Please enable JavaScript.
Coggle requires JavaScript to display documents.
Obstructive Airways Diseases - Coggle Diagram
Obstructive Airways Diseases
Obstructive Airways Diseases
Chronic Obstructive Airways Disease COPD
Chronic Bronchiolitis
Affects the small airways and is an obstructive process
Microscopy
Bronchiolar goblet cell hyperplasia
Airways <2mm
Chronic inflammation - lumen reduced
Peribronchiolar fibrosis - lumen reduced
Cardiac effects
Hypoxia
Pulmonary vasoconstriction
Pulmonary hypertetion with Cor pulmonale (Right HF)
Compensatory Polycythaemia
Chronic Bronchitis
Affects larger airways and is a hypersecretory process
Presentation
BLUE BLOATER
Age: 40-45
Dysnpnoea: Early, copious sputum
Infx: Common
Resp insufficiency: Repeated
Cor pulmonal: Common
Airway resistance: Increased
Elastic recoil: Normal
CXR: Prominent vessels, large heart
Persistent or recurrent excess of secretion in the bronchial tree on most days for at least 3 months in the year, over 3 years
Normal secretions = 100ml / 24hrs
Epidemiology
Middle aged / elderly
M>F
Risk Factors
Cigarette smoke
Air pollution
Dust exposure
Smog
Pathology
Irritants initiate mucus secretion
Excessive sputum production cliically
Pathogens
Haemophilus influenza
Streptococcus pneumoniae
Major cause of death and morbidity
Microscopy
Enlargement of submucosal glands
Shift to pure mucous from mixed sero-mucinous glands
Increased numbers of goblet cells in epithelium
Less ciliated cells in epithelium (clearing airways)
Emphysema
Affects alveoli and is a destructive process
Presentation
PINK PUFFER
Age: 50-75
Dyspnoea: Late, scanty sputum
Infx: Occasional
Rep Insufficiency: Terminal
Cor pulmonal: Rare
Airway resistance: Normal or slightly increased
Elastic recoil: Low
CXR: Hyperinflation, small heart
Features
Abnormal permanent enlargement of airspaces distal to terminal bronchioles
Destruction of airspace walls without fibrosis
Airflow limitation due to premature closure of airways due to dimished elastic recoil
Loss of alveolar walls
Fewer alveolar attachment to bronchioles and preamture closure of these airways on expiration
Severe changes characterised by complete loss of most arspaces, leaving septa and blood vessels
Morphological Types
Centriacinar
Focal lesions confined to the centres of acini
Changes more marked in the upper lobes
Spaces > 1cm known as bullae
Associated with cigarrete smoking
Panacinar
Affects all zones or is worse in the lower zones
Associated with α1-AT deficiency
Paraseptal
Affects airspaces adjacent to septa or pleura
Particular large solitary bullae are apt to form
Prevent expansion of adjacent lung
Liable to rupture - pneumothorax
Pathogenesis
Cigarette smoking inhibition / Inherited deficiency of α1-AT
Imbalance of proteases and antiproteases in the lung
Alveolar wall degradation reduces elastic recoil of lungs
Permanent enlargement of airspaces
Proteases
Neutrophils and macrophages produce elastase
Elastase increased in infx / inflam
Smoking stimulates elastase reclease and enhances activioty
α1-antitrypsin deficiency
Mutations in the SERPINA1 gene chr14
Autosomal recessive
Encompasses 3 conditions: Chronic bronchitis / chronic bronchiolitis / emphysema
Frequently co-exist
Obstruction to air flow
Different mechanisms and parts of resp tree
Symtoms
Increasing shortness of breath
Exercise exacerbates
Nocturnal
Persisten chesty cough with phlegm that never goes away
Freuquent chest infx
Persistent wheezing
Investivations
Pulmonary Function Tests (PFTs)
Reduced FEV1
Limitation of max airflow rates during forced expiration
Asthma
Morphological features
Increased mucus production from goblet cell hypertrophy
Goblet cell hyperplasia
Inflammatory oedema
Infiltration by eosinophils
Thick mucous with eosinophil and charcot-lyden crystals
Bronchial smooth muscle hypertrophy + hyperplasia
Smooth muscle hyperplasia and eosinophils
Basement membrane thickening
Hyper reactive airways leading to episodic reversible bronchoconstriction, owing to increased responsiveness of the tracheobronchial tree to various stimuli
Symptoms
Dyspnoea
Coughing
Wheezing
Types
Extrinisic / Atopic / Allergic
Evidence of allergen sensitisation
Often in patients with allergic rhinitis / eczema
Increased generation of IgE induced by exposure / response to external allergens
Epidemiology
More common
Chi;dhood
M>F
Less severe with age
30% still symptomatic adults
Associated with eczema + rhinitis
Type I (IgE-mediated) Hypersensitivity reaction
Pathogenesis
Antigen sensitisation
IgE production by B-cells (interleukin mediated)
Submucosal mast cells coated in IgE - primed to release granules
Subsequent exposure
Antigen bins to IgE - stimulates mast cell activation
Release of mediators from mast cells
Primary: histamine, chemotactic factors, enzymes
Secondary : leukotrienes, protaglandins, platelet AF
Early phase reaction
Bronchoconstriction - direct stim of subepithelial parasympathetic nerves
Increased mucus production
Vasodilation with increased vascular permeability
Late phase reaction
Inflammation - recruitment of eosinophils, neutrophils, more T cells
Non-Atopic
No evidence of allergen sensitisation
Epidemiology
Adult onset
Chronic worsens with age
Triggered by respiratory tract infx - viral
Family hx uncommon
Serum IgE normal
Viral -induced inflammation may lower threshold of vagal receptors to irritants
Epidemiology
Common in childhood
Genetic
Atopic triad: Eczema, hayevere, asthma
Adult onset after resp tract infection
Possible Rise in asthma due to modern housing, diet, cleanliness
Non-infectious
Increased risk for exposed fetus / child to cigarette smoke
Increased risk when overweight
Chronic disease, may decrease over time
Smoking - Associated Interstitial lung disease
Respiratory Bronchiolitis
Clinical Presentation
Cough
Dyspnoae
Restrictive PFTs
Epidemiology
M>F
40-50
Heavy cigarette smoking
Response to smoking cessation and steroids
Imaging
Patchy upper and lower lobe infiltrates
Microscopy
Accumulation of macrophages containing yellow-brown pigment / smokers macrophages in lumens of distal bronchioles and adjacent alveolar spaces
Mild interstitial thickening
Dequamative Interstitial Pneumonia (DIP)
Similar clinical Presentation to RB-ILD
MOre extensive filling of alveolar spaces by golden brown macrophages
RB-ILD and DIP represent different ends of the spectrum of one disease
Langerhans Cell Histiocytosis LCH
AKA Histocytosis X (HX)
Monoclonal proliferations of immature dendritis cells
Microscopy
Histocytes with clear nuclei with grooves
Abundant vacuolated cytoplasm
Express CD1a and S100 protein
Tennis raket like structures "birbeck granules" on EM
Clinical Syndromes
Lettere-Siwe Disease
Multifocal multisystem LCH
Infants <2
Skin and lung lesions, lymphadenopathy, destructive bone lesions
Eosinophilic granuloma
Unifocal or mutlifocal
Involves bones, skin, lungs, stomach
Often spontaeously regresses
Bone tumour
Pulmonary LCH
Clinical
Smokers
Cough, dysnpnoa, fever, malaise, spontaneous pneumothorax
Imaging
Cysts an nodulesin the upper lobes
Pathology
Discrete stellate nodules centred on bronchioles
Nodules composed of
Langerhan's cells
Eosinophils
Nodules degenerate over time into stellate scars
