NSG 3850 Exam 2 2026-2027 Latest Prep Test
Bank / NSG 3850 Pathophysiology for Nurses II
Exam 2 Latest Practice Test with a Review of 230
Questions and Correct Answers
Airway obstruction in chronic bronchitis is because of
a. thick mucus, fibrosis, and smooth muscle hypertrophy.
b. loss of alveolar elastin.
c. pulmonary edema.
d. hyperplasia and deformation of bronchial cartilage.
ANS: A
Airway obstruction in chronic bronchitis is as a result of thick mucus, fibrosis, and
smooth muscle hypertrophy. Loss of alveolar elastin, pulmonary edema, and
hyperplasia and deformation of bronchial cartilage are not part of the
pathophysiology of chronic bronchitis.
Copious amounts of foul-smelling sputum are generally associated with
a. emphysema.
b. epiglottitis.
c. pulmonary edema.
d. bronchiectasis.
ANS: D
Copious, foul-smelling respiratory secretions are associated with bronchiectasis.
Copious, foul-smelling respiratory secretions are not associated with emphysema,
epiglottitis, or pulmonary edema.
Emphysema results from destruction of alveolar walls and capillaries, which is
because of
a. release of proteolytic enzymes from immune cells.
b. air trapping with resultant excessive alveolar pressure.
c. excessive 1-antitrypsin.
d. autoantibodies against pulmonary basement membrane.
1
,ANS: A
The pathologic changes leading to alveolar destruction are associated with the
release of proteolytic enzymes from inflammatory cells such as neutrophils and
macrophages. While air trapping occurs in emphysema, the destruction of alveolar
walls and capillaries is because of release of proteolytic enzymes. Lack of 1-
antitrypsin can result in emphysema. Autoantibodies are not involved in
destruction of alveolar walls and capillaries in emphysema.
Chronic bronchitis often leads to cor pulmonale because of
a. ventricular hypoxia.
b. increased pulmonary vascular resistance.
c. left ventricular strain.
d. hypervolemia.
ANS: B
Chronic bronchitis often leads to cor pulmonale as a result of increased pulmonary
vascular resistance when right ventricular end-diastolic pressure increases.
Ventricular hypoxia, left ventricular strain, and hypervolemia do not lead to cor
pulmonale.
All obstructive pulmonary disorders are characterized by
a. resistance to airflow.
b. hyperresponsiveness.
c. decreased residual volumes.
d. decreased lung compliance.
ANS: A
Obstructive lung diseases are characterized by increased resistance to airflow. Only
asthma is characterized by hyperresponsiveness. Increased residual volume is
common in obstructive pulmonary disorders. Emphysema is characterized by
increased lung compliance caused by a loss of alveoli and elastic tissue.
Obstructive disorders are associated with
a. low residual volumes.
b. low expiratory flow rates.
c. increased expiratory reserve volume.
d. decreased total lung capacity.
ANS: B
Obstructive disorders are associated with low expiratory flow rates. Obstructive
2
,disorders are associated with high residual volume. Increased expiratory reserve
volume and decreased total
lung capacity are not characteristic of obstructive disorders.
COPD leads to a barrel chest, because it causes
a. pulmonary edema.
b. muscle atrophy.
c. prolonged inspiration.
d. air trapping.
ANS: D
Destruction of alveolar walls reduces lung elastic recoil, which allows airway
collapse during exhalation. Air enters the alveoli during inhalation, but has
difficulty escaping during exhalation. When air is trapped in the alveoli, residual
volume increases, causing a barrel chest. Destruction of alveolar walls does not
cause pulmonary edema, muscle atrophy, or prolonged inspiration.
Lack of -antitrypsin in emphysema causes
a. chronic mucous secretion and airway fibrosis.
b. destruction of alveolar tissue.
c. pulmonary edema and increased alveolar compliance.
d. bronchoconstriction and airway edema.
ANS: B
Lack of a1-antitrypsin in emphysema causes destruction of alveolar tissue, as it is a
protective enzyme that prohibits proteolytic breakdown of alveolar tissue. Lack of
alpha1-antitrypsin does not cause chronic mucous secretion and airway fibrosis,
pulmonary edema and increased alveolar compliance, or bronchoconstriction and
airway edema.
The hypersecretion of mucus resulting for chronic bronchitis is the result of
a. recurrent infection.
b. destruction of alveolar septa.
c. reduced inflammation.
d. barrel chest.
ANS: A
Mucus provides a hospitable environment for bacterial colonization and recurrent
infection. Destruction of alveolar septa and reduced inflammation are not
3
, complications of chronic bronchitis. Hypersecretion of mucus does not contribute
to barrel chest.
When preparing for the admission of a client diagnosed with bronchiectasis, the
nurse will
a. put a sputum cup and a box of tissues on the bedside table.
b. remove the telephone to reduce myocardial oxygen demand.
c. add a box of surgical masks to the nursing supplies near the door.
d. remove the water pitcher to comply with anticipated fluid restrictions.
ANS: A
People who have bronchiectasis have a productive cough, usually with foul-
smelling sputum. Bronchiectasis is not contagious or a cardiac condition. Fluid
restriction is not part of the treatment for bronchiectasis.
Which assessment would support a diagnosis of type A COPD rather than type B
COPD
a. Copious sputum, dyspnea, cor pulmonale
b. Noisy breath sounds, fatigue, high PaCO2, overweight
c. Normal PaCO2, scant sputum, accessory muscle use, barrel chest
d. Barrel chest, productive cough, cyanosis, very decreased PaO2
ANS: C
Barrel chest and obvious respiratory effort that maintains near normal blood gases
are consistent with type A COPD in the early stages. Copious sputum, dyspnea,
and cor pulmonale are consistent with type B COPD. Noisy breath sounds, fatigue,
high PaCO2, and overweight are consistent with type B COPD. Barrel chest,
productive cough, cyanosis, and very decreased PaO2 are not consistent with type
A COPD.
To best prevent emphysema, a patient is instructed to stop smoking since cigarette
smoke
a. impairs 1-antitrypsin, allowing elastase to predominate.
b. paralyzes the cilia, causing impaired mucociliary clearance.
c. predisposes to respiratory infections.
d. introduces carcinogens into the lungs.
ANS: A
Cigarette smoking impairs 1-antitrypsin, allowing elastase to predominate and
destroy lung tissue, causing emphysema. Although cigarette smoking does
4
Bank / NSG 3850 Pathophysiology for Nurses II
Exam 2 Latest Practice Test with a Review of 230
Questions and Correct Answers
Airway obstruction in chronic bronchitis is because of
a. thick mucus, fibrosis, and smooth muscle hypertrophy.
b. loss of alveolar elastin.
c. pulmonary edema.
d. hyperplasia and deformation of bronchial cartilage.
ANS: A
Airway obstruction in chronic bronchitis is as a result of thick mucus, fibrosis, and
smooth muscle hypertrophy. Loss of alveolar elastin, pulmonary edema, and
hyperplasia and deformation of bronchial cartilage are not part of the
pathophysiology of chronic bronchitis.
Copious amounts of foul-smelling sputum are generally associated with
a. emphysema.
b. epiglottitis.
c. pulmonary edema.
d. bronchiectasis.
ANS: D
Copious, foul-smelling respiratory secretions are associated with bronchiectasis.
Copious, foul-smelling respiratory secretions are not associated with emphysema,
epiglottitis, or pulmonary edema.
Emphysema results from destruction of alveolar walls and capillaries, which is
because of
a. release of proteolytic enzymes from immune cells.
b. air trapping with resultant excessive alveolar pressure.
c. excessive 1-antitrypsin.
d. autoantibodies against pulmonary basement membrane.
1
,ANS: A
The pathologic changes leading to alveolar destruction are associated with the
release of proteolytic enzymes from inflammatory cells such as neutrophils and
macrophages. While air trapping occurs in emphysema, the destruction of alveolar
walls and capillaries is because of release of proteolytic enzymes. Lack of 1-
antitrypsin can result in emphysema. Autoantibodies are not involved in
destruction of alveolar walls and capillaries in emphysema.
Chronic bronchitis often leads to cor pulmonale because of
a. ventricular hypoxia.
b. increased pulmonary vascular resistance.
c. left ventricular strain.
d. hypervolemia.
ANS: B
Chronic bronchitis often leads to cor pulmonale as a result of increased pulmonary
vascular resistance when right ventricular end-diastolic pressure increases.
Ventricular hypoxia, left ventricular strain, and hypervolemia do not lead to cor
pulmonale.
All obstructive pulmonary disorders are characterized by
a. resistance to airflow.
b. hyperresponsiveness.
c. decreased residual volumes.
d. decreased lung compliance.
ANS: A
Obstructive lung diseases are characterized by increased resistance to airflow. Only
asthma is characterized by hyperresponsiveness. Increased residual volume is
common in obstructive pulmonary disorders. Emphysema is characterized by
increased lung compliance caused by a loss of alveoli and elastic tissue.
Obstructive disorders are associated with
a. low residual volumes.
b. low expiratory flow rates.
c. increased expiratory reserve volume.
d. decreased total lung capacity.
ANS: B
Obstructive disorders are associated with low expiratory flow rates. Obstructive
2
,disorders are associated with high residual volume. Increased expiratory reserve
volume and decreased total
lung capacity are not characteristic of obstructive disorders.
COPD leads to a barrel chest, because it causes
a. pulmonary edema.
b. muscle atrophy.
c. prolonged inspiration.
d. air trapping.
ANS: D
Destruction of alveolar walls reduces lung elastic recoil, which allows airway
collapse during exhalation. Air enters the alveoli during inhalation, but has
difficulty escaping during exhalation. When air is trapped in the alveoli, residual
volume increases, causing a barrel chest. Destruction of alveolar walls does not
cause pulmonary edema, muscle atrophy, or prolonged inspiration.
Lack of -antitrypsin in emphysema causes
a. chronic mucous secretion and airway fibrosis.
b. destruction of alveolar tissue.
c. pulmonary edema and increased alveolar compliance.
d. bronchoconstriction and airway edema.
ANS: B
Lack of a1-antitrypsin in emphysema causes destruction of alveolar tissue, as it is a
protective enzyme that prohibits proteolytic breakdown of alveolar tissue. Lack of
alpha1-antitrypsin does not cause chronic mucous secretion and airway fibrosis,
pulmonary edema and increased alveolar compliance, or bronchoconstriction and
airway edema.
The hypersecretion of mucus resulting for chronic bronchitis is the result of
a. recurrent infection.
b. destruction of alveolar septa.
c. reduced inflammation.
d. barrel chest.
ANS: A
Mucus provides a hospitable environment for bacterial colonization and recurrent
infection. Destruction of alveolar septa and reduced inflammation are not
3
, complications of chronic bronchitis. Hypersecretion of mucus does not contribute
to barrel chest.
When preparing for the admission of a client diagnosed with bronchiectasis, the
nurse will
a. put a sputum cup and a box of tissues on the bedside table.
b. remove the telephone to reduce myocardial oxygen demand.
c. add a box of surgical masks to the nursing supplies near the door.
d. remove the water pitcher to comply with anticipated fluid restrictions.
ANS: A
People who have bronchiectasis have a productive cough, usually with foul-
smelling sputum. Bronchiectasis is not contagious or a cardiac condition. Fluid
restriction is not part of the treatment for bronchiectasis.
Which assessment would support a diagnosis of type A COPD rather than type B
COPD
a. Copious sputum, dyspnea, cor pulmonale
b. Noisy breath sounds, fatigue, high PaCO2, overweight
c. Normal PaCO2, scant sputum, accessory muscle use, barrel chest
d. Barrel chest, productive cough, cyanosis, very decreased PaO2
ANS: C
Barrel chest and obvious respiratory effort that maintains near normal blood gases
are consistent with type A COPD in the early stages. Copious sputum, dyspnea,
and cor pulmonale are consistent with type B COPD. Noisy breath sounds, fatigue,
high PaCO2, and overweight are consistent with type B COPD. Barrel chest,
productive cough, cyanosis, and very decreased PaO2 are not consistent with type
A COPD.
To best prevent emphysema, a patient is instructed to stop smoking since cigarette
smoke
a. impairs 1-antitrypsin, allowing elastase to predominate.
b. paralyzes the cilia, causing impaired mucociliary clearance.
c. predisposes to respiratory infections.
d. introduces carcinogens into the lungs.
ANS: A
Cigarette smoking impairs 1-antitrypsin, allowing elastase to predominate and
destroy lung tissue, causing emphysema. Although cigarette smoking does
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