Pathology of Asthma and COPD Flashcards
(32 cards)
1
Q
What is COPD?
A
- Chronic Obstructive Pulmonary Disease
- Umbrella term for:
- -> Emphysema (pink puffer)
- -> Chronic bronchitis (blue bloater)
2
Q
What is the shared aetiology for COPD?
A
- Cigarette smoking
- Marijuana smoke
- Atmospheric pollution
- Occupation dust exposure (e.g. factory work)
3
Q
How is spirometry used to show COPD?
A
- Monitoring lung function
- Lung function test
- How much air the patient can quickly expire
4
Q
How is an obstructive disease shown in spirometry?
A
- Amount of air in is normal
- Pathological expiration
5
Q
How is a restrictive disease shown in spirometry?
A
- Air breathed in is pathological
6
Q
What are the clinical syndromes of emphysema?
A
- Pink puffer
- Rapid, shallow breathing
- Thin
- Subjectively breathless
- Active effort used to maintain normal blood gases
- Often low BMI
- Not associated with lung infections- not hyper inflammatory
- Exercise intolerance
7
Q
What are the clinical syndromes of chronic bronchitis?
A
- Blue bloater
- Productive cough to produce sputum (clear, white or purulent)
- Obese and oedematous
- Hypoxic
- Polycythaemia
- Congestive cardiac failure
- Exercise intolerance
- Insufficiency respiratory drive (hypoxia and carbon dioxide retention)- leading to cyanosis
- Predisposition to infection
8
Q
What complications are involved with COPD?
A
- Bronchopneumonia (comorbidities mean that they may not make a full recovery)
- Cardiac failure (respiratory failure), right sided failure
- Pulmonary thromboembolism
- Increased risk of lung cancer
9
Q
Describe the epidemiology of COPD?
A
- Major worldwide cause of mobility and mortality due to respiratory insufficiency
- Current/former smokers
- 35 year+ onset
- Gender distribution matches that of smoking
10
Q
What is emphysema?
A
- Destructive process involving alveoli
- Lung-abnormal increase of air spaces (abnormally dilated)
- Space greater than 1cm = bulla
- Pathological inflation of affected tissue
11
Q
How does air trapping occur in emphysema?
A
- Air flow limitation due to atrophy/expiratory collapse of airways with decreased elastic recoil and less alveolar attachments
- Barrel chest phenotype and hyperinflation
- Reduced alveolar SA for GE- pathological enlargement of each alveolus
- May be associated with small airway disease, with inflammation and narrowing of bronchioles
12
Q
What are the morphological changes that occur due to smoke?
A
- Normal acinus contains respiratory bronchiole and alveolar ducts/alveoli
- Smoke particles deposited into respiratory bronchiole
- Centrilobular emphysema- alveoli surrounding bronchi dilated
- Panacinar emphysema- all alveoli enlarged
13
Q
What is the aetiology of emphysema
A
- Centracinar- cigarette smoking
- Primary panacinar- may also be due to genetic α-1-antitrypsin deficiency
14
Q
What happens with a genetic α-1-antitrypsin deficiency?
A
- May lead to early-onset emphysema
- Unopposed action leukocyte elastase on lung connective tissue (elastase breaks down elastin)
- too much breakdown results in loss of elastic recoil
- Autosomal recessive inheritance
- Association with hepatitis and cirrhosis
15
Q
How does cigarette smoking lead to emphysema?
A
- Activates alveolar macrophages
- Increased macrophages release proteolytic enzymes
- Neutrophil chemotactic factors
- Free radicals
- Reactive oxygen species
16
Q
What is the protease/anti-protease hypothesis?
A
- Protease causes damage to lung tissue, inflammatory response in response
- May also cause inhibition through free radicals
17
Q
What is chronic bronchitis?
A
- Hypersecretory process involving conducting airways
- Airflow limitation due to inflammation of wall and intermittent mucous plugging
- Persistent/ recurrent excess of bronchial secretion on most days for at least 3 moths in the year, over at least 2 years
18
Q
What is the pathogenesis of chronic bronchitis?
A
- Directly actin irritants cause mucus hypersecretion
- Neural reflexes activated by sensory nerve endings in airways further promote this effect
- Up-regulation of mucin genes and epidermal growth factor
- Increase in acidic muffins, leading to more viscous and thick sputum
19
Q
What does bronchial asthma?
A
- Inflammatory condition of airways associated with bronchial hyperresponsivess with reversible airways obstruction
- Affects 5% of population
- Prevalence is increasing
- Manageable condition with inhalers but it can also be fatal
20
Q
What is bronchoconstriction in bronchial asthma?
A
- Narrowed passages conducting air from trachea to alveoli
21
Q
What does episodic mean in bronchial asthma?
A
- No symptoms between attacks (normal lung function)
22
Q
What does reversible mean in bronchial asthma?
A
- Bronchoconstriction can be reversed with appropriate treatment
23
Q
What is the aetiology of bronchial asthma?
A
- Inhaled substance (e.g. pollen, animal dander, house dust, food, drugs etc.)
- Exacerbating factos of asthma:
- -> Lung infections
- -> Exercise
- -> Emotional stress
- -> Cold air
24
Q
What is the relationship between bronchial asthma and IgE?
A
- Low conc in plasma, bound to receptor on mast cell and basophil leukocyte membranes
- Synthesis depends on genetic background, cytokine milieu, nature and timing of allergen exposure
- Cross-linkage of receptors by allergen causes mast cell degranulaiton
25
Describe the effects of type 1 hypersensitivity in asthma
- Presented by dendritic cells to Th2 cells (which promote IgE production)
- Stimulated specific receptors on B cells, which become plasma cells secreting IgE specific for allergen
26
What does subsequent exposure cause?
- Mast cell degranulation
- Antigen presented to Th2 cells by dendritic cells
- Release of cytokines to activate B cells
- B cells differentiate to plasma cells and produce IgE
- IgE attaches to mast cells causing degranulation
27
What acute changes occur to the bronchi in asthma?
- Mast cell degranulation via IgE (release of granule-derived mediators, leukotriene C4, prostaglandin D2 and cytokines)
- T cell activation (Th2)
- Cytokine release
- Eosinophil leukocyte recruitment
- Epithelial cell damage
28
What chronic changes occur to the bronchi in asthma?
- Epithelial damage
- Thickening of airway wall
- Increased vascularity
- Smooth muscle hypertrophy and hyperplasia
- Mucus gland hyperplasia
29
What are the causes of airway obstruction in asthma?
- Smooth muscle contraction
- Vascular congestion
- Oedema of airway wall
- Mucus secretion
- Epithelial damage
30
What is the pathogenesis of asthma?
- Increase contraction of smooth muscle in airways
- Increased mucus production
- Increased vascular permeability (collection of oedema fluid)
31
What happens to smooth muscle in asthma?
- Hyperplastic or hypertrophic
- Enlarged
- Increased contraction
32
What happens to mucous glands in asthma?
- Hyperplasia
| - Increased mucous production
