Renal Physiology Practice Questions

Q: What is true about the H+ secretion by the proximal convoluted tubule (PCT)?

It is meant for reabsorption of the filtered bicarbonate.. In the Proximal Convoluted Tubule (PCT), H+ secretion is primarily coupled with the reabsorption of filtered bicarbonate ($HCO_3^-$), a process essential for maintaining acid-base balance. ### Why Option C is Correct: Approximately 85-90% of filtered bicarbonate is reabsorbed in the PCT. This occurs via the **$Na^+$-$H^+$ Exchanger (NHE3)** on the apical membrane, which secretes $H^+$ into the lumen. In the lumen, $H^+$ combines with filtered $HCO_3^-$ to form $H_2CO_3$. **Carbonic Anhydrase (Type IV)** on the brush border breaks this into $CO_2$ and $H_2O$, which diffuse into the cell. Inside, **Carbonic Anhydrase (Type II)** reforms $HCO_3^-$, which is then transported into the blood. Thus, $H^+$ secretion here is a "shuttle" for bicarbonate reabsorption rather than a means to excrete acid. ### Why Other Options are Incorrect: * **Option A:** Acidification of urine (lowering pH to ~4.5) occurs in the **Alpha-Intercalated cells** of the distal tubule and collecting duct via $H^+$-ATPase. The PCT does not significantly lower urine pH. * **Option B:** $H^+$ secretion in the PCT is **not** against a steep concentration gradient. The luminal pH in the PCT remains relatively high (~6.7-7.0). Active transport against a steep gradient occurs only in the distal nephron. * **Option D:** Diffusion trapping (ammoniagenesis) primarily occurs in the **collecting ducts**, where $NH_3$ combines with $H^+$ to form $NH_4^+$, which is "trapped" and excreted. ### High-Yield Facts for NEET-PG: * **Acetazolamide** (Carbonic Anhydrase Inhibitor) acts on the PCT, blocking this $H^+$ secretion and leading to bicarbonate loss (Proximal Renal Tubular Acidosis/Type 2 RTA). * **NHE3** is the primary transporter for $H^+$ secretion in the PCT. * The PCT is responsible for the **bulk reabsorption** of $HCO_3^-$, while the distal nephron is responsible for **net acid excretion** and the generation of "new" bicarbonate.

Q: Maximum phosphate is reabsorbed in which part of the nephron?

Proximal Convoluted Tubule (PCT). **Explanation:** The **Proximal Convoluted Tubule (PCT)** is the primary site for the reabsorption of the majority of solutes filtered by the glomerulus. Approximately **80% of filtered phosphate** is reabsorbed in the PCT. **Why PCT is the correct answer:** Phosphate reabsorption in the PCT occurs via **Sodium-Phosphate cotransporters (NaPi-IIa and NaPi-IIc)** located on the apical membrane. This process is secondary active transport, driven by the sodium gradient established by the Na+/K+ ATPase pump. The PCT is the only segment where significant, regulated phosphate transport occurs, making it the most critical site for phosphate homeostasis. **Why other options are incorrect:** * **Distal Convoluted Tubule (DCT) & Collecting Duct:** Only a negligible amount of phosphate (approx. 5-10%) is reabsorbed in the distal segments. These areas are more focused on fine-tuning electrolytes like sodium, potassium, and calcium under hormonal influence (e.g., Aldosterone). * **Loop of Henle:** This segment is primarily involved in the concentration of urine and the reabsorption of sodium, chloride, and water (Thin Descending and Thick Ascending Limbs), but it plays no significant role in phosphate reabsorption. **High-Yield Clinical Pearls for NEET-PG:** 1. **Parathyroid Hormone (PTH):** PTH is the most important regulator of phosphate. It **inhibits** phosphate reabsorption in the PCT by causing the internalization of NaPi-IIa transporters, leading to **phosphaturia**. 2. **FGF-23:** A phosphatonin that also inhibits PCT phosphate reabsorption. 3. **Fanconi Syndrome:** A generalized dysfunction of the PCT resulting in the loss of phosphate (hypophosphatemia), glucose, amino acids, and bicarbonate in the urine. 4. **Threshold:** Phosphate is a "threshold substance"; once the plasma concentration exceeds the transport maximum (TmP), the excess is rapidly excreted in the urine.

Q: Aldosterone exerts its action on which part of the nephron?

Collecting duct. ### Explanation **Correct Option: D. Collecting duct** Aldosterone is a mineralocorticoid hormone secreted by the adrenal cortex. Its primary site of action is the **Principal cells (P-cells)** of the **late distal tubule** and the **collecting duct** (specifically the cortical collecting duct). **Mechanism of Action:** Aldosterone binds to intracellular mineralocorticoid receptors, leading to the synthesis and insertion of: 1. **ENaC (Epithelial Sodium Channels)** on the apical membrane. 2. **Na+/K+ ATPase pumps** on the basolateral membrane. This results in **sodium reabsorption** and **potassium secretion**. It also acts on the **α-intercalated cells** to promote **H+ secretion**, which is why excess aldosterone leads to metabolic alkalosis. --- ### Why other options are incorrect: * **A. Proximal tubule:** This is the site for bulk reabsorption (65% of Na+ and water), primarily regulated by Angiotensin II and Carbonic Anhydrase, not aldosterone. * **B. Early distal tubule:** This segment is the "diluting segment," where Na+ is reabsorbed via the **NCC (Na+/Cl- cotransporter)**. This is the site of action for Thiazide diuretics. * **C. Loop of Henle:** The thick ascending limb is responsible for 25% of Na+ reabsorption via the **NKCC2 transporter** (site of action for Loop diuretics). Aldosterone has no significant physiological effect here. --- ### High-Yield Facts for NEET-PG: * **Primary Stimuli:** Hyperkalemia (most potent) and Angiotensin II. * **Conn’s Syndrome:** Primary hyperaldosteronism characterized by the triad of **Hypertension, Hypokalemia, and Metabolic Alkalosis.** * **Spironolactone/Eplerenone:** These are aldosterone antagonists used as potassium-sparing diuretics that act on the collecting duct. * **Liddle’s Syndrome:** A genetic condition causing overactive ENaC channels, mimicking high aldosterone levels (Pseudohyperaldosteronism).

Q: Where is angiotensinogen produced?

Liver. ### Explanation **Correct Answer: A. Liver** The **Renin-Angiotensin-Aldosterone System (RAAS)** is a critical hormonal cascade for regulating blood pressure and fluid balance. **Angiotensinogen** is a large $\alpha_2$-globulin protein synthesized and constitutively secreted into the plasma primarily by the **liver**. It serves as the essential precursor in the RAAS pathway. When blood pressure drops, the enzyme **renin** (secreted by the kidneys) cleaves angiotensinogen to form Angiotensin I, which is subsequently converted to Angiotensin II by ACE (Angiotensin-Converting Enzyme) in the lungs. **Why the other options are incorrect:** * **B. Kidney:** The kidney (specifically the Juxtaglomerular cells) produces **Renin**, not angiotensinogen. Renin is the rate-limiting enzyme that acts *upon* angiotensinogen. * **C. Hypothalamus:** The hypothalamus produces **ADH (Vasopressin)** and **Oxytocin**. While it regulates thirst and fluid balance, it is not the source of angiotensinogen. * **D. Atrium:** The cardiac atria produce **Atrial Natriuretic Peptide (ANP)** in response to stretch. ANP actually antagonizes the RAAS system to lower blood pressure. **High-Yield Clinical Pearls for NEET-PG:** * **Rate-limiting step of RAAS:** The secretion of **Renin** from the JG apparatus. * **Stimulants for Angiotensinogen:** Production in the liver is increased by corticosteroids, estrogens, thyroid hormones, and Angiotensin II itself. * **Clinical Correlation:** The increase in angiotensinogen levels due to **estrogen** (e.g., in pregnancy or Oral Contraceptive Pill use) can sometimes lead to hypertension. * **Site of ACE:** Primarily the luminal surface of vascular endothelial cells, especially in the **lungs**.

Question 1

Filtration barriers have pores of what approximate size?

Accepted Answer

4-6 nm

Answer

1-2 nm

Answer

8-10 nm

Answer

10-12 nm

Question 2

What is true about the H+ secretion by the proximal convoluted tubule (PCT)?

Accepted Answer

It is meant for reabsorption of the filtered bicarbonate.

Answer

It is for acidification of urine.

Answer

It occurs against the concentration gradient for H+.

Answer

It is an example of diffusion trapping.

Question 3

Maximum phosphate is reabsorbed in which part of the nephron?

Accepted Answer

Proximal Convoluted Tubule (PCT)

Answer

Distal Convoluted Tubule (DCT)

Answer

Loop of Henle

Answer

Collecting Duct

Question 4

Aldosterone exerts its action on which part of the nephron?

Accepted Answer

Collecting duct

Answer

Proximal tubule

Answer

Early distal tubule

Answer

Loop of Henle

Question 5

Renin secretion is increased by all of the following except:

Accepted Answer

Sympathetic nerve stimulation

Answer

Sodium load in the proximal convoluted tubule (PCT)

Answer

Low afferent arteriolar pressure

Answer

Sodium load in the distal convoluted tubule (DCT)

Question 6

Glomerular feedback for decreased GFR is mediated by which mechanism?

Accepted Answer

Increase in renin release from the juxtaglomerular complex

Answer

Increased vasopressin activity

Answer

Increased PCT permeability

Answer

Increase in renal sympathetic activity

Question 7

In the micturition reflex, what is the first change to occur?

Accepted Answer

Relaxation of perineal muscles

Answer

Trigone relaxation

Answer

Detrusor contraction

Answer

Decreased urethral pressure

Question 8

Which of the following is defective in renal glucosuria?

Accepted Answer

SGLT-2

Answer

GLUT-1

Answer

GLUT-2

Answer

SGLT-1

Question 9

Where is angiotensinogen produced?

Accepted Answer

Liver

Answer

Kidney

Answer

Hypothalamus

Answer

Atrium

Question 10

What is the effect of acute metabolic acidosis on urinary potassium excretion?

Accepted Answer

Decreases urinary potassium excretion

Answer

Has a biphasic effect on potassium excretion

Answer

Does not affect potassium excretion

Answer

Increases urinary potassium excretion

Renal Physiology — MCQs

Renal Physiology — MCQs

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