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Phase 2a Jill Hogan Sarah Crudden The Peer Teaching Society is not liable for false or misleading information…
Aims
• To give a brief overview of the following topics: – – Asthma COPD – Pulmonary fibrosis (interstitial lung disease) • Apply knowledge to practice exam papers The Peer Teaching Society is not liable for false or misleading information…
Introduction
• • Obstructive defect: FEV 1 (↓↓↓) is reduced more than FVC (↓). FEV 1 /FVC ratio is <75%. – COPD, Asthma Restrictive defect: FVC (↓↓↓) is reduced more than the FEV normal or >80%. 1 (↓). FEV 1 /FVC ratio is – Pulmonary fibrosis, pleural effusion, interstitial pneumonias The Peer Teaching Society is not liable for false or misleading information…
Asthma
• Common chronic relapsing/episodic inflammatory condition of the lung airways • • • Three Characteristics: Airflow limitation Airway hyper-responsiveness Inflammation of the bronchi The Peer Teaching Society is not liable for false or misleading information…
Classification
Onset in childhood atopy Often accompanied by asthma Extrinsic In adults Occupational β-blockers NSAID intolerance Positive skin prick test Type 1 hypersensitivity reaction Often starts in middle age No Causatory agent found Intrinsic Not immunologically mediated The Peer Teaching Society is not liable for false or misleading information…
Aetiology
• • • •
Atopy:
Type 1 hypersensitivity reaction Increase in IgE antibodies- allergen specific Trait run in families Environmental factors include: o Hygiene hypothesis o Childhood exposure to allergens o Maternal smoking •
Increased responsiveness of the airways of the lung:
To stimuli such as inhaled histamine and methacholine The Peer Teaching Society is not liable for false or misleading information…
The Peer Teaching Society is not liable for false or misleading information…
Pathogenesis
Airway Obstruction
Inflammation Mucus and oedema Bronchoconstriction
Airway remodelling
Epithelium Smooth muscle Basement membrane • Narrowing of the airway due to smooth muscle contraction • Thickening of the airway wall by cellular infiltration and inflammation • Presence of secretions within the airway lumen The Peer Teaching Society is not liable for false or misleading information…
1.Inflammation
The Peer Teaching Society is not liable for false or misleading information… Allergen exposure T-helper cells(CD4) -release IL4 IgE produced Mast cell activation Histamine release Note: IL5 Eosinophils Involved in sustained inflammation
2. Bronchoconstriction
IgE + histamine= bronchoconstriction Blocks β-adrenoceptor in smooth muscles surrounding the airways
3. Mucus and Oedema
Vascular permeability (oedema) Histamine Bronchial secretions (mucus plugs) Smooth muscle contraction The Peer Teaching Society is not liable for false or misleading information…
Remodelling
Smooth Muscle • Hypertrophy • Hyperplasia Basement Membrane • Collagen deposition + Matrix proteins deposited = thickened BM Epithelium • Loss of ciliated columnar cells • Metaplasia- ↑ mucus secreting goblet cells The Peer Teaching Society is not liable for false or misleading information…
Clinical features:
Symptoms
Intermittent Dyspnoea Wheeze Cough (often nocturnal) Sputum Chest tightness Ask about: Triggers at home/at work Diurnal variation Other atopic disease
Signs
Tachypnoea Audible wheeze Hyperinflated chest Hyperresonant percussion note Decreased air entry Widespread, polyphonic wheeze The Peer Teaching Society is not liable for false or misleading information…
Investigations
• • • • Respiratory function tests: Spirometry- ↓FEV1/FVC Peak expiratory flow- diurnal variation >20% on 3days/week for 2 weeks 15% improvement in either following β2 agonist Exercise tests Skin prick tests- may help to identify allergens The Peer Teaching Society is not liable for false or misleading information…
Long-term management
• • Conservative: Stop smoking Avoid precipitants Education: Ensure good inhaler technique PEFR monitoring Self-management The Peer Teaching Society is not liable for false or misleading information…
Management of chronic asthma
Step 1 • Occasional short-acting inhaled β2-agonist as required for symptom relief • If used more than once daily, or night-time symptoms, go to step 2
Salbutamol
Step 2 • Add inhaled corticosteroid
Beclomethasone
Step 3 • Add long-acting β2-agonist
Salmeterol
Step 4 • High dose Corticosteroid • Consider leukotriene receptor antagonist
Monteleukast
Step 5 • Add daily oral corticosteroids and continue with inhaled steroids • Refer to asthma clinic
Prednisolone
Start at the step most appropriate to severity; move to next step if needed, or back if control is good for >3months The Peer Teaching Society is not liable for false or misleading information…
Management of acute severe asthma
• O 2 therapy- maintain sats at 94-98% • Nebulized salbutamol or terbutaline with O 2 • Hydrocortisone IV or prednisolone PO • CXR to exclude pneumothorax • Magnesium sulphate if life-threatening The Peer Teaching Society is not liable for false or misleading information…
COPD
• Common, progressive disorder characterised by airflow obstruction with little or no
reversibility
Obstructive: ↓FEV1 (<80% of predicted) ↓FEV1/FVC (<0.7 of predicted) The Peer Teaching Society is not liable for false or misleading information…
Bronchitis vs Emphysema
• Bronchitis (Bronchi): clinically defined as cough and sputum production on most days for 3 months of 2 successive years • Emphysema (Alveoli): histologically defined as enlarged air spaces distal to terminal bronchioles, with destruction of alveolar walls The Peer Teaching Society is not liable for false or misleading information…
Aetiology
• • •
Cigarette smoking
Chronic exposure to pollutants at work (mining, building and chemical industries) Outdoor air pollution • Alpha-1 antitrypsin deficiency-causes early onset COPD The Peer Teaching Society is not liable for false or misleading information…
Pathophysiology
Inactivation of α1-antitrypsin by cigarette smoke Infiltration of the bronchi/bronchiole walls with inflammatory cells Neutrophils and CD8 lymphocytes Granulocytes release elastases and proteases Ulceration, scarring & columnar cells are replaced by squamous cells When disease is predominantly in the small airways and at an early stage it is reversible The Peer Teaching Society is not liable for false or misleading information…
Pathophysiology
Squamous cell metaplasia progressive Fibrosis of bronchial walls Mucus gland hypertrophy Airflow limitation/narrowing The Peer Teaching Society is not liable for false or misleading information…
Chronic Bronchitis
• • • Hypersecretion of mucus due to marked hypertrophy of mucus-secreting glands and hyperplasia of goblet cells Initially small airways are affected and this initial inflammation is reversible, whereas in later stages larger airways become affected and the process is no longer reversible Epithelial layer becomes ulcerated and squamous epithelium may be replaced by columnar cells, resulting in increased gas diffusion distance The Peer Teaching Society is not liable for false or misleading information…
Emphysema
• • • Abnormal dilation of air spaces with destruction of alveolar walls Inflammation and scarring, reducing size of lumen of airways and reducing lung elasticity Hypersecretion of mucus, again reducing lumen size and increasing distances for gas diffusion The Peer Teaching Society is not liable for false or misleading information…
Clinical features
Symptoms
Cough Sputum Dyspnoea Wheeze
Signs
Tachypnoea Use of accessory muscles of respiration Hyperinflation ↓Cricosternal distance (<3cm) ↓ Chest Expansion Resonant or hyperresonant percussion note Quiet breath sounds Wheeze Cyanosis Cor Pulmonale The Peer Teaching Society is not liable for false or misleading information…
The Peer Teaching Society is not liable for false or misleading information…
The Peer Teaching Society is not liable for false or misleading information…
Investigations
• • • • • Lung function tests (↓FEV1:FVC, ↓ PEFR) CXR- may be normal or show evidence of hyperinflated lungs, reduced peripheral lung markings and bullae High resolution CT- show emphysematous bullae Haemoglobin and PCV (packed cell volume) may be high as a result of persistent hypoxaemia and secondary polycythaemia ABG-may be normal or show hypoxia +/- hypercapnia in advanced disease The Peer Teaching Society is not liable for false or misleading information…
Classification of severity
Stage of COPD
Stage I, Mild Stage II, Moderate Stage III, Severe Stage IV, Very severe
Function
FEV1/FVC <70% FEV1 ≥ 80% predicted FEV1/FVC <70% 50% ≤ FEV1<80% predicted FEV1/FVC <70% 30% ≤ FEV1<50% predicted FEV1/FVC <70% FEV1<30% predicted or FEV1<50% predicted plus respiratory failure
Symptoms
Chronic cough, none/ mild breathlessness Breathlessness on exertion Breathlessness on minimal exertion. May be weight loss and depression Breathless at rest The Peer Teaching Society is not liable for false or misleading information…
• • • • • • •
Management
STOP SMOKING- slow rate of deterioration Exercise and weight loss if required or high-calorie dietary supplements in those with low BMI Influenza and pneumococcal vaccination and to receive prompt antibiotic treatment for exacerbations Cardiopulmonary rehabilitation Broncho-pulmonary exercises Caution with flying (increased risk of pneumothorax with altitude) Steroid Trial The Peer Teaching Society is not liable for false or misleading information…
Management
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COPD vs Asthma
COPD
Smoker or ex-smoker Symptoms under age 35 Atopic Features (rhinitis,eczema) Cellular infiltrate Most Rare Uncommon Cough and sputum Breathlessness Night-time symptoms Significant diurnal or day to-day variability of symptoms Bronchodilator response (FEV1 & PEFR) Macrophages, neutrophils, CD8+ T cells Daily/common Persistent and progressive Uncommon Uncommon <15%
Asthma
Possibly Common Common Eosinophils, CD4+ T cells Intermittent Variable Common Common >15%
Pulmonary fibrosis
• • • • • Causes: Secondary to infarction, TB and pneumonia Idiopathic pulmonary fibrosis
Extrinsic allergic alveolitis Sarcoidosis Occupational (industrial dust diseases)
– – – Coal workers pneumoconiosis Silicosis Asbestosis The Peer Teaching Society is not liable for false or misleading information…
Extrinsic allergic alveolitis
• • • • Inhalation of allergens provokes a hypersensitivity
reaction
Acute phase- alveoli infiltrated with acute inflam cells i.e. neutrophils Chronic exposure- small granuloma formation
Clinical features
– 4-6 hrs post exposure- fever, rigors, dry cough, dyspnoea, crackles (no wheeze) – Chronic- weight loss, exertional dyspnoea, type 1 respiratory failure, cor pulmonale. The Peer Teaching Society is not liable for false or misleading information…
• • Most common cause is farmer’s lung (spores) Others: – Pigeon fancier’s lung (proteins in bird droppings) – Malt worker’s lung (aspergillus clavatus) – Bagassosis/sugar worker’s lung (sugar cane fibres) ↑ ↑ EAA is also regarded as an ‘occupational lung disease’!
CXR- upper zone mottling/consolidation. Honeycomb lung in very advanced cases Treat- Remove allergen, O2, oral prednisolone (steroids)
Honey comb lung The Peer Teaching Society is not liable for false or misleading information…
Gell-Coomb classification
• • Type I – IgE mediated (mast cells and basophils) –
Anaphylaxis, hayfever, asthma
Type II – Antibody mediated (IgM or IgG) –
Goodpasture’s syndrome, haemolytic anaemia, Grave’s disease
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• • Type III – Immune complex formation – Antigen-antibody complexes are deposited in various areas of the body.
– Both acute and chronic inflammation occur –
Extrinsic allergic alveolitis, SLE, rheumatoid arthritis.
Type IV – T-lymphocyte mediated – Delayed hypersensitivity reaction – Formation of granulomas (T-cells and macrophages) –
TB and sarcoidosis
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Sarcoidosis
• • • Multisystem granulomatous disorder of unknown cause.
More common in women. Usual age between 20-40.
Symptoms: dry cough, progressive SOB, ↓ exercise tolerance and chest pain.
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• • Other non pulmonary clinical features: • Skin and eye lesions- uveitis, conjunctivitis • Erythema nodosum • Hepatomegaly • Hypercalcaemia Investigate: • CXR- Bilateral hilar lymphadenopathy and pulmonary infiltration (sever fibrosis- honeycomb lung appearance) • Bloods- raised ESR, raised liver function tests, raised calcium, raised Immunoglobulins • Lung function tests- reduced lung volume, restrictive
ventilatory defect.
• Tissue biopsy- non caseating granuloma The Peer Teaching Society is not liable for false or misleading information…
• Treat: Bed rest, NSAIDs and prednisolone Erythema nodosum The Peer Teaching Society is not liable for false or misleading information…
Occupational lung disorders
• Coal workers pneumoconiosis – Coal dust phagocytosed by the alveolar macrophages. Black pigment in lung due to inhaled carbon.
– Two types: Simple CWP (nodular shadowing on cxr usually upper lobes, bilaterally) and progressive massive fibrosis (large irregular nodules with scarring >10mm, necrotic central cavities, severe emphysema and cor pulmonale) – Treat: avoid exposure, claim compensation The Peer Teaching Society is not liable for false or misleading information…
The Peer Teaching Society is not liable for false or misleading information…
• Silicosis – Inhalation of silicon dioxide/silicates-abundant in stone and sand – Stone masons, sand blasters, pottery and ceramic workers – Nodules form in upper and mid zones of lungs after many years of exposure. – Increased risk of reactivation of TB!
– Eggshell calcification (streaks) at hilar lymphnodes on Xray – Treat: avoid exposure, claim compensation. The Peer Teaching Society is not liable for false or misleading information…
• Asbestosis – White asbestos least fibrogenic, blue asbestos most.
– – Pipe lagging, roofing felt, electrical wire insulation Progressive SOB (
long latent period before symptoms develop
), fine end inspiratory crackles, clubbing.
– – Fibres collect in alveoli at lung bases Degree of asbestos exposure is related to degree of pulmonary fibrosis.
– ↑ risk of mesothelioma (and bronchial adenocarcinoma.) – Latent period may be up to 45 years between exposure and development of the tumour – Treat: symptomatic (chemotharepy if tumour develops), claim compensation The Peer Teaching Society is not liable for false or misleading information…
The Peer Teaching Society is not liable for false or misleading information…
Sample Questions
1. A 67 year old man is seen in outpatients with a 4 year history of progressive shortness of breath. He has worked for 12 years in a power station and was regularly exposed to all types of dust.
Answer :
C
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Practice Question
2. An 18-year-old hairdresser apprentice was seen by her GP with a 12 hour history of wheeze and shortness of breath. She was wheezy on examination with a pulse rate of 120 bpm, and had a recorded peak flow at 30% of her predicted value just prior to a nebuliser of salbutamol.
Answer
:
B
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Practice Question
Answer:
C
The Peer Teaching Society is not liable for false or misleading information…
Practice Question
Answer:
I
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Questions?
• Email with any queries or concerns for the phase 2a exams and we will try our best to help!
The Peer Teaching Society is not liable for false or misleading information…