Acid-Base Regulation by the Kidneys — MCQs

10 questions

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

Hyperaldosteronism is associated with all, except:

A patient in renal failure exhibits metabolic acidosis. What compensatory mechanism is most likely activated?

Calcitriol is formed in:

What is the physiological response of the kidney during shock?

Which of the following statements about gluconeogenesis is true?

Which of the following increases uric acid excretion?

In a normally functioning kidney, which part of the nephron has the lowest permeability to water during antidiuresis?

Which one of the following statements concerning gluconeogenesis is correct?

Q10

Which of the following is the primary mechanism that drives sodium reabsorption in the proximal tubule?

Acid-Base Regulation by the Kidneys Indian Medical PG Practice Questions and MCQs

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

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.

Question 2: Hyperaldosteronism is associated with all, except:

A. Hypernatremia
B. Hypertension
C. Hypokalemia
D. Metabolic acidosis (Correct Answer)

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].

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

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.

Question 4: Calcitriol is formed in:

A. Glomerulus
B. Bowman's capsule
C. PCT (Correct Answer)
D. DCT

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.

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)

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

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

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.

Question 7: Which of the following increases uric acid excretion?

A. Probenecid (Correct Answer)
B. Allopurinol
C. Aspirin
D. Colchicine

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.

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

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.

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.

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.

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)

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.

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