Acid-Base and Electrolyte Balance Practice Questions

Q: Which of the following is a precursor of the molecule shown in the illustration?

Insulin. ***Insulin*** - The molecule shown is **C-peptide**, which is produced during **insulin biosynthesis** when **proinsulin** is cleaved to form insulin and C-peptide. - **Insulin** serves as the direct precursor in this pathway: **Preproinsulin** → **Proinsulin** → **Insulin + C-peptide**, making insulin the correct answer. *Glucagon* - **Glucagon** is synthesized from **proglucagon** through a completely separate biosynthetic pathway in pancreatic **alpha cells**. - It has **opposing metabolic effects** to insulin and does not contribute to **C-peptide formation**. *Somatostatin* - **Somatostatin** is derived from **prosomatostatin** in pancreatic **delta cells** and hypothalamic neurons. - It functions as a **growth hormone inhibitor** and has no role in the **insulin-C-peptide** biosynthetic pathway. *Lipase* - **Pancreatic lipase** is a **digestive enzyme** synthesized as **prolipase** and activated in the small intestine. - It is involved in **fat digestion**, not hormone biosynthesis, and has no connection to **C-peptide formation**.

Q: A 40-year-old male presents with recurrent bouts of vomiting for 9 months because of pyloric obstruction. What is the compensatory biochemical change?

Paradoxical aciduria with hyponatremia and hypochloremia. ### **Explanation** **Underlying Concept:** Pyloric obstruction leads to persistent vomiting, causing a massive loss of gastric hydrochloric acid (HCl). This results in **Metabolic Alkalosis** (due to loss of H⁺) and **Hypochloremia** (due to loss of Cl⁻). To compensate for the volume loss (dehydration), the body activates the Renin-Angiotensin-Aldosterone System (RAAS). **Why Option C is Correct:** 1. **Hyponatremia & Hypochloremia:** Vomiting directly removes Na⁺ and Cl⁻. 2. **The "Paradox":** Normally, in alkalosis, the kidneys should excrete bicarbonate (alkaline urine) to restore pH. However, in pyloric obstruction, the body prioritizes volume over pH. 3. **Mechanism:** To conserve Na⁺ (and water), the distal tubule reabsorbs Na⁺ in exchange for H⁺ (via the H⁺/Na⁺ exchanger) and K⁺. This occurs because Cl⁻ is unavailable to be reabsorbed with Na⁺. Consequently, H⁺ ions are secreted into the urine, making it **acidic** despite the systemic **alkalosis**. This is termed **Paradoxical Aciduria**. **Why Other Options are Incorrect:** * **A & B (Respiratory Changes):** While the lungs may attempt a minor compensatory hypoventilation (increasing CO₂), the primary biochemical hallmark and "paradox" of this condition is renal, not respiratory. * **D (Metabolic Acidosis):** Vomiting gastric contents causes a loss of acid, leading to alkalosis, not acidosis. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Hypochloremic, hypokalemic, metabolic alkalosis with paradoxical aciduria. * **Key Electrolyte Shift:** Hypokalemia occurs because K⁺ is shifted into cells and excreted in the urine to save Na⁺. * **Treatment:** The definitive initial management is **Isotonic Saline (0.9% NaCl)**. The chloride in the saline allows the kidney to stop secreting H⁺, thus correcting the paradoxical aciduria.

Q: Low calcium and high phosphate is seen in which condition?

Hypoparathyroidism. ### Explanation The correct answer is **Hypoparathyroidism**. **1. Why Hypoparathyroidism is correct:** The Parathyroid Hormone (PTH) is the primary regulator of calcium and phosphate homeostasis. In hypoparathyroidism, there is a deficiency of PTH, leading to: * **Hypocalcemia:** PTH normally increases bone resorption and renal calcium reabsorption. Its absence leads to low serum calcium. * **Hyperphosphatemia:** PTH is a potent **phosphaturic hormone** (it inhibits phosphate reabsorption in the proximal convoluted tubule). Without PTH, the kidneys retain phosphate, leading to high serum levels. **2. Why the other options are incorrect:** * **Hyperparathyroidism:** This is the exact opposite. Excess PTH causes **Hypercalcemia** (increased bone resorption) and **Hypophosphatemia** (increased urinary phosphate excretion). * **Hyperthyroidism:** While severe thyrotoxicosis can cause mild hypercalcemia due to increased bone turnover, it does not typically present with the classic low calcium/high phosphate pattern. * **Hypothyroidism:** Thyroid hormones have minimal direct impact on acute calcium and phosphate balance compared to PTH. **3. NEET-PG High-Yield Pearls:** * **Pseudohypoparathyroidism:** Presents with the same biochemical profile (Low Ca²⁺, High PO₄³⁻) but with **elevated PTH** levels due to end-organ resistance. * **Chronic Kidney Disease (CKD):** Also shows Low Ca²⁺ and High PO₄³⁻, but is distinguished by elevated PTH (Secondary Hyperparathyroidism) and history of renal failure. * **Vitamin D Deficiency:** Characterized by **Low Ca²⁺ and Low PO₄³⁻** (because PTH rises secondary to low calcium and flushes out phosphate). * **Mnemonic for PTH:** "PTH Puts Phosphate in the Urine" (Phosphaturic action). If PTH is low, phosphate stays in the blood.

Q: Which of the following conditions is typically associated with a normal anion gap?

Renal tubular acidosis. **Explanation:** Metabolic acidosis is categorized based on the **Anion Gap (AG)**, calculated as: $Na^+ - (Cl^- + HCO_3^-)$. The normal range is 8–12 mEq/L. **1. Why Renal Tubular Acidosis (RTA) is correct:** RTA is a classic cause of **Normal Anion Gap Metabolic Acidosis (NAGMA)**, also known as hyperchloremic metabolic acidosis. In RTA, there is either a failure to excrete $H^+$ (Type 1) or a failure to reabsorb $HCO_3^-$ (Type 2). To maintain electroneutrality as bicarbonate is lost, the kidneys retain **Chloride ($Cl^-$)**. Since the increase in chloride offsets the decrease in bicarbonate, the calculated anion gap remains within the normal range. **2. Why other options are incorrect:** * **Diabetic Ketoacidosis (DKA):** Characterized by the accumulation of unmeasured anions (acetoacetate and beta-hydroxybutyrate), which increases the AG. * **Lactic Acidosis:** Occurs due to tissue hypoxia or sepsis; the accumulation of lactate (an unmeasured anion) leads to a High Anion Gap Metabolic Acidosis (HAGMA). * **Starvation Ketoacidosis:** Similar to DKA, the production of ketone bodies increases the concentration of unmeasured anions, resulting in HAGMA. **Clinical Pearls for NEET-PG:** * **Mnemonic for HAGMA:** **MUDPILES** (Methanol, Uremia, DKA, Propylene glycol, Iron/INH, Lactic acidosis, Ethylene glycol, Salicylates). * **Mnemonic for NAGMA:** **USED CARP** (Ureterosigmoidostomy, Saline infusion, Endocrine (Addison’s), **Diarrhea**, **RTA**, Pancreatic fistula). * **Key Distinction:** Diarrhea is the most common cause of NAGMA globally, while RTA is the classic renal cause.

Q: Metabolic alkalosis is seen in which of the following conditions, except?

Methanol poisoning. **Explanation:** The correct answer is **Methanol poisoning**, as it causes **High Anion Gap Metabolic Acidosis (HAGMA)**, not alkalosis. **1. Why Methanol Poisoning is the Correct Answer:** Methanol is metabolized by alcohol dehydrogenase into **formaldehyde** and subsequently by aldehyde dehydrogenase into **formic acid**. The accumulation of formic acid leads to a significant increase in hydrogen ions, resulting in metabolic acidosis. This is typically associated with an increased anion gap and an osmolar gap. **2. Analysis of Other Options (Causes of Metabolic Alkalosis):** * **Vomiting:** Gastric juice is rich in Hydrochloric acid (HCl). Loss of stomach acid leads to a relative increase in bicarbonate levels in the blood, causing "chloride-responsive" metabolic alkalosis. * **Cushing’s Disease:** Excess cortisol has mineralocorticoid effects, leading to increased sodium reabsorption and increased secretion of Potassium ($K^+$) and Hydrogen ($H^+$) ions in the distal renal tubules. The loss of $H^+$ ions results in metabolic alkalosis. * **Diuretic Therapy:** Loop and thiazide diuretics cause the excretion of $Na^+$, $Cl^-$, and water. This leads to "contraction alkalosis" and increased distal delivery of sodium, which promotes $H^+$ secretion. **Clinical Pearls for NEET-PG:** * **Mnemonic for HAGMA:** **MUDPILES** (Methanol, Uremia, DKA, Paraldehyde, Iron/INH, Lactic acidosis, Ethylene glycol, Salicylates). * **Conn’s Syndrome & Cushing’s:** Both are classic endocrine causes of metabolic alkalosis associated with hypokalemia. * **Vomiting:** Characterized by **Hypochloremic, Hypokalemic Metabolic Alkalosis** with paradoxical aciduria.

Q: Which of the following is NOT a component of Oral Rehydration Salts (ORS)?

Glucose without salt. **Explanation:** The core principle of Oral Rehydration Salts (ORS) is the **SGLT-1 (Sodium-Glucose Linked Transporter)** mechanism in the small intestine. This transporter facilitates the coupled absorption of one molecule of glucose with two ions of sodium. As these solutes are absorbed, they create an osmotic gradient that pulls water into the bloodstream. Therefore, **glucose without salt** is ineffective for rehydration because, in the absence of sodium, the co-transport mechanism cannot function, and water absorption remains minimal. **Analysis of Options:** * **Sodium (A):** Essential for the SGLT-1 transporter and for replacing extracellular fluid volume lost during diarrhea. * **Potassium (B):** Crucial for replacing intracellular losses and preventing hypokalemia, which is common in diarrheal diseases. * **Glucose with salt (C):** This is the fundamental combination required to drive the active transport of water across the intestinal mucosa. **High-Yield Clinical Pearls for NEET-PG:** * **WHO Reduced Osmolarity ORS:** The current standard has a total osmolarity of **245 mOsm/L** (reduced from the older 311 mOsm/L) to decrease the risk of hypernatremia and reduce stool output. * **Composition (per Liter):** Sodium Chloride (2.6g), Glucose anhydrous (13.5g), Potassium Chloride (1.5g), and Trisodium Citrate (2.9g). * **Trisodium Citrate:** Added specifically to correct **metabolic acidosis** resulting from bicarbonate loss in stools. * **Zinc Supplementation:** Often given alongside ORS (20mg/day for 10-14 days) to reduce the duration and severity of diarrhea.

Q: Normal anion gap is seen in all of the following conditions except:

Methanol poisoning. ### Explanation The **Anion Gap (AG)** is calculated as $[Na^+] - ([Cl^-] + [HCO_3^-])$. A **Normal Anion Gap Metabolic Acidosis (NAGMA)** occurs when the loss of bicarbonate is compensated by a proportional increase in chloride (Hyperchloremic acidosis). In contrast, **High Anion Gap Metabolic Acidosis (HAGMA)** occurs when unmeasured acid anions (like lactate or ketoacids) accumulate. **Why Methanol Poisoning is the Correct Answer:** Methanol poisoning causes **HAGMA**. Methanol is metabolized by alcohol dehydrogenase into **formic acid**. The accumulation of formate ions (unmeasured anions) increases the anion gap. This is typically associated with an "Osmolar Gap" as well. **Analysis of Incorrect Options (Causes of NAGMA):** * **Renal Tubular Acidosis (RTA):** Characterized by either the inability to reabsorb bicarbonate (Type 2) or secrete hydrogen ions (Type 1/4), leading to bicarbonate loss and compensatory hyperchloremia. * **Diarrhoea:** The most common cause of NAGMA. Gastrointestinal secretions are rich in $HCO_3^-$; their loss leads to a relative increase in serum chloride. * **Ureterosigmoidoscopy:** In this procedure, ureters are diverted into the sigmoid colon. The intestinal mucosa exchanges $Cl^-$ for $HCO_3^-$, leading to bicarbonate loss and hyperchloremic acidosis. **NEET-PG High-Yield Pearls:** 1. **Mnemonic for HAGMA:** **MUDPILES** (Methanol, Uremia, DKA, Propylene glycol, Iron/INH, Lactic acidosis, Ethylene glycol, Salicylates). 2. **Mnemonic for NAGMA:** **USED CARP** (Ureterosigmoidoscopy, Saline infusion, Endocrine/Addison’s, Diarrhoea, Carbonic anhydrase inhibitors, Ammonium chloride, RTA, Pancreatic fistula). 3. **Normal Anion Gap range:** 8–12 mEq/L. 4. **Gold Standard:** In methanol poisoning, look for **optic disc hyperemia** (snow-blindness) on fundoscopy.

Q: What is the commonest cause of metabolic alkalosis?

Pyloric stenosis. **Explanation:** **Pyloric stenosis** is the most common cause of metabolic alkalosis in clinical practice, particularly in the pediatric population. The underlying mechanism is the persistent loss of gastric secretions due to projectile vomiting. Gastric juice is rich in **Hydrochloric acid (HCl)** and **Potassium (KCl)**. 1. **Loss of H+:** For every proton lost in vomitus, a bicarbonate ion ($HCO_3^-$) is added to the blood (the "alkaline tide"), leading to **Metabolic Alkalosis**. 2. **Loss of Cl-:** This leads to **Hypochloremia**. To maintain electrical neutrality, the kidneys reabsorb bicarbonate instead of chloride, worsening the alkalosis. 3. **Volume Depletion:** Dehydration activates the Renin-Angiotensin-Aldosterone System (RAAS). Aldosterone promotes $Na^+$ reabsorption at the expense of $H^+$ and $K^+$ excretion in the distal tubule, leading to **Paradoxical Aciduria** (acidic urine despite systemic alkalosis). **Analysis of Incorrect Options:** * **A. Cancer of the stomach:** While it can cause obstruction, it is less common than pyloric stenosis and often presents with achlorhydria (lack of acid production). * **C. Small-bowel obstruction:** Obstruction distal to the ampulla of Vater results in the loss of both acidic gastric juice and alkaline pancreatic/biliary secretions, often leading to a **neutral pH** or **metabolic acidosis** (if primarily lower bowel). * **D. Diuretics:** Loop and thiazide diuretics cause metabolic alkalosis (contraction alkalosis), but they are a secondary cause compared to the classic presentation of pyloric stenosis. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Hypochloremic, Hypokalemic, Metabolic Alkalosis with Paradoxical Aciduria. * **Management:** The priority is fluid resuscitation with **0.9% Normal Saline** (to provide $Cl^-$) and Potassium supplementation before surgical correction (Ramstedt’s Myotomy).

Q: A solution contains 2x10^-3 mol/L of a weak acid (pK=3.5) and 2x10^-3 mol/L of its conjugate base. Its pH is best approximated by which one of the following?

3.5. ### Explanation **1. Why the Correct Answer is Right (The Henderson-Hasselbalch Equation)** The pH of a buffer solution is determined by the ratio of the concentration of the conjugate base ([A⁻]) to the weak acid ([HA]). This relationship is expressed by the **Henderson-Hasselbalch equation**: $$pH = pK_a + \log \frac{[Conjugate\ Base]}{[Weak\ Acid]}$$ In this question: * $[Conjugate\ Base] = 2 \times 10^{-3}\ mol/L$ * $[Weak\ Acid] = 2 \times 10^{-3}\ mol/L$ * $pK_a = 3.5$ Since the concentrations of the acid and base are **equal**, the ratio is 1. Because the $\log(1) = 0$, the equation simplifies to **$pH = pK_a$**. Therefore, the pH is exactly **3.5**. **2. Why the Incorrect Options are Wrong** * **Options A (4.1) and B (3.9):** These values are higher than the $pK_a$. This would only occur if the concentration of the conjugate base was significantly higher than the acid (making the solution more alkaline). * **Option D (3.1):** This value is lower than the $pK_a$. This would only occur if the concentration of the weak acid was higher than the conjugate base (making the solution more acidic). **3. Clinical Pearls & High-Yield Facts for NEET-PG** * **Maximum Buffering Capacity:** A buffer is most effective at resisting pH changes when the **$pH = pK_a$**. This occurs when the acid and conjugate base are in equal concentrations. * **Effective Buffer Range:** Generally, a buffer system functions effectively within **$\pm 1$ pH unit** of its $pK_a$. * **Bicarbonate Buffer System:** The most important extracellular buffer in humans. Though its $pK_a$ is 6.1 (far from physiological pH 7.4), it is effective because the body can independently regulate $CO_2$ (via lungs) and $HCO_3^-$ (via kidneys). * **Intracellular Buffer:** Phosphate ($pK_a \approx 6.8$) and Proteins (specifically **Histidine** residues) are the primary intracellular buffers.

Question 1

Which of the following is a precursor of the molecule shown in the illustration?

Accepted Answer

Insulin

Answer

Glucagon

Answer

Somatostatin

Answer

Lipase

Question 2

A 40-year-old male presents with recurrent bouts of vomiting for 9 months because of pyloric obstruction. What is the compensatory biochemical change?

Accepted Answer

Paradoxical aciduria with hyponatremia and hypochloremia

Answer

Respiratory Alkalosis

Answer

Respiratory acidosis

Answer

Metabolic acidosis

Question 3

Low calcium and high phosphate is seen in which condition?

Accepted Answer

Hypoparathyroidism

Answer

Hyperparathyroidism

Answer

Hyperthyroidism

Answer

Hypothyroidism

Question 4

Which of the following conditions is typically associated with a normal anion gap?

Accepted Answer

Renal tubular acidosis

Answer

Diabetic ketoacidosis

Answer

Lactic acidosis

Answer

Starvation ketoacidosis

Question 5

Lysis of cells causes which of the following electrolyte abnormalities?

Accepted Answer

Hypercalcemia

Answer

Hyperuricemia

Answer

Hyperphosphatemia

Answer

Hyperkalemia

Question 6

Metabolic alkalosis is seen in which of the following conditions, except?

Accepted Answer

Methanol poisoning

Answer

Cushing's disease

Answer

Vomiting

Answer

Diuretic therapy

Question 7

Which of the following is NOT a component of Oral Rehydration Salts (ORS)?

Accepted Answer

Glucose without salt

Answer

Sodium

Answer

Potassium

Answer

Glucose with salt

Question 8

Normal anion gap is seen in all of the following conditions except:

Accepted Answer

Methanol poisoning

Answer

Ureterosigmoidoscopy

Answer

Renal tubular acidosis

Answer

Diarrhoea

Question 9

What is the commonest cause of metabolic alkalosis?

Accepted Answer

Pyloric stenosis

Answer

Cancer of the stomach

Answer

Small-bowel obstruction

Answer

Diuretics

Question 10

A solution contains 2x10^-3 mol/L of a weak acid (pK=3.5) and 2x10^-3 mol/L of its conjugate base. Its pH is best approximated by which one of the following?

Accepted Answer

3.5

Answer

4.1

Answer

3.9

Answer

3.1

Acid-Base and Electrolyte Balance — MCQs

Acid-Base and Electrolyte Balance — MCQs

On this page

Practice by Chapter

Want unlimited practice?