USMLE Step 2 Quiz
Practice Acid Base And Electrolyte Disorders in USMLE Step 2 with focused quiz questions that help you check what you know, review explanations, and build confidence with test-style prompts.
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A 67-year-old man with end-stage renal disease who missed his last two hemodialysis sessions presents with generalized weakness and palpitations. His ECG shows peaked T waves, a PR interval of 240 ms, and a QRS duration of 140 ms. His serum potassium is 7.5 mEq/L.
Which of the following is the most appropriate immediate step in management?
This quiz focuses on Acid Base And Electrolyte Disorders, giving you a quick way to practice the rules, question types, and explanations that matter most for USMLE Step 2.
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A 67-year-old man with end-stage renal disease who missed his last two hemodialysis sessions presents with generalized weakness and palpitations. His ECG shows peaked T waves, a PR interval of 240 ms, and a QRS duration of 140 ms. His serum potassium is 7.5 mEq/L.
Which of the following is the most appropriate immediate step in management?
Explanation: This patient has severe hyperkalemia with significant ECG changes (peaked T waves, PR prolongation, QRS widening), which indicate cardiac membrane instability and a high risk of life-threatening arrhythmias. The most important first step is to stabilize the cardiac membrane. Intravenous calcium gluconate (or calcium chloride) is administered for this purpose. It does not lower the serum potassium level but directly antagonizes the toxic effects of hyperkalemia on the myocyte cell membrane, preventing arrhythmias. After membrane stabilization, therapies to shift potassium into cells (insulin/glucose, albuterol, sodium bicarbonate) and to remove potassium from the body (diuretics, cation exchange resins, hemodialysis) can be initiated.
A 75-year-old woman with heart failure (ejection fraction 35%), type 2 diabetes, and stage 3 chronic kidney disease is evaluated in clinic. Her medications include lisinopril, metformin, and furosemide. Two weeks ago, she was started on spironolactone. Today, she complains of new-onset weakness. A fingerstick glucose is 140 mg/dL. Her serum potassium is 6.2 mEq/L.
The addition of which medication most likely precipitated her hyperkalemia?
Explanation: This patient has multiple risk factors for hyperkalemia, including chronic kidney disease and the use of an ACE inhibitor (lisinopril). The most likely precipitant for her acute worsening is the recent addition of spironolactone. Spironolactone is a potassium-sparing diuretic that acts as an aldosterone antagonist. Aldosterone normally promotes potassium excretion; by blocking its effect, spironolactone can cause significant potassium retention. The combination of an ACE inhibitor (which also increases potassium by reducing aldosterone production) and spironolactone in a patient with underlying CKD is a well-known cause of severe hyperkalemia. Furosemide is a loop diuretic that causes potassium wasting.
A 58-year-old woman with a 2-month history of fatigue is found to have a blood pressure of 165/100 mm Hg on multiple readings. She is not taking any medications. Laboratory studies show: Sodium: 145 mEq/L Potassium: 3.1 mEq/L Chloride: 98 mEq/L Bicarbonate: 32 mEq/L Urine chloride: 45 mEq/L Plasma renin activity: Suppressed Plasma aldosterone: Elevated
The patient's acid-base and electrolyte abnormalities are most likely due to which of the following conditions?
Explanation: This patient presents with hypertension, hypokalemia, and metabolic alkalosis. The high urine chloride (>20 mEq/L) suggests a saline-unresponsive cause. The combination of suppressed renin and elevated aldosterone is diagnostic for primary hyperaldosteronism (e.g., from an adrenal adenoma). Aldosterone promotes sodium reabsorption and potassium/hydrogen ion excretion in the distal tubule, leading to hypertension, hypokalemia, and metabolic alkalosis. Renovascular hypertension would cause secondary hyperaldosteronism with elevated renin. Thiazide use and Bartter syndrome cause hypokalemia and alkalosis but are typically associated with normal or low blood pressure.
A 65-year-old man with severe emphysema has a baseline arterial pCO₂ of 65 mm Hg. He is clinically stable and at his usual state of health. His pH is 7.36.
Which of the following bicarbonate (HCO₃⁻) levels would be most expected in this patient?
Explanation: This patient has chronic respiratory acidosis due to CO₂ retention from emphysema. The kidneys compensate by retaining bicarbonate to normalize the pH. The rule of thumb for chronic respiratory acidosis is that for every 10 mm Hg increase in pCO₂ above 40, the bicarbonate increases by 3-4 mEq/L. The patient's pCO₂ is 25 mm Hg above normal (65 - 40 = 25). The expected increase in bicarbonate would be 2.5 * (3 to 4) = 7.5 to 10 mEq/L. Adding this to a normal bicarbonate of 24 mEq/L gives an expected range of 31.5 to 34 mEq/L. The value of 34 mEq/L falls within this range and is consistent with full renal compensation.
A 52-year-old man with a history of alcohol use disorder is admitted to the hospital for acute pancreatitis. His initial labs show a potassium level of 2.6 mEq/L. Despite receiving 120 mEq of intravenous potassium chloride over 24 hours, his potassium level only rises to 2.8 mEq/L.
The refractory nature of his hypokalemia is most likely due to a deficiency of which of the following?
Explanation: Hypomagnesemia is a common finding in patients with alcohol use disorder and is a frequent cause of refractory hypokalemia. Magnesium is a crucial cofactor for the Na-K-ATPase pump, which maintains the intracellular potassium concentration. Additionally, magnesium blocks the renal outer medullary potassium (ROMK) channels in the collecting duct, preventing potassium secretion. In a state of hypomagnesemia, this inhibition is lost, leading to continuous renal potassium wasting. Therefore, in a patient with refractory hypokalemia, especially with risk factors like alcoholism, magnesium levels must be checked and repleted before potassium can be effectively corrected.
A 65-year-old man with a history of small cell lung cancer presents with a 1-week history of fatigue and nausea. He has no edema and his mucous membranes are moist. His blood pressure is 125/80 mm Hg. Laboratory results are as follows: Serum sodium: 119 mEq/L Serum potassium: 4.1 mEq/L Serum creatinine: 0.9 mg/dL Serum osmolality: 250 mOsm/kg H₂O Urine osmolality: 500 mOsm/kg H₂O Urine sodium: 50 mEq/L
Which of the following is the most appropriate initial treatment for this patient's hyponatremia?
Explanation: This patient's presentation is classic for the syndrome of inappropriate antidiuretic hormone secretion (SIADH), which is a common paraneoplastic syndrome associated with small cell lung cancer. The diagnosis is supported by euvolemic hyponatremia, low serum osmolality, inappropriately concentrated urine (urine osmolality > 100 mOsm/kg), and elevated urine sodium (>40 mEq/L). The patient is asymptomatic or has mild symptoms (fatigue, nausea). The first-line treatment for mild to moderate SIADH is fluid restriction. This reduces the free water intake, allowing the serum sodium to rise gradually. 0.9% saline can worsen hyponatremia in SIADH. 3% saline is reserved for severe symptoms like seizures. Desmopressin is used to treat central diabetes insipidus.
A 68-year-old man with a long history of chronic obstructive pulmonary disease (COPD) is brought to the emergency department with worsening shortness of breath and increasing somnolence over the past two days. He is using his accessory muscles to breathe. An arterial blood gas is obtained: pH: 7.25 pCO₂: 70 mm Hg HCO₃⁻: 28 mEq/L
Which of the following best describes the patient's acid-base status?
Explanation: The patient has an acidosis (pH < 7.35) with a high pCO₂ (70 mm Hg), indicating a respiratory acidosis. To determine if it is acute, chronic, or acute-on-chronic, we assess the bicarbonate level. In acute respiratory acidosis, bicarbonate increases by about 1 mEq/L for every 10 mm Hg increase in pCO₂ above 40. In chronic respiratory acidosis, it increases by 3-4 mEq/L for every 10 mm Hg increase. This patient's pCO₂ is 30 mm Hg above normal. An acute process would result in a bicarbonate of ~24 + 3 = 27 mEq/L. A chronic process would result in a bicarbonate of ~24 + (3 * 3.5) = ~34.5 mEq/L. The patient's bicarbonate of 28 mEq/L is higher than expected for a purely acute process but lower than expected for full compensation, indicating an acute exacerbation superimposed on his chronic CO₂ retention (acute-on-chronic respiratory acidosis).
A 60-year-old man with hypokalemia (serum K⁺ 2.7 mEq/L) requires intravenous potassium repletion due to inability to tolerate oral supplements. He has a peripheral IV line in his forearm.
What is the generally accepted maximum rate of potassium chloride infusion through a peripheral intravenous line to minimize the risk of phlebitis and pain?
Explanation: Intravenous potassium chloride is caustic to peripheral veins and can cause significant pain, phlebitis, and tissue necrosis if it extravasates. To minimize these risks, the rate of infusion through a peripheral line should generally not exceed 10 mEq/hour. The concentration should also be limited, typically to no more than 40 mEq/L. Higher rates (e.g., 20 mEq/hour or more) require a central venous catheter and continuous cardiac monitoring due to the risk of inducing life-threatening hyperkalemia and arrhythmias.
A 25-year-old man who sustained a severe traumatic brain injury in a motor vehicle accident is now in the ICU. On day 5, his urine output increases to 6 L/day. He is receiving isotonic IV fluids. Laboratory studies show: Serum sodium: 154 mEq/L Serum osmolality: 315 mOsm/kg H₂O Urine osmolality: 150 mOsm/kg H₂O
Which of the following interventions is most likely to confirm the suspected diagnosis?
Explanation: This patient's presentation of hypernatremia, polyuria, and inappropriately dilute urine following a head injury is highly suggestive of central diabetes insipidus (DI), caused by decreased ADH secretion. A water deprivation test is the classic diagnostic test but may be dangerous in a critically ill patient with high urine output. A more practical approach in this setting is to administer a therapeutic and diagnostic trial of desmopressin (an ADH analog). In central DI, administration of desmopressin will lead to a rapid decrease in urine output and an increase in urine osmolality, confirming the diagnosis. In nephrogenic DI, there would be no significant response.
A 45-year-old woman with Sjögren syndrome presents with several months of progressive fatigue and generalized muscle weakness. She denies vomiting, diarrhea, or use of diuretics. Physical examination is unremarkable. Laboratory studies show: Sodium: 140 mEq/L Potassium: 2.9 mEq/L Chloride: 112 mEq/L Bicarbonate: 16 mEq/L Urine pH: 6.5
Which of the following is the most likely diagnosis?
Explanation: This patient has a normal anion gap metabolic acidosis (NAGMA) calculated as 140 - (112 + 16) = 12. The presence of hypokalemia and NAGMA suggests either diarrhea or a renal tubular acidosis (RTA). The inappropriately high urine pH (>5.5) in the setting of systemic acidosis is the hallmark of Type 1 (distal) RTA, which is caused by impaired H⁺ secretion in the distal tubule. Sjögren syndrome is a known cause of Type 1 RTA. Type 2 RTA involves impaired bicarbonate reabsorption and the urine can be acidified. Type 4 RTA is associated with hyperkalemia. Diarrhea would cause a NAGMA with hypokalemia, but the urine would be appropriately acidic (pH <5.5).
An 80-year-old woman is brought from her nursing home with confusion. She has a history of hypertension treated with hydrochlorothiazide. On examination, she is lethargic with dry mucous membranes and poor skin turgor. Her blood pressure is 100/70 mm Hg, and pulse is 105/min. Laboratory studies show: Serum sodium: 122 mEq/L Serum osmolality: 255 mOsm/kg H₂O Urine sodium: 15 mEq/L Urine osmolality: 450 mOsm/kg H₂O
Which of the following is the most appropriate initial fluid management?
Explanation: This patient has hypovolemic hyponatremia. Her clinical signs (lethargy, dry mucous membranes, hypotension, tachycardia) point to volume depletion. The hyponatremia is likely caused by her hydrochlorothiazide use, which impairs the kidney's ability to dilute urine and causes volume loss. The low urine sodium (<20 mEq/L) is consistent with the kidneys trying to conserve sodium in a volume-depleted state. The initial treatment for hypovolemic hyponatremia is to restore volume with isotonic (0.9%) saline. This will correct the hypovolemia, which will turn off the non-osmotic ADH stimulus, allowing the kidneys to excrete free water and correct the sodium. 3% saline is for severe, symptomatic hyponatremia. Water restriction is for euvolemic (SIADH) or hypervolemic hyponatremia. D5W would worsen the hyponatremia.
A 24-year-old woman with a history of type 1 diabetes mellitus is brought to the emergency department by her roommate due to increasing confusion over the past 24 hours. She has had a 'stomach flu' for 2 days with nausea and poor oral intake, and she has been taking less insulin than usual. On examination, she is drowsy and breathing rapidly and deeply. Her temperature is 37.1°C (98.8°F), blood pressure is 98/60 mm Hg, pulse is 120/min, and respirations are 28/min. Laboratory studies show: Sodium: 130 mEq/L Potassium: 5.8 mEq/L Chloride: 92 mEq/L Bicarbonate: 8 mEq/L BUN: 30 mg/dL Creatinine: 1.5 mg/dL Glucose: 550 mg/dL Arterial blood gas shows pH 7.15 and pCO₂ 20 mm Hg.
Which of the following best describes the patient's primary acid-base disorder?
Explanation: The patient's presentation is classic for diabetic ketoacidosis (DKA). The low pH (7.15) and low bicarbonate (8 mEq/L) indicate a metabolic acidosis. The anion gap is calculated as Na⁺ - (Cl⁻ + HCO₃⁻) = 130 - (92 + 8) = 30 mEq/L (normal is 8-12 mEq/L). This high anion gap is due to the accumulation of ketoacids (beta-hydroxybutyrate and acetoacetate). The low pCO₂ (20 mm Hg) represents appropriate respiratory compensation (Kussmaul respirations) for the metabolic acidosis, not a primary respiratory disorder.
A 19-year-old woman is brought to the emergency department for evaluation of weakness and dizziness. She has a history of an eating disorder. Her blood pressure is 90/60 mm Hg, and her pulse is 110/min. Physical examination reveals dry mucous membranes and decreased skin turgor. Laboratory studies show: Sodium: 138 mEq/L Potassium: 2.8 mEq/L Chloride: 85 mEq/L Bicarbonate: 34 mEq/L pH: 7.50 pCO₂: 46 mm Hg Urine chloride: <10 mEq/L
Which of the following is the most appropriate initial step in management?
Explanation: The patient has a metabolic alkalosis (high pH, high bicarbonate) with appropriate respiratory compensation (increased pCO₂). The clinical signs of dehydration (hypotension, tachycardia, dry mucous membranes) and the very low urine chloride (<20 mEq/L) indicate a saline-responsive metabolic alkalosis, most likely due to surreptitious vomiting. This condition is caused by volume depletion and loss of gastric acid (HCl). The cornerstone of treatment is volume repletion with isotonic (0.9%) saline, which corrects the volume depletion and provides chloride, allowing the kidneys to excrete the excess bicarbonate.
A 22-year-old graduate student presents to the urgent care clinic with a 30-minute episode of lightheadedness, palpitations, and tingling around her mouth and in her fingertips. She states she has been under immense stress due to final exams. Her vital signs are normal, and her physical examination is unremarkable. An arterial blood gas reveals a pH of 7.52, pCO₂ of 28 mm Hg, and HCO₃⁻ of 23 mEq/L.
Which of the following is the most appropriate next step in management?
Explanation: The patient's symptoms (perioral and digital paresthesias, lightheadedness) and ABG results (high pH, low pCO₂) are classic for acute respiratory alkalosis caused by hyperventilation, likely secondary to a panic attack given her history of stress. The paresthesias are caused by decreased ionized calcium due to the alkalosis. The most appropriate initial management is to calm the patient and address the hyperventilation. Having the patient rebreathe into a paper bag increases the inspired CO₂, which helps correct the respiratory alkalosis and alleviates the symptoms. While a pulmonary embolism can cause respiratory alkalosis, her presentation is much more consistent with a panic attack, making CT angiography unnecessary at this point. IV lorazepam is too aggressive for a first step. A non-rebreather mask would worsen the alkalosis.
A 72-year-old man with diabetes is admitted to the ICU with urosepsis. He is hypotensive, tachycardic, and tachypneic. His lactate level is 6.2 mmol/L. An arterial blood gas is drawn: pH: 7.20 pCO₂: 24 mm Hg HCO₃⁻: 9 mEq/L
Which of the following best describes this patient's acid-base disturbance?
Explanation: This patient has sepsis-induced lactic acidosis causing a high anion gap metabolic acidosis (low pH, low HCO₃⁻, elevated lactate). Sepsis also directly stimulates the respiratory center, causing a primary respiratory alkalosis (low pCO₂) independent of metabolic compensation. This mixed disorder - metabolic acidosis with concurrent respiratory alkalosis - is classic in sepsis. Using Winter's formula for pure metabolic acidosis compensation: Expected pCO₂ = (1.5 × 9) + 8 = 21.5 mm Hg. The actual pCO₂ of 24 mm Hg is close but the clinical context of sepsis makes a mixed disorder most likely, as sepsis independently causes respiratory alkalosis through direct CNS stimulation.
A 28-year-old woman is brought to the emergency department after being found confused at home with an empty bottle of aspirin next to her. On presentation, she is agitated and tachypneic. An arterial blood gas is obtained: pH: 7.42 pCO₂: 20 mm Hg HCO₃⁻: 12 mEq/L
This patient's acid-base status is most consistent with toxicity from which substance?
Explanation: Salicylate (aspirin) toxicity classically causes a mixed acid-base disorder. Salicylates directly stimulate the medullary respiratory center, leading to hyperventilation and a primary respiratory alkalosis (low pCO₂). They also uncouple oxidative phosphorylation, leading to the accumulation of organic acids (ketoacids, lactate) and a primary high anion gap metabolic acidosis (low HCO₃⁻). This patient's ABG shows a near-normal pH, a significantly low pCO₂ (respiratory alkalosis), and a significantly low HCO₃⁻ (metabolic acidosis), which is the hallmark of this mixed disorder. Ethylene glycol and methanol cause a profound metabolic acidosis without a primary respiratory alkalosis. Benzodiazepines would cause respiratory acidosis from respiratory depression.
A 35-year-old man with uncontrolled type 1 diabetes mellitus presents with diabetic ketoacidosis. His serum bicarbonate is 12 mEq/L.
According to Winter's formula, what is the expected partial pressure of carbon dioxide (pCO₂) as a compensatory response?
Explanation: In a primary metabolic acidosis, the respiratory system compensates by hyperventilating to 'blow off' CO₂, thereby raising the pH. Winter's formula is used to predict the expected degree of respiratory compensation. The formula is: Expected pCO₂ = (1.5 × HCO₃⁻) + 8 ± 2. In this case, Expected pCO₂ = (1.5 × 12) + 8 = 18 + 8 = 26 mm Hg. The expected range would be 24-28 mm Hg. Therefore, 26 mm Hg is the expected pCO₂.
A 70-year-old man with severe congestive heart failure (ejection fraction 20%) is admitted with worsening dyspnea and 4+ pitting edema in his lower extremities. His weight has increased by 5 kg in the past week. Laboratory studies show a serum sodium of 124 mEq/L.
In addition to diuretic therapy, which of the following is the most important intervention for managing his hyponatremia?
Explanation: This patient has hypervolemic hyponatremia secondary to severe congestive heart failure. The low cardiac output leads to activation of the renin-angiotensin-aldosterone system and release of ADH, causing retention of both salt and, disproportionately, water. This results in a dilutional hyponatremia despite an increase in total body sodium. The primary management involves treating the underlying heart failure (e.g., with diuretics) and restricting both water and sodium intake. Giving saline or sodium tablets would worsen the volume overload. Demeclocycline is a second-line therapy for SIADH and is not typically used in heart failure.
An 88-year-old resident of a nursing home is brought to the emergency department due to altered mental status. She has had a fever and poor oral intake for three days. On examination, she is lethargic. Temperature is 38.5°C (101.3°F), blood pressure is 92/60 mm Hg, and pulse is 125/min. Her mucous membranes are parched. Laboratory results show a serum sodium of 168 mEq/L.
Which of the following is the most appropriate initial intravenous fluid for resuscitation?
Explanation: This patient has severe hypernatremia and is hemodynamically unstable (hypotensive, tachycardic), indicating significant hypovolemia. The immediate priority in any patient with circulatory collapse is to restore intravascular volume. Isotonic (0.9%) saline is the fluid of choice for initial resuscitation in hypovolemic patients, regardless of their serum sodium concentration. Once the patient is hemodynamically stable, the focus can shift to correcting the free water deficit using hypotonic fluids like 0.45% saline or D5W. Starting with hypotonic fluids in a hypotensive patient could worsen the hypotension. 3% saline is used for hyponatremia and is contraindicated here.
A 45-year-old man with chronic alcoholism is admitted with a seizure. His serum sodium is found to be 108 mEq/L. The decision is made to treat him with hypertonic saline.
To minimize the risk of osmotic demyelination syndrome, the serum sodium level should not be corrected by more than how much in the first 24 hours?
Explanation: Rapid correction of chronic hyponatremia (>48 hours duration) can lead to osmotic demyelination syndrome (formerly central pontine myelinolysis), a devastating neurologic condition. Brain cells adapt to chronic hyponatremia by extruding osmolytes to prevent cerebral edema. If the serum sodium is raised too quickly, water will shift out of the brain cells, leading to their shrinkage and demyelination. Current guidelines recommend a correction rate of no more than 8-10 mEq/L in any 24-hour period, and no more than 18 mEq/L in any 48-hour period. In high-risk patients (like this one with alcoholism), a slower rate of 4-6 mEq/L per 24 hours is often targeted.