This document discusses asthma, including its pathogenesis, triggers, diagnosis, and treatment. Asthma is a chronic inflammatory airway disease characterized by recurrent wheezing, breathlessness, chest tightness, and coughing. It involves inflammation caused by various cells and mediators that leads to reversible airway obstruction. Treatment includes short-acting bronchodilators for acute attacks and long-term controllers like inhaled corticosteroids to prevent symptoms and exacerbations. Proper management requires education, monitoring, and follow-up according to guidelines.

1. Mrs Khushbu K. Patel
Asst. Professor

2. INTRODUCTION

3. Chronic inflammatory disorder of the airways in
which many cells and cellular elements play a
role.
In susceptible individuals, this inflammation
causes recurrent episodes of wheezing,
breathlessness, chest tightness, and coughing,
particularly at night or in the early morning.
These episodes are associated with widespread
but variable airflow obstruction that is reversible
either spontaneously, or with treatment.

6. PATHOGENESIS OFASTHMA
The early reaction is
immediate
bronchoconstriction
produced by histamine,
tryptase, and other
neutral proteases,
leukotrines C4 and D4
and prostaglandins
These agents diffuse
throughout the airway
wall and cause vascular
leakage

7. PATHOGENESIS OFASTHMA
Late
bronchoconstriction
occurs after 2-8
hours by TH2
lymphocytes and
interleukins 4, 5,
9 and 13, attracting
and activating
eosinophils and
stimulating IgE
production by B
lymphocytes

8. ■ Allergens
■ Dust mites, mold spores, animal dander, cockroaches,
pollen, indoor and outdoor pollutants, irritants (smoke,
perfumes, cleaning agents).
■ Pharmacologic agents; ASA, beta-blockers.
■ Physical triggers (exercise, cold air, distilled water,
and sulfur dioxide)
■ Diseases; GERD, viral and bacterial URI, rhinitis
■ Physiologic factors

9. Global Initiative for Asthma (6-point plan)
■ Educate patients to develop a partnership in asthma
management
■ Assess and monitor asthma severity with symptom
reports and measures of lung function as much as
possible
■ Avoid exposure to risk factors
■ Establish medication plans for chronic management in
children and adults
■ Establish individual plans for managing exacerbations
■ Provide regular follow-up care

11.  Asthma attacks are due to release of various mediators and
other condition.
 Various classes of agents are available for treatment of
asthma.
 Drugs used for asthma can be administrated by inhalation
because,
 Enhance therapeutic effects
 Minimize systemic effects
 Rapid relief of acute attacks
 2 type inhalation are used:
(1). Dry Powder inhalers
(2). Nebulizers

13. A) Short term relievers used for relief of acute
bronchodilators:
1. Beta Adrenergic agonists
2. Methylxanthines/Phosphodiesterase inhibitors
3. Anrimuscrinic agents
B) Long term controllers for reduction of symptoms
and prevention of attacks:
1. Corticosteroids
2. Leukotriene pathway antagonists
3. Inhibitors of mast cell degranulation

14. 1. Beta Adrenergic agonists:
(i) Drugs acting on both β1 and β2receptors:
Epinephrine
Ephedrine
Isoproterenol
ii) Beta2 selective drugs:
Albuterol
Terbutaline
Metaproterenol
Pirbuterol
Bitolterol
Salmoterol
Formoterol

15. MECHANISM OF Β-ADRENERGIC RECEPTOR
• β receptors are the predominant receptors in bronchial
smooth muscle. Selective β2 agonist are now widely used
for treatment of asthma.
Stimulate adenylyl cyclase,
which leads to relaxation of bronchial smooth muscle and
inhibition of release of mediators of immediate
hypersensitivity.
.
which increases synthesis of cAMP
Inhibits release of mast cell mediators such as histamine,
leukotrienes, and prostaglandin-D2.

16. Salbutamol
Terbutaline
Epinephrin
e
Formoterol

17.  Smooth muscle relaxation
(bronchodilation).
 Suppression of the response of
the airways to stimuli.
 Increases force of contraction
of diaphragmatic muscles.
■ Theophylline
■ Theobromine
■ Caffeine
■ Aminophylline
Mechanism of action:

18. Theophyllin
e
Caffeine
Theobromine

19. Mechanism of Action:
 Muscarinic antagonists
competitively inhibit
the effect of
acetylcholine at
muscarinic receptors
ie block the
contraction of airway
smooth muscle
and the increase in the
secretion of mucus.

20. Ipratropium Bromide
Tiotropium bromide

21.  Mainly used for prophylaxis of chronic asthama.
 Mechanism of Action:
 Decreasing the synthesis and release of of inflammatory mediators.
 Decrease infiltration and activity of inflammatory cells.
 Decrease oedema of airway mucosa.
 Decrease airway mucus production.
CORTICOSTEROIDS:

22. Corticosteroids:
Prednisolone
Hydrocortisone
Beclomethasone
Triamcinolone
Fluticasone
Budesonide

23. Mechanism of Action
Zileuton

24. Montelukast
Zileuton
Zafirlukast

25.  Mechanism of action
 They act by stabilizing mast cells and preventing mast cells from
secreting form their internal granules and such mediators of
inflammation e.g. histamine and leukotriens.
Nedocromil
Cromonyl
sodium