Examkin

Nephrology

337 questions

All types337Multiple choice169Numeric81Matching87
Question 281Question →

A 45-year-old woman is brought to the emergency department by her husband due to progressive lethargy over the past 12 hours. The patient has a history of Crohn disease and has been experiencing severe, watery diarrhea for the past five days. Yesterday, she took multiple doses of a friend's prescription oxycodone to help manage her severe abdominal cramping. On physical examination, her temperature is 37.1°C (98.8°F), blood pressure is 105/65 mmHg, heart rate is 110/min, and respiratory rate is 8/min. She is somnolent but arouses to verbal stimuli. Mucous membranes are dry.

Laboratory studies show the following:

ParameterValue
Sodium138 mEq/L
Potassium3.2 mEq/L
Chloride112 mEq/L
Bicarbonate14 mEq/L
Arterial pH7.20
Arterial pCO240 mmHg
Arterial pO268 mmHg

Based on the provided laboratory data, which of the following best characterizes this patient's acid-base status?

Show answer & explanation

Answer: Concurrent normal anion gap metabolic acidosis and respiratory acidosis

Answer

Concurrent normal anion gap metabolic acidosis and respiratory acidosis
The patient's laboratory values reveal an acidemia (pH 7.20) with a low bicarbonate (14 mEq/L), indicating a primary metabolic acidosis. The anion gap is calculated as Na+−(Cl−+HCO3−)=138−(112+14)=12 mEq/LNa^+ - (Cl^- + HCO_3^-) = 138 - (112 + 14) = 12 \text{ mEq/L}. Because a normal anion gap is typically 8-12 mEq/L, she has a normal anion gap metabolic acidosis, primarily driven by her severe diarrhea (gastrointestinal bicarbonate loss). Next, Winter's formula must be applied to determine if the respiratory compensation is adequate: ExpectedpCO2=(1.5×HCO3−)+8±2Expected pCO_2 = (1.5 \times HCO_3^-) + 8 \pm 2. For this patient, ExpectedpCO2=(1.5×14)+8±2=29±2 mmHgExpected pCO_2 = (1.5 \times 14) + 8 \pm 2 = 29 \pm 2 \text{ mmHg}. Her measured pCO2 is 40 mmHg, which is significantly higher than the expected range of 27-31 mmHg. This indicates that she is retaining carbon dioxide, representing a concurrent respiratory acidosis. This is clinically supported by her depressed respiratory rate (8/min) following oxycodone ingestion.

Step-by-Step Solution

1
Calculate the anion gap.
138−(112+14)=12 mEq/L138 - (112 + 14) = 12 \text{ mEq/L}
To determine the etiology of the metabolic acidosis. A result of 12 mEq/L is a normal gap, which is consistent with severe bicarbonate loss from diarrhea.
2
Calculate the expected pCO2 using Winter's formula.
(1.5×14)+8=29±2 mmHg(1.5 \times 14) + 8 = 29 \pm 2 \text{ mmHg}
To assess if the respiratory system is appropriately compensating for the metabolic acidosis.
3
Compare measured pCO2 to the expected pCO2.
The measured pCO2 (40 mmHg) is significantly higher than the expected range (27-31 mmHg).
A higher than expected pCO2 indicates inadequate respiratory compensation, defining a concurrent primary respiratory acidosis (due to opiate-induced hypoventilation).

Key Concept

Patients with a primary metabolic acidosis require calculation of expected pCO2 using Winter's formula to identify whether a secondary respiratory acid-base disorder is present.
Estimated Time:1m 30s
Question 282Question →

A 24-year-old man with a history of type 1 diabetes mellitus is evaluated in the intensive care unit. He was admitted 12 hours ago for the management of diabetic ketoacidosis. Initial therapy included a continuous intravenous regular insulin infusion and aggressive volume resuscitation with a total of 6 liters of 0.9% sodium chloride. He is now alert and reports feeling much better. Vital signs are temperature 37.0°C (98.6°F), blood pressure 118/76 mm Hg, heart rate 88/min, and respiratory rate 20/min.

Laboratory results are as follows:
Serum sodium: 142 mEq/L
Serum potassium: 4.1 mEq/L
Serum chloride: 112 mEq/L
Serum bicarbonate: 10 mEq/L
Blood glucose: 190 mg/dL

Arterial blood gas on room air:
pH: 7.26
PaCO2: 23 mm Hg
PaO2: 95 mm Hg

Which of the following best describes this patient's current acid-base status?

Show answer & explanation

Answer: High anion gap metabolic acidosis and concurrent normal anion gap metabolic acidosis

Answer

The patient has a mixed high anion gap metabolic acidosis and a concurrent normal anion gap metabolic acidosis.
This patient's arterial blood gas and electrolyte panel reveal a primary metabolic acidosis (pH 7.26, HCO3−HCO_3^- 10 mEq/L). The anion gap is calculated as 142−(112+10)=20142 - (112 + 10) = 20, indicating a high anion gap metabolic acidosis (HAGMA) due to his presenting diabetic ketoacidosis. Respiratory compensation is appropriate, as Winter's formula (1.5×10+8=231.5 \times 10 + 8 = 23) perfectly predicts his actual PaCO2PaCO_2 of 23 mm Hg. However, comprehensively evaluating a patient with a HAGMA requires a delta-delta calculation to rule out hidden metabolic disorders. The delta anion gap is 20−12=820 - 12 = 8, and the delta bicarbonate is 24−10=1424 - 10 = 14. The delta ratio (814\frac{8}{14}) is approximately 0.57. A delta ratio less than 0.8 indicates that the bicarbonate level has decreased significantly more than the anion gap has increased, which mathematically proves that a concurrent normal anion gap metabolic acidosis (NAGMA) is present. In patients treated for DKA, aggressive fluid resuscitation with 0.9% sodium chloride (which has a high chloride content) routinely causes a superimposed hyperchloremic NAGMA.

Step-by-Step Solution

1
Identify the primary acid-base disorder by evaluating the pH and serum bicarbonate.
The pH is 7.26 (acidemia) and HCO3−HCO_3^- is 10 mEq/L, indicating a primary metabolic acidosis.
A pH < 7.35 defines acidemia, and a concurrently low bicarbonate level confirms the metabolic etiology.
2
Calculate the anion gap (AG) to determine the type of metabolic acidosis.
AG=Na+−(Cl−+HCO3−)=142−(112+10)=20AG = Na^+ - (Cl^- + HCO_3^-) = 142 - (112 + 10) = 20. The AG is elevated (normal is typically 12±212 \pm 2).
An elevated anion gap identifies the presence of a high anion gap metabolic acidosis (HAGMA), which in this patient is secondary to resolving diabetic ketoacidosis.
3
Assess for appropriate respiratory compensation using Winter's formula.
Expected PaCO2=1.5×10+8±2=23±2PaCO_2 = 1.5 \times 10 + 8 \pm 2 = 23 \pm 2 mm Hg. The actual PaCO2PaCO_2 is 23 mm Hg, which falls exactly within the expected range.
If the actual PaCO2PaCO_2 matches the expected value calculated by Winter's formula, there is no concurrent primary respiratory acid-base disorder.
4
Calculate the delta ratio to evaluate for a hidden, concurrent metabolic disorder.
ΔAG=20−12=8\Delta AG = 20 - 12 = 8. ΔHCO3−=24−10=14\Delta HCO_3^- = 24 - 10 = 14. ΔRatio=814≈0.57\Delta Ratio = \frac{8}{14} \approx 0.57.
In a pure HAGMA, the rise in AG should roughly equal the drop in bicarbonate (ratio ~1.0). A ratio < 0.8 means bicarbonate has dropped more than expected, indicating an additional normal anion gap metabolic acidosis (hyperchloremia from the massive 0.9% NaCl resuscitation).

Key Concept

Identifying a mixed high anion gap and normal anion gap metabolic acidosis using the delta-delta gap ratio.
Question 283Question →

A 68-year-old man is admitted to the medical ward following a 4-day history of worsening diarrhea and generalized weakness. He states he has been unable to keep fluids down. His past medical history is significant for hypertension and osteoarthritis. His temperature is 37.0°C (98.6°F), blood pressure is 98/60 mm Hg, and pulse is 108/min. Jugular venous pressure is decreased, and skin turgor is poor. A Foley catheter is placed, yielding a small amount of concentrated urine.

Laboratory evaluation reveals the following:

ParameterValue
Serum sodium140 mEq/L140\text{ mEq/L}
Serum potassium3.2 mEq/L3.2\text{ mEq/L}
Blood urea nitrogen45 mg/dL45\text{ mg/dL}
Serum creatinine1.5 mg/dL1.5\text{ mg/dL}
Urine sodium14 mEq/L14\text{ mEq/L}
Urine creatinine30 mg/dL30\text{ mg/dL}

What is this patient's fractional excretion of sodium?

Show answer & explanation

Answer: 0.5

Answer

0.5
The fractional excretion of sodium (FeNa) measures the percentage of filtered sodium that is excreted in the urine. It is an essential calculation used to differentiate between prerenal and intrinsic etiologies of acute kidney injury. The formula is FeNa=(UNa/PNa)×(PCr/UCr)×100FeNa = (U_{Na} / P_{Na}) \times (P_{Cr} / U_{Cr}) \times 100. Substituting the provided laboratory values yields (14/140)×(1.5/30)×100=0.1×0.05×100=0.5%(14 / 140) \times (1.5 / 30) \times 100 = 0.1 \times 0.05 \times 100 = 0.5\%. A value less than 1%1\% indicates avid sodium retention by the kidneys, which is characteristic of a prerenal state such as hypovolemia secondary to severe diarrhea.

Step-by-Step Solution

1
Identify the standard equation for fractional excretion of sodium.
FeNa=UNa×PCrPNa×UCr×100FeNa = \frac{U_{Na} \times P_{Cr}}{P_{Na} \times U_{Cr}} \times 100
This formula is used to differentiate the etiology of acute kidney injury.
2
Extract the specific patient values from the clinical vignette.
UNa=14 mEq/LU_{Na} = 14\text{ mEq/L}, PNa=140 mEq/LP_{Na} = 140\text{ mEq/L}, PCr=1.5 mg/dLP_{Cr} = 1.5\text{ mg/dL}, UCr=30 mg/dLU_{Cr} = 30\text{ mg/dL}
These are the four variables required to complete the calculation.
3
Substitute the parameters into the equation.
FeNa=(14140)×(1.530)×100FeNa = \left(\frac{14}{140}\right) \times \left(\frac{1.5}{30}\right) \times 100
To set up the mathematical calculation.
4
Complete the mathematical operation.
FeNa=0.1×0.05×100=0.5%FeNa = 0.1 \times 0.05 \times 100 = 0.5\%
To find the final diagnostic value, which supports a prerenal etiology.

Key Concept

Fractional Excretion of Sodium (FeNa) Calculation
Question 284Question →

Match each of the following urinalysis sediment findings with the most likely underlying renal etiology or clinical condition.

Click a left item, then click its matching right item

Items

Muddy brown granular casts
Red blood cell (RBC) casts and dysmorphic RBCs
White blood cell (WBC) casts and eosinophiluria
Broad, waxy casts
Fatty casts and oval fat bodies

Matches

Show answer & explanation

Answer

Muddy brown granular casts match with Acute tubular necrosis; RBC casts match with Glomerulonephritis; WBC casts and eosinophiluria match with Acute interstitial nephritis; Broad, waxy casts match with Advanced chronic kidney disease; Fatty casts match with Nephrotic syndrome.
Each specific cast and cellular finding in the urine sediment is a direct consequence of the anatomical site and nature of the kidney injury. Muddy brown casts form from necrotic tubular cells (ATN). RBC casts form when RBCs traverse a damaged glomerular basement membrane (Glomerulonephritis). WBC casts with eosinophils reflect an allergic interstitial reaction (AIN). Broad waxy casts form in the enlarged tubules of failing kidneys (CKD). Fatty casts are composed of lipids that pass into the urine due to the severe glomerular permeability seen in nephrotic syndrome.

Step-by-Step Solution

1
Identify the cellular origin of the muddy brown granular casts.
They represent necrotic tubular epithelial cells.
This confirms acute tubular necrosis (ATN) as the underlying etiology.
2
Evaluate the presence of RBC casts and dysmorphic RBCs.
These elements indicate bleeding originating from the glomerulus.
Glomerular inflammation is the hallmark of glomerulonephritis (nephritic syndrome).
3
Assess the clinical significance of WBC casts combined with eosinophiluria.
This specific combination points to an allergic inflammatory process in the renal interstitium.
Acute interstitial nephritis (AIN) is the classic match, usually medication-induced.
4
Determine the pathophysiology behind broad, waxy casts.
They are formed in dilated tubules with low urine flow.
This is characteristic of advanced chronic kidney disease (CKD).
5
Correlate fatty casts and oval fat bodies with a disease state.
They result from severe lipiduria.
Nephrotic syndrome is characterized by massive proteinuria, leading to compensatory hyperlipidemia and subsequent lipiduria.

Key Concept

Correlation of specific microscopic urinalysis (urine sediment) findings with underlying renal pathologies is essential for diagnosing intrinsic kidney diseases.
Estimated Time:1m 0s
Question 285Question →

Emergency medical responders transport a 54-year-old male to the emergency department after his neighbor found him unresponsive. The patient has a known history of severe chronic obstructive pulmonary disease and alcohol use disorder. On physical examination, he is obtunded and taking slow, shallow breaths.

Vital signs include:
Temperature: 36.5 °C (97.7 °F)
Blood pressure: 92/58 mmHg
Heart rate: 108/min
Respiratory rate: 8/min

Laboratory studies display the following results:

TestValue
Sodium142 mEq/L
Potassium4.5 mEq/L
Chloride100 mEq/L
Bicarbonate12 mEq/L
Blood urea nitrogen30 mg/dL
Creatinine1.8 mg/dL

An arterial blood gas sample on room air shows:

TestValue
pH7.15
pCO2pCO_235 mmHg
pO2pO_260 mmHg

Which of the following best describes this patient's acid-base disturbances?

Show answer & explanation

Answer: Elevated anion gap metabolic acidosis with a concurrent respiratory acidosis

Answer

Elevated anion gap metabolic acidosis with a concurrent respiratory acidosis
The patient's presentation and lab results indicate a mixed acid-base disorder. First, the primary process is a metabolic acidosis, given the low pH and low bicarbonate. The anion gap is calculated as Na+−(Cl−+HCO3−)=142−(100+12)=30Na^+ - (Cl^- + HCO_3^-) = 142 - (100 + 12) = 30 mEq/L. Since this is greater than the normal 8-12 mEq/L range, there is an elevated anion gap metabolic acidosis (likely due to lactic acidosis from hypoperfusion or alcoholic ketoacidosis). Next, Winter's formula must be applied to evaluate respiratory compensation: expected pCO2=1.5×12+8±2=26±2pCO_2 = 1.5 \times 12 + 8 \pm 2 = 26 \pm 2 mmHg. Because the patient's actual pCO2pCO_2 (35 mmHg) is higher than the expected range of 24-28 mmHg, the patient is retaining CO2CO_2. This relative hypoventilation (consistent with his obtunded state and history of COPD) indicates a concurrent primary respiratory acidosis.

Step-by-Step Solution

1
Calculate the anion gap.
Anion Gap = Na+−(Cl−+HCO3−)Na^+ - (Cl^- + HCO_3^-) = 142−(100+12)=30142 - (100 + 12) = 30 mEq/L.
An elevated anion gap (> 12 mEq/L) identifies the presence of an unmeasured anion driving the metabolic acidosis.
2
Calculate the expected respiratory compensation using Winter's formula.
Expected pCO2pCO_2 = 1.5×[HCO3−]+8±21.5 \times [HCO_3^-] + 8 \pm 2 = 1.5×12+8±2=26±21.5 \times 12 + 8 \pm 2 = 26 \pm 2 mmHg. The expected range is 24 to 28 mmHg.
This determines if the respiratory system is adequately blowing off CO2CO_2 to compensate for the metabolic acidemia.
3
Compare the actual pCO2pCO_2 to the expected pCO2pCO_2.
The actual pCO2pCO_2 is 35 mmHg, which is higher than the upper limit of the expected range (28 mmHg).
A pCO2pCO_2 higher than the expected compensatory range indicates a concurrent primary respiratory acidosis (hypoventilation).

Key Concept

Evaluation of mixed acid-base disorders using the anion gap and Winter's formula.
Question 286Question →

A 19-year-old college student is evaluated in the emergency department for confusion, nausea, and bilateral ringing in her ears. Her roommate reports that the patient ingested a large, unknown quantity of over-the-counter pain-relieving pills earlier in the day following a stressful exam. Temperature is 37.8°C (100.0°F), blood pressure is 112/68 mm Hg, pulse is 115/min, and respirations are 28/min. Physical examination shows a diaphoretic young woman with deep, rapid breathing.

Laboratory studies show:
Serum sodium: 140 mEq/L
Serum chloride: 104 mEq/L
Serum bicarbonate: 14 mEq/L
Blood urea nitrogen: 18 mg/dL
Serum creatinine: 0.9 mg/dL

Arterial blood gas (room air):
pH: 7.45
pCO2: 21 mm Hg
pO2: 98 mm Hg

Which of the following best describes this patient's acid-base status?

Show answer & explanation

Answer: Mixed high anion gap metabolic acidosis and respiratory alkalosis

Answer

Mixed high anion gap metabolic acidosis and respiratory alkalosis
The correct answer identifies that this patient has two concurrent primary acid-base disorders, which is classic for salicylate (aspirin) toxicity. First, calculate the anion gap: 140−(104+14)=22140 - (104 + 14) = 22 mEq/L. Because this is greater than 12 mEq/L, a primary high anion gap metabolic acidosis (HAGMA) is present. Next, use Winter's formula to determine if the respiratory compensation is adequate: ExpectedpCO2=(1.5×14)+8=29±2Expected pCO_2 = (1.5 \times 14) + 8 = 29 \pm 2 mm Hg. The patient's actual pCO2 is 21 mm Hg. Because the actual pCO2 is lower than the expected range, the patient is hyperventilating beyond what is required for compensation, indicating a concurrent primary respiratory alkalosis. This dual disorder creates a relatively normal or slightly alkalemic pH (7.45 in this case) despite severe metabolic derangements.

Step-by-Step Solution

1
Calculate the anion gap to evaluate the metabolic component.
AnionGap=Na+−(Cl−+HCO3−)=140−(104+14)=22Anion Gap = Na^+ - (Cl^- + HCO_3^-) = 140 - (104 + 14) = 22 mEq/L.
An elevated anion gap (> 12 mEq/L) confirms the presence of a primary high anion gap metabolic acidosis (HAGMA), regardless of the serum pH.
2
Calculate the expected pCO2 using Winter's formula to check for appropriate compensation.
ExpectedpCO2=1.5×[HCO3−]+8±2=1.5×14+8=29±2Expected pCO_2 = 1.5 \times [HCO_3^-] + 8 \pm 2 = 1.5 \times 14 + 8 = 29 \pm 2 (range 27-31 mm Hg).
Winter's formula determines if the respiratory response to a metabolic acidosis is appropriate. If the actual pCO2 falls outside the expected range, a secondary mixed disorder is present.
3
Compare the actual pCO2 to the expected pCO2 to identify the mixed disorder.
The actual pCO2 is 21 mm Hg, which is lower than the expected 27-31 mm Hg.
Because the actual pCO2 is lower than what would be expected from compensatory hyperventilation alone, the patient has an independent, concurrent primary respiratory alkalosis.

Key Concept

Patients with salicylate toxicity classically present with a mixed primary high anion gap metabolic acidosis (due to uncoupling of oxidative phosphorylation) and a primary respiratory alkalosis (due to direct central medullary stimulation). Winter's formula is essential for identifying these concurrent primary disorders.
Estimated Time:1m 30s
Question 287Question →

A 34-year-old man is brought to the emergency department by emergency medical services after his partner witnessed him having an episode of rhythmic limb jerking and loss of consciousness lasting approximately 5 minutes. On arrival, he is deeply lethargic and only moans to painful stimuli. His temperature is 37.2∘C37.2^\circ\text{C} (99.0∘F99.0^\circ\text{F}), blood pressure is 118/76118/76 mmHg, pulse is 112112/min, and respirations are 1212/min. Physical examination reveals a laceration on the lateral aspect of his tongue and generalized muscle tenderness.

Laboratory studies show:
Sodium: 140140 mEq/L
Potassium: 4.64.6 mEq/L
Chloride: 104104 mEq/L
Bicarbonate: 1212 mEq/L
Blood urea nitrogen: 1616 mg/dL
Creatinine: 1.11.1 mg/dL
Glucose: 118118 mg/dL

Arterial blood gas (room air):
pH: 7.177.17
pCO 2_2: 3434 mmHg
pO 2_2: 7878 mmHg

Which of the following best describes this patient's primary acid-base disorder(s)?

Show answer & explanation

Answer: High anion gap metabolic acidosis and concurrent respiratory acidosis

Answer

High anion gap metabolic acidosis and concurrent respiratory acidosis
The correct answer accurately synthesizes the laboratory data. First, the patient has an acidemia (pH 7.17) driven by a low bicarbonate (12 mEq/L), indicating a primary metabolic acidosis. The anion gap is calculated as 140−(104+12)=24140 - (104 + 12) = 24, confirming a high anion gap metabolic acidosis, which is classically seen following generalized tonic-clonic seizures due to intense muscle exertion producing lactic acid. Next, appropriate respiratory compensation must be evaluated using Winter's formula: pCO2=(1.5×12)+8±2=26±2pCO_2 = (1.5 \times 12) + 8 \pm 2 = 26 \pm 2 mmHg. The patient's measured pCO2 is 34 mmHg. Since the measured pCO2 is higher than the expected range of 24-28 mmHg, the patient has a concurrent, superimposed respiratory acidosis. This is clinically consistent with the patient's low respiratory rate of 12/min and deep lethargy, representing a post-ictal depression of the central respiratory drive.

Step-by-Step Solution

1
Determine the primary acid-base disorder by looking at the pH and bicarbonate.
The pH is 7.17 (acidemia) and the bicarbonate is 12 mEq/L (low), which indicates a primary metabolic acidosis.
Establishing the primary disturbance directs the choice of subsequent diagnostic formulas.
2
Calculate the serum anion gap using the formula: AG=Na+−(Cl−+HCO3−)AG = Na^+ - (Cl^- + HCO_3^-).
AG=140−(104+12)=140−116=24AG = 140 - (104 + 12) = 140 - 116 = 24. The normal range is typically 10-14, so this is a high anion gap metabolic acidosis.
Determining the anion gap identifies the cause of the metabolic acidosis (e.g., lactic acidosis from the recent seizure).
3
Calculate the expected respiratory compensation using Winter's formula: Expected pCO2=(1.5×HCO3−)+8±2Expected\ pCO_2 = (1.5 \times HCO_3^-) + 8 \pm 2.
Expected pCO2=(1.5×12)+8±2=18+8±2=26±2Expected\ pCO_2 = (1.5 \times 12) + 8 \pm 2 = 18 + 8 \pm 2 = 26 \pm 2 mmHg. The expected pCO2 range is 24 to 28 mmHg.
Winter's formula determines if the respiratory system has appropriately compensated for the primary metabolic acidosis.
4
Compare the expected pCO2 to the measured pCO2 on the arterial blood gas.
The measured pCO2 is 34 mmHg, which is significantly higher than the expected range of 24-28 mmHg.
Because the measured pCO2 is higher than the expected compensatory range, the patient is retaining carbon dioxide (likely due to a post-ictal depressed respiratory drive), indicating a concurrent respiratory acidosis.

Key Concept

Interpretation of a mixed acid-base disorder requires calculating the anion gap to identify unmeasured anions and applying Winter's formula to determine if respiratory compensation for a metabolic acidosis is appropriate.
Question 288Question →

Correlate the following clinical conditions with their most characteristic acid-base and electrolyte laboratory profile.

Click a left item, then click its matching right item

Items

Surreptitious vomiting
Primary hyperaldosteronism
Thiazide diuretic abuse
Severe acute diarrhea

Matches

Show answer & explanation

Answer

Surreptitious vomiting is matched with low urine chloride metabolic alkalosis; Primary hyperaldosteronism with high urine chloride metabolic alkalosis and hypertension; Thiazide abuse with high urine chloride metabolic alkalosis and normotension; Severe acute diarrhea with normal anion gap metabolic acidosis.
Surreptitious vomiting causes saline-responsive alkalosis (low urine chloride). Thiazide abuse causes saline-resistant alkalosis (high urine chloride) with volume depletion. Primary hyperaldosteronism causes saline-resistant alkalosis (high urine chloride) with volume expansion (hypertension). Diarrhea causes a non-anion gap metabolic acidosis due to direct gastrointestinal base loss.

Step-by-Step Solution

1
Differentiate the causes of hypokalemic metabolic alkalosis based on blood pressure.
Hypertension points to mineralocorticoid excess (Primary hyperaldosteronism). Normotension or hypotension points to volume contraction (vomiting or diuretic use).
Volume status helps narrow down the etiology of metabolic alkalosis.
2
Differentiate the volume-contracted causes of metabolic alkalosis using urine chloride.
Urine chloride <20< 20 mEq/L indicates an extrarenal cause of chloride loss where the kidneys are functioning properly to retain chloride (surreptitious vomiting). Urine chloride >20> 20 mEq/L indicates renal chloride wasting (thiazide diuretic abuse).
Urine chloride distinguishes saline-responsive (extrarenal) from saline-resistant (renal) chloride losses.
3
Identify the primary acid-base disorder caused by severe lower gastrointestinal fluid loss.
Loss of bicarbonate-rich fluid results in a normal anion gap metabolic acidosis.
Unlike gastric fluid which is acidic, lower gastrointestinal fluid is rich in bicarbonate and potassium.

Key Concept

Differentiation of acid-base disorders using volume status, blood pressure, and urine chloride.
Estimated Time:1m 30s
Question 289Question →

A rapid response team is called to evaluate a 45-year-old woman on the general medical ward due to acute-onset lethargy. The patient was admitted 24 hours ago for a severe exacerbation of ulcerative colitis, presenting with numerous large-volume, watery bowel movements per day. Over the past 12 hours, she has received three doses of intravenous hydromorphone to manage severe abdominal cramping. On physical examination, her temperature is 37.1°C (98.8°F), blood pressure is 105/65 mmHg, pulse is 112/min, and respiratory rate is 8/min with shallow breathing. She is difficult to arouse but withdraws appropriately to painful stimuli.

Stat laboratory studies reveal the following:
Serum sodium: 135 mEq/L
Serum potassium: 3.1 mEq/L
Serum chloride: 115 mEq/L
Serum bicarbonate: 10 mEq/L
Blood urea nitrogen: 42 mg/dL
Serum creatinine: 1.8 mg/dL

Arterial blood gas analysis on room air shows:
pH: 7.10
PaO2: 68 mmHg
PaCO2: 36 mmHg

Which of the following best describes this patient's current acid-base disturbance?

Show answer & explanation

Answer: Normal anion gap metabolic acidosis and concurrent respiratory acidosis

Answer

Normal anion gap metabolic acidosis and concurrent respiratory acidosis
This patient's severe diarrhea has caused massive gastrointestinal bicarbonate loss, leading to a primary normal anion gap metabolic acidosis (NAGMA). The calculated anion gap is normal at 10 mEq/L (135−(115+10)135 - (115 + 10)). To determine if respiratory compensation is adequate, Winter's formula must be applied: Expected PaCO2=1.5×[HCO3−]+8±2PaCO_2 = 1.5 \times [HCO_3^-] + 8 \pm 2. Given a bicarbonate of 10 mEq/L, the expected PaCO2PaCO_2 is 21 to 25 mmHg. The patient's actual PaCO2PaCO_2 is 36 mmHg. Because the measured PaCO2PaCO_2 is significantly higher than the expected range, the patient has a concurrent, superimposed respiratory acidosis. Clinically, this is explained by opiate-induced hypoventilation, as evidenced by her somnolence and a respiratory rate of 8/min following hydromorphone administration.

Step-by-Step Solution

1
Identify the primary acid-base disorder by looking at the pH and serum bicarbonate.
The pH is 7.10 (acidemia) and the HCO3−HCO_3^- is 10 mEq/L (low). This indicates a primary metabolic acidosis.
Establishing the primary disturbance is the first step in analyzing any mixed acid-base disorder.
2
Calculate the serum anion gap (AG).
AG = Na+−(Cl−+HCO3−)Na^+ - (Cl^- + HCO_3^-) = 135−(115+10)=10135 - (115 + 10) = 10 mEq/L. This is within the normal range (8-12 mEq/L), confirming a normal anion gap metabolic acidosis (NAGMA).
Differentiating between a normal and high anion gap determines the etiology of the metabolic acidosis (in this case, gastrointestinal bicarbonate loss from diarrhea).
3
Use Winter's formula to calculate the expected PaCO2PaCO_2 for respiratory compensation.
Expected PaCO2=(1.5×HCO3−)+8±2PaCO_2 = (1.5 \times HCO_3^-) + 8 \pm 2. For this patient: (1.5×10)+8=23±2(1.5 \times 10) + 8 = 23 \pm 2 mmHg. The expected range is 21 to 25 mmHg.
Winter's formula determines if the lungs are appropriately compensating for the metabolic acidosis by hyperventilating and blowing off CO2CO_2.
4
Compare the expected PaCO2PaCO_2 to the patient's measured PaCO2PaCO_2.
The measured PaCO2PaCO_2 is 36 mmHg, which is significantly higher than the expected maximum of 25 mmHg.
Because the measured PaCO2PaCO_2 is higher than the expected compensated value, there is a concurrent primary respiratory acidosis. This is clinically consistent with the patient's low respiratory rate (8/min) following hydromorphone administration.

Key Concept

Diagnosis of mixed acid-base disorders using the anion gap and Winter's formula
Question 290Question →

An unresponsive 52-year-old male is transported to the triage area by paramedics after being found in a mechanic's garage. According to bystanders, he had been drinking an unidentified liquid from a jug. His temperature is 36.5°C (97.7°F), blood pressure is 150/92 mm Hg, pulse is 108/min, and respirations are 24/min and deep. He responds only to painful stimuli.

Laboratory studies show the following:
Sodium: 139139 mEq/L
Potassium: 4.84.8 mEq/L
Chloride: 104104 mEq/L
Bicarbonate: 1010 mEq/L
Blood urea nitrogen (BUN): 1414 mg/dL
Creatinine: 1.81.8 mg/dL
Glucose: 9090 mg/dL
Measured serum osmolality: 318318 mOsm/kg H2OH_2O

Arterial blood gas (room air):
pH: 7.227.22
PCO2PCO_2: 2323 mm Hg
PO2PO_2: 9898 mm Hg

Based on the provided laboratory data, what is the patient's serum osmolar gap?

Show answer & explanation

Answer: 30

Answer

30
The patient presents with an unexplained high anion gap metabolic acidosis (anion gap = 139−(104+10)=25139 - (104 + 10) = 25) and altered mental status in a context suspicious for toxic alcohol ingestion (e.g., ethylene glycol). To confirm the presence of an unmeasured osmotically active substance, the serum osmolar gap must be calculated. The standard formula for calculated serum osmolality is 2×[Na+]+BUN2.8+Glucose182 \times [Na^+] + \frac{BUN}{2.8} + \frac{Glucose}{18}. Plugging in the patient's laboratory values yields 2(139)+142.8+9018=278+5+5=2882(139) + \frac{14}{2.8} + \frac{90}{18} = 278 + 5 + 5 = 288 mOsm/kg. The osmolar gap is the measured osmolality minus the calculated osmolality: 318−288=30318 - 288 = 30 mOsm/kg. A normal osmolar gap is typically less than 10 mOsm/kg; an elevated gap of 30 mOsm/kg strongly supports the diagnosis of toxic alcohol poisoning.

Step-by-Step Solution

1
Calculate the expected serum osmolality.
288288 mOsm/kg
Expected osmolality must be determined using the formula 2×[Na+]+BUN2.8+Glucose182 \times [Na^+] + \frac{BUN}{2.8} + \frac{Glucose}{18} to serve as a baseline for identifying unmeasured osmoles.
2
Determine the osmolar gap.
3030 mOsm/kg
The osmolar gap is the difference between the measured serum osmolality and the calculated expected serum osmolality (318−288318 - 288).

Key Concept

Calculation of the serum osmolar gap to evaluate high anion gap metabolic acidosis associated with suspected toxic alcohol ingestion.
Question 291Question →

A 35-year-old woman presents to the emergency department with profound weakness in her legs that began earlier today. She reports difficulty standing from a seated position. Her medical history is significant for Sjögren syndrome and recurrent nephrolithiasis. She denies recent diarrhea, vomiting, or changes in her medications. Her temperature is 37.0°C (98.6°F), blood pressure is 110/70 mm Hg, pulse is 88/min, and respiratory rate is 16/min with shallow breaths. Physical examination reveals 2/5 motor strength in the bilateral lower extremities and diminished deep tendon reflexes.

Laboratory results are as follows:

TestValue
Sodium138 mEq/L
Potassium2.1 mEq/L
Chloride114 mEq/L
Bicarbonate14 mEq/L
Blood urea nitrogen14 mg/dL
Creatinine0.9 mg/dL

Arterial blood gas on room air:

TestValue
pH7.23
PCO2PCO_234 mm Hg
PO2PO_285 mm Hg

Which of the following best describes this patient's acid-base disturbance?

Show answer & explanation

Answer: Normal anion gap metabolic acidosis and respiratory acidosis

Answer

Normal anion gap metabolic acidosis and respiratory acidosis
This patient's primary disturbance is a normal anion gap metabolic acidosis (NAGMA), evidenced by a low bicarbonate (14 mEq/L), low pH (7.23), and a normal anion gap (138−[114+14]=10138 - [114 + 14] = 10 mEq/L). In the context of Sjögren syndrome and severe hypokalemia, this is highly characteristic of Type 1 (distal) renal tubular acidosis. To assess respiratory compensation, Winter's formula must be applied: Expected PCO2=(1.5×14)+8±2=29±2Expected\ PCO_2 = (1.5 \times 14) + 8 \pm 2 = 29 \pm 2 mm Hg (range 27-31 mm Hg). Because the patient's measured PCO2PCO_2 is 34 mm Hg, which is higher than the expected range, she has a concomitant respiratory acidosis. This occurs physiologically because her profound hypokalemia (K+=2.1K^+ = 2.1 mEq/L) has caused respiratory muscle weakness (evidenced by shallow breaths and limb weakness), limiting her ability to generate the deep, rapid breathing (Kussmaul respirations) required for adequate respiratory compensation.

Step-by-Step Solution

1
Calculate the serum anion gap.
AG=Na+−(Cl−+HCO3−)=138−(114+14)=10AG = Na^+ - (Cl^- + HCO_3^-) = 138 - (114 + 14) = 10 mEq/L.
To determine whether the primary metabolic acidosis is high anion gap or normal anion gap. An AG of 10 is normal, confirming a normal anion gap metabolic acidosis (NAGMA).
2
Calculate the expected respiratory compensation using Winter's formula.
Expected PCO2=(1.5×14)+8±2=21+8±2=29±2Expected\ PCO_2 = (1.5 \times 14) + 8 \pm 2 = 21 + 8 \pm 2 = 29 \pm 2 mm Hg (Range: 27-31 mm Hg).
To assess if the physiological respiratory response to the metabolic acidosis is appropriate, or if a secondary respiratory disorder exists.
3
Compare the actual PCO2PCO_2 to the expected PCO2PCO_2 range.
Actual PCO2PCO_2 (34 mm Hg) is greater than the maximum expected PCO2PCO_2 (31 mm Hg).
Because the actual PCO2PCO_2 is higher than expected, the patient is relatively hypoventilating, indicating a superimposed respiratory acidosis.

Key Concept

Acid-base interpretation using Winter's formula to identify a mixed normal anion gap metabolic acidosis and respiratory acidosis.
Question 292Question →

A 2nd-year internal medicine resident is preparing a presentation on inherited and acquired renal tubular disorders. Match each of the following tubulopathies with its primary pathophysiological defect or defining molecular characteristic.

Click a left item, then click its matching right item

Items

Fanconi syndrome
Bartter syndrome
Gitelman syndrome
Liddle syndrome
Syndrome of apparent mineralocorticoid excess

Matches

Show answer & explanation

Answer

Fanconi syndrome matches with the generalized proximal tubule defect; Bartter syndrome matches with the Na+-K+-2Cl- cotransporter defect; Gitelman syndrome matches with the Na+-Cl- cotransporter defect; Liddle syndrome matches with the ENaC gain-of-function mutation; Syndrome of apparent mineralocorticoid excess matches with the 11-beta-hydroxysteroid dehydrogenase type 2 enzyme deficiency.
Renal tubulopathies are characterized by specific transporter or enzymatic defects along the nephron. Fanconi syndrome causes global proximal tubular dysfunction. Bartter syndrome affects the NKCC2 transporter in the thick ascending limb. Gitelman syndrome involves the NCC transporter in the distal convoluted tubule. Liddle syndrome is driven by an overactive ENaC in the collecting duct. Finally, the syndrome of apparent mineralocorticoid excess results from a deficiency in 11-beta-hydroxysteroid dehydrogenase type 2, which normally prevents circulating cortisol from acting on mineralocorticoid receptors in the kidney.

Step-by-Step Solution

1
Identify the primary defect location for Fanconi syndrome.
It involves the proximal tubule.
This leads to a failure in reabsorbing essential filtered solutes, resulting in glycosuria, phosphaturia, and aminoaciduria.
2
Differentiate Bartter and Gitelman syndromes based on their respective transporters.
Bartter syndrome affects the thick ascending limb (NKCC2), while Gitelman syndrome affects the distal convoluted tubule (NCC).
Bartter mimics the effects of loop diuretics; Gitelman mimics the effects of thiazide diuretics.
3
Determine the mechanism behind Liddle syndrome.
Constitutive activation of ENaC in the collecting duct.
This causes unregulated sodium retention, severe hypertension, and hypokalemia, while suppressing endogenous aldosterone.
4
Identify the pathophysiology of the Syndrome of apparent mineralocorticoid excess (SAME).
Deficiency in the 11-beta-HSD2 enzyme.
Cortisol is not converted to inactive cortisone and instead binds to and over-activates the mineralocorticoid receptor.

Key Concept

Understanding the specific anatomical and molecular defects of renal tubulopathies is essential for predicting their clinical and laboratory manifestations.
Question 293Question →

A 27-year-old female with a history of type 1 diabetes mellitus and asthma is evaluated in the emergency department for a three-day history of worsening cough, fever, and shortness of breath. She has been unable to eat and has missed several doses of her basal insulin. On physical examination, her temperature is 38.5∘C38.5^{\circ}\text{C} (101.3∘F101.3^{\circ}\text{F}), blood pressure is 105/65 mmHg, pulse is 118/min, and respirations are 32/min. The patient appears lethargic and is using accessory muscles for respiration.

Laboratory studies reveal the following:

TestResult
Sodium136 mEq/L136 \text{ mEq/L}
Potassium4.8 mEq/L4.8 \text{ mEq/L}
Chloride100 mEq/L100 \text{ mEq/L}
Bicarbonate12 mEq/L12 \text{ mEq/L}
Blood urea nitrogen28 mg/dL28 \text{ mg/dL}
Creatinine1.2 mg/dL1.2 \text{ mg/dL}
Glucose512 mg/dL512 \text{ mg/dL}

Arterial blood gas analysis on room air:

TestResult
pH7.187.18
PaCO2PaCO_235 mmHg35 \text{ mmHg}
PaO2PaO_270 mmHg70 \text{ mmHg}

Based on these laboratory findings, which of the following best describes this patient's acid-base status?

Show answer & explanation

Answer: High anion gap metabolic acidosis and concurrent respiratory acidosis

Answer

High anion gap metabolic acidosis and concurrent respiratory acidosis
This patient presents with diabetic ketoacidosis (DKA) triggered by an underlying respiratory infection, leading to a primary high anion gap metabolic acidosis. The anion gap is elevated at 24 mEq/L24 \text{ mEq/L} (136−(100+12)136 - (100 + 12)). In a primary metabolic acidosis, the lungs should compensate by hyperventilating to blow off CO2CO_2 (Kussmaul respirations). The expected PaCO2PaCO_2 can be calculated using Winter's formula: Expected PaCO2=1.5×[HCO3−]+8±2PaCO_2 = 1.5 \times [HCO_3^-] + 8 \pm 2. For this patient, the expected PaCO2PaCO_2 is (1.5×12)+8=26±2 mmHg(1.5 \times 12) + 8 = 26 \pm 2 \text{ mmHg}. The patient's actual PaCO2PaCO_2 is 35 mmHg35 \text{ mmHg}, which is substantially higher than the expected target range of 24−28 mmHg24 - 28 \text{ mmHg}. This relative CO2CO_2 retention indicates a concurrent primary respiratory acidosis. Clinically, this is consistent with respiratory muscle fatigue secondary to her asthma exacerbation and severe work of breathing, preventing her from achieving the necessary compensatory hyperventilation.

Step-by-Step Solution

1
Calculate the anion gap to evaluate the metabolic acidosis.
Anion gap = Na+−(Cl−+HCO3−)=136−(100+12)=24 mEq/LNa^+ - (Cl^- + HCO_3^-) = 136 - (100 + 12) = 24 \text{ mEq/L}.
An anion gap >12 mEq/L>12 \text{ mEq/L} confirms the presence of a primary high anion gap metabolic acidosis (HAGMA), consistent with her diabetic ketoacidosis.
2
Determine the expected respiratory compensation using Winter's formula.
Expected PaCO2=(1.5×12)+8±2=18+8±2=26±2 mmHgPaCO_2 = (1.5 \times 12) + 8 \pm 2 = 18 + 8 \pm 2 = 26 \pm 2 \text{ mmHg} (Range: 24−28 mmHg24 - 28 \text{ mmHg}).
In a primary metabolic acidosis, the lungs should compensate by hyperventilating to lower PaCO2PaCO_2. Winter's formula determines if this response is adequate.
3
Compare the expected PaCO2PaCO_2 to the patient's actual PaCO2PaCO_2.
The actual PaCO2PaCO_2 is 35 mmHg35 \text{ mmHg}, which is significantly higher than the expected maximum of 28 mmHg28 \text{ mmHg}.
Because the actual PaCO2PaCO_2 is higher than the calculated compensatory target, there is relative CO2CO_2 retention, diagnosing a concurrent primary respiratory acidosis superimposed on the HAGMA.

Key Concept

Mixed Acid-Base Disorders: Utilizing Winter's Formula in High Anion Gap Metabolic Acidosis
Question 294Question →

A 68-year-old female is admitted to the hospital from an assisted living facility due to five days of severe, voluminous watery diarrhea. On presentation, she is lethargic with dry mucous membranes and delayed capillary refill. Her blood pressure is 88/54 mm Hg and her heart rate is 115/min. Laboratory studies are obtained:

TestResult
Serum sodium140 mEq/L
Serum potassium3.2 mEq/L
Serum chloride106 mEq/L
Serum bicarbonate14 mEq/L
Blood urea nitrogen58 mg/dL
Serum creatinine3.5 mg/dL

Assuming a normal anion gap of 12 mEq/L and a normal serum bicarbonate of 24 mEq/L, what is this patient's delta-delta ratio (ΔAGΔHCO3−\frac{\Delta AG}{\Delta HCO_3^-})?

Show answer & explanation

Answer: 0.8

Answer

0.8
The patient's delta-delta ratio is 0.8. She has a high anion gap metabolic acidosis (HAGMA) due to acute kidney injury (uremia from hypovolemia) combined with a normal anion gap metabolic acidosis (NAGMA) driven by severe bicarbonate loss from diarrhea. In a pure HAGMA, for every 1 mEq/L increase in the anion gap, there should be a roughly 1 mEq/L drop in bicarbonate, resulting in a delta-delta ratio between 1.0 and 2.0. A ratio below 1.0 indicates that the bicarbonate has dropped more than expected for the degree of unmeasured anions, signaling an additional, concurrent non-anion gap metabolic acidosis.

Step-by-Step Solution

1
Calculate the patient's current anion gap (AG)
AG=20 mEq/LAG = 20 \text{ mEq/L}
The anion gap is required to determine the presence of a high anion gap metabolic acidosis and to calculate the delta gap. Formula: Na+−(Cl−+HCO3−)Na^+ - (Cl^- + HCO_3^-)
2
Calculate the delta anion gap (ΔAG\Delta AG)
ΔAG=8 mEq/L\Delta AG = 8 \text{ mEq/L}
This value represents how much the patient's anion gap has risen above the normal baseline (12 mEq/L).
3
Calculate the delta bicarbonate (ΔHCO3−\Delta HCO_3^-)
ΔHCO3−=10 mEq/L\Delta HCO_3^- = 10 \text{ mEq/L}
This value represents how much the patient's serum bicarbonate has fallen from the normal baseline (24 mEq/L) due to buffering.
4
Calculate the delta-delta ratio
0.80.8
Dividing ΔAG\Delta AG by ΔHCO3−\Delta HCO_3^- reveals the proportional change, helping identify mixed acid-base disorders.

Key Concept

The delta-delta ratio (ΔAGΔHCO3−\frac{\Delta AG}{\Delta HCO_3^-}) is utilized to identify mixed acid-base disorders in the presence of a high anion gap metabolic acidosis. A ratio < 1.0 (or < 0.8 depending on the criteria) suggests a concurrent normal anion gap metabolic acidosis.
Question 295Question →

A 62-year-old man is brought to the emergency department after falling from a 10-foot ladder while cleaning his gutters. He states he was lying on the ground for approximately 12 hours before a neighbor found him. He complains of severe, sharp pain in his right lower chest that significantly worsens when he takes a deep breath. His temperature is 36.8°C (98.2°F), blood pressure is 115/75 mmHg, pulse is 112/min, and respiratory rate is 16/min with shallow breaths. Physical examination reveals bruising and marked point tenderness over the right 7th and 8th ribs. Decreased breath sounds are noted at the right lung base.

Laboratory results are as follows:

Serum ChemistryValue
Sodium140140 mEq/L
Potassium5.25.2 mEq/L
Chloride104104 mEq/L
Bicarbonate1212 mEq/L
Blood urea nitrogen5555 mg/dL
Creatinine3.13.1 mg/dL
Creatine kinase18,50018,500 U/L
Arterial Blood Gas (Room Air)Value
pH7.167.16
PaCO2P_aCO_23535 mmHg
PaO2P_aO_26868 mmHg

Which of the following best describes this patient's acid-base disturbance?

Show answer & explanation

Answer: High anion gap metabolic acidosis and concurrent respiratory acidosis

Answer

High anion gap metabolic acidosis and concurrent respiratory acidosis
This patient has a mixed acid-base disorder: a high anion gap metabolic acidosis (HAGMA) and a concurrent respiratory acidosis. The primary disturbance is a metabolic acidosis, evidenced by severe acidemia (pH 7.167.16) and low bicarbonate (1212 mEq/L). The anion gap is elevated at 2424 mEq/L (140−[104+12]140 - [104 + 12]), confirming a HAGMA. Clinically, this is likely secondary to acute kidney injury from rhabdomyolysis (markedly elevated CK and creatinine) following his prolonged immobilization. To assess respiratory compensation, Winter's formula must be applied: ExpectedPaCO2=1.5×HCO3−+8±2Expected P_aCO_2 = 1.5 \times HCO_3^- + 8 \pm 2. For this patient, the expected PaCO2=1.5×12+8=26±2P_aCO_2 = 1.5 \times 12 + 8 = 26 \pm 2 mmHg (range: 24−2824-28 mmHg). The patient's actual PaCO2P_aCO_2 is 3535 mmHg. Because the actual PaCO2P_aCO_2 is significantly higher than the expected range, he has inadequate respiratory compensation, defining a concurrent respiratory acidosis. This hypoventilation is clinically consistent with splinting due to severe pain from his rib fractures.

Step-by-Step Solution

1
Determine the primary acid-base disturbance.
The pH is 7.167.16 (acidemia) and HCO3−HCO_3^- is 1212 mEq/L (low), indicating a primary metabolic acidosis.
The direction of the pH change matches the direction of the HCO3−HCO_3^- change, defining a metabolic primary process.
2
Calculate the anion gap (AG) to classify the metabolic acidosis.
AG=Na+−(Cl−+HCO3−)=140−(104+12)=24AG = Na^+ - (Cl^- + HCO_3^-) = 140 - (104 + 12) = 24 mEq/L.
A normal AG is 10−1410-14 mEq/L. An AG of 2424 indicates a high anion gap metabolic acidosis (HAGMA), likely due to uremia secondary to rhabdomyolysis-induced acute kidney injury.
3
Apply Winter's formula to determine the expected respiratory compensation.
ExpectedPaCO2=1.5×(HCO3−)+8±2Expected P_aCO_2 = 1.5 \times (HCO_3^-) + 8 \pm 2. Thus, 1.5×(12)+8=26±21.5 \times (12) + 8 = 26 \pm 2 mmHg (range: 2424 to 2828 mmHg).
Winter's formula predicts the appropriate compensatory hyperventilation (decrease in PaCO2P_aCO_2) for a given severity of metabolic acidosis.
4
Compare the actual PaCO2P_aCO_2 to the expected PaCO2P_aCO_2.
The actual PaCO2P_aCO_2 is 3535 mmHg, which is significantly higher than the expected range of 24−2824-28 mmHg.
When actual PaCO2P_aCO_2 is higher than expected, it indicates inadequate ventilation and a concurrent respiratory acidosis (due to pain splinting from rib fractures in this patient).
5
Check the delta-delta ratio for any occult metabolic alkalosis.
ΔAG=24−12=12\Delta AG = 24 - 12 = 12. ΔHCO3−=24−12=12\Delta HCO_3^- = 24 - 12 = 12. Ratio = 12/12=1.012 / 12 = 1.0.
A ratio between 11 and 22 implies a pure HAGMA without an additional metabolic component.

Key Concept

Patients with a primary metabolic acidosis should hyperventilate to decrease PaCO2P_aCO_2. If the actual PaCO2P_aCO_2 is higher than the expected PaCO2P_aCO_2 calculated by Winter's formula (1.5×HCO3−+8±21.5 \times HCO_3^- + 8 \pm 2), a concurrent respiratory acidosis is present.
Estimated Time:2m 0s
Question 296Question →

A medical team is reviewing arterial blood gas and basic metabolic panel results for several patients in the intensive care and step-down units. Match each patient's clinical presentation with their most likely primary acid-base disturbance.

Click a left item, then click its matching right item

Items

A 22-year-old with recurrent vomiting due to severe gastroparesis, presenting with dehydration and muscle cramps
A 28-year-old presenting with perioral numbness and carpopedal spasm during a severe panic attack
A 45-year-old with a high-output ileostomy presenting with lethargy and profound weakness
A 55-year-old with acute mesenteric ischemia presenting with an acute abdomen and hypotension
A 65-year-old with a severe exacerbation of chronic bronchitis presenting with somnolence and a depressed respiratory drive

Matches

Show answer & explanation

Answer

The correct pairings match upper GI losses to metabolic alkalosis, hyperventilation to respiratory alkalosis, lower GI losses to normal anion gap acidosis, tissue ischemia to high anion gap acidosis, and hypoventilation to respiratory acidosis.
Each clinical scenario uniquely maps to a single primary acid-base disturbance: vomiting causes H+ loss (alkalosis), hyperventilation blows off CO2 (respiratory alkalosis), an ileostomy loses HCO3- (normal AG acidosis), ischemia generates lactate (high AG acidosis), and hypoventilation retains CO2 (respiratory acidosis).

Step-by-Step Solution

1
Analyze the acid-base impact of recurrent vomiting.
Metabolic alkalosis.
Loss of gastric acid (H+) and volume depletion-induced aldosterone release lead to net bicarbonate retention and chloride loss.
2
Analyze the acid-base impact of hyperventilation.
Respiratory alkalosis.
An increased respiratory rate directly blows off CO2, lowering PaCO2 and raising pH.
3
Analyze the acid-base impact of lower gastrointestinal fluid losses (e.g., via an ileostomy).
Normal anion gap metabolic acidosis.
Direct loss of bicarbonate-rich fluid from the lower GI tract causes a non-anion gap acidosis, which is balanced by renal chloride retention.
4
Analyze the acid-base impact of acute mesenteric ischemia.
High anion gap metabolic acidosis.
Tissue ischemia rapidly produces lactate, an unmeasured anion that consumes bicarbonate and increases the anion gap.
5
Analyze the acid-base impact of a COPD exacerbation with hypoventilation.
Respiratory acidosis.
Hypoventilation and worsened ventilation-perfusion mismatch lead to acute CO2 retention in the blood.

Key Concept

Different clinical scenarios produce distinct primary acid-base disturbances based on the underlying mechanism (e.g., GI loss of acid vs. base, tissue hypoxia, ventilation changes).
Question 297Question →

An 18-year-old college freshman visits the campus health center complaining of a constant "ringing" sound in his ears, generalized nausea, and three episodes of nonbloody emesis since last night. He states he has been feeling extremely overwhelmed by his upcoming final examinations. On physical examination, he appears anxious and is breathing rapidly and deeply.

Vital signs:
Temperature: 37.8∘C37.8^\circ C (100.0∘F100.0^\circ F)
Blood pressure: 112/70112/70 mm Hg
Pulse: 114114/min
Respirations: 2828/min

Laboratory results:
Serum chemistry:
Sodium: 140140 mEq/L
Potassium: 3.83.8 mEq/L
Chloride: 104104 mEq/L
Bicarbonate: 1414 mEq/L
Blood urea nitrogen: 1818 mg/dL
Creatinine: 0.80.8 mg/dL

Arterial blood gas (room air):
pH: 7.477.47
PaCO2PaCO_2: 2020 mm Hg
PaO2PaO_2: 9898 mm Hg

Based on the laboratory results, which of the following best characterizes this patient's acid-base status?

Show answer & explanation

Answer: Mixed primary high anion gap metabolic acidosis and primary respiratory alkalosis

Answer

Mixed primary high anion gap metabolic acidosis and primary respiratory alkalosis
This patient's clinical presentation (tinnitus, nausea, tachypnea) is classic for salicylate (aspirin) toxicity. The laboratory values reveal a mixed primary high anion gap metabolic acidosis and primary respiratory alkalosis. First, the anion gap is elevated at 2222 mEq/L (140−[104+14]140 - [104 + 14]), confirming a primary high anion gap metabolic acidosis (HAGMA). Next, Winter's formula is applied to determine if the respiratory response is appropriate: Expected PaCO2=(1.5×14)+8=29±2PaCO_2 = (1.5 \times 14) + 8 = 29 \pm 2 mm Hg. Because the patient's measured PaCO2PaCO_2 (2020 mm Hg) is significantly lower than the expected range (2727-3131 mm Hg), there is an independent, primary respiratory alkalosis driving the PaCO2PaCO_2 down further.

Step-by-Step Solution

1
Calculate the anion gap to check for a primary metabolic acidosis.
AG=Na+−(Cl−+HCO3−)=140−(104+14)=22AG = Na^+ - (Cl^- + HCO_3^-) = 140 - (104 + 14) = 22 mEq/L.
An elevated anion gap (>12>12 mEq/L) confirms the presence of a primary high anion gap metabolic acidosis (HAGMA).
2
Apply Winter's formula to determine the expected respiratory compensation for the metabolic acidosis.
Expected PaCO2=(1.5×HCO3−)+8±2=(1.5×14)+8±2=29±2PaCO_2 = (1.5 \times HCO_3^-) + 8 \pm 2 = (1.5 \times 14) + 8 \pm 2 = 29 \pm 2 mm Hg (Range: 2727 to 3131 mm Hg).
This establishes the predicted normal physiologic respiratory response to the patient's low bicarbonate level.
3
Compare the measured PaCO2PaCO_2 to the expected PaCO2PaCO_2 range.
The measured PaCO2PaCO_2 is 2020 mm Hg, which is significantly lower than the expected lower limit of 2727 mm Hg.
A PaCO2PaCO_2 lower than the expected compensatory range indicates that the patient is hyperventilating beyond physiologic compensation, confirming an independent, coexisting primary respiratory alkalosis.

Key Concept

Salicylate toxicity classically presents with a mixed primary high anion gap metabolic acidosis (due to uncoupling of oxidative phosphorylation) and a primary respiratory alkalosis (due to direct stimulation of the medullary respiratory center).
Question 298Question →

A 45-year-old man is evaluated in the intensive care unit for worsening kidney function. Three days ago, he was admitted with severe sepsis secondary to right lower lobe pneumonia and required vasopressor support for 48 hours. His blood pressure is now stable off vasopressors. Urine output over the last 12 hours has been 250 mL.

Laboratory studies are obtained:

Lab TestValue
Serum sodium140 mEq/L
Serum creatinine2.0 mg/dL
Blood urea nitrogen40 mg/dL
Urine sodium84 mEq/L
Urine creatinine60 mg/dL

What is the patient's fractional excretion of sodium (FeNaFe_{Na}) expressed as a percentage?

Show answer & explanation

Answer: 2

Answer

2.0
The patient's fractional excretion of sodium (FeNaFe_{Na}) is calculated as 2.0%2.0\%. In the context of a patient with recent hypotension/shock, an FeNa≥2%Fe_{Na} \ge 2\% strongly points toward established Acute Tubular Necrosis (ATN) as the cause of acute kidney injury, reflecting the damaged tubules' inability to effectively reabsorb sodium.

Step-by-Step Solution

1
Recall the formula for Fractional Excretion of Sodium (FeNaFe_{Na}).
FeNa=UNa×PCrPNa×UCr×100Fe_{Na} = \frac{U_{Na} \times P_{Cr}}{P_{Na} \times U_{Cr}} \times 100
This formula relates sodium clearance to creatinine clearance and is essential for distinguishing intrinsic renal disease from prerenal azotemia.
2
Extract the relevant values from the laboratory panel.
UNa=84U_{Na} = 84 mEq/L
PCr=2.0P_{Cr} = 2.0 mg/dL
PNa=140P_{Na} = 140 mEq/L
UCr=60U_{Cr} = 60 mg/dL
Accurate variable identification prevents common substitution errors, such as mistakenly using Blood Urea Nitrogen (BUN) instead of serum creatinine.
3
Substitute the values into the formula and calculate the numerator and denominator.
Numerator: 84×2.0=16884 \times 2.0 = 168
Denominator: 140×60=8400140 \times 60 = 8400
Breaking the calculation into intermediate steps reduces mathematical errors.
4
Divide the numerator by the denominator and multiply by 100.
1688400=0.02\frac{168}{8400} = 0.02
0.02×100=2.0%0.02 \times 100 = 2.0\%
Multiplying by 100 converts the raw fraction into the standard percentage format used in clinical practice.

Key Concept

Fractional Excretion of Sodium (FeNa) calculation and interpretation in Acute Kidney Injury

Alternative Method

You can also conceptualize FeNaFe_{Na} conceptually as the ratio of sodium clearance to creatinine clearance: FeNa=(CNa/CCr)×100Fe_{Na} = (C_{Na} / C_{Cr}) \times 100. This helps derive the equation intuitively without pure memorization.
Estimated Time:1m 0s
Question 299Question →

A 42-year-old woman is brought to the emergency department with sudden-onset shortness of breath and right-sided pleuritic chest pain. Her medical history includes ulcerative colitis, and she reports experiencing a severe disease flare with 6 to 8 watery bowel movements daily for the past week. Vital signs show a temperature of 37.6°C (99.7°F), heart rate of 115/min, blood pressure of 112/68 mm Hg, and respiratory rate of 28/min. Pulse oximetry is 88% on room air. Physical examination reveals clear lungs bilaterally but right calf swelling and tenderness. A computed tomography pulmonary angiogram confirms a segmental pulmonary embolism. Laboratory studies are as follows:

LabValue
Sodium138 mEq/L138 \text{ mEq/L}
Potassium3.4 mEq/L3.4 \text{ mEq/L}
Chloride118 mEq/L118 \text{ mEq/L}
Bicarbonate10 mEq/L10 \text{ mEq/L}

Arterial blood gas (room air):
pH: 7.39
PaCO2\text{PaCO}_2: 17 mm Hg17 \text{ mm Hg}
PaO2\text{PaO}_2: 55 mm Hg55 \text{ mm Hg}

Based on these results, which of the following best characterizes this patient's acid-base status?

Show answer & explanation

Answer: Non-anion gap metabolic acidosis and an additional respiratory alkalosis

Answer

Non-anion gap metabolic acidosis and an additional respiratory alkalosis
The correct answer identifies a non-anion gap metabolic acidosis and a concurrent primary respiratory alkalosis. This patient presents with an acidemic pH (7.39) and a low bicarbonate (10 mEq/L10 \text{ mEq/L}), which establishes a primary metabolic acidosis driven by gastrointestinal bicarbonate losses from her ulcerative colitis flare. The anion gap is calculated as Na+−(Cl−+HCO3−)=138−(118+10)=10 mEq/L\text{Na}^+ - (\text{Cl}^- + \text{HCO}_3^-) = 138 - (118 + 10) = 10 \text{ mEq/L}. Because this falls within the normal range (8−12 mEq/L8-12 \text{ mEq/L}), the disorder is a non-anion gap metabolic acidosis. To determine if there is a mixed disorder, Winter's formula must be applied: Expected PaCO2=1.5×[HCO3−]+8±2\text{Expected PaCO}_2 = 1.5 \times [\text{HCO}_3^-] + 8 \pm 2. For this patient, the expected PaCO2\text{PaCO}_2 is (1.5×10)+8=23±2 mm Hg(1.5 \times 10) + 8 = 23 \pm 2 \text{ mm Hg} (range 21−25 mm Hg21-25 \text{ mm Hg}). Her measured PaCO2\text{PaCO}_2 is 17 mm Hg17 \text{ mm Hg}, which is significantly lower than the expected compensatory range. A PaCO2\text{PaCO}_2 lower than expected indicates an additional primary respiratory alkalosis. In this clinical scenario, the superimposed respiratory alkalosis is caused by hypoxia and pain-driven hyperventilation secondary to her acute pulmonary embolism.

Step-by-Step Solution

1
Identify the primary acid-base disorder from the pH and bicarbonate.
The pH is acidemic (7.39) and the bicarbonate is low (10 mEq/L10 \text{ mEq/L}), establishing a primary metabolic acidosis.
pH < 7.40 defines acidemia, and a low bicarbonate indicates a metabolic origin.
2
Calculate the serum anion gap.
Anion gap = 138−(118+10)=10 mEq/L138 - (118 + 10) = 10 \text{ mEq/L}. This is normal, confirming a non-anion gap metabolic acidosis.
Differentiating between normal and elevated anion gap metabolic acidosis helps identify the underlying etiology (gastrointestinal losses in this case).
3
Apply Winter's formula to determine the expected respiratory compensation.
Expected PaCO2=(1.5×10)+8±2=23±2 mm Hg\text{Expected PaCO}_2 = (1.5 \times 10) + 8 \pm 2 = 23 \pm 2 \text{ mm Hg} (range: 21−25 mm Hg21-25 \text{ mm Hg}).
Winter's formula evaluates if the respiratory response to metabolic acidosis is appropriate.
4
Compare the measured PaCO2\text{PaCO}_2 to the expected range.
The measured PaCO2\text{PaCO}_2 (17 mm Hg17 \text{ mm Hg}) is lower than the expected range (21−25 mm Hg21-25 \text{ mm Hg}).
A PaCO2\text{PaCO}_2 lower than expected indicates excessive hyperventilation, revealing a concurrent primary respiratory alkalosis (due to the pulmonary embolism).

Key Concept

Identifying mixed acid-base disorders requires calculating the anion gap to classify metabolic acidosis and applying Winter's formula to determine if respiratory compensation is appropriate or if a secondary respiratory disorder exists.
Question 300Question →

A 35-year-old man is brought to the urgent care clinic by his roommate because of confusion and an inability to keep fluids down for the past 4 days. The roommate reports the patient has a history of type 1 diabetes mellitus but lost his insurance recently and started rationing his insulin. Over the last 96 hours, the patient has had severe nausea and vomited more than 10 times daily. He appears lethargic and is difficult to arouse. His temperature is 37.1°C (98.8°F), blood pressure is 92/56 mm Hg, pulse is 124/min, and respirations are 16/min. Examination shows deeply sunken eyes, dry oral mucosa, and delayed capillary refill.

Laboratory TestResult
Serum sodium138 mEq/L
Serum potassium2.9 mEq/L
Serum chloride80 mEq/L
Serum bicarbonate25 mEq/L
Blood urea nitrogen52 mg/dL
Serum creatinine2.1 mg/dL
Plasma glucose640 mg/dL
Arterial Blood Gas (Room Air)Result
pH7.42
pCO241 mm Hg
pO292 mm Hg

Analysis of these laboratory findings most accurately indicates which of the following underlying acid-base disturbances?

Show answer & explanation

Answer: Mixed high anion gap metabolic acidosis and metabolic alkalosis

Answer

Mixed high anion gap metabolic acidosis and metabolic alkalosis
The correct answer is mixed high anion gap metabolic acidosis (HAGMA) and metabolic alkalosis. Despite a normal pH (7.42) and bicarbonate (25 mEq/L), this patient's anion gap is markedly elevated at 33 mEq/L (138−(80+25)=33138 - (80 + 25) = 33). This indicates the presence of a HAGMA, which in this clinical context is diabetic ketoacidosis. To determine if another metabolic disorder is present, the delta-delta concept must be applied. The expected original bicarbonate is calculated by adding the delta anion gap (ΔAG=33−12=21\Delta AG = 33 - 12 = 21) to the measured bicarbonate: 25+21=4625 + 21 = 46 mEq/L. Because this value is much higher than the normal bicarbonate range (22-26 mEq/L), there is a concurrent metabolic alkalosis. Clinically, the HAGMA is driven by ketoacid accumulation, while the metabolic alkalosis is driven by profound gastric acid and chloride loss from intractable vomiting.

Step-by-Step Solution

1
Evaluate the primary acid-base status using pH, pCO2pCO_2, and HCO3−HCO_3^-.
The pH is 7.42 (normal), pCO2pCO_2 is 41 mm Hg (normal), and HCO3−HCO_3^- is 25 mEq/L (normal).
To identify any overt acidemia or alkalemia and primary respiratory or metabolic disturbances.
2
Calculate the serum anion gap (AG=Na+−(Cl−+HCO3−)AG = Na^+ - (Cl^- + HCO_3^-)).
AG=138−(80+25)=33AG = 138 - (80 + 25) = 33 mEq/L.
An anion gap must be calculated in all critically ill patients, regardless of a normal pH, to detect hidden metabolic acidosis.
3
Calculate the delta gap (ΔAG=MeasuredAG−NormalAG\Delta AG = Measured AG - Normal AG) and expected original bicarbonate.
ΔAG=33−12=21\Delta AG = 33 - 12 = 21 mEq/L. Expected original HCO3−=MeasuredHCO3−+ΔAG=25+21=46HCO_3^- = Measured HCO_3^- + \Delta AG = 25 + 21 = 46 mEq/L.
To determine if a second concurrent metabolic disturbance is present alongside the high anion gap metabolic acidosis.
4
Interpret the delta-delta result.
An expected original HCO3−HCO_3^- of 46 mEq/L is significantly greater than the normal range (22-26 mEq/L), indicating a concurrent metabolic alkalosis.
The large excess in bicarbonate points to a second process adding bicarbonate to the serum, consistent with the patient's severe vomiting.

Key Concept

Patients with a normal pH and bicarbonate can still have severe, opposing mixed acid-base disorders. Calculating the anion gap and delta-delta ratio is essential to uncover a hidden high anion gap metabolic acidosis that is masked by a concurrent metabolic alkalosis.

Alternative Method

Instead of calculating the expected original bicarbonate, the Δ\Delta Ratio can be used: ΔRatio=ΔAGΔHCO3−=33−1224−25=21−1\Delta Ratio = \frac{\Delta AG}{\Delta HCO_3^-} = \frac{33 - 12}{24 - 25} = \frac{21}{-1}. A negative denominator (because measured bicarbonate is higher than the normal baseline) or a ratio >2.0> 2.0 strongly indicates a concurrent metabolic alkalosis.
Estimated Time:1m 30s
PreviousPage 15 / 17Next
Nephrology Practice Questions — USMLE Step 2 CK — Page 15 | Examkin