Restrictive and Obstructive Lung Disease (Respiratory) Flashcards
When do the small airways begin and when does gas exchange begin?
Generation 8, generation 17.
What is some asthma terminology (how would we characterise different types)?
early onset/late onset, atopic/non-atopic, extrinsic (extrinsic trigger factor)/intrinsic (no obvious extrinsic trigger factor).
What is the asthma triad (what are the 3 main parts to asthma)?
Reversible airflow obstruction, airway hyperresponsiveness, airway inflammation.
Describe the dynamic evolution of asthma (what happens in the short and long term).
Broncho-constriction (brief symptoms) -> chronic airway inflammation (exacerbations and airway hyperresponsiveness) -> airway remodelling (fixed airway obstruction)
What is the inflammatory cascade in asthma (what are the stages/causes of inflammation in asthma)?
Inherited or acquired factors, eospinophilic inflammation, mediators and Th2 cytokines, and twitch smooth muscle.
What drugs are used to treat each stage of the inflammatory cascade in asthma?
Eosinophilic inflammation (anti-inflammatory medication e.g. corticosteroids, cromones, theophylline). Mediators and Th2 cytokines (antileukotrienes or antihistamines, monoclonal antibodies e.g. anti-IgE and anti IL-5). Twitchy smooth muscle (bronchodilators e.g. B2 agonists and M3 antagonists).
What should you use as well as a B2 agonist in the treatment of asthma?
A corticosteroid.
What are the features of the clinical syndrome of asthma (what would give us hints that someone has asthma)?
Episodic symptoms and signs, diurnal variability, non-productive cough, wheeze, triggers, associated with atopy (rhinitis, conjunctivitis, eczema), blood eosinophils >3%, responsive to steroids or beta-agonists, family history of asthma, wheezing due to turbulent airflow.
How would we diagnose asthma (what sort of testing could we do)?
History and examination, diurnal variation in peak flow, reduced FEV1/FVC (forced expiratory ratio), reversibility to inhaled salbutamol (>15%), provocation testing to produce bronchospasm (using exercise or histamine/methacholine/mannitol).
Describe the development of COPD (the main stages).
Noxious particles or gases e.g. smoking -> neutrophilic inflammation, mucociliary dysfunction, tissue damage -> obstruction and ongoing disease progression -> disease characteristics (exacerbations and reduced lung function) and symptoms (breathlessness and worsening quality of life).
How does the immune response to noxious agents cause COPD?
Alveolar macrophages release substances (neutrophil chemotactic factors, cytokines (IL-8), mediators (LTB4) and oxygen radicals) -> activates neutrophil -> produces proteases -> alveolar wall destruction (emphysema) and mucus hypersecretion (chronic bronchitis) -> progressive airflow limitation.
Describe the 2 main parts of COPD e.g. their features.
Chronic bronchitis: chronic neutrophilic inflammation, mucus hypersecretion, mucociliary dysfunction, altered lung microbiome, smooth muscle spasm and hypertrophy, partially reversible. Emphysema: alveolar destruction, impaired gas exchange, loss of bronchial support, irreversible.
Describe the protease imbalance in emphysema.
Protease usually overwhelms antiprotease which causes alveolar destruction and emphysema.
How do we assess COPD and what are indicators of high risk?
Assess symptoms, degree of airflow limitation using spirometry, risk of exacerbations and comorbidities. High risk: 2 exacerbations in 1 year or FEV1<50%.
What are the features of the clinical syndrome of COPD (what clues are there that someone might have it)?
Chronic symptoms, smoking, non-atopic, daily productive cough, progressive breathlessness, frequent infective exacerbations, chronic bronchitis (wheezing), emphysema (reduced breath sounds).
Describe the chronic cascade (what will happen as the disease gets worse) and what can arrest further decline of lung volume?
Progressive fixed airflow obstruction, impaired alveolar gas exchange, respiratory failure (less PaO2 and more PaCO2), pulmonary hypertension, right ventricular hypertrophy/failure (cor pulmonare, pulmonary heart disease), death. Stopping smoking.
What is it difficult to distinguish ACOS (asthma COPD overlap syndrome) between?
Asthmatic smokers who have airway remodelling (reduced FVC).
What does the non-pharmacological management of COPD involve?
Smoking cessation, immunisation (influenza/pneumococcal), physical activity, oxygen. Uncommon nowadays: venesection, lung volume reduction and stenting.
What does the pharmacological management of COPD involve?
LAMA or LABA mono, LAMA/LABA combo, ICS/LABA combo, ICS/LABA/LAMA combo.
How from someones cough do we know that they have chronic bronchitis?
They have a productive cough that lasts for at least 3 months each year for at least 2 years.
What are some skeletal causes of thoracic restriction?
Vertebral: thoracic kyphoscoliosis (bent spine in both coronal and sagittal plane), ankylosing spondylitis (inflammation of joints in spine). Ribs: traumatic multiple rib fracture.
Weaknesses in what muscles cause thoracic restriction and what diseases can cause this?
Intercostal or diaphragmatic. Myaesthenia Gravis, Guillan Barre, motor neurone disease, poliomyelitis.
How does abdominal obesity/ascites (abnormal collection of fluid in the abdomen), cause thoracic respiration?
Compresses the thoracic contents.
What does thoracic restriction due to causes outwith the lungs result in?
Chronic alveolar under-ventilation with low PaO2 and raised PaCO2 and reduced lung volumes.
