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Pathology > COPD > Flashcards

COPD Flashcards

1
Q

Group of disorders characterized by airflow obstruction?

A

COPD

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2
Q

What happens to FEV in COPD?

A

Decreased

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3
Q

What happens to FVC in COPD?

A

Decreased

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4
Q

What happens to the FEV:FVC ratio in COPD?

A

Decreased

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5
Q

What are the three main diseases that constitute COPD?

A

Chronic bronchitis, emphysema, and bronchial asthma.

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6
Q

What causes increased sensitivity of air passages in asthma? (bronchial asthma)

A

Stimuli that lead to bronchial hyperreactivity.

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7
Q

What are the two main types of asthma?

A

Extrinsic (immune) and Intrinsic (non-immune).

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8
Q

What mediates extrinsic asthma?

A

Type I hypersensitivity response (IgE binding to mast cells).

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9
Q

When does extrinsic asthma typically begin?

A

Childhood

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10
Q

What is intrinsic asthma associated with?

A

Chronic bronchitis, exercise, or cold-induced asthma.

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11
Q

When does intrinsic asthma typically begin?

A

Adult life

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12
Q

What happens to the smooth muscle of the bronchi in asthma?

A

Hypertrophy

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13
Q

What happens to bronchial submucosal glands and goblet cells in asthma?

A

Hyperplasia

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14
Q

What happens to the basement membranes in asthma?

A

Thickening & hyalinisation.

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15
Q

What inflammatory cell proliferates in asthma?

A

Eosinophils

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16
Q

What are Curschmann spirals?

A

Whorl-like accumulations of epithelial cells found in airways.

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17
Q

What are Charcot-Leyden crystals?

A

Crystalloids of eosinophil-derived proteins found in viscid mucus.

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18
Q

What are the hallmark symptoms of asthma?

A

Episodic dyspnoea and wheezing expiration due to airway stenosis.

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19
Q

Name three potential complications of asthma.

A

Superimposed infection, chronic bronchitis, and pulmonary emphysema.

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20
Q

What is status asthmaticus?

A

Prolonged bouts of asthma lasting days, unresponsive to therapy, and potentially fatal.

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21
Q

What are the main causative agents in chronic bronchitis?

A

Environmental irritants (e.g., cigarette smoke, air pollution).

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22
Q

What are the key histological changes in chronic bronchitis?

A

Hypertrophy of mucous glands in the trachea & main bronchi.
Increased mucin-secreting goblet cells in smaller bronchi & bronchioles.
Inflammation with infiltration of CD8+ lymphocytes, macrophages, & neutrophils.

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23
Q

What are the two main mechanisms leading to airflow obstruction in chronic bronchitis?

A

Small airway disease (goblet cell metaplasia, mucous plugging, inflammation, and fibrosis).
Coexistent emphysema.

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24
Q

What are the hallmark symptoms of chronic bronchitis?

A

Prominent cough.
Production of sputum.

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25
Q

What are the signs of COPD development in chronic bronchitis?

A

Hypercapnia (elevated CO2 levels).
Hypoxaemia (low blood oxygen levels).
Cyanosis (“blue bloaters”).

26
Q

What are the major complications of chronic bronchitis?

A

Pulmonary hypertension → Cor pulmonale → Cardiac failure.
Recurrent infections.
Respiratory failure.

27
Q

What are the gross findings in the mucosal lining of larger airways in chronic bronchitis?

A

Hyperaemic and swollen mucosa (edema fluid).
Mucosa covered by mucinous or muco-purulent secretion.

28
Q

What is the Reid index and its significance in chronic bronchitis?

A

Ratio of submucosal gland thickness to bronchial wall thickness.
A Reid index >0.4 indicates gland enlargement in chronic bronchitis.

29
Q

What inflammatory cells are mainly seen in chronic bronchitis?

A

Mononuclear inflammatory cells with variable numbers of neutrophils.

30
Q

What are the microscopic findings in chronic bronchiolitis?

A

Goblet cell metaplasia.
Mucous plugging.
Inflammation.
Fibrosis.

31
Q

What is bronchiolitis obliterans?

A

A chronic scarring process of small airways, leading to progressive airway obliteration and obstructive lung disease.

32
Q

What is the definition of emphysema?

A

Irreversible enlargement of airspaces distal to the terminal bronchiole, with destruction of their walls & no obvious fibrosis.

32
Q

What is the main cause of emphysema?

A

Smoking

33
Q

How does cigarette smoking contribute to emphysema?

A

Attracts neutrophils & macrophages (sources of elastase).
Inactivates alpha1-antitrypsin, promoting elastase activity & elastin destruction.

34
Q

What are the key clinical features of emphysema?

A

“Pink puffer” (emphysema dominant) vs. “Blue bloater” (chronic bronchitis dominant).
Barrel chest (increased anteroposterior diameter).
Increased total lung capacity.
Hypoxia, cyanosis, and respiratory acidosis

35
Q

What enzyme is central to the pathogenesis of emphysema?

A

Elastase, which destroys elastin in the alveolar wall.

36
Q

What neutralizes elastase?

A

Alpha1-antitrypsin

37
Q

What are the complications of emphysema?

A

Chronic bronchitis.
Interstitial emphysema (air leakage into connective tissue).
Rupture of a surface bleb (apical bulla) → pneumothorax.

38
Q

What are the main types of emphysema?

A

Centri-acinar, Pan-acinar, Distal acinar, Irregular, Bullous, and Interstitial.

39
Q

What parts of the acini are affected in centric acinar?

A

Central/proximal parts (respiratory bronchioles), sparing distal alveoli.

40
Q

What is centri-acinar associated with?

A

Heavy cigarette smoking and chronic bronchitis.

41
Q

Where is centri acinar most common?

A

Upper lobes, particularly apical segments.

42
Q

What is present in walls of the emphysematous spaces in centri acinar?

A

Large amounts of black pigment

43
Q

What parts of the acini are affected in pan lobular?

A

Entire acinus (respiratory bronchioles, alveolar ducts, and alveoli).

44
Q

What is pan lobular emphysema associated with?

A

Alpha1-antitrypsin deficiency.

45
Q

Where is pan lobular emphysema most severe?

A

Lower zones and anterior lung margins.

46
Q

What part of the acinus is affected in distal acinar?

A

Distal portion (alveoli & alveolar ducts), with normal proximal portions.

47
Q

What complications can distal acinar cause?

A

Pneumothorax due to large sub-pleural bullae or blebs.

48
Q

What is a characteristic feature of irrefular emphysema?

A

Airspace enlargement with fibrosis due to scarring from inflammation.

49
Q

What are bullae?

A

Large sub-pleural blebs (>1 cm) due to localized emphysema accentuation.

50
Q

What conditions can bullous emphysema be associated with?

A

Old tuberculous scarring or other lung damage.

51
Q

How does air enter connective tissue in interstitial emphysema?

A

Due to coughing, bronchial obstruction, or alveolar tears.

52
Q

What external injuries can cause interstitial emphysema?

A

Chest wounds or fractured ribs puncturing lung parenchyma.

53
Q

A disease characterized by permanent dilation of bronchi and bronchioles due to destruction of the muscle & elastic tissue, often associated with chronic necrotizing infections.

A

Bronchiectasis

54
Q

What causes bronchiectasis?

A

Destruction of muscle and elastic tissue due to chronic necrotizing infections.

55
Q

What are the main predisposing factors for bronchiectasis?

A

Post-infectious conditions (e.g., necrotizing pneumonia caused by bacteria, viruses, fungi).
Bronchial obstruction (e.g., tumors).
Cystic fibrosis.
Kartagener Syndrome (Primary Ciliary Dyskinesia).
Rheumatoid arthritis.
Systemic lupus erythematosus (SLE).
Inflammatory bowel disease (IBD).

56
Q

What are the key features of Kartagener Syndrome?

A

Sinusitis.
Bronchiectasis.
Situs inversus.
Hearing loss.
Male sterility (impaired sperm motility).

57
Q

Where in the lungs is bronchiectasis most commonly localized?

A

Usually in the lower lobes, bilaterally.
Most severe in the distal bronchi and bronchioles.

58
Q

What are the macroscopic features of bronchiectasis?

A

Dilated airways (up to 4x normal size).
Bronchi and bronchioles’ lumens extend up to the pleural surface.
Cut surface: Dilated bronchi appear as cysts filled with muco-purulent secretions.

59
Q

What are the microscopic findings in bronchiectasis?

A

Intense acute and chronic inflammatory exudation in bronchial and bronchiolar walls.
Desquamation of the lining epithelium.
Necrotizing ulceration.
Pseudo-stratification of columnar cells or squamous metaplasia in preserved epithelium.
Complete necrosis of bronchial/bronchiolar walls → lung abscess.
Fibrosis of bronchial and bronchiolar walls and peri-bronchiolar regions → subtotal or total lumen obliteration.

60
Q

What are the clinical features of bronchiectasis?

A

Severe, persistent cough.
Expectoration of foul-smelling, sometimes bloody sputum.
Dyspnea and orthopnea (severe cases).
Obstructive respiratory insufficiency → marked dyspnea and cyanosis.
Recurrent pulmonary infections → lung abscess.
Occasionally, life-threatening hemoptysis.

61
Q

What are the complications of bronchiectasis?

A

Cor pulmonale.
Brain abscesses.
Amyloidosis (less frequent).

Pathology (26 decks)

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