A patient with severe COPD has an arterial blood gas: pH 7.36, PaCO 65
mmHg, HCO 36 mEq/L. Which statement best characterizes this acid-base
status?
A. Acute respiratory acidosis with no metabolic compensation
B. Chronic respiratory acidosis with full renal compensation
C. Mixed respiratory acidosis and metabolic alkalosis
D. Compensated metabolic alkalosis with respiratory acidosis
Correct Answer: B - Chronic respiratory acidosis with full renal
compensation
RATIONALE
The elevated PaCO indicates respiratory acidosis; the markedly
elevated HCO with near-normal pH reflects renal compensation that
takes days to develop, consistent with chronic respiratory acidosis.
Acute respiratory acidosis would show minimal HCO elevation.
Mixed disorders would show pH outside the expected range or
disproportionate compensation.
Question 2
Which pathophysiologic mechanism best explains the hypoxemia seen in a
patient with acute respiratory distress syndrome (ARDS) that is refractory to
supplemental oxygen?
A. Diffusion limitation due to alveolar-capillary membrane thickening
B. Right-to-left intrapulmonary shunt from flooded alveoli
C. Hypoventilation from decreased respiratory drive
D. V/Q mismatch from bronchospasm
Correct Answer: B - Right-to-left intrapulmonary shunt from
flooded alveoli
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, RATIONALE
ARDS causes alveolar flooding and collapse, leading to true
right-to-left shunting where blood bypasses non-ventilated alveoli; this
shunt is refractory to oxygen. Diffusion limitation and V/Q mismatch
typically improve with supplemental oxygen. Hypoventilation would
also raise PaCO, which is not the primary mechanism in early ARDS.
Question 3
A patient with nephrotic syndrome has a serum albumin of 2.1 g/dL and
generalized edema. Which Starling force alteration is the primary driver of the
edema?
A. Increased capillary hydrostatic pressure
B. Decreased capillary oncotic pressure
C. Increased interstitial oncotic pressure
D. Lymphatic obstruction
Correct Answer: B - Decreased capillary oncotic pressure
RATIONALE
Nephrotic syndrome causes heavy proteinuria and hypoalbuminemia,
reducing plasma oncotic pressure and favoring fluid movement into
the interstitium. Increased hydrostatic pressure is characteristic of
heart failure or venous obstruction. Lymphatic obstruction and
increased interstitial oncotic pressure are less central in nephrotic
edema.
Question 4
Which laboratory finding best distinguishes prerenal azotemia from intrinsic
acute tubular necrosis (ATN) in a hypovolemic patient?
A. Fractional excretion of sodium (FENa) < 1%
B. Urine sodium > 40 mEq/L
C. Urine osmolality < 350 mOsm/kg
D. BUN/creatinine ratio < 10:1
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, Correct Answer: A - Fractional excretion of sodium (FENa) < 1%
RATIONALE
Prerenal azotemia features avid sodium and water reabsorption,
yielding FENa < 1% and concentrated urine. Intrinsic ATN shows
tubular damage with FENa > 2%, high urine sodium, and isosthenuria.
A low BUN/creatinine ratio is not typical of prerenal states.
Question 5
Which statement best describes the primary defect in nephrogenic diabetes
insipidus?
A. Impaired ADH secretion from the posterior pituitary
B. Renal tubular resistance to ADH action
C. Excessive ADH secretion causing water retention
D. Defective thirst mechanism leading to hypodipsia
Correct Answer: B - Renal tubular resistance to ADH action
RATIONALE
Nephrogenic diabetes insipidus results from the kidney's inability to
respond to ADH, often due to lithium or genetic defects in
aquaporin-2. Central diabetes insipidus involves deficient ADH
secretion. SIADH causes water retention, and hypodipsia is a separate
disorder.
Question 6
A patient with a large pulmonary embolism develops sudden hypoxemia and
increased dead space. Which V/Q alteration is most characteristic?
A. Increased shunt fraction
B. Increased dead space ventilation
C. Diffusion limitation
D. Alveolar hypoventilation
Correct Answer: B - Increased dead space ventilation
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