Respiratory Flashcards
1
Q
What is the pathophysiology of COPD?
A
- Increased numbers of mucus-secreting goblet cells within the bronchial mucosa, especially in the larger bronchi
- In advanced cases, the bronchi become overtly inflamed and pus in seen in the lumen
- Most have emphysema and chronic bronchitis and the combination of these severely limits airflow
- V/Q mismatch from damage and mucus plugging
- Cigarette smoke causes mucus gland hypertrophy in larger airways, leading to an increase in neutrophils, macrophages and lymphocytes in the airways
- These cells release inflammatory mediator, attracting inflammatory cells, inducing structural changes and breaking down connective tissue in the lung → emphysema
2
Q
What are the risk factors of COPD?
A
- CIGARETTE SMOKING
- Pollutants at work (mining, building and chemical industries)
- Outdoor air pollution
- Inhalation of smoke from biomass fuels
3
Q
What is the clinical presentation of COPD?
A
- Characteristic symptoms are productive cough with white or clear sputum, wheeze and breathlessness (usually follows many years of a smoker’s cough)
- Colds seem to settle on the chest and frequent infective exacerbations occur with purulent sputum (contains pus)
- Symptoms worsened by cold or damp weather and atmospheric pollution
- Systemic effects: hypertension, osteoporosis, depression, weight loss, reduced muscle mass with general weakness
- Severe disease = breathless at rest with prolonged expiration, poor chest expansion and hyperinflated lungs (barrel chest)
- Pursed lips on expiration (helps to prevent airway collapse)
- Later stages are characterised by respiratory failure
- May develop pulmonary hypertension in advanced disease
4
Q
What are the differential diagnoses of COPD?
A
- Asthma
- Congestive heart failure
- Bronchiectasis
- Allergic fibrosing alveolitis
- Pneumoconiosis
- Asbestosis
5
Q
How is COPD diagnosed?
A
- Based on a history of breathlessness and sputum production in a chronic smoker
- If there is no history of smoking, it’s more likely to be asthma unless there’s a family history suggesting alpha-1 antitrypsin deficiency
- Lung function tests show progressive airflow limitation with increasing severity and breathlessness
6
Q
How is COPD managed?
A
- SMOKING CESSATION
- Bronchodilators: inhaled tiotropium bromide with salbutamol
- Corticosteroids in symptomatic patients with moderate/severe COPD prednisolone daily
- Oxygen therapy
- Antimucolytic agents can reduce sputum viscosity
- Diuretics
- Pulmonary rehabilitation to increase exercise capacity
- Good diet to reduce weight
- Alpha-1 antitrypsin replacement
7
Q
What is the pathophysiology of chronic bronchitis?
A
- Airway narrowing and airway limitation from hypertrophy and hyperplasia of mucus secreting glands of the bronchial tree, bronchial wall inflammation and mucosal oedema
- Infiltration of the bronchi/bronchiole walls with acute and chronic inflammatory cells
- Epithelial layer becomes ulcerated and eventually squamous epithelium replaces the columnar cells (=squamous metaplasia) when the ulcer heals
- Inflammation is followed by scarring and thickening of the walls, narrowing the small airways
- Small airways are particularly affected in early disease
- Initial inflammation is reversible so improvement in airway function can happen is smoking is stopped early (in later stages, inflammation continues even if smoking is stopped)
8
Q
What is the classic clinical presentation of chronic bronchitis?
A
- ‘Blue bloaters’
- Cough with phlegm
- Cor pulmonale
- Respiratory failure (usually T2)
9
Q
What is the pathophysiology of emphysema?
A
- Dilatation and destruction of the lung tissue distal to the terminal bronchioles
- Results in loss of elastic recoil, causing expiratory airflow limitation and air trapping
- Premature closure of airways limits expiratory flow while the loss of alveoli decrease capacity for gas transfer
10
Q
What is the classic clinical presentation of emphysema?
A
- ‘Pink puffers’
- Weight loss
- Breathless
- Maintained pO2
11
Q
What is the aetiology of asthma?
- Allergic/ eosinophilic
- Non allergic/ non-eosinophilic
- Genetic factors
- Environmental factors
A
Two main categories:
- Atopy: IgE antibodies readily produced against common exposures.
- Increased responsiveness of airways to inhaled stimuli: histamine and methacholine
ALLERGIC/ EOSINOPHILIC:
- Allergens (e.g. fungal allergens and pets etc) and atopy
NON-ALLERGIC/ NON-EOSINOPHILIC:
- Exercise, cold air and stress
- Smoking and non-smoking associated
- Obesity associated
GENETIC FACTORS:
- No single gene, but several genes in combination with environmental factors
- Genes controlling the production of different cytokines
- ADAM33 is associated with hyper-responsiveness and tissue remodelling
ENVIRONMENTAL FACTORS:
- Early childhood exposure to allergens and maternal smoking has a major influence on IgE production
- Growing up in a ‘clean’ environment may predispose towards an IgE response to allergens
12
Q
What is the pathophysiology of asthma? (Inflammation and muscular changes)
A
INFLAMMATION:
- Triggers cause an inflammatory cascade in the bronchial tree
- Mast cells, eosinophils, T lymphocytes and dendritic cells increased in bronchial wall, membranes and secretions
- Lymphocytes produce ILs to start cascade → IgE produced
MUSCULAR:
- Increased contraction of smooth muscle in bronchial wall
- Remodelling causes more muscle mass in wall and increased number of goblet cells
13
Q
What are the risk factors of asthma?
A
- Personal history of atopy
- Family history of asthma or atopy
- Obesity
- Inner-city environment
- Premature birth, socio-economic deprivation
14
Q
What is the clinical presentation of asthma?
General, during attack, uncontrolled attack, severe attack, life threatening attack
A
- Intermittent dyspnoea
- Wheeze
- Cough (especially nocturnal)
- Sputum
- Symptoms worse at night
- Episodic shortness of breath
- Provoking factors: allergens, infection, menstrual cycle, exercise, cold air
DURING ATTACK:
- There is reduced chest expansion
- Prolonged expiratory time
- Bilateral expiratory polyphonic wheezes
- Tachypnoea
UNCONTROLLED ATTACK:
- PEFR < 50% expected
- Resp rate < 25/m
- Pulse < 110bpm
- Normal speech
SEVERE ATTACK:
- Inability to complete sentences
- Pulse > 110bpm
- Resp rate > 25/m
LIFE-TREATENING ATTACK:
- Silent chest
- Confusion and exhaustion
- Cyanosis (PaO2 < 8kPa)
- Bradycardia
- PEFR < 33%
15
Q
What are the differential diagnoses of asthma?
A
- Pulmonary oedema
- COPD (may co-exist)
- Large airway obstruction caused by a foreign body/ tumour
- Pneumothorax
- Bronchiectasis
16
Q
How is asthma diagnosed?
A
- History and evidence of obstruction (PEF/ spirometry) during episodes
- RCP3 questions: recent nocturnal waking, usual symptoms in a day, interference with activities of daily living
- Lung function tests (PEFR, spirometry)
- Exercise tests
- Trial or corticosteroids
- Exhaled nitric oxide (measure of eosinophilic inflammation)
- Blood and sputum tests
- Skin prick tests to identify allergens
17
Q
How is asthma managed?
normal, non-emergency management
A
- Avoid triggers
BRONCHODILATORS: → Beta2-agonists: - SABA last 4h e.g. salbutamol - LABA last 12h e.g. salmeterol → Muscarinic agents: - SAMA e.g. ipratropium - LAMA e.g. tiotropium → Methylxanthines: - Theophylline
ANTI-INFLAMMATORY STEROIDS (inhaled corticosteroids)
- For all patients with regular persistent symptoms
- E.g. prednisolone, beclomethasone, budesonide
18
Q
What is the immediate management for a life-threatening asthma attack?
A
- Oxygen therapy to maintain O2 sat (94-98%)
- Nebulised 5mg salbutamol (+ ipratropium if life threatening) – repeat/ IV infusion
- Prednisolone (± IV hydrocortisone)
- Take ABG and repeat within 2 hours if severe or if deteriorating
- CXR if fails to respond to treatment
- Check PEFR within 15-30m / regularly
- Oximetry to ensure SaO2>92%
19
Q
What is the aetiology of mesothelioma?
A
Asbestos exposure
20
Q
What is the pathophysiology of mesothelioma?
A
- High grade malignancy of the pleura that spreads around pleural surfaces
- Can also start in the pericardial space, peritoneal space and paratesticular space
- Tumour begins as nodules in the pleura which extend as a confluent sheet to surround the lung and extend into fissures
- The chest wall if often invaded with infiltration of intercostal nerves, giving severe intractable pain
- Lymphatics may be invaded, giving hilar node metastases
21
Q
What is the main risk factor for mesothelioma?
A
Asbestos exposure
22
Q
What is the clinical presentation of mesothelioma?
A
- Chest pain
- Dyspnoea
- Weight loss
- Finger clubbing
- Recurrent pleural effusions
- Breathlessness
- Signs of metastases: lymphadenopathy, hepatomegaly, bone pain/tenderness, abdominal pain/obstruction
23
Q
How is mesothelioma diagnosed?
A
- CXR and CT: unilateral pleural effusion, pleural thickening
- Blood/straw coloured pleural fluid
- Pleural biopsy
24
Q
How is mesothelioma managed?
A
- Surgery for extremely localised mesothelioma
- Generally resistant to surgery, chemotherapy and radiotherapy
- Average time from diagnosis to death is 8m
- Refer all mesothelioma deaths to HM coroner
- Poor prognosis
25
Q
What is the pathophysiology of a small cell lung carcinoma?
A
- Often arises from endocrine cells in a central bronchus
- Secretes polypeptide hormones and have early development of widespread metastases
26
Q
What is the pathophysiology of a squamous cell carcinoma (type of non-small cell lung carcinoma)?
A
- Tumours are usually central in location and frequently cavitate with central necrosis
- Arise from epithelial cells and are associated with keratin production
- Cause obstructive lesions of bronchus with post-obstructive infection
- Local spread common and metastases relatively late
27
Q
What is the pathophysiology of an adenocarcinoma (type of non-small cell lung carcinoma)?
A
- May be central or peripheral
- Usually single lesions but they can arise in a multifocal pattern, sometimes bilaterally
- Originate from mucus-secreting glandular cells
- Most common type in non-smokers
- Often cause peripheral lesions on CXR/ CT
- Metastases common to pleura, lymph nodes, brain, bones and adrenal glands
Carcinoid tumours: - Characteristic neuroendocrine secreting cells and relatively low rates of invasion and growth
28
Q
What is the pathophysiology of lymphomas (type of non-small cell lung carcinoma)?
A
- Involve the lung primarily but are usually a component of disseminated disease
- Main lung lymphoma is a B cell lymphoma
29
Q
What is the pathophysiology of benign non-small cell lung tumours (hamartomas)?
A
- Irregular proliferations of benign/normal tissues not normally found in this pattern within the lung
- Most common one in the lung is chondroid hamartoma
30
Q
What are the risk factors for lung cancers?
general, occupational, environmental, host factors
A
- Cigarette smoking (including passive smoking)
- OCCUPATIONAL: asbestos, coal (and products of coal combustion), chromium, arsenic, nickel, petroleum products, iron oxide
- ENVIRONMENTAL: radon exposure, ionising radiation
- HOST FACTORS: pre-existing lung disease such as pulmonary fibrosis, HIV infection, genetic factors
31
Q
What is the clinical presentation of lung cancers? (local and metastatic disease)
A
LOCAL DISEASE:
- Cough
- Breathlessness
- Haemoptysis
- Chest pain
- Wheeze
- Recurrent infections e.g. pneumonia
- Clubbing
METASTATIC DISEASE:
- Bone pain
- Headache
- Seizures
- Neurological deficit
- Hepatic pain
- Abdominal pain
32
Q
How are lung cancers diagnosed?
A
- TNM classification
- CXR: appear as round shadow, edge has a fluffy spiked appearance, hilar enlargement, consolidation, lung collapse, pleural effusion
- CT for staging
- Bronchoscopy to give histology and assess operability
- Cytology for sputum and pleural fluid
- Bloods: low FBC
