Nephrology Practice Questions — USMLE Step 2 CK — Page 11

Question 201Question →

A patient in the surgical intensive care unit develops oliguria on the second day following an elective partial colectomy. Over the past 8 hours, the urinary catheter has drained only 150 mL of highly concentrated urine. The patient has been receiving maintenance intravenous fluids at a conservative rate due to a known history of heart failure with preserved ejection fraction.

Vital signs show a temperature of 37.2°C (99.0°F), heart rate of 105/min, and blood pressure of 102/65 mmHg. Physical examination reveals dry oral mucosa and flat jugular veins.

Laboratory studies are obtained:

Laboratory Parameter	Value
Serum sodium	140 mEq/L
Serum blood urea nitrogen	48 mg/dL
Serum creatinine	2.0 mg/dL
Urine sodium	28 mEq/L
Urine creatinine	80 mg/dL

Based on the provided laboratory values, calculate the patient's fractional excretion of sodium (FENa). (Enter your answer as a percentage.)

Show answer & explanation

Answer: 0.5

Answer

0.5

The correct answer is derived mathematically using the Fractional Excretion of Sodium (FENa) formula. By multiplying the urine sodium by the serum creatinine (28 × 2.0 = 56) and dividing that product by the multiplication of the serum sodium and urine creatinine (140 × 80 = 11200), the resulting ratio is 0.005. Multiplying this decimal by 100 expresses the final FENa as 0.5%. Physiologically, a value below 1% indicates robust tubular sodium reabsorption, which strongly suggests a prerenal mechanism for the patient's oliguria, consistent with volume depletion.

Step-by-Step Solution

1

Identify the formula used to calculate the fractional excretion of sodium.

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 if the renal tubules are appropriately reabsorbing sodium in the setting of decreased renal perfusion.

2

Extract the specific variables needed from the provided laboratory table.

Urine sodium (

U_{Na}

) = 28 mEq/L; Plasma (Serum) creatinine (

P_{Cr}

) = 2.0 mg/dL; Plasma (Serum) sodium (

P_{Na}

) = 140 mEq/L; Urine creatinine (

U_{Cr}

) = 80 mg/dL.

Accurate variable identification prevents common inversion errors during calculation.

3

Substitute the values into the formula and calculate the percentage.

FENa = \frac{28 \times 2.0}{140 \times 80} \times 100 = \frac{56}{11200} \times 100 = 0.005 \times 100 = 0.5

%

Completing the calculation yields the final value, which is less than 1%, clinically supporting a prerenal etiology for the patient's acute kidney injury.

Key Concept

Calculation of the Fractional Excretion of Sodium (FENa) to evaluate and differentiate etiologies of acute kidney injury.

Question 202Question →

A 32-year-old woman is brought to the emergency department by her husband due to progressive lethargy and confusion. She has a history of Crohn disease and has been experiencing frequent, voluminous, watery diarrhea for the past four days. Two days ago, she was prescribed oral hydrocodone-acetaminophen for an acute musculoskeletal back injury. Her husband reports she has been taking the pain medication more frequently than prescribed. Temperature is 37.1°C (98.8°F), blood pressure is 92/60 mm Hg, pulse is 112/min, and respirations are 8/min. Physical examination shows dry mucous membranes, decreased skin turgor, and pinpoint pupils. The patient is somnolent but arousable. Laboratory studies are obtained:

Test	Value
Sodium	136 mEq/L
Potassium	2.8 mEq/L
Chloride	115 mEq/L
Bicarbonate	13 mEq/L

Arterial blood gas on room air:

Test	Value
pH	7.22
$pCO_2$	34 mm Hg
$pO_2$	68 mm Hg

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

Normal anion gap metabolic acidosis and respiratory acidosis

Normal anion gap metabolic acidosis with adequate respiratory compensation

Normal anion gap metabolic acidosis and respiratory alkalosis

High anion gap metabolic acidosis and respiratory acidosis

High anion gap metabolic acidosis with adequate respiratory compensation

Show answer & explanation

Answer: Normal anion gap metabolic acidosis and respiratory acidosis

Answer

Normal anion gap metabolic acidosis and respiratory acidosis

The correct answer is normal anion gap metabolic acidosis and respiratory acidosis. The patient's severe diarrhea causes a loss of bicarbonate, resulting in a primary metabolic acidosis. The first step in evaluating metabolic acidosis is calculating the anion gap (AG):

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

. In this patient,

AG = 136 - (115 + 13) = 8

mEq/L, which is within the normal range (8-12 mEq/L), confirming a normal anion gap metabolic acidosis (NAGMA). The next required step is evaluating for appropriate respiratory compensation using Winter's formula:

Expected\ pCO_2 = (1.5 \times HCO_3^-) + 8 \pm 2

. For this patient, the expected

pCO_2

is

(1.5 \times 13) + 8 = 27.5 \pm 2

mm Hg (range: 25.5 to 29.5 mm Hg). Because the patient's measured

pCO_2

(34 mm Hg) is higher than the expected range, she is retaining more

CO_2

than she should. This indicates a concurrent primary respiratory acidosis. Clinically, this is explained by her recent overuse of hydrocodone-acetaminophen, leading to opiate-induced central respiratory depression (evidenced by lethargy, pinpoint pupils, and a respiratory rate of 8/min).

Step-by-Step Solution

1

Calculate the Anion Gap (AG).

AG = Na^+ - (Cl^- + HCO_3^-) = 136 - (115 + 13) = 8

mEq/L.

To determine the mechanism of the primary metabolic acidosis (diarrhea-induced bicarbonate loss vs. unmeasured anions).

2

Calculate the expected respiratory compensation using Winter's formula.

Expected\ pCO_2 = (1.5 \times 13) + 8 = 19.5 + 8 = 27.5 \pm 2

mm Hg (Range: 25.5 to 29.5 mm Hg).

To determine if the patient has a simple metabolic acidosis or a mixed acid-base disorder.

3

Compare expected

pCO_2

to the measured

pCO_2

.

Measured

pCO_2

(34 mm Hg) is greater than the expected range (25.5 - 29.5 mm Hg).

A measured

pCO_2

higher than expected indicates a superimposed primary respiratory acidosis, driven here by opiate toxicity.

Key Concept

Patients with a primary metabolic acidosis must be evaluated for adequate respiratory compensation using Winter's formula. If the measured

pCO_2

is higher than the calculated expected

pCO_2

, a concurrent primary respiratory acidosis is present.

Question 203Question →

Emergency medical responders transport a $62$ -year-old woman to the emergency department due to progressive lethargy and a four-day history of a productive cough. Her past medical history is significant for severe chronic obstructive pulmonary disease. Upon arrival, her temperature is $38.8^\circ\text{C}$ ( $101.8^\circ\text{F}$ ), blood pressure is $88/54\text{ mm Hg}$ , pulse is $122/\text{min}$ , and respirations are $26/\text{min}$ . Oxygen saturation is $85\%$ on room air. Physical examination reveals a somnolent patient with prominent accessory muscle use, diffuse expiratory wheezing, and bilateral rhonchi. Laboratory results are as follows:

Parameter	Value
Serum sodium	$138\text{ mEq/L}$
Serum potassium	$4.2\text{ mEq/L}$
Serum chloride	$102\text{ mEq/L}$
Serum bicarbonate	$12\text{ mEq/L}$
Blood urea nitrogen	$42\text{ mg/dL}$
Serum creatinine	$1.8\text{ mg/dL}$
Serum lactate	$6.5\text{ mmol/L}$

Arterial blood gas analysis (on room air):

Parameter	Value
pH	$7.12$
$\text{PaO}_2$	$55\text{ mm Hg}$
$\text{PaCO}_2$	$38\text{ mm Hg}$

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

Normal 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 acidosis

High anion gap metabolic acidosis and concurrent respiratory alkalosis

Normal anion gap metabolic acidosis with appropriate respiratory compensation

Show answer & explanation

Answer: High anion gap metabolic acidosis and concurrent respiratory acidosis

Answer

High anion gap metabolic acidosis and concurrent respiratory acidosis

The patient's laboratory results demonstrate a high anion gap metabolic acidosis with a concurrent primary respiratory acidosis. First, the severe acidemia (pH

7.12

) with a low bicarbonate (

12\text{ mEq/L}

) establishes a primary metabolic acidosis. Next, calculating the anion gap (

138 - [102 + 12] = 24\text{ mEq/L}

) confirms a high anion gap metabolic acidosis (HAGMA), which is driven by lactic acidosis from tissue hypoperfusion. Finally, Winter's formula must be applied to determine if the respiratory compensation is appropriate:

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

. For this patient, the expected

\text{PaCO}_2

is

(1.5 \times 12) + 8 = 26 \pm 2\text{ mm Hg}

. Because the measured

\text{PaCO}_2

of

38\text{ mm Hg}

is significantly higher than the expected range of

24-28\text{ mm Hg}

, there is an inadequate respiratory response. This indicates a superimposed primary respiratory acidosis, a life-threatening complication in COPD patients experiencing acute respiratory failure alongside shock.

Step-by-Step Solution

1

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

The pH is

7.12

(acidemia) and the serum bicarbonate is

12\text{ mEq/L}

(markedly low), indicating a primary metabolic acidosis.

Establishing the primary direction of the pH derangement dictates which subsequent diagnostic formulas are required.

2

Calculate the serum anion gap to characterize the metabolic acidosis.

\text{Anion Gap} = \text{Na}^+ - (\text{Cl}^- + \text{HCO}_3^-) = 138 - (102 + 12) = 24\text{ mEq/L}

. This confirms a high anion gap metabolic acidosis (HAGMA).

Differentiation between high and normal anion gap acidosis is essential for uncovering the underlying etiology (in this case, lactic acidosis from sepsis).

3

Apply Winter's formula to assess the adequacy of the respiratory compensation.

\text{Expected PaCO}_2 = (1.5 \times \text{HCO}_3^-) + 8 \pm 2 = (1.5 \times 12) + 8 = 26 \pm 2\text{ mm Hg}

.

Metabolic acidosis stimulates central chemoreceptors to increase alveolar ventilation. Winter's formula predicts the physiologically appropriate

\text{PaCO}_2

for a given bicarbonate level.

4

Compare the measured PaCO2 to the expected PaCO2 range.

The measured

\text{PaCO}_2

is

38\text{ mm Hg}

, which is significantly higher than the maximum expected value of

28\text{ mm Hg}

.

Because the patient is retaining more

\text{CO}_2

than physiologically expected for her level of metabolic acidosis, a concurrent primary respiratory acidosis is present (consistent with her severe COPD exacerbation).

Key Concept

In patients with a primary metabolic acidosis, Winter's formula (

\text{Expected PaCO}_2 = [1.5 \times \text{HCO}_3^-] + 8 \pm 2

) must be used to evaluate if the respiratory compensation is adequate. A measured

\text{PaCO}_2

higher than the expected range indicates a superimposed primary respiratory acidosis.

Question 204Question →

Match each clinical patient presentation with the most likely corresponding urinalysis sediment finding.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The ischemic presentation matches with muddy brown granular casts; the post-infectious nephritic presentation matches with red blood cell casts; the medication-induced allergic presentation matches with white blood cell casts; and the diabetic nephrotic presentation matches with oval fat bodies.

Each correct pairing links a classic clinical presentation to its definitive microscopic urinary finding based on the compartment of the kidney affected. Ischemia affects the tubules (muddy brown casts), inflammation of the glomeruli allows RBC leakage (RBC casts), drug allergies inflame the interstitium (WBC casts), and severe podocyte damage causes massive lipiduria (fatty casts).

Step-by-Step Solution

1

Analyze each clinical vignette to determine the underlying renal pathophysiology.

Identified the four mechanisms: ischemic acute tubular necrosis, nephritic syndrome (glomerulonephritis), acute interstitial nephritis, and nephrotic syndrome.

Accurate diagnosis of the underlying mechanism is required to predict the microscopic findings in the urine.

2

Correlate the identified pathophysiology with its pathognomonic urinalysis sediment finding.

Matched ATN to muddy brown casts, glomerulonephritis to RBC casts, AIN to WBC casts, and nephrotic syndrome to fatty casts.

Different compartments of the kidney (tubules, glomeruli, interstitium) slough specific cellular materials into the urine when injured.

Key Concept

Correlation of distinct acute kidney injury and glomerular disease mechanisms with their classic urinalysis sediment patterns.

Question 205Question →

An emergency medical response team transports a young adult male to the hospital after he was discovered lethargic in his dormitory. The patient, a 22-year-old college student with a known psychiatric history, reportedly ingested a large, unknown quantity of over-the-counter pain relievers earlier in the day. Upon arrival at the triage desk, he is tachypneic and diaphoretic. Vital signs include a temperature of 38.1°C (100.6°F), blood pressure of 112/68 mm Hg, heart rate of 115/min, and respiratory rate of 28/min.

Laboratory evaluation is obtained immediately:

Sodium: $140$ mEq/L
Potassium: $4.2$ mEq/L
Chloride: $103$ mEq/L
Bicarbonate: $13$ mEq/L
Blood urea nitrogen: $18$ mg/dL
Creatinine: $1.0$ mg/dL

Arterial blood gas parameters on room air:
pH: $7.43$
PaCO2: $20$ mm Hg
PaO2: $98$ mm Hg

Based on the provided laboratory parameters, which of the following accurately characterizes the primary acid-base disturbance(s) in this patient?

High anion gap metabolic acidosis with adequate respiratory compensation

Mixed high anion gap metabolic acidosis and respiratory alkalosis

Mixed normal anion gap metabolic acidosis and respiratory alkalosis

Primary respiratory alkalosis with appropriate metabolic compensation

Mixed high anion gap metabolic acidosis and respiratory acidosis

Show answer & explanation

Answer: Mixed high anion gap metabolic acidosis and respiratory alkalosis

Answer

Mixed high anion gap metabolic acidosis and respiratory alkalosis

This patient's clinical presentation (lethargy, tachypnea, ingestion of over-the-counter medication) and laboratory findings are highly characteristic of salicylate (aspirin) toxicity. Salicylates cause a classic mixed acid-base disorder: they directly stimulate the medullary respiratory center to cause a primary respiratory alkalosis, and they disrupt cellular metabolism by uncoupling oxidative phosphorylation, leading to organic acid accumulation and a primary high anion gap metabolic acidosis.

This can be proven mathematically:
1. The pH of

7.43

indicates alkalemia, meaning the dominant primary disorder is a respiratory alkalosis (driven by the PaCO2 of

20

mm Hg).
2. The expected acute metabolic compensation for a PaCO2 drop of

20

mm Hg (from the baseline of

40

) is a

4

mEq/L drop in

HCO_3^-

(

2

mEq/L per

10

mm Hg drop in PaCO2). The expected

HCO_3^-

is therefore

20

mEq/L.
3. The patient's actual

HCO_3^-

is

13

mEq/L, which is far lower than the compensatory

20

mEq/L. This signifies an additional, independent primary metabolic acidosis.
4. The anion gap is calculated as

Na^+ - (Cl^- + HCO_3^-) = 140 - (103 + 13) = 24

mEq/L. Since this is greater than the normal maximum of

12

mEq/L, the metabolic component is specifically a high anion gap metabolic acidosis.

Alternatively, applying Winter's formula to the metabolic acidosis:

Expected\ PaCO_2 = (1.5 \times 13) + 8 = 27.5 \pm 2

mm Hg. Because the measured PaCO2 (

20

mm Hg) is well below this range, a concurrent respiratory alkalosis is definitively present.

Step-by-Step Solution

1

Determine the primary acid-base disorder based on the pH.

The pH is

7.43

, indicating alkalemia. The low PaCO2 (

20

mm Hg) aligns with this, establishing a primary respiratory alkalosis.

Identifying the primary disturbance directs the appropriate compensation formula to use.

2

Calculate the expected metabolic compensation for the primary respiratory alkalosis.

For acute respiratory alkalosis,

HCO_3^-

decreases by

2

mEq/L per

10

mm Hg drop in PaCO2. A drop from

40

to

20

mm Hg (a difference of

20

) should decrease

HCO_3^-

by

4

. Expected

HCO_3^-

is

24 - 4 = 20

mEq/L.

This determines if the low bicarbonate is solely compensatory or represents a concurrent primary metabolic acidosis.

3

Compare the measured bicarbonate to the expected compensatory value.

The measured

HCO_3^-

(

13

mEq/L) is significantly lower than the expected

20

mEq/L, confirming an additional primary metabolic acidosis.

A significant deviation from expected compensation indicates a mixed acid-base disorder.

4

Calculate the anion gap to classify the metabolic acidosis.

Anion Gap =

Na^+ - (Cl^- + HCO_3^-) = 140 - (103 + 13) = 24

mEq/L. Since

24 > 12

, it is a high anion gap metabolic acidosis.

Metabolic acidosis must always be classified as normal or high anion gap to narrow the differential diagnosis.

Key Concept

Salicylate toxicity classically causes a mixed acid-base disorder: a primary respiratory alkalosis due to direct medullary respiratory center stimulation, and a primary high anion gap metabolic acidosis due to uncoupling of oxidative phosphorylation.

Estimated Time:1m 30s

Question 206Question →

A 48-year-old man with a history of severe alcohol use disorder is brought to the emergency department by paramedics after being found obtunded in a park. His temperature is $36.2^\circ\text{C}$ ( $97.2^\circ\text{F}$ ), blood pressure is $110/70\text{ mmHg}$ , pulse is $105/\text{min}$ , and respiratory rate is $18/\text{min}$ . The patient is unarousable and responds only to painful stimuli.

Initial laboratory studies reveal the following:

Laboratory Parameter	Value
Sodium	$138\text{ mEq/L}$
Potassium	$4.2\text{ mEq/L}$
Chloride	$104\text{ mEq/L}$
Bicarbonate	$22\text{ mEq/L}$
Blood urea nitrogen (BUN)	$28\text{ mg/dL}$
Creatinine	$1.1\text{ mg/dL}$
Glucose	$126\text{ mg/dL}$
Ethanol	$92\text{ mg/dL}$
Measured serum osmolality	$340\text{ mOsm/kg H}_2\text{O}$

Based on the provided laboratory results, what is this patient's serum osmolar gap in $\text{mOsm/kg H}_2\text{O}$ ?

Show answer & explanation

Answer: 27

Answer

27

The serum osmolar gap is defined as the difference between the measured serum osmolality and the calculated serum osmolality. The standard formula for calculated serum osmolality in the United States (using

\text{mg/dL}

for glucose and BUN) is

2 \times [\text{Na}^+] + \frac{[\text{Glucose}]}{18} + \frac{[\text{BUN}]}{2.8}

. However, when ethanol is present and measured, its contribution must also be subtracted to isolate the gap caused by other unidentified toxic alcohols (e.g., methanol, ethylene glycol). The conversion factor for ethanol is

4.6

. Therefore, the complete calculation for this patient is

2 \times 138 + \frac{126}{18} + \frac{28}{2.8} + \frac{92}{4.6} = 276 + 7 + 10 + 20 = 313 \text{ mOsm/kg H}_2\text{O}

. Subtracting this from the measured osmolality of

340 \text{ mOsm/kg H}_2\text{O}

gives a gap of

27 \text{ mOsm/kg H}_2\text{O}

.

Step-by-Step Solution

1

Identify the need to calculate the serum osmolar gap.

The patient has altered mental status and a measured serum osmolality of

340 \text{ mOsm/kg H}_2\text{O}

, indicating a potential toxic alcohol ingestion.

Calculating the osmolar gap is essential to unmask the presence of unmeasured osmotically active substances (like methanol, ethylene glycol, or isopropyl alcohol) not accounted for by standard chemistry panels.

2

Calculate the expected (calculated) serum osmolality.

Using the expanded formula:

2 \times 138 + \frac{126}{18} + \frac{28}{2.8} + \frac{92}{4.6} = 276 + 7 + 10 + 20 = 313 \text{ mOsm/kg H}_2\text{O}

.

Because ethanol is present in the patient's blood, its osmotic contribution must be included in the calculation. Failure to include it will result in an artificially elevated osmolar gap.

3

Determine the osmolar gap.

340 \text{ (Measured)} - 313 \text{ (Calculated)} = 27 \text{ mOsm/kg H}_2\text{O}

.

The osmolar gap is the difference between the measured and calculated osmolality. A normal gap is typically less than

10\text{-}15 \text{ mOsm/kg H}_2\text{O}

. A gap of

27

is elevated, suggesting ingestion of an additional toxic alcohol.

Key Concept

Calculation of the serum osmolar gap, including the proper osmotic contribution of ethanol.

Question 207Question →

Match each clinical vignette describing a renal or electrolyte complication of pharmacotherapy with the most likely responsible mechanism or drug effect.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The correct pairings match the anti-pseudomonal therapy complication to aminoglycoside-induced ATN, the encephalitis treatment complication to intratubular acyclovir precipitation, the bipolar treatment complication to lithium-induced nephrogenic diabetes insipidus, and the pneumonia prophylaxis complication to trimethoprim-induced channel blockade.

Each medication causes a unique and predictable pattern of renal impairment. Aminoglycosides directly damage proximal tubular cells causing ATN. Acyclovir is relatively insoluble in urine and precipitates in the tubules. Lithium impairs aquaporin insertion in the collecting duct. Trimethoprim acts on specific transporters without damaging the glomerulus itself.

Step-by-Step Solution

1

Analyze the first vignette featuring a delayed, gradual rise in creatinine and pigmented granular casts during anti-pseudomonal therapy.

Identified as acute tubular necrosis.

Aminoglycosides are classically associated with delayed-onset, non-oliguric ATN characterized by muddy brown casts.

2

Evaluate the second vignette detailing rapid oliguric acute kidney injury and needle-shaped crystals during treatment for viral encephalitis.

Identified as acyclovir crystal nephropathy.

Intravenous acyclovir is notorious for precipitating in the renal tubules, forming birefringent crystals and causing obstructive nephropathy.

3

Assess the third vignette describing polyuria, hypernatremia, and desmopressin-resistant dilute urine in a patient with a psychiatric history.

Identified as lithium-induced nephrogenic diabetes insipidus.

Lithium is a primary cause of acquired nephrogenic diabetes insipidus, which presents with ADH resistance at the collecting duct.

4

Examine the fourth vignette showing isolated hyperkalemia and elevated creatinine without true GFR decline during opportunistic pneumonia prophylaxis.

Identified as trimethoprim effect.

Trimethoprim blocks ENaC in the distal nephron (causing hyperkalemia) and inhibits creatinine secretion (elevating serum creatinine artificially).

Key Concept

Recognizing the distinct clinical presentations, timing, and urinary findings of medication-induced nephrotoxicity and electrolyte derangements.

Estimated Time:1m 30s

Question 208Question →

A 27-year-old woman is brought to the emergency department by her roommate due to severe weakness and four days of intractable vomiting. The patient has type 1 diabetes mellitus but has not administered her insulin for the past two days because she has been unable to tolerate oral intake. On physical examination, she appears lethargic. Her temperature is 37.1°C (98.8°F), blood pressure is 92/58 mm Hg, pulse is 122/min, and respirations are 16/min. Her mucous membranes are notably dry and skin turgor is decreased. Laboratory studies show the following:

Laboratory Test	Result
Sodium	$142 \text{ mEq/L}$
Potassium	$3.8 \text{ mEq/L}$
Chloride	$94 \text{ mEq/L}$
Bicarbonate	$20 \text{ mEq/L}$
Blood urea nitrogen	$35 \text{ mg/dL}$
Creatinine	$1.4 \text{ mg/dL}$
Glucose	$512 \text{ mg/dL}$

An arterial blood gas on room air reveals:

Test	Result
pH	$7.34$
$PaCO_2$	$38 \text{ mm Hg}$
$PaO_2$	$94 \text{ mm Hg}$

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 acidosis

High anion gap metabolic acidosis and normal anion gap metabolic acidosis

Normal anion gap metabolic acidosis and metabolic alkalosis

Show answer & explanation

Answer: High anion gap metabolic acidosis and metabolic alkalosis

Answer

The patient has a mixed acid-base disorder consisting of a high anion gap metabolic acidosis (due to diabetic ketoacidosis) and a concurrent metabolic alkalosis (due to severe vomiting).

This patient presents with a high anion gap metabolic acidosis (HAGMA) driven by diabetic ketoacidosis, evidenced by an anion gap of 28 (normal ~12). Despite the severe HAGMA, her bicarbonate is only mildly depressed at 20 mEq/L. To fully evaluate a HAGMA, the delta gap must be calculated to look for mixed metabolic disorders. The delta gap here is 16 (28 - 12). If HAGMA were the sole disorder, the bicarbonate should drop by an amount equal to the delta gap, resulting in an expected bicarbonate of 8 mEq/L (24 - 16 = 8). Because the patient's actual measured bicarbonate (20 mEq/L) is much higher than 8 mEq/L, there must be a second disorder independently raising the bicarbonate. In this clinical scenario, prolonged vomiting leads to substantial hydrogen ion and chloride loss, generating a concurrent metabolic alkalosis. Finally, Winter's formula calculation (

1.5 \times 20 + 8 = 38

) perfectly matches the patient's measured PaCO2, confirming appropriate respiratory compensation and ruling out any superimposed respiratory disorder.

Step-by-Step Solution

1

Calculate the primary anion gap to determine the core metabolic disorder.

AG = 142 - (94 + 20) = 28

.

An anion gap greater than 12 indicates the presence of a high anion gap metabolic acidosis (HAGMA), which in this patient is due to diabetic ketoacidosis.

2

Calculate the expected respiratory compensation using Winter's formula.

Expected

PaCO_2 = (1.5 \times 20) + 8 = 38 \pm 2 \text{ mm Hg}

. The measured

PaCO_2

is exactly

38 \text{ mm Hg}

.

Because the measured

PaCO_2

falls precisely within the expected range, there is no concurrent respiratory acidosis or alkalosis.

3

Calculate the delta gap (delta-delta) to identify hidden secondary metabolic disorders.

\Delta AG = 28 - 12 = 16

. The expected normal

HCO_3^-

if only HAGMA were present is

24 - 16 = 8 \text{ mEq/L}

. The measured

HCO_3^-

is

20 \text{ mEq/L}

.

Because the measured bicarbonate (

20 \text{ mEq/L}

) is significantly higher than the expected compensated bicarbonate (

8 \text{ mEq/L}

), a second disorder that independently raises bicarbonate must be present—specifically, a metabolic alkalosis.

Key Concept

In a patient with a high anion gap metabolic acidosis, calculating the delta gap is essential to identify hidden concurrent metabolic disorders. If the measured bicarbonate is significantly higher than the expected bicarbonate (calculated as 24 minus the delta gap), a concurrent metabolic alkalosis is present.

Question 209Question →

Match each clinical presentation of hypokalemic metabolic alkalosis with its corresponding underlying pathophysiologic mechanism.

Click a left item, then click its matching right item

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Answer

The presentations map to their underlying mechanisms based on blood pressure and neurohormonal profiles: Bartter syndrome involves the Na⁺-K⁺-2Cl⁻ cotransporter; Gitelman syndrome involves the NaCl cotransporter; Liddle syndrome involves ENaC; Renovascular hypertension involves reduced afferent perfusion; and Conn syndrome involves autonomous adrenal hypersecretion.

Each clinical presentation aligns with the physiologic consequences of its specific cellular defect. Tubular wasting syndromes (Bartter/Gitelman) cause hypokalemia with normal or low blood pressure, and are differentiated by urine calcium levels. Hypertensive syndromes (Liddle, primary, and secondary hyperaldosteronism) are successfully differentiated by analyzing the renin-aldosterone profile.

Step-by-Step Solution

1

Assess the patient's blood pressure status.

Patients with Bartter and Gitelman syndromes are typically normotensive or hypotensive, while those with Liddle syndrome, primary hyperaldosteronism, and secondary hyperaldosteronism present with hypertension.

Blood pressure distinguishes volume-depleted states caused by tubular salt-wasting from volume-expanded states caused by excessive sodium retention.

2

Evaluate the plasma renin activity and aldosterone levels in the hypertensive patients.

High renin and high aldosterone indicate secondary hyperaldosteronism. Low renin and high aldosterone indicate primary hyperaldosteronism. Low renin and low aldosterone indicate an aldosterone-independent mechanism of sodium retention, such as Liddle syndrome.

The renin-angiotensin-aldosterone axis feedback loop localizes the primary defect causing the hypertension.

3

Evaluate urine calcium excretion and serum magnesium in the normotensive/hypotensive patients.

Hypercalciuria points to a thick ascending limb defect (Bartter syndrome), whereas hypocalciuria and hypomagnesemia point to a distal convoluted tubule defect (Gitelman syndrome).

Calcium and magnesium handling differ fundamentally based on the specific renal tubular segment affected.

Key Concept

Differential diagnosis of hypokalemic metabolic alkalosis based on blood pressure, the renin-aldosterone axis, and urine electrolytes.

Estimated Time:2m 0s

Question 210Question →

Which specific glomerular disease diagnosis best corresponds to each of the following patient clinical scenarios?

Click a left item, then click its matching right item

Show answer & explanation

Answer

The synpharyngitic hematuria pairs with IgA nephropathy; the post-impetigo nephritic syndrome pairs with Poststreptococcal glomerulonephritis; the pulmonary-renal syndrome pairs with Goodpasture syndrome; the hepatitis B-associated nephrotic syndrome pairs with Membranous nephropathy; and the childhood pure nephrotic syndrome pairs with Minimal change disease.

Accurate diagnosis of glomerular diseases requires synthesizing patient age, timing of symptom onset relative to triggers, presence of nephritic versus nephrotic syndrome, and specific serologic markers such as complement levels or autoantibodies.

Step-by-Step Solution

1

Analyze the patient age and timeline of symptom onset relative to triggering infections.

Identifies synpharyngitic presentation for IgA nephropathy versus a delayed post-infectious timeline.

Timing is a key discriminator for nephritic syndromes.

2

Evaluate laboratory data, specifically proteinuria levels and serum complement.

Categorizes the presentations into nephritic (hematuria, RBC casts) versus nephrotic (protein

>3.5

g/day) and identifies C3 consumption.

Complement levels differentiate immune-complex mediated glomerulonephritides.

3

Correlate specific systemic symptoms and comorbidities with renal manifestations.

Hemoptysis points to pulmonary-renal syndromes; hepatitis B points to specific secondary nephropathies.

Systemic clues are essential for diagnosing secondary causes of glomerular disease.

Key Concept

Clinical presentation and diagnosis of primary and secondary glomerular diseases

Question 211Question →

A 60-year-old man with a history of peptic ulcer disease is brought to the emergency department due to 5 days of severe, intractable nausea and nonbilious vomiting. He reports being unable to tolerate any oral intake and feels profoundly weak. On physical examination, the patient appears lethargic. His mucous membranes are markedly dry, and capillary refill is prolonged. Temperature is 37.1 C (98.8 F), blood pressure is 88/55 mm Hg, pulse is 118/min, and respirations are 16/min. Laboratory studies are as follows:

Laboratory test	Result	Reference range
Serum sodium	140 mEq/L	136-145 mEq/L
Serum potassium	3.1 mEq/L	3.5-5.0 mEq/L
Serum chloride	86 mEq/L	98-106 mEq/L
Serum bicarbonate	24 mEq/L	22-28 mEq/L
Blood urea nitrogen	75 mg/dL	8-20 mg/dL
Serum creatinine	3.8 mg/dL	0.7-1.3 mg/dL

Arterial blood gas (room air)	Result	Reference range
pH	7.40	7.35-7.45
PaCO2	40 mm Hg	35-45 mm Hg
PaO2	90 mm Hg	75-105 mm Hg

Which of the following is the most accurate interpretation of this patient's acid-base status?

Normal acid-base status with isolated prerenal azotemia

High anion gap metabolic acidosis and metabolic alkalosis

Normal anion gap metabolic acidosis and metabolic alkalosis

Primary metabolic alkalosis with appropriate respiratory compensation

High anion gap metabolic acidosis with appropriate respiratory compensation

Show answer & explanation

Answer: High anion gap metabolic acidosis and metabolic alkalosis

Answer

High anion gap metabolic acidosis and metabolic alkalosis

The correct answer accurately identifies a mixed acid-base disorder by utilizing the anion gap and delta-delta calculations. Even when the pH and bicarbonate are normal, an anion gap must be calculated. The anion gap is significantly elevated at

30 \text{ mEq/L}

(normal is approximately

12 \text{ mEq/L}

), indicating a high anion gap metabolic acidosis (HAGMA) due to poor perfusion and acute kidney injury. The delta gap (

\Delta AG = 30 - 12 = 18

) indicates that the bicarbonate should have fallen by

18 \text{ mEq/L}

to an expected level of

6 \text{ mEq/L}

. Because the measured bicarbonate is

24 \text{ mEq/L}

, there is a concurrent severe metabolic alkalosis perfectly balancing the acidosis. This is consistent with his severe vomiting, which causes hypochloremic metabolic alkalosis via the loss of gastric

H^+

and

Cl^-

.

Step-by-Step Solution

1

Evaluate the primary acid-base values from the arterial blood gas.

The pH is 7.40,

PaCO_2

is 40 mm Hg, and

HCO_3^-

is 24 mEq/L. These values are all within strictly normal limits.

Establishing the baseline acid-base status is the required first step in interpretation, but normal values do not preclude mixed disorders.

2

Calculate the serum anion gap using the formula:

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

.

Anion gap =

140 - (86 + 24) = 140 - 110 = 30 \text{ mEq/L}

.

The anion gap must always be calculated, even if pH and

HCO_3^-

are normal, to avoid missing a hidden high anion gap metabolic acidosis (HAGMA).

3

Calculate the expected bicarbonate level using the delta gap (

\Delta AG

) to check for a mixed disorder.

Expected

HCO_3^- = 24 - (\text{Measured AG} - \text{Normal AG}) = 24 - (30 - 12) = 6 \text{ mEq/L}

. Since measured

HCO_3^-

(24 mEq/L) is much higher than the expected

HCO_3^-

(6 mEq/L), there is a concurrent metabolic alkalosis.

A delta gap analysis reveals additional metabolic disturbances that are masked by opposing effects on the serum bicarbonate level.

4

Correlate the calculated mixed acid-base disorder with the patient's clinical presentation.

The HAGMA is driven by lactic acidosis (hypoperfusion) and uremia (acute kidney injury), while the metabolic alkalosis is driven by severe vomiting (loss of

H^+

and

Cl^-

).

Clinical correlation confirms the pathophysiologic etiology of the identified disorders.

Key Concept

In patients with severe vomiting and hypoperfusion, opposing acid-base disturbances (metabolic alkalosis and HAGMA) can result in a deceptively normal pH and bicarbonate. Calculating the anion gap and delta gap is essential to unmask the mixed disorder.

Alternative Method

The delta ratio (

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

) can also be used to evaluate mixed disorders. Delta ratio =

\frac{30 - 12}{24 - 24} = \frac{18}{0}

. As the denominator approaches zero, the ratio approaches infinity. Any delta ratio

> 2.0

strongly indicates a concurrent metabolic alkalosis.

Estimated Time:1m 30s

Question 212Question →

Emergency medical services bring a 47-year-old mechanic to the hospital after he was found deeply lethargic in his workshop. His coworkers report that he had been working alone on a vehicle's cooling system and seemed disoriented before collapsing. On presentation, his temperature is $36.8^\circ C$ ( $98.2^\circ F$ ), blood pressure is $105/65$ mmHg, pulse is $112$ /min, and respiratory rate is $24$ /min. Physical examination reveals an unarousable patient with deep, rapid breathing. Arterial blood gas analysis on room air shows a pH of 7.21, $PaCO_2$ of 24 mmHg, and $PaO_2$ of 95 mmHg.

Laboratory evaluation reveals the following:

Parameter	Value
Sodium	$142$ mEq/L
Potassium	$4.8$ mEq/L
Chloride	$104$ mEq/L
Bicarbonate	$10$ mEq/L
Blood urea nitrogen	$14$ mg/dL
Creatinine	$1.6$ mg/dL
Glucose	$90$ mg/dL
Measured serum osmolality	$334$ mOsm/kg $H_2O$

Based on the provided laboratory results, what is the patient's calculated serum osmolar gap in mOsm/kg $H_2O$ ?

Show answer & explanation

Answer: 40

Answer

40

The correct answer is 40. The serum osmolar gap is defined as the difference between the directly measured serum osmolality and the calculated serum osmolality. The formula for calculated serum osmolality in conventional units (mg/dL) is:

Calculated\ Osmolality = 2 \times [Na^+] + \frac{[Glucose]}{18} + \frac{[BUN]}{2.8}

. Using the patient's values, this is computed as

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

mOsm/kg

H_2O

. The measured osmolality is 334 mOsm/kg

H_2O

. Subtracting the calculated value from the measured value yields an osmolar gap of

334 - 294 = 40

mOsm/kg

H_2O

. A normal osmolar gap is typically less than 10 to 15 mOsm/kg

H_2O

. In a patient with central nervous system depression, high anion gap metabolic acidosis, and exposure to automotive fluids, a markedly elevated osmolar gap strongly suggests intoxication with an unmeasured osmotically active alcohol, such as ethylene glycol (antifreeze).

Step-by-Step Solution

1

Calculate the expected serum osmolality using the standard formula for conventional units.

294

mOsm/kg

H_2O

This establishes the baseline osmolality contributed by the primary endogenous osmoles (sodium, glucose, and urea).

2

Subtract the calculated osmolality from the measured serum osmolality.

334 - 294 = 40

mOsm/kg

H_2O

An elevated difference (gap >10 mOsm/kg) indicates the presence of unmeasured exogenous osmotically active substances, such as ethylene glycol.

Key Concept

Calculation and interpretation of the serum osmolar gap in toxic alcohol ingestion.

Question 213Question →

A 68-year-old man is evaluated in the hospital for decreased urine output. He was admitted 3 days ago for severe community-acquired pneumonia and has been receiving intravenous antibiotics. His blood pressure is 98/60 mm Hg and heart rate is 102/min. Physical examination shows dry mucous membranes and flat jugular veins. Laboratory studies are obtained to evaluate his acute kidney injury:

Laboratory Test	Result
Serum sodium	135 mEq/L
Serum creatinine	1.5 mg/dL
Blood urea nitrogen	38 mg/dL
Urine sodium	27 mEq/L
Urine creatinine	60 mg/dL

What is the patient's fractional excretion of sodium (FeNa) expressed as a percentage?

Show answer & explanation

Answer: 0.5

Answer

0.5

The correct calculation yields a fractional excretion of sodium (FeNa) of exactly 0.5%. A FeNa of < 1% indicates a prerenal etiology for acute kidney injury. In this patient, signs of volume depletion (hypotension, tachycardia, dry mucous membranes) point toward prerenal azotemia secondary to dehydration, leading the kidneys to avidly reabsorb sodium and water in an attempt to restore intravascular volume.

Step-by-Step Solution

1

Identify the formula for Fractional Excretion of Sodium (FeNa).

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

This formula relates the amount of sodium excreted to the amount of creatinine excreted, thereby correcting for urine concentration.

2

Extract the necessary values from the provided laboratory table.

U_{Na} = 27

mEq/L,

P_{Cr} = 1.5

mg/dL,

P_{Na} = 135

mEq/L, and

U_{Cr} = 60

mg/dL.

These specific variables are required for the FeNa equation. The Blood Urea Nitrogen (BUN) value of 38 mg/dL is a distractor for this specific calculation.

3

Substitute the values into the FeNa equation.

FeNa = \frac{27 \times 1.5}{135 \times 60} \times 100

Plugging the values into the correct positions in the numerator and denominator ensures mathematical accuracy.

4

Perform the arithmetic calculation.

\frac{40.5}{8100} \times 100 = 0.005 \times 100 = 0.5

This yields the final FeNa value as a percentage, which can then be interpreted clinically.

Key Concept

Calculation and interpretation of Fractional Excretion of Sodium (FeNa) in the evaluation of Acute Kidney Injury.

Question 214Question →

A 64-year-old woman is brought to the emergency department by her family due to profound weakness and confusion. She has had 5 days of severe, voluminous watery diarrhea. Her medical history includes type 2 diabetes mellitus and hypertension. On examination, blood pressure is 82/50 mm Hg, heart rate is 118/min, and respiratory rate is 24/min. She has dry mucous membranes, flat neck veins, and delayed capillary refill.

Laboratory studies show:
Serum $Na^+$ : 140 mEq/L
Serum $K^+$ : 3.2 mEq/L
Serum $Cl^-$ : 112 mEq/L
Serum $HCO_3^-$ : 8 mEq/L
Blood urea nitrogen: 54 mg/dL
Serum creatinine: 2.8 mg/dL (baseline 0.9 mg/dL)
Serum lactate: 5.2 mmol/L (Normal: 0.5-1.0 mmol/L)
Serum albumin: 4.0 g/dL

Assuming a reference anion gap of 12 mEq/L and a normal serum bicarbonate of 24 mEq/L, what is this patient's calculated delta ratio (also known as the $\Delta/\Delta$ ratio)?

Show answer & explanation

Answer: 0.5

Answer

0.5

The correct answer is 0.5. This patient presents with hypovolemic shock (hypotension, tachycardia, poor perfusion) secondary to severe watery diarrhea, leading to an elevated lactate level. Therefore, she has a mixed acid-base disorder: a high anion gap metabolic acidosis (HAGMA) from lactic acidosis, and a normal anion gap metabolic acidosis (NAGMA) from gastrointestinal bicarbonate losses. The delta ratio is used to uncover this mixed disorder. It is calculated by dividing the excess anion gap (

\Delta AG = 20 - 12 = 8

) by the bicarbonate deficit (

\Delta HCO_3^- = 24 - 8 = 16

). The resulting ratio of 0.5 falls between 0.4 and 0.8, which is the classic diagnostic range for a mixed HAGMA and NAGMA.

Step-by-Step Solution

1

Calculate the serum anion gap.

20

mEq/L

Determines the presence and magnitude of unmeasured anions contributing to the acidosis.

2

Calculate the

\Delta AG

.

8

mEq/L

Quantifies the excess gap above the normal baseline (

20 - 12

).

3

Calculate the

\Delta HCO_3^-

.

16

mEq/L

Quantifies the total deficit of bicarbonate below the normal baseline (

24 - 8

).

4

Divide

\Delta AG

by

\Delta HCO_3^-

.

0.5

Provides the delta ratio, which identifies complex mixed acid-base disorders.

Key Concept

In patients with a high anion gap metabolic acidosis (HAGMA), the delta ratio (

\Delta AG / \Delta HCO_3^-

) is calculated to identify concurrent concealed acid-base disorders. A ratio < 0.8 indicates a concurrent normal anion gap metabolic acidosis (NAGMA), which in this patient is due to severe diarrhea.

Question 215Question →

A 35-year-old woman presents to the clinic for evaluation of generalized muscle weakness and fatigue over the past several weeks. She also reports a recent history of passing two kidney stones. Her past medical history is significant for Sjögren syndrome, for which she uses artificial tears and saliva substitutes. Vital signs are within normal limits. Laboratory evaluation reveals the following:

Test	Value
Sodium	139 mEq/L
Potassium	2.7 mEq/L
Chloride	115 mEq/L
Bicarbonate	14 mEq/L
Blood urea nitrogen	14 mg/dL
Creatinine	0.9 mg/dL

Urinalysis:
- pH: 6.5
- Specific gravity: 1.015
- Protein: Negative
- Blood: Negative
- Glucose: Negative

Which of the following is the most likely underlying mechanism for this patient's laboratory findings?

Impaired hydrogen ion secretion in the distal tubule

Defective bicarbonate reabsorption in the proximal tubule

Decreased aldosterone production or renal responsiveness

Excessive gastrointestinal loss of bicarbonate-rich fluids

Accumulation of unmeasured endogenous organic acids

Show answer & explanation

Answer: Impaired hydrogen ion secretion in the distal tubule

Answer

Impaired hydrogen ion secretion in the distal tubule

The correct mechanism is impaired hydrogen ion secretion in the distal tubule, which is the pathophysiology of Type 1 (distal) renal tubular acidosis (RTA). The patient has a metabolic acidosis with a normal anion gap (139 - 115 - 14 = 10). In the presence of a hypokalemic normal anion gap metabolic acidosis, the urine pH must be assessed. The alpha-intercalated cells in the distal tubule normally secrete

H^+

to acidify the urine. In Type 1 RTA, this mechanism fails, resulting in an inability to acidify the urine below a pH of 5.5 (patient's urine pH is 6.5). The alkaline urine promotes calcium phosphate precipitation, leading to recurrent kidney stones. Type 1 RTA is highly associated with autoimmune disorders, particularly Sjögren syndrome and rheumatoid arthritis.

Step-by-Step Solution

1

Calculate the serum anion gap.

AG = Na^+ - (Cl^- + HCO_3^-) = 139 - (115 + 14) = 10

mEq/L.

Determining the anion gap is the essential first step in evaluating any metabolic acidosis to differentiate between HAGMA (>12 mEq/L) and NAGMA (8-12 mEq/L).

2

Evaluate the serum potassium in the context of a Normal Anion Gap Metabolic Acidosis (NAGMA).

The patient has severe hypokalemia (

K^+ = 2.7

mEq/L).

Serum potassium levels help narrow the differential diagnosis of a NAGMA. Type 4 RTA is associated with hyperkalemia, whereas Type 1 RTA, Type 2 RTA, and gastrointestinal losses typically present with hypokalemia.

3

Assess the urine pH to differentiate the causes of hypokalemic NAGMA.

The urine pH is

6.5

, which is inappropriately alkaline in the face of severe systemic academia.

In Type 2 RTA and severe diarrhea, the distal nephron is intact and maximally excretes

H^+

, lowering urine pH to

< 5.5

. A urine pH

> 5.5

in a hypokalemic NAGMA is diagnostic of Type 1 (distal) RTA.

Key Concept

Type 1 (distal) renal tubular acidosis presents as a normal anion gap metabolic acidosis, hypokalemia, and an inappropriately alkaline urine pH (> 5.5), often complicated by calcium phosphate nephrolithiasis. It is strongly associated with autoimmune diseases like Sjögren syndrome.

Estimated Time:1m 30s

Question 216Question →

Match each clinical presentation of acute renal dysfunction with the most characteristic finding expected on microscopic urinalysis.

Click a left item, then click its matching right item

Show answer & explanation

Answer

Ischemic hypotension causes muddy brown granular casts; ethylene glycol toxicity produces calcium oxalate crystals; cryoglobulinemic glomerulonephritis leads to red blood cell casts; and nafcillin-induced interstitial nephritis generates white blood cell casts.

Urinary sediment serves as a 'liquid biopsy' that non-invasively distinguishes the anatomical compartment of renal injury. Ischemic damage exclusively targets tubular cells (ATN), yielding granular casts. Toxic ingestions like ethylene glycol have specific metabolites (oxalate) that crystallize. Glomerular inflammation (glomerulonephritis) uniquely allows red blood cells to cross the damaged basement membrane, forming RBC casts. Finally, allergic tubulointerstitial reactions (AIN) recruit inflammatory cells, forming WBC casts.

Step-by-Step Solution

1

Analyze the hypotensive surgical patient.

Identified ischemic acute tubular necrosis (ATN), which corresponds to muddy brown granular casts.

Hypoperfusion deprives the metabolically active renal medulla of oxygen, leading to tubular cell necrosis and sloughing.

2

Analyze the toxic ingestion with severe metabolic acidosis.

Identified ethylene glycol poisoning, which corresponds to envelope-shaped calcium oxalate crystals.

The toxic alcohol is metabolized by alcohol dehydrogenase into toxic metabolites, including oxalate, which crystallizes in the renal tubules.

3

Analyze the hepatitis C patient with purpura and low complement.

Identified mixed cryoglobulinemia causing glomerulonephritis, which corresponds to red blood cell casts.

Immune complex deposition in the glomeruli causes severe inflammation, allowing RBCs to leak and become trapped in Tamm-Horsfall protein within the tubules.

4

Analyze the patient with a rash and fever after starting nafcillin.

Identified drug-induced acute interstitial nephritis (AIN), which corresponds to white blood cell casts.

Beta-lactam antibiotics can act as haptens, triggering a delayed hypersensitivity reaction in the renal interstitium that recruits leukocytes.

Key Concept

Correlation of acute kidney injury etiologies with specific urinary sediment findings.

Question 217Question →

A 52-year-old man with a history of obesity hypoventilation syndrome and type 2 diabetes mellitus is brought to the emergency department by his wife due to profound weakness and confusion. For the past 4 days, he has had severe, watery diarrhea with up to 10 bowel movements daily, accompanied by abdominal cramping. He has not been able to tolerate oral intake. His temperature is $37.1^\circ\text{C}$ ( $98.8^\circ\text{F}$ ), blood pressure is $90/60\text{ mm Hg}$ , pulse is $112\text{/min}$ , and respirations are $14\text{/min}$ . Physical examination shows dry mucous membranes and decreased skin turgor. The patient appears somnolent but is arousable.

Laboratory studies show:
Serum sodium: $135\text{ mEq/L}$
Serum potassium: $3.2\text{ mEq/L}$
Serum chloride: $113\text{ mEq/L}$
Serum bicarbonate: $12\text{ mEq/L}$
Blood urea nitrogen: $42\text{ mg/dL}$
Serum creatinine: $1.6\text{ mg/dL}$
Serum albumin: $4.0\text{ g/dL}$

Arterial blood gas analysis on room air:
pH: $7.08$
$\text{PaCO}_2$ : $42\text{ mm Hg}$
$\text{PaO}_2$ : $65\text{ mm Hg}$

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

Mixed normal anion gap metabolic acidosis and respiratory acidosis

Simple normal anion gap metabolic acidosis with appropriate respiratory compensation

Mixed normal anion gap metabolic acidosis and respiratory alkalosis

Mixed high anion gap metabolic acidosis and respiratory acidosis

Simple high anion gap metabolic acidosis with appropriate respiratory compensation

Show answer & explanation

Answer: Mixed normal anion gap metabolic acidosis and respiratory acidosis

Answer

Mixed normal anion gap metabolic acidosis and respiratory acidosis

This patient has a mixed normal anion gap metabolic acidosis and respiratory acidosis. The primary metabolic acidosis is diagnosed by the low pH (

7.08

) and low bicarbonate (

12\text{ mEq/L}

), caused by profound bicarbonate loss from severe diarrhea. The anion gap is calculated as

\text{Sodium} - (\text{Chloride} + \text{Bicarbonate})

, which is

135 - (113 + 12) = 10\text{ mEq/L}

. Since this is within the normal range of

8-12\text{ mEq/L}

, the primary disorder is a normal anion gap (hyperchloremic) metabolic acidosis. Next, Winter's formula must be applied to determine if respiratory compensation is adequate: Expected

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

. For this patient, the expected

\text{PaCO}_2

is

(1.5 \times 12) + 8 = 26 \pm 2\text{ mm Hg}

(range

24-28\text{ mm Hg}

). The patient's actual

\text{PaCO}_2

is

42\text{ mm Hg}

. Because the actual

\text{PaCO}_2

is significantly higher than the expected range, he has a superimposed primary respiratory acidosis. This indicates a failure to mount the necessary hyperventilatory response, perfectly aligning with his history of obesity hypoventilation syndrome and current somnolent state.

Step-by-Step Solution

1

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

The pH is

7.08

(severe acidemia) and the serum bicarbonate is

12\text{ mEq/L}

(low), indicating a primary metabolic acidosis.

Determining the primary disorder is the critical first step in any acid-base evaluation.

2

Calculate the serum anion gap.

Anion Gap =

\text{Na}^+ - (\text{Cl}^- + \text{HCO}_3^-)

=

135 - (113 + 12) = 10\text{ mEq/L}

. This is within the normal range (

8-12\text{ mEq/L}

).

Differentiating between normal and high anion gap metabolic acidosis narrows the differential diagnosis. This patient's profound diarrhea caused a normal anion gap metabolic acidosis due to gastrointestinal bicarbonate loss.

3

Calculate the expected respiratory compensation using Winter's formula.

Expected

\text{PaCO}_2 = (1.5 \times \text{HCO}_3^-) + 8 \pm 2 = (1.5 \times 12) + 8 \pm 2 = 26 \pm 2\text{ mm Hg}

. The actual

\text{PaCO}_2

is

42\text{ mm Hg}

, which is significantly higher than the expected range.

If the actual PaCO2 is higher than the expected PaCO2, there is a concurrent primary respiratory acidosis. This patient's obesity hypoventilation syndrome and somnolence prevent him from adequately hyperventilating to compensate for the acidemia.

Key Concept

Evaluating complex acid-base disorders requires a stepwise approach: identify the primary disturbance, calculate the anion gap, and apply Winter's formula to determine if respiratory compensation is appropriate.

Question 218Question →

An 82-year-old man is brought to the emergency department due to sudden-onset, severe abdominal pain. He has a history of hypertension, type 2 diabetes mellitus, and atrial fibrillation for which he takes apixaban; however, he admits to missing several doses over the past week. During transport, paramedics administered intravenous morphine for pain control. On arrival, he appears drowsy but is arousable. Temperature is $37.1^\circ\text{C}$ ( $98.8^\circ\text{F}$ ), blood pressure is $102/60\text{ mmHg}$ , pulse is $118/\text{min}$ and irregular, and respiratory rate is $14/\text{min}$ . The abdomen is slightly distended with absent bowel sounds, and there is minimal tenderness to palpation.

Laboratory results are as follows:

Parameter	Value
Sodium	$140\text{ mEq/L}$
Potassium	$4.5\text{ mEq/L}$
Chloride	$104\text{ mEq/L}$
Bicarbonate	$12\text{ mEq/L}$
Blood urea nitrogen	$30\text{ mg/dL}$
Creatinine	$1.4\text{ mg/dL}$

Arterial blood gas (on room air):

Parameter	Value
pH	$7.16$
$\text{PaCO}_2$	$34\text{ mmHg}$
$\text{PaO}_2$	$72\text{ mmHg}$

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

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 and concurrent respiratory acidosis

Primary respiratory acidosis with appropriate metabolic compensation

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's clinical presentation (atrial fibrillation off anticoagulation with abdominal pain out of proportion to exam) is classic for acute mesenteric ischemia, leading to lactic acidosis. The pH is

7.16

(acidemia) and bicarbonate is

12\text{ mEq/L}

, defining a primary metabolic acidosis. The anion gap is elevated at

24

(

140 - [104 + 12]

), categorizing it as a high anion gap metabolic acidosis (HAGMA). To assess respiratory compensation, Winter's formula is utilized:

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

. For this patient, the expected

\text{PaCO}_2 = (1.5 \times 12) + 8 = 26 \pm 2\text{ mmHg}

. Because the patient's actual

\text{PaCO}_2

is

34\text{ mmHg}

(which is

>28\text{ mmHg}

), he has an inadequate respiratory response. This relative hypoventilation, likely secondary to the recent administration of intravenous morphine, indicates a concurrent primary respiratory acidosis.

Step-by-Step Solution

1

Determine the primary acid-base disturbance.

The patient has an acidemia (pH

7.16

). The

\text{HCO}_3^-

is low (

12\text{ mEq/L}

), confirming a primary metabolic acidosis.

pH < 7.40 indicates acidemia, and a matched decrease in bicarbonate establishes the primary metabolic nature of the disturbance.

2

Calculate the serum anion gap.

\text{Anion Gap} = \text{Na}^+ - (\text{Cl}^- + \text{HCO}_3^-) = 140 - (104 + 12) = 140 - 116 = 24

.

Differentiating between normal (8-12) and high anion gap metabolic acidosis is the required next step in evaluating any metabolic acidosis.

3

Calculate expected respiratory compensation using Winter's formula.

\text{Expected PaCO}_2 = 1.5 \times [\text{HCO}_3^-] + 8 \pm 2 = 1.5 \times 12 + 8 \pm 2 = 18 + 8 \pm 2 = 26 \pm 2\text{ mmHg}

(Range: 24-28 mmHg).

In primary metabolic acidosis, the lungs compensate by hyperventilating to blow off

\text{CO}_2

. Winter's formula predicts the appropriate

\text{PaCO}_2

response.

4

Compare actual

\text{PaCO}_2

to expected

\text{PaCO}_2

.

The actual

\text{PaCO}_2

(

34\text{ mmHg}

) is greater than the expected range (

24-28\text{ mmHg}

).

An actual

\text{PaCO}_2

higher than the expected compensated range indicates an inadequate respiratory drive, confirming a concurrent primary respiratory acidosis.

Key Concept

Calculation of Anion Gap and Winter's Formula to diagnose mixed acid-base disorders.

Question 219Question →

Match each clinical scenario describing a patient with newly detected hyponatremia to the most accurate expected pattern of laboratory findings, focusing on serum and urine osmolar characteristics.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The heart failure patient represents hypervolemic hypotonic hyponatremia with sodium avidity. The lung mass patient exhibits SIADH with sodium wasting. The psychiatric patient has primary polydipsia with a maximally dilute urine. The DKA patient presents with hypertonic translocational hyponatremia. The patient with severe hypertriglyceridemia demonstrates isotonic pseudohyponatremia.

The algorithmic approach to hyponatremia mandates beginning with measured serum osmolality. Severe hypertriglyceridemia increases the non-aqueous phase of blood, causing an artifactual drop in sodium (isotonic pseudohyponatremia). Hyperglycemia acts as a potent osmole, pulling water into the extracellular space, causing a dilutional, hypertonic hyponatremia. True hypotonic hyponatremia requires interrogating ADH activity via urine osmolality. Primary polydipsia suppresses ADH, yielding a maximally dilute urine (<100 mOsm/kg H₂O). If ADH is active (urine osmolality >100 mOsm/kg H₂O), the urine sodium determines the drive: decreased effective arterial volume (e.g., heart failure) causes intense sodium avidity (urine Na <20 mEq/L), whereas SIADH (e.g., from small cell lung cancer) is characterized by relative volume expansion and obligate sodium wasting (urine Na >40 mEq/L).

Step-by-Step Solution

1

Evaluate the measured serum osmolality.

Categorizes the hyponatremia as isotonic (pseudohyponatremia from lipids/proteins), hypertonic (glucose, mannitol), or true hypotonic hyponatremia.

True hyponatremia must represent a state of hypotonicity. DKA creates hypertonicity, while hypertriglyceridemia creates isotonicity.

2

For patients with true hypotonicity, evaluate the urine osmolality.

Determines whether Antidiuretic Hormone (ADH) is appropriately suppressed.

If urine osmolality is <100 mOsm/kg H₂O, ADH is suppressed, pointing to primary polydipsia or advanced renal failure. If it is >100 mOsm/kg H₂O, ADH is active.

3

For patients with active ADH (urine osmolality >100 mOsm/kg H₂O), assess clinical volume status and urine sodium.

Differentiates appropriate ADH response from inappropriate ADH response.

A low effective arterial volume (heart failure, cirrhosis) triggers RAAS, reducing urine sodium to <20 mEq/L. Euvolemic states like SIADH suppress RAAS, causing urine sodium to exceed 40 mEq/L.

Key Concept

The diagnostic algorithm for hyponatremia relies on sequentially evaluating measured serum osmolality, urine osmolality, and urine sodium to determine the underlying pathophysiology.

Question 220Question →

Match each patient's clinical presentation and initial diagnostic findings with the most accurate underlying pathophysiologic mechanism or defining etiology.

Click a left item, then click its matching right item

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Answer

The correct matches map Goodpasture syndrome to autoantibodies against the alpha-3 chain of type IV collagen; Alport syndrome to genetic mutations in type IV collagen assembly; Mixed cryoglobulinemia to cold-precipitable immune complexes with classical complement activation; Poststreptococcal glomerulonephritis to alternate complement pathway activation; and Collapsing FSGS to viral-associated podocyte injury linked to APOL1.

Each clinical vignette contains pathognomonic markers for a specific glomerular disease. Identifying the precise pattern of complement consumption, genetic history, or specific immunofluorescence findings allows for accurate matching to the underlying pathophysiology.

Step-by-Step Solution

1

Analyze the immunofluorescence, complement levels, and demographic clues in each vignette.

Identified five distinct glomerular syndromes: Anti-GBM disease, Alport syndrome, Cryoglobulinemia, PSGN, and Collapsing FSGS.

Accurate diagnosis of nephritic and nephrotic syndromes requires integrating clinical history with specific biopsy and serologic findings.

2

Differentiate between the two diseases involving type IV collagen.

Linked the patient with hemoptysis to autoimmune destruction (Goodpasture) and the patient with hearing loss to genetic structural defects (Alport).

Both conditions involve type IV collagen, but their mechanisms (autoimmune vs. congenital mutation) dictate vastly different clinical presentations.

3

Differentiate between the causes of hypocomplementemia.

Linked the Hepatitis C patient with low C4 to classical pathway activation (Cryoglobulinemia) and the post-impetigo patient to alternate pathway activation (PSGN).

Complement profiling (C3 vs. C4 levels) is a critical step in narrowing down the differential diagnosis for immune complex glomerulonephritis.

Key Concept

Pathophysiological mechanisms and histopathological correlates of primary and secondary glomerular diseases.

Nephrology

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