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
What are the main causes of HAP
60% of HAP is caused by gram negative bacteria = klebsiella, E. coli, pseudomonas
S. aureus and s. pneumoniae are also important causes
What patients are at risk of aspiration pneumonia
Intoxicated patients
Acute stroke patients with impaired swallowing
Septic patients with reduced conciousness
What organisms cause aspiration pneumonias
Usually mixed infections including anaerobes
What are the causative organisms of pneumonia in the immunocompromised
- conventional respiratory pathogens are still common, but the infection is often more severe
- fungi = pneumocystis, candida, aspergillus
- mycobacterial infection = M. tuberculosis
- viruses = CMV, HSV
What are diffuse parenchymal lung diseases
A large group of conditions characterised by inflammation centres on the interstitium of alveolar walls.
What is the lung interstitium
The tissue lying between the alveoli and containing pulmonary artery capilliaries. Normally it is a thin layer, allowing for the alveoli and the capilliaries to lie very close to one another enabling optimal diffusion
What is the pathophysiology behind DPLD
The interstitium becomes expanded by an inflammatory cell infiltrate (pneumonitis / alveolitis) which impairs gas exchange and causes breathlessness.
Episodes of pneumonitis may be followed by complete regeneration without residual damage to alveoli OR it may repair via scarring (destroys the functional units of the lungs) = ineffective gas exchange and therefore resulting in worsening breathlessness. The scarring means that the lungfs are converted into a mass of cystic air spaces separated by dense scarring (honeycomb lung)
What is pneumonitis
Inflammation of the lung parenchyma (eg. alveoli)
What is the difference between pneumonia and pneumonitis
Both are inflammation of the lung parenchyma, but pneumonia is specifically due to an infective agent.
What are the causes of DPLD
1) Unknown - ideopathic pulmonary fibrosis
2) pneumoconioses - inhaled dusts = asbestosis
3) extrinsic allergic alveolitis - inhaled organic particles = pidgeon fancier’s lung
4) side effects of treatment - amiodarone
5) multisystem diseases - SLE/sarcoid
What would investigations of a patient with DPLD show
1) CXR may show reticulation
2) spirometry = restrictive
3) high res CT = reticulation
What are long term complications of DPLD
pulmonary HTN
cor pulmonale
What is the second most common cancer in the UK
Lung cancer
Who gets lung cancer
50-60 y/o
85% cases due to smoking
What is the most common type of lung cancer
Carcinomas.
- 25% squamous cell carcinoma
- 40% adenocarcinoma
- 15% small cell
Where is the most common site of metastatic tumours
Lung
Lung cancer - Squamous cell carcinoma:
1) Where does it arise?
2) How does it arise?
1) larger airways near the hilum
2) a well defined metaplasia-dysplasia-carcinoma sequence leads to its development
What types of lung cancer are most associated with smoking
Small cell carcinoma = strongest association
Squamous cell = strong association
Adenocarcinoma = commonest in non-smokers (linked to EGFR gene)
Lung cancer - Adenocarcinoma:
1) Where does it arise?
Peripheral smaller airways
Lung cancer - small cell carcinoma:
1) Where does it arise?
2) How is it graded?
1) A central location
2) It isn’t, by definition it is highly aggressive
What genetic mutations are targets for therapy in lung cancer
- Tyrosine kinase inhibitors = gefitinib for EGFR mutations
- Immunotherapy = pembrolizumab for PD-L1 mutations, a key regulator of T cells
How do you sample lung cancers
Central lesions = bronchoscopy
Peripheral lesions = CT guided
How is lung cancer staged
TNM
CT for T staging
PET or PET-CT for N +M
How can lung cancer present
- cough
- haemopytsis
- stridor / wheeze
- hoarse voice (invasion of left recurrent laryngeal nerve)
- breathlessness
- chest wall pain
- non-resolving pneumonia
- SVC obstruction
- B symptoms
- symptoms of mets
What is the most common cause of SVC obstruction
Right-sided lung cancer (often small cell carcinoma)
A right sided lung cancer results in SVC obstruction. What is the result of this?
Increased venous pressure = interstitial oedema and retrograde collateral flow
What are the most common symptoms of SVC obstruction
SOB!!!
- facial swelling
- head fullness
- cough
- arm swelling
- chest pain
- dysphagia
- hoarseness
- stridor
Why is SVC obstruction an emergency
- laryngeal oedema
- cerebral oedema
- decreased CO
What is Pancoast’s tumour
A cancer in the apex of the lung which involves the 8th cervical and 1st and 2nd thoracic nerves.
How might Pancoast’s tumour manifest
Pancoast’s syndrome (shoulder pain radiating in an ulnar distribution down the arm) or horner’s syndrome
What is Horner’s syndrome
Due to sympathetic nerve infiltration by tumour.
What are the clinical features of Horner’s syndrome
- endophthalmos (eyeball depression)
- ptosis (droop) of upper eyelid
- miosis (pupil constriction)
- anhidrosis (absence of sweating)
A patient with lung cancer is found to have hypercalcaemia, what is the likely cause?
Bony mets
Can be a paraneoplastic effect (more common in squamous cell carcinoma)
What is SIADH
A paraneoplastic syndrome.
Syndrome of inappropriate antidiuretic hormone secretion. Mainly seen with small cell carcinomas.
Initially asymptomatic but will progress to cerebral oedema (clumsy + tired –> drowsy + confused)
List the main paraneoplastic syndromes and the cancers they are associated with
1) hypercalcaemia - squamous cell carcinoma
2) SIADH - small cell carcinoma
3) Ectopic ACTH production - small cell carcinoma
4) Lambert Eaton myasthenic syndrome - small cell carcinoma
What is Lambert Eaton myasthenic syndrome?
A paraneoplastic syndrome where autoantibodies block VGCC in the presynaptic membrane and block ACh release
How do you manage small cell lung cancer
Usually highly aggressive at presentation + many mets
Initially they respond to chemotherapy - after a few months they become resistant
Surgery is a possibility if the disease is a low stage
What is mesothelioma
A malignant tumour of the pleura associated with asbestos exposure. there is a long latency period (40yr) between exposure and development
60M presents with breathlessness and chest pain, and a pleural effusion. SHx: Shipyard worker.
What is the likely diagnosis?
Mesothelioma
How do you diagnose mesothelioma
Cytological examination of pleural fluid / histological examination of pleural biopsy
How is mesothelioma graded
It isn’t, by definition it is highly aggressive
What is the prognosis of mesothelioma
18 months from diagnosis
What diseases are related to asbestos exposure
- Mesothelioma
- Lung cancer
- Asbestosis - a type of DPLD
