Pathophysiology, 5th Edition By Lee-Ellen C. Copstead
Pathophysiology, 5th Edition By Lee-Ellen C. Copstead
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Chapter 22: Obstructive Pulmonary Disorders
Complete Chapter Questions With Answers
Sample Questions Are Posted Below
MULTIPLE CHOICE
| a. | hyporesponsiveness of airways. |
| b. | unknown precipitating factors. |
| c. | IgE-mediated airway inflammation. |
| d. | irreversible airway obstruction. |
ANS: C
Extrinsic (allergic) asthma is mediated by IgE triggers. Allergic (extrinsic) asthma involves hyperresponsiveness of the airways. Antigens are the precipitating factors. Airway obstruction is reversible.
REF: Pg. 476
| 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.
REF: Pgs. 489-490
| a. | release of proteolytic enzymes from immune cells. |
| b. | air trapping with resultant excessive alveolar pressure. |
| c. | excessive a1-antitrypsin. |
| d. | autoantibodies against pulmonary basement membrane. |
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 due to release of proteolytic enzymes. Lack of a1-antitrypsin can result in emphysema. Autoantibodies are not involved in destruction of alveolar walls and capillaries in emphysema.
REF: Pg. 487
| a. | ventricular hypoxia. |
| b. | increased pulmonary vascular resistance. |
| c. | left ventricular strain. |
| d. | hypervolemia. |
ANS: B
Chronic bronchitis often leads to cor pulmonale due to increased pulmonary vascular resistance when right ventricular end-diastolic pressure increases. Ventricular hypoxia, left ventricular strain, and hypervolemia do not lead to cor pulmonale.
REF: Pgs. 483-484
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