30. Asthma Flashcards
What is asthma?
What is it characterised by?
What are the sympathetic and parasympathetic airway receptors?
Chronic obstructive inflammatory disorder of airways. 3 factors contribute to airway narrowing: bronchial muscle contraction (triggered by variety of stimuli), mucosal swelling (bronchial hypertrophy)/inflammation (caused by mast cell and basophil degranulation resulting in release of inflammatory mediators), increased mucus production (goblet cell metaplasia).
Episodes of dyspnoea, cough, chest tightness and wheeze.
Sympathetic: β2 receptors -> bronchodilation + mucocillary clearance
Parasympathetic: muscarinic receptors -> bronchoconstriction
What are the causes of asthma (theories)
a) extrinsic
b) intrinsic
c) occupational
What is the general pathology of asthma?
a) air pollution, allergen exposure, maternal smoking, dietary changes, hygiene hypothesis (more common in urban developed than less developed rural societies), genetics - inheritable component
b) non-allergic (no actual cause), less responsive
c) allergens at work e.g. Baker’s asthma
Increase in eosinophils (NB. COPD mostly neutrophils), CD4+ve T cells, mast cells, neutrophils. Thickened basement membrane. Epithelial disruption. Mucus gland hypertrophy. Vessel formation.
What might you see in acute and late phase asthma?
What are some differential dx of wheeze for pts with airflow obstruction?
What are some differential dx of wheeze for pts without airflow obstruction?
What features may increase the probability of asthma?
Acute: mast cells -> histamine -> bronchospasm, oedema, mucus.
Late: Th2 helper cells -> B cells -> IgE and eosinophils -> constriction and mucosecretion.
COPD, bronchiectasis, inhaled foreign body/obstruction, obliterative bronchiolitis, large airway stenosis, lung cancer, sarcoidosis. Pulmonary oedema. Anaphylaxis.
Cough syndromes, hyperventilation syndrome, vocal cord dysfunction, rhinitis, GORD (can occur with asthma), cardiac failure, pulmonary fibrosis.
Hx/family hx of asthma/atopic disorder e.g. eczema. Wheeze/breathlessness/chest tightness/cough esp worse at night and morning, occur with allergen, exercise or cold, after aspirin or β-blocker. Unexplained eosinophilia and low PEF or FEV1. NB. consider NSAIDs and asthma (asprin intolerant asthma, associated wtih nasal polyps), exercise-induced asthma.
No single Ix can dx asthma; what are some ix?
Bronchiectasis is more common than generally thought. What is the consistent feature and how is it dx?
What are some upper airway diseases that can co-exist with asthma and whose symptoms may be cofused with asthma?
1) FBC: eosinophil count
2) PEFR/FEV1 (most imp): PEFR variation (look for 15% fall in FEV1), reversability in spirometry, bronchial provacation challenge testing
3) Treatment trial: FEV1 reversability testing
4) Allergy: skin prick test (only supports dx), specific IgE/total IgE in blood
5) Inflammation: inhaled FENO (fractional exhaled NO)
6) CXR
Presence of cough + productive sputum. Dx by high resolution CT.
Rhinitis, sinusitis.
What are some primary prevention strategies for asthma?
What is the non-pharmacological tx/mx?
Describe the pharmacological treatment ladder for asthma.
Allergen avoidance. Breastfeeding. Microbial exposure. Avoidance of tobacco smoke.
Avoid smoking exposures. Wt reduction. Pt education and self mx. Breathing control exercises (buteyko)
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How does salbutamol work? What are the SEs?
What are the 5 main classes of drugs used to treat asthma? Give examples.
β2 agonist: bronchodilator and mucocillary clearance. Relaxes SM. Relieves bronchospasm. SEs: tremor, tachycardia, seweats, agitiation.
1) SABA: salbutamol, terbutaline
2) LABA: salmeterol, formoterol
3) Inhaled corticosteroids: beclametasone, budesonide, fluticasone
4) Leukotriene receptor antagonists: monteleukast
5) Anti IgE: omalizumab
Also: phosphodiesterase inhibitor - theophyllines. And anticholinergics eg. tiotopium (also used in COPD).
How does anti-IgE therapy work? When is it’s use indicated?
OSCE questions:
- Explain to a patiet the difference between a reliever and preventer inhaler
- Demonstrate the use of a metered dose inhaler with and without a spacer
Omalizumab - monoclonal ab to IgE -> decreases free IgE. Indications: maximum inhaled therapy (step 4/5 of ladder), impaired lung function, symptomatic, frequent exacerbations, raised IgE but <700 iu/L. 24 weekly subcutaneous injections.
- Preventor inhalers (usually brown/orange) used once or twice a day to stop asthma symptoms occuring. Contain corticosteroid e.g. beclometasone which reduces airway inflammation and sensitivity. Recommended if asthma symptoms >2xweek. Don’t work immediately so keep using blue inhaler to start with. Reliever inhalers (blue) relieve symptoms fast, contain beta2 agonist e.g salbutamol. Works for about 15mins, shouldn’t need to use it much
- Remove cap and shake inhaler. Breathe out gently. Put mouthpiece in mouth, and as being to breathe in (slow + deep) press down canister and continue to inhale. Remove inhaler from mouth and continue to hold breath for 10s or as long as comfortable. Breathe out gently. Wait 30s before taking another dose if needed.
Spacer: remove caps from inhaler and spacer, shake inhaler and insert in back of spacer. Breathe out gently. Put mouthpiece in mouth, press canister once to release dose of medicine. Take deep slow breath in. Hold breath for 10s or as long as comfortable. Breathe out gently.
Self management: written asthma action plans improve outcomes and should be given prior to discharge. What should they include information on?
What are the main ways asthma and COPD differ?
Nature of disease and tx, areas where pt most wants tx to have effect, how to use tx, developing self monitoring/assessment skills, goals, recognition and mx of exacerbations, allergen/trigger avoidance.
Asthma: daily FEV1 variation, reversibility. COPD: older, smoking hx, sputum production.
What are the risk factors for fatal and near fatal asthma?
What are some precipitating factors?
What are the 5 different severity classifications of asthma?
Previous near fatal. Previous admission for asthma esp in last year. Needing 3 or more classes of asthma meds. Heavy use of β2 agonists. Repeated attendance at AandE for asthma care esp if in last yr. Brittle asthma. Non-complisnce. DNAs. Self-discharge. Psychosis, depression or SH. Denial. Alcohol/drug use. Obesity. Learning difficulties. Employment/social/income problems etc.
Viral infection, dust/house mite, animal dander, pollen, smoke/pollution, exercise, atm conditions e.g. lightning
Near-fatal, life-threatening, acute severe, moderate, brittle. (bold=admit)
When would you discharge regarding admission for an asthma attack?
Define the following acute asthma exacerbations:
a) near fatal
b) life-threatening
c) acute severe
d) moderate
e) brittle
PEF >75% after 1hr UNLESS significant symptoms, compliance concerns, live alone, psychological/physical/learning problems, previous near fatal/brittle asthma, pre-existing steroids, night, pregnant.
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Life threatening/severe asthma attacks are admitted after what initial tx?
What bronchodilators and steroids are used in these attacks?
Briefly, how would a severe asthma attack of an adult in A and E be treated?
ABC. Keep pt alive with bronchodilators (MDI + large vol spacer) while steroids decrease inflammation. O2 (high flow, aim sats ≥92% (94-98%), O2 driven nebs (if COPD, need to be air driven instead)). IV fluids (rehydration, correct electrolyte imbalance). Reasess every 15 mins with PEFR.
- *Salbutamol** or terbutaline nebulised/large volume spacer. Ipratropium if concerned salbut. not working. IV magnesium suphate some evidence of value. IV salbuamol/aminophylline no evidence.
- *Oral prednisolone** 40 or 50mg/d. Or IV hydrocortisone 100 qds.
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A systemic review of aminophylline showed no overall evidence of benefit in acute asthma attack treatment. What are some SEs?
How is an acute asthma attack monitored?
What are signs of life-threatening/acute severe not improving asthma?
Increased incidence of palpitations, arrhythmias, nausea. Narrow therapeutic index.
Regular PEFR, O2 sats, ABG (at outset and repeat at 1hr if hypoxic, normo-hypercapnoeic, pt deteriorates), serum (K, glucose and theophylline if used).
Decreased PEFR, persistent/worse hypoxia, increased PaCO2, decreased pH, exhaustion/feeble respiration, drowsiness/confusion, resp arrest.
