Dr Rickbir Singh Randhawa
FY1
Definition:
Asthma
 Chronic inflammatory airway disease characterised by
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reversible airway obstruction, airway hyperresponsiveness and bronchial inflammation.
Three factors contribute to reversible airway narrowing:
1. Bronchial smooth muscle contraction triggered by a
variety of stimuli
2. Mucosal swelling/inflammation caused by mast cell and
basophil degranulation- release of inflammatory mediators
3. Increased mucus production
Definition:
COPD
 Chronic progressive lung disorder characterized by
airway obstruction with little or no reversibility. It
includes the following:
 Emphysema: defined histologically as permanent
destructive enlargement of air spaces distal to the terminal
bronchioles
 Chronic Bronchitis: defined clinically as a chronic cough
with sputum production on most days for 3 months per
year over 2 successive years.
Aetiology
Asthma
 Genetic factors +VE family Hx, atopic (eczema, allergic rhinitis), linkages
to multiple chromosomal locations genetic heterogeneity
 Environmental triggers Allergens (House dust mite, pollen, pets (fur)), cigarette
smoke, viral URTI, occupational allergens (isocyanatesspray paints, epoxy resins-adhesives/fibreglass fabrics)
Aetiology/Risk factors
COPD
 Bronchial and alveolar damage due to environmental
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toxins- smoking (cigarette smoke)
Indoor air pollution (such as solid fuel used for cooking
and heating)
Outdoor air pollution
Occupational dusts and chemicals (vapours, irritants, and
fumes)
Frequent lower respiratory infections during childhood.
Rare cause is α1-antitrypsin deficiency (<1%) consider in
non smokers or in younger patients
History
Asthma
 Intermittent wheeze
 Breathlessness (dyspnoea)
 Cough (often nocturnal)
 Occasionally sputum
 Diurnal variation in symptoms/ peak flow- morning dips
of peak flow recordings
History
Asthma: Precipitating factors
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Cold air
Exercise
Allergens (house dust mite, pollen, pets-animal fur)
Emotions
Smoking/passive smoking exposure
Viral URTI
Hx of atopy (eczema/hayfever-allergic rhinitis)
FHx
Drugs (Beta blockers, NSAIDS- ask OTC meds)OSCE !
History
Asthma: things to also ask!
 Precipitating factors if present
 Compliance with medication
 Reliever usage (inhaler) – gauge severity
 Occupational Hx-cause
 Sleep- interference? Severity
 Smoking Hx
 Eczema/hayfever- atopy
 Days off school/work – gauge severity
 Remember CROSSED mnemonic!
History
COPD
 Chronic breathlessness
 Chronic Cough/sputum production
 Wheeze
 Smoker!
 Minimal diurnal variation in symptoms compared to
asthma
 Age of onset >35 years (Rare cause is α1-antitrypsin
deficiency (<1%) consider in non smokers or in younger
patients)
Clinical signs O/E
Asthma
 Tachypnoea
 Use of accessory muscles of
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respiration
Hyper inflated chest (reduced
chest expansion)
Hyper resonant percussion note
Reduced air entry
Polyphonic wheeze
COPD
 Tachypnoea
 Use of accessory muscles of
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respiration
Purse lip breathing
Hyper inflated chest (reduced
chest expansion)
Hyper resonant percussion note
Reduced air entry-prolonged
expiration
Wheeze, crackles if infective
exacerbation
cyanosis
Severity of Asthma
 Moderate exacerbation:
 Increasing symptoms
 PEF >50-75% of best or predicted
 No features of severe asthma
 Severe exacerbation:
 Unable to complete sentences in one breath
 PEF 33-50% of best or predicted
 RR ≥ 25/min
 HR ≥110/min
Severity of Asthma
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Life threatening attack: Any of
PEF <33% of best or predicted
Silent chest
Cyanosis
Feeble respiratory effort
Hypotension
Exhaustion/confusion/coma (CO2 retention)
ABG:
normal or high CO2 (normal PaCO2 4.6-6.0 kPa)
PaO2 <8kPa/O2 sats <92%
Low pH <7.35 acidosis (CO2 retention)
Severity of COPD
Severity
FEV1 (% predicted)
Mild
Moderate
≥80%
But FEV1/FVC <70%
50-79%
Severe
30-49%
Very Severe
<30%
Investigations
Asthma
 Acute exacerbation:
 Peak flow- PEF reading to classify the severity
 Basic Obs include pulse oximetry- classify severity
 ABG-respiratory failure
 CXR- exclude differentials i.e. pneumothorax, pneumonia
 Bloods- FBC (raised WCC infective exacerbation), U+E’s,
CRP
 Blood culture (febrile)
 Sputum culture
Investigations
Asthma
 Chronic Asthma:
 PEF monitoring with peak flow diary- diurnal variation >20%
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on ≥3days a week for 2 weeks with morning dips in readings.
Pulmonary function test- obstructive defect with improvement
of FEV1 usually >15% improvement after a trial of a Beta 2
agonist.
Bloods- eosinophilia, raised IgE levels in atopic asthma.
Skin prick tests- help identify any allergens
Aspergillus antibody titres- for allergic aspergillus lung disease
Investigations
COPD
 Acute exacerbation:
 ABG- respiratory failure
 Bloods- FBC (raised WCC infection),U+Es, CRP
 Bloods cultures if febrile
 Sputum culture
 CXR –exclude differential i.e. pneumothorax, pneumonia
 ECG- cor pulmonale right axis deviation (RVH)
Investigations
COPD
 Chronic COPD:
 Spirometry/pulmonary function tests- obstructive defect
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FEV1/FVC <70% also with FEV1<80% predicted
CXR- normal or show lung hyperinflation( >6 anterior ribs
seen, flat hemi-diaphragms), large central pulmonary arteries,
decreased peripheral vascular markings
ABG- hypoxia and/or hypercapnia
Bloods- FBC (increased Hb and PCV due to secondary
polycythaemia secondary to hypoxia).
ECG and echocardiogram- cor pulmonale, pulmonary
hypertension
α1-antitrypsin levels- in young patients or with minimal
smoking Hx
Obstructive vs Restrictive defect
Spirometry/PFT
FEV1
FVC
FEV1/FVC
Obstructive lung
disease
Decreased (<80%)
Decreased
Decreased
(<0.7)
Restrictive lung
disease
Decreased
Decreased (<80%)
Normal (>0.7) or
increased
Management
Acute life threatening Asthma
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Start Rx before Ix ABCDE!
Oxygen 15L NRB- sit patient up, 02 sats 94-98%/intubate
Salbutamol- 5mg Nebulised, back to back Nebs
Hydrocortisone 100mg IV
Ipratropium bromide 0.5mg nebulised
Theophylline (aminophylline) IV
Magnesium sulphate 2mg IV if no improvement
Remember OSHIT! Mnemonic
Normal or high CO2 is a very worrying sign- get early
anaesthetic/ITU r/v
Management Chronic Asthma
Chronic Asthma
Chronic Asthma Management
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Asthma Management The BTS Stepwise Approach
Rx started at the step most appropriate to the severity
STEP 1: SABA
STEP 2: Step 1 + ICS
STEP 3: Step 2 + LABA &/or ↑ ICS dose
STEP 4: Step 3 + leukotriene receptor antagonist
(montelukast)/theophylline
STEP 5: Step 4 + oral steroids- refer to asthma clinic
Step down Rx if symptom control is good for >3 months
Educate on proper inhaler techniques and routine
monitoring of peak flow.
Develop an individual Mx plan to avoid triggers
Management
Acute exacerbation COPD
 ABCDE approach!
 Controlled oxygen therapy 24-28% Venturi mask vary
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according to ABG- target sats 88-92%
Nebulized bronchodilators- salbutamol 5mg (back to back
NEBS) and ipratopium bromide 0.5mg (4-6 hourly)
Steroids- IV hydrocortisone 200mg or PO prednisolone
40mg (7-14 days)
Abx- if evidence of infection see local guidelines
NIV- if severe respiratory acidosis or medical Rx shows
no improvement e.g. BIPAP- type 2 respiratory failure
Management
Chronic COPD
 Non Pharmacological Mx
 Smoking Cessation
 Nutrition- Rx poor nutrition e.g. fortisips
 Obesity- healthy diet/lifestyle, regular exercise
 Pulmonary Rehabilitation- graded exercise therapy to
increased exercise tolerance
Chronic Management COPD
Chronic Management COPD
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Mucolytics- aid chronic productive cough
CBT/Antidepressants- chronic illness
Criteria for LTOT:
Only for those stopped smoking- fire risk!
PaO2<7.3 kPa clinically stable- this value should be stable on
two occasions >3 weeks apart
 PaO2 7.3-8.0 kPa with signs of pulmonary hypertension/cor
pulmonale
 Terminally ill patients
 Surgical Mx- bullectomy (recurrent pneumothoraces), lung
volume reduction surgery
Inhalers-Quick run through
SABA-e.g. salbutamol (ventolin) “blue inhaler”
LABA-e.g. salmeterol (serevent)
SAMA- e.g. ipratopium bromide (atrovent)
LAMA-e.g. tiotropium bromide (spiriva)
IC Steroids:
Becotide (beclometasone), Pulmicort (budesonide),
Flixotide (fluticasone)
 Combination ICS:
 Seretide (fluticastone + salmeterol)
 Symbicort (budesonide + formoterol)
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Inhaler:
Explaining how to use it
 1. Remove the dust cap from the inhaler device.
 2. Shake the device. Remember the canister holds a suspension of drug, and this
needs to be shaken to ensure a uniform distribution of the drug particles.
 3. If you have not used the inhaler for a week or more, or it is the first time you have
used the inhaler, spray it into the air before using it to check that it works.
 4. Hold the inhaler upright with you forefinger on the top of the canister.
 5. Breathe out as far as is comfortable.
 6. Place the mouthpiece in your mouth between your teeth, and close your lips around
it.
 7. Start to breathe in slowly and deeply, and at the same time, activate the inhaler by
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pressing down on the canister. When the canister is pushed down, a valve delivers a
measured dose of drug in a fine mist.
8. Hold your breath for as long as is comfortable, then breathe out as normal.
9. If you are instructed to take 2 puffs, wait for about 30 seconds and repeat this
process.
10. Do not release two puffs at the same time. This will increase the likelihood of
deposition at the back of the throat and reduce the amount of drug reaching the lungs.
11. Finally, replace the cap on the inhaler.
Clinical scenario
 A 64 year old gentleman presents to A&E with increasing
SOB over the last 3 days. This is associated with a cough
productive of thick, green sputum. He has a past medical
history of “asthma”, but he has smoked 50 cigarettes a day
for the past 40 years. On examination he is tachypnoeic,
tachycardic, O2 sats 85% on air, he is using his accessory
muscles to breathe. Auscultation reveals bilateral diffuse
coarse crepitations and widespread wheeze
Questions
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What are your main differential diagnoses for this gentleman?
How would you investigate this gentleman?
Initial management in acute setting?
Long-term management?
Can you tell me about the pathophysiology of COPD? ie.
Clinical and histopathological definitions
 Can you tell me some risk factors for COPD?
 What are the criteria for mild, moderate, severe and very severe
COPD?
 What are the criteria for use of long term oxygen therapy
(home oxygen)?
ANY QUESTIONS?