Emphysema & COPD Pathophysiology
Q1. A client with emphysema has hyperresonance on percussion and a flattened diaphragm. Which pathophysiologic change BEST explains these findings?
A. Increased surfactant production B. Loss of elastic recoil causing air trapping C. Bronchial smooth muscle hypertrophy D. Increased pulmonary capillary perfusion
B. Loss of elastic recoil causing air trapping
Emphysema destroys alveolar walls and the elastin fibers that normally allow the lungs to recoil during exhalation. Without elastic recoil, the bronchioles collapse prematurely during expiration, trapping air in the distal alveoli. This trapped air causes:
Hyperinflation → increased lung volume
Flattened diaphragm → diaphragm is pushed downward by overinflated lungs
Hyperresonance → excess air increases the percussion note
This is the hallmark of emphysema.
A: Surfactant is not increased; surfactant dysfunction is not the primary issue.
C: Smooth muscle hypertrophy is characteristic of asthma, not emphysema.
D: Emphysema reduces pulmonary capillary perfusion due to capillary destruction.
A child with extrinsic asthma develops bronchospasm after exposure to dust mites. Which immune mechanism is responsible?
A. IgG-mediated complement activation
B. IgE-mediated mast cell degranulation
C. T‑cell cytotoxicity
D. Immune complex deposition
B. IgE-mediated mast cell degranulation
Extrinsic asthma is a type I hypersensitivity reaction. Allergen exposure triggers:
IgE production
IgE binds to mast cells
Re-exposure → mast cell degranulation
Release of histamine, leukotrienes, prostaglandins
Bronchoconstriction, mucus production, airway edema
This is the classic allergic asthma pathway.
A, C, D: These describe type II, IV, and III hypersensitivity, not asthma.
Q11. A client with pneumonia has perfusion without ventilation. What is this called?
A. Dead space
B. Shunt
C. Hyperventilation
D. Diffusion block
In pneumonia, alveoli are filled with fluid, so they are perfused but not ventilated. This is a shunt — blood passes through the lungs without being oxygenated.
A: Dead space = ventilation without perfusion (PE).
C: Not a V/Q mismatch.
D: Not the correct physiologic term.
Q17. Why do clients with CF develop recurrent infections?
A. Excess surfactant
B. Thick mucus impairs ciliary clearance
C. Increased macrophage activity
D. Increased airway diameter
B. Thick mucus impairs ciliary clearance
Thick mucus traps bacteria and prevents normal mucociliary clearance → chronic infection.
A: Surfactant is not increased.
C: Macrophages are overwhelmed.
D: Airways narrow, not widen.
Q21. A client with tension pneumothorax has tracheal deviation. What causes this?
A. Lung hyperinflation
B. Air trapping in pleural space shifting mediastinum
C. Increased venous return
D. Bronchospasm
B. Air trapping in pleural space shifting mediastinum
Air enters pleural space and cannot escape → pressure builds → pushes mediastinum and trachea away from affected side.
Q2. A client with emphysema has a PaCO₂ of 58 mmHg and uses pursed‑lip breathing. What is the PRIMARY purpose of pursed‑lip breathing?
A. Increase respiratory rate
B. Create back‑pressure to prevent airway collapse
C. Strengthen the diaphragm
D. Reduce tidal volume
B. Create back‑pressure to prevent airway collapse
In emphysema, small airways collapse during expiration because of the loss of elastic recoil. Pursed‑lip breathing:
Creates positive end‑expiratory pressure (PEEP)
Prevents premature airway collapse
Improves CO₂ elimination
Reduces air trapping
Slows respiratory rate, improving ventilation efficiency
It is a compensatory technique that patients instinctively adopt.
A: Respiratory rate actually slows.
C: It does not strengthen the diaphragm.
D: Tidal volume often increases because breathing becomes more efficient.
Q7. Which trigger is MOST associated with intrinsic asthma?
A. Pollen
B. Cat dander
C. Cold air
D. Dust mites
C. Cold air
Intrinsic asthma is non‑immune mediated and triggered by:
Cold air
Exercise
Stress
Viral infections
Irritants
It does not involve IgE or allergens.
A, B, D: Classic extrinsic triggers.
Q12.
A client with pulmonary embolism has which V/Q pattern?
A. Low V/Q
B. High V/Q
C. Normal V/Q
D. Zero V/Q
B. High V/Q
PE blocks blood flow → ventilation without perfusion → dead space → high V/Q.
A: Low V/Q = pneumonia.
D: Zero V/Q = complete shunt.
Q18. A client with chronic CO₂ retention relies on which respiratory drive?
A. Central chemoreceptor CO₂ drive
B. Peripheral chemoreceptor hypoxic drive
C. Stretch receptor drive
D. Voluntary drive
B. Peripheral chemoreceptor hypoxic drive
Chronic CO₂ retention desensitizes central chemoreceptors. The body shifts to hypoxic drive, relying on low PaO₂ to stimulate breathing.
Q22. Which finding is MOST consistent with pleural effusion?
A. Hyperresonance
B. Dullness to percussion
C. Tympany
D. Crackles
B. Dullness to percussion
Fluid in pleural space → dullness, decreased breath sounds, decreased expansion.
Q3. A client with chronic bronchitis has polycythemia. What mechanism causes this?
A. CO₂ retention stimulates RBC production
B. Chronic hypoxemia triggers erythropoietin release
C. Mucus production destroys RBCs
D. Hypercapnia causes hemoconcentration
B. Chronic hypoxemia triggers erythropoietin release
Chronic bronchitis causes persistent airway obstruction from mucus, inflammation, and edema. This leads to chronic hypoxemia. The kidneys sense low oxygen levels and respond by releasing erythropoietin, which stimulates the bone marrow to produce more RBCs. This compensatory mechanism increases oxygen‑carrying capacity.
A: CO₂ retention does not stimulate erythropoiesis.
C: Mucus does not destroy RBCs.
D: Hemoconcentration is not the mechanism; RBC mass truly increases.
Q8. A client with asthma has a “silent chest.” What does this indicate?
A. Improvement
B. Severe airway obstruction with minimal airflow
C. Hyperventilation
D. Pneumonia
B. Severe airway obstruction with minimal airflow
A “silent chest” is an ominous sign. It means:
Airflow is so limited that no wheezing is produced
The client is tiring
Respiratory failure is imminent
This requires immediate intervention.
A: Not improvement.
C: Hyperventilation produces loud wheezing.
D: Pneumonia produces crackles, not silence.
Q13. Which condition MOST reduces diffusion capacity?
A. Increased surface area
B. Pulmonary edema
C. Increased partial pressure gradient
D. Increased hemoglobin affinity
B. Pulmonary edema
Pulmonary edema thickens the alveolar‑capillary membrane, increasing diffusion distance and impairing oxygen movement.
A & C: Improve diffusion.
D: Affects oxygen unloading, not diffusion.
Q19. Which oxygen saturation target is appropriate for chronic CO₂ retainers?
A. 100%
B. 95–100%
C. 88–92%
D. <80%
C. 88–92%
Higher saturations can suppress hypoxic drive → CO₂ narcosis. 88–92% maintains oxygenation without suppressing ventilation.
Q23. A client with pneumothorax suddenly becomes hypotensive. Why?
A. Increased preload
B. Compression of vena cava
C. Increased cardiac output
D. Increased lung compliance
B. Compression of vena cava
Tension pneumothorax compresses vena cava → decreased venous return → shock.
Q4. Which finding is MOST characteristic of emphysema rather than chronic bronchitis?
A. Cyanosis
B. Productive cough
C. Increased AP diameter
D. Purulent sputum
C. Increased AP diameter
Emphysema causes hyperinflation due to air trapping. Over time, this expands the rib cage and increases the anterior‑posterior diameter, producing the classic barrel chest.
A & D: Cyanosis and purulent sputum are more typical of chronic bronchitis (“blue bloater”).
B: Chronic productive cough is the hallmark of chronic bronchitis.
Q9.
Which ABG is MOST consistent with early asthma exacerbation?
A. pH 7.50, PaCO₂ 30
B. pH 7.32, PaCO₂ 55
C. pH 7.40, PaCO₂ 40
D. pH 7.28, PaCO₂ 25
A. pH 7.50, PaCO₂ 30
Early asthma → hyperventilation due to anxiety and increased work of breathing. Hyperventilation blows off CO₂, causing:
Respiratory alkalosis (high pH)
Low PaCO₂
As the attack worsens, CO₂ rises (respiratory acidosis).
B: Late asthma with fatigue.
C: Normal.
D: Metabolic acidosis compensation.
Q14. A client with ARDS has severe hypoxemia unresponsive to oxygen. What is the cause?
A. Decreased respiratory rate
B. Widespread shunting
C. Increased dead space
D. Increased surfactant production
B. Widespread shunting
ARDS fills alveoli with protein‑rich fluid → no ventilation despite perfusion → shunt. Oxygen cannot reach blood even with 100% FiO₂.
C: Dead space is PE.
D: Surfactant is decreased, not increased.
Q20. Which finding is MOST concerning in CF?
A. Chronic cough
B. Purulent sputum
C. Hemoptysis
D. Tachypnea
C. Hemoptysis
Hemoptysis indicates erosion of bronchial vessels from chronic infection and inflammation. It can be life‑threatening.
Which intervention is PRIORITY for tension pneumothorax?
A. Chest x‑ray
B. Needle decompression
C. High‑flow oxygen
D. ABG analysis
B. Needle decompression
Tension pneumothorax is fatal within minutes. Needle decompression immediately relieves pressure. Imaging delays treatment.
Q5. A client with emphysema has decreased diffusing capacity (DLCO). Which structural change causes this?
A. Thickened alveolar membrane
B. Loss of alveolar surface area
C. Increased pulmonary blood flow
D. Increased mucus production
B. Loss of alveolar surface area
Emphysema destroys alveolar walls and capillary beds, dramatically reducing the surface area available for gas exchange. DLCO directly measures how well gases diffuse across the alveolar‑capillary membrane, so loss of surface area → decreased DLCO.
A: Thickening occurs in pulmonary edema or fibrosis, not emphysema.
C: Perfusion decreases in emphysema.
D: Mucus is a chronic bronchitis feature.
Q10. Which finding differentiates extrinsic from intrinsic asthma?
A. Bronchoconstriction
B. Mucus production
C. IgE involvement
D. Airway hyperresponsiveness
C. IgE involvement
Only extrinsic asthma is IgE-mediated. Intrinsic asthma has the same symptoms but no allergic component.
A, B, D: Occur in both types.
Q15. Which ABG indicates V/Q mismatch from early pneumonia?
A. Low PaO₂, low PaCO₂
B. High PaO₂, high PaCO₂
C. Normal PaO₂, high PaCO₂
D. Low PaO₂, high PaCO₂
A. Low PaO₂, low PaCO₂
Early pneumonia → hypoxemia → tachypnea → blowing off CO₂ → low PaCO₂.
D: Occurs later when fatigue sets in.
Q16. A client with emphysema has hyperresonance on percussion and a flattened diaphragm. Which pathophysiologic change BEST explains these findings?
A. Increased surfactant production
B. Loss of elastic recoil causing air trapping
C. Bronchial smooth muscle hypertrophy
D. Increased pulmonary capillary perfusion
B. Loss of elastic recoil causing air trapping
Emphysema is defined by destruction of alveolar walls and the elastin fibers that normally allow the lungs to recoil during exhalation. When elastin is lost:
The bronchioles collapse prematurely during expiration, especially during forced exhalation.
This traps air in the distal alveoli, leading to progressive hyperinflation.
Hyperinflation pushes the diaphragm downward, causing the classic flattened diaphragm seen on imaging.
Excess air in the thorax produces hyperresonance on percussion because sound travels more easily through air than through tissue.
This is the fundamental mechanical problem in emphysema: the lungs can get air in, but they cannot get air out.
Why the other options are wrong:
A: Surfactant is not increased in emphysema; surfactant dysfunction is not the primary pathology.
C: Smooth muscle hypertrophy is a hallmark of asthma, not emphysema.
D: Emphysema actually reduces pulmonary capillary perfusion because capillary beds are destroyed along with alveolar walls.
Q25. Pleural effusion impairs ventilation by:
A. Filling alveoli with fluid
B. Increasing intrapleural pressure and restricting lung expansion
C. Destroying alveolar walls
D. Causing bronchoconstriction
B. Increasing intrapleural pressure and restricting lung expansion
Fluid in pleural space compresses lung tissue → prevents expansion → reduces ventilation.