Pathophysiology Quiz: Acid Base Disorders
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Acid Base DisordersQuestion 1 of 20

A 50-year-old patient with a history of Crohn's disease is admitted with a 4-day history of severe diarrhea. An ABG shows: pH 7.28, PaCO2 32 mmHg, HCO3- 15 mEq/L. Serum electrolytes are: Na+ 138 mEq/L, Cl- 115 mEq/L.

The metabolic acidosis observed in this patient is primarily characterized by which underlying mechanism?

Accumulation of unmeasured anions due to systemic hypoperfusion.
Renal retention of hydrogen ions secondary to acute kidney injury.
Direct loss of bicarbonate from the gastrointestinal tract, leading to a hyperchloremic state.
Hypoventilation-induced retention of CO2 with secondary metabolic effects.
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Pathophysiology Quiz

Pathophysiology Quiz: Acid Base Disorders

Practice Acid Base Disorders in Pathophysiology with focused quiz questions that help you check what you know, review explanations, and build confidence with test-style prompts.

What this quiz covers

This quiz focuses on Acid Base Disorders, giving you a quick way to practice the rules, question types, and explanations that matter most for Pathophysiology.

How to use this quiz

Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

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Question 1

A 50-year-old patient with a history of Crohn's disease is admitted with a 4-day history of severe diarrhea. An ABG shows: pH 7.28, PaCO2 32 mmHg, HCO3- 15 mEq/L. Serum electrolytes are: Na+ 138 mEq/L, Cl- 115 mEq/L.

The metabolic acidosis observed in this patient is primarily characterized by which underlying mechanism?

  1. Accumulation of unmeasured anions due to systemic hypoperfusion.
  2. Renal retention of hydrogen ions secondary to acute kidney injury.
  3. Direct loss of bicarbonate from the gastrointestinal tract, leading to a hyperchloremic state. (correct answer)
  4. Hypoventilation-induced retention of CO2 with secondary metabolic effects.
Explanation: This patient has a metabolic acidosis (low pH, low HCO3-). To characterize it, we calculate the anion gap: AG = 138 - (115 + 15) = 8 mEq/L. This is a normal anion gap. Severe diarrhea causes the loss of bicarbonate-rich intestinal fluid. To maintain electroneutrality, the kidneys reabsorb more chloride, resulting in a normal anion gap, or hyperchloremic, metabolic acidosis. Accumulation of unmeasured anions (A) would cause a high anion gap.

Question 2

An unresponsive patient is brought to the emergency department after being found down for an unknown amount of time. The patient is in cardiopulmonary arrest.

Which complex acid-base disorder is most likely to be present upon initial blood gas analysis?

  1. A pure metabolic acidosis from uremia.
  2. A severe, uncompensated respiratory alkalosis.
  3. A mixed respiratory acidosis and metabolic acidosis. (correct answer)
  4. A triple disorder of respiratory alkalosis, metabolic acidosis, and metabolic alkalosis.
Explanation: Cardiopulmonary arrest involves the simultaneous failure of both ventilation and circulation. The cessation of breathing (apnea) leads to the immediate retention of CO2, causing a severe respiratory acidosis. Concurrently, the lack of circulation leads to profound tissue hypoxia and a switch to anaerobic metabolism, resulting in the rapid production and accumulation of lactic acid, which causes a severe metabolic acidosis. Therefore, the characteristic acid-base profile of a patient in cardiac arrest is a mixed respiratory and metabolic acidosis.

Question 3

A patient with a history of alcohol abuse presents with severe abdominal pain. Laboratory results are as follows: pH 7.29, HCO3- 11 mEq/L, Na+ 138 mEq/L, K+ 4.8 mEq/L, Cl- 95 mEq/L. The patient's PaCO2 is 25 mmHg.

Which combination of acid-base disorders best explains this clinical picture?

  1. Normal anion gap metabolic acidosis with appropriate respiratory compensation.
  2. High anion gap metabolic acidosis with appropriate respiratory compensation. (correct answer)
  3. High anion gap metabolic acidosis and a concurrent primary respiratory alkalosis.
  4. Normal anion gap metabolic acidosis and a concurrent primary respiratory acidosis.
Explanation: First, calculate the anion gap: AG = [Na+] - ([Cl-] + [HCO3-]) = 138 - (95 + 11) = 32 mEq/L. This is significantly elevated (normal is 8-12 mEq/L), indicating a high anion gap metabolic acidosis (HAGMA), likely from alcoholic ketoacidosis or lactic acidosis. Second, assess compensation using Winter's formula: Expected PaCO2 = (1.5 × 11) + 8 = 24.5 mmHg. The patient's PaCO2 of 25 mmHg is within the expected range (24.5 ± 2), indicating appropriate respiratory compensation without a second primary respiratory disorder.

Question 4

A 60-year-old male with a gastric outlet obstruction from peptic ulcer disease has had persistent vomiting for three days. His ABG results are: pH 7.55, PaCO2 50 mmHg, HCO3- 45 mEq/L.

Which statement most accurately evaluates the compensatory response in this patient?

  1. The respiratory response is appropriate for the degree of metabolic alkalosis. (correct answer)
  2. The respiratory response is insufficient, indicating a concurrent primary respiratory alkalosis.
  3. The patient has a primary respiratory acidosis with renal compensation.
  4. The respiratory response is excessive, indicating a concurrent primary respiratory acidosis.
Explanation: The patient has a metabolic alkalosis (high pH, high HCO3-), likely from loss of HCl through vomiting. The compensatory response is hypoventilation to increase PaCO2. The expected PaCO2 can be estimated: PaCO2 should increase by about 0.7 mmHg for every 1 mEq/L increase in HCO3- above 24 mEq/L. The HCO3- is elevated by 45 - 24 = 21 mEq/L. The expected PaCO2 increase is 21 × 0.7 = 14.7 mmHg. Thus, the expected PaCO2 is 40 + 14.7 = 54.7 mmHg. The patient's actual PaCO2 of 50 mmHg is within the expected range, indicating an appropriate compensatory response.

Question 5

A patient is admitted with metabolic alkalosis secondary to diuretic therapy and volume depletion. An ABG shows pH 7.52, PaCO2 48 mmHg, and HCO3- 38 mEq/L.

What is the expected effect of this acid-base disturbance on ionized calcium and serum potassium levels?

  1. Increased ionized calcium and hyperkalemia.
  2. Decreased ionized calcium and hypokalemia. (correct answer)
  3. Increased ionized calcium and hypokalemia.
  4. Decreased ionized calcium and hyperkalemia.
Explanation: Metabolic alkalosis has two key effects on electrolytes. First, alkalosis increases the binding of calcium to albumin, thereby decreasing the concentration of physiologically active ionized calcium, which can lead to symptoms of hypocalcemia. Second, in an effort to buffer the extracellular alkalosis, hydrogen ions (H+) move out of cells in exchange for potassium ions (K+), which move into cells. This transcellular shift results in hypokalemia. Diuretic therapy also directly contributes to potassium loss.

Question 6

A 22-year-old is brought to the emergency department with tinnitus, confusion, and tachypnea after ingesting a large quantity of aspirin. Laboratory results are: pH 7.48, PaCO2 20 mmHg, HCO3- 15 mEq/L.

What is the most accurate description of this patient's acid-base status?

  1. Partially compensated respiratory alkalosis.
  2. Partially compensated metabolic acidosis.
  3. A mixed primary respiratory alkalosis and primary metabolic acidosis. (correct answer)
  4. A mixed primary metabolic alkalosis and primary respiratory acidosis.
Explanation: Salicylate toxicity classically causes a mixed acid-base disorder. The salicylates directly stimulate the medullary respiratory center, causing hyperventilation and a primary respiratory alkalosis (low PaCO2, increased pH). They also uncouple oxidative phosphorylation, leading to the accumulation of organic acids (ketoacids, lactate) and a primary high anion gap metabolic acidosis (low HCO3-). The near-normal but slightly alkalemic pH with a very low PaCO2 and a low HCO3- is characteristic of this mixed disorder.

Question 7

A patient is brought to the ICU in septic shock. Initial labs show a pH of 7.15 and a serum lactate of 8 mmol/L. An intravenous infusion of sodium bicarbonate is administered.

Administration of sodium bicarbonate in this setting can lead to which of the following unintended consequences?

  1. A significant decrease in intracellular pH despite an increase in extracellular pH. (correct answer)
  2. A rapid increase in serum ionized calcium levels causing tetany.
  3. An improvement in cardiac contractility due to correction of acidemia.
  4. A decrease in venous PCO2, signaling effective buffering of the acid load.
Explanation: When sodium bicarbonate (NaHCO3) is administered, it dissociates and buffers H+ in the blood, producing carbonic acid (H2CO3), which then becomes CO2 and H2O. This rapidly increases serum CO2. While serum pH rises, the highly lipid-soluble CO2 can freely diffuse across cell membranes, including into myocardial and cerebral cells. This influx of CO2 can worsen intracellular acidosis, potentially impairing cardiac contractility and CNS function, even as the extracellular pH improves. This phenomenon is known as paradoxical intracellular acidosis.

Question 8

A mountaineer has been living at an altitude of 14,000 feet for three weeks. A routine medical evaluation is performed.

Which set of arterial blood gas values would be most expected in this individual?

  1. pH 7.48, PaCO2 25 mmHg, HCO3- 24 mEq/L
  2. pH 7.35, PaCO2 55 mmHg, HCO3- 35 mEq/L
  3. pH 7.44, PaCO2 28 mmHg, HCO3- 18 mEq/L (correct answer)
  4. pH 7.25, PaCO2 30 mmHg, HCO3- 14 mEq/L
Explanation: At high altitude, chronic hypoxia stimulates hyperventilation, leading to a primary respiratory alkalosis (low PaCO2). Over several days to weeks, the kidneys compensate by decreasing H+ secretion and increasing bicarbonate (HCO3-) excretion. This metabolic compensation lowers the serum HCO3- and brings the pH back towards the normal range. Choice C shows a low PaCO2, a low HCO3-, and a pH that is slightly alkalemic but close to normal, which is the hallmark of chronic, compensated respiratory alkalosis. Choice A represents an acute, uncompensated state.

Question 9

A patient is experiencing a severe asthma exacerbation, leading to fatigue of respiratory muscles.

Which sequence of ABG changes is most likely to occur as the patient progresses from initial presentation to impending respiratory failure?

  1. Initial respiratory acidosis followed by metabolic acidosis.
  2. Initial metabolic acidosis followed by respiratory alkalosis.
  3. Initial respiratory alkalosis followed by respiratory acidosis. (correct answer)
  4. Initial metabolic alkalosis followed by respiratory acidosis.
Explanation: In the early stages of an asthma attack, tachypnea and hyperventilation occur as the body tries to overcome bronchoconstriction, leading to a primary respiratory alkalosis (low PaCO2). As the patient fatigues and airway obstruction worsens, ventilation becomes inadequate. CO2 can no longer be effectively cleared, and PaCO2 begins to rise. A 'normalizing' or rising PaCO2 in a tired, tachypneic asthmatic is an ominous sign of impending respiratory failure, which manifests as a primary respiratory acidosis.

Question 10

A 68-year-old female with a long history of severe chronic obstructive pulmonary disease (COPD) presents for a routine check-up. Her recent ABG results are: pH 7.36, PaCO2 60 mmHg, HCO3- 36 mEq/L.

Which physiological process is most responsible for the observed bicarbonate level in this patient?

  1. Acute hyperventilation driven by peripheral chemoreceptors responding to chronic hypoxia.
  2. Intracellular buffering from hemoglobin and other proteins in response to elevated CO2.
  3. Decreased hepatic metabolism of lactate, leading to an increase in serum buffers.
  4. Increased renal synthesis of new bicarbonate and enhanced tubular H+ secretion over several days. (correct answer)
Explanation: The patient has chronic respiratory acidosis, characterized by elevated PaCO2. The pH is near normal (7.36), indicating full metabolic compensation. This long-term compensation is achieved by the kidneys, which, over days to weeks, increase the secretion of hydrogen ions (H+) and enhance both the reabsorption of filtered bicarbonate and the synthesis of new bicarbonate. This renal response is powerful but slow, distinguishing it from acute buffering systems.

Question 11

A patient's ABG results are: pH 7.44, PaCO2 55 mmHg, HCO3- 39 mEq/L.

What is the most likely primary acid-base disturbance?

  1. Fully compensated metabolic alkalosis. (correct answer)
  2. Fully compensated respiratory acidosis.
  3. Acute on chronic respiratory acidosis.
  4. The values represent a normal acid-base status.
Explanation: Although the pH is within the normal range (7.35-7.45), it is not truly normal because the PaCO2 and HCO3- are significantly abnormal. This indicates a fully compensated disorder. To determine the primary process, we see which side of 7.40 the pH falls on. Since the pH is 7.44 (alkalemic), the primary process must be an alkalosis. With a high HCO3-, this is a primary metabolic alkalosis. The elevated PaCO2 represents the respiratory compensation. If it were a primary respiratory acidosis (B), the compensated pH would be on the acidotic side of 7.40 (e.g., 7.36).

Question 12

A patient with diabetic ketoacidosis has the following ABG: pH 7.30, PaCO2 20 mmHg, HCO3- 9 mEq/L.

How is this acid-base state best interpreted?

  1. Simple metabolic acidosis with adequate respiratory compensation.
  2. Metabolic acidosis with a superimposed primary respiratory alkalosis. (correct answer)
  3. Metabolic acidosis with a superimposed primary respiratory acidosis.
  4. Primary respiratory alkalosis with incomplete metabolic compensation.
Explanation: The primary disorder is metabolic acidosis (low pH, low HCO3-). Using Winter's formula to check compensation: Expected PaCO2 = (1.5 × [HCO3-]) + 8 = (1.5 × 9) + 8 = 13.5 + 8 = 21.5 mmHg. The patient's actual PaCO2 is 20 mmHg, which is lower than the expected value (range ~19.5-23.5 mmHg). This indicates that the degree of hyperventilation is greater than what would be expected as compensation for the metabolic acidosis alone. Therefore, there must be a coexisting primary respiratory alkalosis.

Question 13

A patient has a severe, pure metabolic acidosis.

What is the physiological limit to respiratory compensation for this condition?

  1. Compensation is limited by the maximum rate of renal bicarbonate generation.
  2. Hyperventilation cannot lower the PaCO2 below the level of inspired CO2, which is approximately 5 mmHg.
  3. The drive to hyperventilate is limited by the development of cerebral vasoconstriction and hypoxia.
  4. The maximal compensatory response cannot typically lower the PaCO2 below 10-15 mmHg. (correct answer)
Explanation: While the respiratory system can respond very rapidly to metabolic acidosis by increasing ventilation to blow off CO2, there is a physiological limit to this compensation. Even with maximal stimulation of central and peripheral chemoreceptors, mechanical and physiological constraints prevent the PaCO2 from falling indefinitely. The widely accepted physiological limit for compensatory hyperventilation is a PaCO2 of approximately 10-15 mmHg. Further decreases are generally not achievable.

Question 14

A patient with a history of alcohol abuse presents with severe abdominal pain. Laboratory results are as follows: pH 7.29, HCO3- 11 mEq/L, Na+ 138 mEq/L, K+ 4.8 mEq/L, Cl- 95 mEq/L. The patient's PaCO2 is 25 mmHg.

Which combination of acid-base disorders best explains this clinical picture?

  1. Normal anion gap metabolic acidosis with appropriate respiratory compensation.
  2. High anion gap metabolic acidosis with appropriate respiratory compensation. (correct answer)
  3. High anion gap metabolic acidosis and a concurrent primary respiratory alkalosis.
  4. Normal anion gap metabolic acidosis and a concurrent primary respiratory acidosis.
Explanation: First, calculate the anion gap: AG = [Na+] - ([Cl-] + [HCO3-]) = 138 - (95 + 11) = 32 mEq/L. This is significantly elevated (normal is 8-12 mEq/L), indicating a high anion gap metabolic acidosis (HAGMA), likely from alcoholic ketoacidosis or lactic acidosis. Second, assess compensation using Winter's formula: Expected PaCO2 = (1.5 × 11) + 8 = 24.5 mmHg. The patient's PaCO2 of 25 mmHg is within the expected range (24.5 ± 2), indicating appropriate respiratory compensation without a second primary respiratory disorder.

Question 15

A patient with diabetic ketoacidosis has been vomiting for the past 12 hours. Labs are: Na+ 140, Cl- 90, HCO3- 15. A normal anion gap is 12 mEq/L and normal bicarbonate is 24 mEq/L.

Analysis of the delta gap (ΔAG/ΔHCO3-) would most likely reveal the presence of what additional disorder?

  1. A concurrent non-anion gap metabolic acidosis.
  2. A concurrent respiratory acidosis.
  3. A pure high anion gap metabolic acidosis.
  4. A concurrent metabolic alkalosis. (correct answer)
Explanation: This question requires a multi-step analysis. First, calculate the anion gap (AG): 140 - (90 + 15) = 35. This is a HAGMA. Next, calculate the delta gap ratio. The change in AG (ΔAG) is 35 - 12 = 23. The change in HCO3- (ΔHCO3-) is 24 - 15 = 9. The ratio is ΔAG/ΔHCO3- = 23/9 ≈ 2.56. In a pure HAGMA, the drop in bicarbonate should roughly equal the rise in the anion gap (ratio 1-2). A ratio > 2 suggests that the bicarbonate is higher than expected for the degree of HAGMA, which implies a coexisting metabolic alkalosis, in this case due to vomiting (loss of HCl).

Question 16

A 22-year-old is brought to the emergency department with tinnitus, confusion, and tachypnea after ingesting a large quantity of aspirin. Laboratory results are: pH 7.48, PaCO2 20 mmHg, HCO3- 15 mEq/L.

What is the most accurate description of this patient's acid-base status?

  1. Partially compensated respiratory alkalosis.
  2. Partially compensated metabolic acidosis.
  3. A mixed primary respiratory alkalosis and primary metabolic acidosis. (correct answer)
  4. A mixed primary metabolic alkalosis and primary respiratory acidosis.
Explanation: Salicylate toxicity classically causes a mixed acid-base disorder. The salicylates directly stimulate the medullary respiratory center, causing hyperventilation and a primary respiratory alkalosis (low PaCO2, increased pH). They also uncouple oxidative phosphorylation, leading to the accumulation of organic acids (ketoacids, lactate) and a primary high anion gap metabolic acidosis (low HCO3-). The near-normal but slightly alkalemic pH with a very low PaCO2 and a low HCO3- is characteristic of this mixed disorder.

Question 17

A 50-year-old patient with a history of Crohn's disease is admitted with a 4-day history of severe diarrhea. An ABG shows: pH 7.28, PaCO2 32 mmHg, HCO3- 15 mEq/L. Serum electrolytes are: Na+ 138 mEq/L, Cl- 115 mEq/L.

The metabolic acidosis observed in this patient is primarily characterized by which underlying mechanism?

  1. Accumulation of unmeasured anions due to systemic hypoperfusion.
  2. Renal retention of hydrogen ions secondary to acute kidney injury.
  3. Direct loss of bicarbonate from the gastrointestinal tract, leading to a hyperchloremic state. (correct answer)
  4. Hypoventilation-induced retention of CO2 with secondary metabolic effects.
Explanation: This patient has a metabolic acidosis (low pH, low HCO3-). To characterize it, we calculate the anion gap: AG = 138 - (115 + 15) = 8 mEq/L. This is a normal anion gap. Severe diarrhea causes the loss of bicarbonate-rich intestinal fluid. To maintain electroneutrality, the kidneys reabsorb more chloride, resulting in a normal anion gap, or hyperchloremic, metabolic acidosis. Accumulation of unmeasured anions (A) would cause a high anion gap.

Question 18

A patient is admitted with metabolic alkalosis secondary to diuretic therapy and volume depletion. An ABG shows pH 7.52, PaCO2 48 mmHg, and HCO3- 38 mEq/L.

What is the expected effect of this acid-base disturbance on ionized calcium and serum potassium levels?

  1. Increased ionized calcium and hyperkalemia.
  2. Decreased ionized calcium and hypokalemia. (correct answer)
  3. Increased ionized calcium and hypokalemia.
  4. Decreased ionized calcium and hyperkalemia.
Explanation: Metabolic alkalosis has two key effects on electrolytes. First, alkalosis increases the binding of calcium to albumin, thereby decreasing the concentration of physiologically active ionized calcium, which can lead to symptoms of hypocalcemia. Second, in an effort to buffer the extracellular alkalosis, hydrogen ions (H+) move out of cells in exchange for potassium ions (K+), which move into cells. This transcellular shift results in hypokalemia. Diuretic therapy also directly contributes to potassium loss.

Question 19

A patient with diabetic ketoacidosis has the following ABG: pH 7.30, PaCO2 20 mmHg, HCO3- 9 mEq/L.

How is this acid-base state best interpreted?

  1. Simple metabolic acidosis with adequate respiratory compensation.
  2. Metabolic acidosis with a superimposed primary respiratory alkalosis. (correct answer)
  3. Metabolic acidosis with a superimposed primary respiratory acidosis.
  4. Primary respiratory alkalosis with incomplete metabolic compensation.
Explanation: The primary disorder is metabolic acidosis (low pH, low HCO3-). Using Winter's formula to check compensation: Expected PaCO2 = (1.5 × [HCO3-]) + 8 = (1.5 × 9) + 8 = 13.5 + 8 = 21.5 mmHg. The patient's actual PaCO2 is 20 mmHg, which is lower than the expected value (range ~19.5-23.5 mmHg). This indicates that the degree of hyperventilation is greater than what would be expected as compensation for the metabolic acidosis alone. Therefore, there must be a coexisting primary respiratory alkalosis.

Question 20

A patient is experiencing a severe asthma exacerbation, leading to fatigue of respiratory muscles.

Which sequence of ABG changes is most likely to occur as the patient progresses from initial presentation to impending respiratory failure?

  1. Initial respiratory acidosis followed by metabolic acidosis.
  2. Initial metabolic acidosis followed by respiratory alkalosis.
  3. Initial respiratory alkalosis followed by respiratory acidosis. (correct answer)
  4. Initial metabolic alkalosis followed by respiratory acidosis.
Explanation: In the early stages of an asthma attack, tachypnea and hyperventilation occur as the body tries to overcome bronchoconstriction, leading to a primary respiratory alkalosis (low PaCO2). As the patient fatigues and airway obstruction worsens, ventilation becomes inadequate. CO2 can no longer be effectively cleared, and PaCO2 begins to rise. A 'normalizing' or rising PaCO2 in a tired, tachypneic asthmatic is an ominous sign of impending respiratory failure, which manifests as a primary respiratory acidosis.