌

• Involves systematic investigation to produce new knowledge. Not related to explaining an illness to an individual patient.

• Qualitative research is specifically designed to explore the subjective experiences, beliefs, perceptions, and motives behind human behavior.

• It seeks to answer “why” people think or act in a certain way, not just “what” or “how much”.

• Methods often include interviews, focus groups, case studies, and observation, focusing on depth of understanding rather than numbers.

Why the Other Options Are Wrong

Quantitative research ❌

• Deals with numerical data, statistics, and measurable outcomes.

• Answers “what,” “how much,” or “how many,” not “why.”

Medical research ❌

• A broad term that covers all forms of research in medicine (both qualitative and quantitative). Not specific to human motives/experiences.

Hospital-based research ❌

• Refers to the setting where research is conducted (hospital environment). It can be clinical, epidemiological, or basic — but not necessarily focused on subjective experiences.

Clinical research ❌

• Involves studying patients, treatments, and outcomes, usually quantitative, with the aim of improving diagnosis or therapy.

• The patient presents with chronic urinary symptoms (flank pain, dysuria), constitutional signs (fever, anorexia, weakness, ill-health), and a very high ESR (125).

• Urine microscopy shows many pus cells (pyuria) but the culture is negative → this is called sterile pyuria, which is a hallmark of genitourinary tuberculosis (renal TB).

• Mycobacterium tuberculosis is the classic cause of this presentation.

Why the Other Options Are Wrong

Escherichia coli ❌

• Most common cause of acute bacterial UTIs.

• Would typically show positive urine culture, not sterile pyuria.

Proteus mirabilis ❌

• Causes alkaline urine and struvite stones (triple phosphate crystals), not sterile pyuria with constitutional symptoms.

Staphylococcus aureus ❌

• Rare cause of UTI, more linked with hematogenous spread (abscesses). Would not usually cause sterile pyuria.

Klebsiella pneumoniae ❌

• Can cause hospital-acquired UTIs but culture would be positive.

• Proteus mirabilis is a urease-positive organism that splits urea into ammonia + CO₂, making the urine alkaline.

• Alkaline urine favors the precipitation of magnesium ammonium phosphate (struvite) crystals, seen in this patient as triple phosphate crystals.

• This can lead to recurrent urinary tract infections and the formation of staghorn calculi.

Why the Other Options Are Wrong

Pseudomonas aeruginosa ❌

• Can cause complicated UTIs, especially in catheterized patients, but it does not typically produce alkaline urine with triple phosphate crystals.

Serratia ❌

• Rare cause of UTIs; not strongly associated with crystal formation.

Klebsiella pneumoniae ❌

• Urease-positive but less commonly linked with struvite stones compared to Proteus.

• Proteus is the classic and most important cause.

Enterobacter ❌

• Can cause UTIs, especially in hospital settings, but no link to triple phosphate crystals.

• In elderly men, the most common cause of bladder outlet obstruction is benign prostatic hyperplasia (BPH), also known as nodular prostatic hyperplasia.

• BPH arises in the periurethral (transition) zone of the prostate and compresses the urethra, leading to:

  • Difficulty initiating urination

  • Weak stream

  • Urinary frequency/urgency

  • Acute urinary retention (complete inability to void)

• Recurrent urinary tract infections (as in this case) occur because incomplete emptying of the bladder favors bacterial growth.

Why the Other Options Are Wrong

Prostatic adenocarcinoma ❌

• Common in older men, but it usually arises in the peripheral zone of the prostate.

• Rarely causes obstruction until very late, because the urethra is not compressed early.

Urethral stricture ❌

• Can cause obstruction, but more common in younger men with prior trauma, infections, or instrumentation—not the typical cause in elderly patients.

Urothelial cell carcinoma of the bladder ❌

• Presents with painless hematuria, not recurrent cystitis + retention.

• It obstructs only if very advanced, which is less likely here.

Nephrogenic metaplasia ❌

• A rare reactive lesion of bladder mucosa after injury; does not cause obstruction.

• The most common immunologic mechanism in glomerular diseases is antibody-mediated injury.

• This occurs in two main ways:

  1. In situ formation of immune complexes → antibodies react with antigens within the glomerulus (e.g., anti-GBM disease, Goodpasture syndrome).

  2. Deposition of circulating immune complexes → preformed antigen–antibody complexes get trapped in the glomeruli (e.g., post-streptococcal glomerulonephritis, lupus nephritis).

• Both mechanisms lead to complement activation, recruitment of inflammatory cells, and glomerular injury.

• This explains why immune complex deposition and antibody-mediated processes are central to most glomerulopathies.

Why the Other Options Are Wrong

Type-1 hypersensitivity reaction ❌

• IgE-mediated (allergic reactions, anaphylaxis).

• Not the mechanism in glomerular injury.

Activation of alternative complement pathway ❌

• Plays a role in certain rare glomerulopathies (e.g., dense deposit disease), but not the most common mechanism overall.

Cell-mediated injury ❌

• T-cell mediated mechanisms contribute to some kidney diseases (e.g., minimal change disease), but the majority involve antibody/immune complex mechanisms.

Activation of intrinsic coagulation pathway ❌

• Can cause thrombosis and ischemic injury but is not a primary immunologic mechanism of glomerular disease.

• Uremia is the clinical syndrome that occurs when blood urea and creatinine levels are elevated and accompanied by clinical features due to accumulation of nitrogenous waste products.

• Clinical manifestations: fatigue, anorexia, nausea, vomiting, pruritus, pericarditis, neuropathy, and in severe cases altered mental status → uremic coma.

• It represents the symptomatic, systemic expression of advanced renal failure.

Why the Other Options Are Wrong

Uremic coma ❌

• A severe late complication of uremia, when toxin accumulation leads to unconsciousness.

• Not the general term for raised urea/creatinine with features.

Azotemia ❌

• Refers simply to elevated blood urea nitrogen (BUN) and creatinine without necessarily having clinical features.

• Can be pre-renal, renal, or post-renal.

Renal failure ❌

• A broader term for loss of kidney function; may cause azotemia/uremia but is not the specific name for the clinical syndrome.

Chronic pyelonephritis ❌

• A specific chronic infection/inflammation of the kidney; may lead to scarring and renal failure but not the definition of raised urea/creatinine with systemic features.

Proteus mirabilis is a urease-producing organism → splits urea to ammonia, making urine alkaline (pH 7.5). Alkaline urine promotes precipitation of magnesium ammonium phosphate (struvite) → triple phosphate crystals and formation of a staghorn calculus that can occupy the renal pelvis and calyces. The CVA tenderness, pyuria, and recurrent UTIs fit this classic picture.

Why the Other Options Are Wrong

Acute tubular necrosis ❌

• Typically follows ischemia/toxins with muddy brown granular casts and acute kidney injury. Not characterized by alkaline urine and triple phosphate crystals.

Malignant nephrosclerosis ❌

• Due to malignant hypertension; shows flea-bitten kidneys, hyperplastic arteriolosclerosis—not UTI-driven, crystal-forming disease.

Papillary necrosis ❌

• Seen with analgesic abuse, diabetics, sickle cell disease, severe pyelonephritis; presents with sloughed papillae and hematuria, but not specifically with struvite/triple phosphate crystals.

Renal cell carcinoma ❌

• May cause hematuria and mass, but doesn’t explain alkaline urine with triple phosphate crystals or the long history of Proteus UTIs.

• The normal plasma potassium concentration is about 3.5 – 5.0/5.4 mEq/L.

• Potassium is the major intracellular cation, but a small fraction in plasma is tightly regulated because even slight deviations can cause dangerous cardiac arrhythmias and neuromuscular disturbances.

👉 Clinical points:

• Hypokalemia (<3.5 mEq/L) → muscle weakness, arrhythmias, metabolic alkalosis.

• Hyperkalemia (>5.5 mEq/L) → peaked T-waves, risk of ventricular fibrillation, metabolic acidosis.

Why the Other Options Are Wrong

1 – 2.2 mEq/L ❌

• This would be dangerously low (severe hypokalemia), not normal.

5.5 – 7.6 mEq/L ❌

• This range indicates moderate to severe hyperkalemia, not normal.

1.5 – 2.5 mEq/L ❌

• Again, severe hypokalemia, incompatible with normal physiology.

6.5 – 7.7 mEq/L ❌

• Severe hyperkalemia, often life-threatening, not a normal value.

• Sodium (Na⁺) is the predominant cation in plasma and extracellular fluid (ECF).

• Normal plasma sodium concentration: 135–145 mEq/L.

• Sodium is the main determinant of ECF osmolarity and plays a central role in:

  • Maintaining fluid balance

  • Generating membrane potentials

  • Facilitating nerve impulse transmission and muscle contraction

Why the Other Options Are Wrong

Ca²⁺ ❌

• Plasma calcium concentration is only about 9–11 mg/dL (≈ 2.2–2.7 mM), much lower than sodium.

• Important in bone, coagulation, and signaling, but not the main plasma cation.

Mg²⁺ ❌

• Plasma magnesium is very low (~1.5–2.5 mEq/L).

• Plays a role in enzyme activity and neuromuscular function, but not predominant.

Fe²⁺ ❌

• Iron is not a major plasma cation; it is mostly bound to hemoglobin or transferrin.

K⁺ ❌

• Potassium is the major intracellular cation, not extracellular.

• Plasma K⁺ is normally 3.5–5.0 mEq/L, much lower than sodium.

• Water undergoes slight ionization:
  H2O⇌H++OH−H₂O ⇌ H⁺ + OH⁻H2​O⇌H++OH−

• The concentration of hydrogen ions [H+][H⁺][H+] is the foundation of the pH scale, which is defined as:
  pH=−log⁡[H+]pH = -\log[H⁺]pH=−log[H+]

• At 25°C, pure water has [H+]=1×10−7M[H⁺] = 1 × 10⁻⁷ M[H+]=1×10−7M, giving a pH of 7 (neutral).

• This concept is critical in understanding acids, bases, and buffer systems in physiology and chemistry.

Why the Other Options Are Wrong

Solubility ❌

• Solubility depends on polarity and intermolecular interactions, not directly on ionization of water.

Viscosity ❌

• Refers to resistance to flow, determined by hydrogen bonding and molecular interactions, not ionization.

Diffusion ❌

• Movement of molecules down a concentration gradient, unrelated to water’s ionization.

Adsorption ❌

• Adhesion of molecules to a surface, not linked to ionization of water.

• Total body water in an average adult ≈ 60% of body weight (≈ 42 liters in a 70-kg person).

• Distribution of this water:

  • Intracellular compartment (ICF) → ~ 28 liters (≈ 2/3 of total body water)

  • Extracellular compartment (ECF) → ~ 14 liters (≈ 1/3 of total body water)

    • Plasma (intravascular): ~3 liters

    • Interstitial fluid: ~11 liters

    • Transcellular fluids (CSF, aqueous humor, etc.): small amounts

👉 Thus, the largest portion of water is in the intracellular compartment (~28 liters).

Why the Other Options Are Wrong

Blood ❌

• Plasma volume is ~3 liters; even with RBCs, total blood volume is ~5 liters, far less than intracellular water.

Cerebrospinal fluid ❌

• Very small volume (~150 ml), negligible compared to intracellular water.

Extracellular compartment ❌

• Holds ~14 liters total, less than intracellular (28 liters).

Interstitial compartment ❌

• Holds ~11 liters, still much less than intracellular.