Resp Week 7 Flashcards
Provide a brief comparison between restrictive and and obstructive lung disease
RLD = reduction in volume due to pathology in lungs/pleura/structures of thoracic cage
W/a
OLD = airway obstruction resulting in lung volume being normal or high due to overinflation
What are 5 broad causes of restrictive lung disease
Pleural pathologies
Alveolar pathologies
Interstitial pathologies
Neuromuscular pathologies
Thoracic cage abnormality pathologies
Outline interstitial lung disease
Arises from conditions affecting the lung parenchyma such as pulmonary fibrosis which causes scarring and stiffening of lung tissue
Outline extrapulmonary restrictive lung disease
Occurs due to factors outside the lungs that limit lung expansion, such as obesity, neuromuscular disorders or chest wall deformities
What are 3 types of intrinsic restrictive lung disease
Interstitial lung disease
Alveolar conditions
Diffuse cellular infiltrates
What are 3 types of extrinsic restrictive lung disease
Low respiratory muscle tone
Chest wall deformities
Space occupying
What are 4 symptoms of RLD and provide a brief outline of their pathophysiology
Dyspnea - reduced lung compliance > increased work of breathing > SOB
Cough - increased interstitial lung tissue stiffness triggers cough reflex
Malaise - chronic hypoxia + decreased lung function > systemic fatigue and general discomfort
Muscle weakness - prolonged hypoxia + respiratory muscle overuse > decrease muscle strength
What are 5 findings in a physical exam for RLD and provide a brief outline of the pathophysiology of them
Reduced chest expansion - stiffened lung parenchyma restricts thoracic mvmt
Tachypnea - increased RR compensates for reduced lung volume
Decreased breath sounds - reduced lung volumes reduce airflow > quieter breaths
Inspiratory crackles - alveolar + interstitial fibrosis > popping sounds during inspiration due to sudden opening of collapsed airways
Cyanosis - inadequate oxygenation of skin and mucous membranes
Explain the effect RLD on ventilation and perfusion
RLD leads to impaired ventilation which results in reduced lung capacity and TV, limiting the amount of air that can be inhaled per breath
The thickening of alveolar capillary membrane in RLD hinders efficient gas exchange, which causes hypoxaemia
Despite these ventilation issues, perfusion in the lungs may remain relatively unaffected or even increase as pulmonary blood flow continues
Outline ventilation-perfusion mismatch in RLD
Lead to areas of lung receiving less O2 than they should, resulting in hypoxaemia
Alveolar hypoxia may cause vasoconstriction in pulmonary arterioles, diverting blood away from poorly ventilated areas
Over time chronic hypoxaemia can lead to pulmonary HTN and RH strain due to increased resistance in pulmonary circulation
What are 5 classifications of interstitial lung disease
Inorganic exposure - caused by exposure to non-organic substances e.g asbestos
Organic exposure - exposure to organic materials e.g mould
Smoking - inhalation of toxins from tobacco smoke
Rare forms of ILD - uncommon types from unique causes
Idiopathic - unknown cause
What are 3 types of occupational lung diseases
Asbestosis - caused by inhalation of asbestos fibres resulting in lung scarring and impaired respiratory fn
Mesothelioma - rare + aggressive cancer that primarily affects the lining the lungs, abdomen, or heart (strongly associated with asbestos exposure)
Pleural disease - conditions affect pleura e.g pleuritis, pleural effusions, pleural plaques
Outline results of pulmonary function tests in RLD
Low FVC
Reduced TLC
FEV1/FVC ratio will be increased or normal
Diffusing capacity is also reduced
ABG - hypoxia
What are 3 investigations that can be undertaken for RLD
CXR
Spirometry
ABG
What are 5 Rx options for RLD
Minimise exposure if known aetiology
Steroids
Lung transplant
Pulmonary rehab
Education
What are 5 layers of defence in the respiratory system against infection
Mucous layer - traps pathogens
Epithelium - has goblet cells
Lamina propria - has immune cells
Type 1 pneumocytes - physical barrier b.w lung + airway
Type 2 pnemocytes - secrete surfactant
What are 3 harmful substances to the lung and provide a brief description of each
Microbes - bacteria, parasites etc
DAMPs - released from damaged cells > stress
Foreign bodies - trigger hypersensitivity reactions
What are 3 causes of compromised immunity and provide a brief description of each
Defective mucous - inability for lung to trap pathogens
Dysfunctional cilia - e.g caused by smoking
Immune cell defects - e.g impaired action of T lymphocytes
What are 7 causes of lung inflammation and provide an example of each
Infection e.g pneumonia caused by strep agents
Pollutants e.g smog
Allergens e.g pollen
Foreign bodies e.g aspiration of small objects
Autoimmune e.g ILD associated w rheumatoid arthritis
Occupational e.g chronic bronchitis from long term exposure to coal dust
Lifestyle e.g lung diseases caused by chronic smoking
Describe the process of acute pulmonary inflammation
Step 1 - immune cells detect pathogens through PRRs and TLRs and NLRs
Step 2 - macrophages, ILCs and dendritic cells recognise PAMPs and DAMPs through their PRRs > triggers activation of these cells > release cytokines e.g IL-6 and TNF and IL-10 and TGF- beta > vasodilation
Step 3 - dendritic cells and B cells present pathogen fragments to T cells > activate them > CD8+ cells directly kill infected cells and CD4+ cells act as helper cells for B cells releasing IgG antibodies
Step 4 - macrophages remove intra-alveolar debris / lymphatic system resorbs extravascular fluid / macrophages release TGF-beta which stimulates fibroblast proliferation and collagen deposition leading to fibrosis of alveolar walls > fibrotic tissues helps stabilise damaged area but can also affect normal lung function / type 2 pneumocytes proliferate to replace damaged type 1 pneumocytes and facilitate restoration of alveolar lining
Describe the process of chronic pulmonary inflammation
TLRs on immune cells detect patterns shared by pathogens which leads to activation of inflammatory cells
Then, this activation triggers NF-kappa B signalling pathway which drives the production of growth factors, chemokines and proinflammatory cytokines
Then, these mediators recruit and sustain inflammatory cells in the affected tissue, increasing the inflammatory response
Then, over time chronic inflammation can lead to ongoing tissue damage and remodelling, where the tissue undergoes structural changes due to continuous inflammation and repair processes =
Then, the resolution phase aims to restore tissue homestasis
What is a granuloma
Organised collection of macrophages that have transformed into epithelioid cells forming a compact cluster
These epithelioid cells are surrounded by a rim of lymphocytes and occasionally multinucleated giant cells, which are formed by the fusion of macrophages
The core centre of the granuloma may exhibit caseous necrosis which is basically a cheese like appearance due to cell death and tissue destruction
They are typically found in chronic inflammatory conditions e.g TB
What are 4 key structures in the respiratory system that undergo inflammation
Alveoli
Bronchi
Interstitium
Parenchyma
Outline the link between alveoli inflammation and associated symptoms
Inflammation impairs gas exchange, causing symptoms like shortness of breath and hypoxaemia
