Acid-Base Balance — MCQs

Acid-Base Balance Indian Medical PG Practice Questions and MCQs

Question 101: Which of the following can cause metabolic alkalosis?

A. Furosemide (Correct Answer)
B. Addison's disease
C. Hyperkalemia
D. Hyponatremia

Explanation: **Explanation:** **Correct Answer: A. Furosemide** Furosemide is a loop diuretic that inhibits the $Na^+-K^+-2Cl^-$ symporter in the thick ascending limb of Henle. It causes metabolic alkalosis through three primary mechanisms: 1. **Contraction Alkalosis:** Loss of isotonic fluid (sodium and water) leads to extracellular fluid volume depletion, concentrating the existing bicarbonate. 2. **Increased Distal Delivery:** Increased $Na^+$ delivery to the distal tubule stimulates $Na^+$ reabsorption in exchange for $H^+$ and $K^+$ ions (via aldosterone activation), leading to net acid loss. 3. **Hypokalemia:** Diuretic-induced potassium loss causes a transcellular shift where $K^+$ moves out of cells and $H^+$ moves in, further raising extracellular pH. **Why the other options are incorrect:** * **B. Addison’s Disease:** This is primary adrenal insufficiency (low aldosterone). Aldosterone deficiency leads to decreased $H^+$ secretion in the distal tubule, resulting in **Normal Anion Gap Metabolic Acidosis**, not alkalosis. * **C. Hyperkalemia:** High serum potassium causes $K^+$ to enter cells in exchange for $H^+$ moving into the extracellular fluid. This intracellular buffering results in **Metabolic Acidosis**. * **D. Hyponatremia:** While often associated with various acid-base disturbances, hyponatremia itself is an electrolyte imbalance and not a direct cause of metabolic alkalosis. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Metabolic Alkalosis:** "CLEVER" (Contraction, Licorice, Endocrine [Conn’s/Cushing’s], Vomiting, Excess Alkali, Renal [Bartter/Gitelman/Diuretics]). * **Chloride Status:** Diuretic-induced alkalosis is typically **Saline-Responsive** (Urinary $Cl^-$ < 20 mEq/L). * **Bartter vs. Gitelman:** Bartter syndrome mimics Loop diuretics (Furosemide), while Gitelman syndrome mimics Thiazide diuretics; both present with metabolic alkalosis.

Question 102: All are useful for the treatment of metabolic alkalosis except?

A. Sodium chloride
B. Potassium chloride
C. Hydrochloric acid
D. Ammonium hydroxide (Correct Answer)

Explanation: **Explanation:** Metabolic alkalosis is characterized by an increase in plasma bicarbonate ($HCO_3^-$) and a rise in arterial pH. Treatment focuses on reversing the underlying cause and providing chloride ions to facilitate bicarbonate excretion. **Why Ammonium Hydroxide is the Correct Answer:** Ammonium hydroxide ($NH_4OH$) is a **strong base**. Administering a base to a patient already in a state of alkalosis would worsen the condition by further increasing the pH. In contrast, **Ammonium Chloride** ($NH_4Cl$) is used to treat severe metabolic alkalosis because the liver converts it into urea and **Hydrochloric acid (HCl)**, which provides the necessary $H^+$ ions to neutralize excess bicarbonate. **Analysis of Incorrect Options:** * **Sodium Chloride (NaCl):** Most cases of metabolic alkalosis are "chloride-responsive" (e.g., due to vomiting or NG suction). Saline restores ECF volume and provides $Cl^-$, allowing the kidneys to excrete $HCO_3^-$. * **Potassium Chloride (KCl):** Alkalosis often causes hypokalemia (due to $H^+/K^+$ exchange). Replacing potassium is crucial because hypokalemia maintains alkalosis by promoting $H^+$ secretion in the distal tubule. * **Hydrochloric Acid (HCl):** In severe, life-threatening alkalosis (pH > 7.55) where saline/potassium replacement is insufficient or contraindicated, dilute HCl can be infused via a central line to directly lower the pH. **High-Yield Clinical Pearls for NEET-PG:** * **Chloride-Responsive Alkalosis:** Urinary $Cl^-$ < 10 mmol/L (e.g., vomiting, diuretics). Responds to NaCl. * **Chloride-Resistant Alkalosis:** Urinary $Cl^-$ > 20 mmol/L (e.g., Conn’s syndrome, Cushing’s). Does not respond to NaCl; requires treating the mineralocorticoid excess. * **Acetazolamide:** A carbonic anhydrase inhibitor that can be used to treat metabolic alkalosis by inducing bicarbonate diuresis.

Question 103: Aerial blood gases obtained while the patient is receiving oxygen reveal the following values: pH 7.30; PCO2 39; bicarbonate 18 mEq/L; oxygen saturation 85%. What is the acid-base status of the patient?

A. Respiratory acidosis
B. Combined metabolic and respiratory acidosis
C. Metabolic acidosis (Correct Answer)
D. Compensated metabolic acidosis

Explanation: ### Explanation To solve acid-base problems, follow a systematic three-step approach: **1. Analyze the pH:** The normal pH range is 7.35–7.45. A pH of **7.30** indicates **acidemia**. **2. Identify the Primary Process:** * **Metabolic:** Look at Bicarbonate ($HCO_3^-$). Normal is 22–26 mEq/L. Here, it is **18 mEq/L (Low)**. Low bicarbonate matches the acidic pH. * **Respiratory:** Look at $PCO_2$. Normal is 35–45 mmHg. Here, it is **39 mmHg (Normal)**. Since the $HCO_3^-$ is the parameter deviating in the direction of the pH, the primary diagnosis is **Metabolic Acidosis**. **3. Evaluate Compensation:** In metabolic acidosis, the body compensates by hyperventilating to lower $PCO_2$ (Winters' Formula). Here, the $PCO_2$ is 39 mmHg (within the normal range), meaning respiratory compensation has not yet occurred or is insufficient. Therefore, it is uncompensated metabolic acidosis. --- ### Why the other options are incorrect: * **Option A (Respiratory Acidosis):** This would require a high $PCO_2$ (>45 mmHg) and a low pH. * **Option B (Combined Acidosis):** This would require both a low $HCO_3^-$ and a high $PCO_2$. Here, the $PCO_2$ is normal. * **Option D (Compensated Metabolic Acidosis):** For "compensation" to be the label, the pH must return toward the normal range (7.35–7.45), and the $PCO_2$ must be significantly lower than 40 mmHg. --- ### NEET-PG High-Yield Pearls: * **Winters’ Formula:** Expected $PCO_2 = (1.5 \times HCO_3^-) + 8 \pm 2$. If the measured $PCO_2$ is higher than expected, a concurrent respiratory acidosis exists. * **Anion Gap (AG):** Always calculate AG in metabolic acidosis ($Na^+ - [Cl^- + HCO_3^-]$). Normal is 12 ± 2. * **Golden Rule:** The lungs compensate for metabolic issues quickly (minutes to hours), while the kidneys compensate for respiratory issues slowly (2–3 days).

Question 104: Hyperventilation may lead to which of the following?

A. Tetany (Correct Answer)
B. Respiratory alkalosis
C. Metabolic acidosis
D. Metabolic alkalosis

Explanation: **Explanation:** The correct answer is **Tetany**. **Mechanism:** Hyperventilation causes excessive "washout" of Carbon Dioxide ($CO_2$), leading to **Respiratory Alkalosis**. In an alkaline state (high pH), there is a decrease in the concentration of free hydrogen ions ($H^+$). This causes more $H^+$ ions to dissociate from plasma proteins (like albumin) to buffer the pH. Consequently, more binding sites on albumin become available for **Calcium ($Ca^{2+}$)**. As more ionized calcium binds to albumin, the level of **ionized (free) calcium** in the blood decreases (**Hypocalcemia**), even though total body calcium remains normal. Low ionized calcium increases the permeability of neuronal membranes to sodium ions, leading to progressive depolarization and neuromuscular irritability, which manifests as **Tetany** (carpopedal spasm). **Analysis of Incorrect Options:** * **B. Respiratory Alkalosis:** While hyperventilation *causes* respiratory alkalosis, the question asks what it *leads to* (the clinical manifestation). In NEET-PG, if both the physiological state and the clinical sign are present, the clinical consequence (Tetany) is often the preferred answer for "leads to." * **C & D. Metabolic Acidosis/Alkalosis:** These are primary metabolic disturbances involving bicarbonate ($HCO_3^-$) levels, not primarily driven by ventilation changes. **High-Yield Clinical Pearls:** * **Chvostek’s sign** (facial twitching) and **Trousseau’s sign** (carpal spasm with BP cuff) are classic indicators of hypocalcemic tetany. * **Management:** Breathing into a paper bag helps the patient re-breathe $CO_2$, reversing the alkalosis and restoring ionized calcium levels. * **Rule of thumb:** Alkalosis = Hypocalcemia (symptoms); Acidosis = Hypercalcemia (protective against tetany).

Question 105: Interpret the following ABG values: PaCO2-40 mmHg, HCO3-55 mEq/L, and pH-7.7?

A. Uncompensated metabolic alkalosis (Correct Answer)
B. Mixed respiratory and metabolic acidosis
C. Combined respiratory and metabolic acidosis
D. Compensated respiratory acidosis

Explanation: To interpret any ABG, follow a systematic three-step approach: **1. Analyze the pH:** The normal pH range is 7.35–7.45. A pH of **7.7** indicates a profound **alkalemia**. **2. Identify the Primary Cause:** * The **HCO₃⁻ is 55 mEq/L** (Normal: 22–26 mEq/L). An elevated bicarbonate level is consistent with metabolic alkalosis. * The **PaCO₂ is 40 mmHg** (Normal: 35–45 mmHg). Since the PaCO₂ is within the normal range, there is no respiratory contribution to the alkalemia. **3. Determine Compensation:** In metabolic alkalosis, the body should compensate by hypoventilating to retain CO₂ (increasing PaCO₂). Since the PaCO₂ remains at a perfect 40 mmHg despite a high pH, **no compensation** has occurred yet. Therefore, the diagnosis is **Uncompensated Metabolic Alkalosis.** **Analysis of Incorrect Options:** * **B & C (Acidosis):** These are incorrect because the pH (7.7) is alkaline, not acidic. * **D (Compensated Respiratory Acidosis):** In respiratory acidosis, the primary change is an *increase* in PaCO₂ (>45 mmHg) with a *low* pH (<7.35). Compensation would involve the kidneys retaining HCO₃⁻ to bring the pH back toward normal. Here, the pH is high and PaCO₂ is normal. **High-Yield Clinical Pearls for NEET-PG:** * **The "Rule of Thumb":** For every 1 mEq/L rise in HCO₃⁻, the PaCO₂ should rise by approximately **0.7 mmHg**. * **Common Causes:** Vomiting (loss of HCl), nasogastric suction, and diuretic use (contraction alkalosis). * **Limits of Compensation:** Respiratory compensation for metabolic alkalosis is limited because hypoxia (due to hypoventilation) eventually triggers the drive to breathe, rarely allowing PaCO₂ to rise above 55 mmHg.

Question 106: In chronic respiratory alkalosis, HCO3- falls by how many mmol/L for every 10 mm Hg decrease in PCO2?

A. 1
B. 2
C. 3
D. 4 (Correct Answer)

Explanation: ### Explanation **1. Understanding the Concept** In respiratory alkalosis, the primary disturbance is a decrease in $PCO_2$ (hypocapnia). To maintain a normal pH, the body compensates by decreasing the concentration of $HCO_3^-$ through renal excretion. The degree of compensation differs significantly between acute and chronic stages: * **Acute Phase:** Compensation relies on immediate chemical buffering (minimal). * **Chronic Phase (2–5 days):** Compensation relies on the kidneys decreasing $H^+$ secretion and $HCO_3^-$ reabsorption. This is much more effective. For every **10 mmHg decrease in $PCO_2$**, the $HCO_3^-$ levels drop by: * **Acute:** 2 mmol/L * **Chronic:** 4 mmol/L (The "Rule of 2 and 4") **2. Analysis of Options** * **Option A (1):** Incorrect. This value is not part of the standard compensation rules for respiratory alkalosis. * **Option B (2):** Incorrect. This represents the $HCO_3^-$ drop in **acute** respiratory alkalosis. * **Option C (3):** Incorrect. While some texts suggest a range (3–5), the standard "High-Yield" rule for exams is 4 mmol/L. * **Option D (4):** **Correct.** This is the established physiological compensation rate for chronic respiratory alkalosis. **3. High-Yield Clinical Pearls for NEET-PG** * **The 1-2-4-5 Rule (for every 10 mmHg change in $PCO_2$):** * **Acute Resp. Acidosis:** $HCO_3^-$ increases by **1** * **Chronic Resp. Acidosis:** $HCO_3^-$ increases by **3.5 to 4** (often simplified to **4**) * **Acute Resp. Alkalosis:** $HCO_3^-$ decreases by **2** * **Chronic Resp. Alkalosis:** $HCO_3^-$ decreases by **4 to 5** (standard answer is **4**) * **Common Cause:** High altitude (chronic) or hyperventilation/anxiety (acute). * **Limit of Compensation:** In chronic respiratory alkalosis, $HCO_3^-$ can drop to as low as 12–15 mmol/L.

Question 107: In renal failure, metabolic acidosis is primarily due to which of the following mechanisms?

A. Increased hydrogen ion production
B. Loss of bicarbonate
C. Decreased ammonia synthesis (Correct Answer)
D. Use of diuretics

Explanation: **Explanation:** In chronic renal failure (CRF), the primary mechanism leading to metabolic acidosis is the **impairment of ammoniagenesis**. **1. Why "Decreased ammonia synthesis" is correct:** The kidneys maintain acid-base balance by excreting $H^+$ ions, primarily buffered by ammonia ($NH_3$) to form ammonium ($NH_4^+$). In renal failure, there is a progressive loss of functioning nephrons. While the remaining nephrons increase their individual workload, the total renal mass becomes insufficient to produce enough ammonia. This leads to a failure in excreting the daily metabolic acid load, resulting in a **Normal Anion Gap Metabolic Acidosis (NAGMA)** in early stages, which progresses to a **High Anion Gap Metabolic Acidosis (HAGMA)** as phosphate and sulfate excretion also fails. **2. Why other options are incorrect:** * **A. Increased hydrogen ion production:** This occurs in conditions like Diabetic Ketoacidosis (DKA) or Lactic Acidosis, not primarily in renal failure. In renal failure, the problem is **excretion**, not production. * **B. Loss of bicarbonate:** This is the hallmark of Proximal Renal Tubular Acidosis (Type 2 RTA) or diarrhea. While some bicarbonate wasting can occur in CRF, it is not the primary driver. * **C. Use of diuretics:** Most diuretics (like Loop or Thiazides) actually cause **metabolic alkalosis** due to contraction alkalosis and increased $H^+$ secretion. Acetazolamide is an exception but is not the mechanism for acidosis *in* renal failure. **High-Yield Clinical Pearls for NEET-PG:** * **The "Trade-off" Hypothesis:** In early CKD, $NH_4^+$ excretion per functioning nephron actually increases, but the absolute total excretion decreases. * **Anion Gap Transition:** Acidosis in renal failure starts as NAGMA (due to low $NH_3$) and converts to HAGMA when the GFR drops below **15-20 mL/min** (due to retention of unmeasured anions like phosphates/sulfates). * **Type 4 RTA:** Often associated with early diabetic nephropathy, characterized by hyperkalemia and decreased ammonia production.

Question 108: Which of the following neurons inhibits the deep cerebellar nuclei?

A. Golgi cells
B. Purkinje cells (Correct Answer)
C. Stellate cells
D. Basket cells

Explanation: **Explanation:** The cerebellum operates through a complex circuit of excitatory and inhibitory inputs. The **Purkinje cells** are the functional centerpiece of this circuit and represent the **sole output** from the cerebellar cortex. 1. **Why Purkinje cells are correct:** Purkinje cells receive excitatory inputs from climbing and mossy fibers. However, their own axons project downwards to the **Deep Cerebellar Nuclei (DCN)**—such as the dentate, emboliform, globose, and fastigial nuclei—where they release **GABA (Gamma-Aminobutyric Acid)**. This makes them the primary inhibitory influence on the DCN, modulating the final motor output of the cerebellum. 2. **Why other options are incorrect:** * **Golgi cells (A):** These are inhibitory interneurons located in the granular layer. They inhibit **Granule cells**, not the deep nuclei. * **Stellate cells (C) and Basket cells (D):** These are inhibitory interneurons located in the molecular layer. They provide lateral inhibition to the **Purkinje cells** themselves (feed-forward inhibition) to sharpen the signal, but they do not project to the DCN. **High-Yield Clinical Pearls for NEET-PG:** * **All cells** in the cerebellar cortex are **inhibitory (GABAergic)** except for the **Granule cells**, which are excitatory (Glutamatergic). * **Afferent inputs:** Mossy fibers (from various sources) and Climbing fibers (exclusively from the Inferior Olivary Nucleus) are both excitatory. * **Clinical Correlation:** Damage to Purkinje cells or the DCN leads to ipsilateral cerebellar signs, such as hypotonia, ataxia, and intention tremors.

Question 109: A 19-year-old girl develops sudden-onset non-bloody diarrhea. She was previously well, is not taking any medications, and has not traveled recently. Her abdomen is soft and non-tender on examination, and the anion gap is normal. For this patient, what is the most likely acid-base disorder?

A. Metabolic acidosis (Correct Answer)
B. Metabolic alkalosis
C. Respiratory acidosis
D. Respiratory alkalosis

Explanation: ### Explanation **Correct Option: A. Metabolic Acidosis** The primary mechanism behind acid-base disturbances in diarrhea is the **loss of bicarbonate (HCO₃⁻)**. Intestinal secretions below the stomach (pancreatic, biliary, and intestinal fluids) are rich in bicarbonate. When a patient has significant diarrhea, this bicarbonate is lost from the body, leading to a decrease in serum pH. Furthermore, the question specifies a **Normal Anion Gap (NAGMA)**. In diarrhea, as bicarbonate is lost, the kidneys retain Chloride (Cl⁻) to maintain electroneutrality. This results in a **Hyperchloremic Metabolic Acidosis**, which is the classic presentation of GI-related base loss. **Why Incorrect Options are Wrong:** * **B. Metabolic Alkalosis:** This occurs with the loss of acid (H⁺), typically seen in **persistent vomiting** or nasogastric suction, where gastric HCl is lost. * **C. Respiratory Acidosis:** This is caused by alveolar hypoventilation (e.g., COPD, opioid overdose) leading to CO₂ retention, not GI losses. * **D. Respiratory Alkalosis:** This results from hyperventilation (e.g., anxiety, high altitude) leading to excessive CO₂ washout. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for NAGMA (USED CARP):** **U**reterosigmoidostomy, **S**aline infusion, **E**ndocrine (Addison’s), **D**iarrhea, **C**arbonic anhydrase inhibitors, **A**mmonium chloride, **R**enal tubular acidosis (RTA), **P**ancreatic fistula. * **Anion Gap Calculation:** $Na^+ - (Cl^- + HCO_3^-)$. Normal range is 8–12 mEq/L. * **Vomiting vs. Diarrhea:** Vomiting = Metabolic Alkalosis (Loss of H⁺); Diarrhea = Metabolic Acidosis (Loss of HCO₃⁻).

Question 110: All of the following are seen in persistent vomiting EXCEPT?

A. Hypokalemia
B. Decreased K+ in urine (Correct Answer)
C. Elevated pH of blood
D. Metabolic alkalosis

Explanation: **Explanation:** Persistent vomiting leads to a complex acid-base and electrolyte disturbance known as **Metabolic Alkalosis**. **Why "Decreased K+ in urine" is the correct answer (The Exception):** In persistent vomiting, despite the body being in a state of total body potassium depletion (hypokalemia), there is actually **increased K+ excretion in the urine** (Paradoxical Kaliuresis). This occurs due to two main reasons: 1. **Secondary Hyperaldosteronism:** Loss of fluid and Cl- in vomitus leads to volume depletion, activating the Renin-Angiotensin-Aldosterone System (RAAS). Aldosterone acts on the distal tubule to reabsorb Na+ at the expense of secreting K+ into the urine. 2. **Bicarbonaturia:** The high blood pH leads to increased filtration of HCO3-. To maintain electrical neutrality, the kidney excretes K+ along with the negatively charged bicarbonate. **Why the other options are incorrect:** * **Elevated pH & Metabolic Alkalosis:** Loss of gastric HCl (H+ ions) directly increases blood pH, leading to primary metabolic alkalosis. * **Hypokalemia:** Potassium is lost directly in the gastric juice and, more significantly, through the kidneys due to the RAAS activation mentioned above. **High-Yield Clinical Pearls for NEET-PG:** * **Paradoxical Aciduria:** In severe cases, the kidney prioritizes Na+ reabsorption over H+ excretion to maintain volume. This results in acidic urine despite systemic alkalosis. * **The "Classic" Picture:** Metabolic alkalosis, Hypochloremia, Hypokalemia, and Paradoxical Aciduria. * **Treatment:** The mainstay of treatment is **Normal Saline (0.9% NaCl)** to restore volume and chloride levels, which shuts down the RAAS drive.

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Acid-Base Chemistry

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Respiratory Regulation of Acid-Base Balance

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Renal Regulation of Acid-Base Balance

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Bicarbonate Buffer System

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Non-Bicarbonate Buffer Systems

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Respiratory Acidosis and Alkalosis

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Metabolic Acidosis and Alkalosis

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Mixed Acid-Base Disorders

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Compensatory Mechanisms

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Clinical Assessment of Acid-Base Status

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