ASTHMA Flashcards
What is asthma characterised by?
Chronic inflammatory condition of lung airways characterised by reversible airflow obstruction and bronchospasm
What 3 characteristic physiology happen?
- Reversible airflow limitation (spontaneously or with treatment)
- Airway hyper-responsiveness
- Inflammation of the bronchi with T cells, mast cells, eosinophils and smooth muscle hypertrophy, mucus plugging and epithelial damage
What is intrinsic asthma?
o definite external cause
o often starts in middle-age (late onset) though these pts often have a Hx of respiratory problems indicative of asthma
What is extrinsic/ atopic asthma?
o no causative agent found
o frequent in atopic individuals
o late onset in adults causes may be via sensitization of chemicals at work
What % of population?
5-8%
How many adults/ children receiving treatment in UK?
1 in 12 children and 1 in 10 adults are receiving treatment for asthma in UK
What causes intrinsic asthma?
no causative agent
Starts middle age (late onset)
What causes extrinsic asthma?
definite cause identified
• More common atopic individuals
• Positive skin prick for common inhaled antigens
• 90% children and 50% adults with asthma
What are the causes of asthma?
- Atopy – atopic triad of hayfever (allergic rhinitis), atopic eczema and asthma
- Genetic
- Environment
o Allergen exposure – especially in early childhood
o Air pollution exposure
o Maternal smoking
o Viral respiratory infections e.g. RSV, rhinovirus
o Occupational sensitizers eg isocyanates
o Extreme exertion – exercise
Hygiene hypothesis
Describe the Type I (IgE mediated) Hypersensitivity Reaction
• Bronchoconstriction/bronchospasm (SM spasm narrowing airway)
• Inflammation
o Caused by mast cells, eosinophils, dendritic cells and lymphocytes
• Mast cells increased in epithelium and surface secretions
• Histamine, prostaglandin D2 and leukotriene C4 released
• Eosinophils found large numbers in bronchial walls and secretions – attracted to region by cytokines (IL3, IL5) and chemokines
o Combined with bronchial hyper responsiveness
• Hyperresponsive – incr in IgE leads to increased responsiveness of the airway
• Increased mucous production (plugging airways)
• Airway remodelling
o Loss of ciliated cells due to epithelial damage
o Increase in mucous-secreting goblet cells due to metaplasia in response to epithelial damage
o Thickened basement membrane due to deposition of repair collagens
o Smooth muscle hyperplasia causes more sustained contraction
o Nerves contribute to irritability of asthmatic airways
• Paroxysmal and reversible obstruction of the airways
Risk factors
Anti-inflamm drugs Hx of atopy Obesity Air pollutant Beta-blockers Early exposure to broad-spectrum antibiotics Smoking Childhood viral infections Premature and low birth weight
Symptoms
- Recurrent episodes
- Wheezing
- Coughing (often nocturnal)
- Sputum – can appear pus-like due to white cells; can be hard to bring up
- SOB
- Chest tightness
- Triggered by cold air, URTIs, exercise, pollution, allergens, occupation
- Intermittent/ Nocturnal dyspnoea – diurnal variation; morning dipping
Signs
- Tachypnoea
- Wheeze - widespread polyphonic (audible)
- Hyperinflated chest
- Hyper-resonant to percussion
- Decreased air entry
- Severe attack: inability to complete sentences, pulse >110, RR >25, PEFR (peak expiratory flow rate) 33-55% predicted
- Life-threatening attack: silent chest, cyanosis, bradycardia, exhaustion, confusion, feeble respiratory effort, PEFR <33%
Signs of severe attack
Inability to complete sentences
Pulse >110
RR >25
PEF 33-50% of predicted
Signs of life-threatening attack
Silent chest Cyanosis Bradycardia Exhaustion PEF <33%predicted Confusion Feeble resp effort
Investigations of acute asthma
PEF Sputum culture Bloods: FBC, U&Es, CRP, cultures ABG – normal or slightly red PaO2 and low PaCO2 (hyperventilating). If PaCO2 raised – refer ICU CXR – exclude infection or pneumothorax
Investigations of chronic asthma
PEF monitoring: diurnal variation of >20%on >3d a week for 2 weeks
Spirometry: obstructive defect (decr FEV1/FVC – FEV1 more decr than FVC. Usually improvement in FEV1 >15%following B2 agonists or steroid trial
CXR: hyperinflation
Skin prick tests – allergens
Histamine or methacholine challenge
Ạspergillus serology
What steps are there in investigating?
- Peak Flow
- Spirometry – measures volume of air pt able to expel after full inspiration; differentiates between obstructive and restrictive disease; can give indication of severity; shows reversibility
- Exercise tests
- Prednisolone trial
- CXR
- Skin prick tests – help identify allergic cause
- Allergen provocation tests
What results would you see in peak flow?
o Not a definitive test
o Useful for monitoring and management
o Best done with patient standing
o Peak flow reduced
What results would you see in spirometry?
o Patient sat down, breathes in fully, then breathes out as fast and hard as possible and keeps going until nothing left
o If FEV1 improves more than 12% following bronchodilator therapy then asthma likely
o Can be normal when asymptomatic so does not exclude
o If normal while symptomatic then asthma is unlikely
What results would you see in exercise tests?
o Widely used for diagnosis in children
o Run for 6mins on a treadmill so HR >160bpm
o Or cold air challenge but a –ve result doesn’t rule out asthma.
What results would you see in prednisone trial?
o Prednisolone 30mg daily for 2wks with lung function measured before and immediately after the course
o >15% improvement diagnostic
What results would you see in CXR?
o Usually normal
o May be hyperinflation
o Useful to rule out other causes
What management?
Avoid allergens. Quit smoking. Stop beta blockers. Avoid NSAIDs
What is the acute response to acute asthma attack?
Warn ITU
Sit patient up and give high dose O2 in 100%non-rebreathing bag
Salbutamol 5mg (ŏr terbutaline 10mg) plus ipratropium bromide 0.5mg neb with O2
Hydrocortisone 100mg IV or pred 40-50mg PO or both if very ill
CXR to exclude pneumothorax
What else would you do after acute response to acute asthma attack?
Add MgSO4 1.2-2g IV over 2 mins
Give salbutamol nebs every 15 mins or 10mg cont per hr. Watch ECG and check arrhythmias
What management would you consider in chronic asthma?
Stop smoking
Avoid triggers
Check inhaler technique
Peak flow 2xdaily and self manage to alter medication accordingly
Specific advice on what to do in an emergency
Consider teaching relaxed breathing to avoid dysfunctional breathing
What is step 1 in chronic asthma treatment?
Step 1: Occasional short acting inhaled B2 agonist eg salbutamol 100-200mcg/6h as required for symptom relief. Is used more than once daily or night time symptoms = step 2
What is step 2 in chronic asthma treatment?
Step 2: Add standard dose inhaled steroid eg beclomethasone 100-400mcg/12hr or start at dose appropriate to disease severity
What is step 3 in chronic asthma treatment?
Step 3: Add long acting B2-agonist eg salmetrol 50mcg/12hr. If benefit but still inadequate control, continue and incr dose beclomethasone to 400mcg/12hr. If no effect of long acting B2 agonsit, stop it. Leukotriene receptor antagonist or oral theophylline may be trialled
What is step 4 in chronic asthma treatment?
Step 4: Consider trials of beclomethasone up to 1000mcg/12h; modified release oral theophylline; modified release oral B2 agonist; oral leukotriene receptor antagonist. Modified release B2 agonist tablets
What is step 5 in chronic asthma treatment?
Step 5: Add regular oral prednisolone (1 dose daily at lowest dose) and refer to asthma clinic
What do Beta 2 adrenoceptor agonists do?
Relax bronchial smooth muscle
How quickly do Beta 2 adrenoceptor agonists act?
Act within mins
How do you give Beta 2 adrenoceptor agonists?
Best as inhaler but can be given PO or IV
What are the side effects of Beta 2 adrenoceptor agonists?
tachyarrhythmia’s, decr K+, tremor, anxiety
Why do you give long acting Beta 2 adrenoceptor agonists?
help nocturnal symptoms and reduce morning dips
What are the side effects of long acting Beta 2 adrenoceptor agonists?
paradoxical bronchospasm
How do Corticosteroids work?
decr bronchial mucosal inflammation
How do you give Corticosteroids?
Best inhaled
Can also be given PO or IV
How quickly do Corticosteroids work?
Act over days
What do you have warn patients of, then giving them Corticosteroids?
Rinse mouth after taking to reduce oral candida
Describe the use of Corticosteroids acutely
Oral steroids used acutely eg pred 40mg/24hr PO for 7 d and longer term in lower doses 5-10mg/24hr
What are the side effects of Corticosteroids?
pancreatitis, candida, oesophageal ulceration, myopathy, osteoporosis, fractures, growth suppression, adrenal suppression, Cushing’s syndrome, aggravated epilepsy, cataracts, glaucoma, depression, papilledema, increased susceptibility to and severity of infections.
What does Aminophylline do?
Decreases bronchoconstriction by increasing levels cAMP
What else do you need to know about Aminophylline?
- Met to theophylline
- Take at night to prevent morning dipping
- Barrow therapeutic ratio
- Check theophylline levels and do ECG monitoring
What are the side effects of Aminophylline?
arrhythmias, GI upset and fits
When would you give Aminophylline IVI?
Can be given IVI in acute severe asthma.
Check plasma levels after 24hrs
What does Cromoglicate do?
mast cell stabilizer, and is commonly marketed as the sodium salt sodium cromoglicate or cromolyn sodium. This drug prevents the release of inflammatory chemicals such as histamine from mast cells
When would you use Cromoglicate?
prophylaxis in mild and exercise induced asthma
Often used in children
How do administer Cromoglicate?
Always inhaled
What is the caution in Cromoglicate?
May ppt asthma
Is a chronic productive cough common or uncommon?
Uncommon
Is night time waking with SOB common or uncommon?
Common
Is significant diurnal/ day-to-day variation common or uncommon?
Common
What are the differentials? And would distinguish them?
- COPD
- Pulmonary oedema (cardiac asthma) – haemoptysis/pink, frothy sputum; end-inspiratory crackles; acute attack; cardiovascular Hx
- Large airway obstruction – acute attack; unilateral
- SVC obstruction – face/arm swelling; venous distention; light-headedness
- Pneumothorax – no cough
- PE – haemoptysis; risk factors
- Bronchiectasis – productive cough; purulent sputum
What is the prognosis?
Most childhood asthmatics grow out of it in adolescence or suffer much less as adults.
Prognosis is generally good.
1000 asthma deaths in UK in 2009, 50% of which in >65s.
