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Flashcards in COPD Deck (55):

What is COPD?

A condition characterised by airflow reduction that may be partially reversible with bronchodilators but which gets progressively worse. Clinically divided into emphysema and bronchitis.


What features does bronchitis have?

Inflammation of bronchi and bronchioles.
Cough, clear mucous sputum, infections with purulent sputum and increasing breathlessness.


What are some features of emphysema?

Distension and damage to alveoli.
Destruction of acinial pouching in the alveolar sacs.


What can obstruct a hollow viscous?

Extrinsic compression.
thickening of the wall.
internal obstruction.


What type of airway obstruction is important in emphysema?

Loss of alveolar attachment and support of small airways.


What is the functional classification of lung diseases?

Obstructive and restrictive lung diseases.
Obstructive diseases are of the airways
restrictive are of the lungs.


What types of airway narrowing can cause obstruction?

Muscle spasm,
mucosal oedema,
airway collapse due to loss of support or
localised obstruction due to tumour or foreign body.


What are the main categories of obstructive disease?

Asthma, COPD, chronic bronchitis (obstructive airway disease).
COPD and asthma can overlap aka COPD with reversibility.


What are the three categories of COPD and do they occur in isolation?

Chronic bronchitis.
Respiratory bronchiolitis.

Symptomatic patients often have all of these.


What is the overall pathogenesis of COPD?

Noxious particles or gasses cause mucociliary dysfunction, inflammation, and tissue damage leading to development of obstruction and ongoing disease progression.


What are the characteristics of COPD?

Exacerbations and reduced lung function.


What are the symptoms of COPD?

Breathlessness and worsening quality of life.


What is the pathogenesis of COPD at the immune cell level?

Cigarette smoke comes in contact with alveolar macrophages.
neutrophil chemotactic factors are released e.g. Cytokines, mediators and O2 radicals.
Neutrophils come and release protease inhibitors.
This causes alveolar wall destruction and mucus hypersecretion, resulting in progressive airflow limitation.


What symptoms are indicative/diagnostic of chronic bronchitis?

Cough productive of sputum on most days for 3 months of at least 2 successive years.


What is happening to the airways in chronic bronchitis?

Chronic irritation produces an increase in mucus production, causing an increased number of epithelial cells, especially goblet cells.
Causes an increased susceptibility to infection and non reversible obstruction.
They can get chronic neutrophil inflammation, smooth muscle spasm and hypertrophy which is partially reversible.


What is the aetiology of airway obstruction in COPD?

Loss of support
muscle spasm
mucosal swelling
mucus in the irregular lumen.


What part do the small airways play in chronic bronchitis?
What happens to them?

Play an important role.
They Undergo goblet cell metaplasia, macrophage accumulation and fibrosis around bronchioles which may generate functional obstruction.


What two factors play the biggest part in triggering COPD?

Smoking and genetics.


What happens in emphysema?

Loss of alveolar gas exchange and loss of bronchial support which is irreversible.


What is the definition of pulmonary emphysema?

Permanent, abnormal dilatation of airways distal to the terminal bronchioles I.e. The gas exchange part of the lung.


What two factors cause the apparent dilatation of the lung in emphysema?

Partly due to weakening of the alveolar connective tissue matrix and loss of elastic recoil.
Partly an effect of loss by destruction of alveolar walls leaving a hole in the pulmonary parenchyma.


What does alveolar destruction lead to in emphysema?

Impaired gas exchange and loss of bronchial support that is irreversible.


How do we diagnose emphysema?

Very difficult to diagnose in life apart from when it is extreme, but CT can cause alterations in lung density.


What types of emphysema are there and what are the differences between them?

Centriacinar - dilatation based around respiratory bronchioles with preservation of distal alveoli.
Panacinar emphysema - diffuse enlargement across the respiratory acini.


What are some of the causes of emphysema and what parts of the lung do they commonly affect?

Alpha 1 anti trypsin deficiency - classical cause, may show a lower lone predominance.
Ritalin lung.
Swyer James syndrome - affects one lung.
Obliterating bronchiolitis.


What causes protease imbalance in emphysema and what does this result in?

Genetic cause decreased antiproteases.
Smoking causes an increase in proteases which causes alveolar destruction and lead to emphysema.


How does emphysema lead to impaired respiratory function?

Diminished alveolar surface area, loss of elastic recoil and support of small airways leading to a tendency to collapse and obstruct.


What happens to PaO2 as the disease advances and what symptoms does this cause?

Decreased PaO2.
Leads to dyspnoea and increased RR.
This causes pulmonary vasoconstriction and pulmonary hypertension.


What happens to elastic tissue in COPD?

Sensitive to changes by elastases produced by neutrophils and macrophages.
Alpha 1 anti trypsin acts as an anti elastase.
Imbalance in either arm of this predisposes to destruction of elastic alveolar walls.


What does smoking do to alpha1 anti trypsin?

Increases the number of neutrophils and macrophages in the lung. Promotes neutrophil de granulation and inhibits alpha1 antitrypsin.


How do we assess COPD?

Assess the symptoms and the degree of airflow limitation using spirometry.
Also assess the risk of exacerbations.


What are predictors of high risk in COPD?

Two or more exacerbations in the last year.
An FEV1 of under 50% of predicted values.


What difference in breath sounds do we get between chronic bronchitis and emphysema?

CB - wheeze.
E- reduced breath sounds.


What is the chronic cascade in COPD?

Progressive fixed airflow obstruction,
impaired gas exchange,
type 2 respiratory failure,
pulmonary hypertension,
cor pulmonale and death.


How can we arrest further decline in lung function in COPD?

Stopping smoking.


What is the non pharmacological treatment of COPD?

flu jab, home O2, venesection (blood removal), lung volume reduction surgery and stenting.
Weight optimisation. Pulmonary rehab. Smoking cessation. Exercise.


What pharmacological treatments do we use for COPD?

SABA's B2 e.g. Salbutamol inhaler and anticholinergics e.g. Ipratropium inhaler.
LABAs B2 e.g. Salmeterol inhaler and anticholinergics e.g. Tiotropium.

Inhaled corticosteroids if FEV under 50% of predicted or several flare ups.
Oxygen if hypoxic.
Roflumilast - enzyme PDE4 inhibitor.
Carbocystiene - antioxidant
Azithromycin - antibiotic for prevention of flare up.


What drugs do we give for palliative care of COPD?

Opiates and benzo's.


What should we look for in examination of a COPD patient?

Assess severity.
RR, cyanosis, tachycardia, bp, breath sounds and oedema.


What investigations should we do for COPD exacerbations?

CXR, ABGs, FBC, U and Es, ECG, sputum cultures if purulent.


What treatment should we give for a COPD exacerbation?

Nebulised bronchodilators,
controlled O2 aiming for says over 90.
Antibiotics if there is an infection.
Systemic steroids.
Consider non invasive ventilation.


What should we aim for when giving COPD patients O2?

Sats above 90 and a balance between hypoxia and hypercarbia and acidosis.


What non infective causes should we consider for a COPD flare up?

PE, HF or pneumothorax.


What is acute bronchitis preceded by?

The cold.


What are clinical features of acute bronchitis?

Productive cough, fever in a minority of cases, normal chest examination, normal CXR and may have a transient wheeze.


What is the treatment for acute bronchitis?

Rest and hydration etc.
Antibiotics only recommended if underlying chronic lung disease.


What are the clinical features of an acute exacerbation of chronic bronchitis? What is it preceded by?

Usually preceded by upper respiratory infection. Worsening of sputum production which is now purulent, become more wheezy and breathless.


What will we find on examination of an acute exacerbation of bronchitis?

Breathlessness, wheeze, coarse crackles, may be cyanosed and in advanced disease we will see ankle oedema.


How are acute exacerbations of Chronic bronchitis managed in primary care?
And in hospital?

Bronchodilator inhalers.
Some cases need a short coarse of steroids.

Hospital same as above but also ABG's, CXR and O2 in respiratory failure.


When should acute exacerbations of Chronic bronchitis be sent to hospital?

Evidence of respiratory failure and not coping at home.


What are the causes of exacerbation of COPD in order of highest to lowest frequency?

Following Viral infections
Undetermined e.g. Falling temperature and increased humidity.


What are the most common bacterial organisms in COPD?

Haemophilus influenza.
Streptococcus pneumonia.
Moraxella catarrhalis.

All three are commensals but take effect when the body is weak.


What type of bacteria is moraxella catarrhalis?

Gram negative dipplococcus.


When should we give antibiotics in COPD exacerbations?

If increased sputum purulence
Consolidation on CXR
Signs of pneumonia.


What are the first and second line antibiotics for COPD exacerbations?

1st amoxicillin
2nd doxycycline