PBL Topic 2 Case 3 Flashcards
Outline four characteristics of COPD
- Airflow limitation
- Not fully reversible
- Progressive
- Abnormal inflammatory response
What are the main cause of COPD in developed countries and developing countries respectively?
- Cigarette smoking
- Smoke from biomass fuels
Outline the pathophysiology of COPD
- Mucus gland hyperplasia
- Infiltration of neutrophils and CD8 lymphocytes
- Squamous metaplasia
- Loss of interstitial support
Define emphysema
- Abnormal, permanent enlargement of air spaces
- Distal to the terminal bronchioles
- Accompanied by destruction of their walls without obvious fibrosis
Describe centri-acinar emphysema
- Destruction concentrated around the respiratory bronchioles
- Distal alveolar ducts and alveoli well preserved
Define pan-acinar emphysema
- Destruction of the whole acinus
- Associated with a1-Antitrypsin deficiency
Outline the other type of emphysema
- Irregular emphysema
- Damaging and scarring of lungs in a patchy manner independent of acinar structure
Identify 2 ways in which Va/Q mismatch occurs in emphysema
- Mucous plugging of smaller airways from inflammation
- Closure of small airways due to loss of elastic support
Explain why hypoxaemia develops in emphysema
- Va/Q mismatch leads to increased work of ventilation
- PaCO2 increases
- Patients become insensitive to CO2 and come to depend on hypoxaemia to drive their ventilation
(in normal people, the drive for ventilation is high CO2, though these patients become insensitive so low O2 drives their ventilation)
Explain why polycythaemia develops in emphysema
- Renal hypoxia
- Fluid retention and erythrocyte production
Identify the clinical features of polycythaemia
- ‘Blue Bloater’
- Barrel chest and dyspneic
- Hunched over
- Breathes through pursed lips ‘pink puffers’
What is the role of a1-Antitrypsin
- Antiprotease secreted by liver
- Inhibits neutrophil elastase
- Maintain lung elasticity
What is the effect of cigarette smoke on a1-Antitrypsin?
- Inactivates a1-Antitrypsin
- Leads to emphysema
Respiratory failure is said to occur when:
- PaO2 < [A]
- PaCO2 > [B]
- [A] = 8 kPa (60 mm Hg)
- {B] = 7 kPa (55 mm Hg)
What are the effects of hypoxia and hypercapnia?
- Constriction of pulmonary arterioles
- Pulmonary hypertension (Cor Pulmonale)
What is the cause of pulmonary hypertension (cor pulmonale)
- Renal hypoxia
- Failure of excretion of sodium and water
- Leads to fluid retention
What are the clinical features of pulmonary hypertension (cor pulmonale)
- Cyanosed and breathless
- Ankle oedema
- Parasternal heave
- Elevated JVP due to incompetence of pulmonary valve
‘During nocturnal hypoxia, PaO2 may fall as low [A], especially during the [B] phase of sleep’
- [A] = 2.5 kPa (19 mm Hg)
- [B] = Rapid Eye Movement (REM)
During nocturnal hypoxia, outline three causes that result in alveolar hyperventilation
- Inhibition of intercostal and accessory muscles in REM sleep
- Shallow breathing
- Increase in upper airway resistance due to reduced muscle tone
What is the main cause of death in COPD patients?
- Most deaths occur at night
- From cardiac arrhythmias
- Due to hypoxaemia
Explain why patients with nocturnal hypoxia suffer from daytime sleepiness?
- Desaturation is terminated by waking up
- This occurs many times in the night
- Amount of sleep is therefore reduced
Outline the main treatment of nocturnal hypoxia and why sleeping tablets should not be given.
- Nocturnal administration of oxygen by nasal mask and BiPAP
- Sleeping tablets further depress respiratory drive
Outline characteristic symptoms of COPD
- Cough with clear sputum
- Wheeze and breathlessness
- Infections with purulent symptoms
- All made worse by cold / foggy weather
Outline characteristic signs of COPD
- Tachypnea
- Hyperinflation of lungs
- Heart failure and oedema as terminal events
Diagnosis of COPD requires demonstration of flow obstruction by spirometry and is established when:
- FEV1 < 80% predicted value
- FEV1/FVC ratio < 70%
Outline the management of COPD
- Smoking cessation
- Bronchodilators (B-adrenergic agonists, theophylline, antimuscarinic drugs)
- Anti-inflammatories (corticosteroids, phosphodiesterase type 4 inhibitors)
- Antibiotic treatment
- Oxygen therapy
Outline when oxygen therapy will be beneficial to patients:
- PaO2 < 55 mm Hg
- PaO2 < 60 mm Hg with secondary polycythaemia
- Carboxyhaemoglobin < 3%
What is the BODE Index?
- Determine prognosis of COPD
- B = Body Mass
- O = Obstruction
- D = Dyspnoea
- E = Exercise Capacity
How does a BODE index of 0-2 differ to that of a BODE index of 7-10
- 0-2: 4 year mortality rate of 10 %
- 7 - 10: 4 year mortality rate of 80%
Define bronchiectasis
- Permanently dilated airways
- Irreversible damage of airways
- Impaired mucociliary transport mechanism
Outline two causes of bronchiectasis
- Genetic defect e.g. cystic fibrosis
- Infection e.g. tuberculosis
Outline four clinical features of bronchiectasis
- Clubbing
- Yellow or green sputum (following infection)
- Breathlessness (airflow limitation)
- Haemoptysis
Identify investigations carried out for bronchiectasis
- HRCT/CXR = Dilated Airways
- Sputum culture = Bacterial Infection
- Sinus X rays
- Sweat test = Cystic Fibrosis
Outline the treatment of bronchiectasis
- Postural drainage
- Ceftazidime for P.aeruginosa
- Flucloxacillin for S.aureus
- Surgery: embolisation and surgical resection
Outline complications of bronchiectasis
- Pulmonary Tuberculosis
- Pneumonia
- Pneumothorax
- Emphysema
What is Pneumonia
- Inflammation of the substance of the lungs
Identify three classifications of Pneumonia
- Community-acquired (CAP)
- Hospital-acquired (HAP)
- Immunocompromised host