COPD Flashcards
What id the definition of COPD? (WHO)
preventable and treatable disease characterised by persistant respiratory symptoms and air flow limitation and/or alveolar abnormalities, usually caused by significant exposuire to noxious particles or gases. Exacerbations and comorbidities contribute to the overall sevcerity in individual patients.
What is the GOLD 2023 definition of COPD?
Chronic obstructive pulmonary disease is a heterogenous lung condition characterised by chronic respiratory symptoms due to abnormalities in the airways (bronchitis, bronchioloitis) and/or alveoli (emphysema) that cause persistant, often progressive airflow obstruction
What chronic respiratory symptoms generally present in COPD?
- dyspnea (medical word for short of breath)
- Cough
- Sputum production
What symptoms prompt initial seekign of medical attention in COPD?
can’t run like before, feeling very breathless from activities that didn’t used to be so difficult, coughing and difficulty expelling mucus. Feeling cold
Clear exacerbations such as frominhaling pollution from cars, second hand smoke etc
What is the prevalence of COPD in the UK?
2% of the population (1.17 million people).
Globally 6%.
What are the missing millions referring to in COPD statistics?
About 2 million people likely to be walking around with COPD who are undiagnosed and have not sought medical treatment
What community and environmental factors directly relate to prevalence of COPD?
Prevalence is directly related to prevalence of risk factors in the community e.g. tobacco smoke, coal dust exposure, use of biomass fuels and age of population being studied.
95% of UK cases due to tobacco smoke exposure and is the most significant risk factor for COPD and is a dose response to duration and quantity smoked.
Unusual to get COPD from less than 10 pack years (1 pack year = 20 cigs/day for a year). There is individual susceptability.
List noted environmental factors for developing COPD?
- indoor air pollution - cooking with biomass fuels in low income countries (i.e. Kyrgyzstan)
- Occupational exposures - coal dust, silica, cadmium
- Low birth weight - may reduce maximally attained lung function in young adult life - there is an established link between COPD and low birth weight.
- Lung growth - childhood infections or maternal smoking may affect growth of lung during childhood = a lower maximally attained lung function in adult life
- Infections - recurrent infection can accelarate decline in FEV1 - persistant adenovirus in lung tissue can alter inflammatory response = predisposing to lung damage; HIV infection is associated with emphysema
- Low socioeconomic status
- Cannabis smoking
What host factors are associated with COPD development?
- Genetics - Alph-1-trypsin deficiency
- Airway hyperreactivity
What are the 2 main conditions under the umbrella term COPD?
- Bronchitis
- Emphysema
What is emphysema?
Destruction of the alveoli leading to abnormal and permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by the destruction of their walls.
How is chronic bronchitis defined?
a cough and sputum for >3 months in each of 2 consequtive years
What are the names of the 3 enlarged air spaces in COPD?
- Centriacnar
- Panacinar
- Paraseptal
What is a bullae and what impact does it have on breathing?
Bullae = a permanent air filled space within the lung that is >1 cm in diameter.
Results in impaired gas exchange and respiratory failure.
Describe simple pathophysiology of COPD
Pulmonary + systemic components.
The presence of airflow limitation combined with premature airway closure leads to gas trapping and hyperinflation - adversely affects pulmonary and chest wall compliance.
Pulmonary hyperinflation flattens diaphragmatic muscles and leads to an increasingly horizontal alignment of muscles= mechanical disadvantage for breathing ability.
Therefore the work of breathing is increased - initially on exercise when the time for expiration is further shortened and then with disease progression, at rest.
Describe the pathophysiology of Bronchitis
- Irritants enter the airway
- Mucus glands hypertrophy (get bigger)
- Leads to an increase in mucus gland secretion
- Increases polymorphism in the promoter region of inflammatory mediators in the airways
- Airways narrow (especially in bronchioles)
Describe the pathophysiology of Emphysema
- Loss of cell walls of alveoli leading to reduced surface area for gas exchange
- There is a loss of elastic supporting tissue as it starts to disintegrate
- Leads to hyperinflation (barrel shaped chest)
- As a result patients can become very hypoxic
Describe the inflammatory mechanisms involved in COPD
- Irritant enters airways
- Comes into contact with epithelial cells of airways, which activates the CD8 lymphocyte and neutrophils
- CD8 lymphocyte and neutrophil stimulates the destruction of alveolar wall destruction, proteases and fibroblast proliferation
- CD8 inhibits mucus hypersecretion
- The fibroblasts stimulate abnormal tissue repair
- Irritant stimulates macrophage response. Neutrophil chemotactic factors, cytokines and mediators.
- These can also react with oxidants which then inhibit protease inhibitors which inhibits proteases which stimulates alveolar wall destruction , and also stimulates alveloar wall destruction directly as well as mucus hypersecretion
What are some of the consequences of herpinflation in COPD?
- reduced ventilation
- Type 2 respiratory failure = respiratory muscles get stretched so don’t work effectively.
What are some of the consequences of Emphysema in COPD?
- reduced gas exchange
- hypoxia
- Typ1 1 respiratory failure
What are some of the consequences of Bronchitis in COPD?
Airway inflammation causes hyperinflation and sputum production
What are some of the consequences of exacerbations in COPD?
- development of resistant infections due to being on so many antibiotics for infections that they become antibiotic resistant
- hospitalisation
What are some of the systemic consequences of COPD?
- muscle weakness and cachexia
- heart failure
- pulmonary hypertension
- weight changes - excess and weight loss
- Metabolic syndrome
- Cardiovascular disease
- Osteoporosis
- Depression
- Lung Cancer
- Systemic inflammation: Cytokine IL-6 and TNF-alpha
WHat is the difference between type 1 and type 2 respiratory failure?
Type 1 = 1 problem of low oxygen levels (hypoxic)
Type 2 = Type 1 + hypercapnic (high levels of carbondioxide levels circulating)
Describe pulmonary features of COPD
- Pulmonary vascular remodelling and impaired cardiac performance
- Enlargement of mucus-secreting glands (hypertrophy) and an increase in the number of goblet cells, accompanied by an inflammatory cell infiltrate resulting in increased sputum production = leading to chronic bronchitis
- Loss of elastic tissue, inflammation and fibrosis of the airway wall resulting in premature airway closure, gas trapping and dynamic hyperinflation leading to changes in pulmonary and chest wall comliance.
- Unopposed action of proteases and oxidants leading to destruction of alveoli and appearance of emphysema
Describe systemic features of COPD
- Muscular weakness reflecting deconditioning and cellular changes in sekeletal muscles
- Increased circulating inflammatory markers
- Impaired salt and water excretion leading to peripheral oedema
- Altered fat metabolism contributing to weight loss
- An increased prevalence of osteoporosis
How is COPD diagnosed?
- Patient lifestyle and symptom history
- Clinical signs and symptoms
- Sputum test
- Walking test (how far can they walk in a certain time frame) (VO2max)
- Spirometry
What is heamoptysis and what implications does it have on COPD?
Haemoptysis = coughing up of blood.
May complicate COPD exacerbations.
How can you quantify dyspnoea in COPD patients?
Should be quantified in relation to history of patient to observe decline in condition.
dyspnoea = breathlessness
mMRC = The Modified Medical Research Council dyspnoea scale can be useful
Name 2 signs that may be present in advanced disease?
- oedema
- morning headaches (suggestive of hypercapnia)
What does crackling in breathing sounds indicate?
Bronchiectasis is persistant.
Infection if not persistant.
What is cor pulmonae?
Pitting oedema from salt and water retention caused by renal hypoxia and hypercapnia
Why is BMI important in COPD?
BMI has prognostic significance therefore try to keep within ‘normal range’ 18.5 - 24.9 kg/m2
What are the 2 classic phenotypes of COPD?
Pink puffers = typically thing and breathless. They maintain a normal PaCO2 until late stage disease
Blue Bloaters = develop or tolerate hypercapnia earlier and may develop oedema and secondary polycythaemia
What is PaCO2? What relation does it have with COPD?
Partial pressure of carbon dioxide = Increased levels can result in respiratory acidosis in advanced COPD which may lead to respiratory failure
What is polycythaemia?
Abnormally high number of red blood cells
What investigations are used for identifying COPD?
- Chest x-ray to rule out other causes of chest symptoms i.e. cardiac failure, lung cancer and the presence of bullae
- Full blood coung - Exclude anaemia or identify polycthaemia. Can be used to screen for alpha-1-tryspin deficiency (genetic cause)
- Spirometry to assess airflow obstruction
- oximetry (on finger) (significant is <93%)
- Blood gases (measure oxygen and carbondioxide concentrations)
- Biomarkers can distinguish between asthma and COPD
- Exercise tolerance tests
How is spirometry used to diagnose COPD?
when FEV1/FVC = <70%
Severity of COPD is defined in relation to post-bronchodilator FEV1.
How can lung volume be determined in COPD? Why is it significant?
Lung volume measurement provides assessment of hyperinflation.
can be performed in 2 ways:
1. Helium dilation technique
2. Plethysmography (useful in severe COPD where large bullae are suspected because helium method can underestimate lung volumes)
WHat is the role of exercise tolerence tests in identifying and managing COPD?
can provide a baseline to judge response to bronchodilator therapy or pulmonary rehab programmes. Can also be used to assess disease progression and prognosis.
What questionnaires can be helpful in measuring disease progression in COPD
COPD assessment test (CAT test) or mMrc test
The COPD control Questionnaire
In research SGRQ is used but a bit moer difficult to administer in clinic.
How is spirometry performed and what is it measuring?
Using a machine, the person fills their lungs completely and exhales as fast as possible to get as much air out as possible. Complete 3 x .
Normal = get most of air out in the first second and continues to get more out.
In COPD people can’t breathe out as fast and their out-breath scallops but if they keep breathing out for longer they may get more ait volume out than normal measure due to hyperinflation.
How is COPD severity assessed?
Defined in relation to predicted FEV1 for age, sex and stature.
Also assess impact of symptoms on limitations of activity they experience and if they suffer frequent or significant exacerbations.
> 80% = mild/stage 1
50 - 79% = Moderate/Stage 2
30 - 49% = Severe/Stage 3
< 30 % = very severe/stage 4
Describe Grade 0 of mMRC Dyspnea scale
No breathlessness except with streneous exercise
Describe Grade 1 of mMRC Dyspnea scale
Breathlessness when hurrying on a level or walking up a slight hill
Describe Grade 2 of mMRC Dyspnea scale
Walks slower than contemporaries on level ground because of breathlessness or has to stop for breathe when walking at own pace
Describe Grade 3 of mMRC Dyspnea scale
Stops for breath after walking ~100m or after a few minutes on level ground
Describe Grade 4 of mMRC Dyspnea scale
Too breathless to leave the house or breathless when dressing/undressing
What does BODE assessment take into account when assessing prognosis of COPD
Helps estimate survival rate
Body mass index
Obstruction of airflow - FEV1 % of predicted
Dyspnoea - mMRC scale
Exercise Capacity - 6 minute distance walk test
What interventions are useful in managing COPD
- vaccinations (flu, covid-19 and pneumonia as well as; chicken pox, shingles for >70yrs; whooping cough)
- Smoking cessation therapy
- Pulmonary rehabilitation interventions
- Inhalers (Tiotropium and LABA = long acting bronchodilator)
What are the 4 types of inhalers used in COPD?
- SAMA - short acting muscarinic antagonist
- SABA - short acting bronchdilator combinations
- LAMA - long acting muscarinic antagonist
- LABA - long acting beta-2 agonist (manages sputum)
How do SABA and LABA inhalers work?
On the sympathetic nervous system via beta-2 receptors.
They encourage bronchodilation and speed things up
How do SAMA and LAMA inhalers work?
On the parasympathetic nervous system; mucus secretion and bronchoconstriction inhibitors. Therefore slow things down and calm things down.
What are the fundamentals of COPD care?
- stop smoking support/treatment
- vaccines - pneumococcal and influenza
- pulmonary rehab
- co-develop self management plan
- optimise treatment of co-morbidities
When do you start inhaler therapies in COPD?
once fundamentals have been addressed and:
- inhaled therapies needed to relieve breathlessness and exercise limitation
- theyve been trained in how to use inhaler and demonstrate correct technique (offer SABA or SAMA as needed)
If persdon is limited by symptoms or has exacerbations despite treatment, what would be offered?
- Without asthmatic features or features suggesting steroid responsiveness = LABA and LAMA
- if person has day to day symptoms adversely affecting quality of life OR has 1 severe or 2 moderate exacerbations in 1 yr = 3 month trial of LABA + LAMA + ICS - if no improvement revert to LABA + LAMA - With asthmatic features or features suggesting steroid responsiveness = LABA + ICS b
POINT = try to avoid corticosteroid inhalers in COPD because they increase pneumonia risk in COPD patients.
List other treatment options for COPD
- Oxygen therapy - delivered by an O2 concentrator using environmental air (air must be good quality,eg, not smoky)
- Home non-invasive ventilation = attached to breathing machine with tight fitting mask
- Singing - helps improve breathing control
- Nebulisers = usually inhospital for administering antibiotics and typotenic saline
- lung volume reduction via resection/surgery allowing healthy lung to expand into that space
- lung transplantation
- Endobronchial valves = a valve put into the airway that lets air out but not in and helps with hyperinflation
- Telemonitoring
- self management plans including exercise and at home rescue pack with steroids and antibiotics for use during exacerbation reducing response time
- Long term antibiotics
- Airway clearance (physio for those with bronchitis to clear sputum and reduce infection risk/frequency)
Definition of COPD exacerbation
defined as an event characterised by increased dyspnea and/or cough and sputum that worsens in <14 days which may be accompanied by tachypnea and/or tachycardia and is often associated with increased local and systemic inflammation caused by infection, pollution or other insult to the airway
What are signs of exacerbation?
increased breathing work
increased shortness of breath
more sputum production
more coughing
fatigure
lightheadedness
Commone causes of exacerbation?
infection - viral and bacterial
smoking - relapse in cessation
asthma and hayfever if relevent
How is severity of exacerbation measured?
Use pulse oximetry and compare to patients baseline measurement.
Assess frailty, cardiorespiratory complications and co-morbidities.
How is mild exacerbation defined and managed?
INcreased need for medications and can be managed in normal environment. Use SABA
How is moderate exacerbation defined and managed?
sustained worsening of respiratory status that requires treatment with systemic corticosteroids and/or antibiotics. Can also treat with additional SABA. Treatment in community.
How is severe exacerbation defined and managed?
rapid deterioration in respiratory status requiring hospitalisation. May be associated with acute respiratory failure.
Treatment options for exacerbation include:
- antibiotics
- steroids
- oxygen - controlled O2 therapy and ventrivalve (need to know baseline 02%)
- NIV if indicated (if type 2 respiratory faiulre and they’re acidotic)
- End of life care
- manage comorbidities (e.g. heart faiulre with diuretics to reduce water retention)
Why do COPD patients lose weight?
- systemic inflammation
- hypermetabolic state
- hypoxaemia (increases metabolic rate)
- oxidative stress
- breathlessness (increases energy requirement - kcal)
What is impact of weight loss on COPD?
- increased mortality with lower BMI
- CO2 retention
- Type 2 respiratory failure
Why do COPD patients gain weight?
- reduced physical activity
- corticosteroid use
- cor pulmonale (or pulmonary hypertension = weight gain because of water retention/oedema)
What are benefits of nutritional support in COPD?
- not shown to improve survival or exercise test BUT
- is shown to increase BMI and increase peak workload in exercise and improve scores on Quality of Life indices.
- BMI = unreliable in older age due to loss of fat free muscle mass and age related changes in height posture and ratio of fat to muscle
What weight change should be acted upon for nutritional support in COPD? and why.
Any change greater than 3kg because indicated cancer risk
