Respiratory Flashcards
What is COPD
Progressive airway obstruction which does not change markedly over several months. It is characterised by persistent airflow obstruction that is poorly reversible and usually progressive.
What is chronic bronchitis
Clinically as a cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease
What is emphysema
Permanent dilatation of the airways distal to the terminal bronchiole. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
In emphysema there is a permanent dilatation of the distal airways.
What causes airway obstruction in COPD
Damage to the small conducting airways and alveoli. It is almost always caused by tobacco smoking, but may also be related to occupation (mining) and alpha-1 antitrypsin deficiency
Describe the effects of smoking on the bronchi
Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium = increased sputum production
Describe the effects of smoking on the small airways
Chronic inflammation = healing by fibrosis = stenosis of airways
Describe the effects of smoking on the respiratory bronchioles
Destruction of the walls with loss of the elastic tissue but without significant fibrosis = airway dilatation = emphysema
Effects of destruction:
(1) Loss of pulmonary SA for gas exchange = hypoxia
(2) Loss of the elastic tissue of the terminal airways results in loss of the natural recoil of the lungs = contributes to airflow obstruction (reduces airflow on expiration)
Explain the protease-antiprotease hypothesis
May account for the lung destruction in emphysema. Smoking causes
A) increased numbers of activated neutrophils in the lung where they release protease enzymes (eg. elastate)
B) Inhibits the lungs natural protease inhibitor enzymes (alpha-1 antitrypsin)
Essentially + smoking = + elastases = - elastin = destruction and enlargement of the distal airspaces
Describe alpha-1 antitrypsin deficiency and its effects
An inherited deficiency of alpha-1 antitrypsin leads to the premature onset of COPD due to widespread emphysematous change in the lungs (alpha-1 antitrypsin is a protease inhibitor).
Patients may also develop liver cirrhosis.
Describe the clinical presentation of COPD
Varying, depending on where the obstruction is:
- larger aiways = cough and sputum
- smaller airways = breathlessness
Usually the large airways are first affected - progression of symptoms:
- cough + sputum
- breathlessness on exertion
- breathless at minimal exertion
- breathless at rest
What is the biggest cause of death with COPD
- bronchopneumonia
- respiratory failure
- heart failure
How is a diagnosis of COPD confirmed
Spirometry - demonstrates airflow obstruction
What is an acute exacerbation of COPD defined as
Sudden sustained worsening in a patient’s symptoms that is beyond their normal day to day variation = worsening breathlessness + cough, increased sputum production
What are the causes of an acute exacerbation of COPD
Infection - bacterial / viral Pneumothorax PE LVF Lung carcinoma
What are the differences between an infective exacerbation of COPD, and pneumonia
Infective exacerbation = always underlying COPD, airways are the focus infection, CXR shows clear lung fields, most common causes = H influenzae, M catarrhalis, S pneumoniae, viruses
Pneumonia = sometimes underlying COPD, alveoli are the focus of infection, CXR shows consolidation, most common causes = S pneumoniae, H influenzae, viruses, atypicals
A patient with COPD presents with an increase in their productive cough. Their CXR shows clear lung fields.
What are the likely causative organisms?
This is likely to be an infective exacerbation of COPD.
H influenzae, M catarrhalis, S pneumonia, viruses
A patient with COPD presents with an increase in their productive cough. Their CXR shows consolidation.
What are the likely causative organisms?
Although the patient has COPD, this is likely to be pneumonia and not an infective exacerbation due to the consolidation seen on the CXR.
S pneumoniae, H influenzae, viruses, atypicals
What are the long term complications of COPD
- cor pulmonale
- changes in the pulmonary circulation = A) emphysema causes loss of pulmonary arterioles and capillaries B) chronic hypoxia causes pulmonary artery vasoconstriction C) chronic hypoxia causes increased EPO, resulting in erythropoesis and increased blood viscosity
These all cause the gradual development of pulmonary HTN
What is pneumonia
Inflammation of the lung parenchyma (ie. alveolar spaces) due to an infective agent.
What is bronchopneumonia
Characterised by widespread patchy inflammation centred on the airways. It is often bilateral.
What is lobar pneumonia
Characterised by diffuse inflammation affecting an entire lobe or lobes.
Becomes consolidated due to accumulation of acute inflammatory exudate within the alveoli. There is abrupt demarcation at the interlobar fissure.
What is consolidation
On a CXR it refers to the replacement of air in alveolar fluid by fluid or other material with preservation of the underlying alveolar architecture.
In the case of pneumonia, the air is replaced by acute inflammatory exudate. There is no destruction of the underlying architecture.
What are the most common causative organisms in CAP
- Strep pneumoniae (MOST COMMON)
- Influenza + other viruses
- chlamydia pneumoniae
- Mycoplasma pneumoniae
- Legionella pneumonia
- Haemophilus influenzae
A patient has mild CAP. What is the most likely cause?
Strep pneumoniae
A patient has severe CAP. What are the common causes?
S. pneumoniae
Legionella
S. Aureus
What score is used to assess the severity of CAP
CURB-65
What is CURB-65
C = confusion of new onset (AMT <8) U = urea > 7mmol/L R = RR > 30 B = BP <90 systolic / <60 diastolic 65 = being older than 65
What is HAP
Occurs 2 days after admission to hospital
