COPD Flashcards

(53 cards)

1
Q

Definition of COPD

A

A chronic, progressive respiratory disease characterized by airflow limitation.

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2
Q

Causes of COPD

A

Long-term exposure to irritants such as tobacco smoke, air pollution, chemical fumes, and dust.

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3
Q

Main Types of COPD

A

Chronic bronchitis and emphysema.

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4
Q

Symptoms of COPD

A

Chronic cough, sputum production, shortness of breath (dyspnea), wheezing, and chest tightness.

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5
Q

Pathophysiology of COPD

A

Chronic inflammation leads to structural changes in the airways, destruction of alveoli, and mucus hypersecretion.

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6
Q

Chronic Bronchitis

A

Inflammation of the bronchial tubes, leading to excessive mucus production and chronic cough.

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7
Q

Emphysema

A

Damage to alveoli, leading to reduced gas exchange and air trapping.

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8
Q

Risk Factors for COPD

A

Smoking, exposure to secondhand smoke, occupational exposures, and genetic factors (e.g., alpha-1 antitrypsin deficiency).

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9
Q

Alpha-1 Antitrypsin Deficiency

A

A genetic condition that can cause COPD by reducing lung protection from proteolytic enzymes.

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10
Q

Diagnosis of COPD

A

Based on spirometry, showing reduced FEV1/FVC ratio (< 0.7), along with clinical symptoms.

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11
Q

COPD Stages (GOLD Classification)

A

Based on FEV1: mild (≥80%), moderate (50-79%), severe (30-49%), and very severe (<30%).

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12
Q

Treatment of COPD

A

Includes smoking cessation, bronchodilators, corticosteroids, oxygen therapy, and pulmonary rehabilitation.

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13
Q

Bronchodilators

A

Medications that relax airway muscles, including beta-agonists (e.g., salbutamol) and anticholinergics (e.g., tiotropium).

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14
Q

Corticosteroids in COPD

A

Used to reduce inflammation, especially in patients with frequent exacerbations (e.g., inhaled budesonide).

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15
Q

Oxygen Therapy

A

Indicated in severe COPD with hypoxemia (PaO2 < 55 mmHg or SaO2 < 88%).

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16
Q

Exacerbations of COPD

A

Acute worsening of symptoms, often triggered by infections or environmental pollutants.

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17
Q

COPD and Respiratory Failure

A

Severe COPD can lead to hypoxic (type 1) or hypercapnic (type 2) respiratory failure.

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18
Q

Complications of COPD

A

Pulmonary hypertension, right-sided heart failure (cor pulmonale), and frequent infections.

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19
Q

Prevention of COPD Exacerbations

A

Vaccinations (influenza, pneumococcal), proper inhaler technique, and avoidance of triggers.

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20
Q

COPD and Forensic Considerations

A

In post-mortem cases, signs of COPD like hyperinflated lungs, bullae, and airway remodeling are noted in forensic pathology.

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21
Q

What are common obstructive lung diseases?

A

Chronic obstructive pulmonary disease (COPD), asthma, and bronchiectasis.

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22
Q

What are the two major clinicopathologic manifestations of COPD?

A

Emphysema and chronic bronchitis.

23
Q

What is the WHO’s definition of COPD?

A

“A common, preventable and treatable disease characterized by persistent respiratory symptoms and airflow limitation due to airway and/or alveolar abnormalities caused by exposure to noxious particles or gases.”

24
Q

What is the primary etiologic factor for COPD?

A

Cigarette smoking.

25
What percentage of heavy smokers develop COPD?
35% to 50% of heavy smokers.
26
Which groups are more susceptible to COPD?
Women and African Americans who smoke heavily.
27
What additional risk factors are associated with COPD?
Poor lung development early in life, exposure to environmental pollutants, airway hyperresponsiveness, certain genetic polymorphisms.
28
What are the two main types of emphysema that cause airflow obstruction?
Centriacinar and panacinar emphysema.
29
Describe centriacinar emphysema.
Most common form, affecting central parts of acini in heavy smokers; upper lobes are more affected.
30
Describe panacinar emphysema.
Associated with α1-antitrypsin deficiency; acini uniformly enlarged from respiratory bronchiole to terminal alveoli.
31
What is distal acinar emphysema associated with?
Underlies many cases of spontaneous pneumothorax in young adults; proximal acinus is normal, distal part is involved.
32
What characterizes irregular emphysema?
Irregularly involved acini associated with scarring; usually clinically insignificant.
33
What are the mechanisms contributing to the development of emphysema?
Toxic injury from inhaled particles, protease-antiprotease imbalance, oxidative stress, infection.
34
What role does toxic injury and inflammation play in emphysema?
Inhaled smoke damages respiratory epithelium, causing inflammation and parenchymal destruction.
35
How does protease-antiprotease imbalance contribute to emphysema?
Deficiency of protective antiproteases leads to excessive connective tissue breakdown.
36
What is oxidative stress and its role in emphysema?
Oxidants from tobacco smoke cause tissue damage and inflammation.
37
How can infections affect emphysema?
Infections can exacerbate existing disease but do not initiate tissue destruction.
38
What is the significance of α1-antitrypsin deficiency in emphysema?
Patients with genetic deficiency have enhanced emphysema risk, especially with smoking.
39
What are the clinical features of advanced emphysema?
Barrel-chested, dyspneic, prolonged expiration, low diffusion capacity, relatively normal blood gas values, significant weight loss.
40
What is chronic bronchitis defined as?
Persistent cough with sputum production for at least 3 months in 2 consecutive years.
41
What are the primary factors contributing to chronic bronchitis?
Exposure to noxious inhaled substances like tobacco smoke and dust.
42
What is mucus hypersecretion in chronic bronchitis?
Hypersecretion of mucus in large airways; associated with gland enlargement and increased goblet cells.
43
How does smoking affect mucus secretion and airway function?
Smoking damages airway-lining cells, leading to inflammation and reduced ciliary action.
44
What are the gross and microscopic features of chronic bronchitis?
Hyperemia, swelling, edema of mucous membranes, chronic inflammation, goblet cell hyperplasia, enlarged mucus-secreting glands.
45
What is the Reid index, and how does it relate to chronic bronchitis?
The ratio of the thickness of the mucous gland layer to the thickness of the airway wall; increased in chronic bronchitis.
46
What clinical features are associated with COPD?
Slowly increasing dyspnea, chronic cough, sputum production; often worsens with superimposed infections.
47
What are the two extremes of COPD presentation?
"Pink puffers" (emphysema dominates) and "blue bloaters" (chronic bronchitis dominates).
48
What are the treatment options for COPD?
Smoking cessation, oxygen therapy, long-acting bronchodilators, inhaled corticosteroids, antibiotics, surgery.
49
What can lead to pulmonary hypertension in COPD patients?
Pulmonary hypertension, cor pulmonale, and heart failure.
50
What is compensatory hyperinflation?
Dilation of alveoli in response to loss of lung substance elsewhere.
51
What is obstructive overinflation?
Lung expands due to trapped air; caused by obstruction or congenital issues.
52
What is bullous emphysema?
Large subpleural blebs or bullae; can rupture leading to pneumothorax.
53
What is interstitial emphysema?
Air enters connective tissue stroma of the lung or mediastinum.