Renal – 2019

Why the other options are incorrect

Oral contraceptive pill

• Pills are used, but far less frequently than condoms in Pakistan. Their percentage among modern methods is lower. PMC+2dhsprogram.com+2

Intrauterine device (IUD)

• IUDs are used, but the percentage is small relative to condoms and sterilization. For example, in the 2012-13 DHS, IUD usage among married women is about 2-3%.

Contraceptive ring

• This method is hardly used or rarely reported in Pakistan in national data; not among the prevalent choices.

Diaphragm

• Diaphragm usage is very rare in Pakistan; most surveys do not even list it prominently among common methods.

✅ Answer

The most common contraceptive method used in Pakistan is condoms.

Hypovolemia refers to a reduced blood volume, usually due to bleeding, dehydration, or fluid loss.

• 0.9% normal saline (isotonic saline):

  • Has a similar osmolarity to plasma (~308 mOsm/L)

  • Expands extracellular fluid volume without causing major fluid shifts between compartments

  • Preferred initial fluid for rapid volume replacement

Other options:

• 2/3% or 1/3% saline: Hypotonic; can cause cellular swelling and hyponatremia

• 5% dextrose: Initially isotonic but quickly metabolized → becomes hypotonic → not ideal for immediate volume expansion

Pure water (distilled water):

1. Solvent properties:

   • Water is known as the “universal solvent” because it can dissolve many ionic and polar substances.

2. Electrical conductivity:

   • Pure water lacks ions → very low electrical conductivity → bad conductor of electricity

   • Conductivity increases if impurities or electrolytes are present

Other options:

• Acts as a solute: False; water is the solvent in most biological and chemical systems

• Good conductor: False; pure water is a poor conductor

• None of these: Incorrect

Xanthogranulomatous pyelonephritis (XGP) is a rare, chronic renal infection characterized by:

• Destruction of renal parenchyma

• Accumulation of lipid-laden macrophages (xanthoma cells)

• Formation of granulomatous tissue

Causative organisms:

• Most commonly Proteus species

• Occasionally E. coli

• Frequently associated with obstructing renal calculi

Other options:

• Klebsiella: Rare cause

• Neisseria gonorrhoeae / Salmonella: Not associated

• E. coli: Can cause chronic pyelonephritis but less commonly XGP

MPGN is a chronic glomerular disease characterized by:

1. Proliferation of glomerular cells (mesangial and endothelial cells)

2. Infiltration of leukocytes

3. Deposition of immune complexes in the mesangium and along the glomerular basement membrane (GBM)

4. Histologically: “Tram-track” appearance of GBM on light microscopy

Clinical features:

• Mixed nephritic and nephrotic features: hematuria, proteinuria, and sometimes renal insufficiency

Why the Other Options Are Incorrect:

• Nephritic syndrome: Clinical syndrome, not a specific histologic pattern

• Poststreptococcal glomerulonephritis: Immune complex deposition in GBM, usually diffuse and subepithelial, not primarily mesangial proliferation

• Focal segmental glomerulosclerosis: Segmental sclerosis of glomeruli; no significant immune complex deposition

• None of these: Incorrect; MPGN fits the description

Explanation:

• The hilum of the kidney is the entry/exit point for the renal artery, vein, and ureter.

• Left kidney:

  • Usually lies slightly higher than the right kidney because of the liver on the right side.

  • Hilum level:

    • Transpyloric plane (approx. L1 vertebral level)

    • About 5 cm lateral to the midline

• Clinical relevance:

  • Knowledge of hilum location is important for surgical approaches, imaging, and catheterization.

Why the Other Options Are Incorrect:

• Junction of midclavicular line and transtubercular plane: Too low; transtubercular plane ~L5

• Subcostal plane: Around L3; hilum is higher

• Transtubercular plane, 5 cm from median plane: Too low

• Interspinous plane: Around S1; far below kidney

Creatinine is a breakdown product of creatine phosphate in muscle.

• Renal handling:

  • Creatinine is freely filtered at the glomerulus.

  • A small portion is secreted by the proximal tubule into the tubular fluid.

  • It is not reabsorbed.

• Clinical relevance:

  • Because creatinine is mostly filtered and slightly secreted, its plasma levels slightly overestimate GFR.

  • This tubular secretion increases as kidney function declines, which is important to consider when estimating renal function.

Why the Other Options Are Incorrect:

• Excreted by the tubule: Excretion is mostly due to filtration, not active tubular excretion.

• Reabsorbed by the tubule: False; creatinine is not reabsorbed.

• Neither secreted nor reabsorbed: False; there is minor tubular secretion.

• Secreted and reabsorbed: False; only secretion occurs.

Reference :- Laiq Hussain Histology Page 224

Distance between adjacent podocyte cell bodies or foot processes

• This refers to the overall spacing from one podocyte process to the next, including the cytoplasmic extensions and the intervening slit region.

• Width: approximately 40 nm.

• It represents the center-to-center distance between adjacent foot processes — broader than the slit pore itself.

Hence, the filtration slit refers to the overall space between the pedicels, while the filtration slit pores refer to the tiny openings within the slit diaphragm that control molecular passage.

Together with the fenestrated endothelium and glomerular basement membrane (GBM), this structure forms the tripartite glomerular filtration barrier — a selective sieve preventing protein loss while allowing water and small solutes to pass.

⚖️ Summary Comparison

Renal cortex histology:

1. Proximal convoluted tubules (PCT):

   • Lined by simple cuboidal epithelium with a brush border (microvilli)

   • Brush border increases surface area for reabsorption of water, electrolytes, and nutrients

2. Distal convoluted tubules (DCT):

   • Lined by simple cuboidal epithelium without a prominent brush border

3. Glomerulus:

   • Contains capillaries and podocytes, but podocytes are part of the visceral layer of Bowman’s capsule, not an epithelial lining of tubules

Why the Other Options Are Incorrect:

• Cuboidal epithelium lining Bowman’s capsule: Only the parietal layer; not a functional feature like PCT

• Simple columnar epithelium in DCT: DCT is cuboidal, not columnar

• Glomerulus containing podocytes: True, but not considered a tubular cortical histological feature

• None of these: Incorrect

In de novo purine synthesis, the ribose sugar for the nucleotide is donated by phosphoribosyl pyrophosphate (PRPP).

• PRPP:

  • Synthesized from ribose-5-phosphate (from the pentose phosphate pathway)

  • Provides the ribose-phosphate backbone to which purine bases are attached to form IMP, AMP, GMP

Other options:

• Glutamine: Donates nitrogen atoms for purine ring

• Inosine monophosphate (IMP): Intermediate nucleotide, not a ribose donor

• Tetrahydrofolate: Donates one-carbon groups (formyl groups)

• Aspartate: Donates nitrogen and carbon in ring formation

Blood pressure regulation involves multiple hormones and systems:

• Renin-angiotensin-aldosterone system (RAAS):

  • Renin converts angiotensinogen → angiotensin I

  • ACE converts angiotensin I → angiotensin II

  • Angiotensin II: potent vasoconstrictor, increases blood pressure

  • Stimulates aldosterone release → increases Na⁺ and water reabsorption → raises blood volume and pressure

Other options:

• Atrial natriuretic peptide (ANP): Decreases blood pressure by promoting natriuresis and vasodilation

• Erythropoietin: Stimulates RBC production; minor effect on blood viscosity, not primary BP regulator

• Nitric oxide: Vasodilator → lowers blood pressure

• Prostaglandin E: Vasodilator → lowers blood pressure

Acute gout is caused by deposition of monosodium urate (MSU) crystals in joints, triggering inflammation.

• Definitive diagnosis: Identification of MSU crystals in synovial fluid obtained by joint aspiration.

  • Crystals are needle-shaped and show negative birefringence under polarized light microscopy.

Other tests:

• Serum uric acid: May be elevated but can be normal during an acute attack; not diagnostic alone.

• Radiology: Shows chronic changes; early attacks may appear normal.

• MRI: Not required for diagnosis; nonspecific.

• Acute phase reactants: Elevated (e.g., CRP, ESR) but nonspecific.

Megaloblastic anemia is caused by impaired DNA synthesis, often due to defective nucleotide metabolism.

• Orotic aciduria:

  • Rare autosomal recessive disorder

  • Caused by deficiency of UMP synthase, an enzyme in de novo pyrimidine synthesis

  • Leads to accumulation of orotic acid and defective DNA synthesis → megaloblastic anemia

  • Not responsive to vitamin B12 or folate (distinguishing feature)

Other options:

• Lesch-Nyhan syndrome (LNS): Purine salvage defect → hyperuricemia, neurological symptoms, not anemia

• Hyperuricemia and gout: Result of purine degradation, unrelated to anemia

• Adenosine deaminase deficiency: Causes SCID, not megaloblastic anemia

Purine de novo synthesis occurs mainly in cells that have high proliferative and metabolic activity. Here’s the correct picture:

• Liver: Major site of de novo purine synthesis, producing nucleotides for the whole body. ✅

• Muscle: Has some limited capacity but mainly relies on salvage pathways; however, it can perform some de novo synthesis. ✅

• Brain: Cannot perform significant de novo purine synthesis; it depends almost entirely on the salvage pathway to recycle purine bases for nucleotides. ❌

Explanation

The brain lacks some of the enzymes required for the full de novo pathway, so it cannot synthesize purines from scratch. Instead, it salvages hypoxanthine and guanine via HGPRT and APRT to form nucleotides.

Answer: Brain

In most mammals (non-primate species), uric acid is further metabolized by the enzyme uricase (urate oxidase) into allantoin, a compound that is much more soluble in water and thus more easily excreted in urine.

The reaction is as follows:

Uric acid+O2+H2O→Allantoin+H2O2+CO2\text{Uric acid} + O_2 + H_2O → \text{Allantoin} + H_2O_2 + CO_2Uric acid+O2​+H2​O→Allantoin+H2​O2​+CO2​

Humans and higher primates lack the uricase enzyme, which is why uric acid remains the end product of purine metabolism and must be excreted directly. This evolutionary loss is associated with higher serum uric acid levels — beneficial as an antioxidant but also predisposing to gout when levels become excessive.

❌ Explanation of Incorrect Options

•  Glyoxylic acid:
  Involved in glycine and oxalate metabolism, not purine catabolism. It has no connection to uric acid breakdown.

•  Ammonia:
  Ammonia arises mainly from amino acid deamination, not from uric acid oxidation. Uric acid metabolism involves oxidative steps, not deamination.

•  Urea:
  Urea is produced in the urea cycle from ammonia and CO₂ — not from uric acid. The two processes are distinct: urea cycle handles nitrogen disposal, while uric acid metabolism handles purine degradation.

•  It is excreted directly in urine without being converted:
  This is true only for humans and higher primates, not for most mammals. Other mammals convert uric acid into allantoin before excretion.

Loop diuretics act on the thick ascending limb of the loop of Henle:

• Mechanism: Inhibit the Na⁺-K⁺-2Cl⁻ symporter, causing significant sodium, chloride, and water excretion.

• Examples:

  • Furosemide

  • Bumetanide

  • Torsemide

Other options:

• Indapamide, Chlorthalidone, Metolazone, Hydrochlorothiazide: Thiazide or thiazide-like diuretics

  • Act on distal convoluted tubule

  • Less potent than loop diuretics

Why the Other Options Are Incorrect:

• Thiazides: Moderate diuretic effect; act more distally; not loop diuretics.

Post-streptococcal glomerulonephritis (PSGN) is an immune-mediated kidney disorder that occurs after a streptococcal infection (usually pharyngitis or skin infection).

Key features:

• Hematuria: Often cola-colored urine

• Oliguria: Reduced urine output

• Mild proteinuria (not massive, unlike nephrotic syndrome)

• Edema and hypertension

• Lab findings:

  • Low complement levels (C3) temporarily

  • Immune complex deposits seen on biopsy

Classification:

• PSGN is a nephritic syndrome because it is associated with:

  • Hematuria

  • Hypertension

  • Mild proteinuria

  • Edema

Why the Other Options Are Incorrect:

• Urinary tract infection: PSGN is not caused by active infection of the urinary tract.

• Alport syndrome: Genetic disorder affecting collagen in GBM; not post-infectious.

• Nephrolithiasis: Kidney stones; unrelated.

• Nephrotic syndrome: Characterized by heavy proteinuria (>3.5 g/day), hypoalbuminemia, edema, which is not typical of PSGN.

Acute renal failure (ARF), also called acute kidney injury (AKI), can result from:

1. Pre-renal causes: Decreased renal perfusion (hypovolemia, shock)

2. Intrinsic renal causes: Damage to kidney tissue

3. Post-renal causes: Obstruction of urinary tract

Most common cause of intrinsic AKI: Acute tubular necrosis (ATN)

• Etiology: Ischemia (prolonged hypoperfusion) or nephrotoxins (drugs, toxins)

• Pathophysiology: Death of tubular epithelial cells → impaired filtration and reabsorption

• Clinical clue: Oliguria/anuria, muddy brown granular casts in urine

Other options:

• Renal papillary necrosis: Less common, associated with analgesic overuse or diabetes

• Polycystic kidney disease: Chronic, not acute

• Acute interstitial nephritis: Allergic/drug-induced, less common than ATN

• Decreased blood flow to kidney: Pre-renal cause; can lead to ATN if prolonged

Why the Other Options Are Incorrect:

• Renal papillary necrosis: Rare, usually secondary to another condition

• Polycystic kidney disease: Chronic disease, not acute

• Acute interstitial nephritis: Accounts for a smaller percentage of AKI cases

• Decreased renal blood flow: Pre-renal, often reversible; ATN is the leading intrinsic cause

Metabolic acidosis can be classified based on the anion gap (AG):

AG=[Na+]−([Cl−]+[HCO3−])AG=[Na+]−([Cl−]+[HCO3−​])

• Normal AG (~12 ± 4 mEq/L) → hyperchloremic metabolic acidosis

• Increased AG → accumulation of organic acids (lactic acidosis, ketoacidosis, uremia)

Renal tubular acidosis (RTA):

• Defect in renal tubular H⁺ secretion (distal RTA) or HCO₃⁻ reabsorption (proximal RTA)

• Leads to normal AG metabolic acidosis because Cl⁻ rises to maintain electroneutrality (hyperchloremic)

• Commonly associated with hypokalemia

Other conditions:

• Chronic kidney disease: Usually high AG acidosis due to retained sulfates, phosphates

• Lactic acidosis: High AG

• Ketoacidosis: High AG

Why the Other Options Are Incorrect:

• Chronic kidney disease: Accumulation of organic acids → high AG

• Lactic acidosis / Ketoacidosis: High AG metabolic acidosis

• None of these: Incorrect because RTA clearly produces normal AG acidosis

Clues from the case:

1. Patient: 12-year-old girl

2. Symptoms:

   • Periorbital edema → typical of nephrotic syndrome

3. Urinalysis:

   • Proteinuria (dipstick positive)

   • No hematuria → favors nephrotic over nephritic syndrome

4. Microscopy:

   • Oval fat bodies → suggest lipiduria, characteristic of nephrotic syndrome

5. Serum creatinine: 2.3 mg/dL → indicates some degree of renal impairment

6. Electron microscopy:

   • Effacement of foot processes → classic for minimal change disease

Other features of MCD:

• Most common cause of nephrotic syndrome in children

• Often idiopathic or triggered by allergies/viral infections

• Usually normal complement levels

Why the Other Options Are Incorrect:

• Poststreptococcal glomerulonephritis: Nephritic syndrome → hematuria, hypertension, low complement

• Pyelonephritis / Cystitis: Infection → fever, dysuria, WBCs in urine; does not cause heavy proteinuria or foot process effacement

• Acute kidney injury: Can occur secondary to various insults; does not explain isolated nephrotic features with foot process effacement

Pyelonephritis is a bacterial infection of the kidney, usually ascending from the lower urinary tract.

• Most common cause: Escherichia coli (~70–90% of cases)

  • Normally part of the gut flora; can colonize the urethra and ascend the urinary tract.

• Other organisms:

  • Klebsiella species: Less common, opportunistic infections.

  • Staphylococcus saprophyticus: Usually causes cystitis in young women, rarely pyelonephritis.

  • Enterococcus faecalis: Can cause UTIs but uncommon as a cause of pyelonephritis.

  • Proteus mirabilis: Often associated with struvite stones; less common cause of pyelonephritis.

Urea transporters in the kidney are important for urea recycling and medullary hyperosmolarity, which are essential for concentrating urine.

• UT-A1 and UT-A3:

  • Located in the inner medullary collecting ducts.

  • Their activity is upregulated by antidiuretic hormone (ADH / vasopressin).

  • ADH increases urea permeability, allowing urea to move into the medullary interstitium → contributes to hyperosmotic medulla → water reabsorption.

• Other transporters (UT-A2, UT-A4): Less influenced by ADH and mainly in other nephron segments.

Why the Other Options Are Incorrect:

• UT-A2 and UT-A4: ADH has minimal effect.

• No urea transporter is affected: Incorrect; UT-A1 and UT-A3 are ADH-sensitive.

• UT-A2 and UT-A3 / UT-A1 and UT-A2: Only part of the correct pair is ADH-sensitive.

Aspartate enters the TCA cycle after undergoing transamination — a reversible reaction where it donates its amino group to α-ketoglutarate, forming glutamate and oxaloacetate.

Aspartate+α-ketoglutarate⇌Oxaloacetate+Glutamate\text{Aspartate} + \alpha\text{-ketoglutarate} ⇌ \text{Oxaloacetate} + \text{Glutamate}Aspartate+α-ketoglutarate⇌Oxaloacetate+Glutamate

This reaction is catalyzed by aspartate transaminase (AST or GOT).
Oxaloacetate then serves as an intermediate of the TCA cycle, condensing with acetyl-CoA to form citrate in the first step of the cycle.

Thus, aspartate contributes to the anaplerotic replenishment of oxaloacetate, helping maintain TCA cycle function — a vital link between amino acid metabolism and cellular respiration.

❌ Explanation of Incorrect Options

•  α-Ketoglutarate:
  This is the recipient of aspartate’s amino group during transamination, not the product. Aspartate helps form α-ketoglutarate indirectly via glutamate, but it itself becomes oxaloacetate.

•  Succinic acid (succinate):
  Formed later in the TCA cycle from fumarate, not directly from aspartate. Aspartate doesn’t bypass into this step.

•  Fumarate:
  Produced from aspartate in the urea cycle, not in the TCA cycle. Specifically, in the argininosuccinate lyase step, aspartate contributes to fumarate formation — but that fumarate then enters the TCA cycle secondarily, not directly.

• Citrate:
  Citrate is the first product of the TCA cycle, formed from oxaloacetate and acetyl-CoA. Aspartate never directly becomes citrate — it first must become oxaloacetate.

During purine degradation:

1. Inosine monophosphate (IMP) and guanosine monophosphate (GMP) are nucleotides, which must first be converted to nucleosides.

2. 5′-nucleotidase removes the phosphate group from IMP and GMP → forming inosine and guanosine, respectively.

3. These nucleosides are then further broken down:

   • Inosine → hypoxanthine → xanthine → uric acid

   • Guanosine → guanine → xanthine → uric acid

Why the Other Options Are Incorrect:

• Guanylate kinase: Converts GMP → GDP (phosphorylation), not degradation.

• Adenosine deaminase: Acts on adenosine → inosine, not IMP or GMP.

• Ribonucleotide reductase: Converts ribonucleotides → deoxyribonucleotides, not degradation.

• Xanthine oxidase: Acts later in the pathway (xanthine → uric acid), not at the nucleotide-to-nucleoside step.

Lesch-Nyhan syndrome is a rare X-linked recessive disorder caused by a deficiency of the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRT).

• HGPRT is critical for the purine salvage pathway, which recycles hypoxanthine and guanine into IMP and GMP.

• Defect in HGPRT → purine bases cannot be salvaged → increased degradation of purines to uric acid → hyperuricemia.

• Clinical features:

  • Gout / uric acid stones

  • Neurological dysfunction (self-mutilation, dystonia)

  • Developmental delay

Why the Other Options Are Incorrect:

• Purine biosynthesis: De novo synthesis is unaffected.

• Purine degradation: Degradation is actually increased, not defective.

• Pyrimidine degradation / synthesis: Unrelated to Lesch-Nyhan syndrome.

Inosine monophosphate (IMP) is the branch-point intermediate in de novo purine synthesis.

• From IMP, two key purine nucleotides are synthesized:

  • Adenosine monophosphate (AMP)

  • Guanosine monophosphate (GMP)

Other options:

• Uric acid: End product of purine catabolism, not a precursor.

• Phosphoribosyl pyrophosphate (PRPP): Donates ribose-phosphate in the first step of purine synthesis but is not the immediate precursor of AMP/GMP.

• Glutamine: Nitrogen donor in purine synthesis, not a direct precursor.

• Orotate: Precursor in pyrimidine synthesis, not purines.

The renal medulla contains pyramids, which are triangular structures of tubules and collecting ducts.

• Renal columns (of Bertin):

  • Extensions of cortical tissue that project between the renal pyramids.

  • Provide structural support and contain blood vessels supplying the cortex and medulla.

Other structures:

• Renal pyramids: Medullary tissue containing loops of Henle and collecting ducts.

• Medullary rays: Straight tubules extending from the cortex into the medulla, not cortical extensions.

• Major calices / Minor calices: Collect urine from the pyramids; part of the collecting system.

Chronic renal failure (CRF), also called chronic kidney disease (CKD), is a progressive loss of kidney function over months to years.

Most common causes worldwide:

1. Diabetes mellitus (type 1 or type 2):

   • Causes diabetic nephropathy, leading to glomerular sclerosis.

2. Hypertension:

   • Causes hypertensive nephrosclerosis, damaging renal arterioles and glomeruli.

• Together, these two conditions account for the majority of chronic renal failure cases.

Why the Other Options Are Incorrect:

• Central or nephrogenic diabetes insipidus: Cause polyuria, not progressive kidney failure.

• Hypotension: May cause acute kidney injury, not chronic kidney disease.

• None of these: Incorrect because diabetes and hypertension are well-established major causes.

Antidiuretic hormone (ADH / vasopressin) is secreted by the posterior pituitary in response to:

1. Increased plasma osmolality:

   • Detected by osmoreceptors in the hypothalamus.

   • ADH promotes water reabsorption in the collecting ducts → dilutes plasma, concentrating urine.

2. Decreased blood volume or pressure (less sensitive trigger):

   • Detected by baroreceptors in atria and large vessels.

Opposing factors:

• Decreased osmolality: Inhibits ADH release.

• Atrial natriuretic peptide (ANP): Inhibits ADH to promote sodium and water excretion.

• Increased blood pressure / volume: Inhibits ADH to prevent further water retention.

Why the Other Options Are Incorrect:

• Decreased osmolality: Reduces ADH secretion.

• Atrial natriuretic peptide: Antagonizes ADH.

• Increase in blood pressure/volume: Inhibits ADH, opposite effect.

Diuretics increase urine output by inhibiting sodium and water reabsorption at different sites of the nephron. Their potency depends on how much sodium they block from being reabsorbed.

• Furosemide: A loop diuretic that acts on the thick ascending limb of the loop of Henle.

  • Inhibits the Na⁺-K⁺-2Cl⁻ symporter.

  • Can cause excretion of up to 20–25% of filtered sodium, making it the most powerful diuretic.

• Other diuretics:

  • Spironolactone: Potassium-sparing, acts on collecting ducts, weak natriuretic effect.

  • Amiloride: Potassium-sparing, acts on collecting ducts, weak diuretic.

  • Acetazolamide: Carbonic anhydrase inhibitor in proximal tubule; mild diuretic.

Why the Other Options Are Incorrect:

• Spironolactone / Amiloride: Weak diuretics; primarily prevent potassium loss.

• Acetazolamide: Mild diuretic; mostly used for glaucoma, altitude sickness, or metabolic alkalosis.

• None of these: Incorrect because furosemide is clearly the strongest.

• The filtrate in Bowman’s capsule is formed by glomerular filtration of plasma.

• Since filtration is non-selective for water and small solutes, the osmolarity of the filtrate is roughly equal to plasma osmolarity.

• Normal plasma osmolarity: ~285–295 mOsm/L → filtrate ≈ 300 mOsm/L.

Key point:

• At the start of the nephron, filtrate is isotonic with plasma, and further modification occurs along the tubules depending on reabsorption and secretion.

Why the Other Options Are Incorrect:

• 100, 200 mOsm/L: Too dilute; filtrate hasn’t undergone dilution yet.

• 400 mOsm/L: Slightly hypertonic; not typical at Bowman’s capsule.

• 1200 mOsm/L: Maximal urine concentration, occurs at the tip of the collecting duct, not at the start.

Concentrated urine formation depends on two main factors:

1. Antidiuretic hormone (ADH / vasopressin):

   • Increases water permeability of the collecting ducts by inserting aquaporin-2 channels, allowing water to be reabsorbed into the medullary interstitium.

2. Hyperosmotic medullary interstitium:

   • Created by the countercurrent multiplier system in the loop of Henle and urea recycling.

   • This osmotic gradient pulls water out of the collecting ducts when ADH is present, concentrating urine.

Why the Other Options Are Incorrect:

• Aldosterone and renin: Mainly regulate Na⁺ and K⁺, not directly responsible for urine concentration.

• ADH and hypoosmotic medullary interstitium: Wrong because water needs a hyperosmotic gradient to be reabsorbed.

• Aldosterone and cortical nephrons: Cortical nephrons don’t significantly contribute to the medullary osmotic gradient.

• Aldosterone and hyperosmotic medullary interstitium: Aldosterone affects sodium, not water reabsorption via ADH.

The kidneys concentrate urine to conserve water, depending on hydration status and antidiuretic hormone (ADH) levels.

• Normal plasma osmolality: ~285–295 mOsm/L

• Maximally concentrated urine: ~1200 mOsm/L

  • Achieved in the collecting ducts under the influence of ADH, which increases water reabsorption.

• Maximally dilute urine: ~50–100 mOsm/L

Why the Other Options Are Incorrect:

• 200, 300, 400, 600 mOsm/L: These values are below the maximal concentrating capacity; they represent normal or slightly concentrated urine, not the most concentrated.

The urachus is a fetal structure connecting the apex of the bladder to the umbilicus, which normally obliterates after birth to form the median umbilical ligament.

Failure to close completely can lead to:

1. Patent urachus (urachal fistula):

   • Entire urachus remains open

   • Urine flows from the bladder directly to the umbilicus

2. Urachal cyst:

   • Central portion remains patent, ends closed

   • Does not allow urine to escape

3. Urachal sinus:

   • Umbilical end remains patent, but bladder end closed

   • May drain mucus, but not urine

4. Renal agenesis / ectopic kidney:

   • Unrelated to urachal patency

Why the Other Options Are Incorrect:

• Urachal cyst: Closed at both ends → no urine discharge

• Urachal sinus: Closed at bladder → only mucus may drain

• Renal agenesis / ectopic kidney: Kidney anomaly, unrelated to urachal urine leakage

Isotonic solutions have an osmolarity similar to plasma (~285–295 mOsm/L) and do not cause significant fluid shifts between compartments.

• 0.9% normal saline (NS): Isotonic (~308 mOsm/L) ✅

• 5% dextrose (D5W): Isotonic in the bag but becomes effectively hypotonic after metabolism of glucose; still often classified as isotonic initially. ✅

• Lactated Ringer’s (LR): Isotonic (~273 mOsm/L) ✅

3% normal saline is hypertonic (~1027 mOsm/L) → draws water out of cells → not isotonic.

Why the Other Options Are Incorrect:

• 0.9% NS: True isotonic solution.

• 5% dextrose: Initially isotonic.

• Lactated Ringer’s: Isotonic solution.

• None of these: Incorrect because 3% saline is clearly hypertonic.

The urinary bladder has a wall composed of:

1. Mucosa: Lined by transitional epithelium (urothelium), which can stretch as the bladder fills.

2. Muscular layer: Smooth muscle arranged in three layers (inner longitudinal, middle circular, outer longitudinal) called the detrusor muscle, responsible for bladder contraction during urination.

3. Adventitia/serosa: Outer connective tissue layer depending on location.

Key points:

• No skeletal muscle is present in the bladder wall; voluntary control occurs via the external urethral sphincter.

• Pseudostratified columnar epithelium is not present in the bladder.

Why the Other Options Are Incorrect:

• Outer smooth, inner skeletal muscle: Wrong arrangement; bladder has only smooth muscle.

• Skeletal muscle layer lined by transitional epithelium: Skeletal muscle is absent in the bladder wall.

• None of these: Incorrect because one option is true.

• Smooth muscle lined by pseudostratified columnar epithelium: Incorrect epithelial type.

The macula densa is a specialized group of cells in the distal convoluted tubule that senses sodium (Na⁺) and chloride (Cl⁻) concentrations in the tubular fluid.

• Low Na⁺/Cl⁻ in the distal tubule → macula densa signals the juxtaglomerular (JG) cells of the afferent arteriole to release renin.

• Renin then catalyzes the conversion of angiotensinogen → angiotensin I, eventually leading to angiotensin II formation, which:

  • Constricts efferent arterioles

  • Stimulates aldosterone secretion from the adrenal cortex

  • Increases sodium and water reabsorption

This is part of the tubuloglomerular feedback and renin-angiotensin-aldosterone system (RAAS).

Why the Other Options Are Incorrect:

• Cause systemic vasodilation: Incorrect; angiotensin II causes vasoconstriction, not dilation.

• Release angiotensin-converting enzyme (ACE): ACE is produced in endothelial cells, not by macula densa.

• Stimulate JG cells to produce erythropoietin: Erythropoietin is produced by interstitial fibroblasts in the kidney, not JG cells.

• Inhibit JG cells to prevent prostaglandin release: Opposite effect; macula densa stimulates, not inhibits.

Glomerular filtration is determined by the net filtration pressure (NFP) across the glomerular capillaries. The forces involved are:

Favoring filtration:

• Glomerular capillary hydrostatic pressure (GCHP): Pressure of blood within glomerular capillaries pushing water and solutes into Bowman’s space.

Opposing filtration:

• Bowman’s capsule hydrostatic pressure: Pushes fluid back into capillaries.

• Glomerular capillary colloid osmotic pressure: Due to plasma proteins, pulls water back into capillaries.

Peritubular capillary hydrostatic pressure and Bowman’s capsule colloid osmotic pressure are not significant contributors to glomerular filtration.

Why the Other Options Are Incorrect:

• Peritubular capillary hydrostatic pressure: Affects reabsorption in the peritubular capillaries, not filtration.

• Bowman’s capsule colloid osmotic pressure: Normally negligible (very few proteins in filtrate).

• Glomerular capillary colloid osmotic pressure: Opposes filtration.

• Bowman’s capsule hydrostatic pressure: Opposes filtration.

Water is lost from the body through several routes:

1. Skin (sweat): Insensible and sensible perspiration.

2. Lungs: Water vapor lost during respiration.

3. Kidneys: Water excreted in urine.

4. Nose: Insensible water loss through humidification of inhaled air.

Skeletal muscles, however, do not directly contribute to water loss. While muscles contain water and metabolic activity produces heat, they do not secrete water externally.

Why the other options are incorrect:

• Nose: Water lost via exhaled air.

• Skin: Primary route of insensible water loss and sweat.

• Lungs: Water vapor exhaled with each breath.

• Kidneys: Major route of regulated water excretion via urine.

The kidney plays a vital role in vitamin D metabolism.

• The proximal tubules of the kidney convert 25-hydroxycholecalciferol (calcidiol) into 1,25-dihydroxycholecalciferol (calcitriol) through the enzyme 1α-hydroxylase.

• Calcitriol is the active form of vitamin D and:

  • Increases calcium absorption in the intestines.

  • Enhances phosphate absorption.

  • Works synergistically with parathyroid hormone (PTH) to regulate calcium homeostasis.

Why the other options are incorrect:

• 24,25-dihydroxycholecalciferol: Less active form, not significant for calcium absorption.

• Calcidiol: Precursor stored in the liver; not biologically active in absorption.

• Erythropoietin: Stimulates RBC production; unrelated to calcium metabolism.

• All of these: Incorrect since only 1,25-dihydroxycholecalciferol is directly responsible.

Glutamine is a key nitrogen donor in nucleotide synthesis:

• Purine synthesis: Donates nitrogen for positions N3 and N9 in the purine ring.

• Pyrimidine synthesis: Donates nitrogen for N3 of the pyrimidine ring.

Other amino acids contribute in a more limited or specific way:

• Aspartate: Nitrogen donor mainly in pyrimidine synthesis (N1).

• Glycine: Contributes nitrogen only in purine synthesis.

• Valine: Not involved in nucleotide nitrogen donation.

Thus, glutamine is unique in donating nitrogen to both purine and pyrimidine rings.

Metabolic alkalosis is characterized by a primary increase in plasma bicarbonate (HCO₃⁻), which raises blood pH.

• Compensation: The body responds via respiratory compensation:

  • Hypoventilation occurs to retain CO₂, which acts as an acid to partially neutralize the alkalosis.

  • As a result, pCO₂ rises above normal.

Key points:

• The compensation does not fully normalize pH, it only mitigates it.

• The kidneys may also eventually adjust by excreting HCO₃⁻, but respiratory compensation is rapid and primary.

Why the Other Options Are Incorrect:

• HCO₃⁻ increased, pCO₂ decreased – This pattern is seen in metabolic acidosis with respiratory compensation, not alkalosis.

• HCO₃⁻ decreased, pCO₂ increased – Opposite pattern (metabolic acidosis or respiratory alkalosis).

• Both decreased – Seen in primary metabolic acidosis without compensation.

• Both increased – Correct pattern for compensated metabolic alkalosis.

• HCO₃⁻ increased, pCO₂ normal – This represents uncompensated metabolic alkalosis, not compensated.

The parallelogram of Morris is a surface landmark used to approximate the position of the kidneys on the posterior abdominal wall. Its borders are:

• Vertical lines:

  • 9.5 cm from the midline (spinal column)

  • 2.5 cm from the midline

• Horizontal lines:

  • Superior: Tips of the spinous processes of T11

  • Inferior: Spinous process of L3

The kidney lies roughly between T12 and L3 vertebral levels, so L1 is not used as a horizontal border of the parallelogram.

Why the Other Options Are Correct:

• Vertical line 9.5 cm from midline – Part of the parallelogram.

• Horizontal border at T11 tips – Superior boundary.

• Vertical line 2.5 cm from midline – Medial boundary.

• Horizontal border at L3 spinous process – Inferior boundary.

Acute pyelonephritis is an infection of the renal pelvis and parenchyma, usually bacterial in origin (commonly E. coli). Complications can arise if the infection is severe or recurrent.

Papillary necrosis is a recognized complication, especially in:

• Diabetes mellitus

• Urinary tract obstruction

• Analgesic abuse

• Severe or recurrent pyelonephritis

It involves ischemic necrosis of the renal papillae, which may slough into the urinary tract and cause hematuria, obstruction, or infection.

Why the Other Options Are Incorrect:

• Pulmonary embolism: Not a direct complication of pyelonephritis.

• Necrotic syndrome: Likely referring to nephrotic syndrome; not caused by acute infection.

• Cholecystitis: Inflammation of the gallbladder; unrelated.

• Chronic renal failure: Can result from recurrent or chronic pyelonephritis, but not a complication of a single acute episode.

Urolithiasis (kidney stones) requires imaging for diagnosis. Among available modalities:

• Non-contrast CT scan of the kidneys, ureters, and bladder (NCCT KUB) is the most sensitive and specific test for detecting urinary stones.

  • Detects stones as small as 1–2 mm.

  • Identifies stone location, size, and density.

  • Can detect stones of all compositions except very rare radiolucent stones (like some uric acid stones).

• X-ray (KUB) – Can detect radio-opaque stones (like calcium stones) but misses radiolucent stones.

• Intravenous pyelogram (IVP) – Older method; uses contrast to outline urinary tract; less commonly used now due to CT availability and speed.

• MRI – Poor for stones; not used routinely for urolithiasis.

• Blood test – Cannot reliably detect stones; may show secondary effects like elevated creatinine or uric acid, but not diagnostic.

Kidney stones (renal calculi) can form or get lodged in areas where urine collects or flows, such as the renal pelvis, calyces, ureter, or bladder. These are parts of the urinary tract that deal with the passage or storage of urine, making them common sites for stone obstruction.

The nephron, however, is the microscopic functional unit of the kidney that filters blood and forms urine. It is too small for stone formation or retention — stones are far larger than the microscopic tubules of the nephron.

Why the other options are incorrect:

• Ureter: Narrow tubes — stones often get stuck here.

• Bladder: Stones can form or accumulate here, especially in urinary retention.

• Calyces: Stones often form in the minor or major calyces where urine first collects.

• Pelvis: Common site for stone lodging before entering the ureter.

Aldosterone, a hormone secreted by the zona glomerulosa of the adrenal cortex, acts mainly on the principal cells of the distal convoluted tubule and collecting ducts of the nephron.

Its effects are:

• Increased reabsorption of Na⁺ (sodium) and Cl⁻ (chloride), leading to water retention and increased blood volume/pressure.

• Increased excretion of K⁺ (potassium) into the urine, helping regulate serum potassium levels.

• Indirectly increases H⁺ excretion, affecting acid-base balance.

Why the other options are incorrect:

• Decreases Na⁺ and Cl⁻ reabsorption, and K⁺ excretion: Opposite of aldosterone’s actual function.

• Increases Na⁺ and K⁺ reabsorption: Incorrect because aldosterone increases K⁺ excretion, not reabsorption.

• Increases Na⁺ and Cl⁻ excretion, and K⁺ reabsorption: This reverses aldosterone’s effects.

• Increases Na⁺, Cl⁻, and K⁺ excretion: Completely opposite of aldosterone’s primary role in sodium retention.

The ureters are muscular tubes that connect each kidney to the urinary bladder.

• They originate from the renal pelvis at the hilum of the kidney.

• They descend retroperitoneally along the posterior abdominal wall.

• They finally enter the bladder at the posterolateral angles, allowing urine to flow from the kidney to the bladder for storage before excretion.

Why the other options are incorrect:

• Transversalis fascia: This is a fascial layer of the abdominal wall, not involved in urinary drainage.

• Lumbar nodes: These are lymph nodes, not a physical connection between kidney and bladder.

• Perinephric fat: This surrounds and protects the kidney but doesn’t connect it to the bladder.

• Aorta: The main artery of the body; supplies blood but is unrelated to urine transport.

In the proximal convoluted tubule (PCT), the reabsorption and secretion of H⁺ ions are closely tied to sodium (Na⁺) handling. This happens mainly through the Na⁺/H⁺ exchanger (NHE3) in the apical membrane of tubular cells:

• Na⁺ enters the tubular cells from the lumen in exchange for H⁺ secretion into the tubular fluid.

• This process is crucial for:

  • Bicarbonate (HCO₃⁻) reabsorption

  • Acid-base balance

  • Maintaining sodium balance in the body

Why the other options are incorrect:

• K⁺: Potassium is regulated in later segments of the nephron, like the distal tubule and collecting duct.

• OH⁻: Not directly involved in ion exchange in the PCT.

• Mg²⁺: Mostly reabsorbed in the loop of Henle, not in the PCT.

• Cl⁻: Reabsorbed passively in the PCT but not coupled directly with H⁺ secretion.

The nephron is the basic structural and functional unit of the kidney, responsible for filtering blood, reabsorbing essential substances, and excreting waste products in urine. Each kidney contains about 1 to 1.5 million nephrons, consisting of the renal corpuscle (Bowman’s capsule and glomerulus) and the renal tubule.

Why other options are incorrect:

• Minor calices: These are part of the collecting system that collects urine from papillary ducts, not functional filtration units.

• Renal corpuscles: These are part of nephrons but are not the entire functional unit.

• Medullary rays: These are bundles of straight tubules and collecting ducts within the cortex, not complete functional units.

• Renal pyramids: These are anatomical structures in the medulla, containing loops of Henle and collecting ducts, but they are not individual functional units.

The urinary bladder is a muscular sac that stores urine until micturition. Its mucosal lining is made up of transitional epithelium (urothelium), which is specialized to stretch as the bladder fills and recoils after emptying.

Why the Other Options Are Incorrect:

• “It has a layer of skeletal muscle” – Incorrect. The bladder wall contains smooth muscle called the detrusor muscle, not skeletal muscle.

• “It consists of four muscular layers” – Incorrect. The bladder has three layers of smooth muscle (inner longitudinal, middle circular, and outer longitudinal), not four.

• “None of these” – Incorrect because one option is true.

• “It stores urine and has pseudostratified columnar epithelium” – Incorrect. The lining is transitional epithelium, not pseudostratified.

Xanthine oxidase is an enzyme involved in purine metabolism, converting hypoxanthine → xanthine → uric acid.

• Allopurinol is a structural analog of hypoxanthine and acts as a competitive inhibitor of xanthine oxidase.

• By inhibiting this enzyme, it reduces the production of uric acid, making it the drug of choice for conditions like gout and hyperuricemia (including tumor lysis syndrome).

Why the Other Options Are Incorrect:

• Mycophenolic acid – Inhibits inosine monophosphate dehydrogenase, blocking de novo guanine nucleotide synthesis (used as an immunosuppressant).

• 5-fluorouracil (5-FU) – Inhibits thymidylate synthase, interfering with pyrimidine synthesis.

• Methotrexate – Inhibits dihydrofolate reductase, blocking folate metabolism and purine/pyrimidine synthesis.

• Hydroxyurea – Inhibits ribonucleotide reductase, preventing DNA synthesis, often used in sickle cell disease.

Water reabsorption in the nephron occurs in two main ways:

1. Obligatory Reabsorption – Happens in the proximal convoluted tubule (PCT) and descending loop of Henle. This process is independent of hormonal control and reabsorbs about 80–85% of filtered water.

2. Facultative Reabsorption – Takes place in the collecting ducts (including the duct of Bellini) and is regulated by antidiuretic hormone (ADH). When ADH levels rise, it increases the insertion of aquaporin-2 channels into the apical membrane of the collecting duct cells, allowing additional water reabsorption depending on the body’s hydration needs.

Why the Other Options Are Incorrect:

• Loop of Henle – Mainly involved in creating a medullary osmotic gradient; not where ADH-dependent reabsorption occurs.

• Proximal convoluted tubule – Handles obligatory water reabsorption, not facultative.

• Bowman’s capsule – Site of filtration, not reabsorption.

• None of these – Incorrect, because the collecting ducts (duct of Bellini) are the actual site.

In nephrolithiasis (kidney stones), pain is caused by obstruction of the urinary tract, leading to spasmodic ureteral contractions and increased intraluminal pressure. This results in renal colic, a sharp, severe, and colicky pain that:

• Starts in the flank or back region (costovertebral angle)

• Radiates towards the groin, lower abdomen, or genitalia, following the path of the ureter

• Often associated with nausea, vomiting, and hematuria.

Why the Other Options Are Incorrect:

• No pain is felt – False; renal stones are typically very painful unless completely non-obstructive.

• Pain is mild and is only felt when urinating – This describes urethral irritation, not nephrolithiasis.

• Pain is localized to kidneys – Incorrect; the pain radiates along the ureter.

• None of these – Incorrect, since the characteristic radiation pattern is well known.

The ureters develop from the ureteric bud, which is an outgrowth of the mesonephric (Wolffian) duct during week 5 of embryonic development.

• The ureteric bud gives rise to:

  • Ureter

  • Renal pelvis

  • Major and minor calyces

  • Collecting ducts

Meanwhile, the metanephric mesenchyme (blastema) forms the nephrons (glomerulus, proximal tubule, loop of Henle, and distal tubule).

Why the Other Options Are Incorrect

• Ureteric bud from metanephric duct – The metanephric duct does not exist; the metanephric tissue is mesenchyme, not a duct.

• Mesenchymal condensation posterior to cloaca – This is associated with other pelvic structures, not the ureter.

• Ureteric bud from allantois – The allantois contributes to the urachus and bladder apex, not the ureter.

• None of these – Incorrect because the first option is the accurate description.

The ureters are lined by transitional epithelium, also called urothelium.

• This specialized epithelium allows the ureters to stretch and recoil as urine passes through.

• It has multiple layers:

  • Basal cells (small and cuboidal)

  • Intermediate cells (columnar or polygonal)

  • Superficial umbrella cells (large, dome-shaped), which can flatten when the ureter is distended.

This property is critical for maintaining a barrier against urine while allowing expansion.

Why the Other Options Are Incorrect

• Simple squamous epithelium – Found in areas like alveoli or endothelium, not in ureters.

• Stratified squamous non-keratinized – Seen in the esophagus or vagina, not the urinary tract.

• Stratified squamous keratinized – Found in the skin (epidermis), not in ureters.

• Pseudostratified columnar epithelium – Seen in respiratory tract, not in urinary system.

In de novo purine synthesis, the purine ring is built atom by atom using specific amino acids and other molecules as nitrogen and carbon donors.

Sources of Nitrogen in Purine Synthesis:

• Glutamine → Provides nitrogen for N3 and N9 positions.

• Aspartate → Provides nitrogen for N1.

• Glycine → Contributes to the ring as part of N7 (and carbon skeleton too).

Alanine, however, does not contribute nitrogen to the purine ring.

Why the Other Options Are Incorrect

• Aspartate – Direct contributor to purine nitrogen.

• Glycine – Supplies nitrogen and carbon atoms.

• Glutamine – Important nitrogen donor in several steps.

• All of these are a source – Wrong because alanine is not a donor.

The first step in pyrimidine synthesis is the formation of carbamoyl phosphate, catalyzed by the enzyme carbamoyl phosphate synthetase II (CPS-II) in the cytosol.

Pathway overview:

1. Formation of carbamoyl phosphate – by CPS-II using glutamine, CO₂, and 2 ATP. ✅ (First and rate-limiting step)

2. Formation of carbamoyl aspartate – by aspartate transcarbamoylase.

3. Cyclization to form orotate.

4. Combination with PRPP to form orotidine monophosphate (OMP).

5. Conversion of OMP to UMP and eventually other pyrimidine nucleotides.

Why the Other Options Are Incorrect

• Formation of carbamoylaspartate: This is the second step, not the first.

• Formation of orotate: Happens later in the pathway after ring closure.

• Formation of PRPP: Belongs to purine and pyrimidine synthesis but is not the first committed step in pyrimidine synthesis.

• None of these: Incorrect because formation of carbamoyl phosphate is indeed the first step.

Carbamoyl phosphate synthetase II (CPS-II) is the rate-limiting enzyme of the de novo pyrimidine synthesis pathway.

• Location: Cytosol

• Function: Catalyzes the reaction:

  Glutamine + CO₂ + 2 ATP → Carbamoyl phosphateGlutamine + CO₂ + 2 ATP → Carbamoyl phosphate

Regulation:

• Activated by: PRPP (phosphoribosyl pyrophosphate) → promotes pyrimidine synthesis.

• Inhibited by: UTP (uridine triphosphate) → negative feedback to prevent excessive pyrimidine production.

Why the Other Options Are Incorrect

• UMP (Uridine monophosphate): Not a direct inhibitor; inhibition occurs mainly by UTP.

• PRPP: Activates, not inhibits, CPS-II.

• UDP (Uridine diphosphate): Intermediate but does not regulate CPS-II directly.

• ATP: Provides energy for the reaction but doesn’t regulate enzyme activity.

The ureters are muscular tubes (~25–30 cm long) that transport urine from the renal pelvis to the urinary bladder.

Key features:

• Retroperitoneal: They lie behind the peritoneum throughout their course.

• Originate at the renal pelvis: At the hilum of the kidney (posteriorly, not anteriorly).

• Constriction sites (three):

  1. Ureteropelvic junction – where the renal pelvis becomes the ureter.

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

  3. Vesicoureteral junction – where ureter enters the bladder.

Why the Other Options Are Incorrect

• “Arise from anterior side…” – Incorrect; they arise posteriorly at the hilum, not anteriorly.

• “Ureters are intraperitoneal” – Incorrect; they are retroperitoneal.

• “They are constricted at two regions” – Incorrect; there are three constriction sites, not two.

• “None of these” – Incorrect, because the statement about being retroperitoneal is true.

The kidney coverings (from inside to outside) are arranged in layers:

1. Fibrous capsule –

   • The innermost covering.

   • A thin, tough, fibrous membrane that directly adheres to the kidney surface, providing protection and structural integrity.

2. Perinephric fat (perirenal fat) –

   • Surrounds the fibrous capsule and acts as a cushion.

3. Renal fascia (Gerota’s fascia) –

   • Encloses the perinephric fat and kidney, anchoring them in place.

4. Paranephric fat (pararenal fat) –

   • Outermost fat layer, providing additional support and insulation.

Why the Other Options Are Incorrect

• Paranephric fat – Outermost fat, not innermost.

• Renal fascia – Lies outside perinephric fat, not the first layer.

• Perinephric fat – Surrounds but doesn’t directly touch the kidney.

• None of these – Incorrect, as fibrous capsule is the true innermost covering.

The renal corpuscle filters blood based on size, charge, and shape through the glomerular filtration barrier, which consists of:

• Fenestrated endothelium

• Basement membrane (negatively charged)

• Podocyte slit diaphragm

Among the given components:

• Albumin (~66 kDa, negatively charged) is the least filtered due to:

  • Its large size

  • Its negative charge, which is repelled by the negatively charged glomerular basement membrane.

• In a healthy kidney, almost no albumin is found in the filtrate (only trace amounts).

Why the Other Options Are Incorrect

• Lactic acid – Small molecule, freely filtered.

• Water – Freely filtered due to its small size.

• Glucose – Freely filtered; later reabsorbed in the proximal tubule.

• Amino acids – Freely filtered and then reabsorbed in the proximal tubule.

Net Filtration Pressure (NFP) Calculation
The Net Filtration Pressure (NFP) in the kidney glomerulus is the force that drives plasma from the glomerular capillaries into Bowman’s space, starting urine formation. It is determined by Starling forces.

Net Filtration Pressure Formula
NFP = P_GC – P_BS – π_GC

Where:
P_GC = Glomerular capillary hydrostatic pressure (≈ 55 mmHg)
P_BS = Bowman’s space hydrostatic pressure (≈ 15 mmHg)
π_GC = Glomerular oncotic pressure (≈ 30 mmHg)

Step-by-Step Calculation
Substitute the values into the formula:

NFP = 55 – 15 – 30
NFP = 40 – 30
NFP = 10 mmHg

Conclusion
The net filtration pressure is 10 mmHg, which drives the filtration of plasma into the nephron.

Why Other Options Are Incorrect
15 mmHg, 20 mmHg, 25 mmHg, 30 mmHg – These overestimate NFP. Although the glomerular hydrostatic pressure is high, the opposing pressures (Bowman’s space hydrostatic pressure + glomerular oncotic pressure) reduce the effective filtration pressure to only 10 mmHg.

The renal blood flow (RBF) represents the amount of blood that the kidneys receive relative to the total cardiac output.

• The kidneys are highly perfused organs despite their small size (~0.5% of body weight).

• They receive about 20–25% of cardiac output, which translates to approximately 1.2 liters per minute in a healthy adult.

This high perfusion is crucial for:

• Effective filtration of blood

• Excretion of waste products

• Regulation of fluid and electrolyte balance

Why the Other Options Are Incorrect

• 45–50% – Too high; no organ receives nearly half the cardiac output.

• 1–2% – Too low; such values are closer to perfusion of skeletal muscles at rest, not kidneys.

• 30–50% – Still an overestimation; kidneys do not receive that much.

• 10–15% – Underestimation; less than what is physiologically normal.

The glomerular filtration rate (GFR) is the volume of plasma filtered by the kidneys per minute, and it is a key indicator of kidney function.

• In a healthy adult, the normal GFR is:

  • 125 ml/min

  • ≈ 180 liters per day

This value is usually normalized to 1.73 m² body surface area for comparison between individuals.

Why the Other Options Are Incorrect

• 100 ml/min – Slightly below the normal range; may indicate reduced renal function.

• 150 ml/min – Higher than normal; not typical unless in certain physiological states like pregnancy.

• 155 ml/min – Too high for average adults.

• 175 ml/min – Unrealistically high for a normal, healthy kidney.

This patient presents with symptoms consistent with Diabetic Ketoacidosis (DKA), which is most commonly seen in Type 1 Diabetes Mellitus.

Key findings in the scenario:

• Altered mental status (delirium) – due to metabolic acidosis and dehydration.

• Deep and labored breathing (Kussmaul respiration) – a compensatory mechanism for metabolic acidosis.

• Sweet/fruity breath odor – due to ketone body production (acetone).

• Blood glucose: 256 mg/dL – moderate hyperglycemia (not extremely high, but high enough with ketosis to trigger DKA).

• Ketonuria: +2 – confirms significant ketone body formation.

Pathophysiology:
In Type 1 DM, lack of insulin → increased lipolysis → excess free fatty acids → hepatic ketogenesis → metabolic acidosis.

Why the Other Options Are Incorrect

• Lactic acidosis – Causes metabolic acidosis and rapid breathing but does not produce ketones or fruity breath.

• Addison’s disease – Features hypotension, hyperpigmentation, and electrolyte imbalances but no hyperglycemia or ketonuria.

• Acute renal failure – Would show decreased urine output, elevated creatinine, but not ketones or fruity breath.

• Type 2 diabetes mellitus – Usually presents with hyperosmolar hyperglycemic state (HHS), characterized by very high glucose (>600 mg/dL) and minimal or no ketosis.

Nephrotic syndrome is a kidney disorder characterized by heavy protein loss in the urine due to increased permeability of the glomerular filtration barrier.

The diagnostic threshold for proteinuria in nephrotic syndrome is:

• >3.5 grams of protein per 24 hours per 1.73 m² body surface area

Other key features of nephrotic syndrome include:

• Hypoalbuminemia

• Generalized edema (anasarca)

• Hyperlipidemia and lipiduria

Why the Other Options Are Incorrect

• >9.4 g/day – Too high; while severe proteinuria may reach these levels, the diagnostic cutoff is 3.5 g/day.

• >5.7 g/day – Same reason; not the standard diagnostic cutoff.

• >30 g/day – Unrealistically high for most clinical scenarios.

• >50 g/day – Impossible and incompatible with life.

The posterior relations of the kidney include muscles, nerves, and fascia that are located behind the kidney in the retroperitoneal space.

Posterior structures of the kidney:

• Muscles:

  • Psoas major

  • Quadratus lumborum

  • Transversus abdominis

• Nerves:

  • Subcostal nerve

  • Iliohypogastric nerve

  • Ilioinguinal nerve

The quadratus femoris muscle, however, is a deep gluteal muscle located in the hip region, not in the posterior abdominal wall where the kidneys are located.

Why the Other Options Are Incorrect

• Transversus abdominis – Lies posterior-laterally to the kidney.

• Ilioinguinal nerve – Runs posterior to the kidney along with iliohypogastric nerve.

• Iliohypogastric nerve – Posterior to the kidney in the retroperitoneal space.

• Psoas major – Lies medially and posteriorly to the kidney.

The pronephros is the most primitive of the three stages of kidney development (pronephros → mesonephros → metanephros).

• It appears early in the 4th week of gestation.

• It is nonfunctional in humans and degenerates by the end of the 4th week, while the mesonephros takes over as the interim kidney until the permanent metanephros develops around the 5th week.

Why the Other Options Are Incorrect

• End of 6th week – Too late; by then, the pronephros has already degenerated and the metanephros is beginning to mature.

• End of 3rd week – Too early; pronephros only starts to appear around the early 4th week.

• End of 5th week – Incorrect; degeneration has already occurred by then.

• End of 2nd week – Far too early; kidney structures are not forming yet.

The ascending limb of the loop of Henle, especially the thick ascending limb (TAL), has a key role in urine concentration:

• It is impermeable to water under all conditions, even in the presence of antidiuretic hormone (ADH).

• Actively reabsorbs Na⁺, K⁺, and Cl⁻ through the Na⁺-K⁺-2Cl⁻ symporter.

• This creates a hyperosmotic medullary interstitium and allows the countercurrent multiplier system to function.

Why the Other Options Are Incorrect

• Permeability to water is affected by ADH – False; this happens in the collecting ducts, not in the ascending limb.

• Permeable to water – False; only the descending limb is permeable to water.

• Impermeable to sodium – False; sodium is actively reabsorbed here.

• Impermeable to potassium – False; potassium is also reabsorbed along with sodium and chloride.

Urea is a waste product of protein metabolism that is freely filtered at the glomerulus.

• About 50% of the filtered urea is passively reabsorbed in the proximal tubule along with water.

• In the loop of Henle and medullary collecting ducts, additional urea recycling occurs under the influence of antidiuretic hormone (ADH), which helps maintain the medullary concentration gradient for water reabsorption.

• The rest (~50%) is excreted in urine daily.

Why the Other Options Are Incorrect

• 20% – Too low; more urea is reabsorbed.

• 1% – Far too low; much more is reabsorbed before excretion.

• 99.9% – Incorrect; not all urea is reabsorbed because some must be excreted as waste.

• 30% – Too low; actual reabsorption is around 50%.

For patients with a latex allergy, the preferred alternative material for Foley’s catheters is silicone.

• Silicone catheters are:

  • Hypoallergenic (safe for latex-sensitive patients)

  • Biocompatible and flexible

  • Suitable for long-term catheterization due to less encrustation and irritation.

Why the Other Options Are Incorrect

• Plastic – Non-flexible, uncomfortable, and not commonly used for standard Foley catheters.

• Polyvinyl chloride (PVC) – Often contains latex additives; not ideal for latex-allergic individuals.

• Teflon – Sometimes used as a coating, but not typically the primary material; also not the standard alternative for latex allergy.

• Silver – Used for antimicrobial coating on catheters but still often applied over a latex base, so it doesn’t eliminate allergy risk.