Pharmacology of asthmatic drugs
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Pharmacology of asthmatic drugs

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Pharmacology of asthmatic drugs Presentation Transcript

  • 1. Asthmatics Drugs Pharmacology and Therapy I Fadel Muhammad Garishah Diponegoro University School of Medicine
  • 2. Case I
    • A 56-year-old man presents to ED with the history of shortness of breath for 45 minutes. He reports that he was feeling well and in his usual state of health until about an hour ago, when he smelled something burning. Twenty minutes later, he began to fell short of breath and was wheezing. He tried using his albuterol inhaler without success, so he proceeded to the ED. At the ED, he was tachycardia, tachypnea, wheezing and hypertensive. His O2 sats on RA were 87% to 88%. His last admission for an asthma attack was 2 months ago.
    • What is his acute asthma management?
    • Long term managements?
  • 3. Bronchial Asthma
    • Asthma
      • Asthma is defined as recurrent reversible airway obstruction, with attacks of wheeze, shortness of breath and often nocturnal cough. Severe attacks cause hypoxaemia and are life-threatening.
    • Asthmatic patients experience intermittent attacks of wheezing, shortness of breath-with difficulty especially in breathing out-and sometimes cough.
    • Essential features include:
      • airways inflammation, which causes
      • bronchial hyper-responsiveness, which in turn results in
      • recurrent reversible airway obstruction.
  • 4.
    • Pathogenesis involves exposure of genetically disposed individuals to allergens; activation of Th2 lymphocytes and cytokine generation promote:
      • differentiation and activation of eosinophils
      • IgE production and release
      • expression of IgE receptors on mast cells and eosinophils.
    • Important mediators include leukotriene B4 and cysteinyl leukotrienes (C4 and D4); interleukins IL-4, IL-5, IL-13; and tissue-damaging eosinophil proteins.
  • 5.
    • Inflammatory cells releasing Growth factors act on smooth muscle cells
      • causing hypertrophy and hyperplasia , and the smooth muscle can itself release proinflammatory mediators and autocrine growth factors schematically the changes that take place in the bronchioles.
      • Epithelial cell loss means that irritant receptors and C fibres are more accessible to irritant stimuli-an important mechanism of bronchial hyper-reactivity.
  • 6. Asthma Pathogenesis cysteinyl leukotrienes IgE
  • 7. Airway Narrowing: Acute Asthmatic Attacks
    • Contraction of airway smooth muscle
    • Inspissation of viscid mucus plugs in the airway lumen
    • Thickening of bronchial mucosa from edema, cellular infiltration, and hyperplasia of secretory, vascular, and smooth muscle cells.
    • Which is easily reversed? Requires sustained treatment?
    • Easily reversed : Contraction of Airway Smooth Muscle by giving Bronchodilator drugs
    • Sustained treatment? Mucus Hypersecretion and Thickening mucosa due to immune cells infiltration maintained with antiinflammatory drugs
  • 8.  
  • 9.
    • Antiasthmatic drugs include:
      • bronchodilators
      • anti-inflammatory agents.
    • Treatment is monitored by measuring forced expiratory volume in 1 second (FEV1) or peak expiratory flow rate and, in acute severe disease, oxygen saturation and arterial blood gases.
  • 10. Antiinflammatory drugs Bronchodilators Antiinflammatory drugs
  • 11.
    • Severe acute asthma is a medical emergency requiring hospitalisation.
    • Treatment includes (Bronchodilators reverse the bronchospasm of the immediate phase; anti-inflammatory agents inhibit or prevent the inflammatory components of both phases )
      • oxygen (in high concentration, usually ≥ 60%),
      • inhalation of nebulised salbutamol , and
      • intravenous hydrocortisone followed by a course of oral prednisolone .
      • Additional measures occasionally used include nebulised ipratropium ,
      • intravenous salbutamol or aminophylline ,
      • and antibiotics (if bacterial infection is present).
      • Monitoring is by PEFR or FEV 1 , and by measurement of arterial blood gases and oxygen saturation.
  • 12.
    • Oxygen
    • Salbutamol: β 2 -Adrenoceptor agonists act as physiological antagonists of the spasmogenic mediators but have little or no effect on the bronchial hyper-reactivity
    • Glucocorticoids: These reduce the inflammatory component in chronic asthma and are life-saving in status asthmaticus (acute severe asthma).
    • Theophylline (often formulated as aminophyllin) relaxant effect on smooth muscle has been attributed to inhibition of phosphodiesterase (PDE) isoenzymes, with resultant increase in cAMP and/or cGMP
    • ipratropium: Muscarinic receptor antagonists
    • Cysteinyl leukotriene receptor antagonists
    • Histamine H1-receptor antagonists
  • 13.
    • Cromoglicate and nedocromil: Given prophylactically, they reduce both the immediate- and late-phase asthmatic responses and reduce bronchial hyper-reactivity.
    • Omalizumab is a humanised monoclonal anti-IgE antibody. It is effective in patients with allergic asthma as well as in allergic rhinitis. It is of considerable theoretical interest (see review by Holgate et al., 2005), but it is expensive and its place in therapeutics is unclear