Chapter 20: Management of Patients With Chronic Pulmonary Disease

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Flashcards covering key concepts from COPD, asthma, cystic fibrosis, and bronchiectasis, including pathophysiology, risk factors, clinical manifestations, diagnostics, management, and nursing care.

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53 Terms

1
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What is chronic obstructive pulmonary disease (COPD)?

A slowly progressive, largely irreversible respiratory disease characterized by chronic and recurrent airflow obstruction.

2
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Which two primary disorders make up COPD?

Chronic bronchitis and emphysema.

3
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Is COPD preventable, treatable, or reversible?

It is preventable and treatable but not fully reversible.

4
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Describe the basic pathophysiology of COPD.

Progressive airflow limitation caused by abnormal inflammatory response to noxious particles/gases, leading to airway narrowing, parenchymal destruction, and pulmonary vascular changes.

5
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List four common pathophysiologic characteristics of COPD.

Mucus hypersecretion, ciliary dysfunction, lung hyperinflation, and gas-exchange abnormalities.

6
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Name five major risk factors for developing COPD.

Cigarette smoking, advanced age, severe recurring respiratory infections, occupational/environmental pollution, and genetic (familial) tendency including alpha-1 antitrypsin deficiency.

7
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Define chronic bronchitis (clinical definition).

Excessive mucus production with a chronic productive cough for at least 3 months in each of 2 consecutive years.

8
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State two key structural changes in chronic bronchitis.

Thickened bronchial walls with increased size/number of mucus glands and decreased ciliary function.

9
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Why are patients with chronic bronchitis nicknamed “blue bloaters”?

They often exhibit hypoxia, cyanosis, polycythemia, peripheral edema, and right-sided heart failure.

10
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Identify three common assessment findings in chronic bronchitis.

Peripheral edema, productive cough with rhonchi/crackles, and hypercapnia.

11
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Define emphysema.

Abnormal, permanent enlargement of distal air spaces with destruction of alveolar walls and loss of lung elasticity.

12
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Explain the role of alpha-1 antitrypsin in emphysema.

It normally inhibits elastase; deficiency allows unchecked elastase activity, destroying elastic fibers and leading to emphysema.

13
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Differentiate centrilobular and panlobular emphysema.

Centrilobular affects respiratory/terminal bronchioles; panlobular involves entire acinus including peripheral alveoli.

14
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Why are emphysema patients called “pink puffers”?

They maintain near-normal oxygenation (pink) but have dyspnea with pursed-lip breathing (puffers).

15
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List three classic physical findings in emphysema.

Barrel-shaped chest, prolonged expiration with pursed-lip breathing, and use of accessory muscles.

16
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State two typical pulmonary function test (PFT) results in emphysema.

Increased residual volume/total lung capacity and decreased forced expiratory volume (FEV1).

17
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Give six key elements of COPD management.

Smoking cessation, pharmacologic therapy, oxygen therapy, pulmonary rehabilitation, vaccination (influenza/pneumococcal), and management of exacerbations.

18
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What is the primary goal of oxygen therapy in COPD?

Provide adequate oxygenation while decreasing work of breathing and cardiac stress.

19
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Define hypoxemia versus hypoxia.

Hypoxemia = low arterial oxygen tension; hypoxia = diminished oxygen supply to tissues/cells.

20
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At what concentration and duration can oxygen toxicity occur?

FiO2 >50% for prolonged periods.

21
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List four complications of oxygen therapy.

Combustion risk, CO2 narcosis, oxygen toxicity, absorption atelectasis, and infection.

22
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Name three major drug classes used as bronchodilators in COPD.

Beta-adrenergic agonists, anticholinergics (muscarinic antagonists), and combination agents.

23
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What surgical options exist for advanced COPD?

Bullectomy, lung volume-reduction surgery, and lung transplantation.

24
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Identify four common complications of COPD.

Pneumonia, respiratory failure, cor pulmonale, and pneumothorax.

25
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What is the most common trigger of a COPD exacerbation?

Respiratory infection.

26
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List two nursing interventions to promote oxygenation in COPD.

Incentive spirometry and postural drainage with chest percussion/vibration.

27
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Give four components of an education plan for patients with COPD.

Smoking cessation, proper medication use, breathing/exercise techniques, and emergency management guidelines.

28
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Define asthma.

A chronic inflammatory airway disease with variable, reversible airflow obstruction, hyperresponsiveness, and mucus production.

29
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What triad of pathophysiologic events causes airway obstruction in asthma?

Bronchospasm, mucosal edema, and mucus hypersecretion.

30
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What is the strongest predisposing factor for asthma?

Allergy.

31
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List at least five asthma risk factors or triggers.

Family history, pollen, air pollution, occupational hazards, viral infections, smoking, and obesity.

32
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Name three hallmark clinical manifestations of asthma.

Cough, wheezing, and dyspnea (shortness of breath).

33
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Differentiate quick-relief and long-acting asthma medications.

Quick-relief: short-acting beta2 agonists, anticholinergics; Long-acting: inhaled corticosteroids, LABAs, leukotriene modifiers.

34
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What is the purpose of the stepwise approach in asthma management?

To escalate or de-escalate therapy based on symptom control and severity.

35
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List four key teaching points for asthma self-management.

Trigger avoidance, proper inhaler technique, peak-flow monitoring, and action plan implementation.

36
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What does a “silent chest” indicate in asthma?

Severely diminished breath sounds after prior wheezing—an impending life-threatening airway obstruction.

37
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State two criteria that characterize severe life-threatening asthma.

Respiratory rate >30/min and inability to speak due to dyspnea (with signs such as diaphoresis, confusion).

38
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Identify four possible complications of asthma.

Status asthmaticus, mucus plugs, barotrauma, and respiratory failure or cardiovascular complications.

39
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What is cystic fibrosis (CF)?

The most common autosomal recessive disorder among Caucasians caused by CFTR gene mutation leading to thick, dehydrated secretions.

40
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Explain the basic pathophysiology of CF.

Defective chloride transport results in thick mucus that obstructs ducts in lungs, pancreas, and other organs, causing infection and organ dysfunction.

41
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List four respiratory manifestations of CF.

Persistent productive cough with thick mucus, wheezing, recurrent lung infections, and chronic hypoxia.

42
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Name three gastrointestinal manifestations of CF.

Steatorrhea (foul greasy stools), poor weight gain, and intestinal obstruction such as meconium ileus.

43
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How does CF affect male fertility?

Nearly all males are infertile due to absent or mucus-blocked vas deferens.

44
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What is the gold-standard diagnostic test for CF?

Sweat chloride test demonstrating elevated chloride concentration.

45
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Give five components of medical management in CF.

Antibiotics, inhaled bronchodilators, mucolytics, pancreatic enzyme replacement, and CFTR modulators.

46
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State three nursing strategies to promote secretion clearance in CF.

Chest physiotherapy, breathing exercises, and adequate hydration.

47
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Does lung transplantation cure CF?

No; it prolongs life but does not eliminate systemic disease or infection risk.

48
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List two categories of common CF complications beyond the lungs.

Gastrointestinal (nutritional deficiencies, diabetes) and musculoskeletal (osteoporosis).

49
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Define bronchiectasis.

Chronic, irreversible dilation and destruction of bronchi/bronchioles due to inflammation and impaired mucus clearance.

50
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Give three causes or contributing factors to bronchiectasis.

Recurrent pulmonary infections, airway obstruction, and genetic or immune disorders.

51
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State three clinical manifestations of bronchiectasis.

Chronic cough, copious purulent sputum, and digital clubbing.

52
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List three elements of medical management for bronchiectasis.

Postural drainage with chest physiotherapy, antimicrobial therapy, and bronchodilators/mucolytics.

53
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What patient teaching topics are essential in bronchiectasis?

Smoking cessation, recognizing early infection signs, energy conservation, and effective airway clearance techniques.