25 slides

1. WELCOME

2. ANTIASTHMATICS Presented by P.Pavani 10T22SO112 Under The Guidence of Mr. J. Anoop

4. Bronchial hyper-reactivity/hyper-responsivness

6. PATHOPHYSIOLOGY:

7. MORPHOLOGICAL FEATURES: 1.The mucus plugs contain normal or degenerated respiratory epithelium forming twisted strips called “Curschmann’ssprials”. 2.The sputum usually contains numerous eosinophils and diamond-shaped crystals derived from eosinophils called “Charcot-Leyden crystals”. 3. Airway remodeling.

9. Severe Asthma Episode Symptoms personal Severe coughing, wheezing, Shortness of breath or tightness in the chest Difficulty talking or concentrating Walking causes shortness of breath Breathing may be shallow and fast or slower than usual Hunched shoulders (posturing) Nasal flaring Retractions Cyanosis .

11. Physical examination

12. Supportive diagnostic tests:*Pulmonary funcion tests Spirometery Peak flow meter Methacholine challenge test *Allergic test *Chest x-ray *GERD assesment test

13. APPROACHES TO TREATMENT: 1.Prevention of AG:AB reactions 2.Neutralisation of IgE antibody eg: Omalizumab 3.Suppresssion of inflamation and bronchial hyperreactivity eg: cotricosteriods 4.Prevention of realease of mediators eg: mast cell stabilisers 5.Antagonism of realeased mediators eg: leukotrieneantagonists 6.Blocked of constictor neurotransmitters eg:anticholinergics 7.Mimicking dilator neurotransmitter eg:sympathomimetics. 8.Directly acting bronchodilators eg:methylxanthines

15. STEPWISE MANAGEMENT OF ASTHMA: Mild intermittent asthma ↓ Regular preventer therapy ↓ Add -on therapy ↓ Persistent poor control ↓ Continuous or frequent use of oral steriod

16. SHORT -ACTING ß2 AGONISTS: Eg: Salbutamol, T erbutaline These are mainstay of asthma management M.O.A: ß2 Receptor stimulation ->↑edcAMP in bronchial muscle cell -> relaxation Route of administration: By inhalation of aerosol, powder. Salbutamol is given as intravenous infusion in status asthmaticus. Adverse reactions: Down regulation of bronchial ß2 receptors Tachycardia , palpitations

17. CORTICOSTEROIDS: Corticosteriods afford more complete and sustained symptomatic relief than bronchodialators and others M.O.A: Decrease formation of cytokines(Th2), that recruit and activate eosinophils and are responsible for promoting the production of IgE and expression of IgE receptors. INHALED CORTICOSTERIODS: Eg: Beclomethasone, fluticasone, ciclesonide 1ST choice in patients with any degree of persistent asthma

18. ROUTE OF ADMINISTRATION: Inhalation by MDI SLOWLY and DEEPLY inhalation for solution type inhalers QUICKLY and DEEPLY inhalation for dry powdet inhalers ADVERSE REACTIONS: Hoarseness Oral or pharyngeal candidiasis Adrenal suppression ICS directly targets underlying airway inflammation

19. . SYSTEMIC STERIODS EG: Hydrocortisone, prednisolone These are oral steriods Used in status asthmaticus. ADVERSE REACTIONS: Adrenal suppression Cushing syndrome Growth suppression in children

20. ANTI-IgE ANTIBODY: Eg: Omalizumab M.O.A: This drug leads to ↓ed binding of IgE to high affinity IgE receptors on surface of mast cells and basophils and limits realease of mediators of allergic response USES: ◦In moderate to severe asthma patients who are poorly controlled with conventional therapy. ◦Reduces steriod requirements

22. Status asthmaticus can vary from a mild form to a severe form with bronchospasm.

24. coughing and wheezing are not common, because there is not enough airflow

25. advanced symptoms include little or no breath sounds

27. heavy sweating

29. The initial treatment starts with supplemental oxygen to increase blood oxygen levels.

30. Inhaled or intravenous bronchodilator to open the airways.

31. large doses of corticosteroids drugs and bronchodilators to reduce inflammation.

33. Conclusion: Asthma is a curable disease, so it is needed to take proper medication and there is a need to follow the medication therapy systematically.