Diseases Of The Pulmonary System Flashcards

1
Q

What is COPD?

A

A disease characterized by persistent airway limitation that is usually progressive and associated with chronic inflammatory response in the airways.

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2
Q

What are the 2 classic types of COPD?

A
  1. Chronic bronchitis: a clinical diagnosis characterized by chronic cough productive of sputum for at least 3 months per year for at least 2 consecutive years.
  2. Emphysema: a pathologic diagnosis characterized by permanent enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls.

Both often coexist.

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3
Q

What are the clinical features of COPD?

A
  1. Any combination of cough, sputum production, and dyspnea
  2. Prolonged expiratory time with pursed lip breathing
  3. End-expiratory wheezes on forced expiration, decreased breath sounds and/or inspiratory crackles
  4. Tachypnea, tachycardia
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4
Q

How is COPD diagnosed

A
  1. PFT: definitive diagnostic test
    • The FEV1/FVC ratio is <0.7
    • FEV1 is decreased (the lower the rate the more severe it is)
    • TLC is increased (excess volume is not useful because it all becomes residual volume)
    • Residual volume is increased (doesn’t contribute in gas exchange)
  2. CXR: low sensitivity to diagnosed COPD as only severe emphysema shows changes
    • Hyperinflation, flattened diaphragm, enlarged retrosternal space, diminished vascular markings
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5
Q

What are the treatment modalities for COPD?

A
  1. Smoking cessation (prolongs survival rate, but doesn’t result in complete reversal)
  2. Inhaled anticholinergic drugs (ipratropium bromide)
  3. Inhaled beta-2 agonist
  4. Combination of 2 and 3 are more efficacious
  5. Inhaled corticosteroids
  6. Theophylline (oral)
  7. Oxygen therapy: shown to improve survival and quality of life in patients with COPD and chronic hypoexmia
  8. Pulmonary rehabilitation
  9. Antibiotics for acute exacerbation
  10. Surgery: lung resection or transplant
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6
Q

What are the treatment guidelines for COPD?

A
  1. Low risk of exacerbation (0-1 time per year):
    • Short-acting bronchodilator as needed in MDI
    • Add long-acting bronchodilator if more symptomatic
    • Inhaled glucocorticoids may be used
  2. High risk of exacerbation (2 or more times per year):
    • Regular use of long-acting bronchodilator
    • Add inhaled corticosteroid if more symptomatic
    • Continuous oxygen therapy
    • Pulmonary rehabilitation
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7
Q

How is acute COPD exacerbation managed?

A
  1. CXR
  2. Beta-2 agonist with or without anticholinergics
  3. Systemic corticosteroids: if hospitalized
  4. Antibiotics: if moderate or severe exacerbation
  5. Supplemental oxygen: used to keep O2 sat 88%-92%
  6. NPPV
  7. Intubation and mechanical ventilation
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8
Q

What is asthma?

A

A chronic inflammatory disease of the respiratory system characterized by bronchial hyper-responsiveness, episodic exacerbation, acute reversible airflow obstruction; manifests with reversible cough, wheezing, and dyspnea.

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9
Q

What are the typical features of asthma?

A
  1. Persistent dry cough that worsens at night, with exercise, or on exposure to triggers/irritants
  2. End-expiratory wheezes
  3. Chest tightness
  4. Prolonged expiratory phase on auscultation
  5. Hyperresonance to lung percussion
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10
Q

What are the signs of acute severe asthma?

A
  1. Tachypnea
  2. Diaphoresis
  3. Wheezing
  4. Speaking in incomplete sentences
  5. Use of accessory muscles of respiration
  6. Paradoxic movement of the abdomen and diaphragm on inspiration is sign of impending respiratory failure
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11
Q

How is asthma diagnosed?

A
  1. Typical clinical features of asthma
  2. PFT:
    • Decreased peak expiratory flow rate during asthma exacerbations
    • Decreased FEV1
    • Decreased FEV1/FVC ratio
    • Obstruction is reversible with a bronchodilator (increase in FEV1 >12%)
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12
Q

What is pleural effusion?

A

It is the accumulation of fluid inside the pleural sac. Caused by either increased drainage of fluid into pleural space, increased production of fluid by cells in the pleural space, or decreased drainage of fluid from the pleural space

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13
Q

What are the 2 types of pleural effusion?

A
  1. Transudative effusions
  2. Exudative effusions: have at least one of the following Light’s criteria
    • Pleural protein/serum protein >0.5
    • Pleural LDH/serum LDH >0.6
    • LDH > two-third the upper limit of normal serum LDH
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14
Q

What are the findings of pleural effusion on examination?

A
  1. Stony dullness on percussion
  2. Decreased or diminished breath sounds over the effusion
  3. Decreased tactile fremitus and chest expansion
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15
Q

How is pleural effusion diagnosed?

A
  1. CXR: PA and lateral, but lateral decubitus is more reliable
    • Blunting of costophrenic angle + meniscus sign
  2. CT chest: more reliable than CXR
  3. Thoracocentesis: indicated for evaluation of all new pleural effusions
    • 5 bottles taken for: micro culture & gram stain, biochemistry (protein, glucose, LDH), cell count & differential, cytology, TB
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16
Q

How is pleural effusion managed?

A
  1. Transudative effusions:
    • Diuretics and sodium restriction
    • Therapeutic thoracentesis if massive effusion causing dyspnea
  2. Exudative effusion: treat underlying cause
  3. Parapneumonic effusion: which is effusion in the presence of pneumonia
    • Most cases require antibiotic alone for up to 6 weeks
    • If complicated (empyema) chest tube drainage may be required
17
Q

What is empyema?

A

Pus within the pleural space which occurs if exudative pleural effusion is left untreated.

18
Q

What is interstitial lung disease?

A

Inflammatory process involving the alveolar wall that can lead to irreversible fibrosis, distortion of lung architecture, and impaired gas exchange.

19
Q

What is sarcoidosis?

A

A chronic systemic granulomatous disease characterized by noncaseating granulomas, often involving multiple organ systems such as lungs, skin, eyes, heart, musculoskeletal system and nervous system.

20
Q

How is sarcoidosis diagnosed?

A
  1. Clinical features:
    • Typical presentation of a young patient with constitutional symptoms, respiratory complaints, erythema nodosum, blurred vision, and bilateral hilar adenopathy.
  2. CXR: bilateral hilar adenopathy is the hallmark of the disease, but is not specific
  3. Skin anergy with tuberculin skin test
  4. Elevated angiotensin-converting enzyme: helps in supporting diagnosis, but lacks sensitivity and specificity
  5. Definitive diagnosis requires transbronchial biopsy showing noncaseating granulomas with clinical features
21
Q

How is sarcoidosis managed?

A

Most resolve spontaneously in 2 years, but systemic corticosteroids is the treatment of choice (Prednisone 30 mg for 6 weeks)

22
Q

What is pulmonary langerhans cell histiocytosis?

A

Chronic interstitial pneumonia caused by abnormal proliferation of histiocytes. Honeycomb appearance on CXR and cystic lesions on CT scan.

23
Q

When does acute respiratory failure occur?

A

Results when there is inadequate oxygenation of blood or inadequate ventilation (elimination of CO2) or both

24
Q

What is acute respiratory distress syndrome?

A

A diffuse inflammatory process involving both lungs, neutrophil activation in the systemic or pulmonary circulations is the primary mechanism.

25
Q

What is the pathophysiology of ARDS?

A
  1. Massive intrapulmonary shunting of blood: severe hypoxemia with no significant improvement on 100% O2
  2. Decreased pulmonary compliance
  3. Increased dead space
  4. Low vital capacity
26
Q

How is ARDS diagnosed?

A
  1. Hypoxemia that is refractory to oxygen therapy
  2. Bilateral diffuse pulmonary infiltrates on CXR
  3. No evidence of CHF clinically or PCWP <18 mmHg
  4. Respiratory symptoms that develop within 1 week of known insult
27
Q

What is pulmonary hypertension?

A

A mean arterial pressure greater than 25 mmHg at rest.

28
Q

What is Cor Pulmonale?

A

Right ventricular hypertrophy with eventual RV failure resulting from pulmonary HTN, secondary to pulmonary disease. Most commonly secondary to COPD.

29
Q

What is pulmonary embolism?

A

A thrombus in another region of the body embolizes to the pulmonary vascular tree via the RV and pulmonary artery. Blood flow distal to the embolus is obstructed. Majority of cases are silent

30
Q

How is PE diagnosed?

A
  1. Venous duplex ultrasound of the lower extremities: helpful when positive, but little value when negative
  2. CTA: test of choice, but contraindicated in patients wit significant renal insufficiency because of IV contrast
  3. Pulmonary angiography: gold standard, definitively diagnoses or excludes PE but invasive.
  4. D-dimer assay: if pretest probability of PE is low, D-dimer is a good noninvasive test to rule out PE
31
Q

How is PE managed?

A
  1. Supplemental oxygen
  2. Acute anticoagulation therapy (heparin)
  3. Oral anticoagulation (warfarin) started with heparin on day 1
  4. Thrombolytic therapy: use is not well defined
  5. Inferior vena cava interruption (IVC filter placement): indicated in certain patients
  6. Surgical thombectomy: consider in patients with hemodynamic compromise