Management of asthma and copd

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A chronic inflammatory disorder of the airway

Infiltration of mast cells, eosinophils and lymphocytes

Airway hyperresponsiveness Recurrent episodes of wheezing,

coughing and shortness of breath Widespread, variable and often

reversible airflow limitation

Predisposing Factors Atopy

Causal Factors Indoor Allergens

Domestic mites Animal Allergens Cockroach Allergens Fungi

Outdoor Allergens Pollens Fungi

Occupational Sensitizers

Contributing Factors

Respiratory infections

Small size at birth Diet Air pollution

– Outdoor pollutants– Indoor pollutants

Smoking– Passive Smoking– Active Smoking

Genetic factors

Environmental factors

Atopic sensitization

Structural changes

Mucosal inflammation

Phenotype

1. Extrinsic or allergic: History of `atopy` in childhood Family history of allergies Positive skin test Raised IgE level Below 30 years of age Less prone to status asthmaticus

2. Intrinsic or Idiosyncratic: No family history of allergy Negative skin test No rise in IgE level Middle age onset Prone to status asthmaticus

STEP 4Severe

Persistent

STEP 3Moderate Persistent

STEP 2Mild

Persistent

STEP 1Intermitte

nt

The presence of one of the features of severity is sufficient to place a patient in that category.

Global Initiative for Asthma (GINA) WHO/NHLBI, 2002

SymptomsNighttimeSymptoms

PEF

CLASSIFY SEVERITYClinical Features Before Treatment

ContinuousLimited physical activityDailyUse 2-agonist dailyAttacks affect activity>1 time a week but <1 time a day

< 1 time a weekAsymptomatic and normal PEF between attacks

Frequent

>1 time week

>2 times a month

<2 times a month

<60% predictedVariability >30%>60%-<80% predictedVariability >30%>80% predictedVariability 20-30%>80% predictedVariability <20%

GINA Guideline clearly states that THERE IS NO CURE FOR ASTHMA, But appropriate management most often leading to CONTROL of asthma

Relievers Preventers Peak Flow meter Patient education

- Rescue medications- Quick relief of symptoms- Used during acute attacks- Action lasts 4-6 hrs

Short acting 2 agonistsSalbutamolLevosalbutamol

Anti-cholinergicsIpratropium bromide

XanthinesTheophylline

Adrenaline injections

Selective 2 agonist

ATP

cAMP

Theophyline

5’-AMP

Relaxation

Ach

Ipratopium

Vagus nerve

- Prevent future attacks- Long term control of asthma- Prevent airway remodelling

Corticosteroids Anti-leukotrienesPrednisolone, Betamethasone Montelukast,

ZafirlukastBeclomethasone, Budesonide

Fluticasone Xanthines

Theophylline SR

Long acting 2 agonists Mast cell stabilisersBambuterol, Salmeterol Sodium cromoglycateFormoterol

COMBINATIONS

Salmeterol/FluticasoneFormoterol/Budesonide

Salbutamol/Beclomethasone

SALBUTAMOL INHALER100 mcg:1 or 2 puffs as necessary

LEVOSALBUTAMOL INHALER 50 mcg :1 or 2 puffs as necessary

Formoterol ( fast relief and sustained relief ) +

Budesonide ( twice or even once daily use )

Dose: 1- 4 puffs ( OD/BD )

Another combination

Salmeterol + Fluticasone

Metered dose inhalers

Dry powder inhalers

(Rotahaler)

Spacers / Holding

chambers

SpacerDry PowderInhaler

Metered Dose inhaler

Step I: When symptoms are less than once daily - occasional inhalation of a short acting Beta-2 agonist – salbutmol, terbutaline. If used more than once daily – step II (Mild episodic asthma)

Step II: Regular inhalation of low-dose steroids. Alternatively, cromoglycates. Beta-2 agonist as and whenever required (Mild chronic asthma)

Step III: Inhalation of high dose of steroids (800 mcg) + Beta-2 agonist. Sustained release theophylline may be added. LT inhibitors may be tried instead of steroids (Moderate asthma with frequent exacerbations) - spacers

Step IV: Higher dose of steroid (800 to 200 mcg) + regular beta-2 agonist (long acting salmeterol)

Additional treatment with oral drugs – LT antagonist or SR theophylline or oral beat-2 agonist

allergenavoidance

indicated when possible

allergenavoidance

indicated when possible

pharmacotherapysafety

effectivenesseasy to be administered

pharmacotherapysafety

effectivenesseasy to be administered

immunotherapyeffectiveness

specialist prescription may alter the natural course of the disease

immunotherapyeffectiveness

specialist prescription may alter the natural course of the disease

patient'seducation

always indicated

patient'seducation

always indicated

ARAR

Older siblings:Many infections

[TH1 stimuli]

TH1No allergies

Still TH2Allergies

Only child:Few infections

AllergenExposure

Source: Busse WW, Lemanske RF. N Engl J Med 2001.

Birth:TH2

Patients diagnosed with allergic asthma

Patients diagnosed with allergies such as hay fever

Patients diagnosed with sinusitis that predisposes them to asthma

Patients diagnosed with insect sting allergy

COPD is characterized by airflow limitation caused by chronic bronchitis or emphysema often associated with long term tobacco smoking

This is usually a slowly progressive and largely irreversible process

Consists of increased resistance to airflow, loss of elastic recoil, decreased expiratory flow rate, and overinflation of the lung.

COPD is clinically defined by a low FEV1 value that fails to respond acutely to bronchodilators, a characteristic that differentiates it from asthma.

Chronic Bronchitis is characterized by Chronic inflammation and excess mucus

production Presence of chronic productive cough

Emphysema is characterized by Damage to the small, sac-like units of the lung

that deliver oxygen into the lung and remove the carbon dioxide

Chronic cough

*Source: Braman, S. Update on the ATS Guidelines for COPD. Medscape Pulmonary Medicine. 2005;9(1):1.

Normal versus Diseased Bronchi

Smoking Air pollution genetic (hereditary) risk

Night time waking with breathlessness or wheeze is common in asthma and uncommon in COPD.

COPD is rare before the age of 35 whilst asthma is common in under-35.

Classification of COPD Severity by Spirometry

Stage I: Mild FEV1/FVC < 0.70 FEV1 > 80% predicted

Stage II: Moderate FEV1/FVC < 0.70 50% < FEV1 < 80% predicted

Stage III: Severe FEV1/FVC < 0.70 30% < FEV1 < 50% predicted

Stage IV: Very Severe FEV1/FVC < 0.70 FEV1 < 30% predicted or

FEV1 < 50% predicted plus chronic respiratory failure

Physical examinationSigns of heavy smokers Observe for clubbing Distended neck vein on expiration The presence of barrel chest Observe for abdominal breathing The use of pursed lips breathing and

chest movement Auscultate the chest& listen for musical

wheezes characteristics of chronic bronchitis

Symptoms Physical examination Sample of sputum Chest x-ray High-resolution CT (HRCT scan) Pulmonary function test (spirometery) Arterial blood gases test Pulse oximeter

Give antibiotics to treat infection

Give bronchodilators to relieve bronchospasm, reduce airway obstruction, mucosal edema and liquefy secretions.

Chest physiotherapy and postural drainage to improve pulmonary ventilation.

Proper hydration helps to cough up secretions or tracheal suctioning when the patient is unable to cough.

Steroid therapy if the patient fails to respond to more conservative treatment.

Stop smoking

Oxygenation with low concentration during the acute episodes

In asthma adrenaline ( epinephrine) SC if the bronchospasm not relieved.

Aminophylins IV if the above treatment does not help.

IV corticosteroids for patients with chronic asthma or frequent attack.

Sedative or tranquilizers to calm the patient.

Increase fluids intake to correct loss of diaphoresis and inaccessible loss of hyperventilation.

Intubations and mechanical ventilation if there is respiratory failure.

Oxygen therapy Used as long-term continuous therapy, during

exercise, or to relieve acute dyspnea Improves survival in COPD patients with severe

hypoxemia (partial pressure of oxygen [pO2] < 55 mm Hg or oxygen saturation [sO2] <88%) (Strength of Recommendation [SOR]: A) When used for >15 hours daily

Does not improve survival in patients with moderate hypoxemia or desaturation at nightCranston, 2008

GOLD, 2009

Annual flu vaccine Reduces risk of flu and its complications

Pneumonia vaccine Reduces risk of common cause of pneumonia

lobal Initiative for Chronic

bstructive

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lobal Initiative for Chronic

bstructive

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G

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November 19, 2006World COPD Day, Kyoto Japan

Definition, Classification Burden of COPD Risk factors Pathogenesis, pathology,

pathophysiology Management Practical Considerations

Definition, Classification Burden of COPD Risk factors Pathogenesis, pathology,

pathophysiology Management Practical ConsiderationsRevised 2006

THANK YOU

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