Week 7: Respiratory Flashcards
Restrictive Lung disease
-Reduction in lung volume due to a pathology in the lungs, pleura, or surrounding strcutures
Causes of Restrictive Lung disease
** PAINT**
P Pleural Pathologies
A Alveolar Pathologies
I Interstitial Pathologies
N Neuromuscular Patholgies
T Thoracic cage abnormalities
Intrinsic vs extrinsic causes of Restricitve lung disease
Intrinsic: Intersitial, alveolar, diffuse cellular infiltrates
Extrinsic: Low Resp muscle tone, chest wall defomities, space occupying
Symptoms of Restrictive Lung disease
Dyspnoea: reduced lung compliance = increased work of breathing
Cough: Increased interstitial lung tissues stiffness triggers reflex
Malaise: Chronic hypoxia
Muscle weakness: Prolonged hypoxia and Resp muscle overuse
Sings of RLD
Reduced chest expansion
Tachypnoea
Decreased breath sounds upon auscultation
Inspiratory crackles (due to fibrosis)
Cyanosis
RLD Ventilation and perfusion
Impaired Ventilation: Stiff, less compliant lung tissue restricts lung expansion, decreasing total lung capacity and tidal volume.
Gas Exchange Issues: Thickened alveolar-capillary membrane slows oxygen diffusion, causing hypoxemia, especially during physical exertion.
Perfusion: Lung perfusion may remain normal or increase, but uneven ventilation worsens hypoxemia.
Dyspnea: Patients experience increased shortness of breath, particularly during activities that raise oxygen demands.
RLD: V/Q mismatch
Mismatch Impact: Areas of the lung receive inadequate oxygen, leading to hypoxemia.
Hypoxic Vasoconstriction: Alveolar hypoxia causes pulmonary arteriolar constriction, diverting blood flow from poorly ventilated areas.
Long-term Effects: Chronic hypoxemia can lead to pulmonary hypertension and right heart strain.
RLD Feature: V/Q mismatch is a hallmark of restrictive lung diseases, affecting gas exchange and oxygen delivery.
hypoxaemia
Low oxygen in blood
Interstitial Lung disease (ILD)
- Effects the tissues between the capilary endothelium and alveolar endothelium
- can progress to pulmonary fibrosis
Classifications of ILD
- Inorganic exposure: non organic substances eg asbestos or silica dust
- Organic exposure:
- Smoking
- Rare forms of ILD: eg LAM or vasculitis
- Idiopathic: unknown cause
How does asbestos cause ILD
inhalation of asbestos fibres, resulting in lung scarring and impaired respiratory function.
Mesothelioma
A rare and aggressive cancer that primarily affects the lining of the lungs, abdomen, or heart, and is strongly associated with asbestos exposure.
Diagnosing RLD
Chest X-Ray: reduced lung volume, flattened diaphragm, other abnormailites
Spirometry: decreased TLC, VC, FVC
aterial blood gas: reduced PaO2, normal or low PaCO2
Management of RLD
- Minimise exposure
- Steroids: to reduce inflammation
- Lung transplantation
- Pulmonary rehab, eduction + Resp muscle conditioning
Management of RLD
- Minimise exposure
- Steroids: to reduce inflammation
- Lung transplantation
- Pulmonary rehab, eduction + Resp muscle conditioning
Management of RLD
- Minimise exposure
- Steroids: to reduce inflammation
- Lung transplantation
- Pulmonary rehab, eduction + Resp muscle conditioning
Mucous Layer as a Immune Defence
Traps pathogens and/or foreign particles; expels them via the muco-ciliary escalator
Epithelium as a resp immune defence
Contains goblet cells that secrete mucous; creates a physical barrier
Lamina Propria as resp immune defence
Contains immune cells (e.g., macrophages, dendritic cells)
Type I Pneumocytes role in immune defence
Physical barrier between the lung and the airway
Type II Pneumocytes role in immune defence
Secrete surfactant to protect the lung against collapse and/or infection
Compromised resp immunity causes
Defective mucous Inability for the lung to trap/remove pathogens (e.g., in cystic fibrosis)
Dysfunctional cilia E.g., dysfunction caused by smoking or drug use
Immune cell defects
Process of Acute Pulmonary Inflamation
Recognition, Innate Immunity, Adaptive Immunity, Repair phase
Process of Acute Pulmonary Inflamation - Recognition
Innate immune cells detect threats using pattern recognition receptors, such as Toll-like receptors (TLRs) and NOD-like receptors (NLRs), which identify pathogen- associated molecular patterns (PAMPs) from pathogens and damage-associated molecular patterns (DAMPs) from damaged or dying cells.