Acid-Base Regulation by the Kidneys Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Acid-Base Regulation by the Kidneys. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Acid-Base Regulation by the Kidneys Indian Medical PG Question 1: Use the following laboratory values to find the best option that describes the acid-base disorder: Plasma pH = 7.12, Plasma PCO2 = 60 mm Hg, Plasma HCO3- = 19 mEq/L
- A. Combined metabolic and respiratory acidosis (Correct Answer)
- B. Metabolic alkalosis with respiratory compensation
- C. Combined metabolic and respiratory alkalosis
- D. Respiratory acidosis with renal compensation
Acid-Base Regulation by the Kidneys Explanation: ***Combined metabolic and respiratory acidosis***
- The **pH of 7.12** indicates profound **acidemia**, meaning the blood is more acidic than normal.
- The **PCO2 of 60 mm Hg** (normal 35-45 mm Hg) indicates **respiratory acidosis** as the elevated CO2 drives the pH down; the **HCO3- of 19 mEq/L** (normal 22-26 mEq/L) indicates **metabolic acidosis** as the decreased bicarbonate also drives the pH down, making both components contribute to the acidemia.
*Metabolic alkalosis with respiratory compensation*
- This would present with an **elevated pH** (alkalemia) and an **elevated HCO3-**, compensated by an elevated PCO2.
- The given values show a **low pH** and a **low HCO3-**, which contradicts metabolic alkalosis.
*Combined metabolic and respiratory alkalosis*
- This would involve an **elevated pH** with both a **low PCO2** (respiratory alkalosis) and an **elevated HCO3-** (metabolic alkalosis).
- The patient's pH is very low, unequivocally ruling out any form of alkalosis.
*Respiratory acidosis with renal compensation*
- While respiratory acidosis is present due to the high PCO2, the **low bicarbonate (19 mEq/L)** indicates a **metabolic acidosis** rather than renal compensation.
- In compensated respiratory acidosis, the kidneys would retain bicarbonate, leading to an **elevated HCO3-**, which is not seen here.
Acid-Base Regulation by the Kidneys Indian Medical PG Question 2: Hyperaldosteronism is associated with all, except:
- A. Hypernatremia
- B. Hypertension
- C. Hypokalemia
- D. Metabolic acidosis (Correct Answer)
Acid-Base Regulation by the Kidneys Explanation: ***Metabolic acidosis***
- **Hyperaldosteronism** leads to increased **potassium and hydrogen ion excretion** in the kidneys [1], resulting in **metabolic alkalosis**, not acidosis [2].
- The increased loss of hydrogen ions causes a rise in blood pH and bicarbonate levels [2].
*Hypernatremia*
- Aldosterone promotes **sodium reabsorption** in the renal tubules, leading to increased plasma sodium concentration [1], [3].
- This increased sodium reabsorption contributes to the expansion of extracellular fluid volume and **hypertension** [3].
*Hypokalemia*
- Aldosterone stimulates the **secretion of potassium ions** into the renal tubules, leading to excessive potassium loss in the urine [1].
- This sustained potassium excretion often results in **low serum potassium levels**.
*Hypertension*
- The increased reabsorption of **sodium and water** due to aldosterone action expands the extracellular fluid volume [3].
- This volume expansion directly contributes to elevated blood pressure, making hypertension a hallmark feature of **hyperaldosteronism** [2].
Acid-Base Regulation by the Kidneys Indian Medical PG Question 3: A patient in renal failure exhibits metabolic acidosis. What compensatory mechanism is most likely activated?
- A. Hyperventilation (Correct Answer)
- B. Hypoventilation
- C. Increased renal HCO3- reabsorption
- D. Increased K+ excretion
Acid-Base Regulation by the Kidneys Explanation: ***Hyperventilation***
- In metabolic acidosis, the body responds by increasing **respiratory rate and depth** to exhale more CO2, thereby reducing carbonic acid levels and raising pH.
- This is a rapid compensatory mechanism to counteract the drop in blood pH caused by the accumulation of non-volatile acids or loss of bicarbonate.
- In renal failure, this becomes the **primary compensatory mechanism** since renal compensation is impaired.
*Hypoventilation*
- **Hypoventilation** leads to CO2 retention, which would worsen metabolic acidosis by increasing carbonic acid and lowering pH further.
- This mechanism is characteristic of primary respiratory acidosis, not a compensatory response to metabolic acidosis.
*Increased renal HCO3- reabsorption*
- While increased **renal bicarbonate reabsorption** and hydrogen ion excretion are fundamental renal compensatory mechanisms for metabolic acidosis, these are impaired in a patient with **renal failure**.
- The kidneys are failing to perform this crucial function, which is the underlying cause of the metabolic acidosis in this scenario.
- This is why respiratory compensation becomes the only available mechanism.
*Increased K+ excretion*
- **Increased K+ excretion** (or retention) is primarily a response to changes in potassium balance, though acid-base disturbances can influence it.
- It is not a direct or primary compensatory mechanism for metabolic acidosis, although some renal tubular processes related to acid-base balance can affect potassium handling.
Acid-Base Regulation by the Kidneys Indian Medical PG Question 4: Calcitriol is formed in:
- A. Glomerulus
- B. Bowman's capsule
- C. PCT (Correct Answer)
- D. DCT
Acid-Base Regulation by the Kidneys Explanation: ***PCT***
- The final step in calcitriol (active vitamin D) synthesis, 1-alpha hydroxylation, primarily occurs in the **proximal convoluted tubule (PCT)** cells of the kidney.
- This enzymatic step converts **25-hydroxyvitamin D** into the potent hormone **1,25-dihydroxyvitamin D (calcitriol)**, which regulates calcium and phosphate homeostasis.
*Glomerulus*
- The **glomerulus** is primarily responsible for **filtering blood** to form ultrafiltrate, not for hormone synthesis.
- While vitamin D precursors are filtered, the enzymatic conversion to calcitriol does not occur here.
*Bowman's capsule*
- **Bowman's capsule** surrounds the glomerulus and collects the filtered fluid, acting as a passive receiver.
- It plays no direct role in the synthesis or metabolism of vitamin D.
*DCT*
- The **distal convoluted tubule (DCT)** is involved in fine-tuning reabsorption of ions like calcium and sodium, responding to hormones.
- It is not the primary site for the **1-alpha hydroxylation** required for calcitriol synthesis.
Acid-Base Regulation by the Kidneys Indian Medical PG Question 5: What is the physiological response of the kidney during shock?
- A. GFR decreases
- B. Perfusion of kidney decreases
- C. Afferent arteriole resistance increases
- D. Renal blood flow decreases (Correct Answer)
Acid-Base Regulation by the Kidneys Explanation: ***Renal blood flow decreases***
- During shock, the **primary and most fundamental** physiological change affecting the kidney is a marked **reduction in renal blood flow (RBF)**.
- Shock triggers intense **sympathetic activation** and **renin-angiotensin system (RAS) activation**, causing preferential **vasoconstriction** of renal vessels to redirect blood to vital organs (brain, heart).
- RBF can drop to as low as **20-30% of normal** in severe shock, making this the hallmark renal response.
- This reduction in RBF is the **upstream event** that triggers all other renal changes during shock.
*Perfusion of kidney decreases*
- While technically correct, "decreased perfusion" is **essentially synonymous** with decreased blood flow in this context.
- The term "renal blood flow" is the **standard physiological terminology** used in medical literature to describe this phenomenon, making it the more precise answer.
*Afferent arteriole resistance increases*
- This is a **mechanism** by which RBF decreases, not the overall response itself.
- Increased afferent arteriolar resistance is **secondary** to sympathetic activation and angiotensin II effects during shock.
- It describes the "how" rather than the "what" of the kidney's response.
*GFR decreases*
- GFR reduction is a **consequence** of decreased RBF and increased afferent arteriolar resistance.
- While clinically important (oliguria/acute kidney injury), it's a **downstream effect** rather than the primary physiological response.
- The relationship: ↓RBF → ↓Glomerular hydrostatic pressure → ↓GFR
Acid-Base Regulation by the Kidneys Indian Medical PG Question 6: Which of the following statements about gluconeogenesis is true?
- A. Occurs only in liver
- B. Uses ATP (Correct Answer)
- C. Activated by insulin
- D. Uses only lactate as a substrate
Acid-Base Regulation by the Kidneys Explanation: ***Uses ATP***
- Gluconeogenesis is an **anabolic process** that synthesizes glucose from non-carbohydrate precursors, requiring significant energy input in the form of **6 ATP and 2 GTP molecules per glucose molecule**.
- Key energy-consuming reactions include **pyruvate carboxylase** (uses ATP) and **phosphoenolpyruvate carboxykinase (PEPCK)** (uses GTP).
- This high energy requirement distinguishes it from glycolysis, which produces ATP.
*Occurs only in liver*
- This is **incorrect** as gluconeogenesis occurs predominantly in the **liver (90%)** but also takes place in the **renal cortex (10%)** and to a minimal extent in the epithelial cells of the small intestine.
- The liver's role is crucial for maintaining **blood glucose homeostasis** during fasting or starvation.
*Activated by insulin*
- Gluconeogenesis is **inhibited by insulin**, which signals a state of high blood glucose and promotes glucose utilization and storage.
- It is primarily **activated by glucagon and cortisol**, hormones that signal low blood glucose and energy deficit states.
*Uses only lactate as a substrate*
- This is **incorrect** as gluconeogenesis utilizes multiple substrates, not just lactate.
- Key substrates include **lactate** (via the Cori cycle), **amino acids** (especially alanine via the glucose-alanine cycle), **glycerol** (from lipolysis), and **propionate**.
- This substrate diversity allows glucose production from various metabolic pathways during fasting.
Acid-Base Regulation by the Kidneys Indian Medical PG Question 7: Which of the following increases uric acid excretion?
- A. Probenecid (Correct Answer)
- B. Allopurinol
- C. Aspirin
- D. Colchicine
Acid-Base Regulation by the Kidneys Explanation: **Probenecid**
- **Probenecid** is a **uricosuric agent** that increases renal excretion of uric acid by inhibiting its reabsorption in the proximal tubule.
- It is used in the treatment of **chronic gout** to lower serum uric acid levels.
*Allopurinol*
- **Allopurinol** works by inhibiting **xanthine oxidase**, an enzyme responsible for uric acid synthesis, thereby reducing its production.
- It does not increase uric acid excretion but rather decreases its formation, making it suitable for **overproducers** of uric acid.
*Aspirin*
- **Low-dose aspirin** can actually *decrease* uric acid excretion by interfering with tubular secretion of uric acid.
- **High-dose aspirin** has a uricosuric effect, but it is not typically used for gout due to side effects and more effective alternatives.
*Colchicine*
- **Colchicine** is an **anti-inflammatory agent** used to treat acute gout flares by inhibiting neutrophil chemotaxis and activation.
- It does **not affect uric acid synthesis or excretion** directly, but rather mitigates the inflammatory response to uric acid crystals.
Acid-Base Regulation by the Kidneys Indian Medical PG Question 8: In a normally functioning kidney, which part of the nephron has the lowest permeability to water during antidiuresis?
- A. Distal Convoluted Tubule
- B. Proximal Convoluted Tubule
- C. Thick Ascending Limb of Loop of Henle (Correct Answer)
- D. Collecting Duct
Acid-Base Regulation by the Kidneys Explanation: ***Thick Ascending Limb of Loop of Henle***
- This segment is **completely impermeable to water** regardless of the presence of ADH, making it the segment with the lowest water permeability in the nephron.
- Its primary function is to actively reabsorb solutes like **Na+, K+, and Cl-** via the Na-K-2Cl cotransporter, diluting the tubular fluid without water following.
- This impermeability is critical for establishing and maintaining the **medullary osmotic gradient**.
*Proximal Convoluted Tubule*
- The **proximal convoluted tubule** is highly permeable to water, responsible for reabsorbing about **65% of filtered water** through constitutively expressed aquaporin-1 (AQP-1) channels.
- Water reabsorption here is obligatory and **not regulated by ADH**.
*Distal Convoluted Tubule*
- The **distal convoluted tubule** has low water permeability in the absence of ADH but can be increased when ADH is present (though less responsive than the collecting duct).
- Its primary role is in fine-tuning electrolyte reabsorption, particularly **sodium and calcium**.
*Collecting Duct*
- The **collecting duct** has variable water permeability that is highly **ADH-dependent**.
- During antidiuresis (high ADH), aquaporin-2 channels are inserted into the apical membrane, making it highly permeable to water for final urine concentration.
- Without ADH, it has low permeability, but it's never as impermeable as the thick ascending limb.
Acid-Base Regulation by the Kidneys Indian Medical PG Question 9: Which one of the following statements concerning gluconeogenesis is correct?
- A. It occurs primarily in the liver.
- B. It is stimulated by elevated levels of acetyl CoA.
- C. It is important in maintaining blood glucose during the normal overnight fast. (Correct Answer)
- D. It is primarily inhibited by insulin.
Acid-Base Regulation by the Kidneys Explanation: ***It is important in maintaining blood glucose during the normal overnight fast.***
- **This is the BEST answer** as it emphasizes the **primary physiological role** of gluconeogenesis in human metabolism.
- During the **overnight fast** (8-12 hours), hepatic glycogen stores become depleted, making gluconeogenesis the **critical mechanism** to maintain blood glucose for glucose-dependent tissues like the **brain** (requires ~120g glucose/day) and **red blood cells**.
- Without gluconeogenesis, blood glucose would drop dangerously during fasting, leading to hypoglycemia and neurological dysfunction.
*It occurs primarily in the liver.*
- This statement is **technically correct** - the liver accounts for approximately **90%** of total gluconeogenesis under normal conditions.
- However, the **kidney cortex** also contributes significantly (10% normally, up to 40% during prolonged fasting), and the **intestine** plays a minor role.
- While true, this is more of a **anatomical fact** rather than highlighting the critical physiological importance of the pathway, making it a less comprehensive answer than Option 1.
*It is stimulated by elevated levels of acetyl CoA.*
- This statement is **biochemically correct** - **Acetyl-CoA** is an important **allosteric activator** of **pyruvate carboxylase**, the first committed enzyme of gluconeogenesis.
- However, this represents just **one regulatory mechanism** at the enzymatic level, not the overall physiological significance.
- Primary regulation occurs through **hormones** (glucagon, cortisol, epinephrine) that coordinate the entire pathway, making this a narrower answer than Option 1.
*It is primarily inhibited by insulin.*
- This statement is also **correct** - **Insulin** is the primary hormonal **inhibitor** of gluconeogenesis.
- Insulin suppresses gluconeogenesis by inhibiting key enzymes (PEPCK, glucose-6-phosphatase) and decreasing transcription of gluconeogenic genes.
- However, this describes **inhibition** rather than the positive physiological role, making it less representative of gluconeogenesis's essential function than Option 1.
**Note:** All four statements are technically correct, but Option 1 best captures the **essential physiological importance** of gluconeogenesis in human metabolism, which is why it is the preferred answer for this question.
Acid-Base Regulation by the Kidneys Indian Medical PG Question 10: Which of the following is the primary mechanism that drives sodium reabsorption in the proximal tubule?
- A. Sodium reabsorption through cotransport with amino acids at the luminal membrane.
- B. Sodium reabsorption through cotransport with glucose at the luminal membrane.
- C. Sodium reabsorption through countertransport with hydrogen ions at the luminal membrane.
- D. Active sodium transport via the Na+-K+-ATPase pump at the basolateral membrane. (Correct Answer)
Acid-Base Regulation by the Kidneys Explanation: ***Active sodium transport via the Na+-K+-ATPase pump at the basolateral membrane.***
- This pump **actively transports sodium out of the cell** into the interstitial fluid, creating a low intracellular sodium concentration.
- The **Na+-K+-ATPase** is the primary driver of sodium reabsorption throughout the nephron, creating the electrochemical gradient for other sodium transporters.
*Sodium reabsorption through cotransport with amino acids at the luminal membrane.*
- While **sodium-amino acid cotransport** does occur in the proximal tubule, it accounts for only a fraction of total sodium reabsorption.
- The primary driving force for this cotransport is the **low intracellular sodium concentration** maintained by the Na+-K+-ATPase.
*Sodium reabsorption through cotransport with glucose at the luminal membrane.*
- **Sodium-glucose cotransporters (SGLTs)** are crucial for glucose reabsorption in the proximal tubule, moving glucose into the cell along with sodium.
- However, glucose cotransport represents a specific mechanism for glucose handling, not the overarching mechanism for sodium reabsorption.
*Sodium reabsorption through countertransport with hydrogen ions at the luminal membrane.*
- The **Na+-H+ exchanger (NHE3)** is significant for exchanging sodium for hydrogen ions at the luminal membrane in the proximal tubule.
- This mechanism is important for **acid-base balance** and some sodium reabsorption, but it is secondary to the Na+-K+-ATPase in driving the overall sodium gradient.
More Acid-Base Regulation by the Kidneys Indian Medical PG questions available in the OnCourse app. Practice MCQs, flashcards, and get detailed explanations.
