WGU D236 Pathophysiology OA Actual Exam
2026/2027 | Questions with Verified Answers |
100% Correct | Pass Guaranteed
SECTION 1: Cellular Biology & Foundations
Q1: A patient presents with severe diarrhea. Arterial blood gas reveals: pH 7.28, PaCO₂
38 mm Hg, HCO₃⁻ 16 mEq/L. What is the primary pathophysiological process?
A. Respiratory acidosis
B. Respiratory alkalosis
C. Metabolic acidosis
D. Metabolic alkalosis
Correct Answer: C
Rationale: Disease/Process: Metabolic acidosis due to bicarbonate loss.
Pathophysiological Sequence: Severe diarrhea (etiology) causes excessive loss of
bicarbonate-rich intestinal fluids (pathogenesis), depleting the body's base buffer
(HCO₃⁻), leading to an increase in H⁺ concentration and a low pH with a correspondingly
low HCO₃⁻ (clinical manifestation/ABG finding). The normal PaCO₂ indicates the lungs
are not compensating yet. Distractor Analysis: A & B are incorrect because the primary
disturbance is metabolic (abnormal HCO₃⁻), not respiratory (PaCO₂ is normal). D is
incorrect because diarrhea causes acid gain/base loss, not alkali gain.
,Q2: A 68-year-old man with COPD develops increased work of breathing. ABG: pH 7.34,
PaCO₂ 65 mm Hg, HCO₃⁻ 35 mEq/L. Which statement best explains his acid-base
status?
A. Acute respiratory acidosis with no compensation
B. Chronic respiratory acidosis with renal compensation
C. Metabolic alkalosis with respiratory compensation
D. Mixed respiratory and metabolic acidosis
Correct Answer: B
Rationale: Disease/Process: Chronic hypercapnic respiratory failure. Pathophysiological
Sequence: Long-standing COPD (etiology) reduces alveolar ventilation → CO₂ retention
→ ↑PaCO₂ (respiratory acidosis). Over days, kidneys increase HCO₃⁻ reabsorption (renal
compensation) to buffer excess H⁺, returning pH toward normal (7.34 vs expected <7.3
in acute). HCO₃⁻ 35 mEq/L >24 indicates renal compensation. Distractor Analysis: Acute
(A) would show pH <7.35 with HCO₃⁻ near 24; metabolic alkalosis (C) would have
elevated HCO₃⁻ but low PaCO₂ as compensation; mixed acidosis (D) would show lower
pH and possibly elevated anion gap.
Q3: A 45-year-old woman with Sjögren syndrome presents with muscle cramps and
perioral numbness. Labs: Na⁺ 139 mEq/L, K⁺ 3.2 mEq/L, HCO₃⁻ 28 mEq/L, Ca²⁺ 7.8
mg/dL, phosphate 2.0 mg/dL. Which underlying mechanism best explains her
hypocalcemia?
A. Renal calcium wasting due to metabolic acidosis
B. Decreased intestinal calcium absorption due to autoantibody-mediated destruction of
exocrine glands → vitamin D malabsorption
C. Increased bone deposition secondary to hyperphosphatemia
D. Hypoalbuminemia from chronic inflammation
,Correct Answer: B
Rationale: Disease/Process: Hypocalcemia secondary to malabsorption in Sjögren
syndrome. Pathophysiological Sequence: Autoimmune destruction of salivary/lacrimal
glands (etiology) extends to exocrine pancreas/gut mucosa → ↓pancreatic enzymes &
bile acids → impaired fat-soluble vitamin (D) absorption → ↓25-OH vitamin D →
↓intestinal Ca²⁺ absorption → hypocalcemia (clinical manifestation). Mild metabolic
alkalosis (HCO₃⁻ 28) from vomiting/diuretic use further lowers ionized Ca²⁺. Distractor
Analysis: Renal wasting (A) is not typical in Sjögren unless RTA present; phosphate is
low (not high) ruling out increased bone deposition (C); Ca²⁺ is total but symptoms
suggest ionized hypocalcemia, not purely albumin-bound (D).
Q4: A 30-year-old man with sickle cell trait exercises vigorously in hot weather and
develops dark urine. Urinalysis shows ≥3+ blood on dipstick but 0–2 RBCs/hpf
microscopy. Which pathophysiological process is responsible?
A. Glomerular inflammation causing hematuria
B. Intravascular hemolysis releasing hemoglobin filtered in urine
C. Myoglobin release from rhabdomyolysis
D. Urate crystal-induced nephropathy
Correct Answer: B
Rationale: Disease/Process: Hemoglobinuria due to exertional hemolysis in sickle cell
trait. Pathophysiological Sequence: Dehydration and acidosis during exertion (etiologic
triggers) promote sickling of a minority of RBCs (pathogenesis) → intravascular
hemolysis → free hemoglobin in plasma → filtered by glomeruli → hemoglobin-positive
dipstick with few intact RBCs (clinical picture). Distractor Analysis: Glomerular disease
(A) would show dysmorphic RBCs/casts; rhabdomyolysis (C) would elevate CK/aldolase
and cause myoglobinuria (tea-colored urine) but dipstick equally positive—however
, clinical context here emphasizes hemolysis; urate nephropathy (D) causes crystalluria
and AKI, not isolated hemoglobinuria.
Q5: A 55-year-old diabetic patient on dialysis misses two treatments and becomes
confused. ABG: pH 7.24, PaCO₂ 28 mm Hg, HCO₃⁻ 12 mEq/L, anion gap 24 mEq/L.
Which mechanism best explains the acid-base disorder?
A. Accumulation of urea leading to respiratory acidosis
B. Accumulation of organic acids (phosphates, sulfates) and lactic acid →
high-anion-gap metabolic acidosis with respiratory compensation
C. Loss of bicarbonate in dialysate causing non-anion-gap acidosis
D. Hyperchloremic acidosis from normal saline infusion
Correct Answer: B
Rationale: Disease/Process: High-anion-gap metabolic acidosis (HAGMA) due to
missed dialysis. Pathophysiological Sequence: Missed sessions (etiology) → retention
of protein-bound acids, phosphates, sulfates, and possible lactic acid (pathogenesis) →
consumption of bicarbonate → HAGMA (anion gap >12) and acidemia →
hyperventilation (respiratory compensation) lowers PaCO₂. Distractor Analysis: Urea is
not an acid and does not cause acidosis (A); loss of bicarbonate (C) would yield normal
anion gap; hyperchloremic acidosis (D) also presents with normal gap and is unrelated
to missed dialysis.
Q6: A 60-year-old woman with chronic liver disease develops increasing abdominal girth
and shortness of breath. Albumin 2.1 g/dL, total protein 4.8 g/dL. Which Starling force
alteration is primarily responsible for ascites formation?
A. Increased plasma oncotic pressure
B. Decreased plasma oncotic pressure → net filtration exceeds reabsorption in
peritoneal capillaries
2026/2027 | Questions with Verified Answers |
100% Correct | Pass Guaranteed
SECTION 1: Cellular Biology & Foundations
Q1: A patient presents with severe diarrhea. Arterial blood gas reveals: pH 7.28, PaCO₂
38 mm Hg, HCO₃⁻ 16 mEq/L. What is the primary pathophysiological process?
A. Respiratory acidosis
B. Respiratory alkalosis
C. Metabolic acidosis
D. Metabolic alkalosis
Correct Answer: C
Rationale: Disease/Process: Metabolic acidosis due to bicarbonate loss.
Pathophysiological Sequence: Severe diarrhea (etiology) causes excessive loss of
bicarbonate-rich intestinal fluids (pathogenesis), depleting the body's base buffer
(HCO₃⁻), leading to an increase in H⁺ concentration and a low pH with a correspondingly
low HCO₃⁻ (clinical manifestation/ABG finding). The normal PaCO₂ indicates the lungs
are not compensating yet. Distractor Analysis: A & B are incorrect because the primary
disturbance is metabolic (abnormal HCO₃⁻), not respiratory (PaCO₂ is normal). D is
incorrect because diarrhea causes acid gain/base loss, not alkali gain.
,Q2: A 68-year-old man with COPD develops increased work of breathing. ABG: pH 7.34,
PaCO₂ 65 mm Hg, HCO₃⁻ 35 mEq/L. Which statement best explains his acid-base
status?
A. Acute respiratory acidosis with no compensation
B. Chronic respiratory acidosis with renal compensation
C. Metabolic alkalosis with respiratory compensation
D. Mixed respiratory and metabolic acidosis
Correct Answer: B
Rationale: Disease/Process: Chronic hypercapnic respiratory failure. Pathophysiological
Sequence: Long-standing COPD (etiology) reduces alveolar ventilation → CO₂ retention
→ ↑PaCO₂ (respiratory acidosis). Over days, kidneys increase HCO₃⁻ reabsorption (renal
compensation) to buffer excess H⁺, returning pH toward normal (7.34 vs expected <7.3
in acute). HCO₃⁻ 35 mEq/L >24 indicates renal compensation. Distractor Analysis: Acute
(A) would show pH <7.35 with HCO₃⁻ near 24; metabolic alkalosis (C) would have
elevated HCO₃⁻ but low PaCO₂ as compensation; mixed acidosis (D) would show lower
pH and possibly elevated anion gap.
Q3: A 45-year-old woman with Sjögren syndrome presents with muscle cramps and
perioral numbness. Labs: Na⁺ 139 mEq/L, K⁺ 3.2 mEq/L, HCO₃⁻ 28 mEq/L, Ca²⁺ 7.8
mg/dL, phosphate 2.0 mg/dL. Which underlying mechanism best explains her
hypocalcemia?
A. Renal calcium wasting due to metabolic acidosis
B. Decreased intestinal calcium absorption due to autoantibody-mediated destruction of
exocrine glands → vitamin D malabsorption
C. Increased bone deposition secondary to hyperphosphatemia
D. Hypoalbuminemia from chronic inflammation
,Correct Answer: B
Rationale: Disease/Process: Hypocalcemia secondary to malabsorption in Sjögren
syndrome. Pathophysiological Sequence: Autoimmune destruction of salivary/lacrimal
glands (etiology) extends to exocrine pancreas/gut mucosa → ↓pancreatic enzymes &
bile acids → impaired fat-soluble vitamin (D) absorption → ↓25-OH vitamin D →
↓intestinal Ca²⁺ absorption → hypocalcemia (clinical manifestation). Mild metabolic
alkalosis (HCO₃⁻ 28) from vomiting/diuretic use further lowers ionized Ca²⁺. Distractor
Analysis: Renal wasting (A) is not typical in Sjögren unless RTA present; phosphate is
low (not high) ruling out increased bone deposition (C); Ca²⁺ is total but symptoms
suggest ionized hypocalcemia, not purely albumin-bound (D).
Q4: A 30-year-old man with sickle cell trait exercises vigorously in hot weather and
develops dark urine. Urinalysis shows ≥3+ blood on dipstick but 0–2 RBCs/hpf
microscopy. Which pathophysiological process is responsible?
A. Glomerular inflammation causing hematuria
B. Intravascular hemolysis releasing hemoglobin filtered in urine
C. Myoglobin release from rhabdomyolysis
D. Urate crystal-induced nephropathy
Correct Answer: B
Rationale: Disease/Process: Hemoglobinuria due to exertional hemolysis in sickle cell
trait. Pathophysiological Sequence: Dehydration and acidosis during exertion (etiologic
triggers) promote sickling of a minority of RBCs (pathogenesis) → intravascular
hemolysis → free hemoglobin in plasma → filtered by glomeruli → hemoglobin-positive
dipstick with few intact RBCs (clinical picture). Distractor Analysis: Glomerular disease
(A) would show dysmorphic RBCs/casts; rhabdomyolysis (C) would elevate CK/aldolase
and cause myoglobinuria (tea-colored urine) but dipstick equally positive—however
, clinical context here emphasizes hemolysis; urate nephropathy (D) causes crystalluria
and AKI, not isolated hemoglobinuria.
Q5: A 55-year-old diabetic patient on dialysis misses two treatments and becomes
confused. ABG: pH 7.24, PaCO₂ 28 mm Hg, HCO₃⁻ 12 mEq/L, anion gap 24 mEq/L.
Which mechanism best explains the acid-base disorder?
A. Accumulation of urea leading to respiratory acidosis
B. Accumulation of organic acids (phosphates, sulfates) and lactic acid →
high-anion-gap metabolic acidosis with respiratory compensation
C. Loss of bicarbonate in dialysate causing non-anion-gap acidosis
D. Hyperchloremic acidosis from normal saline infusion
Correct Answer: B
Rationale: Disease/Process: High-anion-gap metabolic acidosis (HAGMA) due to
missed dialysis. Pathophysiological Sequence: Missed sessions (etiology) → retention
of protein-bound acids, phosphates, sulfates, and possible lactic acid (pathogenesis) →
consumption of bicarbonate → HAGMA (anion gap >12) and acidemia →
hyperventilation (respiratory compensation) lowers PaCO₂. Distractor Analysis: Urea is
not an acid and does not cause acidosis (A); loss of bicarbonate (C) would yield normal
anion gap; hyperchloremic acidosis (D) also presents with normal gap and is unrelated
to missed dialysis.
Q6: A 60-year-old woman with chronic liver disease develops increasing abdominal girth
and shortness of breath. Albumin 2.1 g/dL, total protein 4.8 g/dL. Which Starling force
alteration is primarily responsible for ascites formation?
A. Increased plasma oncotic pressure
B. Decreased plasma oncotic pressure → net filtration exceeds reabsorption in
peritoneal capillaries
