ASTHMA AND COPD obstructive lung disease chronic respiratory disease

1. SMS2053

2. Overview
What is COPD?
How do I know if I have COPD?
How common is it?
– General population
– Mining population
What increases my risk of developing
COPD?
How can I prevent getting COPD?
How is COPD treated?

3. What is COPD?
A set of lung diseases that limit air flow
and is not fully reversible.
– COPD patients report they are “hungry” for
air
– Usually progressive and is associated with
inflammation of the lungs as they respond
to noxious particles or gases
– Potentially preventable with proper
precautions and avoidance of precipitating
factors
– Symptomatic treatment is available

4. Two Major Causes of COPD
 Chronic Bronchitis is characterized by
– Chronic inflammation and excess mucus
production
– Presence of chronic productive cough
 Emphysema is characterized by
– Damage to the small, sac-like units of the
lung that deliver oxygen into the lung and
remove the carbon dioxide
– Chronic cough

5. What can cause COPD?
Smoking is the primary risk factor
– Long-term smoking is responsible for 80-90 % of
cases
 Prolonged exposures to harmful particles and
gases from:
– Industrial smoke,
– Chemical gases, vapors, mists & fumes
– Dusts from grains, minerals & other
materials

6. Other Risk Factors for COPD
History of childhood respiratory infections
Genetic makeup
Increasing age

7. Pathogenesis of Chronic Bronchitis and
Emphysema

8. Pathophysiology

9. Emphysema
Pathology (Histology)
– Hyperinflation of alveoli
– Destruction of alveolar walls
– Destruction of alveolar capillary walls
– Narrowed airways
– Loss of lung elasticity
– Small bronchioles become obstructed as a result of
• Mucus
• Smooth muscle spasm
• Inflammatory process
• Collapse of bronchiolar walls

10. Emphysema
 Emphysema is an enlargement of air
spaces caused by destruction of alveolar
walls.
 Air spaces greater than one cm are
bullae.
 This photo shows apical bullous
disease with relatively little involvement
of the rest of the lung.

11. Chronic Bronchitis
Pathology (Histology)
 Pathologic lung changes are:
 Hyperplasia of mucus-secreting glands in trachea and
bronchi
 Increase in goblet cells
 Disappearance of cilia
 Chronic inflammatory changes and narrowing of small
airways
 Hyperplasia of mucus glands
 Inflammatory swelling
 Excess, thick mucus
 Altered of alveolar macrophages infections

12. Normal versus Diseased Bronchi

13. Chronic Bronchitis
Chronic bronchitis:
Scarring or fibrosis of the walls of
the bronchioles causing narrowing of
the airway
Production of excessive quantities
of thick mucus which further plugs
the tubules and compromises
breathing

14. Primary Symptoms
 Chronic Bronchitis
– Chronic cough
– Shortness of breath
– Increased mucus
– Frequent clearing of throat
 Emphysema
– Chronic cough
– Shortness of breath
– Limited activity level
Death from emphysema is related to:
1. Pulmonary failure with respiratory acidosis, hypoxia and coma.
2. Right-sided heart failure.

15. Difference between COPD and Asthma
 In COPD there is permanent damage to the airways.
The narrowed airways are fixed, and so symptoms are
chronic (persistent). Treatment to open up the airways,
is therefore limited.
 In asthma there is inflammation in the airways which
makes the muscles in the airways constrict.
 This causes the airways to narrow. The symptoms
tend to come and go, and vary in severity from time to
time.
 Treatment to reduce inflammation and to open up the
airways usually works well.
 COPD is more likely than asthma to cause a chronic
(ongoing) cough with sputum.

16. Difference between COPD and asthma (cont…)
 Night time waking with breathlessness or
wheeze is common in asthma and uncommon
in COPD.
 COPD is rare before the age of 35 whilst
asthma is common in under-35.

17. COPD
Diagnostic tests
Symptoms
Physical examination
Sample of sputum
Chest x-ray
High-resolution CT (HRCT scan)
Pulmonary function test (spirometery)
Arterial blood gases test
Pulse oximeter

18. Ways to prevent or slow the
progression of COPD
 Stop smoking, if you smoke, to prevent
further damage to your body
– Smoking cessation is critical for all severities of
COPD
 Avoid or protect yourself from exposures to
– Second-hand smoke
and
– Other substances such as chemical
vapors, fumes, mists, dusts, and diesel
exhaust fumes that irritate your lungs

19. How is COPD Treated?
 COPD can be managed, but not cured
 Treatment is different for each individual and
is based on severity of the symptoms
 Early diagnosis and treatment can
– Slow progress of the disease
– Relieve symptoms
– Improve an individual’s ability to stay active
– Prevent and treat complications
– Improve quality of life

20. When should you see your doctor?
 If smoker, see doctor for baseline evaluation of your
lungs
 When first experiencing shortness of breath or having
other lung symptoms
 When your symptoms get worse
 Seek emergency medical treatment if:
 Breathing suddenly becomes more difficult
 If diagnosed with chronic bronchitis, emphysema or
COPD, see doctor 1-2 times yearly to review your
treatment plan

21. What medications are used to
treat symptoms?
Short-acting bronchodilator inhalers
 such as salbutamol and terbutaline
Long-acting bronchodilator inhalers
 such as salmeterol (Seretide), formoterol (flutiform)
Bronchodilators – Theophylline tablets
 Relaxes muscles around airways
Oxygen therapy
 Helps with shortness of breath

22. long-acting β2 agonist and inhaled corticosteroid

23. Chronic Obstructive Pulmonary
Diseases
Bronchial asthma
Chronic relapsing inflammatory disorder
characterized by hyperactive airways leading to
episodic, reversible bronchoconstriction owing to
increased responsiveness of the tracheobronchial
tree to various stimuli.
It has been divided into two basic types:
1. Extrinsic asthma.
2. Intrinsic asthma.

24. Extrinsic Asthma
Initiated by type 1
hypersensivity reaction induced
by exposure to extrinsic
antigen like food, pollen, dust,
etc.
Subtypes include:
a. atopic (allergic) asthma.
b. occupational asthma.
c. allergic bronchopulmonary
aspergillosis.
Develop early in life
Intrinsic Asthma
• Initiated by diverse,
non-immune mechanisms,
including ingestion of
aspirin, pulmonary
infections, cold, inhaled
irritant, stress and exercise.
• No personal or family
history of allergic reaction.
• Develop later in life
CLASSIFICATION OF ASTHMA

27. **Some Potential Asthma Triggers**
Allergens — Pollen, pet dander, fungi, dust mites
Cold air
Fragrances and chemicals
Food and drinks
Pollutants
Cigarette smoke
Strong emotions
Exercise
Respiratory tract infections
Bronchial asthma

28. Extrinsic Asthma
Atopic (allergic) asthma is the most common form,
begins in childhood
Other allergic manifestation: allergic rhinitis, urticaria,
eczema.
Other family member is also affected

29. Pathogenesis of Bronchial Asthma
Exaggerated Bronchoconstriction
Two components:
1. Chronic airway inflammation.
2. Bronchial hyperresponsiveness.
The mechanisms have been best studied in atopic
asthma.

30. Pathogenesis

31. Pathogenesis of Atopic Asthma
• IgE-mediated reaction to inhaled allergens elicits:
1. acute response (within minutes)
2. a late phase reaction (after 4-8 hours)
In the airway – initial sensitization to antigen
(allergen) with stimulation of TH2 type T cells and
production of cytokines (IL-4, IL- 5, and IL-13).

32. Pathogenesis of Atopic Asthma
Acute-phase response
Begin 30 to 60 minutes after inhalation of antigen.
Mast cells on the mucosal surface are activated.
Mediator produced are :
 Leukotrienes C4, D4 & E4 (induce bronchospasm, vascular permeability &
mucous production)
 Prostaglandins D2, E2, F2 (induce bronchospasm and vasodilatation)
 Histamine ( induce bronchospasm and increased vascular permeability)
 Platelet-activating factor (cause agggregation of platlets and release of
histamine)
 Mast cell tryptase (inactvate normal bronchodilator).
Mediators induce bronchospasm, vascular
permeability & mucous production.

33. Pathogenesis of Atopic Asthma
 Late phase reaction:
Recruitment of leukocytes mediated by product of mast
cells including:
1. Eosinophil and neutophil chemotactic factors
2 . IL-4 & IL-5 and induceTH2 subset ofCD4+ T cells
3. Platelet-activating factor
4. Tumor necrosis factor.
Other cell types are involved: activated epithelial cells,
macrophages and smooth muscle.

34. Pathogenesis of Atopic Asthma
Late phase reaction:
The arrival of leukocytes at the site of mast cell
degranulation lead to:
1. Release of more mediators to activate more mast
cells
2. Cause epithelial cell damage .
Eosinophils produce major basic protein, eosinophilic
cationic protein and eosinophil peroxidase ( toxic to
epithelial cells).
These amplify and sustains injury without additional
antigen.

36. Non-Atopic Asthma
Triggered by respiratory tract infection including
viruses and inhaled air pollutants e.g. sulfur dioxide,
ozone.
Positive family history is uncommon.
Serum IgE – normal.
No other associated allergies.
Skin test – negative.
Hyperirritability of bronchial tree.
Subtypes:
1. Drug-induced asthma.
2. Occupational asthma.

37. Morphology of Asthma
Grossly: - Lung over distended
(over inflation), occlusion of bronchi
and bronchioles by thick mucous.
Histological finding:
 mucous contain Curschmann
spirals, eosinophil and Charcot-
Leyden crystals.
Thick BM.
Edema and inflammatory
infiltrate in bronchial wall.
Submucosal glands increased.
Hypertrophy of the bronchial
wall muscle.

38. Normal
Asthma patient
Epithelial remodeling
Apoptosis

39. Curschmann spirals
Coiled, basophilic plugs of mucus formed in the lower
airways and found in sputum and tracheal washings

40. Clinical signs
Classic asthmatic attack –
Dyspnea, Persistent/recurrent cough
Wheezing
Chest tightness
Difficult expiration, progressive hyperinflation of lung and
mucous plug in bronchi.
Status asthmaticus – severe cyanosis and persistent
dyspnea, may be fatal.
May progress to emphysema.

41. 41
Diagnosis
Spirometry
Breathing test which measures the amount and rate at which air
can pass through the airways
Bronchodilator Reversibility Testing
Relaxing tightened muscles around the airways and opening up
airways quickly to ease breathing
Other pulmonary function testing
Diffusion capacity
Chest X-ray
Arterial Blood Gas
Shows oxygen level in blood

42. 42
Asthma Medications: Bronchodilators
β2-adrenergic agonists
Rapid onset: quick relief of bronchoconstriction
Acts in minutes, lasts 4 to 8 hours
Treatment of choice for acute attacks
If used too much causes tremors, anxiety, tachycardia, palpitations,
nausea
Short-acting
 Albuterol(Proventil, Ventolin); metaproterenol (alupent); bitolterol
(tornalate)
Continuous β-adrenergic agonist nebulizer therapy may be given
Bronchodilators : Theophylline (relaxing bronchial
smooth muscle, anti-inflammatory effects)

43. Asthma
Drug Therapy
Antiinflammatory drugs
Corticosteroids (e.g., beclomethasone, budesonide)
 Suppress inflammatory response
 Inhaled form is used in long-term control
 Systemic form to control exacerbations and manage
persistent asthma

44. Emphysema: Dilated air spaces beyond respiratory
arteriols

45. Chronic Bronchitis: Persistent productive cough for at least 3
consecutive months in at least 2
consecutive years, smoking related

46. Asthma: Dyspnea and wheezing

47. Case Study
 A 64 year old gentleman presents to emergency
department with shortness of breath, cyanosed lips and
cough productive of thick, green sputum. He has a past
medical history of asthma as well he has smoked 20
cigarettes a day for the past 40 years. Physical examination
showed heart rate 144, respiratory rate 40, PaO2/Fio2=.21.
.O/E he is using his accessory muscles to breathe,
bilateral diffuse coarse crepitations and widespread
wheeze.
 Identify the diagnosis of the disease and describe the pathogenesis
of both condition.
 Describe the pathological changes in lung section.
 Describe the treatment options for the patient.