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ACEM Primary Written > Respiratory: Pathology - Obstructive airways disease > Flashcards

Respiratory: Pathology - Obstructive airways disease Flashcards

1
Q

What is the difference between obstructive and restrictive airways disease?

A

Obstructive: increased resistance to airflow due to obstruction
Restrictive: decreased expansion of lung parenchyma (decreased total lung capacity)

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2
Q

Give four examples of obstructive lung diseases

A
  1. Chronic bronchitis*
  2. Emphysema*
  3. Asthma
  4. Bronchiectasis
  • COPD is a clinical grouping of chronic bronchitis and emphysema
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3
Q

What is emphysema?

A

Chronic obstructive lung disease charactered by irreversible airspace enlargement distal to terminal bronchioles, with destruction of their walls

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4
Q

Give three risk factors for emphysema

A
  1. Heavy cigarette smoking
  2. Female sex
  3. African American
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5
Q

What % of emphysema sufferers do not smoke?

A

10%

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6
Q

What are the four classifications of emphysema?

A
  1. Centriacinar
  2. Panacinar
  3. Paraseptal (distal acinar)
  4. Irregular (airspace enlargement with fibrosis)
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7
Q

Describe the pathological changes seen in centriacinar emphysema

A

Destruction of central or proximal parts of acini, with sparing of distal alveoli

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8
Q

Describe the pathological changes seen in panacinar emphysema

A

Uniform enlargement of acini

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9
Q

Describe the pathological changes seen in paraseptal emphysema

A

Enlargement of distal acini, sparing proximal
Multiple continuous enlarged airspaces 0.5 to >2cm in diameter
May form cyst-like structures

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10
Q

Describe the pathological changes seen in irregular emphysema

A

Irregular involvement of acinus, with scarring

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11
Q

What parts of the lung are predominantly affected in centriacinar emphysema?

A

Upper lobes and apices

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12
Q

What parts of the lung are predominantly affected in panacinar emphysema?

A

Lower zones and anterior margins
Most severe at bases

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13
Q

What parts of the lung are predominantly affected in paraseptal emphysema?

A

Areas adjacent to pleura, along lobular connective tissue septa, and lobule margins

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14
Q

Which pattern of emphysema is typically seen in heavy smokers?

A

Centriacinar

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15
Q

Which pattern of emphysema is usually caused by a1-antitrypsin deficiency?

A

Panacinar

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16
Q

Which pattern of emphysema may be the underlying cause in spontaneous pneumothorax?

A

Paraseptal

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17
Q

What is the typical clinical presentation seen with irregular emphysema?

A

Often asymptomatic, clinically insignificant

18
Q

Describe the pathogenesis of emphysema in smokers

A

Nicotine and reactive oxygen species from tobacco smoke cause “functional” a1-antitrypsin deficiency due to oxidative damage, and induce transcription of NF-κB
Results in release of chemoattractants for neutrophils and macrophages, which are then activated with subsequent release of proteases and elastase
May also see goblet cell metaplasia with mucus plugging, and peribronchial fibrosis

19
Q

Describe the concept of protease-antiprotease imbalance as it relates to emphysema

A

Hereditary deficiency of a1-antitrypsin (a major protease inhibitor) invariably results in emphysema
In these patients, unchecked proteolytic activity occurs in response to inflammatory stimulus, resulting in destruction of elastic tissue and leading to airway enlargement

20
Q

What % of all patients with emphysema have a1-antitrypsin deficiency?

A

1%

21
Q

Define chronic bronchitis

A

Persistent cough with sputum production for at least 3 months in at least 2 consecutive years, in absence of any other identifiable cause

22
Q

What are some of the potential complications of chronic bronchitis?

A
  1. COPD
  2. Cor pulmonale
  3. Respiratory epithelium metaplasia/dysplasia -> increased risk of cancer
23
Q

What % of chronic bronchitis sufferers are smokers?

A

90%

24
Q

Describe the pathogenesis of chronic bronchitis

A

Chronic airway irritation due to smoking or other inhaled irritants
Earliest feature is mucus hypersecretion and hypertrophy of submucosal glands in large airways (trachea, bronchi): this is stimulated by elastases and MMPs released by neutrophils
Subsequent metaplastic reaction with hyperplasia and hypertrophy of goblet cells of smaller airways (small bronchi, bronchioles), leading to airway obstruction

25
Q

Five morphological changes seen in chronic bronchitis

A
  1. Hyperaemia and oedema of mucous membranes
  2. Mucinous secretions or casts filling airways
  3. Increased mucus gland size (increased Reid index, which is ratio of mucus gland layer to total wall thickness)
  4. Bronchial/bronchiolar mucous plugging, inflammation and fibrosis
  5. Squamous metaplasia/dysplasia of respiratory epithelium
26
Q

What is bronchiolitis obliterans?

A

Obliteration of small airway lumen seen in severe chronic bronchitis as a result of progressive airway fibrosis and narrowing

27
Q

Distinguish between predominant emphysema and predominant bronchitis patterns of COPD, in terms of appearance, age, dyspnoea, cough, infections, respiratory insufficiency, cor pulmonale, airway resistance, elastic recoil, and CXR changes

A
28
Q

What is asthma?

A

Chronic inflammatory disorder characterised by recurrent episodes of wheezing, breathlessness, chest tightness, and cough (often nocturnal and/or early morning)

29
Q

Three hallmarks of asthma

A
  1. Increased airway responsiveness resulting in episodic bronchoconstriction
  2. Inflammation of bronchial walls
  3. Increased mucus secretion
30
Q

What are the four types of asthma? Which are most common?

A
  1. Atopic (most common)
  2. Intrinsic nonreagenic (also common)
  3. Drug-induced
  4. Occupational
31
Q

Describe the immediate and late phase components of the hypersensitivity reaction seen in atopic asthma. What mediates each and what are the features?

A

Acute phase:
- Mediated by binding of Ag to IgE-coated mast cells
- Features include bronchoconstriction, increased mucus secretion, vasodilation with increased vascular permeability

Late phase:
- Inflammation mediated by recruited leukocytes
- Features persistent bronchospasm and oedema, leukocytic infiltration, loss of damaged epithelial cells

32
Q

Three cytokines of importance in atopic asthma

A

All secreted by TH2 cells:
IL-4: IgE production
IL-5: eosinophil activation
IL-13: increased mucus secretion and IgE production

33
Q

What are three typical triggers for intrinsic nonreagenic asthma?

A

Respiratory tract infections
Chemical irritants
Drugs

34
Q

What causes drug-induced asthma?

A

Aspirin, likely related to effects of COX inhibition

35
Q

What causes occupational asthma?

A

Triggered by fume, organic and chemical dusts, gases, and other chemicals
Usually due to repeated exposures

36
Q

Describe the histological findings seen in asthma

A
  1. Curschmann spirals (whorled mucus plugs)
  2. Eosinophilic infiltrate with crystalloid debris of their membranes (Charcot-Leyden crystals)
  3. “Airway remodelling”:
    - Thickening of airway wall with sub-basement membrane fibrosis
    - Hypervascularity
    - Submucosal gland hypertrophy, mucous metaplasia
    - Hypertrophy and/or hyperplasia of bronchial wall muscle
37
Q

What is bronchiectasis?

A

Disease charactered by permanent dilation of bronchi and bronchioles, caused by destruction of muscle and elastic tissue due to chronic necrotising infections

38
Q

Four types of causes of bronchiectasis with examples of each

A
  1. Congenital/hereditary conditions (e.g. CF, primary ciliary dyskinesia)
  2. Postinfectious conditions (e.g. TB, influenza, aspergillosis)
  3. Bronchial obstruction (e.g. due to tumour or FB)
  4. Other causes (e.g. RA, IBD, GVHD)
39
Q

What areas of the lung are predominantly affected in bronchiectasis?

A

Lower lobes
May be localised if due to obstruction, otherwise typically bilateral

40
Q

What is typically grown on sputum culture in bronchiectasis?

A

Mixed flora

ACEM Primary Written (150 decks)

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