Nephrology Practice Questions — USMLE Step 2 CK — Page 14

Question 261Question →

Emergency medical services bring a 72-year-old woman to the hospital after her daughter found her profoundly lethargic at home. According to the daughter, the patient has had severe, watery, non-bloody diarrhea for the past five days. Her past medical history is significant for severe chronic obstructive pulmonary disease requiring home oxygen therapy, hypertension, and osteoarthritis. Upon arrival, the patient is difficult to arouse.

Temperature is $37.2^\circ\text{C}$ ( $99.0^\circ\text{F}$ ), blood pressure is $88/54$ mmHg, pulse is $114$ /min, and respiratory rate is $26$ /min. Physical examination reveals dry mucous membranes, delayed capillary refill, and decreased breath sounds bilaterally with a prolonged expiratory phase.

Arterial blood gas (room air) and serum chemistries are obtained:

Laboratory Parameter	Result
Arterial pH	$7.21$
$\text{PaCO}_2$	$42$ mmHg
$\text{PaO}_2$	$56$ mmHg
Sodium	$139$ mEq/L
Potassium	$3.1$ mEq/L
Chloride	$114$ mEq/L
Bicarbonate	$15$ mEq/L
Blood urea nitrogen (BUN)	$48$ mg/dL
Creatinine	$2.1$ mg/dL

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

Mixed non-anion gap metabolic acidosis and respiratory acidosis

Mixed high anion gap metabolic acidosis and respiratory acidosis

Non-anion gap metabolic acidosis with appropriate respiratory compensation

High anion gap metabolic acidosis with appropriate respiratory compensation

Mixed non-anion gap metabolic acidosis and respiratory alkalosis

Show answer & explanation

Answer: Mixed non-anion gap metabolic acidosis and respiratory acidosis

Answer

Mixed non-anion gap metabolic acidosis and respiratory acidosis

The correct answer is a mixed non-anion gap metabolic acidosis and respiratory acidosis. The first step in evaluating this patient's acid-base status is identifying the primary disorder: the

pH

is

7.21

(acidemia) and the serum bicarbonate is

15

mEq/L (decreased), signifying a primary metabolic acidosis. Next, the anion gap must be calculated:

\text{Na}^+ - (\text{Cl}^- + \text{HCO}_3^-) = 139 - (114 + 15) = 10

mEq/L. Because this falls within the normal physiologic range (

8-12

mEq/L), the patient has a normal anion gap (hyperchloremic) metabolic acidosis, which directly corresponds to her history of profound watery diarrhea causing massive gastrointestinal bicarbonate loss. The final step is assessing the adequacy of respiratory compensation using Winter's formula: Expected

\text{PaCO}_2 = (1.5 \times 15) + 8 \pm 2 = 30.5 \pm 2

mmHg. For appropriate respiratory compensation, her

\text{PaCO}_2

should fall between

28.5

and

32.5

mmHg. However, her measured

\text{PaCO}_2

is

42

mmHg. Because her measured

\text{PaCO}_2

is substantially higher than expected, she is retaining

\text{CO}_2

, representing a superimposed, concurrent primary respiratory acidosis. This occurs because her severe underlying chronic obstructive pulmonary disease and lethargy prevent her from achieving the necessary compensatory hyperventilation.

Step-by-Step Solution

1

Analyze the primary acid-base disorder by looking at pH and bicarbonate.

The arterial pH is

7.21

(acidemia) and serum bicarbonate (

\text{HCO}_3^-

) is

15

mEq/L (low). This indicates a primary metabolic acidosis.

Establishing the direction of the primary disorder dictates which compensatory formula must be applied.

2

Calculate the anion gap (AG) to determine the etiology of the metabolic acidosis.

AG = \text{Na}^+ - (\text{Cl}^- + \text{HCO}_3^-) = 139 - (114 + 15) = 139 - 129 = 10

mEq/L.

A normal AG (

8-12

mEq/L) confirms a non-anion gap metabolic acidosis, which in this patient is due to profound gastrointestinal bicarbonate loss from diarrhea.

3

Determine expected respiratory compensation using Winter's formula.

Expected

\text{PaCO}_2 = (1.5 \times \text{HCO}_3^-) + 8 \pm 2

. Here,

(1.5 \times 15) + 8 = 22.5 + 8 = 30.5 \pm 2

(range

28.5

to

32.5

mmHg).

Winter's formula determines the physiologic

\text{CO}_2

elimination expected in response to a specific degree of metabolic acidosis.

4

Compare the measured

\text{PaCO}_2

to the expected

\text{PaCO}_2

.

The measured

\text{PaCO}_2

is

42

mmHg, which is significantly higher than the maximum expected value of

32.5

mmHg.

An inappropriately elevated

\text{PaCO}_2

indicates a concurrent primary respiratory acidosis, secondary to hypoventilation from her underlying chronic obstructive pulmonary disease and severe fatigue.

Key Concept

Identifying mixed acid-base disorders using the anion gap and Winter's formula

Question 262Question →

A 22-year-old woman with a history of bulimia nervosa and type 1 diabetes mellitus is brought to the emergency department by her roommate due to severe lethargy and confusion. The roommate reports that the patient has been intentionally restricting her insulin doses and has been vomiting frequently over the past 3 days. Temperature is 37.0°C (98.6°F), blood pressure is 100/60 mmHg, pulse is 118/min, and respirations are 24/min.

Laboratory studies show:

Parameter	Value
Serum sodium	142 mEq/L
Serum potassium	3.4 mEq/L
Serum chloride	94 mEq/L
Serum bicarbonate	16 mEq/L
Blood glucose	480 mg/dL

Arterial blood gas on room air:

Parameter	Value
pH	7.32
$pCO_2$	32 mmHg
$pO_2$	95 mmHg

Assuming a baseline normal serum anion gap of 12 mEq/L and a normal serum bicarbonate of 24 mEq/L, what is the calculated delta ratio ( $\frac{\Delta AG}{\Delta HCO_3^-}$ ) for this patient?

Show answer & explanation

Answer: 2.5

Answer

The calculated delta ratio is 2.5.

The delta ratio is calculated by dividing the change in anion gap (

\Delta AG

) by the change in serum bicarbonate (

\Delta HCO_3^-

). For this patient, the measured anion gap is

142 - (94 + 16) = 32

. The

\Delta AG

is

32 - 12 = 20

. The

\Delta HCO_3^-

is

24 - 16 = 8

. Therefore, the delta ratio is

\frac{20}{8} = 2.5

. In an uncomplicated high anion gap metabolic acidosis (like pure diabetic ketoacidosis), the ratio is typically between 1.0 and 2.0. A ratio greater than 2.0 indicates that the bicarbonate level is higher than expected for the degree of anion gap elevation, which signifies a concurrent metabolic alkalosis. In this clinical scenario, the metabolic alkalosis is driven by the patient's frequent vomiting, leading to a loss of

H^+

and

Cl^-

.

Step-by-Step Solution

1

Calculate the patient's measured serum anion gap.

AG = 142 - (94 + 16) = 32

mEq/L.

The first step in evaluating a metabolic acidosis is determining the presence and size of an anion gap.

2

Calculate the change in anion gap (

\Delta AG

).

\Delta AG = 32 - 12 = 20

mEq/L.

This value represents the excess unmeasured anions contributing to the acidosis.

3

Calculate the change in serum bicarbonate (

\Delta HCO_3^-

).

\Delta HCO_3^- = 24 - 16 = 8

mEq/L.

This determines how much the bicarbonate has dropped from the normal baseline.

4

Calculate the delta ratio.

Ratio = \frac{20}{8} = 2.5

.

The delta ratio helps identify mixed acid-base disorders, such as a concurrent metabolic alkalosis.

Key Concept

The delta ratio (

\frac{\Delta AG}{\Delta HCO_3^-}

) is used in high anion gap metabolic acidosis to identify concurrent mixed acid-base disorders, with a ratio > 2.0 indicating an additional metabolic alkalosis.

Alternative Method

The delta gap (expected bicarbonate) can also be calculated as: Measured

HCO_3^-

+

\Delta AG

. Here,

16 + 20 = 36

mEq/L. Since the expected normal bicarbonate (36) is significantly higher than the normal baseline of 24, a concurrent metabolic alkalosis is confirmed.

Estimated Time:1m 30s

Question 263Question →

A 52-year-old man with a history of severe alcohol use disorder is brought to the emergency department after being found unresponsive by his landlord. The landlord reports that the patient had been complaining of severe, intractable vomiting for the preceding three days and was unable to keep any fluids down. On physical examination, the patient appears lethargic and has remarkably dry mucous membranes with delayed capillary refill. Vital signs show a temperature of $37.1^\circ\text{C}$ ( $98.8^\circ\text{F}$ ), blood pressure of $88/55\text{ mm Hg}$ , pulse of $118/\text{min}$ , and respiratory rate of $10/\text{min}$ .

Laboratory studies reveal the following:

Serum sodium: $136\text{ mEq/L}$
Serum potassium: $3.1\text{ mEq/L}$
Serum chloride: $82\text{ mEq/L}$
Serum bicarbonate: $13\text{ mEq/L}$
Blood urea nitrogen: $68\text{ mg/dL}$
Serum creatinine: $3.4\text{ mg/dL}$ (baseline $1.1\text{ mg/dL}$ )

Arterial blood gas (room air):
pH: $7.16$
$PaCO_2$ : $38\text{ mm Hg}$
$PaO_2$ : $68\text{ mm Hg}$

Based on the provided laboratory results, which of the following best characterizes the complete set of primary acid-base abnormalities present in this patient?

Elevated anion gap metabolic acidosis, metabolic alkalosis, and respiratory acidosis

Elevated anion gap metabolic acidosis and respiratory acidosis only

Elevated anion gap metabolic acidosis and metabolic alkalosis with appropriate respiratory compensation

Normal anion gap metabolic acidosis and respiratory acidosis

Elevated anion gap metabolic acidosis, normal anion gap metabolic acidosis, and respiratory acidosis

Show answer & explanation

Answer: Elevated anion gap metabolic acidosis, metabolic alkalosis, and respiratory acidosis

Answer

Elevated anion gap metabolic acidosis, metabolic alkalosis, and respiratory acidosis

The correct answer identifies a triple acid-base disorder. First, the low pH (

7.16

) and low bicarbonate (

13\text{ mEq/L}

) establish metabolic acidosis. The anion gap is calculated as

136 - (82 + 13) = 41\text{ mEq/L}

, revealing an elevated anion gap metabolic acidosis (HAGMA). Next, Winter's formula (

Expected\ PaCO_2 = 1.5 \times [HCO_3^-] + 8

) predicts a

PaCO_2

of

27.5\text{ mm Hg}

. The patient's actual

PaCO_2

of

38\text{ mm Hg}

is significantly higher than expected, indicating a concurrent respiratory acidosis due to hypoventilation. Finally, the delta gap is calculated to find hidden metabolic disorders:

\Delta AG = 41 - 12 = 29

. Adding this

\Delta AG

to the measured bicarbonate gives

29 + 13 = 42\text{ mEq/L}

. Because this is significantly greater than

24\text{ mEq/L}

, a concurrent metabolic alkalosis is also present, consistent with his history of severe vomiting.

Step-by-Step Solution

1

Determine the primary acid-base disturbance using the pH and serum bicarbonate.

The pH is

7.16

(acidemia) and the

HCO_3^-

is

13\text{ mEq/L}

(low). This establishes a primary metabolic acidosis.

Establishing the dominant disorder directs the subsequent formulas needed for full analysis.

2

Calculate the anion gap (AG) to classify the metabolic acidosis.

AG = Na^+ - (Cl^- + HCO_3^-) = 136 - (82 + 13) = 136 - 95 = 41\text{ mEq/L}

.

Since the normal AG is roughly

12\text{ mEq/L}

, a value of

41\text{ mEq/L}

confirms the presence of an elevated anion gap metabolic acidosis (HAGMA).

3

Calculate the expected respiratory compensation using Winter's formula.

Expected\ PaCO_2 = (1.5 \times 13) + 8 = 19.5 + 8 = 27.5 \pm 2\text{ mm Hg}

. The measured

PaCO_2

is

38\text{ mm Hg}

.

Because the measured

PaCO_2

(

38

) is greater than the expected range (

25.5 - 29.5

), there is inadequate respiratory compensation, indicating a concurrent respiratory acidosis (likely due to lethargy/hypoventilation).

4

Perform a delta-delta (

\Delta/\Delta

) calculation to assess for a third, hidden metabolic disorder.

\Delta AG = Measured\ AG - 12 = 41 - 12 = 29

. Adding the

\Delta AG

to the measured

HCO_3^-

yields

29 + 13 = 42\text{ mEq/L}

.

If this were a pure HAGMA, the sum of the

\Delta AG

and measured

HCO_3^-

should equal the normal starting bicarbonate (

\sim 24\text{ mEq/L}

). A value significantly

> 24

(here,

42

) indicates that bicarbonate was added to the system, confirming a concurrent metabolic alkalosis from the severe vomiting.

Key Concept

Evaluation of complex acid-base disorders requires a systematic approach: identifying the primary disturbance, calculating the anion gap, assessing for adequate respiratory compensation using Winter's formula, and utilizing the delta gap (

\Delta/\Delta

) to unmask hidden secondary metabolic abnormalities.

Alternative Method

Instead of adding the delta gap to the measured bicarbonate, you can calculate the delta ratio (

\Delta AG / \Delta HCO_3^-

). Here,

\Delta AG

is

29

(

41 - 12

) and

\Delta HCO_3^-

is

11

(

24 - 13

). The ratio is

29 / 11 = 2.6

. A ratio greater than

2.0

signifies a concurrent metabolic alkalosis.

Estimated Time:2m 0s

Question 264Question →

A 21-year-old woman is brought to the emergency department by her college roommate due to confusion, nausea, and ringing in her ears for the past 6 hours. The roommate reports that the patient was distraught over a recent breakup and may have ingested "a bottle of pills." On physical examination, her temperature is 38.0°C (100.4°F), blood pressure is 115/75 mm Hg, pulse is 112/min, and respiratory rate is 28/min. The patient appears flushed and is breathing deeply and rapidly. Lungs are clear to auscultation bilaterally. Laboratory results show:

Serum sodium: 140 mEq/L
Serum potassium: 3.6 mEq/L
Serum chloride: 102 mEq/L
Serum bicarbonate: 16 mEq/L
Blood urea nitrogen: 14 mg/dL
Serum creatinine: 0.8 mg/dL

Arterial blood gas (room air):
pH: 7.48
$PaCO_2$ : 22 mm Hg
$PaO_2$ : 100 mm Hg

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

Primary high anion gap metabolic acidosis with appropriate respiratory compensation

Primary respiratory alkalosis with appropriate metabolic compensation

Mixed primary respiratory alkalosis and primary high anion gap metabolic acidosis

Mixed primary high anion gap metabolic acidosis and primary metabolic alkalosis

Primary non-anion gap metabolic acidosis with appropriate respiratory compensation

Show answer & explanation

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

Answer

Mixed primary respiratory alkalosis and primary high anion gap metabolic acidosis

The correct answer accurately synthesizes the laboratory data into a mixed disorder. The patient's alkalemic pH (7.48) and low

PaCO_2

(22 mm Hg) indicate a primary respiratory alkalosis. However, calculating the anion gap yields a value of 22 mEq/L (

140 - [102 + 16]

), which confirms the presence of a concurrent primary high anion gap metabolic acidosis. This mixed acid-base derangement is the classic hallmark of salicylate (aspirin) toxicity, consistent with her tinnitus, tachypnea, fever, and history of pill ingestion.

Step-by-Step Solution

1

Analyze the pH to determine the predominant acid-base status.

The pH is 7.48, indicating alkalemia.

Establishing alkalemia (pH > 7.45) directs us to look for a primary alkalosis.

2

Identify the primary process driving the alkalemia by looking at the

PaCO_2

and

HCO_3^-

.

The

PaCO_2

is low at 22 mm Hg. A low

PaCO_2

causes alkalemia, so the primary disorder is a respiratory alkalosis.

Since the

HCO_3^-

is low (16 mEq/L), it cannot be the cause of the alkalemia; rather, it suggests either compensation or a concurrent metabolic acidosis.

3

Calculate the expected metabolic compensation for the acute respiratory alkalosis.

In acute respiratory alkalosis,

HCO_3^-

drops by 2 mEq/L for every 10 mm Hg drop in

PaCO_2

. The

PaCO_2

dropped by 18 (from 40 to 22). Expected

HCO_3^-

drop =

18 \times (2/10) = 3.6

. Expected

HCO_3^- \approx 24 - 3.6 = 20.4

mEq/L.

Because the actual

HCO_3^-

(16 mEq/L) is significantly lower than the expected compensated value (20.4 mEq/L), there must be an additional primary metabolic acidosis.

4

Calculate the serum anion gap to classify the metabolic acidosis.

Anion Gap = Na^+ - (Cl^- + HCO_3^-) = 140 - (102 + 16) = 140 - 118 = 22

mEq/L.

An anion gap > 12 mEq/L confirms the presence of a high anion gap metabolic acidosis (HAGMA).

5

Alternatively, check Winter's formula starting from the metabolic acidosis.

Expected

PaCO_2 = 1.5 \times [HCO_3^-] + 8 \pm 2 = 1.5 \times 16 + 8 = 32 \pm 2

mm Hg. The actual

PaCO_2

(22 mm Hg) is much lower than the 30-34 mm Hg range.

This alternate calculation confirms that the respiratory alkalosis is a primary disorder, not just compensation for the HAGMA.

Key Concept

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

Question 265Question →

A 74-year-old man is brought to the emergency department from a skilled nursing facility due to severe abdominal pain, bloody diarrhea, and altered mental status. His medical history includes peripheral artery disease, hypertension, and a myocardial infarction one year ago. His temperature is 37.8°C (100.0°F), pulse is 118/min, blood pressure is 88/50 mm Hg, and respirations are 28/min. Physical examination shows a lethargic patient taking shallow, rapid breaths. The abdomen is distended and diffusely tender with involuntary guarding.

The following laboratory results are obtained:

Test	Result
Sodium ( $Na^+$ )	138 mEq/L
Potassium ( $K^+$ )	4.8 mEq/L
Chloride ( $Cl^-$ )	98 mEq/L
Bicarbonate ( $HCO_3^-$ )	10 mEq/L
Blood urea nitrogen	45 mg/dL
Creatinine	2.1 mg/dL
Lactic acid	7.2 mmol/L

Arterial blood gas analysis on room air reveals:

Test	Result
pH	7.15
$PaCO_2$	30 mm Hg
$PaO_2$	65 mm Hg

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

Primary high anion gap metabolic acidosis with appropriate respiratory compensation

Primary high anion gap metabolic acidosis and a concurrent respiratory acidosis

Primary high anion gap metabolic acidosis and a concurrent respiratory alkalosis

Primary normal anion gap metabolic acidosis with appropriate respiratory compensation

Primary respiratory acidosis with compensatory metabolic alkalosis

Show answer & explanation

Answer: Primary high anion gap metabolic acidosis and a concurrent respiratory acidosis

Answer

Primary high anion gap metabolic acidosis and a concurrent respiratory acidosis

The correct answer identifies a mixed acid-base disorder. First, the patient has acidemia (pH 7.15) driven by a very low bicarbonate (10 mEq/L), which establishes a primary metabolic acidosis. The anion gap is calculated as

138 - (98 + 10) = 30

mEq/L. Because the anion gap is > 12 mEq/L, this is a high anion gap metabolic acidosis, perfectly consistent with severe lactic acidosis (7.2 mmol/L) secondary to acute mesenteric ischemia. Next, Winter's formula must be used to check for adequate respiratory compensation: Expected

PaCO_2 = (1.5 \times HCO_3^-) + 8 \pm 2

. Using the patient's values, Expected

PaCO_2 = (1.5 \times 10) + 8 \pm 2 = 23 \pm 2

mm Hg. The patient's actual measured

PaCO_2

is 30 mm Hg. Since the actual

PaCO_2

is significantly higher than the expected range of 21-25 mm Hg, the patient has inadequate respiratory compensation, diagnosing a superimposed, concurrent respiratory acidosis. Clinically, this occurs because the patient is lethargic and fatigued, taking shallow breaths that fail to adequately clear carbon dioxide.

Step-by-Step Solution

1

Analyze the pH to determine the primary status.

The pH is 7.15.

A pH < 7.35 indicates primary acidemia.

2

Identify the primary disturbance causing the acidemia.

The

HCO_3^-

is extremely low at 10 mEq/L.

A low bicarbonate matching an acidic pH defines a primary metabolic acidosis.

3

Calculate the serum anion gap.

Anion Gap =

Na^+ - (Cl^- + HCO_3^-) = 138 - (98 + 10) = 30

mEq/L.

An anion gap > 12 mEq/L confirms the presence of a high anion gap metabolic acidosis (HAGMA), in this case due to lactic acidosis from ischemic bowel.

4

Apply Winter's formula to determine the expected respiratory compensation.

Expected

PaCO_2 = (1.5 \times 10) + 8 \pm 2 = 23 \pm 2

mm Hg.

Winter's formula calculates the expected

PaCO_2

response to a primary metabolic acidosis.

5

Compare measured

PaCO_2

to expected

PaCO_2

.

Measured

PaCO_2

(30 mm Hg) is greater than the expected range (21-25 mm Hg).

When the measured

PaCO_2

is higher than the calculated compensatory expected value, a concurrent respiratory acidosis is present, likely due to respiratory muscle fatigue in this critically ill patient.

Key Concept

In a patient with a primary metabolic acidosis, calculating the anion gap and applying Winter's formula are essential to identify mixed acid-base disorders such as a concurrent respiratory acidosis.

Question 266Question →

A 50-year-old man is evaluated in the neuro-intensive care unit. He was admitted four days ago after sustaining a severe closed head injury in a high-speed motor vehicle collision. Over the past 24 hours, the nursing staff reports a dramatic increase in his urine output, totaling 7.5 L of pale, dilute urine. He is currently intubated and sedated. His weight on admission was 72 kg, and his current weight is 70 kg. Vital signs show a blood pressure of 102/64 mm Hg and a heart rate of 118/min. Laboratory studies reveal a serum sodium concentration of 160 mEq/L and a serum osmolality of 330 mOsm/kg $H_2O$ . Urine osmolality is 115 mOsm/kg $H_2O$ . The patient is diagnosed with central diabetes insipidus.

What is this patient's estimated free water deficit in liters?

Show answer & explanation

Answer: 6

Answer

6

The patient has developed severe hypernatremia due to massive free water loss from central diabetes insipidus. To safely correct his sodium levels and formulate an intravenous fluid replacement plan, the free water deficit must be calculated. The standard formula is

FWD = TBW \times (\frac{\text{Measured } Na^+}{140} - 1)

. For a 50-year-old adult male, TBW is estimated as 60% of his current body weight (

0.6 \times 70 \text{ kg} = 42 \text{ L}

). Plugging in the serum sodium of 160 mEq/L yields

42 \times (\frac{160}{140} - 1) = 42 \times \frac{1}{7} = 6

liters.

Step-by-Step Solution

1

Calculate Total Body Water (TBW)

42 L

TBW for an adult male is approximately 60% (0.6) of his lean body weight. Current weight (70 kg) should be used.

2

Set up the Free Water Deficit formula

FWD = 42 \times (\frac{160}{140} - 1)

The standard formula requires the TBW and the ratio of the patient's measured serum sodium to the ideal serum sodium (140 mEq/L).

3

Solve the equation mathematically

6

42 \times (\frac{20}{140})

simplifies to

42 \times \frac{1}{7}

, which equals exactly 6.

Key Concept

Calculation of Free Water Deficit in Hypernatremia

Estimated Time:1m 30s

Question 267Question →

Match each clinical presentation of renal disease with the most likely corresponding glomerular pathology.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The correct matches are: 1) HIV infection matches Focal segmental glomerulosclerosis, 2) Colon cancer matches Membranous nephropathy, 3) Synpharyngitic hematuria matches IgA nephropathy, and 4) Corticosteroid-responsive proteinuria matches Minimal change disease.

Each vignette represents a classic presentation of a specific glomerular disease. HIV infection strongly predisposes patients to HIV-associated nephropathy, a collapsing form of Focal segmental glomerulosclerosis. Solid organ malignancies are a classic secondary cause of Membranous nephropathy. Synpharyngitic hematuria is the hallmark of IgA nephropathy. Finally, sudden-onset, steroid-responsive nephrotic syndrome in a young patient is highly characteristic of Minimal change disease.

Step-by-Step Solution

1

Analyze the clinical presentation and demographics of each patient in the provided vignettes.

Identified key triggers and associations: HIV, solid tumor, concurrent respiratory infection, and pediatric/adolescent steroid-responsive nephrotic syndrome.

Recognizing the classic clinical associations is essential for diagnosing specific glomerular diseases before considering renal biopsy.

2

Correlate each identified clinical trigger with its classic glomerular pathology.

HIV correlates with Focal segmental glomerulosclerosis, solid tumors with Membranous nephropathy, concurrent infections with IgA nephropathy, and steroid responsiveness in youth with Minimal change disease.

These classic epidemiological and clinical links guide the next steps in management and diagnostic confirmation.

Key Concept

Clinical associations of specific glomerular diseases

Question 268Question →

A 68-year-old man is evaluated in the emergency department for a 3-day history of high fever, productive cough, and progressive shortness of breath. His medical history includes type 2 diabetes mellitus and hypertension. He does not smoke. His temperature is 38.9°C (102°F), blood pressure is 90/55 mm Hg, pulse is 122/min, and respirations are 28/min. Pulse oximetry shows 88% on room air. Physical examination reveals a patient in severe respiratory distress with diminished breath sounds and coarse crackles over the right lower lung field.

Laboratory results:
Sodium: 140 mEq/L
Potassium: 4.6 mEq/L
Chloride: 102 mEq/L
Bicarbonate: 14 mEq/L
Blood urea nitrogen: 38 mg/dL
Serum creatinine: 1.6 mg/dL
Lactate: 6.1 mmol/L

Arterial blood gas on room air:
pH: 7.18
PaCO2: 38 mm Hg
PaO2: 58 mm Hg

Which of the following accurately describes this patient's acid-base disorders?

Increased anion gap metabolic acidosis and concurrent respiratory acidosis

Isolated increased anion gap metabolic acidosis

Increased anion gap metabolic acidosis with appropriate respiratory compensation

Normal anion gap metabolic acidosis and concurrent respiratory acidosis

Mixed increased anion gap and normal anion gap metabolic acidosis with concurrent respiratory acidosis

Show answer & explanation

Answer: Increased anion gap metabolic acidosis and concurrent respiratory acidosis

Answer

Increased anion gap metabolic acidosis and concurrent respiratory acidosis

The correct answer accurately identifies that the patient has a dual acid-base disorder consisting of an increased anion gap metabolic acidosis and a concurrent respiratory acidosis. Acid-base analysis begins with identifying the primary disorder: a pH of 7.18 (acidemia) with a low bicarbonate of

14\text{ mEq/L}

defines a metabolic acidosis. Next, the anion gap is calculated as

Na^+ - (Cl^- + HCO_3^-)

, yielding

140 - (102 + 14) = 24\text{ mEq/L}

. Since this is elevated above the standard

12\text{ mEq/L}

, an increased anion gap metabolic acidosis is present. To evaluate respiratory compensation, Winter's formula is applied:

\text{Expected PaCO}_2 = 1.5 \times [HCO_3^-] + 8 \pm 2

, which results in

1.5(14) + 8 = 29 \pm 2\text{ mm Hg}

. The patient's actual PaCO2 is

38\text{ mm Hg}

, which is significantly higher than the expected compensatory range of 27-31 mm Hg. This relative hypoventilation in the setting of severe metabolic acidosis reveals a concurrent primary respiratory acidosis, a consequence of respiratory muscle fatigue from severe community-acquired pneumonia. Finally, the delta ratio (

\Delta AG / \Delta HCO_3^-

) is calculated as

(24-12)/(24-14) = 1.2

; falling between 1.0 and 2.0, this rules out any additional underlying normal anion gap metabolic acidosis or metabolic alkalosis.

Step-by-Step Solution

1

Determine the primary acid-base disorder by evaluating the pH and bicarbonate.

The pH is 7.18 (acidemia) and bicarbonate is

14\text{ mEq/L}

(low), identifying a primary metabolic acidosis.

pH indicates the overall direction of the acid-base derangement, and the corresponding change in bicarbonate confirms its metabolic origin.

2

Calculate the anion gap (AG) to classify the metabolic acidosis.

AG = Na^+ - (Cl^- + HCO_3^-) = 140 - (102 + 14) = 24\text{ mEq/L}

.

The normal AG is

12\text{ mEq/L}

. Since

24 > 12

, an increased anion gap metabolic acidosis is present, driven by the elevated lactate.

3

Calculate the expected respiratory compensation using Winter's formula.

\text{Expected PaCO}_2 = (1.5 \times 14) + 8 \pm 2 = 29 \pm 2\text{ mm Hg}

(Range: 27 to 31 mm Hg).

To determine if the respiratory system has adequately compensated, the measured PaCO2 must be compared to the calculated expected PaCO2.

4

Compare expected and measured PaCO2.

The measured PaCO2 (

38\text{ mm Hg}

) is higher than the expected range (27-31 mm Hg).

A PaCO2 higher than expected indicates that ventilation is inadequate for the degree of metabolic acidosis, diagnosing a concurrent primary respiratory acidosis (likely due to respiratory muscle fatigue).

5

Check for a third disorder using the delta gap ratio (

\Delta AG / \Delta HCO_3^-

).

\Delta AG = 24 - 12 = 12\text{ mEq/L}

.

\Delta HCO_3^- = 24 - 14 = 10\text{ mEq/L}

. Ratio =

12 / 10 = 1.2

.

A ratio between 1.0 and 2.0 indicates a pure increased anion gap metabolic acidosis without an additional normal anion gap metabolic acidosis or metabolic alkalosis.

Key Concept

In patients with severe metabolic acidosis, a 'normal' PaCO2 (35-45 mm Hg) actually indicates inadequate physiological respiratory compensation, establishing the presence of a concurrent primary respiratory acidosis. Winter's formula is essential to identify this mixed disorder.

Question 269Question →

A 38-year-old woman is evaluated in the emergency department for severe, progressive muscle weakness over the past two days. She reports feeling so weak today that she had difficulty standing up from a chair. Her medical history is significant for a 2-year history of dry eyes and dry mouth, for which she uses artificial tears and saliva substitutes. She takes no other medications. Her temperature is 37.0°C (98.6°F), blood pressure is 110/70 mmHg, pulse is 88/min, and respirations are 18/min. Physical examination reveals dry oral mucosa and 4/5 motor strength in the proximal muscles of the upper and lower extremities. Sensation and deep tendon reflexes are intact.

Laboratory studies show the following:

Test	Result
Serum sodium	$140$ mEq/L
Serum potassium	$2.4$ mEq/L
Serum chloride	$115$ mEq/L
Serum bicarbonate	$13$ mEq/L
Blood urea nitrogen	$12$ mg/dL
Serum creatinine	$0.8$ mg/dL

Urine studies:

Test	Result
pH	$6.8$
Sodium	$50$ mEq/L
Potassium	$20$ mEq/L
Chloride	$30$ mEq/L

Based on these findings, which of the following is most likely to be found on further evaluation of this patient?

Bilateral nephrocalcinosis on renal ultrasound

Uric acid crystals on urine microscopy

Impaired proximal tubule reabsorption of amino acids

A negative calculated urine anion gap

Elevated arterial carbon dioxide tension on blood gas analysis

Show answer & explanation

Answer: Bilateral nephrocalcinosis on renal ultrasound

Answer

Bilateral nephrocalcinosis on renal ultrasound

This patient's laboratory profile reveals a normal anion gap metabolic acidosis (NAGMA) with severe hypokalemia. The calculated urine anion gap is positive (

+40

), which indicates a failure of the kidneys to excrete ammonium (

NH_4^+

), ruling out gastrointestinal bicarbonate loss. The urine pH is 6.8, which is inappropriately alkaline in the setting of severe systemic acidemia. This inability to acidify the distal tubule is the hallmark of Type 1 (distal) Renal Tubular Acidosis (RTA), which is strongly associated with autoimmune disorders like Sjögren syndrome (suggested by her dry eyes and mouth). Chronic acidemia buffers against the bone, releasing calcium (hypercalciuria), while the proximal tubule reabsorbs more citrate (hypocitraturia). The triad of hypercalciuria, hypocitraturia, and an alkaline urine pH highly predisposes these patients to the precipitation of calcium phosphate stones, resulting in bilateral nephrocalcinosis on imaging.

Step-by-Step Solution

1

Calculate the serum anion gap (AG).

AG = 140 - (115 + 13) = 12

mEq/L.

Determines if the metabolic acidosis is anion-gap or normal anion-gap. A result of 12 indicates a Normal Anion Gap Metabolic Acidosis (NAGMA).

2

Evaluate the serum potassium level.

Severe hypokalemia is present (

K^+ = 2.4

mEq/L).

Narrows the differential diagnosis of NAGMA to gastrointestinal losses (like diarrhea) or Type 1 / Type 2 Renal Tubular Acidosis (RTA).

3

Calculate the Urine Anion Gap (UAG).

UAG = (Urine\ Na^+ + Urine\ K^+) - Urine\ Cl^- = (50 + 20) - 30 = +40

.

Differentiates GI vs. renal bicarbonate loss. A positive UAG indicates impaired renal ammonium (

NH_4^+

) excretion, confirming a renal etiology (RTA) rather than diarrhea.

4

Assess the urine pH to differentiate the type of RTA.

Urine pH is

6.8

, which is inappropriately alkaline (

> 5.5

) for severe systemic acidemia.

An inability to acidify the urine below a pH of 5.5 confirms a distal

H^+

secretion defect, diagnostic of Type 1 (distal) RTA.

5

Identify downstream complications of Type 1 RTA.

Alkaline urine + hypercalciuria (from bone buffering) + hypocitraturia -> Calcium phosphate stone formation.

Predicts the clinical sequelae that would be found on imaging (nephrocalcinosis).

Key Concept

Diagnosis and complications of Type 1 (Distal) Renal Tubular Acidosis (RTA)

Question 270Question →

Match each clinical vignette describing a patient with a normal anion gap metabolic acidosis to the most likely corresponding serum and urine laboratory profile.

Click a left item, then click its matching right item

Show answer & explanation

Answer

Sjogren syndrome with nephrolithiasis matches to the profile with high urine pH and positive UAG (Type 1 RTA). Multiple myeloma with aminoaciduria matches to positive urine glucose, positive UAG, and low potassium (Type 2 RTA). Diabetic nephropathy on an ACE inhibitor matches to hyperkalemia and positive UAG (Type 4 RTA). Chronic diarrhea matches to negative UAG and low potassium.

The differentiation of normal anion gap metabolic acidosis relies heavily on the urine anion gap (UAG) and serum potassium levels. A negative UAG indicates intact renal ammonium excretion, typical of extrarenal bicarbonate loss like diarrhea. A positive UAG indicates impaired renal ammonium excretion, which is diagnostic of renal tubular acidosis (RTA). Among the RTAs, Type 4 is distinct for hyperkalemia. Type 1 and Type 2 both present with hypokalemia, but Type 1 is characterized by an inability to acidify urine (pH

> 5.5

) leading to calcium phosphate stones, while Type 2 often occurs as part of Fanconi syndrome with glycosuria and allows for an acidic urine pH when systemic acidemia is severe enough to overwhelm the proximal tubule defect.

Step-by-Step Solution

1

Analyze the patient with Sjogren syndrome and nephrolithiasis.

Identified as having Type 1 (distal) Renal Tubular Acidosis.

Type 1 RTA involves a defect in distal

H^+

secretion, resulting in a positive urine anion gap, hypokalemia, and an inability to acidify urine (pH

> 5.5

), which strongly promotes calcium phosphate precipitation.

2

Analyze the patient with multiple myeloma, osteomalacia, and aminoaciduria.

Identified as having Fanconi syndrome causing Type 2 (proximal) Renal Tubular Acidosis.

This defect in proximal bicarbonate reabsorption is accompanied by glycosuria (positive urine dipstick), aminoaciduria, and phosphaturia. Distal acidification is intact, allowing urine pH

< 5.5

when systemically acidemic.

3

Analyze the patient with diabetic nephropathy taking an ACE inhibitor.

Identified as having Type 4 (hyperkalemic) Renal Tubular Acidosis.

Hypoaldosteronism impairs distal sodium reabsorption and potassium/hydrogen secretion. It is uniquely characterized by hyperkalemia alongside a positive urine anion gap.

4

Analyze the patient with chronic profuse watery diarrhea.

Identified as having gastrointestinal bicarbonate loss.

The kidneys respond appropriately by excreting acid as ammonium chloride, resulting in a negative urine anion gap. Potassium is lost in the stool, causing profound hypokalemia.

Key Concept

Normal anion gap metabolic acidosis (NAGMA) differentiation using serum potassium and urine anion gap.

Question 271Question →

A 19-year-old college student is brought to the emergency department by his roommates. They report that he ingested a large amount of a sweet-tasting, brightly colored liquid he found in a garage, believing it was a sports drink. On presentation, he is disoriented and slurring his words. His blood pressure is 120/75 mm Hg and his pulse is 100/min.

Laboratory studies:
- Serum sodium: 142 mEq/L
- Serum chloride: 105 mEq/L
- Serum bicarbonate: 14 mEq/L
- Blood urea nitrogen: 14 mg/dL
- Blood glucose: 90 mg/dL
- Measured serum osmolality: 345 mOsm/kg $H_2O$

What is this patient's serum osmolar gap in mOsm/kg $H_2O$ ?

Show answer & explanation

Answer: 51

Answer

51

The osmolar gap is used to detect the presence of unmeasured, osmotically active substances in the blood, such as toxic alcohols (e.g., ethylene glycol, methanol). It is determined by subtracting the calculated serum osmolality from the measured serum osmolality. The formula for calculated osmolality is

(2 \times Na) + \frac{Glucose}{18} + \frac{BUN}{2.8}

. For this patient, the calculated osmolality is

(2 \times 142) + \frac{90}{18} + \frac{14}{2.8} = 284 + 5 + 5 = 294

mOsm/kg

H_2O

. Subtracting this from the measured osmolality of 345 mOsm/kg

H_2O

yields an osmolar gap of 51 mOsm/kg

H_2O

. A normal gap is typically less than 10; an elevated gap in this context strongly suggests ethylene glycol toxicity.

Step-by-Step Solution

1

Recall the formula for calculated serum osmolality

Calculated Osm = (2 \times Na) + \frac{Glucose}{18} + \frac{BUN}{2.8}

This formula estimates the osmotically active particles normally present in the blood, primarily sodium salts, glucose, and urea.

2

Calculate the estimated serum osmolality

Calculated Osm = (2 \times 142) + \frac{90}{18} + \frac{14}{2.8} = 284 + 5 + 5 = 294

mOsm/kg

H_2O

Accurately applying the patient's lab values yields the expected osmolality without the presence of toxic alcohols.

3

Calculate the osmolar gap

Osmolar Gap = Measured Osm - Calculated Osm = 345 - 294 = 51

mOsm/kg

H_2O

The difference between the measured and calculated osmolality represents the concentration of unmeasured osmoles, which in this case points to ethylene glycol ingestion.

Key Concept

Serum Osmolar Gap Calculation

Alternative Method

In systems using SI units (mmol/L) rather than traditional US units, the formula for calculated osmolality does not require division by 18 or 2.8 and is instead:

2 \times Na + Glucose + Urea

.

Estimated Time:1m 30s

Question 272Question →

An alert 42-year-old female is evaluated in the urgent care clinic for persistent weakness, severe muscle cramps, and three days of voluminous, watery stools after attending a community barbecue. Her past medical history is significant for severe obesity and obstructive sleep apnea, for which she uses continuous positive airway pressure (CPAP) inconsistently at night. Vital signs show a temperature of 37.4°C (99.3°F), pulse of 108/min, respirations of 22/min, and blood pressure of 102/64 mmHg. Physical examination reveals dry mucous membranes and decreased skin turgor. The following laboratory values are reported:

Test	Result
Sodium	$140 \text{ mEq/L}$
Potassium	$3.1 \text{ mEq/L}$
Chloride	$114 \text{ mEq/L}$
Bicarbonate	$14 \text{ mEq/L}$
Blood urea nitrogen	$32 \text{ mg/dL}$
Serum creatinine	$1.2 \text{ mg/dL}$
Arterial pH	$7.24$
Arterial $pCO_2$	$52 \text{ mmHg}$
Arterial $pO_2$	$78 \text{ mmHg}$

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

Normal anion gap metabolic acidosis and respiratory acidosis

Normal anion gap metabolic acidosis with appropriate respiratory compensation

High anion gap metabolic acidosis and respiratory acidosis

Primary respiratory acidosis with metabolic compensation

Normal anion gap metabolic acidosis and respiratory alkalosis

Show answer & explanation

Answer: Normal anion gap metabolic acidosis and respiratory acidosis

Answer

The patient has a mixed acid-base disorder consisting of a normal anion gap metabolic acidosis and a respiratory acidosis.

The correct answer characterizes the presence of two distinct acid-base disorders. First, the patient's arterial pH is

7.24

with a low bicarbonate (

14 \text{ mEq/L}

), confirming a metabolic acidosis. The anion gap is

140 - (114 + 14) = 12

, which is a normal anion gap metabolic acidosis, classically caused by severe gastrointestinal bicarbonate losses (diarrhea). Second, to verify if the respiratory compensation is adequate, Winter's formula must be applied:

\text{Expected } pCO_2 = 1.5 \times [HCO_3^-] + 8 \pm 2

. For a bicarbonate of

14 \text{ mEq/L}

, the expected

pCO_2

is

27-31 \text{ mmHg}

. The patient's measured

pCO_2

is

52 \text{ mmHg}

. Because the actual

pCO_2

is much higher than the expected

pCO_2

, the patient is hypoventilating relative to her metabolic state, indicating a concurrent respiratory acidosis. Her history of severe obesity and obstructive sleep apnea strongly suggests baseline

CO_2

retention (obesity hypoventilation syndrome), explaining the respiratory component.

Step-by-Step Solution

1

Analyze the pH and primary derangement.

The pH is

7.24

(acidemia). Both the

HCO_3^-

(

14 \text{ mEq/L}

) and the

pCO_2

(

52 \text{ mmHg}

) are contributing to acidemia, indicating a mixed disorder or at least a primary metabolic acidosis with abnormal

pCO_2

.

Establishing the direction of pH change and corresponding variables dictates the primary disorder.

2

Calculate the anion gap (AG).

\text{AG} = Na^+ - (Cl^- + HCO_3^-) = 140 - (114 + 14) = 12 \text{ mEq/L}

.

Differentiates the cause of the metabolic acidosis. An AG of

12

is normal, consistent with bicarbonate loss from severe diarrhea.

3

Calculate the expected respiratory compensation using Winter's formula.

\text{Expected } pCO_2 = 1.5 \times [HCO_3^-] + 8 \pm 2 = (1.5 \times 14) + 8 = 29 \pm 2 \text{ mmHg}

.

Determines if the patient's ventilation is appropriately compensating for the metabolic acidosis.

4

Compare the actual

pCO_2

to the expected

pCO_2

.

The actual

pCO_2

is

52 \text{ mmHg}

, which is significantly higher than the expected range of

27-31 \text{ mmHg}

.

An actual

pCO_2

greater than the expected

pCO_2

indicates a superimposed, independent respiratory acidosis (likely due to the patient's obesity hypoventilation and sleep apnea).

Key Concept

Identifying mixed acid-base disorders using the anion gap and Winter's formula for respiratory compensation.

Estimated Time:1m 30s

Question 273Question →

A 62-year-old man with a history of alcohol-associated cirrhosis is brought to the emergency department due to progressive confusion, lethargy, and fever over the past 2 days. His temperature is $38.6^\circ\text{C}$ ( $101.5^\circ\text{F}$ ), blood pressure is $95/60\text{ mm Hg}$ , heart rate is $112/\text{min}$ , and respiratory rate is $22/\text{min}$ . Physical examination is notable for scleral icterus, spider angiomas, a distended abdomen with a positive fluid wave, and bilateral lower extremity pitting edema.

Laboratory studies show:
Sodium: $136\text{ mEq/L}$
Potassium: $3.8\text{ mEq/L}$
Chloride: $104\text{ mEq/L}$
Bicarbonate: $18\text{ mEq/L}$
BUN: $32\text{ mg/dL}$
Creatinine: $1.5\text{ mg/dL}$
Glucose: $98\text{ mg/dL}$
Albumin: $2.0\text{ g/dL}$
Total bilirubin: $4.5\text{ mg/dL}$

Arterial blood gas on room air reveals a pH of $7.32$ and a $PaCO_2$ of $34\text{ mm Hg}$ .

Assuming a reference normal serum albumin of $4.0\text{ g/dL}$ , what is this patient's albumin-corrected serum anion gap in mEq/L?

Show answer & explanation

Answer: 19

Answer

19

This patient has a metabolic acidosis (pH 7.32, low bicarbonate). To accurately assess the etiology, the serum anion gap must be calculated and corrected for his severe hypoalbuminemia. The uncorrected anion gap is

Na^+ - (Cl^- + HCO_3^-) = 136 - (104 + 18) = 14\text{ mEq/L}

. Because albumin is negatively charged, it constitutes a significant portion of the baseline 'unmeasured anions'. A decrease in albumin falsely lowers the calculated anion gap. The standard correction requires adding

2.5\text{ mEq/L}

to the calculated gap for every

1\text{ g/dL}

decrease in albumin below

4.0\text{ g/dL}

. Here, the deficit is

4.0 - 2.0 = 2.0\text{ g/dL}

. The correction is

2.0 \times 2.5 = 5\text{ mEq/L}

. Adding this to the uncorrected gap yields

14 + 5 = 19\text{ mEq/L}

. This reveals a high anion gap metabolic acidosis, likely secondary to lactic acidosis from sepsis.

Step-by-Step Solution

1

Calculate the uncorrected anion gap.

14\text{ mEq/L}

Using the standard formula:

AG = 136 - (104 + 18) = 14\text{ mEq/L}

.

2

Calculate the albumin deficit.

2.0\text{ g/dL}

Subtract the patient's albumin from normal:

4.0\text{ g/dL} - 2.0\text{ g/dL} = 2.0\text{ g/dL}

.

3

Calculate the albumin-corrected anion gap.

19\text{ mEq/L}

Add the correction factor to the uncorrected gap:

14 + (2.0 \times 2.5) = 14 + 5 = 19\text{ mEq/L}

.

Key Concept

Albumin is a major unmeasured anion; in hypoalbuminemic states, the calculated anion gap is falsely lowered and must be corrected by adding

2.5\text{ mEq/L}

for every

1\text{ g/dL}

decrease in serum albumin.

Question 274Question →

A 68-year-old man is evaluated in the intensive care unit for decreased urine output. He was admitted 4 days ago for septic shock secondary to severe community-acquired pneumonia and initially required norepinephrine for blood pressure support. He has been hemodynamically stable off vasopressors for the past 24 hours. His current blood pressure is 118/76 mm Hg and heart rate is 82/min. Laboratory studies show:

Serum sodium: 140 mEq/L
Serum blood urea nitrogen (BUN): 32 mg/dL
Serum creatinine: 2.0 mg/dL

Urine sodium: 63 mEq/L
Urine creatinine: 30 mg/dL

Urinalysis reveals muddy brown granular casts.

Calculate the patient's fractional excretion of sodium (FeNa). (Express the result as a percentage)

Show answer & explanation

Answer: 3

Answer

3.0

The correct Fractional Excretion of Sodium (FeNa) is calculated using the formula

FeNa = \frac{U_{Na} \times P_{Cr}}{P_{Na} \times U_{Cr}} \times 100

. Plugging in the patient's values yields

\frac{63 \times 2.0}{140 \times 30} \times 100

, which simplifies to

\frac{126}{4200} \times 100 = 3.0\%

. In the clinical context of a patient recovering from septic shock, a FeNa greater than 2% strongly points toward intrinsic acute kidney injury—specifically acute tubular necrosis (ATN). This diagnosis is further corroborated by the presence of muddy brown granular casts on urinalysis.

Step-by-Step Solution

1

Identify the standard formula for calculating FeNa.

FeNa = \frac{U_{Na} \times P_{Cr}}{P_{Na} \times U_{Cr}} \times 100

This formula relates the clearance of sodium to the clearance of creatinine to determine the percentage of filtered sodium that is excreted.

2

Substitute the patient's specific serum and urine chemistries into the formula.

FeNa = \frac{63 \times 2.0}{140 \times 30} \times 100

Applying the clinical laboratory values provided in the vignette.

3

Calculate the products in the numerator and the denominator.

Numerator =

126

, Denominator =

4200

To simplify the mathematical expression before final division.

4

Divide the numerator by the denominator and multiply by 100.

\frac{126}{4200} \times 100 = 0.03 \times 100 = 3.0

To obtain the final percentage value for FeNa.

Key Concept

Fractional Excretion of Sodium (FeNa) Calculation

Estimated Time:1m 30s

Question 275Question →

A 52-year-old woman presents to the emergency department with a 2-day history of diffuse abdominal pain, polyuria, and severe, intractable vomiting. She has a history of type 1 diabetes mellitus and states she ran out of her insulin three days ago. Her temperature is 37.2°C (99.0°F), blood pressure is 95/60 mmHg, pulse is 118/min, and respirations are 24/min. Physical examination reveals dry mucous membranes and diffuse, mild abdominal tenderness without rebound or guarding. Laboratory studies show:

Test	Value
Sodium	$140 \text{ mEq/L}$
Potassium	$3.4 \text{ mEq/L}$
Chloride	$90 \text{ mEq/L}$
Bicarbonate	$16 \text{ mEq/L}$
Blood urea nitrogen	$42 \text{ mg/dL}$
Creatinine	$1.8 \text{ mg/dL}$
Glucose	$510 \text{ mg/dL}$

Arterial blood gas on room air reveals:

Parameter	Value
pH	$7.32$
pCO $_2$	$32 \text{ mmHg}$
pO $_2$	$96 \text{ mmHg}$

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

High anion gap metabolic acidosis and metabolic alkalosis

High anion gap metabolic acidosis with appropriate respiratory compensation

High anion gap metabolic acidosis and respiratory alkalosis

High anion gap metabolic acidosis and respiratory acidosis

Non-anion gap metabolic acidosis and metabolic alkalosis

Show answer & explanation

Answer: High anion gap metabolic acidosis and metabolic alkalosis

Answer

High anion gap metabolic acidosis and metabolic alkalosis

The correct answer identifies a mixed metabolic disorder. The patient has acidemia (pH 7.32) and a low bicarbonate (16 mEq/L), indicating metabolic acidosis. The anion gap is 140 - (90 + 16) = 34 mEq/L, confirming a High Anion Gap Metabolic Acidosis (HAGMA) due to DKA. Winter's formula (1.5 × 16 + 8 = 32) perfectly matches the measured pCO2, ruling out a primary respiratory disorder. However, a delta ratio must be performed for any HAGMA. The change in anion gap (34 - 12 = 22) compared to the change in bicarbonate (24 - 16 = 8) gives a delta ratio of 2.75. A ratio >2.0 means the bicarbonate has not fallen as much as expected given the accumulation of acids, which reveals a concurrent primary metabolic alkalosis caused by the patient's severe vomiting.

Step-by-Step Solution

1

Determine the primary disorder based on pH and bicarbonate.

pH is 7.32 (acidemia) and bicarbonate is low (16 mEq/L), indicating a primary metabolic acidosis.

Establishing the primary direction of the pH derangement dictates the subsequent calculation steps.

2

Calculate the serum anion gap.

Anion Gap = Na - (Cl + HCO3) = 140 - (90 + 16) = 34 mEq/L.

An elevated anion gap (>12 mEq/L) confirms the presence of a High Anion Gap Metabolic Acidosis (HAGMA), highly consistent with Diabetic Ketoacidosis in this patient.

3

Assess for appropriate respiratory compensation using Winter's formula.

Expected pCO2 = 1.5 × HCO3 + 8 ± 2 = 1.5 × 16 + 8 = 32 ± 2 mmHg. The measured pCO2 is 32 mmHg, meaning respiratory compensation is appropriate and there is no concurrent primary respiratory disorder.

A pCO2 outside the expected range would indicate an additional mixed respiratory disorder, but this patient's ventilation appropriately matches the metabolic acidosis.

4

Calculate the delta ratio to check for additional hidden metabolic disorders.

Delta Gap = 34 - 12 = 22. Delta Bicarbonate = 24 - 16 = 8. Delta Ratio = 22 / 8 = 2.75.

Because the delta gap is significantly larger than the drop in bicarbonate, the ratio is >2.0. This indicates an independent process is adding bicarbonate to the blood, signifying a concurrent metabolic alkalosis (caused by the patient's severe vomiting).

Key Concept

In patients with a high anion gap metabolic acidosis, the delta ratio (ΔAG / ΔHCO3) must be calculated to identify hidden, concurrent metabolic disorders; a ratio >2.0 indicates a superimposed metabolic alkalosis.

Estimated Time:2m 0s

Question 276Question →

A thorough urinalysis is a critical non-invasive tool for localizing the site of renal injury in patients with acute or chronic kidney disease. For each characteristic urinalysis sediment finding presented below, what is the most likely associated renal pathology? Match each finding to its correct etiology.

Click a left item, then click its matching right item

Show answer & explanation

Answer

Muddy brown casts indicate acute tubular necrosis; RBC casts indicate proliferative glomerulonephritis; WBC casts indicate acute interstitial nephritis; fatty casts indicate nephrotic syndrome; and broad waxy casts indicate advanced chronic kidney disease.

Urinary casts serve as specific markers that localize the source of renal pathology. Glomerular injury allows RBCs to pass and form RBC casts; tubular necrosis causes epithelial sloughing to form muddy brown casts; interstitial inflammation leads to WBC casts; severe proteinuria enables lipiduria to form fatty casts; and chronic structural dilation from nephron loss produces broad waxy casts.

Step-by-Step Solution

1

Determine the significance of cellular versus acellular casts.

Cellular casts indicate active inflammation or necrosis within the nephron, whereas acellular or degenerative casts often indicate stasis or severe proteinuria.

Casts are formed in the distal nephron when Tamm-Horsfall mucoprotein traps available luminal contents, reflecting the specific pathology occurring upstream.

2

Evaluate the clinical implication of muddy brown granular casts.

They are linked to acute tubular necrosis.

Ischemic or nephrotoxic injury causes tubular cells to die, slough off, and degrade into muddy brown granular material.

3

Evaluate the implication of specific immune cells (RBCs and WBCs) in casts.

RBC casts point to glomerular disease (nephritic syndrome), while WBC casts point to tubulointerstitial disease (AIN or pyelonephritis).

The type of cell trapped in the cast reflects the primary site of structural damage and inflammation.

4

Evaluate the implication of fatty and broad waxy casts.

Fatty casts suggest nephrotic syndrome, and broad waxy casts suggest advanced chronic kidney disease.

Lipiduria accompanies the severe proteinuria seen in nephrotic syndrome. Waxy casts result from extreme stasis in enlarged tubules of failing kidneys over a long period.

Key Concept

Urinalysis Cast Interpretation in Renal Pathologies

Estimated Time:1m 0s

Question 277Question →

A 22-year-old woman is brought to the emergency department by her roommate due to confusion, nausea, and ringing in her ears for the past several hours. The roommate found an empty bottle of over-the-counter pain relievers in her room. On physical examination, her temperature is 37.8°C (100.0°F), blood pressure is 110/70 mm Hg, pulse is 115/min, and respiratory rate is 28/min. She appears agitated and diaphoretic. Laboratory results are as follows:

Laboratory Test	Result
Sodium	140 mEq/L
Potassium	4.1 mEq/L
Chloride	104 mEq/L
Bicarbonate	14 mEq/L
Blood urea nitrogen	18 mg/dL
Creatinine	0.9 mg/dL

Arterial blood gas (room air):

Parameter	Result
pH	7.42
$pCO_2$	22 mm Hg
$pO_2$	95 mm Hg

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

Primary metabolic acidosis with adequate respiratory compensation

Mixed primary metabolic acidosis and primary respiratory acidosis

Primary respiratory alkalosis with adequate metabolic compensation

Mixed primary metabolic acidosis and primary respiratory alkalosis

Mixed primary metabolic acidosis, primary respiratory alkalosis, and primary metabolic alkalosis

Show answer & explanation

Answer: Mixed primary metabolic acidosis and primary respiratory alkalosis

Answer

The patient has a mixed primary metabolic acidosis and primary respiratory alkalosis.

This patient's presentation of tinnitus, tachypnea, agitation, hyperthermia, and an empty bottle of over-the-counter pain relievers is classic for acute salicylate (aspirin) toxicity. Salicylates directly stimulate the medullary respiratory center, causing a primary respiratory alkalosis. Simultaneously, they uncouple oxidative phosphorylation, leading to the accumulation of lactic acid and ketoacids, which causes a primary high anion gap metabolic acidosis. The acid-base analysis confirms this exact mixed disorder: the anion gap is elevated at 22 mEq/L (indicating primary metabolic acidosis), and the measured

pCO_2

of 22 mm Hg is lower than the expected compensatory range of 27-31 mm Hg calculated by Winter's formula (indicating a concurrent primary respiratory alkalosis). The delta-delta calculation yields an expected normal bicarbonate of 24 mEq/L, confirming that these are the only two primary acid-base disorders present.

Step-by-Step Solution

1

Calculate the anion gap to evaluate for a high anion gap metabolic acidosis.

Anion gap =

140 - (104 + 14) = 22

mEq/L. Since this is greater than the normal value of 12 mEq/L, a primary high anion gap metabolic acidosis is present.

An elevated anion gap definitively establishes the presence of a primary metabolic acidosis regardless of the final pH value.

2

Calculate the expected respiratory compensation for the metabolic acidosis using Winter's formula.

Expected

pCO_2 = (1.5 \times 14) + 8 \pm 2 = 29 \pm 2

mm Hg. The calculated expected range is 27 to 31 mm Hg.

Comparing the measured

pCO_2

to the expected

pCO_2

determines if there is an additional primary respiratory disorder.

3

Compare the measured

pCO_2

to the expected

pCO_2

to identify any concurrent respiratory disorder.

The measured

pCO_2

is 22 mm Hg, which is lower than the expected range of 27 to 31 mm Hg. This indicates a concurrent primary respiratory alkalosis.

A measured

pCO_2

below the expected compensatory response means the patient is hyperventilating beyond what is driven by the metabolic acidosis.

4

Calculate the delta gap (delta-delta) to check for a third concurrent metabolic disorder.

Delta gap =

22 - 12 = 10

. Expected normal

HCO_3^- = 14 + 10 = 24

mEq/L. Since this exactly equals a normal baseline bicarbonate, there is no additional metabolic alkalosis or non-anion gap metabolic acidosis.

The delta-delta calculation reveals if the drop in bicarbonate is purely due to buffering the unmeasured anions, effectively ruling out a triple acid-base disorder.

Key Concept

Diagnosis of mixed acid-base disorders using the anion gap, Winter's formula, and delta-delta calculations.

Question 278Question →

A 76-year-old woman is admitted to the intensive care unit with severe, poorly localized abdominal pain out of proportion to physical examination findings, accompanied by bloody diarrhea. Her medical history is significant for atrial fibrillation. She is hypotensive and tachycardic. Laboratory testing reveals a serum lactate of $8.5$ mmol/L. Arterial blood gas and basic metabolic panel results are as follows:

Laboratory test	Result
Serum sodium	$138$ mEq/L
Serum chloride	$102$ mEq/L
Serum bicarbonate	$14$ mEq/L
Arterial $pH$	$7.26$

The physician determines that the patient has a primary high anion gap metabolic acidosis secondary to suspected acute mesenteric ischemia. According to Winter's formula, what is the exact calculated midpoint of the target expected arterial $pCO_2$ (in mmHg) representing appropriate respiratory compensation?

Show answer & explanation

Answer: 29

Answer

29

In the setting of a primary metabolic acidosis, the lungs compensate by increasing ventilation to blow off

CO_2

, thereby raising the

pH

toward normal. Winter's formula (

Expected\ pCO_2 = 1.5 \times [HCO_3^-] + 8 \pm 2

) is used to determine if this respiratory response is appropriate. For this patient with a serum bicarbonate of

14

mEq/L, the calculated midpoint of the target

pCO_2

is

1.5 \times 14 + 8 = 29

mmHg. If the measured

pCO_2

on an arterial blood gas were significantly higher than this target range (

27-31

mmHg), a concomitant respiratory acidosis would be present; if significantly lower, a concomitant respiratory alkalosis would be present.

Step-by-Step Solution

1

Identify the primary acid-base disorder

Primary metabolic acidosis

The patient has a low

pH

(

7.26

) and a low

HCO_3^-

(

14

mEq/L) along with elevated lactate, indicating a metabolic acidosis.

2

Select the appropriate compensation formula

Winter's formula: Expected

pCO_2 = 1.5 \times [HCO_3^-] + 8

Winter's formula is the standard physiological rule used to predict the expected respiratory compensation (hyperventilation) in the setting of primary metabolic acidosis.

3

Calculate the expected target

pCO_2

1.5 \times 14 + 8 = 29

mmHg

Substituting the patient's measured serum bicarbonate of

14

mEq/L yields the exact midpoint of the expected

pCO_2

range.

Key Concept

Calculating expected respiratory compensation for metabolic acidosis using Winter's formula

Question 279Question →

Emergency medical services transport a 41-year-old male to the hospital after his spouse discovered him unresponsive in their garage. Beside him was an open, partially consumed jug of automotive antifreeze. Upon arrival, vital signs demonstrate a temperature of 36.5°C (97.7°F), blood pressure of 105/65 mm Hg, heart rate of 92/min, and a depressed respiratory rate of 10/min. The physical examination is notable for profound lethargy, with the patient only groaning in response to painful stimuli.

Initial laboratory evaluation reveals the following:

Test	Value
Sodium	140 mEq/L
Potassium	4.6 mEq/L
Chloride	102 mEq/L
Bicarbonate	8 mEq/L
Blood urea nitrogen	22 mg/dL
Creatinine	1.5 mg/dL

Arterial blood gas parameters on room air:

Test	Value
pH	7.05
PaCO2	30 mm Hg
PaO2	75 mm Hg

Which of the following best characterizes this patient's underlying acid-base disorder?

High anion gap metabolic acidosis and concurrent respiratory acidosis

High anion gap metabolic acidosis with appropriate respiratory compensation

High anion gap metabolic acidosis and concurrent respiratory alkalosis

Normal anion gap metabolic acidosis with appropriate respiratory compensation

Mixed high and normal anion gap metabolic acidosis

Show answer & explanation

Answer: High anion gap metabolic acidosis and concurrent respiratory acidosis

Answer

High anion gap metabolic acidosis and concurrent respiratory acidosis

The laboratory results reveal severe acidemia (pH 7.05) driven by a significantly reduced bicarbonate level (8 mEq/L), pointing to a primary metabolic acidosis. The anion gap is calculated as

Na^+ - (Cl^- + HCO_3^-)

, which equals

140 - (102 + 8) = 30

mEq/L. Since this value exceeds the normal limit of 12 mEq/L, the patient has a high anion gap metabolic acidosis (HAGMA), which is consistent with antifreeze (ethylene glycol) toxicity. To assess whether the respiratory system is appropriately compensating, Winter's formula must be applied:

Expected PaCO_2 = (1.5 \times [HCO_3^-]) + 8 \pm 2

. For this patient, the expected

PaCO_2

is

(1.5 \times 8) + 8 = 20 \pm 2

mm Hg. The measured

PaCO_2

of 30 mm Hg is substantially higher than the 18 to 22 mm Hg range. This relative hypercapnia indicates that the patient is hypoventilating (likely due to toxic CNS depression, reflected by a respiratory rate of 10/min), confirming a concurrent respiratory acidosis.

Step-by-Step Solution

1

Identify the primary disturbance from the arterial blood gas.

The pH of 7.05 indicates acidemia. The low bicarbonate (

8

mEq/L) identifies the primary disorder as a metabolic acidosis.

Establishing the primary acid-base status is the foundation for all subsequent calculations.

2

Calculate the serum anion gap.

Anion Gap = Na^+ - (Cl^- + HCO_3^-) = 140 - (102 + 8) = 140 - 110 = 30

mEq/L. Since this is greater than

12

mEq/L, there is a High Anion Gap Metabolic Acidosis (HAGMA).

Classifying the metabolic acidosis helps identify the etiology (e.g., toxic alcohol ingestion such as ethylene glycol).

3

Calculate the expected respiratory compensation using Winter's formula.

Expected PaCO_2 = (1.5 \times HCO_3^-) + 8 \pm 2 = (1.5 \times 8) + 8 = 12 + 8 = 20 \pm 2

mm Hg. The expected range is

18

to

22

mm Hg.

Winter's formula determines what the PaCO2 should be if the respiratory system is properly compensating for the metabolic acidosis.

4

Compare the expected

PaCO_2

to the measured

PaCO_2

to check for mixed disorders.

The measured

PaCO_2

(

30

mm Hg) is higher than the expected range (

18

-

22

mm Hg). This indicates a superimposed respiratory acidosis.

A

PaCO_2

higher than the expected compensatory range means the lungs are retaining too much

CO_2

, characteristic of hypoventilation (consistent with the patient's depressed respiratory rate of

10

/min from intoxication).

Key Concept

Diagnosis of mixed acid-base disorders requires calculating the anion gap and applying Winter's formula to determine if respiratory compensation is adequate. A measured PaCO2 higher than predicted indicates a concurrent respiratory acidosis.

Estimated Time:1m 30s

Question 280Question →

Match each clinical presentation with its most likely corresponding arterial blood gas and serum electrolyte panel.

Click a left item, then click its matching right item

Show answer & explanation

Answer

Diabetic ketoacidosis pairs with the high anion gap metabolic acidosis; diarrhea pairs with the normal anion gap metabolic acidosis; COPD exacerbation pairs with the primary respiratory acidosis; and vomiting pairs with the metabolic alkalosis.

Each clinical presentation leads to a classic acid-base and electrolyte disturbance. The patient with a fruity breath odor has diabetic ketoacidosis, producing an elevated anion gap metabolic acidosis (AG = 22 mEq/L). The patient with severe diarrhea loses substantial bicarbonate in the stool, producing a normal anion gap metabolic acidosis (AG = 10 mEq/L) along with severe hypokalemia. The patient with a COPD exacerbation retains CO2, leading to a primary respiratory acidosis with a significantly elevated PaCO2. Finally, the patient with gastric outlet obstruction loses hydrochloric acid through vomiting, resulting in a hypochloremic, hypokalemic metabolic alkalosis with compensatory CO2 retention.

Step-by-Step Solution

1

Identify the primary acid-base disorder for each laboratory panel by evaluating the pH, PaCO2, and HCO3- values.

The first two panels represent metabolic acidosis (low pH, low HCO3-). The third panel represents respiratory acidosis (low pH, high PaCO2). The fourth panel represents metabolic alkalosis (high pH, high HCO3-).

Establishing the primary disorder is the critical first step in interpreting acid-base derangements.

2

Calculate the serum anion gap (

Na^+ - [Cl^- + HCO_3^-]

) for the two metabolic acidoses.

The first panel has an anion gap of 22 mEq/L (High AG). The second panel has an anion gap of 10 mEq/L (Normal AG).

The anion gap distinguishes between different etiologies of metabolic acidosis.

3

Match the clinical scenarios to their corresponding laboratory findings based on pathophysiology.

DKA causes ketone accumulation (high anion gap acidosis). Diarrhea causes direct bicarbonate loss (normal anion gap acidosis). COPD causes ventilation failure (respiratory acidosis). Vomiting causes acid loss (metabolic alkalosis).

Each clinical etiology produces a distinct signature on a basic metabolic panel and arterial blood gas.

Key Concept

Acid-Base Derangements and Electrolyte Abnormalities

Alternative Method

You can also use Winter's formula (

PaCO_2 = 1.5 \times HCO_3^- + 8 \pm 2

) to confirm that the respiratory compensation for the metabolic acidoses in the provided correct panels is appropriate, further reinforcing your diagnostic match.

Estimated Time:2m 0s

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