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ASTHMA
Adapted from source
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Epidemiology in Australia
Prevalence in adults: 10 12%
(England: 15.3%, Germany: 6.9%)
Prevalence in children: 14 16%
More common in women and indigenous
Australians
1.7% of all ED presentations, 0.3% of all deaths,
0.6% of hospital admissions, 2.5% of GPencounters
40% of children with asthma live with smokers
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EtiologyAtopy is largest risk factor for development ofasthma (increased IgE production)
Suspect atopy if there is history or family history ofallergic rhinitis, urticaria, eczema, positive prick test,increased levels of IgE, positive reaction to specificprovocation test.
Pevalence of atopy > 30%, not all atopic peopledevelop symptoms
Allergic asthma: atopic component, earlier onset
(30%) Nonatopic, idiosyncratic asthma: No atopic
characteristics, later onset (> 40 yrs.) 30%
Mixed etiology asthma 40%
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Etiology
Genetic predisposition.
If both parents have allergic asthma,
children have a risk of 60 80 % ofdeveloping it. If one parent has allergic
asthma, risk is 30 40%
25% of patients with allergic rhinitis due to
pollen will develop allergic asthma within
10 years.
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Pathogenesis
Persistent subacute inflammation of
airways
mucous membranes oedematous,
infiltrated with eosinophils, neutrophils and
lymphocytes, elevated capillary density,
glandular hypertrophy and denudation of
epithelium
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3 Characteristics
Airway inflammation (allergens or infection),involvement of mast cells, T lymphocytes,
eosinophils, and mediators of inflammation
(histamin, eosinophil chemotactic factor of
anaphylaxis, leucotriens, bradykinin)
Bronchial hyperreactivity (prevalence 15%, but
only 5% have asthma)
Endobronchial obstruction throughbronchospasm, oedema of mucous membranes
and inflammatory infiltration, large amounts of
thick mucous secretions, airway remodelling
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Cellular sources of inflammatory mediators and
effects
Cells Mediators Effects
Mast cells
Macrophages
E
osinophilsT Lyphocytes
Epithelial cells
Fibroblasts
NeuronsNeutrophils
(Platelets,
Basophils?)
Histamine
Leukotriens
Prostaglandins
ThromboxaneBradykinin
Tachykinins
Adenosine
Anaphylaxotoxins
Endothelins
Nitric Oxide
Cytokines
Growth factors
PAF
Bronchoconstriction
Plasma exudation
Mucus hypersecretion
Structural changes(fibrosis, hyperplasia,
angiogenesis, mucous
hyperplasia)
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Categories of Asthma
Allergic
Pharmacologic
E
nvironmental Occupational
Infectious
Exercise induced
Asthma because of gastrooesophagealreflux
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Pharmacologic
Aspirin and NSAID ~ 10% of asthmatics(mast cell activation through chronic
oversecretion of cysteinyl leukotrienes, not
IgE mediated, leukotrien antagonistsinhibit reaction)
Beta blockers (contraindicated in Asthma)
Sulfur agents, tyramine, glutamate(sanitizing and preserving agents in food,
beverages, drugs, inhalers), mechanism
unknown
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Environmental
Asthma through climatic conditions thatpromote concentration of atmosphericpollutants or antigens
Smog, mostly in densely populated andindustrialised areas
Pollutants are ozone, nitrogen, nitrogen
dioxide, sulfur dioxideGreater effects during periods of highventilation
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Occupational asthma
High mulecular compounds (IgE mediated)
wood and vegetable dusts, pharmaceuticalagents, biologic enzymes, animal andinsect dusts, latex, fish and seafood
Low molecular compounds (direct mastcell degranulation)
metal salts, industrial chemicals andplastics, formaldehyde, persulfates,isocyanates
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Infectious exacerbated asthma
Viral respiratory infections
Upper respiratory tract infections are the mostcommon trigger for exacerbation of allergic
asthma.RS virus, Influenza- and Parainfluenza virus,Rhinovirus
long lasting infection necessary to destabilise
preexisting asthma, T cell derived cytokinesattract inflammatory cells into airway mucousmembranes
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Exercise induced
After exertion, not during exertion
? thermally induced hyperaemia and
capillary leakage in airway wallHigh ventilation of cold air causes more
severe response
Does not cause airway hyperreactivity orlong term sequelae
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Pathophysiology
Reduction in airway diameter
contraction of smooth muscle, vascularcongestion, oedema of bronchial wall, largeamounts of thick mucous secretions
Increase in airway resistance, decreased flow
rates, hyperinflation, increased work ofbreathing, mismatch of ventilation and perfusion
When patient presents for therapy, FEV1 isusually < 40% of predicted
Histologically hypertrophy of smooth muscles,hyperplasia of vessels, mucosal oedema,denudation of epithelium, thickening of basalmembrane, eosinophilic infiltrates, airwayremodelling
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Clinical features during attack
Dynpnoea, cough and wheezing Prolonged expiration, tachypnoea, mild
hypertension
Use of accessory respiratory muscles,
hyperinflation, silent lung, pulsus paradoxus
Curschmans spirals, Charcot Leyden crystals
and eosinophils in sputum
Atelectasis due to mucous plugs, pneumothorax Blood gas analysis necessary to diagnose
impending respiratory failure (CO2 retention)
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Curschmans Spiralstwisted plugs of mucous
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Charcot-Leyden CrystalsEosinophilic needle-shaped crystalline structures
representing breakdown products of eosinophils.
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Symptoms in mild asthma
Nocturnal awakening with dyspnoea or
wheezes
Chronic cough Mild episodes of dypnoea
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Diagnosis Reversible airways obstruction (FEV1 increases
by a minimum of 12% (15%) after inhalation of abeta agonist)
Unspecific bronchial challenge (Histamin,Metacholin, direct challenge, hypertonic saline,
Mannitol, indirect challenge) shows reduction ofthe FEV1 by a minimum of 20% (off steroids for96 hrs, off antihistamines for 48 hrs, offtheophylline, inhaled beta agonists oranticholinergics for 12 hours). Direct challenge
more sensitive, indirect challenge more specific. Peak flow fluctuations during the day of a
minimum of 20% in a minimum of 3 days a weekfor 2 weeks
Sputum eosinophilia
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Diagnosis
History! Work history, contact with
animals, onset of symptoms, family
history,
Total IgE
Skin prick test
Specific IgE
in serum (less sensitive thanprick test, but very specific)
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Treatment
Quick relief (inhibition of smooth muscle contraction)
Adrenergic stimulants (inhalative, iv, oral, Salbutamol, )Theophylline
Anticholinergics (Ipatropiumbromide, Atrovent)
Long term controller medication
Glucocorticoids (oral, iv, inhaled, Budesonide,
Beclomethasone, Fluticasone), improve sensitivity of betareceptors
Combined inhaled glucocorticoid and long acting betaagonist (Serevent, Symbicort)
Leukotrien modifiers (oral, Montelukast, Zafirlukast)
Mast cell stabilising agents (inhaled, Cromolyn, Nedocromil) no evidence
Anti IgE Antibody (s.c. Omalizumab, Xolair)
Cyclosporin A, Methotrexate
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Best strategy for management of acute
exacerbation of asthma is earlyrecognition and intervention, before
attacks become severe and potentially life
threatening.Detailed investigations into the
circumstances surrounding fatal asthma
have often revealed failures of patients
and clinicians to recognize the severity of
disease and to intensify treatment.
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Acute exacerbation, home treatment,
asthma managementplan (peak flow falls
by more than 20% of baseline)
Inhaled or nebulised beta agonists immediately and
20 minutes later. If peak flow increases to > 80% of
baseline, no need for admission. Continue betaagonists, quadruple inhaled steroid dose or add oral
steroids.
Peak flow post betaagonists > 50% 200 l/min: severe obstruction
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Treatment of acute attack
Inhaled betaagonist (Salbutamol), in statusasthmaticus often temporary decreasedsensitivity of beta receptors! 6 doses throughMDI (metered dose inhaler) roughly equal onenebuliser. Repeat 2 after 20 and 40 minutes,
then every 1 to 4 hours. Inhaled ipatropiumbromide (Atrovent)
Oxygen supplementation
Intravenous Hydrocortisone (antiinflammatory,antiallergic, immunosuppressiv, improvessensitivity of beta receptors). Massive dose hasno advantage over large dose (60 125 mg ofmethylprednisolone)
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Treatment of acute ctd.
Continous intravenous Aminophylline alone orcombined with betaagonist (Terbutaline) instatus asthmaticus, additive effect to betaagonists
Magnesium Sulfate iv (2g over 20 min) ?Inhibition of calcium influx into airway smoothmuscle cells.
ABGs necessary to monitor treatment
If peak flow > 25% of normal, hypercapnia isunlikely
Antibiotics in most cases not necessary
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Criteria for hospital admission
FEV1 or Peak Flow < 40% - 50% of best value
FEV1 or Peak Flow > 70% of best value do notneed admission
FEV1 or Peak Flow between 40 and 70% of bestvalue should be admitted ifnew onset asthma
multiple prior hospitalizations for asthma
use of oral corticosteroids at the time of presentationwith acute deterioration
complicating psychosocial difficulties.
Risk of fatal asthma
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Risk of fatal asthma
Previous near fatal asthma
Admission for asthma during last 12months
On 3 or more classes of asthmamedication
Heavy use of beta agonists
Repeated ED presentations during the last12 months
Brittle asthma
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Brittle Asthma Type 1
Patients who consistently demonstrate wide peak flow variation(greater than 40% diurnal variation for at least 50% of days),despite maximal medical therapy including at least 1500 g/dayof inhaled beclomethasone or equivalent, are classified ashaving type 1 brittle asthma.
These patients are typically female and aged between 15 and55 years.
Type 2Patients with type 2 brittle asthma appear to be well controlledbetween attacks which are often sudden in onset (occurring
within minutes) and are associated with loss of or disturbedconsciousness on at least one occasion.
Severe respiratory acidosis develops quickly in an attack and, ifventilated, needs support for relatively short time periods.Equally prevalent in men and women.
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Brittle asthma
90% of patients have atopy
60 % have food intolerance worsening
asthma (dairy products, wheat, fish, citrus,egg, potato, soya, peanut, yeast)
Psychosocial complications common
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Prevention
Avoidance of exposure to allergen
removal of pets, air filtration devices, travel to
non pollinating areas during the critical times,
control of dust mites by use of plastic linedcovers for mattresses, pillows and comforters,
elimination of carpets and drapes, control of
mould by eliminating plants and keeping the
house dry, in extreme cases change of house,eliminate cockroaches.
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Patient Education
Home peak flow measurements
Personal asthma management plan
Exposure avoidance Inhaler use
Relaxation/breathing techniques
Advise of young atopic people regardingfuture job: They should not become
woodworkers or bakers
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