Chronic Obstructive Pulmonary Disorder Flashcards
What is the definition of COPD?
a disease state characterised by airflow limitation that is not fully reversible
the airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases
What 2 conditions is COPD usually a combination of?
BRONCHITIS:
- cough & sputum production on most days for at least 3 months during the last 2 years
EMPHYSEMA:
- enlarged air spaces distal to the terminal bronchioles, with destruction of the alveolar walls
What are the usual causes of COPD?
it is caused by long-term exposure to toxic particles and gases
- cigarette smoking accounts for over 90% of cases
- also inhalation of smoke from biomass fuels used in heating and cooking in poorly ventilated areas
What group of conditions is it important to distinguish COPD from?
How are these conditions defined?
COPD needs to be distinguished from the restrictive pulmonary diseases
these are also chronic respiratory diseases that are characterised by decreased lung capacity where FEV1 and FVC are both decreased proportionally
this results in a normal FEV1 : FVC
What is the FEV1 : FVC ratio in COPD usually?
Is this factor essential for diagnosis?
FEV1 : FVC ratio is <70%
COPD can also be diagnosed in patients with FEV1 : FVC >70% on the basis of clinical signs and symptoms
(e.g. cough, shortness of breath)
around 30% of cases of COPD have normal spirometry at diagnosis
What is the general disease course of COPD typically like?
patients typically follow a slowly progressive course with recurrent exacerbations
this involves short periods of increased shortness of breath, with or without infection
In general, what is involved in the long term management of COPD?
- combinations of inhaled steroids and bronchodilators
- smoking cessation
- pulmonary rehabilitation
- important to prevent exacerbations with flu and pneumonia vaccines
How are COPD exacerbations typically managed?
exacerbations are often mild and can be treated in primary care, but COPD patients sometimes present to the hospital with exacerbations
- oral steroids
- increases in doses of inhaled agents
- oxygen therapy
- most cases are also given antibiotics
What is the prevalence of COPD in the UK?
- affects 1.5million in the UK
- affects at least 1 in 7 people over 40
- it is severely under-diagnosed with airway obstruction affecting 10% of the population, but only 5% being diagnosed with COPD
What % of COPD cases are accountable to smoking?
Why is this important to consider?
smoking accounts for 90-98% of all cases
symptoms will improve in 90% of patients with smoking cessation
What are the characteristics of a typical patient presenting with COPD?
Why is it important to ask about how many cigarettes the patient smokes?
- most commonly seen in ex-smokers > 35 years of age
- most patients do not show symptoms until they are in their 50s
COPD is unlikely to develop with a smoking history less than 10 pack years
What factors are involved in the aetiology of COPD?
- smoking
- coal mining
- exposure to air pollution
- particularly in the developing world - indoor fires & cooking
- genetic predisposition
- a1-antitrypsin deficiency causes emphysema
What are 2 predisposing factors to development of COPD?
- low socioeconomic status
- low birth weight
- associated with reduced maximum lung capacity in adulthood
What % of smokers will develop COPD?
10 - 20% of all smokers will develop COPD
up to 50% of those with a >20 pack year history will develop COPD
not all heavy smokers develop COPD, showing there is some individual susceptibility
What are the characteristic symptoms of COPD?
- cough (may or may not be productive, but usually is)
- wheeze
- dyspnoea (breathlessness)
- usually following many years of a smokers cough
- frequent exacerbations producing purulent spputum
What factors can sometimes worsen symptoms in COPD patients?
- cold, foggy weather
- atmospheric pollution
- in advanced disease, breathless becomes severe even after mild exercise, such as dressing
What are the most common clinical signs of COPD?
- in mild disease, there are no signs apart from “wheeze” throughout the chest
- in severe disease, there is tachypnoea with prolonged expiration
- use of accessory muscles of respiration
- intercostal indrawing on inspiration
- pursing of the lips on expiration
- poor chest expansion
- hyperinflation of the lungs
What is the cricosternal distance?
How is this changed in COPD and why?
the distance between the cricoid cartilage and the sternal angle
it is reduced and is < 3cm in COPD due to hyperinflation
the thorax is raised in relation to the cricoid cartilage
What may chest / breath sounds be like in COPD?
- Resonant chest sounds are suggestive of hyperinflation
- Quiet breath sounds over areas of emphysematous bullae
What is wheeze?
What causes it?
an abnormal high pitched or low pitched breath sound heard on expiration
it is caused by abnormal narrowing of the smaller airways
What type of wheeze is usually present in COPD?
What is the other type and what is this more likely to be?
COPD presents with a POLYPHONIC wheeze
this is made up of many different “notes” as it is caused by many abnormal airways
the other type of wheeze is MONOPHONIC
this is caused by a single airway obstruction, and is more likely to be cancer
Why is wheeze sometimes confused with stridor?
What tends to cause stridor?
stridor is the name for a sound heard on INSPIRATION, rather than expiration
it is typically caused by an UPPER airways obstruction such as an inhaled foreign body or mass (cancer) impinging on the upper airway
Why does someone with COPD have a prolonged expiration?
as their FEV1 is low, they have to have a prolonged expiratory phase to allow for adequate respiration
Why do patients with COPD use a pursed lip breathing technique?
- it creates a smaller opening though which air can exit the respiratory system
- this keeps pressure in the airways higher
- this helps to stop smaller airways from collapsing
- there is a larger surface area for gas exchange than in the absence of pursed lip breathing
Why is pursed lip breathing sometimes called Auto-PEEP?
PEEP stands for positive end expiratory pressure
it is a technique used in intubated and CPAP patients to improve ventilation
pursed-lip breathing provides a small amount of PEEP for patients with COPD
What is meant by the “dynamic closure point” in a COPD patient?
in COPD, some of the airways will collapse at a point proximal to many of the alveoli
this point is the dynamic closure point
it occurs due to destruction of elastin tissue that occurs in emphysema
How can pursed-lip breathing alter the dynamic closure point?
What is the overall effect of this on ventilation and reducing dyspnoea?
- high pressure in the lungs created by pursed lip breathing moves the dynamic closure point to a more distal area of the lung
- this means that ventilation can occur in a greater number of alveoli
- VQ mismatch is reduced
- dyspnoea is reduced
What is the difference in the way COPD patients present depending on whether they remain sensitive to CO2?
those who remain responsive to CO2 are usually breathless and rarely cyanosed
heart failure & oedema are rare features except as terminal events
those who become insensitive to CO2 are often odematous and cyanosed, but rarely breathless
What features may a COPD patient present with if they have hypercapnia?
What can severe hypercapnia lead to?
- peripheral vasodilatation
- bounding pulse
- coarse flapping tremor of the outstretched hand when pCO2 is above 10 kPa
- severe hypercapnia leads to confusion and progressive drowsiness
Why does COPD lead to hyperinflation?
Why is this a problem?
COPD leads to gas trapping which increases the amount of dead space and leads to hyperinflation
this reduces the amount of air exchanged with outside air with each breath
it also leads to reduced chest wall compliance
hyperinflation is exaggerated during exercise
How is a diagnosis for COPD usually made?
it is usually clinical and uses the GOLD criteria
there is a history of breathlessness and sputum production in a lifetime smoker
in the absence of smoking, a working diagnosis of asthma is usual unless there is family history of lung disease suggestive of a1-antitrypsin inhibitor deficiency
What would be expected to be seen on lung function tests (spirometry) in a patient with COPD?
- FVC < 80%
- FEV1 : FVC < 0.7 or < LLN (lower limit of normal)
- increased residual volume (but may also be normal)
- gas transfer coefficient of carbon monoxide is low when significant emphysema is present
What would be expected to be seen on a chest X-ray of someone with COPD?
- possible hyperinflation, but often normal
- flattened hemi-diaphragms
- large central pulmonary arteries
- decreased peripheral vascular markings
- bullae
- cylindrical heart (due to cor pulmonale)
- patchy consolidation may be present if there is an ongoing infective exacerbation
What may be seen on an ECG in someone with severe COPD?
if there is right atrial and ventricular hypertrophy suggestive of cor pulmonale, this will produce large p waves on ECG
this is known as P pulmonale
What do blood gases show in someone with COPD?
they are often normal
in advanced disease there is evidence of hypoxaemia (reduced PaO2) and hypercapnia (increased PaCO2)
What may be seen on a full blood count in someone with COPD?
- raised haemoglobin & PVC as a result of persistent hypoxaemia
- this is secondary polycythaemia
- in this case, the haematocrit is measured and is >45
- normocytic normochromic anaemia of chronic disease has a prevalence of 20%
What other test is performed when investigating COPD?
a1-antitrypsin levels
normal range is 2 - 4 g/L
What is involved in the gas transfer coefficient for carbon monoxide test?
it is a measure of the effectiveness of gas transfer across the alveoli
the patient inhales a known value of carbon monoxide, which has a very high affinity for haemoglobin
in emphysema and severe fibrosis, the gas transfer value is reduced
What test is required for a diagnosis of COPD?
When can these values be a bit less reliable?
spirometry is required to confirm a diagnosis of COPD with a cutoff of FEV1 : FVC ratio of <0.7
in patients >65 and <45 this ratio is not as reliable, and specialist spirometry may be required to clarify the diagnosis in borderline cases
Why can it be difficult to diagnose COPD sometimes?
What can it become confused with?
there are no clinical features that are diagnostic and COPD cannot be diagnosed on the basis of CXR and clinical history alone
- COPD cannot be diagnosed from hyperinflation seen in CXR as asthma may also cause this
- there may appear to be a barrel chest in elderly patients that is actually curvature of the spine due to osteoporosis
In what groups of patients should a diagnosis of COPD be considered?
- patients >35 with symptoms of breathlessness and cough and/or sputum production
- all smokers and ex-smokers > 35
Why does spirometry need to be measured both pre- and post- giving a bronchodilator?
if airflow limitation is reversible
(usually an increase in FEV1 of >12% and >200mls)
this is suggestive of asthma or mixed COPD
if FEV1 increase is >400mls this suggests asthma
What is predicted FEV % and typical symptoms in mild COPD?
FEV predicted 60 - 80%
- symptoms are variable and there are typically few symptoms
- breathlessness on moderate exertion
- no effects on activities of daily living (ADLs)
- may be cough and sputum production
What are the symptoms and predicted FEV % in moderate COPD?
FEV predicted 40 - 60%
- breathlessness when walking on flat ground
- exacerbations
- some limitations of ADLs
What is the predicted FEV and symptoms in severe COPD?
FEV predicted <40%
- breathlessness on minimal exertion
- daily activities severely limited
- frequent and severe exacerbations
What is the most consistent pathological finding associated with COPD?
What is the result of this on lung function?
hypertrophy and increase in the number of mucous-secreting goblet cells of the bronchial tree
this is evenly distributed throughout the lung but mainly seen in larger bronchi
this reduces lumen size and increases distances for gas exchange
What is seen on histology of the bronchi in severe COPD?
the bronchi themselves are obviously inflamed
pus is seen in the lumen
Microscopically, what is seen on pathology in COPD?
What is the end result of these changes?
- infiltration of the walls of the bronchi and bronchioles with acute and chronic inflammatory cells and lymphoid follicles
- epithelial layer may become ulcerated
- when ulcers heal, squamous epithelium replaces columnar cells
- inflammation is followed by scarring and remodelling
- this thickens the walls (increased gas diffusion distance) and leads to widespread narrowing of the small airways
What is the difference in the lymphocyte infiltrate in COPD compared to asthma?
in COPD the lymphocyte infiltrate is predominantly CD8+, rather than CD4+
How does the size of the airways affected by inflammation change as COPD progresses?
How can this be reversed?
- initially, only the small airways are affected
- no significant breathlessness has developed at this stage
- initial inflammation of small airways is reversible
- this accounts for the improvement in airway function if smoking is stopped early
- in later stages, larger airways start to become affected and inflammation continues even if smoking is stopped
Following on from inflammation, if COPD continues to progress, what changes are seen?
What is the consequence of this?
- progressive squamous cell metaplasia
- and fibrosis of the bronchial walls
- inflammation and scarring reduces the size of the lumen of the airways and reduces lung elasticity
- the result of these changes is the development of airflow limitation
How can airflow limitation be made even worse in COPD following brochial fibrosis and squamous cell metaplasia?
resulting airflow limitation is made more severe when it is combined with emphysema
this causes loss of the elastic recoil of the lung
What is the definition of chronic bronchitis?
What 2 features are present on histology?
defined as cough and sputum production on most days for at least 3 months during the last 2 years
there will be presence of:
- an increase in the number of mucus secreting glands (hypertrophy)
- an increase in the number of goblet cells (hyperplasia)
- in extreme cases the bronchial tissue itself becomes inflamed and pus is present in the lumen
What is the result of emphysema on airspaces in the lungs?
emphysema causes enlarged airspaces distal to the terminal bronchioles
destruction of the elastin alveolar walls causes decreased elastic recoil of the lungs
What structures are affected in centri-acinar emphysema?
How disabling is it?
distension and damage of lung tissue is concentrated around the respiratory bronchioles
the more distal alveolar ducts and alveoli tend to be well preserved
this is very common and is not usually associated with disability when it is modest
severe centri-acinar emphysema is associated with substantial airflow limitation
What is pan-acinar emphysema?
What disease is this associated with and what are the consequences?
distension and destruction appear to involve the whole of the acinus
in extreme forms, the lung becomes a mass of bullae
severe airflow limitation and V/Q mismatch occur
this type of emphysema occurs in a1-antitrypsin deficiency
What is para-septal emphysema?
emphysema that tends to affect the more distal alveoli and alveolar ducts
What is irregular emphysema?
there is scarring and damage affecting the lung parenchyma patchily without regard for acinar structure
What are emphysematous bullae?
large closed off air spaces with trapped air inside them
the alveoli distend to form exceptionally large air spaces, especially in the uppermost regions of the lungs
What is meant by a “pink puffer”?
What is their PaO2 and PaCO2 like and why?
they have a _near normal *P*aO2_ and a _normal or low *P*aCO2_ (due to hyperventilation)
they “puff” to increase their alveolar ventilation
by increasing their respiratory effort, they are able to keep their blood gases close to normal
What is meant by a “blue bloater”?
What are their PaO2 and PaCO2 values like?
blue bloaters have _low *P*aO2_ and _high *P*aCO2_
they fail to maintain respiratory efforts
they have decreased alveolar ventilation, and as a result, CO2 levels rise
What are the non-pharmacological approaches to management of long-term COPD?
- pulmonary rehabillitation
- advice for smoking cessation
- this is vital in reducing the speed of disease progression
