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K12, Pa, Pathology of Copd - RTS1-K12
K12, Pa, Pathology of Copd - RTS1-K12
PATHOLOGY OF
CHRONIC
OBSTRUCTIVE
PULMONARY DISEASE
( COPD )
dr. Lidya Imelda Laksmi, M.Ked (PA), Sp.PA
dr. Causa Trisna Mariedina, M.Ked (PA), Sp.PA
Obstructive vs. Restrictive
•OBSTRUCTIVE:
Airflow obstruction with normal or hyper-expansion of lungs
COPD
RESTRICTIVE:
Reduced expansion of the lung (e.g. due to fibrosis or oedema)
Chest wall disorders
Acute or chronic interstitial & infiltrative diseases
Chronic bronchitis
Chronic bronchiolitis (small airways disease)
Emphysema
Asthma
Bronchiectasis
All characterized by airflow limitation, but involve different
mechanisms and parts of the respiratory tract.
Normal
Bronchial
mucus
gland
hyperplasia
Chronic
bronchitis
Acute on Chronic Bronchitis
Loss of airway ‘tapering’ in chronic bronchitis
Chronic Bronchitis
Clinical Features
Complications
PANACINAR
• Uniform injury Panacinar
• Lower lobes > upper emphysema
• Cause: 1-antitrypsin deficiency
PARASEPTAL
• Destruction of distal portion;
normal proximal portion of acinus
(septal / subpleural)
• Upper lobes > lower
• Incidental / Spontaneous
pneumothorax Alpha-1-AT
Neutrophils
Centriacinar Emphysema Paraseptal Emphysema
Paraseptal Emphysema
lung.
Intrinsic / Non-atopic
No exogenous factors identified
Extrinsic Asthma
Atopic (allergic) asthma is the most common form,
begins in childhood
Other allergic manifestation: allergic rhinitis,
urticaria, eczema.
Skin test with antigen result in an immediate
wheel and flare reaction
Other family member is also affected
Serum IgE and eosinophil are increased
immune related, TH2 subset of CD4+ T cells
Pathogenesis of Bronchial Asthma
EXAGGERATED BROCHOCONTRICTION
Two components:
1. Chronic airway inflammation.
2. Bronchial hyperresponsiveness.
The mechanisms have been best studied in
atopic asthma.
Pathogenesis of Atopic Asthma
A classic example of type 1 IgE-mediated
hypersensitivity reaction.
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).
Cytokines promote:
1. IgE production by B cell.
2. Growth of mast cells.
3. Growth and activation of
eosinophils.
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)
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).
Histologic 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.
Curschmann spirals
Caused by destruction
of muscle & elastic
tissue secondary to
recurrent inflammation
Gross examination:
Dilated bronchi exending to pleural surface (characteristic),
surrounding scarring
Microscopy:
Mucosal ulceration, submucosal CI & granulation tissue, adjacent
organising pneumonia
Bronchiectasis
Clinical:
• Fever
• Severe, persistent cough (foul sputum)
• Haemoptysis
• Recurrent infections
• Paroxysmal cough
Worse in morning due to drainage into bronchi of
collected pus
Bronchiectasis
Complications:
Depend on severity & co-existent disease