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Exam 2: NSG 3850 / NSG3850 (Latest 2025 / 2026
Update) Pathophysiology for Nurses II |
Questions and verified Answers | Grade A | 100%
Correct – Galen
The amount of gas remaining in the lungs after a maximal expiration is called the a. residual volume. b. functional residual capacity. c. expiratory reserve volume. d. vital capacity. ANS: A Residual volume is the amount of gas remaining in the lungs after a maximal expiration. Functional residual capacity is the amount of gas left in the lungs at the end of a normal expiration. Expiratory reserve volume is the amount of gas expired beyond tidal volume. Vital capacity is the total volume of gas that can be exhaled during maximal expiration. An increase in filtration of fluid from the pulmonary capillaries into the interstitium occurs with ________ pressure. a. increased capillary colloid b. increased capillary hydrostatic c. decreased capillary hydrostatic d. decreased interstitial colloid ANS: B When capillary hydrostatic pressure exceeds capillary colloid osmotic pressure, fluid moves from the capillary to the interstitium. Increased capillary colloid pressure, decreased capillary hydrostatic pressure, or decreased interstitial colloid pressure would all prevent fluid movement out of the capillaries.
The central chemoreceptors for respiratory control are a. located in the carotid artery. responsive primarily to changes in pH and CO2. b. responsive primarily to hypoxemia. c. less important than the peripheral d. chemoreceptors in maintaining respiration. ANS: B Central chemoreceptors for respiratory control are responsive primarily to changes in pH and CO2. The central chemoreceptors are located in the medullary center, are responsive to pH and CO2, and are more important than the peripheral chemoreceptors in controlling respirations. The peripheral chemoreceptors a. are located in the medulla oblongata. b. lead to hypoventilation when stimulated. c. respond to the arterial oxygen level. d. are unresponsive to pH and CO2 levels. ANS: C The peripheral chemoreceptors respond to reduced arterial oxygen (hypoxemia). The peripheral chemoreceptors are located in the aortic arch and carotid bodies, lead to hyperventilation when stimulated, and respond to pH and CO2 levels in addition to arterial oxygen level. Hypoxic pulmonary vasoconstriction a. diverts blood to hypoxic regions. b. increases blood flow to the base of the lung. c. can lead to secondary pulmonary hypertension. d. is always detrimental to the patient. ANS: C
Surfactant is a phospholipid that reduces a. pulmonary vascular capacitance. b. elastic recoil force. c. alveolar surface tension. d. pulmonary capillary fragility. ANS: C Surfactant reduces alveolar surface tension. Surfactant does not reduce pulmonary vascular capacitance, elastic recoil force, or pulmonary capillary fragility. Secondary pulmonary hypertension is most often caused by a. increased pulmonary blood flow. b. increased pulmonary vascular resistance. c. increased left atrial pressure. d. decreased alveolar compliance. ANS: B Secondary pulmonary hypertension is most often caused by increased pulmonary vascular resistance. Although increased pulmonary blood flow and increased left atrial pressure can lead to secondary pulmonary hypertension, the most common cause is increased pulmonary vascular resistance. Decreased alveolar compliance does not cause pulmonary hypertension. The pulmonary structure that has the least pulmonary blood flow is a. lung apex. b. middle lung. c. lower lung. d. zone 4. ANS: A
Zone 1 (apex) has no perfusion and is equivalent to dead space. Zone 2 (middle lung) is intermittently perfused. Zone 3 (lower lung) is continuously perfused. There is no zone 4. Autonomic nervous system stimulation effects on the respiratory system include a. parasympathetic stimulation dilates airways. b. sympathetic stimulation constricts airways. c. sympathetic stimulation relaxes bronchial smooth muscle. d. the autonomic system has no effect on the respiratory system. ANS: C Sympathetic nervous system stimulation relaxes bronchial smooth muscle. Parasympathetic stimulation constricts airways. Sympathetic stimulation dilates airways. The autonomic nervous system does affect the respiratory system by relaxing the pulmonary blood vessels. Primary pulmonary hypertension is a. more common in men. b. readily treatable. c. caused by genetic mutation. d. rapidly progressive. ANS: D Primary pulmonary hypertension is rapidly progressive. Primary pulmonary hypertension is more common in women and is not responsive to treatment. While primary pulmonary hypertension may be genetic in some individuals, the cause is unknown. Hypoventilation causes a. hypoxemia. b. respiratory alkalosis. c. increased minute ventilation.
hypertension, rather than a complication of it. Chronic pulmonary hypertension does not cause chronic obstructive pulmonary disease; COPD may cause chronic pulmonary hypertension. Virchow's triad can result in a. decreased pulmonary arterial pressure. b. alveolar collapse. c. pulmonary embolus. d. bronchoconstriction. ANS: C Virchow's triad consists of three physiologic factors that can predispose patients to thrombus formation, increasing the risk of PE. In Virchow's triad, pulmonary arterial pressure increases. Alveolar collapse and bronchoconstriction are not a result of Virchow's triad. Right-sided heart failure secondary to pulmonary hypertension is also called a. diastolic heart failure. b. high output failure. c. coronary disease. d. cor pulmonale. ANS: D Cor pulmonale is right-sided heart failure secondary to pulmonary hypertension. Cor pulmonale, not diastolic heart failure, is right-sided heart failure secondary to pulmonary hypertension. High output failure refers to left or biventricular failure caused by high output conditions such as sepsis or anemia. Coronary disease is atherosclerosis of the coronary arteries. "My doctor said I have cor pul-something, which is a heart problem," says Mr. Garabedian. "I thought I just had these bad lungs that can't be fixed. How can that make my heart go bad?" Which mechanism leads to the development of cor pulmonale, which should serve as the basis for your response to Mr. Garabedian?
a. Left ventricular failure causes pulmonary venous congestion and pulmonary edema. b. Pneumothorax causes compression atelectasis, decreased alveolar ventilation, and impaired oxygenation. c. Increased resistance to pulmonary arterial flow leads to compensatory right ventricular hypertrophy. d. Impaired ventilation causes decreased PaO2, which precipitates cardiac dysrhythmias. ANS: C Cor pulmonale is right ventricular hypertrophy that occurs as a compensatory response to chronically increased resistance to pulmonary arterial flow. Left ventricular failure, pneumothorax and compression atelectasis, and cardiac dysrhythmias are not part of the pathogenesis of cor pulmonale. Structure(s) that engage in exchange of respiratory gases include(s) the (Select all that apply.) a. trachea. b. bronchi. c. pulmonary artery. d. pulmonary capillaries. e. alveoli. ANS: A, B, D, E The trachea, bronchi, pulmonary capillaries, and alveoli are all involved in the respiratory gas exchange process. The pulmonary artery is not involved in gas exchange. Which is true about lung compliance? (Select all that apply.) a. Represents lung expandability b. Decreases in the elderly c. Can be decreased by obesity, abdominal distention, pregnancy d. Is decreased in emphysema e. Is affected by body position
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 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.
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 paralyze cilia, this action predisposes to respiratory infections rather than to emphysema. Although cigarette smoking does predispose to respiratory infections, that is not the mechanism that causes emphysema. Carcinogens introduced by cigarette smoking increase the risk of developing lung cancer, but they are not responsible for emphysema. When a client diagnosed with COPD type A asks, "Why is my chest so big and round?", the nurse responds that a. "Loss of elastic tissue in your lungs allows your airways to close and trap air, which makes your chest round." b. "Swelling and mucus in your airways causes air to be trapped in your lungs, which makes your chest round." c. "Coughing caused by your condition has changed the structure of your airways, which makes your chest round." d. "Scar tissue in your lungs makes them stiff and more full of air than usual, which makes your chest round." ANS: A
Loss of elastic tissue in the lungs allows premature airway closure, which traps air, creating a barrel chest. The other answer choices do not describe the pathophysiology that causes barrel chest in persons with COPD type A. 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. Individuals who have chronic bronchitis most often have a. a productive cough. b. normal lung sounds. c. a barrel chest. d. substantial weight loss. ANS: A A productive cough for at least 3 months is the classic sign of chronic bronchitis. People who have chronic bronchitis commonly have abnormal lung sounds resulting from mucus in their airways. Barrel chest is a classic sign of emphysema. Substantial weight loss is characteristic of emphysema, but not of chronic bronchitis. The increased anterior-posterior chest diameter associated with obstructive lung disease is caused by a. increased pulmonary blood flow.
Which is indicative of a left tension pneumothorax? a. Course crackles throughout the left chest b. Tracheal deviation to the left c. Absent breath sounds on the left d. Respiratory acidosis ANS: C A left pneumothorax results in absent breath sounds on the affected side. Crackles will not be heard because breath sounds are not present. Tracheal deviation occurs on the contralateral side. Pneumothorax results in acute respiratory alkalosis. A patient exhibiting respiratory distress as well as a tracheal shift should be evaluated for a. pneumonia. b. pneumothorax. c. pulmonary edema. d. pulmonary embolus. ANS: B Pneumothorax leads to a tracheal shift to the side opposite the pneumothorax. Pneumonia, pulmonary edema, and pulmonary embolus do not lead to tracheal shift. A patient with a productive cough and parenchymal infiltrates on x-ray is demonstrating symptomology of a. bacterial pneumonia. b. viral pneumonia. c. tuberculosis. d. acute respiratory distress syndrome. ANS: A
Bacterial pneumonia produces a productive cough and parenchymal infiltrates (white shadows) on x-ray. Viral pneumonia does not produce a productive cough. Tuberculosis may produce a productive cough but does not show parenchymal infiltrates (white shadows) on x-ray. Acute respiratory distress syndrome produces a non-productive cough. The organism that causes pulmonary tuberculosis is a. Mycobacterium tuberculosis. b. Haemophilus tuberculosis. c. Tuberculosis tuberculoci. d. Mycococcidio tuberculosis. ANS: A Mycobacterium tuberculosis causes pulmonary tuberculosis. Haemophilus tuberculosis, Tuberculosis tuberculoci, and Mycococcidio tuberculosis do not cause pulmonary tuberculosis. Which clinical manifestation is not likely the result of a tuberculosis infection? a. Productive cough b. Low-grade fever c. Night sweats d. Cyanosis ANS: D Cyanosis is not a typical manifestation of tuberculosis infection. A productive cough, low-grade fever, and night sweats are the typical manifestations of tuberculosis infection. Which disorder is caused by inhalation of organic substances? a. Diffuse interstitial lung disease b. Hypersensitivity pneumonitis c. Sarcoidosis
a. myasthenia gravis. b. poliomyelitis. c. Pickwickian syndrome. d. pneumonia. ANS: C Pickwickian syndrome is hypoventilation caused by obesity. Sleep apnea is often a problem in obese individuals. Obstructive sleep apnea is not likely to be found in a patient with myasthenia gravis, poliomyelitis, or pneumonia. The most definitive diagnostic method for active tuberculosis is acquired via a. sputum culture. b. Mantoux skin test. c. chest x-ray. d. blood culture. ANS: A The most definitive diagnostic method for active tuberculosis is via sputum culture to identify the acid-fast bacillus. The Mantoux skin test does not distinguish between active infection and past infection. Although a chest x-ray will show characteristic nodules, a sputum culture is the most definitive diagnostic method for active tuberculosis. Unless a patient is septic (infection in the blood), the tuberculosis organism will not be found in the blood. A major cause of treatment failure in tuberculosis is a. resistant organism. b. allergy to drugs used. c. noncompliance. d. immunosuppression. ANS: C
The major cause of treatment failure in tuberculosis is non-adherence to drug therapy. The major cause of treatment failure in tuberculosis is not a resistant organism, drug allergy, or immunosuppression. Neuromuscular disorders impair lung function primarily because of a. inflammatory events in the lung. b. secondary pneumonia. c. weak muscles of respiration. d. inactivity secondary to the disorder. ANS: C Neuromuscular disorders weaken respiratory muscle function resulting in poor ventilation. Inflammatory events in the lung, secondary pneumonia, and inactivity secondary to the disorder are not the primary reasons neuromuscular disorders impair lung function. Legionnaires disease is characterized by a. presence of systemic illness. b. airborne mechanism of communicability. c. mild symptomatology. d. resolution with or without antimicrobial therapy. ANS: A Legionnaires disease produces system manifestations such as fever, diarrhea, abdominal pain, and pneumonia. The organism that causes Legionnaires disease is transmitted by means of contaminated water. Symptoms are severe, and the disease requires antimicrobial therapy. Bacterial pneumonia leads to hypoxemia caused by a. cardiogenic pulmonary edema. b. upper airway obstruction.
