lec 4+5 Obstructive pulmonary disease Flashcards
Cause and results of Obstructive pulmonary disease:
Anatomic obstruction: Asthma
Loss of elastic recoil: emphysema
result:
-Normal or increased Total lung capacity (because of loss of elastic recoil)
- slightly Decreased **Forced vital capacity (max air you can breathe out)
-Forced expiratory volume (FEV1)** is decreased significantly
Emphysema is:
-permanent enlargment of air spaces distal to the terminal bronchioles in the acinus.
-Acinus : bronchiole, alveolar duct, alveolus
basically, destruction of acni wall but without fibrosis
Types of emphysema and their pathogenisis :
(simple)
Centriacinar
Panacinar
pathogenisis:
1) protease- Antiprotease imbalance
2) Oxidant- Antioxidant imbalance
what is Protease-antiprotease imbalance:
-Protease, elastase and oxidase from inflam cells damage elastic tissue and collagen
-a decrease in antiproteases can produce acini wall damage—-emphysema
can be genetic deficiency or smoking
1) Centriacinar emphysema
-involves proximal acinus
-more severe in upper lobes
-more in male smokers and chronic bronchitis patients.
-presence of bulla is common
2)panacinar emphysema:
-Involves entire acinus
-more severe in lower zones and bases
-more genetic: so a1 antitrypsin deficiency
3)Distal emphysema:
paraseptal
-involves pleural surface and connective tissue of septa
-more in upper lobe and subpleural
-adjacent to fibrosed area
-prescence of multiple bulla
very similar to centriacinar
4)Irregular emphysema
-common but asymptomatic.
-acinus is unlikely involved.
-associated with scarring of healed inflammation.
Conditions related to emphysema:
-enlargment of air spaces w/o destruction of walls
-bullous emphysema : any type with formation of subpleural air filled cysts
Morphology of emphysema:
Destruction of alveolar walls
collapse of adjacent spaces
diminished blood vessles in septa
later—- pulmonary hypertension
Clinical course of emphysema:
-decreased FEV1/FVC ration
-dyspnea is first symptom
-insidious then progressive dyspnea
-tachypnea and hyperventilation (pink puffer)
-Blue bloater (in chronic bronchitis)
-Decreased O2 level and increased CO2 level— cyanosis
Signs of chronic bronchitis:
on level of bronchi
-Productive cough for 3 months, for 2 years consistently
-simple chronic bronchitis—- mucoid sputum , but is not enough to obstruct airflow in early stage
Hypersecretion of mucus is a result of:
1) hypertrophy and hyperplasia of mucus glands
2) increase in goblet cells by metaplasia
3) recurrent infections
Reid index:
-measure of degree of chronic bronchitis
-Thickness of submucosal mucus secreting glands vs thickness between epithelium and cartialage.
<0.4 normally
Morphology of chronic bronchitis:
-Edematous congested mucus
-luminal thick mucus
Microscopic:
-non eosinophillic cell infiltrate
-squamous metaplasia and dysplasia
-inc in mucus glands, and goblet cells
PURE emphysema vs PURE bronchitis:
Bronchitis:
-inflammation and mucus hypersecretion in large airways
-airway obstruction in small airways
Emphysema: Acini wall damage and loss of elastic recoil
Blue bloater vs pink puffer:
Blue bloater (COPD):
* chronic cough
* purulent sputum
* hemoptysis
* cyanosis
* obesity
* secondary polycythemia vera
* hypercapnia
Pink puffer (emphysema):
* minimal cough
* hyperventilation and tachypnea
* cachexia
Bronchiectasis is:
chronic necrotizing inflammation of bronchi AND bronchioles with destruction of the muscle and elastic tissue in the wall.
-leads to PERMANENT enlargment of bronchioles
predisposing conditions of bronchiectasis:
1)Bronchial obstruction
-localized (F.B or tumor)
-generalized (asthma, bronchitis)
2)congenital
-cystic fibrosis
-Immunodeficiency
-kartagners syndrome
3)post necrotizing supparative inflammation
important
Pathogenisis of bronchiectasis:
-Obstruction of bronchus wall+ infection
-continous dialation and exudate accumilation
Asthma is :
A CHRONIC inflammatory process of wheezing (small airway obstruction during expiration)
chest tightness, cough early in the morning or at night
important
Morphology of bronchiectasis:
-more in lower lobes and bilateral
-occurs in distal bronchial tree
-wall shows:
acute and chronic inflam cells
squamous metaplasia of lining
fibrosis
Clinical picture of bronchiectasis:
VERYYYY SIMILAR TO CHRONIC BRONCHITIS
-chronic cough
-purulent sputum
-hemoptysis
-CLUBBING
-core pulmonale
Summary of bronchiectasis:
-irreversibly dialated thick walled bronchi
-honeycombing, tram-line, cystic, signet ring sign can all be seen in imaging
-the vicious cycle and p.aeuroginosa contributes to severity of disease
manifestations of asthma:
episodic attacks
widespread narrowing of airways
Type 1 asthma: allergic asthma
Atopy: largest risk factor for developing asthma
-Rhinitis, eczema, urticaria
-inc IgE
develops early
Clinical features of asthma occur because of:
-Repeated immediate hypersensitivity
-Late phase reactions in lung
these reactions give rise to:
1)intermittent and reversible airway obstruction
2)Chronic bronchial inflammation WITH eosinophils
3)Bronchial smooth muscle cell hypertrophy and hyperreactivity
chronic bronchitis is WITHOUT eosinophils
Type 2-Non atopic asthma
develops later
Normal IgE levels
no allergy history
-suspect is virus or pollutants
Pathogenisis in atopic asthma:
-type 1 hypersensitivity reaction
-linked to abnormalities of TH2 cytokines
-GENETIC PREDISPOSITION (ADAM33):
transmembrane protein implicated in bronchial hyperresponsiveness
mast cell and EOSINOPHIL activation
allergen activates TH2 cells
IL’s turn on IgE, eosinophils—- activate mast cells
bronchoconstriction
2)Protracted late phase: (4-8 hours later)
-antigen in submucosa: more mast cells and neutrophils
-mast cells— chemotactic factors for eosinophils and neutrophils (IL4,5,PAF,TNF)
Prognosis of asthma:
maturation of immune response against asthmatic response, so mortality is low
pathology of asthma:
1)edema, congestion— increase in eosinophils
2)mucus cell and smooth muscle hypertrophy any hyperplasia and goblet cells metaplasia
3)necrosis of surface epithelium
4)lumen of bronchi and bronchioles contain
a)charcot leyden crystals from eosinophil
b)curschmann’s spirals from epithelial necorsis
ways to diagnose asthmatic patient:
-lung function test
-blood gasses
-chest x ray
-skin test
