Bronchial Asthma Etiology Pathogenesis Clinical features Treatment of Bronchial Asthma

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Asthma is a chronic inflammatory disease of airways characterized by increased bronchial responses to a variety of stimuli.
There is widespread narrowing of air passages which is relieved by therapy, or by itself.
The typical clinical picture is paroxysms of dyspnoea, cough; and wheezing.
Most attacks are short-lived, for minutes to hours and patient recovers completely after an attack.
The attack comes in episodes lasting for minutes, hours, days or weeks.
There are symptom-free periods between attacks.
Status asthmaticus severe obstruction persisting for days or weeks continuously.
Serious attacks can result in death ,
Age: Usually occurs before age of 10 years or before 40 years age.
Sex: Amongst children, it is more common in males.

Symptoms of recurrent episodes of airway obstruction or airway hyper-responsiveness may include:
Cough (particularly if worse at night)
Wheeze
Airflow obstruction is at least partially reversible.
Alternative diagnoses are excluded.
Chest tightness
Difficulty breathing
Symptoms are typically precipitated or worsened by exercise, viral infections, irritants such as allergens, changes in weather, stress or strong emotions, and/or menstrual cycles.

It is an atopic disease (genetic) where environmental factors have an important role.
Allergic asthma is associated with rhinitis, urti-caria, eczema, increased IgE, and positive reaction to intradermal antigens.
Some patients have non-atopic asthma (no history of allergy) or idiosyncratic asthma.
Asthma of early life usually has allergic basis. Asthma occurring in later life usually has no history of allergy.

The airways are inflamed, edematous, infiltrated with eosinophils, neutrophils, Iymphocytes.
The cells involved in inflammatory and allergic response are masked cells, eosinophils, Iymphocytes, epithelial lining cells of airways .
The IgE response is controlled by T and B Iymphocytes in allergic asthma.

There is reduction in airway diameter.
FEV₁ is reduced to less than 40% of predicted. .y Peak expiratory flow rate (PEFR) is less than 40% of predicted.
There is hypoxia and ventilatory failure.
There may be hypocapn~ and respiratory alkaI~.
There may be metabolic acidosis in acute severe asthma.
There may be cyanosis.

Clinical features Bronchial Asthma

There is a triad of dyspnoea, cough, wheezing.
· There is tachypnea, sense of constriction in chest,
nonproductive cough, wheezing in inspiration and expiration, prolonged expiration, tachycardia”
systolic hypertension. •
Anteroposterior diameter of thorax is increased.
Wheezing is high-pitched and there is loss of an . sOUnds in severe cases.
Accessory muscles become active.
There is paradoxical pulse due to large negative intrathoracic pressu re.
There may be productive cough with mucus often as casts called Curschmann’s spirals. These are laden with eosinophils and Charcot-Leyden crystals.
Respiration may change from tachypnea to gasping.
Patient then needs ventilatory support.

Quick relief medications: Beta adrenergic agonists, metQylxanthines, anticholinergics.
Beta adrenergic agonists :

These are catecholamines, resorcinols and saligenins.
Catecholamines e.g. epinephrine, isoproterenol.
They are short acting and given by inhalation or parenterally.
Resorsinols e.g. Fenoterol.
Resorsinols have no cardiac side effects.
Saligenins e.g. Albuterol (salbutamol).
Long acting beta 2 agonists e.g. Terbutaline, Salmeterol, Formeterol.
Methyl xanathines e.g.
Theophylline Common side-effects of theophylline are nervousness, nausea, vomiting, anorexia, headache and even seizures and cardiac arrhythmias.

Glucocorticoids, long acting beta 2 aganists, mast cell stailizing agents, leukotriene modifiers, methylxanthines.
Glucocorticoids – have anti-inflammatory and preventive role. Its effects are not immediate and only seen after 6 hrs of administration.
Prednisone is given 60 mg every 6 hours.
In acute asthma methyl prednisolone IV 120180 mg is given 6 hrly.
Inhaled glucocorticoids : These are b.eclomethasone, budesonide, fluticasone.
Mast cell stabilizing agents: Promolin sodium, Nedocromil sodium. Effective in atopic asthma
Leukotrine modifiers: These reduce the synthesis of leukotrines. E.g. Zileuton, Zafirlukast, Montelukast.

· Evaluation of symptoms.
· Monitoring of respiratory parameters.
· Avoidance of allergens.
· For acute cases use short-acting drugs – Inhaled Albuterol, IV Aminophylline.
Beta 2 agonists every 20 minutes by inhalation for 2 – 3 doses.
· Anticholinergics like ipratropium may be added.
· Inhalational agents may be given by jet nebulizer, metered dose inhaler, or dry powder inhalers in acute situations.
· For respiratory emergency like paradoxical pulse, use of accessory muscles, FEV₁ <20% and disturbed arterial blood gases-intensive management, glucocorticoids, ventilatory support may be required.
·If PaCO₂ is elevated, patients need intensive care. In severe airway obstruction 80% helium and 20% oxygen may be useful.
For chronic asthma – mast cell stabilizing agents, g1Ucocorticoids, methylxnnthines, long-acting !5eta 2 agonists may be used.
· Cigarette smoking must be stopped in all asthma patients.