COPD Flashcards
Pathology of COPD
Obstruction due to narrowing of airways - combination of bronchitis and emphysema
Pathology of chronic bronchitis
Causes excess mucous production and inflammation of respiratory tract
Inflammation leads to scarring and fibrosis which thickens the walls of the airways, reducing size of lumen and increases diffusion distance
Pathology of emphysema
Causes increased in airspaces due to dilation or from destruction of the walls without obvious fibrosis
Loss of alveolar tissue means loss of elasticity and thus recoil of the lungs
Chronic bronchitis aetiology
- SMOKING
- Air pollution
- Occupation (dust)
- a-1-antitrypsin deficiency (cant inhibit protease which destroys tissue)
- Effect of age & susceptibility (metabolism of irritants in tobacco smoke)
Smoke paralyses cilia that sweeps debris and mucous out of the airways and smoke irritation increased mucous production - without functional cilia, mucous & debris pool in airways
Morphological changes in chronic bronchitis
Small airways:
- Goblets appear
- Fibrosis and inflammation I along standing disease
Large airways:
- Mucous and goblet cell hyperplasia
- Inflammation and fibrosis
Emphysema aetiology
- SMOKING: protease-antiprotease imbalance
- a-1-antitrypsin deficiency
Describe centri-acinar emphysema
Begins with bronchiolar dilation, then alveolar tissue loss
Enlargement of airways in the proximal part of bronchial tree due to LACK OF ELASTIN
Describe panacinar
a-1-antitrypsin deficiency allows elastase to inhibit elastin, so all acinar structures destroyed
What is a bulla?
Emphysematous space > 1cm
What is a bleb?
A space (bulla) underneath the pleura which can cause a pneumothorax
Effect of hypoxaemia
Low O2 concentration in blood due to airway obstruction which decreased inhaled air in alveoli - alveolar hypoventilation
Most alveoli are hypoxic, so arterioles constrict due to shunt (V/Q mismatch) which increased BP and cause pulmonary HPT
Pul. HPT increases work of RV to pump blood in pul. circulation, causing it to hypertrophy and dilate -> Cor pulmonale
Symptoms of COPD
SOB (decreased gas exchange and abnormal diaphragm mechanism) Cough (cilia impaired) Recurrent chest infection - specific Sputum purulence Wheeze Dyspnoea
Signs
May be normal in early stages
Reduced chest expansion
Wheeze
Hyperinflated chest (gas trapping)
Respiratory failure: Cyanosis Tachypnoea Accessory muscles Pursed lip breathing Peripheral oedema
Cor Pulmonale
Weight loss
Clinical history
PH:
Asthma as child
Ischaemic heart disease
Drugs:
List of current inhalers and doses
Previous meds and effect on breathing (steroids)
Social:
Occupation (exposure to dust, vapours, fumes)
Smoking - pack years
Exacerbating factors
Viral/bacterial infections, sedative drugs, trauma and pneumothorax
Useful Investigations
CXR (flattened diaphragm, hyperinflation: > 6 anterior and > 10 posterior ribs, bullae)
ABG (type I or II res failure)
FBC (high WBC - anaemia, high Hb or eosinophil)
ECG (cor pulmonale)
Sputum culture (Strep. pneumonia, H influenza, M catarrahlis)
Effect of loss of elastic recoil in emphysema
Can cause collapse of the lungs - this makes expiration hard and air is ‘trapped’ -> hyperinflation of lungs
Main pathological changes in the small airways
Goblet cells appear
Inflammation and fibrosis
Main pathological changes in the large airways
Mucous gland hyperplasia
Goblet cell hyperplasia
Inflammation and fibrosis
How does smoking cause COPD?
Tobacco in cigarettes releases a reactive oxygen species - free radicals. This causes the inactivation of antiproteases leading to an increase in neutrophil elastase which cause tissue damage -> emphysema
Paralyses the cilia that sweep debris and mucus out of the airways -> mucous and debris pool in the airways
Why does hypoxaemia occur?
Airway obstruction
Reduced respiratory drive
Loss of alveolar surface area (less gas exchange)
V/Q mismatch - responds well to small increases in FiO2
What other molecules can increase neutrophil elastase?
Nicotine in tobacco
IL-8, LTB4 and TNF from free radicals
Both cause the release of neutrophils causing an increase in neutrophil elastase
What can COPD lead to?
Loss of muscle mass (SOB)
Weight loss
Cardiac disease - R HF then L HF which will decrease CO
Depression, anxiety
How is COPD diagnosed?
Clinical history: cough, SOB, recurrent chest infections, winter bronchitis
Examination: normal or tachypnoea, wheeze, hyper inflated chest
Spirometry: confirms and assesses severity
Interpretation of spirometry
Based on the patient’s FEV1 and its percentage of predicated FEV1
> 80% : mild AFO
50-79% : moderate AFO - cough, SOBOE
30-49% : severe AFO - SOBOE, cough/sputum
<30% : v severe AFO - SOBOE+, wheeze, cough, cor pulmonale
Essential investigations
Spirometry
Full pulmonary function testing
Response to drug therapy
Explain use of PFT
Looking for emphysema
Gas trapping present: increase residual volume and total lung capacity
RV/TLC > 30%
Carbon monoxide gas transfer:
Decreased diffusion of CO sign of emphysema (loss of surface area)
Explain response to drug therapy in COPD
Should show:
Minimal bronchodilator reversibility (salbutamol)
Minimal response to oral corticosteroids
- 30mg prednisone daily for 2 weeks
- Measure baseline and final FEV1
What are 4 exacerbating factors?
Viral/bacterial infection
Sedative drugs
Pneumothorax
Trauma
What are 5 signs of AECOPD?
Confusion Cyanosis SOB Flapping tremor Pyrexia
Aims and interventions of COPD
Prevent progression -> smoking cessation
Relieve SOB -> inhalers
Prevent exacerbation -> inhalers, vaccines, pulmonary rehabilitation
Manage complications -> long term O2 therapy
Non-pharmacological management
Smoking cessation Vaccinations (flu, pneumococcal) Pul. rehab Nutritional assessment Psychological support
Benefits of pharmacological management
Relieves symptoms
Prevent exacerbations
Improves quality of life
Stages to treatment
- SABA
- LABA or LAMA
- Further LABA or LAMA
- Triple therapy: ICS, LABA, LAMA
Name short acting bronchodilators
SABA - salbutamol
SAMA - ipratropium
Name long acting bronchodilators
LABA (long acting B2 agonist) - salmeterol
LAMA (long acting anti-muscarinic agents) - umeclidium
Name inhaled corticosteroids
Revlar
Criteria for long term oxygen (LTOT)
PaO2 < 7.3kPa or PaO2 = 7.3-8 kPa if: polycythaemia nocturnal hypoxia peripheral oedema pul. HPT
Management of AECOPD
SABA (salbutamol) Steroids (prednisone) Antibiotics - if evidence of infection (fever, increase in sputum volume/purulence) Consider hospital: -Tachypneoa -Low O2 sat <92% -Hypotension
Investigations for AECOPD
FBC Biochem and glucose Theophylline concentration ABG Electrocardiograph CXR Blood culture Sputum microscopy, culture and sensitivity
Why do you get a hyper inflated chest in COPD?
Obstruction is usually with air being expired so air trapped in lungs
