Bronchial asthma
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Bronchial asthma

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Bronchial asthma Bronchial asthma Presentation Transcript

  • BRONCHIAL ASTHMA
  • Introducation  Asthma - derived from Greek word To stay awake in order to breath OR Difficulty in breathing
  •  Asthma is a chronic inflammatory disease in which patient suffers with reversible episodes of airway obstruction due to bronchial hyper responsiveness. (Damage of bronchial epithelium (mucous layer) by chemical mediators. So direct expose of bronchi to irritant stimuli)
  • It has 2phases  Early phase (Acute) -Due to bronchial smooth muscle spasm. - Excessive secretion of mucus.  Chronic phase Continuous Inflammation, fibrosis, oedma, necrosis of bronchial epithelial cells.
  • Clinical hallmarks Recurrent episodic coughing  Shortness of breathing  Chest tightness  Wheezing  Symptoms are worsening at night
  • Asthma described as two type  Extrinsic (Atopic extrinsic asthma)  It is associated with exposure of specific allergen It is associated with some non specific stimulants Ex:- House dust, pollen Ex:- chemical It is episodic and less prone to develop to status asthmaticus. Intrinsic (Non atopic extrinsic asthma) irritants It is perenial and prone to develop to status asthmaticus.
  • Pathophysiology Allergen enter (Foreign body) Immunological reaction (AG:AB Complex formation) Circulation in blood Basophiles, Neutrophilis engulf Cause neutralization contd..,
  • Whenever same allergen re exposed Activation of AG:AB complex Reacts with lung mast cells (Degranulation of mast cells) Spasmogens release (Like Histamine,5HT,PGs,LT4, Cytokines)
  • IgE-Antigen Complex Basophil Eosinophil Activation Activation  Mast Cell Degranulation Chemical mediators Histamine, LTC4, LTD4, LTB4, Cytokines, Adenosine, PGD2, PAF, ECP and Neuropeptides Cause inflammation, oedema, bronchospasm, muscus secretion, epithelial damage  In early phase these mediators leads to bronchoconstriction Bronchial Tone In late phase inflammation, pulmonary oedema, mucous secretion bronchial hypersensivity and epithelial damage
  • Asthma therapy  It divided into two categories 1. Short term relievers.( Bronchodilators) 2. Long term controllers.
  • IgE-Antigen Complex SALBUTAMOL Basophil Eosinophil Activation β2 AGONISTS Activation Bronchodilitation 5AMP THEOPHYLLINE PDE cAMP β2 AC Mast Cell Degranulation Chemical mediators Histamine, LTC4, LTD4, LTB4, Cytokines, Adenosine, PGD2, PAF, ECP and Neuropeptides ATP Bronchial Tone THEOPHYLLINE GTP GC β2 AGONISTS Inhibit release Adenosine cGMP Cause inflammation, oedema, bronchospasm, muscus secretion, epithelial damage M3 Bronchoconstriction CARTICOSTEROIDS Bronchial Smooth Muscle
  • IgE-Antigen Complex Eosinophil Basophil Bronchodilitation Activation Activation Mast Cell Degranulation NITRIC OXIDE DONORS SOD. CROMOGLYCATE Bronchial Tone Stabilises Mast Cells Chemical mediators Histamine, LTC4, LTD4, LTB4, Cytokines, Adenosine, PGD2, PAF, ECP and Neuropeptides Leukotrienes LT-ANTAGONIST Cause inflammation, oedema, bronchospasm, muscus secretion, epithelial damage Bronchoconstriction CARTICOSTEROIDS INFECTION Bronchial Smooth Muscle
  • Drugs Used in Bronchial Asthma BRONCHODILATORS Selective β2– Agonists Short acting 1.      Salbutamol, Terbutaline, Remiterol, Fenoterol, Bitolterol Long-acting    Salmeterol, Formoterol, Bambuterol 2. Non-Selective Sympathomimetics  Adrenaline, Ephedrine, Isoprenaline, Orciprenaline (Metaproterenol), Isoetharine    
  • 3. Anticholinergics Ipatropium, Tiotropium, Oxitropium 4. Methyl Xanthines Theophylline, Aminophylline, Diprophylline, Choline theophyllinate Anti inflammatory Drugs (Controllers) Corticosteroids 1. Oral : Prednisolone, Methylprednisolone 2. Parenteral : Methyl prednisolone, Hydrocortisone 3. Inhalational : Beclomethasome, Fluticasone, Triamcinolone, Budesonide, Flunisolide
  •  Mast Cell Stabilisers Sodium Cromoglycate, Nedocromil, Ketotifen  Leukotriene Modulators: 1. 5-Lipoxygenase Inhibitor : Zileuton 2. LT – Receptor Antagonists : Zafirlukast, Montelukast, Iralukast, Pranlukast  Monoclonal Anti-IgE Antibody  Omalizumab Miscellaneous: NO, Calcium channel blockers
  • Sympathomimetic agents     ß2 receptors are present in the airway smooth muscle. These agents acts on ß2 receptors cause bronchodilatation These are only provide relief M.O.A:  cAMP  Bonchodilatation  Release of bronchoconstricting mediators from mast cells  Inhibit macrovascular leakage  Mucociliary clearence
  •  Epinephrine:  Rapid bronchodilator when inj/SC/inhaled(320µg/puff) Onset of action 15min after inhalation Duration of action:60-90min.   ADR:- Acts on β1     receptor cause Tachycardia Arrhythmias Worsening angi So rarely prescribed.
  •   Ephedrine: α,β1, β2 Ephedrine has a longer action  Oral activity  Lower potency  Pronounced central effects.
  • β2 Selective  Short acting : Terbutaline, Salnutamol  On inhalation they have rapid onset(1-5Min) Short duration of action preferred for acute attack Route: Inhalation 100-200µg/6hourly Other MDI, Oral, IM, IV     Terbutaline is the only one drug safely used during the pregnancy.
  • Long acting: Salmeterol, bambutarol Long acting but slow onset of action  Preferred for maintenance therapy  Not useful in acute attack due to slow onset of action Route: Inhalation 50µg twice daily.  Formoterol:  Long acting  Rapid onset  Preferred for prophylaxis due to long acting Route: Inhalation 12-24µg twice daily
  • ADR of Sympathomimetics  By oral route stimulate β2 receptors in skeletal muscle cause tremors, Orthostatic hypotension.  Tachycardia (High dos also stimulate β1 receptors in heart)  Restlessness  Tolarance occurs.
  • Antimuscurnic agent  Less effective then β agonists MOA: By blocking M3 receptors on air way smooth muscle and prevents Ach action. -They acts by cGMP levels in bronchial smooth muscle.  Ipatropium:-Poor absorption from circulation -Do not cross BBB. -Also mucus secretion bronchi into systemic Ipatropium + β2 (Salbutamol) work better in serve asthma and long duration of action
  • Methyl Xanthenes  MOA: i) Inhibition of PDE 3,4. These enzyme are responsible for metabolism of cAMP. ii) Blockade of Adenosine receptors.  Actions:  Theophyline exhibits bronchodilatory action  Anti Inflammatory  Immunomodulator  Respiratory stimulation  Diaphragmatic contractility  Mucociliary clearance
  •  Pharmaco Kinetics:  Oral/Parental  Food delay the rate of absorption  Well distributed  Cross placental & BBB  Metabolized in Liver  Excreted in urine
  • ADR: Low therapeutic window, CNS stimulant drugs Plasma levels 10-20µg/ml, Narrow safety Restlessness, insomnia, headache, tremors CNS Nausea, Vomiting GIT Peptic ulcer 40µg/ml 20µg/ml Xanthenes Diuresis 20µg/ml Heart Tachycardia, palpitation, hypotension, arrythimias Theophyline: potent vasodilator, reflex tachcardia, oral route Aminophyline: Slow IV infusion
  • Corticosteroids (Controllers)  Glucocorticosteriods induce synthesis of lipocotrin which inhibits pholipaseA2 there by preventing formation of mediators such as PGs,TAX2, LTand other mediators.  Actions: Anti allergic, anti inflammatory, immunosuppressant ( AG:AB reactions ), Mucosal oedema, bronchial hyperactivity, Enhance β adrenergic action by up regulation of β2 receptors in lung.
  •  Inhalator glucocorticosteriods such as beclomethasone, budesonide and fluticasone are used as prophylactic agents in asthma.  PK: Well tolerated less systemic side effects.   Common side effects:  Dryness of mouth  Voice change  Oropharangeal candidiats. Systemic are used in acute severe and chronic severe asthma.
  • Mast cell stabilizers Non bronchodilating, Non steroid drugs, used for prophylactic treat. MOA:  Prevent degranulation and release of chemical mediators from the mast cells.  They stabilize the mast cells by preventing transmembarane influx of Ca ions. PK:  Highly ionized  Least systemic absorption  well tolerated. Uses: Allergic asthma, allergic conjunctivitis, allergic rhinitis, allergic dermatitis. Ketotifen (Mast stab.+ Antihistamincs) 
  • LT Modulators         LT are powerful bronchoconstrictors. Action by preventing their synthesis or blocking effect on cys LT receptors Synthesis inhibitors (Lipooxygenase) Zafirlukast,Montelukast PK: Well absorbed after oral administration Highly bound to plasma protein Metabolized by liver Effective for prophylactic treat of mild asthma.
  • ADR:  Head ache  skin rashes  rarely eosinophilia  Zileuton cause hepatic toxicity.
  • Monoclonal anti IgE antibody        MOA:- AG:Ab complex formation by AB action Omalizumab: Recombinant humanized monoclonal antibody. Inhibit the binding site of IgE to mast cells and basophils PK: administered parentarally Uses: Moderate to severe asthma and allergic disorders. Indicated for asthmatic patients who are not adequately controlled by inhalational corticosteroids. ADR: Inj site redness, itching, stinging.
  • Miscellaneous NO: It dilate pulmonary blood vessels and relax airway smooth muscle.  Uses: For acute severe asthma and management of pulmonary hypertension.  Ca channel blockers:  Broncho constriction ultimately involves some degree of ca into cells Nefedpine / Verapamil should provide relief in asthma. 
  • RX Status asthmatics (Acute severe asthma)  Status asthmatics a severe acute asthma, which is a life threatening condition involving exhaustion, cyanosis, bradicardia,hypotension, dehydration and metabolic acidosis.
  •  Humidified O2 inhalation  Inj. Aminophyline 500mg in 10ml of 5% Glucose IV Slow  Neubulized β2 adrenergic agonist + anti cholinergic agent  Systemic glucocorticosteroids IV (Hydrocortisone 200mgIV) immediately  IV fluids to correct dehydration.  K supplements: To correct hypokalemia produced by repeated administration of salbutamol.  NaHCo3 (Sodium bicarbonate) to treat acidosis.  Antibiotics to treat infection (Cap. Ampicillin 250mg 1tab tds-
  • DRUGS TO BE AVOIDED IN ASTHMA  β adrenergic blockers  Cholinergic agents  NSAIDS ( cause hyperapoenia) except paraceatamol.