COPD Flashcards
(90 cards)
What are the most common conditions comprising COPD?
Chronic bronchitis
Emphysema
What is COPD?
Chronic obstructive pulmonary disease
Characterised by airflow limitation which is not fully reversible.
This limitation is usually progressive and assoc. with abnormal inflammatory response of the lungs to noxious particles or gases
Is COPD curable?
No.
COPD can be prevented, but not cured. Treatment is symptomatic and preventing further exacerbations
What is the epidemiology of COPD?
15% of adults in NZ get COPD. This is increasing due to smoking at this point in time
COPD is the 4th leading cause of death in the world
How is chronic bronchitis classified?
“Blue bloater”
There is a chronic cough with copious sputum production for 3months in the last 2 years, irrreversible with a β2 agonist.
There is no allergic component involved.
Onset age often 46-65 years,
Patients often obese with high incidence of cigarette use
Chest diameter is increased- barrel chest (in severe disease)
There may be right ventricular failure (which can be shown by jugular venous distension)
CO2 retention is caused by decreased responsiveness of respiratory centre to prolonged hypoxemia and leads to cyanosis.
How is emphysema classified?
“Pink puffer”
There is an abnormal enlargement of the airspace distal to the terminal bronchioles accompanied by destruction of terminal bronchiole wall.
This leads to impaired ventilation due to loss of anatomical structure integrity of lung and destruction of alveolar sac.
Patients often have dysponea even at rest
Airway function is irreversible with a β2 agonist
There is minimal cough with a scanty sputum production
Patients are usually aged 55-75 , often with barrel chest due to overuse of accessory muscles of chest and neck to assist with breathing.
They Hyperventilate to compensate for hypoxia, leading to a Flushed appearance
What are the risk factors for COPD?
Smoking
Occupational exposure
Pollution
Genetic
Other (SEP, age, gender which are mostly linked to smoking)
How is smoking a risk factor for COPD?
Smoking is the #1 risk factor.
80-90% of COPD is linked to smoking
However NOT all smokers get COPD
How is occupational exposure a risk factor for COPD?
Patients working in coal mining, asbestos, grain handling, potter workers and farming are more likely to get COPD
How is pollution a risk factor for COPD?
Patients living in urban areas are more likely to get COPD due to inhalation of polluting gases e.g. From cars, factories etc.
How is genetic predisposition a risk factor for COPD?
Decreased α-1 antitrypsin increases the risk of COPD
Polymorphisms of SERPINA1 gene result in differences in α-1 antitrypsin production resulting in variant neutrophil elastase inhibition.
What does the SERPINA1 gene code for?
The SERPINA1 gene encodes the anti protease α-1 antitrypsin.
α-1 antitrypsin is higher in the white population and is produced by hepatocytes and mononuclear phagocytes.
It is a major inhibitor of neutrophil elastase which is capable of destroying components of the lung matrix.
M1 ala and M2 alleles have significantly lower elastase inhibitor capacity compared to M1val gene
What is the most common aetiology of COPD?
Most common aetiology is exposure to tobacco smoke although other chronic inhalation all exposures can also lead to COPD
What is the pathophysiology of COPD?
Inhalation of noxious particles and gases stimulate the activation of
- neutrophils
- macrophages
- CD8+ lymphocytes
These release a variety of chemical mediators (TNF-α, IL-8, LTB4)
These lead to widespread destructive changes in the airways, pulmonary vasculature and lung parenchyma
What are the results of the widespread destructive changes caused by TNF-α, IL-8 and LTB4?
Oxidative stress
Inhibition of α-1 antitrypsin activity
Mucous production
Vascular changes
What happens in oxidative stress?
Increased oxidants (generated by cigarette smoke) can react with and damage various proteins and lipids. This results in cell and tissue damage.
Oxidants also promote inflammation directly and exacerbate the protease-anti protease imbalance by inhibiting anti protease activity
What happens when the anti protease α-1 antitrypsin is inhibited?
α-1 antitrypsin inhibits several protease enzymes including neutrophil elastase. Inhibition of this antiprotease will allow increase neutrophil elastase activity. This can lead to damage of the alveolar wall (which comprises of elastin)
What happens in mucous production?
Inflammatory exudate present in the airways lead to an increased number and size of goblet cells and mucous glands.
Mucous secretion will increase, impairing ciliary motility.
The smooth muscle and connective tissues in airways will thicken.
Chronic inflammation results in scarring and fibrosis, limiting expiratory air flow, diffuse airway narrowing occurs (although this is more prominent in small peripheral airways)
What happens in the advanced stages of COPD?
Vasuclar changes occur. This includes
Thickening of pulmonary vessels leading to endothelial dysfunction of pulmonary arteries.
Structural changes increase pulmonary pressures - especially during exercise.
In severe COPD, secondary hypertension results in right sided heart failure due to hypoxia in poorly ventilated lungs, vasoconstrictor peptides produced by the inflammatory cells, and vascular remodelling.
What are the initial symptoms of COPD?
Chronic cough, sputum production
Patients may have these symptoms for several years before dysponea develops
How is COPD diagnosed?
Using the COPD-X framework.
C- confirm diagnosis O- optimise management P- prevent deterioration D- develop support and self management plan X- eXacerbation management
How can COPD be confirmed?
Patient history Physical examination Spirometry Exercise testing Arterial blood gas measurements
What sort of history would confirm a diagnosis of COPD?
History of chronic progressive symptoms Like cough Wheeze Breathlessness Sputum production
History of tobacco use
How would physical examination confirm a diagnosis of COPD?
Physical examination is not good for detecting mild to mod COPD
Common features: Hyperinflation of chest Reduced chest expansion Rales (crackling noises signalling oedema Ronchi (coarse rattling sound) Prolonged expiratory phase
