CMN 571 Unit 3 Test – 2026/2027
Edition – 50 Complete Questions &
Correct Answers
Questions with Step-by-Step Answers | 100% Verified | A+ Graded Review
OVERVIEW:
CMN 571 Unit 3 Test – 2026/2027 focuses on advanced pathophysiology of
pulmonary, renal, acid-base, and immune systems. Topics include asthma, COPD,
ARDS, restrictive lung disease, pneumonia, pleural effusion, acute and chronic
kidney injury, glomerulonephritis, nephrotic versus nephritic syndromes,
electrolyte disorders, metabolic and respiratory acidosis/alkalosis, inflammation,
hypersensitivity, and immunity, emphasizing clinical manifestations and
mechanisms for diagnostic reasoning and management principles.
Answers are in bold Green, with rationales after.
1. Which mediator is primarily responsible for bronchial smooth muscle contraction in
asthma?
A. Surfactant
B. Norepinephrine
C. Acetylcholine esterase
D. Histamine and Leukotrienes C4/D4/E4
Rationale: In asthma, mast cell degranulation releases histamine and cysteinyl
leukotrienes causing bronchoconstriction, vascular permeability, and mucus
secretion. Leukotrienes are 100-1000x more potent bronchoconstrictors than
histamine.
, 2. In COPD, the primary mechanism for alveolar wall destruction (emphysema) is:
A. Pulmonary vasoconstriction
B. Alpha-1 antitrypsin deficiency leading to unchecked elastase activity
C. Hyperplasia of goblet cells
D. Excess collagen deposition
Rationale: Emphysema results from imbalance between proteases (neutrophil
elastase) and antiproteases (alpha-1 antitrypsin). Smoking recruits neutrophils;
elastase destroys elastin in alveolar walls.
3. A patient with acute respiratory distress syndrome (ARDS) shows PaO2/FiO2 <300.
The underlying pathophysiology is:
A. Carbon dioxide retention due to hypoventilation
B. Diffuse alveolar damage with increased alveolar-capillary permeability and
surfactant inactivation
C. Bronchial hyperresponsiveness
D. Pulmonary artery hypertension alone
Rationale: ARDS is non-cardiogenic pulmonary edema due to injury to alveolar-
capillary membrane, leading to protein-rich fluid, surfactant dysfunction, and
refractory hypoxemia.
4. Which acid-base disorder is expected in early acute asthma exacerbation?
A. Mixed metabolic acidosis
B. Metabolic alkalosis
C. Respiratory acidosis
D. Respiratory alkalosis due to hyperventilation
Rationale: Early asthma causes hyperventilation to overcome hypoxia → CO2
washout → respiratory alkalosis. Late, with fatigue and air trapping, it shifts to
respiratory acidosis.
5. Clubbing of fingers is most associated with:
Edition – 50 Complete Questions &
Correct Answers
Questions with Step-by-Step Answers | 100% Verified | A+ Graded Review
OVERVIEW:
CMN 571 Unit 3 Test – 2026/2027 focuses on advanced pathophysiology of
pulmonary, renal, acid-base, and immune systems. Topics include asthma, COPD,
ARDS, restrictive lung disease, pneumonia, pleural effusion, acute and chronic
kidney injury, glomerulonephritis, nephrotic versus nephritic syndromes,
electrolyte disorders, metabolic and respiratory acidosis/alkalosis, inflammation,
hypersensitivity, and immunity, emphasizing clinical manifestations and
mechanisms for diagnostic reasoning and management principles.
Answers are in bold Green, with rationales after.
1. Which mediator is primarily responsible for bronchial smooth muscle contraction in
asthma?
A. Surfactant
B. Norepinephrine
C. Acetylcholine esterase
D. Histamine and Leukotrienes C4/D4/E4
Rationale: In asthma, mast cell degranulation releases histamine and cysteinyl
leukotrienes causing bronchoconstriction, vascular permeability, and mucus
secretion. Leukotrienes are 100-1000x more potent bronchoconstrictors than
histamine.
, 2. In COPD, the primary mechanism for alveolar wall destruction (emphysema) is:
A. Pulmonary vasoconstriction
B. Alpha-1 antitrypsin deficiency leading to unchecked elastase activity
C. Hyperplasia of goblet cells
D. Excess collagen deposition
Rationale: Emphysema results from imbalance between proteases (neutrophil
elastase) and antiproteases (alpha-1 antitrypsin). Smoking recruits neutrophils;
elastase destroys elastin in alveolar walls.
3. A patient with acute respiratory distress syndrome (ARDS) shows PaO2/FiO2 <300.
The underlying pathophysiology is:
A. Carbon dioxide retention due to hypoventilation
B. Diffuse alveolar damage with increased alveolar-capillary permeability and
surfactant inactivation
C. Bronchial hyperresponsiveness
D. Pulmonary artery hypertension alone
Rationale: ARDS is non-cardiogenic pulmonary edema due to injury to alveolar-
capillary membrane, leading to protein-rich fluid, surfactant dysfunction, and
refractory hypoxemia.
4. Which acid-base disorder is expected in early acute asthma exacerbation?
A. Mixed metabolic acidosis
B. Metabolic alkalosis
C. Respiratory acidosis
D. Respiratory alkalosis due to hyperventilation
Rationale: Early asthma causes hyperventilation to overcome hypoxia → CO2
washout → respiratory alkalosis. Late, with fatigue and air trapping, it shifts to
respiratory acidosis.
5. Clubbing of fingers is most associated with:
