Adult asthma

Adult Asthma (Medicine) MohdHanafiRamlee

History Asthma : derived from the Greek aazein, meaning "sharp breath." The word first appears in Homer's Iliad. In 450 BC. Hippocrates: more likely to occur in tailors, anglers, and metalworkers. Six centuries later, Galen: caused by partial or complete bronchial obstruction. 1190 AD, Moses Maimonides: wrote a treatise on asthma, describing its prevention, diagnosis, and treatment 17th century, Bernardino Ramazzini: connection between asthma and organic dust. 1901: The use of bronchodilators started. 1960s: inflammatory component of asthma was recognized and anti-inflammatory medications were added to the regimens.

ASTHMA Chronic inflammatory condition of the airways characterized by; - airflow limitation (reversible with treatment) - airway hyper-responsivenessto a wide range stimuli - inflammation of the bronchi In chronic asthma, inflammation maybe accompanied by irreversible airflow limitation Symptoms are cough, wheeze, chest tightness, and shortness of breathwhich often worse at night

Simple Definition A reversible chronic inflammatory airway disease which is characterized by bronchial hyper-responsiveness of the airways to various stimuli, leading to widespread bronchoconstriction, airflow limitation and inflammation of the bronchi causing symptoms of cough, wheeze, chest tightness and dyspnoea.

Epidemiology Majority of patients(87.3%) had mild asthma; 9.9% had moderate asthma and 2.7% had severe asthma Among severe asthmatics, only 19.4% were on inhaled corticosteroids Common disease with unacceptably high morbidity and mortality Commonly underdiagnosed and undertreated Only 36.1% of adult asthmatics ever had their peak flow measured Higher prevalence in rural (4.5%) than in urban areas (4%),lower educational status(5.6%) and lower income

EPIDEMIOLOGY The prevalence of asthma has increased 61% over the last two decades. Asthma is the leading chronic illness among children. Asthma results in 10 million lost school days and 3 million lost work days. Deaths from asthma have increased by 31% since 1980.

Classification Extrinsic – implying a definite external cause more frequently in atopic inviduals (atopic – individual which tends to develop hypersensitivity by contact with allergens) often starts in childhood - accompanied by eczema Intrinsic/cryptogenic – no causative agent can be identified starts in middle age

Types of Asthma According to the severity: helpful for treatment and management.

Types of Asthma According to pathophysiology Allergic asthma Occupational (allergic) ABPA (allergic) Intrinsic (Non-Allergic) Exercise-induced Steroid-resistant

Pathogenesis Complex, not fully understood numbers of cells, mediators, nerves, and vascular leakage -activated by expose to allergens or several mechanism Inflammation Eosinophils, T-lymphocytes, macrophages and mast cell Remodeling Deposition of repair collagens and matrix proteins-damage Loss of ciliated columnar cells- metaplasia – increase no of secreting goblet cells

Pathologic features of asthma Inflammatory cell infiltration of the airways Increased thickness of the bronchial smooth muscle Partial or full loss of the respiratory epithelium Subepithelialfibrosis Hypertrophy and hyperplasia of the submucosal glands and goblet cells Partial or full occlusion of the airway lumen by mucous plugs Enlarged mucous glands and blood vessels

Pathophysiology Smooth muscle contraction Thickening of airway –cellular infiltration and inflammation Excessive secrection of mucus Genetic factor Cytokine gene complex (chromosome 5)-IL-4 gene cluster control IL-3, IL-4 , IL-5 and IL-13 Environment factor Childhood expose irritants or childhood infection

Pathophysiology Extrinsic asthma: Atopic/allergic, occupational, allergic bronchopulmoaryaspergillosis. Atopic or allergic Dust, pollens, animal dander, food etc. Family history of atopy. ↑ serum IgE. Skin test with Ag  wheal, flare ( Classical IgE mediated response) Exposure of pre-sensitised mast cells to the Ag stimulates chemical mediators from these cells. Type 1 hypersensitivity.

1.Early phase Inhaled Antigen Sensitised mast cells on the mucosal surface  mediator release. Histamine bronchoconstriction, increased vascular permeability. prostaglandin D 2  bronchoconstriction, vasodilatation. Leucotriene C4,D4, E4  Increased vascular permeability, mucus secretion and bronchoconstriction. Direct subepithelialparasympathetic stimulation bronchoconstriction.

2.Late phase starts 4 to 8 hours later Mast cell release additional cytokine Influx of leukocytes(neutrophil,eosinophil) Eosinophils are particularly important- exert a variety of effect

Pathophysiology Atopic Asthma Eosinophil IL5 TH2 cell Trigger Eg.dust,pollen, animal dander IL4 IgE B cell Mast cell Mediators Eg.Histamine, leukotrines IgE antibody Immediate phase(minutes) Bronchospasm Increase vascular permeability Mucus production

Environment factor Genetic prediposition Bronchial inflammation Bronchial hyperreactivity + trigger factors Oedema BronchoC Mucus production Airways narrowing Cough, Wheeze, Breathlessness, Chest tightness

Aetiology and triggers ,[object Object],Genetic factors Allergen exposure house dust mite, household pets, grass pollen Atmospheric polutionsulphurdioxide, ozone, ciggerate smoke, perfume Dietary deficiency of antioxidants  vit E and selenium may protect asthma in children(freshfruits and vegetables)

Aetiology and triggers Occupational sensitizers isocyanates(from industrial coating, spray painting) colophony perfumes(electronic industries) Drugs NSAIDS B-blocker(B1 adrenergic blocker drug such as atenolol is avoided to treat HPT and angina in asthmatic pt Cold air Exercise  exercise-induced wheeze is driven by histamin and leukotrienes which are release from mast cells when epithelial lining fluid of the bronchi become hyperosmolar owing to drying and cooling during exercise Emotion

History Presenting symptoms: Cough ± sputum - time: become worse at night - duration: chronic / acute - associated with wheezing - fever? URTI Wheeze - max during expiration and accompanied by prolonged expiration

Cough History 1.Ask specifically about the symptoms: -Cough?how is the cough? more severe at night or on day? associated symptoms like dyspnea & wheezing? how long is the cough? Recurrent?Any previous similar episode? Aggravated factor?like cough become severe after exercise?or the cough is initiated after exercise?

Cough History 2.If the cough is associated with dyspnea and wheezingis it relieved by bronchodilator? 3.Ask for any precipatating factors -whether the symptoms(cough,dyspnea,wheezing) started after exposure to weather changes, dust, exercise, infection or drugs? 4.Is there any pets,carpet or feather pillow in home?(easily trapped dust and the dust or animal fur will cause exacerbation of asthma)

Dyspnoea History Dyspnoea - onset: after exercise? cold? dust? animal fur? emotion? - severity and pattern: varies from day to day or from hour to hour - no chest pain

History Clinical features Recurrent episodes of wheezing,chesttightness,breathlessness and cough Precipitants- cold,allergen,pollutant,viralurti Exercise tolerance Disturbed sleep Other atopic disease Home-Pet?Carpet? Occupation

History Clinical features ,[object Object]

Mild intermittent asthma-asymptomatic between exacerbation

Persistent asthma-chronic wheeze and breathlessness,[object Object]

History Past medical history: Experienced asthma attack before Taking any medications: NSAIDs / β-blocker / aspirin (non atopic asthma) Family history: Has family history of asthma

History Social history: Occupation: expose to fumes/organic/chemical dust House: near to factory? Pets? Dust? Carpet? Feather pillow? Smoking in any family members

known asthmatic When he was diagnosed with asthma? How the asthma was diagnosed? Who diagnosed it? Whether he is on prophylaxis? What type of prophylaxis? How he get the drugs and how many dosage of the drugs? Whether he know how to deliver the drugs properly? How is his compliance to drugs?

Physical examination General inspection: - tachypnoeic, sign of respiratory distress, effort of breathing, cyanosis (life-threatening) Inspection: - fingers: tar staining - pulse rate: tachycardia and pulsusparadoxus, bradycardia (life-threatening) - used of accessory muscles or recession - wheezing

Chest Percussion: - may be hyperresonance / normal Auscultation: - breath sound: vesicular - ronchi in expiratory phase, may be both in severe asthma - prolonged expiratory phase -vocal resonance decrease / normal Inspection: - shape: hyperinflated in severe asthma - movement of chest/silent chest (life-threatening) - chest deformity: - recession: Palpation: - chest expension may be reduce (hyperinflated)/ normal - apex beat: may be displaced -vocal fremitus: decrease

Clinical features Sign ,[object Object]

Severe attack – inability to complete sentences, pulse >110bpm, RP>25/min, PEF 33-50%

Life-threatening attack- silent chest,cyanosis,bradycardia,exhaustion, PEF < 33%,confusion

Pulsusparadoxus (exaggeration of the normal variation in the pulse volume with respiration, becoming weaker with inspiration and stronger with expiration ),[object Object]

At the onset of an attack, patients experience a sense of constriction in the chest, often with a nonproductive cough.

Respiration becomes audibly harsh; wheezing in both phases of respiration becomes prominent; expiration becomes prolonged; and patients frequently have tachypnea, tachycardia, and mild systolic hypertension.

The lungs rapidly become overinflated.

If the attack is severe or prolonged, there may be a loss of adventitial breath sounds, and wheezing becomes very high pitched.

The accessory muscles become visibly active, and a paradoxical pulse often develops.,[object Object]

Diagnosing asthma ,[object Object], PEF increases more than 15% and 200mls 15 to 20 minsafter inhaling a short acting beta2 agonist, or PEF varies more than 20% from morning measurement upon arising to measurement 12 hours later in patients who are taking a bronchodilator, or PEF decreases more than 15% after 6 mins of running or exercise

Differential diagnosis ,[object Object]

Allergic bronchopulmonaryaspergillosis

Hyperventilation with panic attacks,[object Object]

Specific investigation Specific: - respiratory function test: 1. peak expiratory flow 2. spirometry - exercise tests -histamine/methacholine bronchial provocation test - trial of corticosteroids

Reversibility Test ,[object Object]

An improvement of 15% or more (as measured on the peak flow meter) is diagnostic of asthma.

However, in severe chronic disease or patient who has treated with long-acting bronchodilators, little reversibility will be demonstrated. ,[object Object]

Peak expiratory flow rate Simple and cheap Subject take full inspiration then blow out forcefully into peak flow meter. Best used to monitor progression of the asthma and its treatment. To access possible occupational asthma PEFR value varies with sex, age and height.

Peak Expiratory Flow Rate (PEFR) The maximum rate of air breathed out as hard as possible through a measuring device called a peak flow meter, (after a full breath taken in). Reading is measured in litres/minute (l/min). Take 3 readings and choose the best Reading < 80% - presense of obstruction, but not diagnostic of asthma

Require to take a series of reading - on waking up - prior taking bronchodilator - after taking bronchodilator (before sleep)

PEF measurements During periods of well-being: provides measurement of the patients best PEF value which will provide the target for the doctor and the patient to aim for.Twice daily measurements before any inhaled bronchodilator tx will determine the diurnal variability of airway calibre.Good control of asthma means PEF variability is maintained at less than 10%. During symptomatic episodes: During an attack of asthma PEF fairly accurately measures the degree of bronchospasm.A PEF of less than 50% of normal or best suggests a very severe attack and a PEF of less than 30% suggests a life-threatening attack

Spirometry Test ,[object Object]

- measures the volume of air blown out against time

- gives more specific information about lung function.

A value is calculated for the amount of air blown out in one second - “Forced Expiratory Volume” or FEV1).

This is divided by the total amount of air blown out until all air is expired - Forced Vital Capacity or FVC).

FEV1/FVC expressed as a percentage value,[object Object]

Male Spirometryreading range Mild reduction: 2.5 litres or more Moderate reduction :1.5 to 2.49 litres Severe reduction :Less than 1.5 litre ,[object Object], Mild reduction :2.0 litres or more Moderate reduction: 1.0 to 1.99 litres Severe reduction: Less than 1.0 litre ,[object Object],[object Object]

Exercise Test ,[object Object]

Peak flow reading measured before hand

Ask patient to run for 6 min, to increase HR > 160 beats/min

Cannot run – use cold air challenge, isocapnoiec(CO2) hyperventilation, aerosol challenge with hypertonic solution

After exercise – take readings at intervals of 5, 10 and 15 minutes.

Diagnosed asthma - fall in peak flow of 15% or more, after exercise.,[object Object]

histamine/methacholine bronchial provocation test

Chest X-ray Showed lung hyperinflation. Not diagnostic of asthma Useful to rule out other causes eg. Pneumothorax ----------------------------------------------- Hyperinflation and increased bronchovascular markings

Allergies & Atophy Allergen Provocation Test In suspected occupational asthma and food-allergy related asthma Skin-Prick Test To identify allergens A drop of allergen is placed on skin , site is marked and pricked with needle, measured any weals

Severity assessment for acute setting of AEBA

Management of Chronic Asthma Aims of management ,[object Object]

to restore normal or best possible long term airway function

to reduce morbidity and prevent mortality ,[object Object]

1) Education of patient and family Recognition of features of worsening asthma ,[object Object]

development of nocturnal symptoms

reducing peak flow rates). Self management plan for selected, motivated patients or parents. The danger of non prescribed self medication including certain traditional medicines. Natureof asthma Preventive measures/avoidance of triggers Drugs used and their side-effects Proper use of inhaled drugs Proper use of peak flow meter Knowledge of the difference between relieving and preventive medications

2) Avoidance of precipitating factors The following factors may precipitate asthmatic attacks: ,[object Object]

Aspirin and nonsteroidal anti-inflammatory drugs if known to precipitate asthma, these drugs should be avoided.

Allergens e.g. house dust mites, domestic pets, pollen should be avoided whenever possible.

Occupation should be considered as a possible precipitating factor.

Day to day triggers  such as exercise and cold air. It is preferable to adjust treatment if avoidance imposes inappropriate restrictions on lifestyle.

Food  if known to trigger asthma, should be avoided.,[object Object]

Drug Delivery ,[object Object]

Inhaled medications exert their effects at lower doses

pMDI is suitable for most patients as long as the inhalation technique is correct

Alternative methods include spacer devices,dry powder inhalers and breath-actuated pMDI

Nebulised route is preferred in the management of acute attacks,[object Object]

2. Anti-Inflammatory Drug ,[object Object], Examples: Beclomethasonedipropionate (Becotide, Becloforte, Beclomet, Aldecin, Respocort) Budesonide (Pulmicort) ,[object Object]

Other treatments Anti-histamines including ketotifen AnticholinergicsExamples: Ipratropium bromide (Atrovent) Methylxanthines Examples: Nuelin SR, Theodur, Euphylline

Approach To Drug Therapy - "Stepwise Approach"[step 1] Start at the step most appropriate to severity, moving up if needed or down if control is good for > 3 months. Rescued courses of prednisolone may be needed STEP 1 MILD EPISODIC ASTHMA ,[object Object]

PEF 80-100% predicted Treatment: inhaled beta2 agonist "as needed" for symptom relief. If needed more than once a day, advance to Step 2

Approach To Drug Therapy - "Stepwise Approach"[step 2] STEP 2 MODERATE ASTHMA ,[object Object]

PEF 60-80% predicted Treatment ,[object Object]

inhaled sodium cromoglycate plus

inhaled beta2 agonist "as needed" ,[object Object]

PEF 60% predicted or less Treatment: ,[object Object]

inhaled beta2 agonist as needed plus, if necessary

oral beta2 agonist preferably long acting, or

inhaled long acting beta2 agonist, or

Adult asthma

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