Acid-Base and Electrolyte Disturbances — MCQs

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Acid-Base and Electrolyte Disturbances — MCQs

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Which electrolyte imbalance causes prolonged QT interval?

What is the most common cause of normal anion gap metabolic acidosis?

Which of the following is NOT a cause of hypokalemia?

A patient presents with metabolic acidosis and increased anion gap. Which is most consistent with this presentation?

Best immediate management of hyperkalemia includes all except?

A patient presents with the following arterial blood gas (ABG) and electrolyte values: pH: 7.34, Na: 135 mEq/L, Cl: 93 mEq/L, HCO3: 20 mEq/L, Random Blood Sugar (RBS): 420 mg/dl. What is the most likely acid-base disturbance?

The lab reports of a patient given below: pH = 7.2, HCO3 = 10 mEq/L, PCO2 = 30 mmHg. This exemplifies which of the following disorders?

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?

Treatment of choice in severe dehydration is:

Q10

Which electrolyte abnormality is expected in tumor lysis syndrome?

Acid-Base and Electrolyte Disturbances Indian Medical PG Practice Questions and MCQs

Question 1: Which electrolyte imbalance causes prolonged QT interval?

A. Hypernatremia
B. Hyperkalemia
C. Hypocalcemia (Correct Answer)
D. Hyponatremia

Explanation: ***Hypocalcemia*** - **Hypocalcemia** prolongs the **repolarization phase** of the action potential in cardiac myocytes, leading to a lengthened **QT interval** on an electrocardiogram. - This increased duration of repolarization places the heart at higher risk for **Torsades de Pointes** and other life-threatening arrhythmias [2], [3]. *Hypernatremia* - **Hypernatremia** primarily affects neurological function and can cause symptoms like **confusion** and **seizures**. - It does not typically lead to a **prolonged QT interval**; instead, it can sometimes be associated with a shortened QT interval or other non-specific ECG changes. *Hyperkalemia* - **Hyperkalemia** primarily causes peaked T waves, a widened QRS complex, and eventually **bradycardia** and **asystole** [1]. - While it drastically alters cardiac conduction, it typically **shortens** rather than prolongs the QT interval. *Hyponatremia* - **Hyponatremia** is associated with cerebral edema and neurological symptoms such as **headaches**, **nausea**, and **altered mental status**. - It generally does not cause a **prolonged QT interval**; significant hyponatremia can sometimes be associated with non-specific ECG changes [1] but not a specific lengthening of the QT interval.

Question 2: 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 3: Which of the following is NOT a cause of hypokalemia?

A. Tamoxifen therapy (Correct Answer)
B. ACTH producing tumors
C. Diabetic ketoacidosis
D. Non-bilious vomiting

Explanation: ***Tamoxifen therapy*** - **Tamoxifen**, an estrogen receptor modulator, can cause electrolyte imbalances, but **hypokalemia is not a typical side effect**. - It is more commonly associated with an increased risk of **thromboembolic events** and **endometrial cancer**. *ACTH producing tumors* - **ACTH-producing tumors** lead to increased cortisol production (**Cushing's syndrome**), which can cause **mineralocorticoid effects** [1]. - This results in increased renal potassium excretion, leading to **hypokalemia** [1]. *Diabetic ketoacidosis* - In **diabetic ketoacidosis (DKA)**, potassium shifts from the intracellular to the extracellular space due to **acidosis** and **insulin deficiency**. - Despite elevated serum potassium initially, patients often have significant **total body potassium depletion** and are at risk for **severe hypokalemia** upon insulin and fluid administration. *Non-bilious vomiting* - **Non-bilious vomiting** leads to the loss of **gastric acid (HCl)** [1]. - This causes **metabolic alkalosis**, which promotes potassium shift into cells and increased renal excretion of potassium to conserve hydrogen ions, leading to **hypokalemia** [1].

Question 4: A patient presents with metabolic acidosis and increased anion gap. Which is most consistent with this presentation?

A. Renal tubular acidosis
B. Lactic acidosis (Correct Answer)
C. Hyperaldosteronism
D. Diarrhea

Explanation: ***Lactic acidosis*** - **Lactic acidosis** is a common cause of **high anion gap metabolic acidosis**, resulting from increased lactate production or decreased lactate clearance [1]. - Conditions like **sepsis**, **shock**, and severe hypoxia can lead to increased anaerobic metabolism and subsequent lactic acid accumulation [1]. *Renal tubular acidosis* - This condition is characterized by **metabolic acidosis** but typically presents with a **normal anion gap** (non-anion gap metabolic acidosis) [1]. - It involves impaired acid excretion or bicarbonate reabsorption by the renal tubules, not an accumulation of unmeasured anions [1]. *Hyperaldosteronism* - **Hyperaldosteronism** typically causes **hypokalemia** and **metabolic alkalosis**, not metabolic acidosis [2]. - Excess aldosterone leads to increased sodium reabsorption and potassium/hydrogen ion excretion [2]. *Diarrhea* - Severe **diarrhea** leads to a loss of bicarbonate from the gastrointestinal tract, causing a **normal anion gap metabolic acidosis** [1]. - It does not involve the accumulation of unmeasured acids that would increase the anion gap.

Question 5: Best immediate management of hyperkalemia includes all except?

A. Salbutamol nebulization
B. Insulin drip
C. Calcium gluconate
D. MgSO4 (Correct Answer)

Explanation: ***MgSO4*** - **Magnesium sulfate** is not used for the immediate management of **hyperkalemia**; its primary uses include treating hypomagnesemia, eclampsia, and certain arrhythmias. - While magnesium can have effects on electrolyte balance, it directly addresses calcium or potassium levels in an acute hyperkalemic crisis. *Calcium gluconate* - **Calcium gluconate** is crucial for **cardiac stabilization** in hyperkalemia by protecting the myocardium from potassium's effects [1]. - It does not lower potassium levels but prevents life-threatening arrhythmias by antagonizing the cardiac membrane effects of potassium [1]. *Insulin drip* - An **insulin drip** (often with dextrose) shifts potassium **intracellularly**, thereby lowering serum potassium levels [1]. - This effect is rapid, making it an effective measure for immediate management. *Salbutamol nebulization* - **Salbutamol (albuterol)** nebulization can also help shift potassium into cells, thus reducing serum potassium levels. - It works by stimulating beta-2 adrenergic receptors, which activate the **Na+/K+-ATPase pump**.

Question 6: A patient presents with the following arterial blood gas (ABG) and electrolyte values: pH: 7.34, Na: 135 mEq/L, Cl: 93 mEq/L, HCO3: 20 mEq/L, Random Blood Sugar (RBS): 420 mg/dl. What is the most likely acid-base disturbance?

A. Normal Anion Gap Metabolic Acidosis (NAGMA)
B. Respiratory Acidosis
C. High Anion Gap Metabolic Acidosis (HAGMA) (Correct Answer)
D. Metabolic Alkalosis

Explanation: ### High Anion Gap Metabolic Acidosis (HAGMA) - The **pH (7.34)** indicates **acidemia**, and the **low bicarbonate (20 mEq/L)** suggests a metabolic acidosis [1], [2]. - Calculation of the anion gap: Na - (Cl + HCO3) = 135 - (93 + 20) = 22 mEq/L. An anion gap > 12 mEq/L is considered high, confirming **High Anion Gap Metabolic Acidosis (HAGMA)** [4]. The **RBS of 420 mg/dl** also points towards a likely cause such as **diabetic ketoacidosis** [3]. *Normal Anion Gap Metabolic Acidosis (NAGMA)* - This would be present if the calculated anion gap were within the normal range (typically 8-12 mEq/L). - Causes of NAGMA (e.g., hyperchloremic acidosis) are typically associated with increased chloride levels to compensate for the bicarbonate loss, which is not the primary finding here [4]. *Respiratory Acidosis* - This condition is characterized by a **low pH** and an **elevated PaCO2**, which is not provided but implied by the **low bicarbonate** not fitting a respiratory picture [2]. - While the pH is low, the primary disturbance given the other values (especially the low bicarbonate) is metabolic, not respiratory. *Metabolic Alkalosis* - Metabolic alkalosis is characterized by an **elevated pH** and an **elevated bicarbonate level**, which contradicts the presented values of low pH and low bicarbonate [2]. - This condition would involve a net gain of bicarbonate or a loss of acids, which is the opposite of the findings in this patient.

Question 7: The lab reports of a patient given below: pH = 7.2, HCO3 = 10 mEq/L, PCO2 = 30 mmHg. This exemplifies which of the following disorders?

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

Explanation: ***Metabolic acidosis*** - The pH of 7.2 is acidic, and the **bicarbonate (HCO3) of 10 mEq/L** is significantly low (normal: 22-28 mEq/L), indicating a primary metabolic disturbance causing acidosis. - The **PCO2 of 30 mmHg** is also low (normal: 35-45 mmHg), which represents **partial respiratory compensation** through hyperventilation to blow off CO2 and raise pH. - This is a classic example of **metabolic acidosis with respiratory compensation**. *Metabolic alkalosis* - This condition would be characterized by a **high pH** and a **high bicarbonate (HCO3)** level, which is the opposite of the given values. - The body would attempt to compensate by increasing PCO2 through hypoventilation. *Respiratory acidosis* - This would present with a **low pH** and a **high PCO2** (>45 mmHg), indicating a primary respiratory problem leading to CO2 retention and acid accumulation. - Metabolic compensation would show elevated HCO3, not the low HCO3 (10 mEq/L) seen here. *Respiratory alkalosis* - This condition is characterized by a **high pH** (>7.45) and a **low PCO2**, due to excessive ventilation causing CO2 elimination. - While PCO2 is low in the given scenario, the pH is acidic (7.2), not alkalotic, ruling out this diagnosis.

Question 8: 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].

Question 9: Treatment of choice in severe dehydration is:

A. Plasma
B. Isolyte P
C. Ringer lactate
D. Normal saline (Correct Answer)

Explanation: ***Normal saline*** - **Normal saline (0.9% sodium chloride)** is an isotonic solution, making it the preferred initial intravenous fluid for rapidly correcting severe dehydration and restoring intravascular volume [1]. - Its **electrolyte composition** closely mimics the body's extracellular fluid, minimizing osmotic shifts and providing effective volume expansion [1]. *Plasma* - **Plasma** is primarily used for expanding blood volume in cases of **hemorrhage** or severe **protein deficiency**, not for simple dehydration. - It carries risks of allergic reactions and disease transmission, making it inappropriate for routine dehydration treatment. *Isolyte P* - **Isolyte P** is a hypotonic solution, typically used for maintenance fluid therapy in children, especially in situations where **sodium restriction** is desirable. - It is not suitable for rapid volume expansion in severe dehydration due to its low sodium content, which could worsen hypotonicity in an already depleted patient. *Ringer lactate* - **Ringer's lactate** is an isotonic crystalloid solution often used for fluid resuscitation, but it contains **lactate**, which is metabolized in the liver to bicarbonate. - While generally safe, in severe shock situations with impaired liver function or lactic acidosis, the metabolism of lactate can be compromised, potentially exacerbating acidosis. **Normal saline** avoids this concern as a first-line agent [2].

Question 10: Which electrolyte abnormality is expected in tumor lysis syndrome?

A. Hypocalcemia
B. Hyponatremia
C. Hypernatremia
D. Hyperkalemia (Correct Answer)

Explanation: ***Hyperkalemia*** - **Tumor lysis syndrome (TLS)** leads to the rapid breakdown of malignant cells, releasing their intracellular contents, including a large amount of **potassium**, into the bloodstream. [1] - This excessive release of intracellular potassium overwhelms renal excretion mechanisms, resulting in **hyperkalemia**, which can cause life-threatening cardiac arrhythmias. [1] *Hypocalcemia* - **Hypocalcemia** does occur in TLS but is not due to direct release from lysed cells. It results from the precipitation of **calcium** with the massive release of **phosphate** from the lysed cells. - The elevated phosphate levels bind to free calcium in the serum, forming **calcium phosphate crystals** that deposit in tissues, thereby lowering serum calcium levels. *Hyponatremia* - **Hyponatremia** is not a characteristic feature of tumor lysis syndrome. Sodium is primarily an extracellular ion, and its levels are not directly impacted by massive cell lysis in the same way as potassium or phosphate. - While fluid shifts or renal dysfunction in severe TLS could indirectly affect sodium, it's not a primary or expected electrolyte derangement of the syndrome itself. *Hypernatremia* - **Hypernatremia (elevated sodium)** is not expected in tumor lysis syndrome. The primary electrolyte disturbances involve intracellular components like potassium, phosphate, and uric acid, and secondary effects on calcium. - Hypernatremia would typically be associated with dehydration or impaired water balance, not the massive release of intracellular contents seen in TLS.

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