CH35 - Test prep PDF

Title CH35 - Test prep
Course Pathophysiology
Institution Murray State University
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Chapter 35: Alterations of Pulmonary Function MULTIPLE CHOICE 1. Besides dyspnea, what is the most common characteristic associated with pulmonary disease? a. Chest pain c. Cough b. Digit clubbing d. Hemoptysis ANS: C

Pulmonary disease is associated with many signs and symptoms, and their specific characteristics often help in identifying the underlying disorder. The most common characteristics are dyspnea and cough. Others include abnormal sputum, hemoptysis, altered breathing patterns, hypoventilation and hyperventilation, cyanosis, clubbing of the digits, and chest pain. PTS: 1

REF: Page 1248

2. Sitting up in a forward-leaning position generally relieves which breathing disorder? a. Hyperpnea c. Apnea b. Orthopnea d. Dyspnea on exertion ANS: B

Of the options available, only orthopnea is generally relieved by sitting up in a forwardleaning posture or supporting the upper body on several pillows. PTS: 1

REF: Page 1249

3. Kussmaul respirations as a respiratory pattern may be associated with which characteristic(s)? a. Alternating periods of deep and shallow breathing b. Pulmonary fibrosis c. Chronic obstructive pulmonary disease d. Slightly increased ventilatory rate, large tidal volumes, and no expiratory pause ANS: D

Kussmaul respirations are characterized by a slightly increased ventilatory rate, very large tidal volume, and no expiratory pause. Kussmaul respirations are not associated with any of the other options. PTS: 1

REF: Page 1249

4. Respirations that are characterized by alternating periods of deep and shallow breathing are a

result of which respiratory mechanism? a. Decreased blood flow to the medulla oblongata b. Increased partial pressure of arterial carbon dioxide (PaCO2), decreased pH, and decreased partial pressure of arterial oxygen (PaO2) c. Stimulation of stretch or J-receptors d. Fatigue of the intercostal muscles and diaphragm ANS: A

Alternating periods of deep and shallow breathing are characteristic of Cheyne-Stokes respirations and are the result of any condition that slows the blood flow to the brainstem, which in turn slows impulses that send information to the respiratory centers of the brainstem. None of the remaining options are responsible for the described breathing pattern. PTS: 1

REF: Page 1250

5. With a total hemoglobin of 9 g/dl, how many grams per deciliter of hemoglobin must become

desaturated for cyanosis to occur? a. 3 b. 5

c. 7 d. 9

ANS: B

Cyanosis generally develops when 5 g/dl of hemoglobin is desaturated, regardless of hemoglobin concentration. PTS: 1

REF: Page 1250

6. Which statement is true regarding ventilation? a. Hypoventilation causes hypocapnia. b. Hyperventilation causes hypercapnia. c. Hyperventilation causes hypocapnia. d. Hyperventilation results in an increased partial pressure of arterial carbon dioxide

(PaCO2). ANS: C

Hyperventilation is alveolar ventilation that exceeds metabolic demands. The lungs remove carbon dioxide at a faster rate than produced by cellular metabolism, resulting in decreased PaCO2 or hypocapnia. None of the remaining options are accurate statements. PTS: 1

REF: Page 1250

7. What term is used to describe the selective bulbous enlargement of the distal segment of a

digit that is commonly associated with diseases that interfere with oxygenation of the blood? a. Edema c. Angling b. Clubbing d. Osteoarthropathy ANS: B

Clubbing is the selective bulbous enlargement of the end (distal segment) of a digit (finger or toe) (see Figure 35-1) and is commonly associated with diseases that interfere with oxygenation, such as bronchiectasis, cystic fibrosis, pulmonary fibrosis, lung abscess, and congenital heart disease. None of the remaining options are terms used to identify the condition described. PTS: 1

REF: Page 1250

8. Pulmonary edema and pulmonary fibrosis cause hypoxemia by which mechanism? a. Creating alveolar dead space b. Decreasing the oxygen in inspired gas c. Creating a right-to-left shunt d. Impairing alveolocapillary membrane diffusion

ANS: D

Diffusion of oxygen through the alveolocapillary membrane is impaired if the alveolocapillary membrane is thickened or if the surface area available for diffusion is decreased. Abnormal thickness, as occurs with edema (tissue swelling) and fibrosis (formation of fibrous lesions), increases the time required for diffusion across the alveolocapillary membrane. None of the remaining options accurately describes the mechanism that triggers hypoxemia as a result of pulmonary edema or pulmonary fibrosis. PTS: 1

REF: Pages 1251-1252

9. High altitudes may produce hypoxemia through which mechanism? a. Shunting c. Decreased inspired oxygen b. Hypoventilation d. Diffusion abnormalities ANS: C

The presence of adequate oxygen content of the inspired air is the first factor. Oxygen content is lessened at high altitudes. At high altitudes none of the remaining options would be the cause of hypoxemia. PTS: 1

REF: Page 1251

10. Which condition is capable of producing alveolar dead space? a. Pulmonary edema c. Atelectasis b. Pulmonary emboli d. Pneumonia ANS: B

A pulmonary embolus that impairs blood flow to a segment of the lung results in an area where alveoli are ventilated but not perfused, which causes alveolar dead space. Alveolar dead space is not the result of any of the remaining options. PTS: 1

REF: Page 1252

11. What is the most common cause of pulmonary edema? a. Right-sided heart failure c. Mitral valve prolapse b. Left-sided heart failure d. Aortic stenosis ANS: B

The most common cause of pulmonary edema is heart disease. When the left ventricle fails, filling pressures on the left side of the heart increase and cause a concomitant increase in pulmonary capillary hydrostatic pressure. The remaining options are not common triggers for pulmonary edema. PTS: 1

REF: Page 1260

12. Pulmonary edema usually begins to develop at a pulmonary capillary wedge pressure or left

atrial pressure of how many millimeters of mercury (mm Hg)? a. 10 c. 30 b. 20 d. 40 ANS: B

Pulmonary edema usually begins to develop at a pulmonary capillary wedge pressure or left atrial pressure of 20 mm Hg.

PTS: 1

REF: Page 1260

13. The collapse of lung tissue caused by the lack of collateral ventilation through the pores of

Kohn is referred to as what type of atelectasis? a. Compression c. Absorption b. Perfusion d. Hypoventilation ANS: C

Absorption atelectasis is a result of the gradual absorption of air from obstructed or hypoventilated alveoli or from inhalation of concentrated oxygen or anesthetic agents. The other forms of atelectasis are not a result of the described mechanism. PTS: 1

REF: Pages 1256-1257 | Figure 35-5

14. In what form of bronchiectasis do both constrictions and dilations deform the bronchi? a. Varicose c. Cylindric b. Symmetric d. Saccular ANS: A

Varicose bronchiectasis exists when both constrictions and dilations deform the bronchi. None of the other options involve both constriction and dilation, resulting in bronchi deformity. PTS: 1

REF: Pages 1256-1258

15. Which pleural abnormality involves a site of pleural rupture that acts as a one-way valve,

permitting air to enter on inspiration but preventing its escape by closing during expiration? a. Spontaneous pneumothorax c. Open pneumothorax b. Tension pneumothorax d. Secondary pneumothorax ANS: B

In tension pneumothorax, the site of pleural rupture acts as a one-way valve, permitting air to enter on inspiration but preventing its escape by closing up during expiration. As more and more air enters the pleural space, air pressure in the pneumothorax begins to exceed barometric pressure. None of the other options result from the pathologic condition described. PTS: 1

REF: Page 1254

16. In which type of pleural effusion does the fluid become watery and diffuse out of the

capillaries as a result of increased blood pressure or decreased capillary oncotic pressure? c. Transudative d. Large

a. Exudative b. Purulent ANS: C

In transudative pleural effusion, the fluid, or transudate, is watery and diffuses out of the capillaries as a result of disorders that increase intravascular hydrostatic pressure or decrease capillary oncotic pressure. The described mechanism is not associated with the other forms of pleural effusion. PTS: 1

REF: Page 1254

17. Which condition involves an abnormally enlarged gas-exchange system and the destruction of

the lung’s alveolar walls? a. Transudative effusion b. Emphysema

c. Exudative effusion d. Abscess

ANS: B

Emphysema is abnormal permanent enlargement of gas-exchange airways (acini) accompanied by the destruction of alveolar walls without obvious fibrosis. The described mechanism is not associated with the other options. PTS: 1

REF: Page 1268

18. Which term is used to identify a circumscribed area of suppuration and destruction of lung

parenchyma? a. Consolidation b. Cavitation

c. Empyema d. Abscess

ANS: D

An abscess is a circumscribed area of suppuration and destruction of lung parenchyma. The described pathologic abnormality is not associated with the other options. PTS: 1

REF: Page 1274

19. Which condition is not a cause of chest wall restriction? a. Pneumothorax c. Gross obesity b. Severe kyphoscoliosis d. Neuromuscular disease ANS: A

Unlike the other options that result in chest wall restriction, a pneumothorax is the presence of air or gas in the pleural space caused by a rupture in the visceral pleura (which surrounds the lungs) or the parietal pleura and chest wall. PTS: 1

REF: Page 1254

20. What causes pneumoconiosis? a. Pneumococci bacteria b. Inhalation of inorganic dust particles

c. Exposure to asbestos d. Inhalation of cigarette smoke

ANS: B

Pneumoconiosis represents any change in the lung caused by the inhalation of inorganic dust particles, which usually occurs in the workplace. Pneumoconiosis is not a result of any of the other options. PTS: 1

REF: Page 1259

21. Which condition is a fulminant form of respiratory failure characterized by acute lung

inflammation and diffuse alveolocapillary injury? a. Acute respiratory distress syndrome (ARDS) b. Pneumonia c. Pulmonary emboli d. Acute pulmonary edema ANS: A

ARDS is a fulminant form of respiratory failure characterized by acute lung inflammation and diffuse alveolocapillary injury. The described pathologic characteristics are not associated with the other options. PTS: 1

REF: Page 1261

22. Which structure(s) in acute respiratory distress syndrome (ARDS) release inflammatory

mediators such as proteolytic enzymes, oxygen-free radicals, prostaglandins, leukotrienes, and platelet-activating factor? a. Complement cascade c. Macrophages b. Mast cells d. Neutrophils ANS: D

The role of neutrophils is central to the development of ARDS. Activated neutrophils release a battery of inflammatory mediators, among them proteolytic enzymes, oxygen-free radicals (superoxide radicals, hydrogen peroxide, hydroxyl radicals), arachidonic acid metabolites (prostaglandins, thromboxanes, leukotrienes), and platelet-activating factor. These mediators cause extensive damage to the alveolocapillary membrane and greatly increase capillary membrane permeability. The described responses are not associated with the other options. PTS: 1

REF: Page 1261

23. Pulmonary edema in acute respiratory distress syndrome (ARDS) is the result of an increase

in: a. Levels of serum sodium and water b. Capillary permeability

c. Capillary hydrostatic pressure d. Oncotic pressure

ANS: B

Increased capillary permeability, a hallmark of ARDS, allows fluids, proteins, and blood cells to leak from the capillary bed into the pulmonary interstitium and alveoli. The resulting pulmonary edema and hemorrhage severely reduce lung compliance and impair alveolar ventilation. The other options would not trigger ARDS-associated pulmonary edema. PTS: 1

REF: Page 1261

24. In acute respiratory distress syndrome (ARDS), alveoli and respiratory bronchioles fill with

fluid as a result of which mechanism? a. Compression on the pores of Kohn, thus preventing collateral ventilation b. Increased capillary permeability, which causes alveoli and respiratory bronchioles to fill with fluid c. Inactivation of surfactant and the impairment of type II alveolar cells d. Increased capillary hydrostatic pressure that forces fluid into the alveoli and respiratory bronchioles ANS: C

Lung inflammation and injury damage the alveolar epithelium and the vascular endothelium. Surfactant is inactivated, and its production by type II alveolar cells is impaired as alveoli and respiratory bronchioles fill with fluid or collapse. The other options would not trigger the described response. PTS: 1

REF: Page 1261

25. Which type of pulmonary disease requires more force to expire a volume of air? a. Restrictive c. Acute b. Obstructive d. Communicable ANS: B

Obstructive pulmonary disease is characterized by airway obstruction that is worse with expiration. Either more force (i.e., the use of accessory muscles of expiration) or more time is required to expire a given volume of air. The other options are not associated with a need for an increase of force to expire air. PTS: 1

REF: Page 1263

26. Which immunoglobulin (Ig) may contribute to the pathophysiologic characteristics of asthma? a. IgA c. IgG b. IgE d. IgM ANS: B

Asthma is a familial disorder, and more than 100 genes have been identified that may play a role in the susceptibility of and the pathogenetic mechanisms that cause asthma, including those that influence the production of interleukin (IL)–4, IL-5, and IL-13; IgE; eosinophils; mast cells; adrenergic receptors; and leukotrienes. The pathophysiologic characteristics of asthma are not associated with the other immunoglobulins. PTS: 1

REF: Pages 1263-1264

27. Which statement about the late asthmatic response is true? a. Norepinephrine causes bronchial smooth muscle contraction and mucus secretion. b. The release of toxic neuropeptides contributes to increased bronchial

hyperresponsiveness. c. The release of epinephrine causes bronchial smooth muscle contraction and

increases capillary permeability. d. Immunoglobulin G initiates the complement cascade and causes smooth muscle

contraction and increased capillary permeability. ANS: B

The late asthmatic response begins 4 to 8 hours after the early response when the release of toxic neuropeptides contributes to increased bronchial hyperresponsiveness. This selection is the only option associated with the late asthmatic response. PTS: 1

REF: Page 1264

28. Clinical manifestations of inspiratory and expiratory wheezing, dyspnea, nonproductive

cough, and tachypnea are indicative of which condition? a. Chronic bronchitis c. Pneumonia b. Emphysema d. Asthma ANS: D

At the beginning of an attack, the individual experiences chest constriction, expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, and tachypnea. Severe attacks involve the use of accessory muscles of respiration, and wheezing is heard during both inspiration and expiration. The presentations of none of the other options are consistent with the described symptoms.

PTS: 1

REF: Page 1264 | Page 1266

29. The most successful treatment for chronic asthma begins with which action? a. Avoidance of the causative agent b. Administration of broad-spectrum antibiotics c. Administration of drugs that reduce bronchospasm d. Administration of drugs that decrease airway inflammation ANS: A

Chronic management of asthma begins with the avoidance of allergens and other triggers. The effectiveness of the other options is reliant on the avoidance of triggers. PTS: 1

REF: Page 1266

30. Which factor contributes to the production of mucus associated with chronic bronchitis? a. Airway injury c. Increased Goblet cell size b. Pulmonary infection d. Bronchospasms ANS: C

Continual bronchial inflammation causes bronchial edema and increases the size and number of mucous glands and goblet cells in the airway epithelium. Thick, tenacious mucus is produced and cannot be cleared because of impaired ciliary function (see Figure 35-13). The lung’s defense mechanisms are therefore compromised, increasing a susceptibility to pulmonary infection, which contributes to airway injury. Frequent infectious exacerbations are complicated by bronchospasm with dyspnea and productive cough. PTS: 1

REF: Page 1267

31. Clinical manifestations of decreased exercise tolerance, wheezing, shortness of breath, and

productive cough are indicative of which respiratory disorder? a. Chronic bronchitis c. Pneumonia b. Emphysema d. Asthma ANS: A

The symptoms that lead individuals with chronic bronchitis to seek medical care include decreased exercise tolerance, wheezing, and shortness of breath. Individuals usually have a productive cough (“smoker’s cough”). The described symptoms are not associated with any of the other options. PTS: 1

REF: Page 1267

32. Clinical manifestations that include unexplained weight loss, dyspnea on exertion, use of

accessory muscles, and tachypnea with prolonged expiration are indicative of which respiratory disorder? a. Chronic bronchitis c. Pneumonia b. Emphysema d. Asthma ANS: B

Individuals with emphysema usually have dyspnea on exertion that later progresses to significant dyspnea, even at rest (see Table 35-3). Little coughing and very little sputum are produced. The individual is often thin, has tachypnea with prolonged expiration, and must use accessory muscles for ventilation. The anteroposterior diameter of the chest is increased (barrel chest), and the chest has a hyperresonant sound with percussion. The described symptoms are not associated with any of the other options. PTS: 1

REF: Page 1270

33. Which of the following is the most common route of lower respiratory tract infection? a. Aspiration of oropharyngeal secretions b. Inhalation of microorganisms c. Microorganisms spread to the lung via blood d. Poor mucous membrane protection ANS: A

Aspiration of oropharyngeal secretions is the most common route of lower respiratory tract infection; thus the nasopharynx and oropharynx constitute the first line of defense for most infectious agents. The other options are not common routes of lower respiratory tract infections. PTS: 1

REF: Page 1271

34. What is the initial step in the management of emphysema? a. Inhaled anticholinergic agents c. Cessation of smoking b. Beta agonists d. Surgical reduction of lung volume ANS: C

Chronic management of emphysema begins with smoking cessation. Pharmacologic management includes inhaled anticholinergic agents, and beta agonists should be prescribed. Pulmonary rehabilitation, improved nutrition, and breathing techniques all can improve symptoms. Oxygen therapy is indicated in chronic hypoxemia but must be administered with care. In selected patients, lung volume reduction surgery...


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