Renal Regulation of Acid-Base Balance — MCQs
Mechanism of secretion of ammonia in distal tubule is?
Maximum absorption of HCO3- occurs in:
What is the most common cause of normal anion gap metabolic acidosis?
Aldosterone mainly acts upon
Aldosterone acts chiefly on which of the following parts of the nephron:
Among the following conditions, which is most likely to cause type 4 renal tubular acidosis?
In plasma, if pH is 5, what is the fraction of base to acid?
Which one of the following biochemical abnormalities can be produced by repeated vomiting?
Carbonic anhydrase activity is found in all of the following except?
In a comatose patient with a blood glucose level of 750 mg/dL, which test is most important to perform in addition to serum potassium?
Renal Regulation of Acid-Base Balance Indian Medical PG Practice Questions and MCQs
Question 1: Mechanism of secretion of ammonia in distal tubule is?
- A. Primary active transport
- B. Symport
- C. Antiport
- D. Passive diffusion (Correct Answer)
Explanation: ***Passive diffusion*** - Ammonia (NH3) is a **lipid-soluble molecule** that can readily cross cell membranes, including those of the distal tubule and collecting duct, down its **concentration gradient**. - This process is crucial for regulating **acid-base balance**, as NH3 traps H+ ions to form NH4+, which is then excreted. *Primary active transport* - This mechanism involves the direct use of **ATP hydrolysis** to move ions against their concentration gradient, which is not the primary way ammonia is secreted in the distal tubule. - While NH4+ can be secreted via active transport in some segments (e.g., substituting for K+ on the Na-K-2Cl cotransporter in the thick ascending limb), free ammonia diffusion is distinct. *Symport* - **Symport** involves the co-transport of two or more different molecules or ions in the same direction across a cell membrane, powered by an electrochemical gradient. - This mechanism is not typically involved in the secretion of uncharged, lipid-soluble ammonia. *Antiport* - **Antiport** is a type of coupled transport where two different ions or molecules move in opposite directions across a membrane. - While antiport systems are essential for various renal functions (e.g., Na+/H+ exchanger), they are not the primary mechanism for the secretion of free ammonia in the distal tubule.
Question 2: Maximum absorption of HCO3- occurs in:
- A. DCT
- B. PCT (Correct Answer)
- C. collecting duct
- D. ascending limb of the loop of Henle
Explanation: ***PCT*** - The **proximal convoluted tubule (PCT)** reabsorbs approximately **80-90% of filtered bicarbonate (HCO3-)** from the glomerular filtrate. - This high reabsorption rate is crucial for **maintaining acid-base balance** and preventing bicarbonate loss in urine. *DCT* - The **distal convoluted tubule (DCT)** reabsorbs a much smaller percentage of bicarbonate compared to the PCT. - Its primary role in acid-base balance is often related to **acid secretion** rather than bulk bicarbonate reabsorption. *collecting duct* - The **collecting duct** plays a significant role in the *final regulation* of acid-base balance, including variable bicarbonate reabsorption or secretion, but not the majority of absorption. - Its bicarbonate handling is influenced by the body's acid-base status, with **intercalated cells** being key players. *ascending limb of the loop of Henle* - The **thick ascending limb of the loop of Henle** is primarily responsible for the reabsorption of **sodium, potassium, and chloride** (via the NKCC2 co-transporter). - It has **minimal to no direct reabsorption of bicarbonate**, making it an unlikely site for maximum HCO3- absorption.
Question 3: What is the most common cause of normal anion gap metabolic acidosis?
- A. Ingestion of ammonium chloride
- B. Lactic acidosis
- C. Ethylene glycol intoxication
- D. Renal tubular acidosis
- E. Salicylate intoxication
- F. External pancreatic drainage
- . Diarrhoea (Correct Answer)
- . Chronic renal failure
- . Methanol/Formaldehyde intoxication
- . Uterosigmoidostomy
- . Ketoacidosis
Explanation: ***Diarrhoea*** - Diarrhoea causes a **loss of bicarbonate** from the gastrointestinal tract, leading to a **normal anion gap metabolic acidosis** [2]. - The loss of bicarbonate is compensated by an **increase in chloride reabsorption** in the kidneys, maintaining a normal anion gap. *Ingestion of ammonium chloride* - Ingestion of ammonium chloride leads to **hyperchloremic metabolic acidosis** by contributing to a net gain of hydrogen ions. - While it causes a normal anion gap metabolic acidosis, it is **not the most common cause** in clinical practice. *Lactic acidosis* - Lactic acidosis results from the accumulation of **lactic acid**, an unmeasured anion, leading to a **high anion gap metabolic acidosis** [1]. - This typically occurs in conditions of **tissue hypoxia** or impaired lactate metabolism [1]. *Ethylene glycol intoxication* - Ethylene glycol metabolism produces various organic acids (e.g., **glycolic acid, oxalic acid**), which are unmeasured anions, causing a **high anion gap metabolic acidosis**. - It is often associated with acute **kidney injury** and neurological symptoms. *Renal tubular acidosis* - Renal tubular acidosis (RTA) involves impaired acid excretion or bicarbonate reabsorption by the kidneys, resulting in a **normal anion gap metabolic acidosis** [1]. - While a significant cause, it is **less common globally** than diarrhoea as a cause of normal anion gap metabolic acidosis. *Salicylate intoxication* - Salicylate intoxication initially causes **respiratory alkalosis** due to central respiratory stimulation [1]. - At toxic levels, it can lead to **high anion gap metabolic acidosis** due to the accumulation of organic acids and uncoupling of oxidative phosphorylation. *External pancreatic drainage* - External pancreatic drainage can lead to significant **bicarbonate loss**, as pancreatic fluid is rich in bicarbonate. - This loss causes a **normal anion gap metabolic acidosis**, similar to severe diarrhoea. *Chronic renal failure* - Chronic renal failure can cause metabolic acidosis, but it's typically a **high anion gap metabolic acidosis** due to the accumulation of unexcreted organic acids (e.g., phosphates, sulfates). - In earlier stages, or when accompanied by specific renal tubular defects, it can sometimes present as normal anion gap acidosis. *Methanol/Formaldehyde intoxication* - Methanol and formaldehyde intoxication lead to **high anion gap metabolic acidosis** due to their metabolism into highly toxic substances like **formic acid**. - These are characterized by severe systemic toxicity and visual disturbances. *Uterosigmoidostomy* - Uterosigmoidostomy involves diverting urine into the sigmoid colon, allowing for the reabsorption of **chloride** and the loss of **bicarbonate** from the body. - This results in a **normal anion gap metabolic acidosis**, also known as **hyperchloremic metabolic acidosis**. *Ketoacidosis* - Ketoacidosis (e.g., diabetic ketoacidosis, alcoholic ketoacidosis) is characterized by the overproduction of **ketoacids** (beta-hydroxybutyrate, acetoacetate). - These are unmeasured anions, leading to a prominent **high anion gap metabolic acidosis**.
Question 4: Aldosterone mainly acts upon
- A. Loop of Henle
- B. Distal renal tubule (Correct Answer)
- C. PCT
- D. Glomerulus
Explanation: ***Distal renal tubule*** - Aldosterone primarily acts on the **principal cells** of the **distal convoluted tubule** and collecting duct. - Its main function is to promote **sodium reabsorption** and **potassium excretion** in these segments. *Loop of Henle* - The Loop of Henle is primarily involved in establishing the **medullary osmotic gradient** and reabsorbing water and solutes, but it is **not the primary site** of aldosterone action. - While some sodium is reabsorbed here, this process is largely independent of aldosterone's direct influence. *PCT* - The **proximal convoluted tubule (PCT)** is responsible for the bulk reabsorption of filtered substances, including about 65% of sodium and water. - Aldosterone has **minimal to no direct effect** on the reabsorptive processes occurring in the PCT. *Glomerulus* - The **glomerulus** is the site of **ultrafiltration**, where blood is filtered to form a protein-free filtrate. - Aldosterone has no direct action on the filtration barrier or the cells of the glomerulus.
Question 5: Aldosterone acts chiefly on which of the following parts of the nephron:
- A. DCT (Correct Answer)
- B. Glomerulus
- C. Loop of Henle
- D. PCT
Explanation: ***DCT*** - Aldosterone primarily acts on the **principal cells** in the **distal convoluted tubule (DCT)** and collecting duct. - Its main roles are increasing **sodium reabsorption** and **potassium secretion** from the tubular fluid. *Glomerulus* - The glomerulus is responsible for **filtration** of blood, not hormonal regulation of electrolyte reabsorption. - It is where the initial filtrate is formed, based on pressure gradients. *Loop of Henle* - The Loop of Henle is crucial for establishing the **medullary osmotic gradient**, primarily through reabsorption of water (descending limb) and solutes (ascending limb). - It does not have significant receptors for aldosterone regulation. *PCT* - The proximal convoluted tubule (PCT) is the primary site for the **non-regulated reabsorption** of most filtered solutes, including a large percentage of sodium, glucose, and amino acids. - Its reabsorptive functions are largely independent of aldosterone.
Question 6: Among the following conditions, which is most likely to cause type 4 renal tubular acidosis?
- A. Chronic pyelonephritis
- B. Diabetic nephropathy (Correct Answer)
- C. Systemic lupus
- D. Multiple myeloma
Explanation: ***Diabetic nephropathy*** - **Diabetic nephropathy** is a common cause of **type 4 renal tubular acidosis (RTA)** due to damage to the **juxtaglomerular apparatus** affecting **renin production** and subsequent aldosterone levels. - The resulting **hypoaldosteronism** or **aldosterone resistance** [1] leads to impaired potassium and hydrogen secretion in the **distal tubules**, causing **hyperkalemia** and **metabolic acidosis**. [1] *Chronic pyelonephritis* - While chronic pyelonephritis can lead to **renal scarring** and **chronic kidney disease**, it typically does not directly cause type 4 RTA. - It is more commonly associated with a variety of tubular defects, but not specifically the **hypoaldosteronism** characteristic of type 4 RTA unless severe general renal failure is present. *Systemic lupus* - **Systemic lupus erythematosus (SLE)** can cause **lupus nephritis**, leading to various forms of kidney damage, but it is more commonly associated with **type 1 (distal)** or **type 2 (proximal) RTA**, rather than type 4. - Type 1 RTA in SLE is often due to an **autoimmune attack** on the **distal tubule's ability** to secrete hydrogen ions. *Multiple myeloma* - **Multiple myeloma** is known to cause **renal impairment** primarily through the deposition of **light chains** in the tubules, often leading to **proximal tubular dysfunction** (Fanconi syndrome) or **cast nephropathy**. - This typically results in **type 2 RTA** (proximal RTA) characterized by impaired reabsorption of bicarbonate, amino acids, and phosphate, rather than the distal tubular and aldosterone-related issues seen in type 4 RTA.
Question 7: In plasma, if pH is 5, what is the fraction of base to acid?
- A. 0.01
- B. 0.1 (Correct Answer)
- C. 1
- D. 10
Explanation: ***0.1*** - This question applies the **Henderson-Hasselbalch equation**: pH = pKa + log([base]/[acid]). For the **bicarbonate buffer system** (the primary plasma buffer), pKa ≈ 6.1. - Substituting the given values: $5 = 6.1 + \log([HCO_3^-] / [H_2CO_3])$ - Rearranging: $\log([HCO_3^-] / [H_2CO_3]) = 5 - 6.1 = -1.1$ - Therefore: $[HCO_3^-] / [H_2CO_3] = 10^{-1.1} ≈ 0.079$ - Among the given options, **0.079 is closest to 0.1**, making this the correct answer. - Note: pH 5 in plasma is physiologically impossible (incompatible with life), but this tests theoretical understanding of the buffer equation. *0.01* - This ratio would correspond to an even **more acidic** condition with $\log([base]/[acid]) = -2$. - Using Henderson-Hasselbalch: pH = 6.1 + (-2) = 4.1, which is lower than the given pH of 5. - The calculated ratio of 0.079 is much closer to 0.1 than to 0.01. *1* - A ratio of 1 means **equal concentrations** of base and acid, which occurs when pH = pKa. - This would give pH = 6.1, not the given pH of 5. - This represents a **neutral buffer condition**, not the acidic state described. *10* - This ratio indicates an **alkaline** solution with 10 times more base than acid. - Using Henderson-Hasselbalch: pH = 6.1 + log(10) = 6.1 + 1 = 7.1 (physiological alkalosis). - This contradicts the given acidic pH of 5.
Question 8: Which one of the following biochemical abnormalities can be produced by repeated vomiting?
- A. Metabolic acidosis
- B. Metabolic alkalosis (Correct Answer)
- C. Ketosis
- D. Uraemia
Explanation: ***Metabolic alkalosis*** - Repeated vomiting leads to the loss of **hydrochloric acid (HCl)** from the stomach, causing **hypochloremic metabolic alkalosis** with an increase in serum **bicarbonate (HCO3-)** and a rise in blood pH. - The loss of H+ and Cl- ions results in **compensatory hypokalemia** as the kidneys exchange K+ for H+ to maintain electroneutrality. - **Volume depletion** from vomiting triggers aldosterone secretion, which further promotes K+ loss and H+ excretion, perpetuating the alkalosis (contraction alkalosis). - This is one of the most common causes of metabolic alkalosis in clinical practice. *Metabolic acidosis* - This condition is characterized by a decrease in **serum pH** and **bicarbonate levels**, typically due to excess acid production or bicarbonate loss from diarrhea or renal tubular acidosis. - Vomiting does not directly cause metabolic acidosis; rather, it leads to the opposite effect by removing acidic gastric contents. *Ketosis* - **Ketosis** occurs when the body metabolizes fat for energy, producing **ketone bodies**, common in conditions like uncontrolled diabetes or prolonged starvation. - While severe, prolonged vomiting with reduced oral intake can indirectly lead to starvation ketosis, the primary and most characteristic biochemical abnormality of repeated vomiting is metabolic alkalosis, not ketosis. *Uraemia* - **Uraemia** is a syndrome caused by the accumulation of **nitrogenous waste products** (urea, creatinine) in the blood, primarily due to kidney failure. - Vomiting may be a *symptom* of uraemia, but it does not *cause* uraemia. Kidney function is the primary determinant of urea levels.
Question 9: Carbonic anhydrase activity is found in all of the following except?
- A. Brain
- B. Kidney
- C. RBC
- D. Plasma (Correct Answer)
Explanation: ***Plasma*** - **Carbonic anhydrase** is an intracellular enzyme that catalyzes the rapid interconversion of carbon dioxide and water to carbonic acid, **bicarbonate**, and protons. - It is notably **absent in plasma** in healthy individuals, as it is primarily found within cells where its function is crucial for pH regulation and CO2 transport. *Brain* - Carbonic anhydrase is found in various brain cells, including **neurons**, **oligodendrocytes**, and **astrocytes**. - It plays a vital role in pH regulation, fluid balance, and the production of cerebrospinal fluid (CSF) within the **central nervous system**. *Kidney* - The kidney is rich in carbonic anhydrase, particularly in the **proximal tubules** and collecting ducts. - It is critical for **bicarbonate reabsorption** and proton excretion, essential processes for maintaining acid-base balance. *RBC* - **Red blood cells (RBCs)** contain a high concentration of carbonic anhydrase (specifically CA-I and CA-II isoforms). - This enzyme facilitates the rapid conversion of CO2 to bicarbonate for transport to the lungs and the reverse reaction for **CO2 exhalation**.
Question 10: In a comatose patient with a blood glucose level of 750 mg/dL, which test is most important to perform in addition to serum potassium?
- A. Serum creatinine
- B. Serum sodium
- C. Serum ketones
- D. Arterial blood gases (Correct Answer)
Explanation: ***Arterial blood gases*** - In a comatose patient with severe hyperglycemia (750 mg/dL), **arterial blood gases (ABGs)** are crucial to assess for **acidosis**, which could indicate **diabetic ketoacidosis (DKA)** or **hyperosmolar hyperglycemic state (HHS)** with lactic acidosis [1], [4]. - The **pH**, **bicarbonate (HCO3-)**, and **pCO2** levels from ABGs help determine the severity and type of metabolic derangement, guiding immediate treatment, especially for potential **cerebral edema** [3], [4]. *Serum creatinine* - While important for assessing **kidney function** in hyperosmolar states, it does not directly evaluate the immediate acid-base status that is critical for neurologic function in a comatose patient. - Renal insufficiency can exacerbate electrolyte imbalances and fluid overload but is secondary to the immediate need for acid-base assessment. *Serum sodium* - **Serum sodium** is important for calculating **effective serum osmolality**, which is elevated in both DKA and HHS, contributing to mental status changes [2]. - However, while important, it does not provide information about the **acid-base balance**, which is a more critical determinant of immediate neurologic stability and treatment in deep coma. *Serum ketones* - **Serum ketones** are essential for distinguishing between **DKA** (high ketones) and **HHS** (low or absent ketones) [4]. - While vital for diagnosis, ketones alone do not give the full picture of **acid-base status** (pH, bicarbonate) which is directly assessed by ABGs and more immediately actionable in managing a severely ill, comatose patient [1].
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