Tubular Reabsorption and Secretion — MCQs
Mechanism of action of thiazides is by -
Glucose is reabsorbed in which part of the nephron?
Which of the following statements is MOST true regarding water reabsorption in the nephron?
What happens to the concentration of inulin as fluid passes through the Proximal Convoluted Tubule (PCT)?
Increased aldosterone and ADH secretion following major trauma results in all the following except?
Which of the following statements about the biodisposition of penicillins and cephalosporins is NOT accurate?
Which substance has the least renal clearance?
Mechanism of action of exenatide in diabetes mellitus is
Which of the following is a cause of hypokalemic metabolic alkalosis with hypertension?
The Renal function is best assessed by:
Tubular Reabsorption and Secretion Indian Medical PG Practice Questions and MCQs
Question 1: Mechanism of action of thiazides is by -
- A. Inhibiting Na+K+2Cl- in ascending limb of loop of henle
- B. Inhibiting Na+/Cl- symporter in DCT (Correct Answer)
- C. Inhibiting Na+/Cl- symporter in PCT
- D. Inhibiting Na+K+2Cl- in descending limb of loop of henle
Explanation: **Inhibiting Na+/Cl- symporter in DCT** - Thiazide diuretics primarily act on the **distal convoluted tubule (DCT)** of the nephron [2]. - They inhibit the **Na+/Cl- symporter** (NCC channel) on the apical membrane, preventing reabsorption of sodium and chloride ions [1], [2]. *Inhibiting Na+K+2CI- in descending limb of loop of henle* - The descending limb of the loop of Henle is permeable to water but largely impermeable to solutes; there is no significant Na+K+2Cl- symporter activity here. - This mechanism describes the action of loop diuretics, but they act on the **ascending** limb, not the descending limb. *Inhibiting Na+K+2Cl- in ascending limb of loop of henle* - This mechanism describes the action of **loop diuretics** (e.g., furosemide, bumetanide) [3]. - Loop diuretics inhibit the **Na+K+2Cl- cotransporter (NKCC2)** in the thick ascending limb of the loop of Henle, leading to significant diuresis [3]. *Inhibiting Na+/Cl- symporter in PCT* - The **proximal convoluted tubule (PCT)** is primarily responsible for reabsorbing most of the filtered sodium, chloride, bicarbonate, and other solutes. - While sodium is reabsorbed in the PCT, it's mainly through Na+/H+ exchangers and other mechanisms, not a specific Na+/Cl- symporter that is targeted by thiazides [2].
Question 2: Glucose is reabsorbed in which part of the nephron?
- A. Distal convoluted tubule
- B. Early PCT (Correct Answer)
- C. Henle loop
- D. Collecting duct
Explanation: ***Early PCT*** - The **proximal convoluted tubule (PCT)** is the primary site for the reabsorption of most solutes, including nearly all **glucose** and amino acids. - Approximately **100% of filtered glucose** is reabsorbed here under normal physiological conditions, primarily through **sodium-glucose cotransporters (SGLTs)**. *Distal convoluted tubule* - The **distal convoluted tubule (DCT)** is primarily involved in the fine-tuning of **sodium, potassium, and calcium reabsorption**, influenced by hormones like aldosterone and parathyroid hormone. - It does not significantly reabsorb glucose; by the time filtrate reaches the DCT, all glucose should have been reabsorbed in the PCT. *Henle loop* - The **loop of Henle** is crucial for establishing and maintaining the **medullary osmotic gradient**, which is essential for concentrating urine. - Its main functions are the reabsorption of **water** (descending limb) and **sodium and chloride** (ascending limb), but not glucose. *Collecting duct* - The **collecting duct** plays a significant role in **water reabsorption** (regulated by ADH) and acid-base balance through the reabsorption of bicarbonate and secretion of hydrogen ions. - Like the DCT and loop of Henle, it does not participate in the reabsorption of glucose.
Question 3: Which of the following statements is MOST true regarding water reabsorption in the nephron?
- A. Facultative reabsorption primarily occurs in the collecting ducts.
- B. The bulk of water reabsorption occurs in the proximal tubule secondary to Na+ reabsorption. (Correct Answer)
- C. Obligatory reabsorption occurs regardless of hydration state.
- D. Water reabsorption can vary significantly depending on the body's hydration needs.
Explanation: ***The bulk of water reabsorption occurs in the proximal tubule secondary to Na+ reabsorption.*** - Approximately 65-70% of filtered water is reabsorbed in the **proximal tubule**, largely driven by the active transport of **Na+**, which creates an osmotic gradient. - This process is **obligatory**, meaning it occurs regardless of the body's hydration status, and is essential for maintaining fluid balance. *Facultative reabsorption primarily occurs in the collecting ducts.* - While facultative water reabsorption, **regulated by ADH**, does occur in the **collecting ducts**, this statement is not "most true" because it overlooks the quantitative significance of the proximal tubule. - The collecting ducts are responsible for fine-tuning water reabsorption to match the body's hydration needs, but only a smaller, variable amount compared to the proximal tubule. *Obligatory reabsorption occurs regardless of hydration state.* - This statement is true, but it is not the MOST true statement compared to the option highlighting the bulk reabsorption in the proximal tubule. **Obligatory reabsorption** primarily occurs in the **proximal convoluted tubule** and **loop of Henle**. - It is a constant process that recovers a large, fixed percentage of filtered water, essential for basic volume maintenance **independent of ADH**. *Water reabsorption can vary significantly depending on the body's hydration needs.* - This statement is true, specifically referring to **facultative water reabsorption**, which is regulated by **antidiuretic hormone (ADH)** in the collecting ducts. - However, this variation is only for about 10-20% of total reabsorption, while the *bulk* of reabsorption is constant and occurs in the **proximal tubule**.
Question 4: What happens to the concentration of inulin as fluid passes through the Proximal Convoluted Tubule (PCT)?
- A. Concentration of inulin increases (Correct Answer)
- B. Concentration of urea remains constant
- C. Concentration of HCO3- increases
- D. Concentration of Na+ decreases
Explanation: ***Concentration of inulin increases*** - Inulin is **freely filtered** at the glomerulus and is neither reabsorbed nor secreted along the renal tubule, making it an excellent marker for **glomerular filtration rate (GFR)**. - As water is reabsorbed from the PCT, the volume of tubular fluid decreases, causing the concentration of **unreabsorbed solutes**, like inulin, to increase. *Concentration of urea remains constant* - Urea is **reabsorbed** along the tubule, though passively; its concentration typically **increases** initially in the PCT due to water reabsorption, but then decreases as some is reabsorbed. - The statement is incorrect because urea concentration changes significantly throughout the nephron, particularly increasing as water is reabsorbed and then decreasing with some reabsorption. *Concentration of HCO3- increases* - The majority (approximately 80-90%) of **bicarbonate (HCO3-)** is reabsorbed in the PCT, primarily through its conversion to CO2 within the tubular lumen and then back to HCO3- intracellularly. - Therefore, the concentration of HCO3- in the tubular fluid actually **decreases** significantly as fluid passes through the PCT. *Concentration of Na+ decreases* - **Sodium (Na+)** is actively reabsorbed along the entire nephron, with about 65-70% reabsorbed in the PCT. - While Na+ is reabsorbed, water follows passively, so its concentration in the tubular fluid remains relatively **iso-osmotic** with plasma, meaning its concentration does not significantly decrease as fluid passes through the PCT, remaining fairly constant.
Question 5: Increased aldosterone and ADH secretion following major trauma results in all the following except?
- A. Increased osmolarity of urine
- B. Increased water excretion (Correct Answer)
- C. Increased K+ excretion in urine
- D. Decreased Na+ excretion in urine
Explanation: ***Increased water excretion*** - **ADH (antidiuretic hormone)** increases water reabsorption in the collecting ducts, leading to a *decrease* in water excretion, not an increase. - Increased aldosterone and ADH would promote fluid retention to maintain blood volume following trauma, thus reducing water loss via urine. *Decreased Na+ excretion in urine* - **Aldosterone** acts on the renal tubules to increase **sodium reabsorption** and potassium excretion. - This response is crucial in **conserving sodium** and thereby maintaining extracellular fluid volume after trauma. *Increased K+ excretion in urine* - **Aldosterone** directly stimulates **potassium secretion** into the urine in the principal cells of the collecting ducts. - This is a normal physiological consequence of increased aldosterone levels. *Increased osmolarity of urine* - **ADH** increases the permeability of the collecting ducts to water, leading to **more water reabsorption** back into the bloodstream. - This removal of water from the urine concentrates the solutes, resulting in a **more concentrated (higher osmolarity)** urine.
Question 6: Which of the following statements about the biodisposition of penicillins and cephalosporins is NOT accurate?
- A. Procaine penicillin G is used for intramuscular injection
- B. Nafcillin and ceftriaxone are eliminated mainly by biliary secretion
- C. Oral bioavailability is affected by lability to gastric acid
- D. Renal tubular reabsorption of beta-lactams is inhibited by probenecid (Correct Answer)
Explanation: ***Renal tubular reabsorption of beta-lactams is inhibited by probenecid*** - Probenecid inhibits the **active tubular secretion** of beta-lactam antibiotics, not their reabsorption, thereby increasing their half-life and maintaining higher plasma concentrations [3]. - This interaction is clinically useful for prolonging the antibacterial effect of penicillins and cephalosporins. *Oral bioavailability is affected by lability to gastric acid* - Many early penicillins, such as **penicillin G**, are highly susceptible to degradation by stomach acid, leading to poor oral bioavailability [2]. - This necessitates their administration via intravenous or intramuscular routes, or the development of **acid-stable analogs** like penicillin V [2]. *Procaine penicillin G is used for intramuscular injection* - **Procaine penicillin G** is formulated for intramuscular injection to create a **depot effect**, allowing for slow absorption and prolonged therapeutic plasma concentrations. - The procaine component also acts as a **local anesthetic**, reducing the pain associated with a large-volume intramuscular injection [1]. *Nafcillin and ceftriaxone are eliminated mainly by biliary secretion* - **Nafcillin** and **ceftriaxone** are indeed notable among beta-lactam antibiotics for their significant elimination through the biliary tract. - This route of excretion makes them particularly useful in patients with **renal impairment**, as their elimination is less dependent on kidney function.
Question 7: Which substance has the least renal clearance?
- A. Glucose (Correct Answer)
- B. Inulin
- C. Urea
- D. Creatinine
Explanation: ***Glucose (Correct Answer)*** - Under normal physiological conditions, **glucose is almost completely reabsorbed** in the proximal tubule of the nephron, leading to a **renal clearance of nearly zero**. - While glucose is freely filtered by the glomerulus, the extensive reabsorption mechanisms (via SGLT2 and SGLT1 transporters) ensure that virtually no glucose appears in the urine under normal circumstances. - This makes glucose the substance with the **least renal clearance** among the given options. *Inulin (Incorrect)* - **Inulin** is freely filtered by the glomerulus but is neither reabsorbed nor secreted by the renal tubules. - Its renal clearance equals the **glomerular filtration rate (GFR)** (~125 mL/min), making it an ideal marker for GFR measurement. - Inulin has a **much higher clearance than glucose**. *Urea (Incorrect)* - **Urea** is filtered by the glomerulus, and approximately **50% of the filtered urea** is reabsorbed in the renal tubules, primarily in the proximal tubule and medullary collecting duct. - Its clearance (~60-70 mL/min) is lower than GFR but still **significantly higher than glucose clearance**. *Creatinine (Incorrect)* - **Creatinine** is freely filtered by the glomerulus and is also **secreted by the renal tubules** (approximately 10-20% secreted). - This secretion means its renal clearance (~130-140 mL/min) is slightly **higher than the actual GFR**. - Despite this, creatinine is commonly used as an estimate of GFR due to its relatively stable production and ease of measurement.
Question 8: Mechanism of action of exenatide in diabetes mellitus is
- A. It is DPP-4 inhibitor and results in decreased breakdown of GLP
- B. It is amylin analogue and decreases glucagon
- C. It is analogue of GLP released from gut and increases glucose dependent insulin secretion (Correct Answer)
- D. It inhibits SGLT-2 and causes glucosuria
Explanation: ***It is analogue of GLP released from gut and increase glucose dependant insulin secretion*** - **Exenatide** is a **glucagon-like peptide-1 (GLP-1) receptor agonist**, mimicking the action of naturally occurring GLP-1 [1]. - It stimulates **glucose-dependent insulin secretion**, suppresses glucagon release, slows gastric emptying, and promotes satiety, all contributing to improved glycemic control [2]. *It inhibits SGLT-2 and cause glucosuria* - This describes the mechanism of **sodium-glucose co-transporter 2 (SGLT-2) inhibitors**, such as empagliflozin or canagliflozin, which promote glucose excretion in urine. - **Exenatide** does not directly affect renal glucose reabsorption. *It is DPP-4 inhibitor and result in decreased breakdown of GLP* - This mechanism belongs to **dipeptidyl peptidase-4 (DPP-4) inhibitors** (e.g., sitagliptin, saxagliptin), which prevent the rapid degradation of endogenous GLP-1, thus prolonging its action [1]. - **Exenatide** directly activates GLP-1 receptors rather than modulating the enzyme that breaks down endogenous GLP-1 [1]. *It is amylin analogue and decrease glucagon* - This describes **pramlintide**, an amylin analogue used in diabetes management, which primarily suppresses postprandial glucagon secretion, slows gastric emptying, and promotes satiety. - While **exenatide** also decreases glucagon, its primary mechanism is via GLP-1 receptor agonism [2].
Question 9: Which of the following is a cause of hypokalemic metabolic alkalosis with hypertension?
- A. Liddle syndrome (Correct Answer)
- B. Bartter syndrome
- C. Gitelman syndrome
- D. Renal tubular acidosis
Explanation: ***Liddle syndrome*** - It is an **autosomal dominant** disorder characterized by a mutation in the **ENaC channel**, leading to increased sodium reabsorption and potassium excretion, thus causing **hypokalemia**, **metabolic alkalosis**, and **hypertension**. [1] - This condition mimics **primary hyperaldosteronism** but has **low plasma renin activity** and **low aldosterone levels**. [1] *Bartter syndrome* - This is a genetic disorder affecting the **Na-K-2Cl cotransporter** in the **thick ascending limb** of the loop of Henle, leading to **salt wasting** and compensatory **renin-angiotensin-aldosterone system activation**. - It presents with **hypokalemia**, **metabolic alkalosis**, but typically with **normal or low blood pressure**, not hypertension. *Gitelman syndrome* - This is an autosomal recessive disorder affecting the **thiazide-sensitive Na-Cl cotransporter** in the **distal convoluted tubule**. - It causes **hypokalemic metabolic alkalosis**, hypomagnesemia, and hypocalciuria, but patients are typically **normotensive** or **hypotensive**, distinguishing it from Liddle syndrome. *Renal tubular acidosis* - This is a group of disorders characterized by the **kidneys' inability to excrete acid** or **reabsorb bicarbonate**, leading to **metabolic acidosis**. [2] - While it can cause electrolyte abnormalities, hypokalemia is a feature of certain types (e.g., RTA type 1 and 2), but the defining feature is **metabolic acidosis**, not metabolic alkalosis, and it is not typically associated with hypertension from the primary tubular defect. [2]
Question 10: The Renal function is best assessed by:
- A. Tc 99m DMSA
- B. Tc 99m DTPA
- C. Tc 99m pertechnetate
- D. Tc 99m MAG3 (Correct Answer)
Explanation: ***Tc 99m MAG3*** - **Technetium-99m mercaptoacetyltriglycine (MAG3)** is the **preferred agent for dynamic renal scintigraphy** and assessment of **overall renal function**. - It is a **renal tubular agent** with a high extraction fraction (40-50%) that assesses **effective renal plasma flow (ERPF)** and **tubular secretion**. - **Superior to DTPA** for functional assessment due to better image quality, faster clearance, and excellent performance even in **impaired renal function**. - Provides comprehensive evaluation of **renal perfusion, function, and excretion** in a single study. *Tc 99m DMSA* - **Technetium-99m dimercaptosuccinic acid (DMSA)** is a **cortical imaging agent** used primarily for **static renal imaging**. - Excellent for assessing **renal anatomy**, detecting **cortical scarring**, **pyelonephritis**, and **differential renal function**. - It binds to the cells of the **proximal tubules** and is retained (40-50% at 6 hours), making it unsuitable for dynamic functional studies or excretion assessment. *Tc 99m DTPA* - **Technetium-99m diethylenetriaminepentaacetic acid (DTPA)** is a **glomerular filtration agent** used to measure **GFR**. - Excreted solely by **glomerular filtration** (no tubular secretion), making it the gold standard for **GFR measurement**. - However, it has a **lower extraction fraction (20%)** compared to MAG3, resulting in poorer image quality and less reliable assessment in patients with **impaired renal function**. - MAG3 has largely replaced DTPA as the preferred agent for routine dynamic renal studies. *Tc 99m pertechnetate* - **Technetium-99m pertechnetate** is primarily used for **thyroid imaging** and detecting **Meckel's diverticulum** (taken up by mucous-secreting cells). - **Not used for renal function assessment** as it does not provide reliable information about glomerular or tubular function.
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