Pathology Of Small Airway Diseases

Front 1

define small airways

Back 1

<2 mm diameter:
~ terminal bronchiole, resp. bronchiole, alveolar duct and alveoli

Front 2

compare and contrast asthma and COPD (5)

Back 2

1. Similar functional effects: diffuse small airway narrowing
2. common symptoms, physical findings and acute complications
3. asthma - allergy, COPD - cigarette smoking
4. asthma - acute attacks, COPD - chronic progressive
5. asthma - reversible, COPD - nonreversible

Front 3

Define asthma

Back 3

paroxysmal (sudden recurrence or attack) narrowing of airways that reverses spontaneously or with treatment

Front 4

what is extrinsic asthma? (3)

Back 4

1. allergic conditions in family or patient
2. triggered by common environmental allergens
3. childhood onset

Front 5

what are the patient characteristics (4)

Back 5

1. young
2. SOB
3. 'attacks'
4. mistaken for allergy

Front 6

what type of HS is extrinsic asthma?

Back 6

Type I (raised IgE level against common environmental antigens)

Front 7

give examples of common environmental Ag that raises IgE in asthma (7)

Back 7

1. house dust mite (indoor) ****
2. pollens (outdoor) ~ not that common
3. cats and dogs
4. indoor air pollution (cigarette smoke)
5. occupational agents
6. air pollution aggravates asthma
7. infection aggravates asthma

Front 8

describe PG of asthma (5 features)
2. (3)
3. (3)

Back 8

1. allergen binds to IgE on mast cells

2. mast cells degranulate (histamine, LT, eosinophil chemotactic factor

3a. Mucus hypersecretion
3b. bronchoconstriction (SM contraction)
3c. oedema

Front 9

effects of Type I HS reaction (5)

Back 9

increased airway resistance - small airway obstruction

1. smooth muscle contraction (bronchospasm)
2. vascular dilatation (congestion)
3. oedema of airways
4. inflammatory cell infiltration
5. mucus production

Front 10

what is intrinsic asthma
a) etiology
b) patient presentation
c) reversibility

Back 10

non-atopic (non-allergic) asthma
a) unknown (aspirin, exercise, cold, viral infection, air pollution, stress)
b) hyper-irritable or sensitive airways
c) not as definite as extrinsic asthma

Front 11

what is the prognosis of asthma? (2)

Back 11

~ well-controled extrinsic asthma subsides in adolescence
~ intrinsic asthma doesn't show as dramatic improvement

Front 12

what is COPD?

Back 12

obstructive lung disease characterised by chronically poor airflow.
major, increasing global health problem

Front 13

Aetiology of COPD (4)

Back 13

1. tobacco (80-95%)
2. occupational (coal mining, cadmium, isocyanates, welding)
3. air pollution (SO2, NO, soot) co-factor, increasing risk and duration of hospital state
4. genetics (susceptibility factors) ~50% chronic smokers develop COPD

Front 14

what is the pathogenesis of tobacco-induced COPD? (7)

Back 14

1. smoking (+ contribution from pack-years, genetics)
2. ROS, chemo-attractants, inflammatory mediators (esp NFkB)
3. stimulate neutrophils, activated macrophages, lymphocytes

4a. induce mucus secretion (oedema, inflam exudate, mucosal thickening)
4b. chronic inflamm (attract more inflam cells and release inflammatory mediators)
4c. peribronchiolar fibrosis (bronchiolar epi. repair)
4d. proteolytic enzymes (e.g. MMP, elastase)

Front 15

what are the 3 pathological components of COPD?

Back 15

1. increase mucus of bronchi and bronchioles
2. chronic inflammation, obstruction of small airways
3. emphysema of alveolar tissue

Front 16

what is used to measure mucus production?

Back 16

Reid index (mucus glands/mucosa thickness)

Front 17

in histological specimen, what is seen in COPD? [4]

Back 17

1. increased thickness of mucus gland layer in bronchial mucosa
2. inflammation
3. mucus plug
4. fibrosis

Front 18

what contributes to mucus plugging and chronic inflammation? (3)

Back 18

1. goblet cell hyperplasia

2. mucous gland hyperplasia

3. increased inflammatory cells

Front 19

what contributes to increased mucus?

Back 19

1. impaired ciliary clearance in smokers
2. mucus plugs in bronchi & bronchioles
3. cough & mucoid sputum -> lung infection

Front 20

describe chronic inflammation of small airways. [3]

Back 20

1. cigarette smoke or irritant gas causes chemotaxis of inflammatory cells (LMN) to bronchial & bronchiolar wall

2. chronic inflammation (mucosal oedema, SM spasm, epithelial damage) to attract more inflamm cells. [vicious cycle]

3. Long term~ irreversible, slowly progressive fibrosis, narrowing and obstruction of small airways

Front 21

what is emphysema (2)

Back 21

1. destruction of airspace and alveolar wall
2. abnormal enlargement of airspaces beyond terminal bronchioles.

Front 22

what is the mechanism of emphysema?

Back 22

1. decrease in anti-protease and anti-oxidant
(smoking, hereditary anti-trypsin deficiency)

2. increase protease and oxidants
(smoking)

Front 23

how does smoking increase protease and oxidative damage (3)

Back 23

1. increases PMN, macrophages, reactive O2 radicles
2. increase proteolysis from PMN, macrophages
3. Loss of lung tissue [apoptosis of alveolar tissue cells, degradation of ECM]

Front 24

how does smoking decrease anti-protease activity?

Back 24

1. smoking inhibits alpha-1 antitrypsin

2. alternatively, hereditary alpha-1 antitrypsin deficiency

Front 25

how are alveolar walls affected in emphysema?

Back 25

1. loss of alveolar septa and capillaries

2. enlarged air spaces

Front 26

describe small airways obstruction in emphysema (6)

Back 26

1. loss of elastic recoil of alveoli

2. loss of radial traction on respiratory bronchioles

3. early small airway closure during expiration, impaired expiration & obstruction

4. incomplete emptying of alveoli

5. expanded, voluminous lung (air trapping)

6. pale, soft lung, pits on pressure due to decrease in elasticity

Front 27

what is centrilobular (centriacinar) emphysema?

Back 27

involves alveoli at centre of lobules; advanced cases becomes panacinar (related to smoking)

Front 28

what is panacinar (panlobular) emphysema?

Back 28

involves all air spaces
usually seen in alpha-1 antitrypsin deficiency and smoking (advanced changes)

Front 29

what is the disease course of COPD? (2)
1. initial
2. Chronic

Back 29

1. initially: cough with mucoid sputum

2. chronic bronchitis ~ chronic productive cough w. mucoid sputum at least 3 months per yr, 2 consecutive years, in absence of other lung diseases
~CB and emphysema may co-exist to various extent

Front 30

COPD prognosis
(3)

Back 30

not fully reversible;
individuals may have different degrees of the 3 pathological components;
usually progressive not not completely stopped by smoking cessation

Front 31

genetics in COPD

Back 31

genetic susceptibility factors play role: not all smokers have COPD

Front 32

aggravating factors of COPD

Back 32

1. COPD is an abnormal inflammatory response and bronchospasm to noxious particles and gas

2. acute exacerbations induced by:
Upper RT/bronchial infection/air pollution/irritant gas/dusts

Front 33

Pathophysiological effects of COPD (concerning Lung function)
(4)

Back 33

1. reduced tidal volume
2. increased residual lung volume
3. reduced flow rate in spirometry
4. FEV1/FVC <70%

Front 34

symptoms and signs of small airway obstruction

Back 34

1. expiratory wheeze (narrowed airways cause turbulent airflow)

2. prolonged expiration (expiratory airflow obstruction)
*more noticeable because intercostal muscles and diaphragm relax to reduce volume of thoracic cavity during expiration (which is a passive process usually dependent on elastic recoil of lung)

Front 35

effects of small airway obstruction (2)

Back 35

1. AIR TRAPPING in lungs
2. hyperinflated, 'blown-up' lungs

Front 36

complications of severe asthma and acute COPD exacerbation (3)

Back 36

1. pneumothorax (excessive air-trapping, leakage from weak spots of pleura)

2. pneumonia: superimposed bacterial infection

3. Acute RF (ventilatory failure)

Front 37

long term complications of COPD (4)

Back 37

1. chronic persistent hypoxia
2. pulmonary HT (alveolar hypoxia - pulmonary arterial narrowing)
3. cor pulmonale (right heart failure - high pulmonary BP)
4. increased RBC (polycythaemia, increased viscosity to compensate for decrease PaO2)