Asthma Vpl 2 Edited

8/8/2019 Asthma Vpl 2 Edited

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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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Asthma Vpl 2 Edited

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