COPD Flashcards
What cormobidities are associated with COPD?
CVD Lung cancer Osteoporosis i.e. due to having to take corticosteroids Muscle weakness Cachexia
What is COPD? What causes the obstruction?
Progressive, partially reversible disorder due to airway obstruction caused by chronic bronchitis or emphysema which can be accumpanied with airway hypersensitivity (FEV1/FVC <0.7)
Chronic bronchitis
- inflammation and thickening of the bronchioles
- cough and chronic sputum production on most days for 3 months of the past 2 years
Emphysema
-enlarged airways distal to terminal bronchioles (damaged alveoli)
Causes of obstruction:
- Disrupted alveolar attachments= emphysema
- Mucosal inflammation + Fibrosis
- Mucus hypersecretion
What happens to airways in COPD patients during the expiratory phase?
Degredation of protein and elastin scaffolding due to inflammation and cigarette smoke which normally acts to keep airways patent during expiration
Therefore:
-early collapse of airways during expiration in COPD
Why do COPD patients have “gas trapping”? What is the consequence of this?
Unable to completely expire (due to increased resistance to expiration) before inspiration triggered
Eg. Leads to gas trapping and high residual volume
What are the 2 main phenotypes of COPD? How might patients present differently for the different phenotypes?
Chronic bronchitis= BLUE BLOATER
- chronic sputum production (3+ months for more than 2 consecutive years)
- increased risk of infective exacerbation due to sputum production providing environment for bacteria
- other causes of chronic cough been excluded
- cyanosis due to hypoxaemia
- peripheral oedema due to cor pulmonale
- prolonged expiration
- obese
Emphysema= PINK PUFFER
- breakdown of alveolar tissue leading to enlarged airspaces distal to terminal bronchioles w/o obvious fibrosis
- breathless and hypoxic
- increased minute ventilation
- pink skin + pursed lips
- accessory muscle use and tri-podding
- cachexic
- hyperinflation of chest= barrel chested
What is required for patient to be diagnosed with COPD? How is FEV1 used to grade the severity of COPD?
Spirometric diagnosis of AIRWAY OBSTRUCTION
-FEV1/FVC < 0.7
>80%= mild 50-80%= moderate <50%= severe <30%= very severe
H/O progressive symptoms of:
- SOB
- Chronic cough
- Expiratory wheeze
What is the criteria for asthma patients for be classified as having asthma-COPD overlap syndrome?
When asthma patients develop partially reversible airway obstruction over time
What is the pathophysiology of COPD?
Exposure to noxious particles and gases Consequences: -tissue damage -muco-ciliary dysfunction -chronic inflammation -airway hyper responsiveness -bronchospasm
LEADS TO AIRWAY OBSTRUCTION
How does cigarette smoke lead to tissue damage and inflammation?
Triggers alveolar macrophages which produce chemotactic factors ( IL-8 and LTB4) to recruit neutrophils
Neutrophils secrete proteases which target bacterial infection
Deficiency in protease inhibitors (alpha anti-trypsin deficiency) leads to:
- alveolar wall destruction= emphysema
- mucus hypersecretion= chronic bronchitis
What factors exacerbation mucociliary dysfunction associated with COPD? What are the implications of mucociliary dysfunction?
Tissue damage + inflammation
Increased mucus viscosity
Mucus hypersecretion
Leads to bacterial colonisation due to reduced mucociliary transport of mucus
What are the causes of COPD?
Smoking
Occupations exposure
- industrial dusts
- cotton textile industry
Indoor air pollution and biomass exposure:
Genetics:
-alpha-1 antitrypsin deficiency= inability to neutralise neutrophil proteases
What is the most affective way to improve lung function in COPD patients? What are the possible obstacles?
Smoking cessation i.e. lung function will improve with cessation at all stages of disease
Nicotine dependency
Initial productive unpleasant cough due to re-activating of muco-ciliary escalator
How can the clinical presentation of a COPD patient provide evidence of which type of COPD they have? What are the associated characteristics for both?
BLUE BLOATERS= chronic bronchitis
- overweight
- cyanotic
- elevated Hb
- cor pulmonale= RHF
- peripheral oedema
- rhonchi= low-pitch sound which can be heard in airways
- wheezing due to inflamed airways
PINK PUFFERS= emphysema
- older
- thin (cachexic)
- severe dyspnea
- quiet chest
- CXR w/ hyperinflation and flattened diaphragms
What are the signs and symptoms of COPD?
SOB
- worse on exercising
- MRC breathless scale
Chronic cough w/ sputum
-try to quantify the amount of sputum production per day
Expiratory wheeze
Weight loss
Nocturnal + early morning symptoms
-asthma overlay
Barrel chest
Cyanosis
Abnormal posture
Resp distress
Chronic hypoxaemia signs
- RHF
- signs of cor pulmonale
Why can RHF and cor pulmonale be associated with COPD?
Chronic hypoxaemia can lead to pulmonary circulation shutting down as lung tries to shunt BF away from non-functioning part of lung BUT most of lung affected meaning there is gross vasocontriction:
- leads to increase BV in peripheral circulation which increases the blood return to the right side of the heart
- pulmonary hypertension
THEREFORE= right sided heart failure
What investigations would you want in someone suspected of COPD and why?
BED SIDE
-sputum culture= assess for chronic infection i.e. pseudomonas
- ECG= if RHF or cor pulmonale suspected
- BMI= baseline to assess later changes which might occur with steroids or loss due to cancer
BLOODS:
FBC:
-polycythaemia with chronic hypoxia
Serum alpha-1 antitrypsin (early onset or more severe disease)
Transfer facto for carbon monoxide (TLCO) decreased in COPD
ABG= looking for signs respiratory failure
IMAGING CXR -hyperinflation -flatten diaphragms -dilation of pulmonary vasculature -excluding lung cancer
CT chest
-can help to determine the location of emphysema i.e. different causes of COPD can cause preferential development of emphysema
Eg Alpha 1 Anti-trypsin deficiency= lung bases with apices preserved
What are the goals of COPD management?
Reduce symptoms:
- relieve symptoms
- improve exercise tolerance
- improve health status
Reduce risk:
- prevent disease progression
- prevent and treat exacerbation
- reduce mortality
What are the stages of COPD management?
Smoking cessation
Conservative measures:
- decrease exposure to occupational/environmental exposure
- exercise
- flu and pneumococcal vaccinate
- mucolytic drugs= decreases risk of CX infection
Bronchodilators or antimuscarinics
- SA bronchodilator i.e. occasional use
- LA bronchodilator i.e. regular use for symptom relief
Oral/inhaled corticosteroids
Additional considerations:
- oral theophylline= bronchodilator
- home Neb
- Long term domiciliary oxygen therapy (LTOT)
- pulmonary rehab
- surgical interventions
What is LTOT? What are the possible indications for patient to be considered for LTOT? What is the criteria for this TX?
Long term oxygen therapy (domiscillary oxygen) Improves mortality and morbidity in patients
Indications:
- chronic hypoxia
- polycythaemia
- cyanosis
- cor pulmonale
Criteria:
-resting hypoxia on room air (RA)
I.e. confirmed 2 times over a 3 week period
What is the role of pulmonary rehab for COPD patients?
Physios work with px
Exercise to improve physical reserve and strength
I.e. bike riding and guided squats= need to become moderately breathless for it to be effective
When is NIV (non-invasive nasal ventilation) indicated for COPD patients?
Acidotic patients with CO2 (>6kPa) which remain acidotic after medical intervention
When are surgical interventions indicated for COPD patients? What are examples of the types of intervention that are available?
Criteria:
- need to be fit enough
- marked reduction in daily activity
Lung vol reduction:
-20% of effected lung removed
Lung transplantation
What are the possible complications associated with COPD?
Chronic hypoxaemia
-causes progressive pulmonary hypertension and can lead to development of RHF and cor pulmonale
Pneumothorax
-due to lung popping due to hyperinflation
Type 2 respiratory failure
-due to hypoxic drive
Arrhythmias i.e. AF = common after exacerbation
Infection
Secondary polycythaemia
-due to chronic hypoxia and resp failure
What are the steps of management for acute COPD/asthma exacerbation? (Acronym= O SHIT) What is the slight difference between the management for asthma and COPD?
O
-oxygen= controlled oxygen 24-28% litres via Venturi mask
S
-salbutamol (2.5-5mg NEB)
H
-hydrocortisone 100mg IV
I
-Ipratropium 500 mcg NEB (anticholingergic)
T
-Theophylline: aminophylline infusion 1g in 1L saline
(Xanthine which helps to prevent wheeze, SOB and chest tightness)
Need tight oxygen control in COPD i.e. use of Venturi whereas don’t in asthma
How is COPD diagnosed?
Clinical presentation of:
- chronic SOB
- productive cough i.e. sputum produced
- wheeze
- recurrent respiratory infections
Spirometry:
-obstructive picture= FEV1/FVC ratio <0.7
What results would you expect to see from spirometry of patient with COPD?
Obstructive picture= FEV1/FVC <0.7
- FEV1 (forced expiratory volume)= how quickly patient able to blow air out quickly
- FVC (forced vital capacity) = measures the overall lung capacity
- in COPD= ability to blow out quickly (FEV1) is compromised
No response to reversibility testing with beta-2 agonists i.e. salbutamol during the test
I.e. differentiates from asthma
What is the stepwise escalation of COPD treatment?
STEP 1:
- SA bronchodilators= beta-2 agonists= Salbutamol/terbutaline
- SA anti-muscarinics= Ipratropium bromide
STEP 2:
If patient hasn’t asthmatic or steroid responsive features:
-LABA + LAMA
Eg Anoro ellipta/Ultibro Breezhaler= combination inhalers
If patient has got asthmatic or steroid responsive features:
-LABA + ICS (inhaled corticosteroids)
Eg Fostair/Symbicort
Can escalate to triple therapy if not responsive to dual:
-LABA+LAMA+ICS
Eg Trimbo/Tregely Ellipta
What additional therapy’s are available in more severe cases of COPD?
Salbutamol or ipratropium nebs
Oral mucolytic therapy e.g. Carbocisteine to break down sputum
Saline nebs e.g. things sputum/secretions
LT prophylactic antibiotics e.g. Azithromycin
LTOT
How would someone with an exacerbation of COPD present? What test could you do to confirm it and what would results would you be looking for? What type of respiratory failure is commonly seen in COPD?
Acute worsening of cough and SOB and sputum production
ABG:
- low pH
- low O2
- high CO2 due to increased retention= respiratory acidosis
- high bicarbonate= due to chronic CO2 retention leading to elevating bicarbonate but unable to rise further/quickly enough for acute increase in CO2
Type 2 respiratory failure (2 are abnormal)
- low O2
- high CO2
What investigations would you do in an acute exacerbation of COPD and why?
ABG
CXR:
-pneumonia= consolidation
ECG:
- arrhythmia
- evidence of heart strain
FBC + CRP
- For infection
- distinguish between bacterial and viral infection (bacterial= neutrophilia, viral= lymphocytosis
U+E
-baseline before treating with medication which might affect renal function or relies on renal clearance
Sputum culture
-to determine what best antibiotics
Blood culture
-if septic
Lactate
-if suspecting sepsis
What is included in COPD rescue pack?
Prednisolone
Antibiotics= amoxicillin
Why should high flow oxygen be used with caution in COPD patients? How can this be combated?
COPD cause a shift from normal respiratory drive to hypoxic drive, associated with chronic elevation of CO2
Giving high levels of oxygen means that patient has blunted hypoxic drive because body thinks that ventilating adequately. Results in exacerbated retention of CO2 which can induce type 2 respiratory failure.
Need to balance optimising pO2 whilst preventing pCO2 from rising
Venturi mask so can more accurately titrate oxygen levels to reach targets of 88-92%
What condition can develop in longer term COPD? Why does this occur and what signs and symptoms would a patient present with?
Cor pulmonale (RHF) -Pulmonary vascular remodelling occurs which increases pulmonary hypertension
Occurs due to combined effect of: -hypoxia -inflammation -loss of capillaries (Occurs in severe emphysema)
Presentation:
-SOB (unlikely to be significant indicate because respiratory diseases causing cor pulmonale also give rise to SOB)
-Peripheral oedema
-Syncope
-Chest pain
-Raised JVP
-Hepatomegaly= due to back pressure into the portal system
-Parasternal heave= right ventricular hypertrophy
I.e. RV being anatomically most anterior and therefore closest to the chest wall
