Acid-Base Balance Practice Questions

Q: What is the commonest cause of metabolic alkalosis?

Pyloric stenosis. **Explanation:** **Pyloric stenosis** is the classic cause of metabolic alkalosis due to the persistent vomiting of gastric contents. Gastric juice is rich in hydrochloric acid (HCl). When a patient vomits (as seen in the projectile vomiting of congenital hypertrophic pyloric stenosis), there is a massive loss of hydrogen ions ($H^+$) and chloride ions ($Cl^-$). The underlying mechanism involves: 1. **Loss of $H^+$:** Leads to a direct increase in plasma bicarbonate ($HCO_3^-$). 2. **Hypochloremia:** Loss of $Cl^-$ forces the kidneys to reabsorb $HCO_3^-$ to maintain anionic balance. 3. **Contraction Alkalosis:** Dehydration triggers the Renin-Angiotensin-Aldosterone System (RAAS). Aldosterone promotes $Na^+$ reabsorption at the expense of $K^+$ and $H^+$ excretion in the distal tubule, further worsening the alkalosis (Paradoxical Aciduria). **Analysis of Incorrect Options:** * **A. Cancer of the stomach:** While it can cause obstruction, it is not the *most common* or classic association compared to the specific pathology of pyloric stenosis. * **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 do cause metabolic alkalosis, but in the context of clinical exams and classic surgical/pediatric presentations, pyloric stenosis remains the "textbook" commonest cause cited for profound metabolic alkalosis. **High-Yield NEET-PG Pearls:** * The characteristic electrolyte profile in pyloric stenosis is **Hypochloremic, Hypokalemic, Metabolic Alkalosis with Paradoxical Aciduria.** * **Paradoxical Aciduria** occurs because the body prioritizes volume expansion (reabsorbing $Na^+$) over pH balance, leading to $H^+$ secretion in the urine despite systemic alkalosis.

Q: A patient has a pCO2 of 80 mm Hg and plasma bicarbonate of 33 mEq/L. What is the acid-base disorder?

Respiratory acidosis. **Explanation:** The primary step in analyzing acid-base disorders is identifying the deviation in **pCO2** (normal: 40 mmHg) and **Bicarbonate (HCO3-)** (normal: 24 mEq/L). 1. **Why Respiratory Acidosis is Correct:** The patient has a significantly elevated pCO2 (80 mmHg), which is much higher than the normal 40 mmHg. In physiology, CO2 acts as a volatile acid. An increase in pCO2 (hypercapnia) indicates alveolar hypoventilation, leading to **Respiratory Acidosis**. The elevated bicarbonate (33 mEq/L) represents a compensatory response by the kidneys to buffer the acidity, suggesting this may be a chronic or partially compensated state. 2. **Why Incorrect Options are Wrong:** * **Metabolic Acidosis:** This would be characterized by a *low* bicarbonate (<22 mEq/L) and a low pH. Here, bicarbonate is elevated. * **Respiratory Alkalosis:** This occurs when pCO2 is *low* (<35 mmHg) due to hyperventilation. This patient’s pCO2 is doubled. * **Excessive Renal Bicarbonate Loss:** This mechanism leads to metabolic acidosis (e.g., Renal Tubular Acidosis). In this case, the kidneys are actually *retaining* bicarbonate to compensate for the high CO2. **High-Yield Clinical Pearls for NEET-PG:** * **The 1-2-3-4 Rule for Compensation:** * **Acute Resp. Acidosis:** HCO3 increases by **1** for every 10 mmHg rise in pCO2. * **Chronic Resp. Acidosis:** HCO3 increases by **3.5 to 4** for every 10 mmHg rise in pCO2. * In this case, pCO2 rose by 40 units. If acute, HCO3 should be ~28; if chronic, ~40. At 33 mEq/L, this patient is in a state of partially compensated respiratory acidosis. * **Common Causes:** COPD, Opioid overdose, Guillain-Barré syndrome, and Obstructive Sleep Apnea.

Q: What is the most abundant extracellular buffer in the human body?

Bicarbonate. **Explanation:** The acid-base balance of the body is maintained by various buffer systems. The **Bicarbonate buffer system ($HCO_3^– / CO_2$)** is the most abundant and important buffer in the **extracellular fluid (ECF)**. Its primary strength lies in the fact that it is an "open system": the concentration of $HCO_3^–$ is regulated by the kidneys, while $CO_2$ levels are controlled by the lungs (respiration). This allows the body to rapidly compensate for pH changes. **Analysis of Options:** * **A. Haemoglobin:** This is a potent buffer, but it is located exclusively **intracellularly** (within Red Blood Cells). It is crucial for buffering $H^+$ ions generated during $CO_2$ transport (Bohr effect). * **B. Plasma Proteins:** These act as extracellular buffers due to their amino acid side chains, but their concentration and buffering capacity are significantly lower than the bicarbonate system. * **D. Phosphate:** The phosphate buffer system is highly efficient due to its pKa (6.8) being close to physiological pH. However, it is the **most abundant intracellular buffer** and is also vital in renal tubular fluid. Its concentration in the ECF is too low to be the primary buffer there. **High-Yield Clinical Pearls for NEET-PG:** * **Henderson-Hasselbalch Equation:** $pH = pKa + \log ([HCO_3^-] / [0.03 \times PCO_2])$. * **First line of defense:** Chemical buffers (seconds). * **Second line:** Respiratory system (minutes). * **Third line:** Renal system (hours to days; most powerful). * **Isohydric Principle:** All buffer systems in a common solution are in equilibrium; a change in one affects all others.

Q: Which of the following conditions is associated with normal anion gap metabolic acidosis?

Hyperchloremic acidosis. **Explanation:** Metabolic acidosis is categorized based on the **Anion Gap (AG)**, calculated as $[Na^+] - ([Cl^-] + [HCO_3^-])$. A normal anion gap is typically 8–12 mEq/L. **Why the correct answer is right:** **Hyperchloremic acidosis** is the hallmark of **Normal Anion Gap Metabolic Acidosis (NAGMA)**. In this condition, the loss of bicarbonate ($HCO_3^-$) from the body (via the GI tract or kidneys) is compensated by a proportional increase in serum chloride ($Cl^-$) to maintain electroneutrality. Since the sum of chloride and bicarbonate remains constant, the calculated anion gap does not change. Common causes include diarrhea and Renal Tubular Acidosis (RTA). **Why the incorrect options are wrong:** * **Lactic acidosis (A), Ketoacidosis (B), and Methanol poisoning (C)** are all causes of **High Anion Gap Metabolic Acidosis (HAGMA)**. * In these conditions, metabolic acidosis occurs due to the accumulation of "unmeasured" organic acids (lactate, acetoacetate, or formic acid). As these acids dissociate, the $H^+$ ions consume $HCO_3^-$, but the remaining acid anions are not chloride. This increases the gap between measured cations and anions. **High-Yield NEET-PG Pearls:** * **Mnemonic for NAGMA (USED CARP):** **U**reterosigmoidostomy, **S**aline infusion (large volume), **E**ndocrine (Addison’s), **D**iarrhea, **C**arbonic anhydrase inhibitors (Acetazolamide), **A**mmonium chloride, **R**enal tubular acidosis, **P**ancreatic fistula. * **Mnemonic for HAGMA (MUDPILES):** **M**ethanol, **U**remia, **D**KA, **P**araldehyde, **I**NH/Iron, **L**actic acidosis, **E**thylene glycol, **S**alicylates. * **Gold Standard:** Diarrhea is the most common cause of NAGMA worldwide.

Q: What is the primary determinant of the anion gap?

Proteins. **Explanation:** The **Anion Gap (AG)** represents the difference between measured cations (Sodium) and measured anions (Chloride and Bicarbonate). It reflects the concentration of **unmeasured anions** in the plasma. **Why Proteins are the correct answer:** The formula for the anion gap is: $AG = [Na^+] - ([Cl^-] + [HCO_3^-])$. In a healthy individual, the normal range is 8–12 mEq/L. **Albumin**, a plasma protein, carries a significant negative charge at physiological pH. It accounts for approximately **75-80%** of the normal anion gap. Therefore, proteins are the primary determinant. In clinical practice, if a patient has hypoalbuminemia, the "normal" anion gap must be adjusted downward (decreased by ~2.5 mEq/L for every 1 g/dL drop in albumin). **Analysis of Incorrect Options:** * **B & C (Sulphates and Phosphates):** While these are indeed "unmeasured anions" that contribute to the anion gap, their concentrations in the blood are significantly lower than that of plasma proteins under normal physiological conditions. They only rise significantly in conditions like renal failure. * **D (Nitrates):** Nitrates are not present in the blood in concentrations high enough to significantly influence the anion gap calculation. **High-Yield Clinical Pearls for NEET-PG:** * **MUDPILES:** The classic mnemonic for High Anion Gap Metabolic Acidosis (HAGMA) includes Methanol, Uremia, DKA, Propylene glycol, Iron/INH, Lactic acidosis, Ethylene glycol, and Salicylates. * **Albumin Correction:** Adjusted $AG = \text{Observed } AG + 2.5 \times (4.5 - \text{Measured Albumin})$. * **Goldmark:** A newer mnemonic for HAGMA (Glycols, Oxoproline, L-Lactate, D-Lactate, Methanol, Aspirin, Renal failure, Ketoacidosis).

Q: Why is tetany seen with hyperventilation?

Respiratory alkalosis. ### Explanation **Why Respiratory Alkalosis is the Correct Answer:** Hyperventilation causes excessive "washout" of carbon dioxide ($CO_2$) from the lungs. According to the Henderson-Hasselbalch equation, a decrease in partial pressure of arterial $CO_2$ ($PaCO_2$) leads to an increase in blood pH, resulting in **Respiratory Alkalosis**. The development of **tetany** in this state is due to changes in ionized calcium levels. In an alkalotic state, there is a decrease in hydrogen ions ($H^+$). This causes plasma proteins (primarily albumin) to release $H^+$ ions to buffer the pH. To maintain electrical neutrality, **calcium ions ($Ca^{2+}$) bind to the newly vacant sites on albumin**. This reduces the concentration of **ionized (free) calcium** in the plasma, even though total serum calcium remains normal. Low ionized calcium increases neuronal permeability to sodium ions, leading to progressive depolarization and hyperexcitability of peripheral nerves, manifesting as tetany (e.g., carpopedal spasm). **Analysis of Incorrect Options:** * **Metabolic Alkalosis (A):** While this also causes decreased ionized calcium and tetany, it is caused by primary bicarbonate gain or $H^+$ loss (e.g., vomiting), not by hyperventilation. * **Metabolic Acidosis (C) & Respiratory Acidosis (D):** Acidosis increases ionized calcium levels because $H^+$ ions compete with calcium for albumin binding sites. Therefore, acidosis is protective against tetany. **High-Yield Clinical Pearls for NEET-PG:** * **Trousseau’s Sign:** Induction of carpopedal spasm by inflating a BP cuff above systolic pressure (more sensitive than Chvostek's). * **Chvostek’s Sign:** Tapping the facial nerve leads to twitching of facial muscles. * **Management:** For hyperventilation-induced tetany, breathing into a paper bag helps by rebreathing $CO_2$, which corrects the alkalosis and restores ionized calcium levels.

Q: A 75-year-old woman was recently started on furosemide to treat pedal edema. She describes a loss of energy and a light-headed sensation when arising from a seated position. Her arterial blood gases indicate pH of 7.53, PaCO2 of 52 mmHg, and HCO3- of 32 mEq/L. Serum chemistries show the following levels: Na = 129 mEq/L, Cl- = 90 mEq/L, K = 3.0 mEq/L, Glucose = 120 mg/dL. These findings are suggestive of what acid-base disturbance?

Metabolic alkalosis. ### Explanation **1. Why Metabolic Alkalosis is Correct:** The patient’s arterial blood gas (ABG) shows a **pH of 7.53**, indicating **alkalemia** (pH > 7.45). The primary driver is the elevated **bicarbonate (HCO₃⁻ = 32 mEq/L)**, which defines **metabolic alkalosis**. The PaCO₂ is elevated (52 mmHg) as a compensatory respiratory response to retain acid (CO₂) and bring the pH back toward normal. The clinical trigger here is **Furosemide (a loop diuretic)**. Diuretics cause metabolic alkalosis through three mechanisms: * **Contraction Alkalosis:** Loss of ECF volume (fluid) while the total body bicarbonate remains the same, "concentrating" the HCO₃⁻. * **Hypochloremia:** Loss of Cl⁻ in urine leads to increased HCO₃⁻ reabsorption in the distal tubule. * **Hypokalemia (3.0 mEq/L):** K⁺ shifts out of cells in exchange for H⁺ shifting into cells, raising extracellular pH. **2. Why the Other Options are Incorrect:** * **Metabolic Acidosis:** This would present with a low pH ( 7.45) but with a primary *decrease* in PaCO₂ (usually due to hyperventilation). **3. High-Yield Clinical Pearls for NEET-PG:** * **Diuretic Triad:** Loop and Thiazide diuretics typically cause **Hypokalemic, Hypochloremic, Metabolic Alkalosis**. * **Compensation Rule:** In metabolic alkalosis, for every 1 mEq/L rise in HCO₃⁻, the PaCO₂ should rise by approximately **0.7 mmHg**. * **Orthostatic Hypotension:** The "light-headed sensation when arising" indicates volume depletion (contraction), a common side effect of furosemide. * **Saline Responsiveness:** Most diuretic-induced alkalosis is "Saline Responsive" (Urinary Cl⁻ < 10–20 mEq/L).

Question 1

What is the commonest cause of metabolic alkalosis?

Accepted Answer

Pyloric stenosis

Answer

Cancer of the stomach

Answer

Small-bowel obstruction

Answer

Diuretics

Question 2

Metabolic alkalosis is seen in all of the following conditions except?

Accepted Answer

Ureterosigmoidostomy

Answer

Thiazide diuretic therapy

Answer

Prolonged vomiting

Answer

Cushing's disease

Question 3

A patient has a pCO2 of 80 mm Hg and plasma bicarbonate of 33 mEq/L. What is the acid-base disorder?

Accepted Answer

Respiratory acidosis

Answer

Metabolic acidosis

Answer

Respiratory alkalosis

Answer

Excessive renal bicarbonate loss

Question 4

What is the most abundant extracellular buffer in the human body?

Accepted Answer

Bicarbonate

Answer

Haemoglobin

Answer

Plasma proteins

Answer

Phosphate

Question 5

Which of the following conditions is associated with normal anion gap metabolic acidosis?

Accepted Answer

Hyperchloremic acidosis

Answer

Lactic acidosis

Answer

Ketoacidosis

Answer

Methanol poisoning

Question 6

What is the important role of the distal tubule of the kidney in acid-base balance?

Accepted Answer

Secretion of Ammonia

Answer

Secretion of bicarbonate

Answer

Secretion of HCl

Answer

Absorption of Ammonia

Question 7

What is the primary determinant of the anion gap?

Accepted Answer

Proteins

Answer

Sulphates

Answer

Phosphates

Answer

Nitrates

Question 8

Uncompensated metabolic acidosis shows what pattern of pH and bicarbonate levels?

Accepted Answer

Decreased pH with decreased HCO3-

Answer

Increased pH with increased HCO3-

Answer

Increased pH with decreased HCO3-

Answer

Decreased pH with increased HCO3-

Question 9

Why is tetany seen with hyperventilation?

Accepted Answer

Respiratory alkalosis

Answer

Metabolic alkalosis

Answer

Metabolic acidosis

Answer

Respiratory acidosis

Question 10

A 75-year-old woman was recently started on furosemide to treat pedal edema. She describes a loss of energy and a light-headed sensation when arising from a seated position. Her arterial blood gases indicate pH of 7.53, PaCO2 of 52 mmHg, and HCO3- of 32 mEq/L. Serum chemistries show the following levels: Na = 129 mEq/L, Cl- = 90 mEq/L, K = 3.0 mEq/L, Glucose = 120 mg/dL. These findings are suggestive of what acid-base disturbance?

Accepted Answer

Metabolic alkalosis

Answer

Metabolic acidosis

Answer

Respiratory acidosis

Answer

Respiratory alkalosis

Acid-Base Balance — MCQs

Acid-Base Balance — MCQs

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