BRONCHIAL ASTHMA.

BY
SWETHA. R
B. SC PHYSICIAN ASSISTANT
DEFINITION :

 A disease characterized by increased reactivity

of the trachea and bronchi to various stimuli,
resulting in bronchoconstriction
(bronchospasm), increased mucus production
& swelling of mucosal tissue.
 Asthma is a chronic inflammatory disorder.
 CLASSIFICATION OF ASTHMA :

Based on ANTIGEN :
Based on TRIGGER :
 Early onset • Seasoned. Based on SEVERITY:
asthma ( allergic • EIA.
/ extrinsic). • Mild intermittent.
• Drug induced. • Mild persistent.
 Large onset • Occupational. • Moderate persistent.
asthma (non- • Smokers. • Severe persistent.
allergic / • Cough variant
intrinsic).
asthma.
TRIGGERS :

1. Inhaled allergens.
2. Upper respiratory tract viral infection.
3. Heredity.
4. Psychosocal factors.
5. GERD patients.
6. Exercise(EIA), cold air, hyperventilation.
7. Drugs.
8. Air pollution.
9. Passive smoking.
10. Emotional stress.
RISK FACTORS :

ENDOGENOUS FACTORS :
ENVIRONMENTAL FACTORS :
1. Genetic predisposition.
2. Atopy. 1. Allergens.
3. Airway hyper- responsiveness. 2. Occupational sensitizers.
3. Respiratory infections.
4. Gender & age
5. Ethnicity.
6. Obesity.
7. Early viral infection.
PATHOPHYSIOLOGY :

1. AIRWAY INFLAMMATION. 2.AIRWAY REMODELING.

 Airway Inflammation :

 Inflammation is chronic and involves many types of cells and inflammatory mediators..
 Important cells
•MAST CELLS.
•EOSINOPHILIS.
•DENDRITIC CELLS.
•LYMPHOCYTES.
Airway Remodeling :

Airway remodeling is the group of structural &

functional changes in the bronchial wall due to
repeated bouts of inflammation observed in
chronic asthma.
 Hypertrophy and Hyperplasia of submucosal
glands, bronchial wall smooth muscles,
increased vascularity, deposition of
subepithelial collagen accompained by fibrosis
& thickening of basement membrane.
Changes occur in AIRWAY :
SYMPTOMS :

Commonly patients appear with :

1. Wheeze.
2. Shortness of breathe.
3. Chest tightness.
4. Cough.
SIGNS :

 Paradoxial Pulse.
 Systolic blood plessure is higher than Diastolic blood pressure.
(10mmHg)
 Tachycardia.
 Tachypnea.
 Cyanosis
 ABG level initially reveals hypoxemia.
 Increased level of Eosinophilia.
INVESTIGATION :
 Lung Function test :
1. Spirometry
2. Peak expiratory flow rate.
 Airway Responsiveness :
 Imaging :
1. Chest X-ray.
 Measurement of Allergic Status. :
1. Skin Privk test (SPT).
2. Elevated serum IgE levels.
 Blood & Sputum test.
 Arterial Blood Gas Analysis.
TREATMENT :

 Avoid identified factors /allergens.

 Control of risk factors causing exacerbation.
 Desensitization or Immunotherapy.
 Drug therapy.
Drug therapy :

BRONCHODILATORS :
 Selective β2 adrenergic agonists .
 Methylxanthines.
 Anticholinergics.
 Leukotriene receptor antagonists.
 Mast cell stabilizers.
Bronchodilators :

 Selective β2 adrenergic agonists :

•Salbutamol ( 2-4 mg )
•Terbutaline ( 2.5-5mg )
 Methylxanthines :
•Theophylline
•Aminophylline
 Anticholinergics :
•Ipatropium bromide ( 2 puff of 20 μg )
•Tiotropium bromide ( 2 puff of 9μg )
 Leukotriene Receptor Antagonists :
•Zafirlukast.
•Montelukast.
 Mast cell stabilizers :
•Sodium cromoglycate
•Ketotifin
CONTROLLER THERAPIES :
 Inhaled Corticosteroids :
•Belomethasone (200μg)
•Budesonide (200μg)
•Fluticasone (125μg)
Drugs to be avoided for asthmatic
patients :

 NSAIDS – Aspirin,
Ibuprofen,
Diclofenac.

 βAdrenergic blockers.
 Cholinergic agonists.
COMPLICATIONS :

 Collapse of part or all of the lung.

 Pneumonia.
 Severe Acute Asthma ( status asthmaticus ).
 Respiratory failure.
 Management of severe acute asthma :
•Humidified Oxygen Inhalation.
•Nebulized β2 adernergic agonists. ( salbutamol 5mg /
terbutaline 10mg ) + anticholinergics Agents. ( ipatropium bromide
0.5mg )
•IV fluids to correct dehydration.
•Potassium Supplements is given.
•Sodium bicarbonate is given to treat acidosis.
•Antibiotics to treat infection.
DIFFERENTIAL DIAGNOSIS :

 Congestive heart failure.

 Laryngeal dysfunction.
 Upper airway obstruction.
 Bronchiectasis.
***THANK YOU ALL FOR YOUR ATTENTION ***