COPD Flashcards
What is the major cause of COPD
Cigarette smoking
daily average of cigarettes smoked and years spent smoking
Other then Cigarettes, what else can result in COPD from chronic exposure
• Pollutants at work (mining, building and chemical industries)
• Outdoor air pollution
• Inhalation of smoke from biomass fuels used in heating and cooking in
poorly ventilated areas
What genetic deficiency can cause early COPD
Alpha-1 antitrypsin deficiency (due to proteolytic lung damage)
Pathophysiology of Alpha-1 antitrypsin deficiency
Mutations in the alpha-1 antitrypsin gene on chromosome 14 lead to
reduced hepatic production of alpha-1 antitrypsin which normally inhibits the proteolytic enzyme - neutrophil elastase
(Rare cause of cirrhosis due to accumulation of abnormal protein in the liver)
What is COPD
Chronic Obstructive pulmonary disease
Poorly reversible airflow limitation, usually progressive and persistent inflammatory response
Types of COPD
Blue bloaters
Pink puffers
Underlying pathology of Blue bloaters
Chronic bronchitis
Compensatory increase in Cardiac Output leads to hypoxia
Underlying pathology of Pink puffers
Emphysema
Compensatory hyperventilation prevents hypoxia
Pathophysiology of chronic bronchitis (blue bloaters)
Hypertrophy and hyperplasia of mucus secreting glands in bronchial tree, broncial wall inflammation and mucosal oedema. Ulcerations may cause metaplasia of columnar epithelium -> squamous epithelium. Capillary bed intact; body responds to increased obstruction by decreasing ventilation and increasing cardiac output. Poor ventilation to perfusion mismatch -> hypoxia (blue). Obstruction causes increasing residual lung volume (bloating).
Pathophysiology of pink puffers
Emphysematous:
Dilation and destruction of lung tissue distal to terminal bronchioles
-> loss of elastic recoil.
This usually is what allows airways to remain open following expiration, so causes air trapping.
Also causes damage to capillary bed and loss of alveoli (decreasing capacity for gas transfer)
-> Inability to oxygenate
-> Hyperventilation (puffing)
Are there more cases of emphysema or chronic bronchitis
Most people have a combination which results in severe airflow limitation
Different types of emphysema
Centri-acinar (v common)
Pan-acinar
Irregular
Describe Centri-acinar emphysema
Distension and damage of lung tissue is concentrated around the respiratory bronchioles, whilst the more distal alveolar ducts and alveoli tend to be well preserved
Describe Pan-acinar emphysema
Distension and destruction affect the whole acinus and in severe cases the lung is just a collection of bullae.
Associated with alpha-1 antitrypsin deficiency
Describe irregular emphysema
Scarring and damage that affects the lung parenchyma
patchily, independent of acinar structure
What causes V/Q mismatch in COPD
Partly due to damage and mucus plugging of smaller airways from the chronic inflammation
and partly due to rapid closure of smaller airways in expiration owing to the loss of elastic support
What results from V/Q mismatch in COPD
Fall in PaO2
Increased work or respiration
Why is CO2 excretion sometimes less affected by V/Q mismatch and so PaCO2 is usually normal or low (Type 1 RF)
Due to increasing alveolar ventilation in attempt to correct their hypoxia (pink puffers)
In shorter term for COPD patients, a rise in CO2 leads to stimulation of respiration. How does this change in longer term
Patients often become insensitive to CO2 and come to depend on the hypoxaemia to drive ventilation.
Such patients appear less breathless and because of renal hypoxia, they start
to retain fluid and increase erythrocyte production (leading eventually to polycythaemia) - they become bloated and cyanosed (blue).
Example of precipitating cause of acute exacerbations in COPD
Respiratory infections
Pathogenesis of cigarette smoke
- Causes mucus gland hypertrophy in the larger airways and leads to an increase in neutrophils, macrophages and lymphocytes in the airways and walls of the bronchi and bronchioles
- These cells release inflammatory mediators (elastases, proteases, IL-1,-8 & TNF-alpha) that attracts inflammatory cells (further amplify the process), induce structural changes and break down connective tissue (protease antiprotease imbalance) in the lung resulting in emphysema
- Inactivates the major protease inhibitor alpha-1 antitrypsin
Aetiology of COPD
Chronic inflammation of the airways.
Usually by smoking, also occupational irritants.
This causes the mucous gland hypertrophy, and increase in neutrophils, macrophages and lymphocytes in airways
-> Increase in inflammatory mediators (recurrent cycle)
-> Breakdown of lung tissue.
Respiratory clinical presentation of COPD
Chronic cough, exertional breathlessness, regular sputum production, wheeze.
Non-respiratory clinical presentation of COPD
Abnormal posture (leans forward), drowsiness/mental confusion, underweight, ankle oedema
Signs of COPD
Tachypnoea Use of accessory muscles of respiration Hyperinflation Decreased expansion Decreased cricosternal distance (<3cm) Wheeze Cyanosis Cor pulmonale Quiet breath sounds Resonant percussion note
Symptoms of COPD
Cough
Sputum
Dyspnoea
Wheeze
Epidemiology
Mostly smokers
Rare under 35
Diagnostic tests
CXR
FBC (increased PCV)
ABG (decreased PaO2 with or without hypercapnia)
Spirometry (obstructive and air trapping)
ECG (Right atrial and ventricular hypertrophy - cor pulmonale)
Complications
Respiratory failure Polycythaemia Cor pulmonale (oedema and increased JVP) Pnuemothorax Lung carcinoma
Complications
Respiratory failure Polycythaemia Cor pulmonale (oedema and increased JVP) Pnuemothorax Lung carcinoma Acute exacerbations with or without infection
Management of COPD if FEV1 <50%
- Initiate Short-Acting Beta 2 agonist (SABA) or Short Acting Muscarinic antagonist (SAMA)
- Test FEV1 (<50%)
- Long-acting muscarinic antagonist (LAMA) or Long-acting Beta agonst (LABA) plus inhlaed corticosteroid (ICS) in combined inhaler
- If still then LAMA plus LABA/ICS combination inhaler
COnsider LTOT if PaO2<7.3kPa
When should Long term oxygen therapy be given for COPD
Clinically stable non smokers with PaO2 <7.3kPa (despite maximal Rx)
If PaO2 is between 7.3-8.0 and have pulmonary hypertension, polycythaemia, peripheral oedema or nocturnal hypoxia
Terminaly ill patients
Management of COPD if FEV1 >50%
-Initiate Short-Acting Beta 2 agonist (SABA) or Short Acting Muscarinic antagonist (SAMA)
-Test FEV1 (>50%)
Two options:
1) LABA -> LABA plus Inhlaed Corticosteroid (ICS) -> LAMA plus LABA/ICS combination inhaler
2)LAMA -> LAMA plus LABA/ICS combination inhaler
Other factors in management of COPD
Consider palliative care input
Air travel is risky if FEV1 <50% or PaO2 <6.7kPa on air
Presentation of acute exacerbation of COPD
Increasing cough
Breathlessness
Wheeze
Decreased exercise capacity
Hx of acute exacerbation of COPD
Usual/recent treatments (esp home O2)
Smoking status
Exercise capacity
Differential diagnosis of acute exacerbation of COPD
Asthma Pulmonary oedema Upper resp tract obstruction Pulmonary embolus Anaphylaxis
Investigations of acute exacerbation of COPD
ABG,
CXR (to exclude pneumothorax and infection),
FBC, U and E, CRP,
Theophylline level if patient on therapy at home,
ECG,
Spend sputum for culture if purulent,
Blood cultures if pyrexial
*Management of acute exacerbation of COPD
1) Nebulised bronchodilators: Salbutamol and Ipratropium
Investigate ABG, CXR
2) Controlled oxygen therapy if SaO2 <88% or PaO2 <7kPa
3) Steroids: IV hydrocortisone and oral predinsolone
4) Antibiotics (e.g. amoxicillin or doxycycline)
5) Physiotherapy to aid sputum exacerbation
6) If no response to nebulisers and steroids, consider IV aminophylline
7) If still no response consider non-invasive positive pressure ventilation (NIPPV) or respiratory stimulant drug (e.g. doxapram)
Example of nebulised bronchodilators
Salbutamol and ipratropium
What is the greatest danger in COPD
Hypoxia (bigger killer than hypercapnia)
