COPD Flashcards
Name some key features of COPD
-obstructive spiro
-NOT fully reversible
-airflow obstruction is progressive
-patients experience exacerbations
-may be genetic or environmental factors involved
Define COPD
a heterogenous lung condition characterised by chronic respiratory symptoms due to abnormalities in the airway ( progressive and fixed ariway obstruction)
What terms come under COPD?
-emphysema
-chronic bronchitis
-chronic irreversible asthma
Define chronic bronchitis
the prescence of chronic or recurrent increases in bronchial secretions sufficent to cause expectoration. The secretions are present most days for a min of 3 months per year, at least 2 successive years and cant be attributed to other pulmonary or cardiac causes
Name some key features of emphysema
-abnormal enlargement of alveoli together with destruction of alveolar walls
-Increase in T cells and macrophages
-alveolar walls are destroyed by the loss of epithelial and endothelial cells
-Bulla ( airspaces>1cm) may develop
What are the results of emphysema?
loss of elastic recoil, leading to the development of airways obstruction, reduced surface area and increased dead space
Name some risk factors for COPD
-SMOKING
-occupational exposure to high conc of irritants
-low birth weight
-recurrent resp tract infections
-low socio-economic status
-genetic predisposition ( Alpha-1-antitrypsin deficency)
-chronic IV drug use
describe the key processes involved in the pathophysiology of COPD
-airway inflammation and remodelling
-development of emphysema ( airflow limitation and gas trapping, impairment of gas exchange)
-oxidative stress
Describe the process of airway inflam and remodelling in COPD
-chronic inflam triggered by irritants such as air, pollution, smoking or chronic damage by repeat infections
-immune system has an innate defence system against the toxins
-intact airway epithelium acts as a physcial barrier to foreign bodies
-mucociliary esculator removes many inhaled particles
-acute inflam response is initated which removes pathogens
-long term humoral and cellular responses develop, resulting in tissue healing, but microvascular changes and increased connective tissue matrix leads to proggressive inflam and remodelling
Describe key cells involved in airway inflam and remodelling incolved in COPD
-increased numbers of neutrophils, macrophages and T lymphs in lungs stimulated during the inflam response
Macrophages , neutrophils and airway epithelial cells release-
-cytokines and chemotactic factors such as LTB4 and IL-8
-pro inflam cytokines - TNF- a
-growth factors such as transforming growth factors -TGF-B
-Proteases
Describe the effects of inflam mediators on airways
-airwya narrowing resulting in fibrosis of small airways
-increased mucus production and hyperplasia of goblet cells
-impairment of cillia lining the airways, reducing mucus clearance and increasing infection risk
Describe just airway remodelling
-TGF-B stimulates fibroblast production
-fibroblasts produce collagen and extracellular matrix material
-accumulation of scar tissue
-results in narrowing of small airways
Describe mucociliary dysfunction
-increased number of englarged mucous glands in airway walls
-increased mucous production
-impaired mucociliary transport
-results in accumulation of mucus and reduction in airflow
Describe the effects of inflam mediators on alveolar walls
-normal balance between proteases and antiproteases is upset
-tissue proteases such as elastase digest connective tissue such as elastin and collagen
-destruction of alveolar walls and supporting structures
-increase in bullae
-reduction in lung elasticity
Describe the process of oxidative stress in COPD
-caused by inhaled toxins
-results in inflam, release of proteases such as elastase, inactivation of antiproteases
-protease activation results in alveolar wall destruction, mucous hypersecretion and abnormal tissue repair
-antiproteases such as a1-antitrypsin ( AAT) protect lung tissue from the action of proteases
Describe general oxidative stress
-occurs when free radicals and antioxidants become imbalanced
-free radicals are unstable oxygen- containing molecules, react easily with other molecules resulting in oxidation, which may be harmul to the body
-oxidative stress can be caused by an increase in free radical production or a reduction in antioxidants within the body
What is a1-antitrypsin deficency ( A1AT) ?
-inherited genetic condtion ehich can cause lung and liver damage
A1AT protects the lung tissue from trypsin damage which is a protease
-A1AT def results in protease/antiprotease imbalance
-A1AT is produces by the body but is misshapen and unable to leave the body
-Leads to early development of severe emphysema
Symptoms of COPD
-breathless
-cough
-regular production of sputum
-frequent chest infections
Name some signs of COPD
-accessory muscle use
-hyperinflation of the chest
-wheeze, rhonchi or quiet breath sounds
-ankle oedema or rasied JVP- signs of pulmonary hypertension
-cyanosis
-nail clubbing
name some additional features of COPD
-weight loss
-SOBOE
-wheeze
-waking at night m
-ankle swelling
-fatigue
-chest pain
-haemoptysis
-pulm hypertension
-respiratory failure
Describe what happens to the airways in a patient with emphysema
-loss of elastic recoil results in gas trapping or hyperinflation where air is left in alveolus following expiration
-Airway obstruction increases expiratory time- patients breath more slowly and deeply to maximise ventilation
-patients use pursed lip breathing to increase positive end expiratory pressure (PEEP) to prevent airway collapse
-patient will develop signs of barrel chest dues to chronic overinflation
Describe the effects that emphysema has on ventilation
-destruction of alveolar wall by elastase results in reduced ventilation
-proteases also destroys the pulmonary cappillaries and reduce perfusion
-ventilation and perfusion are both reduced leading to a mismatch
-o2 and co2 levels are relatively well maintained until late stage disease when PO2 drops and PCO2 increases
Describe the effects of chronic bronchitis on ventilation
-bronchoconstriction and increased mucus in bronchioles lead to chronic cough and expiratory wheeze
-inability to ventilate alveoli results in ventilation/perfusion mismatch leads to hypoxaemia and hypercapnia
-hypercapnia leads to respiratory acidosis, reduced blood PH
-hypoxaemia results in an increased RBC ( polycythemia) and HB
-respiratory acidosis+hypoxaemia and polycythaemia results in cyanosis
Describe the effects on chronic bronchitis within the body as a whole
alveolar hypoxia also causes vasoconstriction of pulmonary cappilaries, results in increased pulmonary vascular pressure and pulmonay hypertension
-pulmonary hypertension results in right side HF ( Cor pulmonale) and a reduction in blood returning to the left side of the heart, reducing CO and circulating blood volume
-reduction in blood volume activates the RAAS leading to fluid retention and oedema
Decsribe airway obstruction and small airway disease
<2mm diameter
-mucs plugging and increased number of neutrophils, macrophages, B and T cells
-airways thicken and narrow
-loss of terminal bronchioles and reduced airwya diameter reduces cor sectional area and so increases airway resistance
What is the effect of COPD on spirometry
-narrowed airways, which are prone to collapse on expiration results in reduced blood flow and prolonged expiration
-results in a reduced FEV1, normal FVC, but reduced FEV1/FVC%
-as severity increases, gas trapping and hyperinflation causes an increase in residual volume. May result in a reduced FVC. FEV1/FVC% will still be < LLN
Explain the effect of COPD and lung function
-obstruction spiro
-no reversibility to bronchodilators
-reduced gas transfers due to reduced surface area for gas exchange
-TLC and RV may increase due to hyperinflation
