Renal – 2018

In tabes dorsalis (a form of neurosyphilis), there is degeneration of the dorsal columns and dorsal roots of the spinal cord. This disrupts sensory input required for the micturition reflex → the bladder loses tone and becomes atonic.

• The result is urinary retention with overflow incontinence.

• This is the correctly paired pathophysiology.

❌ Incorrect Answer Breakdown:

• Decreased vesicourethral angle – stress incontinence: Wrong. Stress incontinence is due to increased vesicourethral angle / urethral hypermobility and weak pelvic floor, not decreased angle.

• Decreased detrusor activity – urge incontinence: Wrong. Urge incontinence is caused by increased / uninhibited detrusor activity (detrusor overactivity), not decreased activity.

• Prostatic hyperplasia – large volumes of urine: Wrong. BPH causes urinary retention with small, frequent voids due to obstruction, not large-volume urination.

• Urethral injury – frequent voiding of urine: Wrong. Urethral injury causes urine leakage into surrounding tissues, not increased frequency of urination.

In chronic pyelonephritis, long-standing infection and scarring lead to tubular atrophy. Some atrophic tubules become dilated and filled with eosinophilic colloid-like casts, producing a microscopic appearance similar to thyroid follicles. This change is called “thyroidization of the kidney.” It is a classic feature of chronic pyelonephritis.

❌ Incorrect Answer Breakdown:

• Chicken wire loop pattern of glomerular capillaries – IgA nephropathy: Wrong. The “chicken wire” appearance refers to diffuse membranous glomerulonephritis, not IgA nephropathy.

• Eosinophilic infiltrate in the interstitium – hydronephrosis: Wrong. Eosinophilic infiltrates are typical of drug-induced interstitial nephritis, not hydronephrosis.

• Nodular glomerulosclerosis – hypertensive nephropathy: Wrong. Nodular glomerulosclerosis (Kimmelstiel–Wilson nodules) is pathognomonic of diabetic nephropathy, not hypertension.

• None of these: Incorrect, because one option (thyroidization – chronic pyelonephritis) is correct.

The retropubic space (space of Retzius) lies anterior to the bladder, between the pubic symphysis and the bladder.

• Therefore, it cannot be considered a posterior relation.

• Posterior relations of the bladder differ slightly between males and females but generally include the rectum, rectovesical pouch (male), and uterus/vagina (female).

❌ Incorrect Answer Breakdown:

• Rectovesical pouch: Present posterior to the bladder in males (peritoneal reflection between bladder and rectum).

• Rectum: Lies posterior to the bladder (directly in males; in females, posterior to uterus and vagina which lie between bladder and rectum).

• Uterus: In females, the uterus lies superior/posterior to the bladder (separated by vesicouterine pouch).

• None of these: Wrong, because one option (retropubic space) is clearly not posterior.

Both the ureter and urinary bladder receive dual autonomic innervation:

• Parasympathetic (pelvic splanchnic nerves, S2–S4): stimulates contraction of the detrusor muscle and ureter peristalsis, and relaxes the internal urethral sphincter → promotes urination.

• Sympathetic (from T11–L2 via hypogastric plexus): relaxes the detrusor muscle and ureter, and contracts the internal urethral sphincter → promotes urine storage.
  This balance between sympathetic and parasympathetic input controls both storage and micturition.

❌ Incorrect Answer Breakdown:

• Preganglionic fibers: Too nonspecific; autonomic innervation involves both pre- and postganglionic fibers depending on the pathway.

• Parasympathetic only: Wrong, because sympathetic input is equally important for urine storage.

• Sympathetic only: Wrong, because parasympathetic activity is essential for micturition.

• None of these: Incorrect, since both autonomic divisions are definitely involved.

Both NSAIDs and ACE inhibitors can impair kidney function, especially when used together or in patients with pre-existing renal disease.

• NSAIDs inhibit prostaglandin synthesis → this prevents vasodilation of the afferent arteriole, reducing renal blood flow.

• ACE inhibitors block angiotensin II → this prevents constriction of the efferent arteriole, lowering glomerular filtration pressure.

• When combined, they significantly reduce glomerular filtration rate (GFR), leading to acute kidney injury (AKI).

❌ Incorrect Answer Breakdown:

• Loop diuretics: Cause volume depletion and electrolyte disturbances but are not the direct classic cause of impaired kidney perfusion like NSAIDs + ACE inhibitors.

• Penicillin: Generally safe; rarely may cause allergic interstitial nephritis, but not a common mechanism of impaired renal hemodynamics.

• Thiazides: Mainly cause electrolyte imbalance (hyponatremia, hypokalemia); not typically associated with direct renal impairment in normal kidneys.

• Antacids: Can cause metabolic alkalosis or electrolyte imbalances (e.g., hypermagnesemia, milk-alkali syndrome) if overused, but not the main cause of impaired renal hemodynamics.

The pelvic splanchnic nerves (S2–S4) provide the parasympathetic innervation to the bladder.

• These nerves stimulate the detrusor muscle to contract.

• They also cause relaxation of the internal urethral sphincter, allowing urination (micturition).

• This regulation is considered the autonomous parasympathetic control of the bladder.

❌ Incorrect Answer Breakdown:

• Lumbar splanchnic nerve: Carries sympathetic fibers from L1–L2 that help in bladder relaxation and internal sphincter contraction, not parasympathetic activity.

• Cervical plexus: Innervates structures of the neck (phrenic nerve, etc.); has nothing to do with bladder control.

• None of these: Incorrect, since the correct nerve (pelvic splanchnic) is listed.

• Lumbar plexus: Supplies muscles and skin of the lower limb and parts of the abdominal wall; not responsible for parasympathetic regulation of the bladder.

Xanthogranulomatous pyelonephritis (XGP) is a rare, severe, chronic form of pyelonephritis characterized by:

• Replacement of renal parenchyma with lipid-laden macrophages (xanthoma cells).

• Strong association with urinary tract obstruction and staghorn calculi.

• Most commonly caused by Proteus species (especially Proteus mirabilis) and sometimes Escherichia coli.

• Proteus contributes by producing urease, which alkalinizes urine and promotes stone formation.

❌ Incorrect Answer Breakdown:

• Neisseria gonorrhoeae: Causes sexually transmitted infections and urethritis, not chronic kidney infection.

• Escherichia coli: Common cause of acute pyelonephritis and UTIs, but not the hallmark organism for XGP.

• Klebsiella: Can cause UTIs but is not the typical pathogen in XGP.

• Salmonella: Associated with gastroenteritis, enteric fever, and sometimes bacteremia; not linked to XGP.

Spironolactone is a potassium-sparing diuretic.

• It antagonizes aldosterone in the collecting ducts, preventing sodium reabsorption and potassium secretion.

• As a result, it leads to potassium retention and is often used in conditions like heart failure, cirrhosis, and hyperaldosteronism.

• Because it does not increase potassium excretion, it is the correct answer.

❌ Incorrect Answer Breakdown:

• Ethacrynic acid: A loop diuretic (like furosemide) that increases sodium, potassium, and chloride excretion.

• Acetazolamide: A carbonic anhydrase inhibitor that increases bicarbonate, sodium, and potassium excretion in the proximal tubule.

• Furosemide: A potent loop diuretic that increases potassium excretion by inhibiting the Na⁺/K⁺/2Cl⁻ transporter in the thick ascending limb.

• Mannitol: An osmotic diuretic that increases urine volume, leading to secondary loss of sodium and potassium.

Nucleic acid digestion (DNA and RNA) occurs primarily in the small intestine, especially the duodenum.

• Pancreatic nucleases (DNAse and RNAse) break down nucleic acids into smaller nucleotides.

• These nucleotides are further digested by brush-border enzymes (nucleotidases, nucleosidases) into nitrogenous bases, sugars, and phosphate, which can then be absorbed.

• Minimal digestion occurs in the mouth or stomach; the small intestine is the major site.

❌ Incorrect Answer Breakdown:

• Esophagus: Functions only as a passage for food; no enzymatic digestion occurs here.

• Appendix: A lymphoid organ with immune functions; not involved in digestion.

• Rectum: Stores feces before defecation; no role in digestion.

• Mouth: Only mechanical digestion and some carbohydrate breakdown (salivary amylase). No nucleic acid digestion occurs here.

The renal artery enters the kidney at the hilum, which is the medial concavity of the kidney. The hilum serves as the passage for major structures:

• Renal vein (most anterior)

• Renal artery (middle)

• Renal pelvis/ureter (most posterior)
  This arrangement is remembered by the acronym “VAU” (Vein, Artery, Ureter — from anterior to posterior).

❌ Incorrect Answer Breakdown:

• Glomerulus: A capillary tuft inside the nephron, supplied by afferent arterioles after the renal artery has branched many times. Not the entry site.

• Pyramid: Refers to the renal medullary pyramids. These are deep structures within the kidney, not points of vascular entry.

• Bladder: A separate organ where urine collects; not related to the entry of renal vessels.

• Capsule: The fibrous covering of the kidney. Vessels do not pierce it directly but enter through the hilum.

The pylorus is part of the stomach and lies more medially in the epigastric/right hypochondriac region. It does not come into direct relation with the anterior surface of the right kidney. Instead, it lies anterior to the pancreas and duodenum, not directly touching the kidney.

❌ Incorrect Answer Breakdown:

• Right colic flexure: ✅ Related — the hepatic flexure of the colon is in contact with the lower part of the anterior surface of the right kidney.

• Suprarenal gland: ✅ Related — the right suprarenal gland caps the upper pole of the right kidney anteriorly and medially.

• Duodenum: ✅ Related — specifically the descending part of the duodenum (2nd part) lies in front of the hilum of the right kidney.

• Liver: ✅ Related — the right lobe of the liver covers the upper part of the anterior surface of the right kidney.

The Na⁺-H⁺ exchanger (NHE3) is a counter-transporter in the proximal tubule. It reabsorbs sodium from the tubular lumen into the proximal tubule cell while secreting hydrogen ions into the lumen.

• This process not only contributes to sodium reabsorption but also plays a critical role in bicarbonate reabsorption and maintaining acid–base balance.

• Since sodium moves inward while hydrogen moves outward, it qualifies as a counter-transporter (antiporter).

❌ Incorrect Answer Breakdown:

• Na⁺-glucose transporter: This is a symporter (SGLT) that reabsorbs sodium and glucose together in the proximal tubule, not a counter-transporter.

• Na⁺/K⁺/2Cl⁻ transporter: Found in the thick ascending limb of loop of Henle, not the proximal tubule. It’s a symporter, not a counter-transporter.

• Na⁺-Cl⁻ transporter: Located in the distal convoluted tubule, not the proximal tubule. It is also a symporter.

• Na⁺ channel: Present in the collecting duct (ENaC), not the proximal tubule, and functions as a simple channel, not a transporter.

The female urethra is about 4 cm in length (sometimes described as 3–5 cm). The statement saying it is “20 cm long” is incorrect, because that length applies to the male urethra (approximately 18–20 cm). The short length of the female urethra contributes to a higher risk of urinary tract infections (UTIs).

❌ Incorrect Answer Breakdown (Why the others are correct):

• The area continuous with the labia majora is lined with non-keratinized stratified squamous epithelium: ✅ True — the distal urethra near the external opening is lined with non-keratinized stratified squamous epithelium, continuous with the vulvar epithelium.

• The middle part is surrounded by the external striated muscle sphincter: ✅ True — the urethra passes through the urogenital diaphragm, where it is surrounded by the external urethral sphincter composed of striated muscle.

• It is initially lined with transitional epithelium: ✅ True — the proximal urethra, near the bladder neck, is lined with transitional (urothelium).

• It is approximately 5 cm long: ✅ True — often given as 4 cm, but some sources accept 3–5 cm. This is correct.

An arteriovenous (AV) fistula is a surgical connection between an artery and a vein, usually in the forearm (e.g., radial artery to cephalic vein). The arterial pressure strengthens and enlarges the vein, making it durable for repeated needle punctures. This high-flow access is essential for hemodialysis, and AV fistulas are the preferred long-term access because they last longer and have fewer complications compared to catheters or grafts.

❌ Incorrect Answer Breakdown:

• Arteriolymphatic fistula: Not a real clinical procedure; arteries are not surgically joined to lymphatic vessels.

• Capillary bed: A natural microscopic exchange network; cannot be surgically created for dialysis.

• Foramen ovale: A fetal cardiac opening between atria; unrelated to dialysis or vascular access.

• Portal vein: A natural venous vessel carrying blood from the gut to the liver; not surgically made and irrelevant to dialysis.

During urinary catheterization, certain sterile materials and solutions are required, but Dettol (antiseptic/disinfectant) is not used because it can irritate or damage mucosal tissues of the urethra and bladder.

Items commonly required for catheterization:

• Foley catheter – Flexible tube inserted into the bladder.

• Urine drainage bag – To collect urine.

• Sterile water or saline – Used to inflate the balloon of the Foley catheter.

• Lidocaine jelly – As a lubricant and mild local anesthetic for patient comfort.

• Sterile gloves, drapes, and antiseptic solution (usually povidone-iodine) – For maintaining asepsis.

Why the Other Options Are Correct

• Urine drainage bag – Necessary to collect urine.

• Distilled water – Used to inflate the balloon of the Foley catheter.

• Foley tube – The main device for catheterization.

• Lidocaine – Provides lubrication and reduces discomfort during insertion.

The ureter is a retroperitoneal muscular tube that carries urine from the kidneys to the bladder.

• It lies anterior to the transverse processes of the lumbar vertebrae as it descends vertically along the posterior abdominal wall.

• This relationship is often noted during surgeries like ureteric stent placements or retroperitoneal procedures.

Why the Other Options Are Incorrect

• Esophagus – Located in the posterior mediastinum (thorax), not related to lumbar transverse processes.

• Rectum – Lies in the pelvis, anterior to the sacrum, not along the lumbar vertebral transverse processes.

• Aorta – Runs anterior to the vertebral bodies, not anterior to the transverse processes.

• Bladder – Located in the pelvis, far from the lumbar transverse processes.

The kidneys play a key role in acid–base regulation by secreting H⁺ and reabsorbing HCO₃⁻.

• When HCO₃⁻ absorption decreases, there is less buffering capacity in the blood, leading to reduced H⁺ secretion in the renal tubules.

• This can contribute to acidosis, as the body is unable to excrete enough acid or regenerate adequate bicarbonate.

Why the Other Options Are Incorrect

• Increased HCO₃⁻ absorption – Would increase H⁺ secretion, not decrease it, as the kidneys try to buffer more acid.

• Increased pCO₂ – Seen in respiratory acidosis; this stimulates increased H⁺ secretion by the kidneys to compensate.

• Ammonia synthesis – Ammonia binds to secreted H⁺ in the tubules; more ammonia synthesis means more H⁺ excretion, not less.

• Hypoventilation – Leads to increased CO₂ (respiratory acidosis), which in turn stimulates H⁺ secretion, not decreases it.

Renin is an enzyme secreted by the juxtaglomerular (JG) cells located in the afferent arteriole of the kidney.

• These cells are specialized smooth muscle cells that play a key role in the renin–angiotensin–aldosterone system (RAAS), which regulates:

  • Blood pressure

  • Sodium balance

  • Fluid homeostasis

Triggers for renin release:

• Low renal perfusion pressure (e.g., hypotension)

• Sympathetic nervous system activation (β1 receptors)

• Low sodium delivery sensed by macula densa cells

Why the Other Options Are Incorrect

• Hepatocytes – Produce angiotensinogen, not renin.

• Principal cells – Found in the collecting ducts; involved in water and sodium reabsorption under ADH and aldosterone influence, not renin secretion.

• Alveoli – Function in gas exchange, not hormone secretion.

• Intercalated cells – Located in the collecting ducts; regulate acid-base balance, not renin secretion.

The tip of each renal pyramid is called the renal papilla.

• Urine formed in the nephrons drains through the collecting ducts located in the medulla.

• From the papilla, urine flows into the minor calyx, then into a major calyx, then the renal pelvis, and finally into the ureter for excretion.

Why the Other Options Are Incorrect

• Capsule – The fibrous capsule surrounds the kidney but is not part of the drainage pathway.

• Ureter – Receives urine after it passes through calyces and the renal pelvis; not the direct opening point of the pyramid tips.

• Medulla – This is the region where the pyramids are located, but the openings are at the calyces, not in the medulla tissue itself.

• Cortex – The outer region of the kidney, containing glomeruli and parts of the nephron, but not the drainage point.

The detrusor muscle is the smooth muscle layer of the bladder wall.

• During micturition (urination), the detrusor muscle contracts under parasympathetic control (pelvic splanchnic nerves, S2–S4).

• This contraction increases pressure within the bladder, forcing urine out through the urethra while the internal urethral sphincter relaxes.

Why the Other Options Are Incorrect

• Opens urethral lumen – This is performed by the relaxation of the sphincter muscles, not the detrusor itself.

• Helps fill up the bladder – Filling requires the detrusor to relax, not contract.

• Empties renal pelvis – That is the function of the ureter and peristaltic activity, not the bladder muscle.

• Blocks urethral lumen – Done by the internal and external urethral sphincters, not the detrusor.

The mucosa of the urinary bladder is lined by urothelium, also known as transitional epithelium.

• It is a specialized stratified epithelium that allows the bladder to stretch as it fills with urine and recoil when it empties.

• The superficial layer contains umbrella cells that protect underlying tissues from urine toxicity.

Why the Other Options Are Incorrect

• Adventitia – This is a connective tissue layer found externally around parts of the bladder (except the superior surface). It is not the mucosal lining.

• Serosa – Found only on the superior surface of the bladder, derived from the peritoneum; not the lining of the mucosa.

• Endothelium – Lines blood vessels, not the bladder.

• Renal fascia – Connective tissue around the kidney, unrelated to bladder mucosa.

Goodpasture syndrome is an autoimmune disease where the body produces IgG autoantibodies against the α3 chain of type IV collagen.

• These antibodies attack the basement membranes of the glomeruli in the kidneys and the alveoli in the lungs.

• This results in:

  • Rapidly progressive glomerulonephritis (RPGN) → hematuria, proteinuria, and renal failure

  • Pulmonary hemorrhage → hemoptysis and shortness of breath

Why the Other Options Are Incorrect

• Acetylcholine receptor – Targets in myasthenia gravis, not Goodpasture syndrome.

• Platelet membrane proteins – Seen in immune thrombocytopenic purpura (ITP).

• Red blood cell membrane proteins – Found in conditions like autoimmune hemolytic anemia.

• Thyroid-stimulating hormone receptor – Seen in Graves’ disease, leading to hyperthyroidism.

In respiratory acidosis, there is an increase in arterial CO₂ (PaCO₂) due to hypoventilation or impaired gas exchange (e.g., COPD, airway obstruction).

• CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻
  ↑CO₂ → ↑H⁺ → ↓pH (acidemia)

To compensate:

• The kidneys respond (takes hours to days) by increasing reabsorption of HCO₃⁻ and increasing H⁺ excretion in the urine.

• This raises the blood bicarbonate level, buffering the excess acid and partially restoring the pH.

Why the Other Options Are Incorrect

• Decrease in H⁺ excretion – Wrong; the kidneys actually increase H⁺ excretion to counter the acidity.

• Hyperventilation – Wrong; hyperventilation reduces CO₂, but in respiratory acidosis, the primary problem is hypoventilation.

• Decrease in HCO₃⁻ reabsorption – Wrong; this would worsen acidosis.

• Hypoventilation – Wrong; hypoventilation causes respiratory acidosis, it is not the compensatory response.

Alport syndrome is a primarily hereditary kidney disease caused by mutations in type IV collagen genes (commonly COL4A3, COL4A4, or COL4A5).

• It usually follows an X-linked dominant inheritance pattern, but autosomal dominant and autosomal recessive forms also exist.

• The mutation leads to defective glomerular basement membrane (GBM), causing:

  • Hematuria (often microscopic initially)

  • Progressive renal failure

  • Sensorineural hearing loss

  • Ocular abnormalities (e.g., anterior lenticonus, dot-and-fleck retinopathy)

Why the Other Options Are Incorrect

• Minimal Change Disease (MCD) – Mostly idiopathic or secondary to triggers like infections, NSAIDs, or lymphomas; not hereditary.

• Rapidly Progressive Glomerulonephritis (RPGN) – Often secondary to autoimmune conditions (like Goodpasture syndrome, lupus) or severe post-infectious causes; not genetic.

• Post-Streptococcal Glomerulonephritis (PSGN) – Caused by an immune response after streptococcal infection; acquired, not hereditary.

• Focal Segmental Glomerulosclerosis (FSGS) – Usually secondary to obesity, HIV, heroin use, or adaptive responses, though rare genetic forms exist, it is not primarily hereditary in most cases.

The proximal convoluted tubule (PCT) is the major site of sodium reabsorption in the nephron.

• About 65% of filtered sodium (Na⁺) is reabsorbed here along with water, glucose, amino acids, and other solutes.

• This process is mostly active transport driven by the Na⁺/K⁺ ATPase pump on the basolateral membrane.

• This also contributes to reabsorption of water (via osmotic coupling) and bicarbonate (HCO₃⁻).

Why not the other options?

• 100% – Incorrect. Not all sodium is reabsorbed in the PCT; additional reabsorption occurs in the loop of Henle, distal tubule, and collecting duct.

• 20% – Incorrect. The loop of Henle reabsorbs about 20–25% of Na⁺, not the PCT.

• 40% – Incorrect. The PCT reabsorbs more than 40%, specifically around 65%.

• 80% – Incorrect. Too high; 80–90% of sodium is reabsorbed cumulatively in the nephron, but not in the PCT alone.

Summary Table of Sodium Reabsorption

Osmolarity of extracellular fluid (ECF) depends on the ratio of solutes (mainly sodium and its accompanying anions) to water.

• Edema → This is fluid accumulation in the interstitial space. Osmolarity doesn’t necessarily increase; it depends on the underlying cause. Often fluid is protein-poor and osmolarity is normal.

• Lack of salt consumption → Would lower sodium in the plasma, decreasing or not affecting osmolarity, not increasing it.

• Excess hydration → Dilutes extracellular fluid, decreasing osmolarity.

• Dehydration → Loss of water without proportional solute loss leads to concentrated solutes in the ECF, raising osmolarity.

• Excess salt excretion → Would reduce solute concentration, lowering osmolarity.

Answer breakdown:

• Osmolarity ↑ when water ↓ relative to solutes → dehydration

• Osmolarity ↓ when water ↑ or solutes ↓ → excess hydration, salt loss

• Edema doesn’t directly reflect osmolarity changes

The rate of flow of any fluid is explained by Poiseuille’s law, where flow (Q) is inversely proportional to viscosity (η). Viscosity is a measure of a fluid’s internal resistance to flow. Honey has much higher viscosity than water because of its thicker, more cohesive molecular structure (mainly concentrated sugars and less free water).

• Water has less calories → Irrelevant, caloric content does not determine flow.

• Honey is less heavy per unit volume → Incorrect, honey is actually denser than water, but density isn’t the key factor here.

• Water has a lower boiling point → True fact, but unrelated to flow rate at room temperature.

• Honey has a higher viscosity → Correct, this higher resistance to flow slows it down.

• Honey has a lower density → False, honey’s density is higher than water’s.

If the urethra is obstructed (for example, by a stricture, stone, or enlarged prostate in males), urine cannot be expelled from the bladder. This leads to progressive bladder distension. Since urine cannot leave, pressure builds up and is transmitted back through the ureters, leading to hydroureter and eventually hydronephrosis. This explains the CT findings in the patient.

• Kidney failure → causes oliguria/anuria but does not cause an enlarged bladder or hydronephrosis, because the kidneys themselves are not producing urine.

• Obstruction at ureter → would cause unilateral hydronephrosis and hydroureter, but the bladder would not be significantly enlarged.

• Unilateral kidney stone at pelvis → only blocks one kidney; the other continues to drain, so no bilateral hydronephrosis or massively distended bladder.

• Gardnerella vaginalis infection → a bacterial cause of vaginitis, unrelated to bladder outflow obstruction or hydronephrosis.

Answer breakdown:

• Enlarged bladder + hydronephrosis = lower urinary tract obstruction (urethra)

• Upper tract obstructions = hydronephrosis without bladder distension

• Renal failure = anuria without hydronephrosis or enlarged bladder

• Renal vein –

• • The renal veins drain blood from the kidney after it has already developed in its proper position.

  • They are not located inferior enough to block the ascent.

Thus, they have no role in stopping a horseshoe kidney.

• Renal artery –

• The renal arteries actually form after the kidney reaches its final position in the upper abdomen.

• They branch directly from the abdominal aorta at ~L1–L2.

Since they don’t exist during the ascent, they cannot be the obstacle.

• Inferior mesenteric artery (IMA) –

• The IMA originates at the level of L3, which is below the normal final kidney position (L1–L2).

• When the lower poles of the fused kidney try to ascend, they hit the IMA and can’t move further up.

That’s why horseshoe kidneys are usually found lower in the abdomen (around L3–L5).

• Superior mesenteric artery (SMA) –

• The SMA arises higher, at L1.

• By the time kidneys reach this level, they are already fused and stuck below the IMA.

So the SMA is too high to be the obstructing vessel.

• Celiac trunk –

• The celiac trunk is the highest of all these vessels, arising around T12.

• Kidneys never ascend this high (they normally stop at L1–L2).

• Therefore, it plays no role in stopping ascent.

Answer Breakdown:

• Renal vein →  drains kidney, no obstruction

• Renal artery → ❌ forms later, not during ascent

• Inferior mesenteric artery → ✅ blocks fused kidney’s ascent

• Superior mesenteric artery → ❌ too high, not the obstacle

• Celiac trunk → ❌ way too high, unrelated

• Renal capsule: Thin fibrous covering directly on the kidney surface.

• Perinephric (perirenal) fat: Immediately outside the capsule, cushioning the kidney.

• Renal fascia: Condensation of connective tissue enclosing kidney + adrenal gland + perinephric fat.

• Paranephric (pararenal) fat: Outermost, behind the kidney, between renal fascia and posterior abdominal wall.

Answer breakdown:

• Capsule → perinephric fat → renal fascia → paranephric fat → ✅ Correct

• Paranephric first → ❌ it’s the outermost, not innermost

• Capsule → paranephric fat → ❌ wrong sequence

• Capsule last → ❌ capsule is innermost

• Paranephric before perinephric → ❌ inverted

Hemodialysis is a renal replacement therapy that uses a dialysis machine and dialyzer to filter wastes, excess water, and electrolytes from the blood when the kidneys fail to do so. Its main role is to maintain homeostasis of fluid, electrolytes, and acid-base balance.

• Not erythropoietin → That is produced by the kidneys (peritubular fibroblasts) and must be replaced with injections, dialysis does not restore it.

• Not kidney function → Dialysis replaces lost functions but does not regenerate nephrons.

• Not erythrocytes → Dialysis cannot make RBCs; anemia of CKD requires EPO therapy.

• Not gluconeogenesis → That’s a function of the kidney and liver, unaffected by dialysis.

Answer breakdown:

• Restore erythropoietin → ❌ (requires EPO injections)

• Restore fluid & electrolytes → ✅ (true purpose of dialysis)

• Restore kidney function → ❌ (doesn’t cure kidneys)

• Restore RBC numbers → ❌ (needs EPO/iron therapy)

• Restore gluconeogenesis → ❌ (not related)

The coverings of the kidney from innermost to outermost are:

1. Fibrous capsule – thin layer tightly adherent to kidney.

2. Perinephric (perirenal) fat – surrounds kidney and adrenal gland.

3. Renal fascia (Gerota’s fascia) – fibrous connective tissue enclosing kidney + fat.

4. Paranephric fat – outermost, posterior to the renal fascia.

• Cortex & medulla are internal structures of the kidney, not coverings.

• Pelvis is the funnel-shaped structure inside, collecting urine.

• Perinephric fat is not the outermost, it lies inside the renal fascia.

• The renal fascia is the true outermost layer enclosing the kidney and perinephric fat.

Answer breakdown:

• Renal fascia → Correct (outermost covering of kidney itself)

• Pelvis → inside, collects urine

• Cortex → internal tissue

• Medulla → deeper internal tissue

• Perinephric fat → surrounded by fascia, not outermost

• Acute kidney injury (AKI):

  • A sudden decline in renal function (hours to days).

  • Caused by ischemia, toxins, obstruction, or sepsis.

  • Often reversible if the underlying cause is treated early (e.g., prerenal AKI corrected by fluids, obstruction relieved, nephrotoxin withdrawn).

  • Dialysis may be required temporarily, but not always.

  • Does not require transplantation unless it progresses to chronic, irreversible damage.

• Chronic kidney disease (CKD):

  • Irreversible, progressive scarring of kidney.

  • Often ends in end-stage renal disease, requiring dialysis or transplant.

Answer breakdown:

• Often reversible → Correct

• Requires transplantation → CKD, not AKI

• Is irreversible → False for AKI, true for CKD

• Due to severe progressive scarring → CKD, not AKI

• Requires dialysis → Only sometimes in AKI, not always

• The urogenital sinus has three regions:

  • Vesical part → Forms most of the urinary bladder.

  • Pelvic part → Forms the prostatic urethra in males and the entire urethra in females.

  • Phallic part → Contributes to penile urethra in males and vestibule of vagina in females.

Other options:

• Vagina – Incorrect: Mainly derived from the vaginal plate (endoderm of urogenital sinus + paramesonephric ducts).

• Fallopian tubes – Incorrect: Derived from paramesonephric (Müllerian) ducts, not urogenital sinus.

• Ureter – Incorrect: Develops from the ureteric bud (outgrowth of mesonephric duct).

• Kidneys – Incorrect: Develop from metanephric blastema + ureteric bud, not urogenital sinus.

• The hilum of the kidney lies at the level of L1 vertebra in the transpyloric plane, which passes through:

  • Pylorus of the stomach

  • Fundus of gallbladder

  • Neck of pancreas

  • Origins of the superior mesenteric artery and portal vein

  • Hilum of kidneys

Other options:

• Median plane – Incorrect: Vertical midline plane, not used for kidney hilum location.

• Supine plane – Incorrect: Not an anatomical reference plane.

• Subcostal plane – Incorrect: At L2 level, below the transpyloric plane.

• Transtubercular plane – Incorrect: At L5 level, much lower than the kidneys.

Answer breakdown:

• Transpyloric plane – Correct (L1, passes through renal hilum).

• Others – Incorrect anatomical levels.

• H⁺ secretion: Mainly occurs in the intercalated cells of the collecting duct, via H⁺-ATPase and H⁺/K⁺-ATPase pumps. This process is vital for maintaining acid–base balance and allows the kidney to lower tubular pH to as low as 4.5.

• K⁺ secretion: Primarily occurs in the principal cells of the late distal convoluted tubule and collecting duct, through Na⁺/K⁺-ATPase activity and apical K⁺ channels.

Other nephron segments:

• Proximal tubule: Major site for reabsorption of Na⁺, H₂O, HCO₃⁻, glucose, amino acids. Limited H⁺ secretion occurs here (for bicarbonate reabsorption), but it is not the main site of regulation.

• Loop of Henle (ascending/descending): Primarily handles Na⁺, Cl⁻, and water reabsorption. Not the main site for H⁺/K⁺ secretion.

• Vasa recta: Capillary network involved in counter-current exchange, not secretion.

Answer breakdown:

• Collecting duct – Correct (site of regulated H⁺ and K⁺ secretion).

• Descending loop – Incorrect (mainly water reabsorption).

• Proximal tubule – Incorrect (H⁺ secretion occurs but not the main site; K⁺ secretion does not occur).

• Vasa recta – Incorrect (capillary, not nephron tubule).

• Distal convoluted tubule – Partially true for K⁺, but H⁺ secretion is minimal here).

• Ascending loop – Incorrect (Na⁺, K⁺, 2Cl⁻ transport, no major H⁺ secretion).

The ureter receives blood supply segmentally from nearby arteries as it descends:

• Abdominal ureter: renal artery, gonadal artery, aorta, common iliac artery.

• Pelvic ureter: branches from internal iliac artery, especially superior vesical artery, inferior vesical artery (in males), uterine/vaginal arteries (in females).

• Occasionally, umbilical artery remnants (via superior vesical) also supply.

The inferior mesenteric artery supplies the hindgut (distal colon & rectum), but does not contribute to ureteric supply.

Answer breakdown:

• Inferior mesenteric artery → ✗ does not supply ureter

• Umbilical artery → ✓ via superior vesical branch, supplies pelvic ureter

• Superior vesical artery → ✓ supplies upper pelvic ureter

• Inferior vesical artery → ✓ supplies lower ureter in males

• Internal iliac artery → ✓ main pelvic source

The nephron is the structural and functional unit of the kidney, each kidney containing about 1–1.5 million nephrons.
A nephron consists of:

• Renal corpuscle (glomerulus + Bowman’s capsule) → filtration.

• Tubular system (PCT, loop of Henle, DCT, collecting duct) → reabsorption & secretion.

Together, nephrons maintain fluid balance, electrolytes, acid-base status, and remove nitrogenous waste.

Incorrect options:

• Brain → functional unit is the neuron.

• Heart → functional unit is the cardiac muscle cell/myocyte.

• Spleen → does not have a single defined functional unit.

• Liver → functional unit is the hepatic lobule.

The purine ring is built step by step on ribose-5-phosphate (via PRPP). Several amino acids contribute atoms:

• Aspartate → provides a nitrogen (N1).

• Glutamine → provides two nitrogens (N3, N9).

• Glycine → provides two carbons and a nitrogen (C4, C5, N7).

• Formyl-THF → provides carbons (C2, C8).

• CO₂ → provides one carbon (C6).

So both aspartate and glutamine are crucial in purine nucleotide biosynthesis.

Incorrect options:

• Triglyceride → made from glycerol + fatty acids, not amino acids.

• Ribose → comes from HMP shunt (not amino acids).

• Glucose → synthesized via gluconeogenesis, amino acids contribute carbons but not specifically aspartate + glutamine together.

• Cholesterol → made from acetyl-CoA, not amino acids.

The RIFLE criteria is the standard system used to classify acute kidney injury (AKI).

• It divides AKI into three severity classes:

  • Risk (mildest)

  • Injury

  • Failure (most severe)

• And two outcome classes:

  • Loss (persistent renal failure > 4 weeks)

  • End-stage renal disease (renal failure > 3 months).

This system is based on changes in serum creatinine, GFR, and urine output.

Incorrect options:

• HHELPSS → mnemonic for congenital syphilis features.

• JONES criteria → used for diagnosing rheumatic fever.

• GUN criteria → not a medical classification system.

• HACEK → group of Gram-negative bacteria causing endocarditis (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella).

The counter-current exchange system in the kidney is performed by the vasa recta, the straight capillaries that descend into the renal medulla parallel to the loops of Henle.

• Their slow blood flow and hairpin structure allow for passive exchange of water and solutes between descending and ascending limbs.

• This prevents the “washout” of the medullary osmotic gradient while still delivering oxygen and nutrients.

• This mechanism supports the counter-current multiplier created by the loop of Henle, allowing the kidney to concentrate urine.

Incorrect options:

• Vasa nervosum → tiny vessels supplying peripheral nerves.

• Vasa vasorum → vessels supplying large blood vessel walls.

• Varicose veins → dilated, tortuous veins in the legs; unrelated.

• Venae comitantes → paired veins accompanying arteries, not part of counter-current exchange.

The kidneys have multiple homeostatic functions:

• Short-term BP regulation: Through the renin-angiotensin-aldosterone system (RAAS), kidneys can rapidly increase systemic vascular resistance and sodium/water retention.

• Long-term BP regulation: By controlling extracellular fluid volume and sodium balance, kidneys maintain blood pressure over days to weeks.

• Acid-base balance: Kidneys excrete hydrogen ions and regenerate bicarbonate, keeping plasma pH in a very narrow range (7.35–7.45).

Therefore, the correct choice is the one that includes both BP regulation (short + long term) and acid-base balance.

Incorrect options:

• “Only long-term BP regulation and acid-base balance” → ignores the acute renin-mediated role.

• “Short and long-term BP regulation only” → ignores acid-base role.

• “Blood acid-base balance only” → ignores BP regulation.

• “Only short-term BP regulation and acid-base balance” → ignores the long-term volume/Na⁺ control role.

5) Answer breakdown:

• Only long-term BP regulation + acid-base → ✗

• Short + long-term BP regulation only → ✗

• Acid-base only → ✗

• Only short-term BP regulation + acid-base → ✗

• Short + long-term BP regulation + acid-base → ✓

The kidney has many vital functions beyond filtration and reabsorption. One key endocrine function is the activation of vitamin D. The proximal tubule contains the enzyme 1α-hydroxylase, which converts 25-hydroxycholecalciferol (calcidiol, inactive) into 1,25-dihydroxycholecalciferol (calcitriol, active). This active form increases calcium and phosphate absorption from the gut.

Other options are incorrect:

• Reabsorbs sulfuric and phosphoric acid → incorrect, the kidney excretes hydrogen ions and buffers acids but does not “reabsorb” strong acids.

• Produces erythrocytes → wrong, erythropoietin stimulates bone marrow to produce RBCs, but kidney itself doesn’t make them.

• Activates vitamin K → no, vitamin K activation happens in the liver (for clotting factors).

• Performs glucuronidation → this is a liver detoxification process.

5) Answer breakdown:

• Reabsorbs sulfuric/phosphoric acid → ✗ (actually excretes acids).

• Produces erythrocytes → ✗ (bone marrow’s job).

• Produces active vitamin D → ✓ correct.

• Activates vitamin K → ✗ (liver).

• Performs glucuronidation → ✗ (liver).

In end-stage renal disease (ESRD), the kidneys cannot produce enough erythropoietin (EPO), leading to anemia. Administering exogenous EPO stimulates the bone marrow to increase red blood cell production. This improves oxygen-carrying capacity, but it also increases hematocrit and blood viscosity, which can cause hypertension. This is a well-known side effect of recombinant EPO therapy in chronic kidney disease patients.

5) Answer breakdown:

• Decreased BP → wrong, it tends to raise it.

• Decreased blood volume → wrong, volume effectively increases with more RBC mass.

• Increased BP → ✅ correct, due to higher viscosity and vascular resistance.

• Decreased erythrocyte production → wrong, EPO stimulates production.

• Induces hypoxia → opposite effect, it relieves hypoxia.

Filtration fraction (FF) quantifies the proportion of plasma flow that is filtered through the glomerulus. By definition:

FF=GFRRPFFF=RPFGFR​

Normal values are ~16–20%. It rises with efferent arteriole constriction (↑GFR, ↓RPF), and falls with afferent dilation.

5) Answer breakdown:

• RBF ÷ GFR → wrong, blood includes cells.

• Systemic BP ÷ GFR → unrelated.

• RPF ÷ GFR → inverted.

• GFR ÷ RPF → ✅ correct.

• None of these → incorrect.

The appendix has variable positions, but the retrocecal position is the most common (about 60–65% of cases). Other positions include pelvic, subcecal, preileal, and postileal, but they are less frequent.

• Rectovesicular → pouch between rectum & bladder (in males).

• Rectosigmoid → region at junction of rectum & sigmoid colon.

• Transverse → appendix rarely lies across transversely.

• Rectouterine → pouch of Douglas (in females).

Answer breakdown:

• Rectovesicular – Wrong (male pelvic pouch, not appendix).

• Rectosigmoid – Wrong (appendix not usually here).

• Retrocecal – Correct (most common site, behind cecum).

• Transverse – Wrong (uncommon).

• Rectouterine – Wrong (female pouch, not appendix).

The conversion of phosphoenolpyruvate (PEP) → pyruvate is catalyzed by pyruvate kinase. In this reaction, the phosphate group of PEP is transferred to ADP, generating ATP directly without involvement of the electron transport chain. This process is called substrate-level phosphorylation.

• Isomerization → rearrangement of atoms (e.g., G6P ↔ F6P).

• Phosphorylation → general addition of phosphate group, not necessarily ATP formation.

• Oxidative phosphorylation → ATP generation via ETC and proton gradient.

• Aldol condensation → reaction forming C–C bonds, not relevant here.

Answer breakdown:

• Isomerization – Wrong (this is a transfer, not rearrangement).

• Phosphorylation – Wrong (phosphate isn’t just added, it’s transferred to ADP).

• Oxidative phosphorylation – Wrong (ETC not involved).

• Aldol condensation – Wrong (different pathway).

• Substrate level phosphorylation – Correct (ATP formed directly from PEP).

Mountain sickness occurs at high altitude due to hypoxia. The main issue is respiratory alkalosis from hyperventilation. Acetazolamide, a carbonic anhydrase inhibitor, induces a mild metabolic acidosis by promoting bicarbonate excretion in urine. This counteracts alkalosis and stimulates ventilation, improving oxygenation. It is therefore the drug of choice for both prevention and treatment of acute mountain sickness.

Loop diuretics (Bumetanide, Torsemide, Furosemide, Ethacrynic acid) are not useful for mountain sickness; they act at the thick ascending limb of Henle and are used for edema, hypertension, and hypercalcemia instead.

Answer breakdown:

• Acetazolamide – Correct, DOC for mountain sickness.

• Bumetanide, Torsemide, Furosemide, Ethacrynic acid – Loop diuretics, not effective.

Filtration fraction (FF) is the fraction of renal plasma flow (RPF) that is filtered across the glomeruli: FF = GFR/RPF. In adults, GFR is about 125 mL/min (~180 L/day) and RPF is ~600 mL/min. Thus, FF ≈ 125/600 ≈ 0.20, i.e., 20%.

Why others are wrong:

5% and 10% are far below physiologic norms and would imply very low filtration relative to plasma flow;

30%–40% are too high for healthy kidneys and would suggest abnormally aggressive filtration.

• Dialysis indications are remembered by the rule: AEIOU

  • A → Acidosis (severe metabolic acidosis, refractory)

  • E → Electrolyte imbalance (esp. refractory hyperkalemia)

  • I → Ingestions (toxic substances: methanol, ethylene glycol, lithium, salicylates)

  • O → Overload (fluid overload not responsive to diuretics)

  • U → Uremia (encephalopathy, pericarditis, bleeding, neuropathy)

• Chronic indication: Dialysis is initiated when GFR falls below ~15 ml/min/1.73 m² (≈ <15% of normal).

  • Normal GFR ≈ 90–120.

  • <15 = end-stage renal disease (ESRD).

• Other options explained:

  • Hypokalemia → Not an indication; it’s hyperkalemia that is.

  • Hypernatremia → Managed with fluids, not dialysis (except extreme cases with renal failure).

  • GFR < 50% → Too early, CKD stage 3–4 but not ESRD.

  • Hypovolemia → Contraindication for dialysis (need volume first).

Answer breakdown:

• Hypokalemia → Wrong (dialysis for hyperkalemia).

• Hypernatremia → Wrong.

• GFR < 50% → Too early.

• Hypovolemia → Contraindicated.

• GFR < 15% → Correct.

• In CAPD peritonitis, the main source of infection is contamination of the catheter from skin flora.

• The most common cause is Staphylococcus epidermidis (a coagulase-negative staphylococcus), because it:

  • Colonizes skin.

  • Forms biofilms on catheter surfaces, protecting it from host defenses and antibiotics.

• Other common organisms:

  • Staphylococcus aureus (more virulent, causes severe peritonitis, but less frequent than epidermidis).

  • Gram-negative organisms like Pseudomonas or Proteus occur less commonly, usually in hospital-acquired infections.

• Staphylococcus saprophyticus is a cause of UTIs in young women, not peritonitis.

Answer breakdown:

• Staphylococcus saprophyticus → UTIs, not CAPD.

• Proteus mirabilis → UTI/struvite stones, not main CAPD cause.

• Staphylococcus aureus → possible, but less common than S. epidermidis.

• Pseudomonas aeruginosa → hospital-acquired cases, not most common.

• Staphylococcus epidermidis → correct, most frequent agent of CAPD peritonitis.

• Acute pyelonephritis is an acute suppurative infection of the kidney, usually caused by ascending spread of bacteria from the lower urinary tract.

• The most common organism is E. coli, responsible for ~80–85% of cases.

• It expresses P-fimbriae and other adhesins that allow it to attach to urothelium and ascend against urine flow.

• Other possible organisms:

  • Proteus (especially in patients with urinary stones, since urease activity alkalinizes urine and promotes struvite stones).

  • Klebsiella, Enterobacter, Pseudomonas (hospital-acquired, catheter-associated).

  • Staphylococcus aureus is usually from hematogenous spread, not ascending infection.

Answer breakdown:

• Proteus mirabilis → causes struvite stones, but not the most common.

• Staphylococcus aureus → usually hematogenous spread, rare cause.

• Escherichia coli → correct, most common cause of acute pyelonephritis.

• Enterobacter → possible, but less common.

• Pseudomonas aeruginosa → hospital-acquired, catheter-related, not the leading cause.

• The urinary bladder develops mainly from the vesical part of the urogenital sinus (which gives rise to most of the bladder lining). This portion is highly distensible.

• However, the trigone (the triangular area between the two ureteric orifices and the internal urethral orifice) has a different embryological origin.

• It is formed by the incorporation of the lower ends of the mesonephric ducts into the posterior wall of the developing bladder.

• Since the trigone is derived from mesoderm (mesonephric duct), unlike the rest of the bladder (endodermal origin from urogenital sinus), it is the least distensible part.

• With time, even the trigone becomes overgrown by endodermal epithelium, but its mesodermal origin makes it distinct functionally.

Answer breakdown:

• Phallic part of urogenital sinus → gives rise to penile urethra, not bladder.

• Pelvic part of urogenital sinus → contributes to prostatic and membranous urethra.

• Allantois → becomes urachus → median umbilical ligament.

• Mesonephric duct → correct (forms trigone, least distensible part).

• Vesical part of urogenital sinus → forms most of bladder, highly distensible.

• In the proximal convoluted tubule (PCT), H⁺ is secreted into the tubular lumen mainly via the Na⁺/H⁺ exchanger (NHE3) on the apical membrane.

• This is a secondary active transport process:

  • Na⁺ moves down its electrochemical gradient (into the cell).

  • H⁺ is exchanged out into the lumen.

• The secreted H⁺ combines with filtered HCO₃⁻ → H₂CO₃ → carbonic anhydrase converts it to CO₂ + H₂O → CO₂ diffuses back into the cell, where it reforms HCO₃⁻, which is reabsorbed into the blood.

• The other options are incorrect:

  • Glucose/H⁺ exchanger → doesn’t exist (glucose uses Na⁺-glucose symporter).

  • Cl⁻/H⁺ exchanger → not a PCT mechanism.

  • K⁺/H⁺ exchanger → seen in intercalated cells of collecting duct, not PCT.

  • All of these → wrong, because only Na⁺/H⁺ exchanger works here.

Answer breakdown:

• Na⁺/H⁺ exchanger → correct

• Glucose/H⁺ exchanger → wrong

• Cl⁻/H⁺ exchanger → wrong

• K⁺/H⁺ exchanger → wrong

• All of these → wrong

• The boy has gross hematuria (cola/tea-colored urine), hypertension, edema, and systemic symptoms → the hallmark of nephritic syndrome.

• The key trigger is a streptococcal throat infection 2–3 weeks prior, strongly pointing toward post-streptococcal glomerulonephritis (PSGN).

• Pathology: Immune complex deposition (Type III hypersensitivity) → complement activation → glomerular inflammation.

• Distinguishing features from other options:

  • IgA nephropathy (Berger’s disease): Hematuria appears within 1–2 days of infection, not weeks later.

  • Minimal change disease: Nephrotic syndrome, not nephritic; presents with proteinuria and edema, not hematuria/hypertension.

  • Membranous GN: More common in adults, causes nephrotic syndrome.

  • Wegener’s granulomatosis: Systemic vasculitis with upper/lower respiratory involvement and c-ANCA positivity.

Answer breakdown:

• Nephritic syndrome → correct (fits timing, symptoms, and age).

• IgA nephropathy → wrong (hematuria within days, not weeks).

• Minimal change disease → wrong (nephrotic, not nephritic).

• Membranous GN → wrong (adult nephrotic syndrome).

• Wegener’s granulomatosis → wrong (respiratory + renal, not just post-strep).

• The proximal convoluted tubule (PCT) is where 100% of filtered glucose and amino acids are normally reabsorbed.

• This happens via Na⁺/glucose symporters (SGLT-2 and SGLT-1) in the apical membrane.

• Na⁺ gradient is maintained by Na⁺/K⁺-ATPase on the basolateral side.

• If plasma glucose exceeds ~200 mg/dL → transporters begin to saturate → glycosuria appears.

• Other nephron segments (Loop, DCT, CD) handle electrolytes and water, but not glucose.

• Bowman’s capsule just collects filtrate — no transporters.

Answer breakdown:

• Proximal convoluted tubule → correct (site of Na⁺/glucose symporters).

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

• Collecting duct → water reabsorption (ADH-sensitive), not glucose.

• Loop of Henle → Na⁺, K⁺, Cl⁻, urea handling, not glucose.

• Distal convoluted tubule → Na⁺/Cl⁻ transport, Ca²⁺ regulation, not glucose.

• The juxtaglomerular apparatus (JGA) consists of:

  • Juxtaglomerular (granular) cells → secrete renin.

  • Macula densa → senses NaCl concentration in distal tubule.

  • Extraglomerular mesangial cells → support communication.

• When blood pressure drops or NaCl delivery is low, JGA → renin release.

• Renin converts angiotensinogen → angiotensin I, which is later converted to angiotensin II (a potent vasoconstrictor that also stimulates aldosterone release).

• Net effect → blood pressure rises.

• So: JGA increases blood pressure, not decreases it.

Answer breakdown:

• Angiotensin secretion to reduce BP → wrong, JGA doesn’t directly secrete angiotensin.

• Renin secretion to reduce BP → wrong, renin increases BP.

• Renin secretion to increase BP → correct.

• Angiotensin secretion to increase BP → wrong, renin triggers it but doesn’t secrete angiotensin.

• Angiotensinogen secretion → wrong, that comes from the liver.

• In ultrasound, hyperechoic structures (very dense, like bone or stones) reflect most of the ultrasound waves, so they appear bright white.

• Behind them, there’s an acoustic shadow (dark area) because no sound waves pass through.

• Calculi (stones) are classic examples — they produce a bright echogenic focus with posterior acoustic shadowing.

• Fluid → appears black (anechoic), not bright.

• Cortex/Medulla/Fat → have intermediate echogenicity, not associated with shadowing.

Answer breakdown:

• Fluid → black (anechoic).

• Medulla → hypoechoic relative to cortex, not bright.

• Fat → hyperechoic but doesn’t make strong posterior shadows.

• Cortex → intermediate echogenicity.

• Calculus → bright focus with acoustic shadow → correct.

• Urinary catheterization is generally safe, but the major contraindication is the presence (or suspicion) of urethral trauma or strictures, because inserting a catheter can worsen injury, cause bleeding, or create a false passage.

• Urethral infection is not a contraindication; catheterization may even be required in acute infection with retention.

• Urinary incontinence is an indication, not a contraindication (especially if skin breakdown risk exists).

• Patient refusal is an ethical barrier, not a medical contraindication — but of course, consent is always required.

• Thus, the only true medical contraindication that must be ruled out is urethral strictures/trauma.

Answer breakdown:

• Urethral infection → not a contraindication.

• Urethral strictures → correct, must be ruled out.

• Urinary incontinence → not a contraindication.

• None of these → wrong, because strictures are one.

• Patient refusal → ethical issue, but not the medical contraindication being tested.

• The urinary tract (above the distal urethra) is normally sterile.

• The primary mechanism is the continuous unidirectional flow of urine, which washes away potential pathogens before they can adhere and colonize.

• Other factors help but are secondary:

  • IgA is important in mucosal immunity but plays a bigger role in the gut and respiratory tract than in keeping urine sterile.

  • B cells / T cells are systemic immune players, not the main reason for sterility here.

  • Low pH is important in the vagina (due to lactobacilli), not in the urinary tract.

Thus, the main protective factor = urinary flow.

Answer breakdown:

• B cells → wrong (general immunity, not specific to sterility).

• T cells → wrong (same reason).

• IgA → wrong (important in mucosa, but not the primary urinary defense).

• Urinary flow → correct (mechanical flushing keeps tract sterile).

• Low pH → wrong (important in vagina, not urinary tract).

• Metabolic alkalosis occurs when there is a primary gain of bicarbonate (HCO₃⁻) or a loss of hydrogen ions (H⁺).

• Vomiting causes the loss of large amounts of gastric HCl. This loss of hydrogen ions shifts the body toward alkalosis, and bicarbonate levels rise in the plasma.

• The other options:

  • Carbon monoxide poisoning → causes hypoxia, not alkalosis.

  • Hyperventilation → causes respiratory alkalosis (not metabolic).

  • Diarrhea → causes loss of bicarbonate, leading to metabolic acidosis, not alkalosis.

  • Type 1 diabetes mellitus → leads to ketoacidosis (metabolic acidosis).

So the correct answer is vomiting.

Answer breakdown:

• Carbon monoxide poisoning → wrong (hypoxia).

• Hyperventilation → wrong (respiratory alkalosis).

• Diarrhea → wrong (metabolic acidosis).

• Vomiting → correct (loss of gastric acid → metabolic alkalosis).

• Type 1 diabetes mellitus → wrong (ketoacidosis).

The nephron has specific regions:

• Cortex: Contains the renal corpuscles (glomerulus + Bowman’s capsule), proximal convoluted tubule (PCT), and distal convoluted tubule (DCT). These areas handle filtration and much of selective reabsorption.

• Medulla: Contains the loops of Henle and collecting ducts, which are crucial for concentrating urine.

• Renal papilla/pyramids: Terminal medullary structures, not cortical.

Therefore, the correct structures that lie in the renal cortex are the renal corpuscles, PCT, and DCT.

Answer breakdown:

• Glomeruli, Bowman’s capsule, and loop of Henle → incorrect (loop extends into medulla).

• Collecting tubule, proximal and distal convoluted tubule → incorrect (collecting tubules are medullary).

• Renal corpuscles, proximal and distal convoluted tubule → correct.

• Glomeruli, Bowman’s capsule, and renal papilla → incorrect (papilla is medullary).

• Renal pyramid, glomeruli, and Bowman’s capsule → incorrect (pyramids are medullary).

Catheterization, especially urinary catheterization, breaches natural defenses and provides a direct entry route for microorganisms. The most common complication is urinary tract infection (UTI), which can lead to bacteriuria within a few days. Other listed complications are possible but rare in comparison:

• Febrile reaction → usually blood transfusions, not catheterization.

• Delayed hemolytic reaction → post transfusion, not catheterization.

• Anaphylaxis → severe but rare, more linked to drugs/latex allergy.

• Toxic shock syndrome → possible in indwelling catheters but extremely uncommon.

So infection is by far the most frequent complication of catheterization.

Answer breakdown:

• Delayed hemolytic reaction → transfusion-related, not relevant here.

• Febrile reaction → transfusion-related, not catheter.

• Anaphylaxis → rare, only if latex allergy.

• Toxic shock syndrome → rare but possible.

• Infection → Correct and most common.

Filtration fraction (FF) is defined as GFR ÷ Renal Plasma Flow (RPF).

• Normal GFR ≈ 125 mL/min

• Normal RPF ≈ 600 mL/min
  So, 125 ÷ 600 ≈ 0.2 (20%).

This means that about one-fifth of the plasma that enters the glomerular capillaries gets filtered, while the remaining continues in the peritubular capillaries. FF increases in states where GFR is preserved but RPF decreases (e.g., dehydration, renal artery stenosis due to angiotensin II action).

Answer breakdown:

• 20% → Correct: physiological normal

• 15% → Slightly low, could occur in renal impairment but not the normal value

• 10% → Too low, indicates poor filtration

• 7% → Pathological state, not normal

• 5% → Extremely low, seen only in severe renal failure

The counter-current multiplier mechanism of the kidney is responsible for creating the osmotic gradient in the renal medulla, which is essential for water reabsorption and urine concentration. This function is carried out by the Loop of Henle, specifically because of its differential permeability: the descending limb is permeable to water but not solutes, while the thick ascending limb actively transports Na⁺, K⁺, and Cl⁻ out but is impermeable to water. This arrangement multiplies small differences into a large osmotic gradient. The vasa recta, on the other hand, does not create the gradient but preserves it, and is therefore part of the counter-current exchanger system.

Answer breakdown:

• Loop of Henle → Correct: counter-current multiplier

• Peritubular arteries → Wrong: no role in counter-current mechanism

• Proximal convoluted tubules → Wrong: only bulk reabsorption

• Vasa recta → Wrong here: counter-current exchanger, not multiplier

• Glomerulus → Wrong: only filtration

The kidney’s ability to excrete concentrated urine depends on the medullary osmotic gradient, established by the loop of Henle (countercurrent multiplier) and preserved by the vasa recta (countercurrent exchanger).

• If medullary blood flow is too high, solutes (NaCl, urea) are washed out, reducing the gradient and impairing concentration ability.

• If medullary blood flow is low (but not ischemic low), solute washout is minimized, the gradient is preserved, and the kidney can generate more concentrated urine.

Now analyzing the options:

• Decreasing the activity of the Na⁺-K⁺ pump in the loop of Henle:
  Wrong. The thick ascending limb’s Na⁺-K⁺-2Cl⁻ pump is crucial for generating the osmotic gradient. Reduced activity would decrease, not increase, concentrating ability.

• Decreasing the permeability of the collecting duct to water:
  Wrong. Water reabsorption in the collecting duct (under ADH influence) is essential for concentrating urine. Decreased permeability means more dilute urine.

• Increasing the rate of flow through the loop of Henle:
  Wrong. Faster flow reduces the time for solute reabsorption and disrupts the countercurrent multiplier, leading to less concentration.

• Decreasing the rate of blood flow through the medulla (Correct):
  Right. This reduces solute washout from the interstitium, preserving the high osmolarity needed to draw water out of the collecting duct under ADH.

• Decreasing the permeability of the proximal tubule to water:
  Wrong. The proximal tubule reabsorbs water isosmotically with solutes. Its water permeability is not a determinant of maximal urine concentration — this is regulated later in the collecting ducts.

Glomerulonephritis is characterized by inflammation of the glomeruli, which increases permeability of the filtration barrier. This allows red blood cells to pass into the tubules. Within the tubules, these RBCs become trapped in Tamm–Horsfall protein, forming red cell casts. The presence of red cell casts on urinalysis is considered pathognomonic for glomerulonephritis, distinguishing it from other renal conditions.

Now let’s analyze the options:

• Red cell cast (Correct):
  Highly specific for glomerulonephritis. It signifies that RBCs originated within the nephron, not just from contamination or bleeding elsewhere in the urinary tract.

• Hyaline cast:
  Made up almost entirely of Tamm–Horsfall protein. They can be seen in normal individuals (especially after exercise, fever, or dehydration) and are not specific for glomerulonephritis.

• White cell cast:
  Seen in interstitial nephritis or pyelonephritis, where WBCs migrate into tubules. Not typical of glomerulonephritis.

• Renal tubular cell cast:
  Formed when tubular epithelial cells slough off, seen in acute tubular necrosis (ATN), toxin exposure, or ischemia.

• Granular cast:
  Represent degenerated cellular casts or protein aggregates. Nonspecific, but often associated with acute tubular necrosis or advanced renal disease.