Transcript R1 Simon Berry - Peer Teaching Society

Phase 2
Simon Berry + Liz Stedman
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Aims
• To give a brief overview of the following 3 topics:
– COPD
– Asthma
– Pulmonary Fibrosis (Interstitial Lung Disease)
• Apply the knowledge to practice exam questions
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COPD
Introduction
Chronic Obstructive Pulmonary Disease made up of Chronic bronchitis vs Emphysema
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Chronic Bronchitis (Bronchi) – . Daily productive cough for at least 3 months over
2 years consecutive years. Pathology hyperplasia of mucous glands and infiltration
of the airway wall with inflammatory cells. Bronchial wall thickening.
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Emphysema (alveoli) – permanent enlargement of airspaces distal to terminal
bronchioles. Reduced SA for gas exchange. Reduced recoil, and loss of support =
airway narrowing
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Mainly affects people over 35, more common with increasing age
Men >Women
Very common reason for hospitalisation (1 in 8 admissions)
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Aetiology
• Smoking / occupational exposure / air pollutants  irritation
and inflammation  damage to the airways
• 1 in 10 (20/d) and 1 in 4 (40/d) will develop COPD
• Genetic  alpha-1-antitryspin deficiency (affects the proteins
in the lung, liver and blood disorder). 1 in100
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Pathophysiology
• Defining feature  irreversible airflow limitation during
forced expiration. Result of loss of elastic recoil due to lung
tissue destruction / increase in resistance of conducting
airways (mucus)
• May develop HF  reduced Ox. in blood and changes in lung
tissue leading to increased pressure in pulmonary vasculature.
 increased strain on H. muscles = HF (worsening
Breathlessness and fluid retention)
• Respiratory failure  level of oxygen in blood too low, CO2
builds up in blood stream. May need palliative care
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Symptoms
• Exertional breathlessness (PC) – MRC
breathlessness scale
• Chronic productive Cough (PC) : may start of
episodic persistent
• Wheeze
• Frequent winter ‘bronchitis’ / exacerbations
– Bacteria 1 in 2/3 in COPD
– Vrial 1 in3
• Symptoms all worsen with time if smoking not
stopped!
Signs
• Physical examination in
detecting mild – moderate
COPD is poor.
• Severe disease may show
– Tachypnea and respiratory
distress w/ simple activities
– Accessory muscle usage and
indrawing of lower IC spaces
(Hoover sign
– Cyanosis
– Elevated JVP
– Peripheral Oedema
– Hyperinflation
• Thoracic signs may show
– Hyperinflation (barrel chest)
– Wheezing – forced+ unforced
expiration
– Diffusely decreased breath sounds
– Hyperresonance on percussion
– Prolonged expiration
– Coarse crackles beginning with
inspiration in some cases
Bronchitis vs Emphysema
• CB (blue bloaters)
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alveolar ventilation
Low PaO2
High PaCO2
Cyanosed but not
Breathless
– Rely on hypoxic drive
– Oxygen sats: 88-92%
– May progress to cor
pulmonale
• Emphysema (pink
puffers)
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 alveolar ventilation
near normal PaO2
Normal / low PaCO2
Breathless, but NOT
cyanosed
– May progress to Type
1 RF
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Investigations
• Spirometry  diagnostic. Check FEV1 - postbronchodilator
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FEV1/FVC < 70% or 0.7 = COPD (compared to pred. value / matched control)
Mild (stage 1) FEV1 at least 80% predicted value
Moderate (stage 2) FEV1 50%-79% pv
Severe (stage 3) FEV1 30%-49% pv
Very Severe (stage 4) FEV1 <30% pv
• ABG
– Best clues for acuteness an D. severity / exacerbation
• CXR
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check for lung cancer
Hyperinflation (> 6 ant. Ribs seen above diaphragm and mid-clavicular line)
Flat hemidiaphragms, large central pulmonary arteries
 in peripheral vasc markings, bullae (emphysema)
• High-res CT
Investigations (cont.)
• FBC: anaemia can cause SOB, polycythemia secondary to
COPD (RBC)
• Alpha—antitrypsin levels – if early onset, minimal smoking
Hx, FHx presence
• Steroid trial – see if COPD responsive to steroids
• ECG/Echo – Monitor Cor Pulmonale
• TLCO – Ix symptoms disproportionate to spirometric
impairment
Management
• STOP SMOKING
• Exercise and weight loss
• Influenza and pneumococcal vaccination
• Cardiopulmonary rehabilitation
• Broncho-pulmonary exercises
• Caution with flying (increased risk of pneumothorax with
altitude)
Management (cont.)
• Pulmonary Rehab programme (physiotherapy and broncho-pulmonary
exercises
Stage 1 • SABA or antimuscarinic (Beta agonist or anticholinergic) as needed
• +LABA
Stage 2 • Cardiopulmonary rehab
Stage 3
Stage 4
Stage 5
• Inhale glucocorticoid (if repeated exacerbations)
• Anticholinergic + LABA + inhaled steroid
• + LTOT +?Lung Surgery
Asthma
Introduction
• Paroxysmal and reversible airways obstruction
– Airway hyperresponsiveness
– Inflammation of the bronchi
– Airway remodelling
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Aetiology
• Extrinsic
– Atopic individuals
– Often accompanied by eczema
– Can be IgE related or non-IgE related
• Intrinsic
– Middle age (‘late onset’)
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Precipitants
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Occupational sensitizers
Cold symptoms – upper respiratory tract infection (URTI)
Cold air
Exercise (during or after)
Pollution eg cigarette smoke, car fumes
Infection
Drugs eg beta blockers, NSAIDs
Allergens – pollen exposure, exposure to animals, dust mites
Time of day: natural dip in peak flow overnight
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Symptoms
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Intermittent dyspnoea
Wheeze
Cough (often nocturnal)
Sputum
Ask about:
– Triggers: at home, at work
– Diurnal variation
– Other atopic disease
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Severity
• RCP 3
– Recent nocturnal waking?
– Usual asthma symptoms in day?
– Interference with ADLs?
• Asthma control test (out of 25)
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Signs
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Tachypnoea
Hyperinflated chest
Hyperresonant percussion note
Diminished air entry
Widespread, polyphonic wheeze
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Investigations
• Respiratory Function Tests
– Peak Expiratory Flow (PEF)
• diurnal variation of >20% on 3d a wk for 2wks
– Spirometry
• obstructive defect (↓FEV1/FVC, ↑RV), >15% increase
improvement in FEV1 following beta2 agonists
• Other tests
– Corticosteroid trial
– Skin prick tests
– CXR – exclude pneumothorax/ aspergillosis
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Management of Acute Attack
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100% O2 via non-rebreathing bag
Nebulized salbutamol + ipratropium bromide
Hydrocortisone IV or prednisolone PO
CXR to exclude pneumothorax
Magnesium sulphate if life-threatening
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Long-term Management
• Conservative Management
– DON’T FORGET
– Smoking cessation
– Avoid Precipitants
– Education: Inhaler technique, PEF monitoring,
self-management by altering medications in light
symptoms, advise about oral prednisolone for
rescue therapy
– Asthma action plan
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Long-term Management
Medical Management
Step 1
Step 2
• Inhaled short-acting β2 agonist PRN
• Add inhaled steroid 200-800 mcg/day
• Add inhaled long-acting β2 agonist (LABA)
Step 3 • If LABA fails, increase steroid dose
Step 4
Step 5
• Addition of fourth drug eg leukotriene receptor antagonist, theophylline, cromoglicate,
omalizumab
• Increase inhaled steroid up to 2000 mcg/day
• Prednisolone PO
Asthma vs COPD
• COPD – permanent damage and constriction to airways
• Asthma – reversible constriction of the smooth muscle in
the airways
• COPD more likely to cause productive cough than asthma
• Waking at night with SOB and wheeze  asthma > COPD
• COPD rare <35, asthma common <35
• Asthma, allergies, eczema (atopic conditions)
Pulmonary Fibrosis
Introduction
• Three main types:
– Replacement fibrosis 2ry to lung damage
• Eg infarction, TB and pneumonia
– Focal fibrosis in response to irritants
• Eg coal dust and silica
– Diffuse parenchymal lung disease
• Occurs in idiopathic pulmonary fibrosis (IPF) and
extrinsic allergic alveolitis
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Epidemiology + Aetiology
• Peak age 50-70 yrs. M=F
• Common causes:
– Idiopathic pulmonary fibrosis
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Replacement fibrosis
Pneumoconioses eg silicosis, asbestosis, CWP etc
Extrinsic allergic alveolitis
Granulomatous diseases eg sarcoidosis
Exposure to drugs eg amiodarone
Radiation exposure
Connective tissue diseases eg rheumatoid arthritis, SLE etc
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Presentation
• Dependent on disease process
• May be:
– Acute, with a fulminant, progressive, remitting or
resolving course
– Subacute, with a resolving, remitting, relapsing or
progressive course
– Chronic, insidious and slowly progressive
• May be incidental findings on CXR, spirometry,
occupational risk assessment
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Symptoms
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Dyspnoea
Chronic cough
Wheezing
Haemoptysis
Chest pain
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Signs
• Central cyanosis, fine end-inspiratory
pulmonary crackles
• Nonspecific features eg low grade fever and
myalgia
• Finger clubbing, esp with idiopathic
pulmonary fibrosis and asbestosis
• Signs of pulmonary hypertension and cor
pulmonale
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Investigations
• FBC - ?mild anaemia, ESR / CRP may ↑
• Autoantibodies (antinuclear antibodies, rheumatoid factor)
• ABGs: O2 desaturation is common
• Lung function tests
– Restrictive pattern (but obstruction of airways may also be
present).
– Reduced total lung capacity.
– Reduced residual capacity.
– Reduced residual volume.
– Reduced gas transfer.
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Imaging
• CXR
– May show no abnormality
– Reticular and/or nodular opacities
– Honeycombing is a late finding = severe disease
• High resolution chest CT scanning
– characteristic findings, extent and progression
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Management
• Supportive measures
– Smoking cessation, avoidance of cause, influenza
and pneumococcal vaccine, pulmonary
rehabilitation
• Drug treatment
– Immunosuppressive therapy
• Corticosteroids
• Cytotoxic drugs (azathioprine)
• Lung transplantation
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Complications
• Pulmonary hypertension
• Coronary artery disease
• Lung cancer
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ABGs
Respiratory Failure
• Type 1 Respiratory Failure
– PaO2 LOW < 8kPa
– *PaCO2 LOW/ NORMAL < 6.5kPa*
• Type 2 Respiratory Failure
– PaO2 LOW < 8kPa
– *PaCO2 HIGH > 6.5kPa*
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Respiratory Failure
• Type 1 Respiratory Failure
– Ventilation-perfusion mismatch
• Under-ventilated alveoli eg pulmonary oedema,
pneumonia, pneumothorax, pulmonary fibrosis
• Venous blood bypasses (eg R-L cardiac shunts, PE)
• Type 2 Respiratory Failure
– Inadequate alveolar ventilation eg asthma, COPD
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Practice Questions
Practice Question
• What is the key pathological feature of
asthma?
a)
b)
c)
d)
e)
Collapse of small airways on exhalation
Increased connective tissue deposition
Intermittent, inappropriate bronchoconstriction
Loss of alveolar surface area
Smooth muscle hyperplasia and increased mucus
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Practice Question
1. A young patient with a history of asthma arrives at the accident and
emergency department with acute severe breathlessness, and is
obviously wheezy and distressed. The doctors immediately give him a
treatment which will rapidly improve his arterial oxygenation
Answer: C
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Practice Question
2. The doctors then examine and investigate the same patient
described in question 1 (above) and make a diagnosis of acute severe
asthma. They decide to prescribe the bronchodilator treatment for
initial therapy
Answer: I
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Practice Question
3. Shortly after this the doctors then decide to administer antiinflammatory treatment to the same patient. Which is the most
appropriate treatment?
Answer: G
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Practice Question
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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Hints and Tips
• For phase list:
– Patient.co.uk/patientplus
• For OSCE
– Geeky medics youtube channel
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Thanks for listening!!
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Appendix
Appendix
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Asthma Control Test