COPD Flashcards
Definition?
Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease state characterised by airflow limitation that is not fully reversible. It encompasses both emphysema and chronic bronchitis.
Risk factors strong?
- Smoking
- Advanced age
- Genetics
- Occupational problems
Risk factors weak?
- White
- Air pollution
- Developmental problems
- Male
- Low SE status
Differentials?
- Asthma
- Congestive heart failure
- Bronchiectasis
- Tuberculosis
- Bronchiolitis
- Upper airway dysfunction
- Chronic sinusitis/post-nasal drip
- GORD
- ACE inhibitor induced chronic cough
- Lung cancer
Epidemiology?
Age: over 65’s
Sex: Male-recently equal
Ethnicity: White
Prevalence: Fourth leading cause of death in the world, 3 million in UK
Aetiology?
Smoking induces an inflammatory response, cilia dysfunction and oxidative stress by increasing proteinases that break down the cell lining in bronchioles
Clinical Presentation-common?
- Risk factors
- Cough
- SOB
Clinical Presentation-uncommon?
- Barrel chest
- Hyper-resonance on percussion
- Distant breath sounds and poor air movement
- Wheezing
- Coarse crackles
- Tachypnoea
- Asterixis
- Distended neck veins
- Swelling
- Fatigue
- Headache
- Cyanosis
- Hepatojugular reflux
- Loud P2
- Hepatosplenomegaly
- clubbing
Pathophysiology of Chronic Bronchitis?
• Inflammation causes mucociliary dysfunction and increased goblet cell secretions and numbers so more mucus is made
• Bronchoconstriction and mucus hypersecretion causes airway obstruction and chronic cough and wheezing in expiration
• Airway obs-alveolar hypoxia-V/Q mismatch and pulmonary VC-leads to pulmonary hypertension and backflow to RV and so cor pulmonale and increased JVP
• Also less circulatory volume causes RAAS activation and so extra fluid retention
Obstruction-leads to hypoxaemia and hypercapnia and resp acidosis and polycythaemia and lead to cyanosis
Pathophysiology of Emphysema?
- Inflammatory response due to irritants stimulating macrophages attracting neutrophils and that secrete elastase leading to elastin breakdown in alveoli walls and so recoil is lost so less ventilation
- Or a1 antitrypsin deficiency-more proteases and less anti-proteases-breakdown of elastin/alveoli walls
- Also destruction of capillary beds and alveoli wall leading to decreased perfusion
- Leads to air trapping in alveolus in exhalation-higher end expiratory vol-cant empty lungs and accessory muscle used-barrel chest
- Mismatched V/Q -hypoxaemia and hypercapnia
First line investigations and findings?
- spirometry (FEV1/FVC ratio <0.70),
- pulse oximetry (88-90% or pulse wave),
- ABG (PaCO₂ >50 mmHg and/or PaO₂ of <60 mmHg suggests respiratory insufficiency)
- CXR-increased anteroposterior ratio, flattened diaphragm, increased intercostal spaces, and hyperlucent lungs may be seen.
- FBC-raised haematocrit, possible increased WBC count
- BMI
- ECG-signs of right ventricular hypertrophy, arrhythmia, ischaemia
2nd line investigations and findings?
2nd line: • Pulmonary function tests • Chest CT • Sputum culture • Alpha-1 antitrypsin level • Exercise testing • Sleep study • Resp muscle function
Management group A?
Info, smoking cessation, vaccines, anxiety and depression, management, inhaled therapy
Management group B?
Info, smoking cessation, vaccines, anxiety and depression, management, inhaled therapy, oral therapy and oxygen therapy-LABA and LAMA
Management group C?
Info, smoking cessation, vaccines, anxiety and depression, management, inhaled therapy, oral therapy and oxygen therapy-LABA and LAMA and ICS
