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lecture on Asthma

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  2. 2. BRONCHIAL ASTHMA • Definition • Prevalence • Etiology • Pathogenesis • Pharmacology of anti asthmatic drugs • Management 2
  3. 3. Bronchial asthma Bronchial asthma is a chronic inflammatory disorder of the airways associated with airway hyper responsiveness presents with: • Wheezing • Breathlessness • Chest tightness • Nighttime or early morning cough Airway obstruction is reversible either spontaneously or with treatment. 3
  4. 4. Bronchial asthma • Bronchial asthma is a disease of the lungs in which an obstructive ventilation disturbance of the respiratory passages evokes a feeling of shortness of breath. • The cause is a sharply elevated resistance to airflow in the airways. • Despite its most strenuous efforts, the respiratory musculature is unable to provide sufficient gas exchange. • The result is a characteristic asthma attack, with spasms of the bronchial musculature, edematous swelling of the bronchial wall and increased mucus secretion. 4
  5. 5. WHO Definition of Asthma • "A chronic inflammatory disorder of the airways in which many cells play a role, in particular mast cells, eosinophils, and T lymphocytes. In susceptible individuals this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and cough particularly at night and/or in the early morning. These symptoms are usually associated with widespread but variable airflow limitation that is at least partly reversible either spontaneously or with treatment. The inflammation also causes an associated increase in airway responsiveness to a variety of stimuli." 5
  6. 6. • 235-330 million affected individuals • 1% -18% - global prevalence rate • 2,50,000-3,45,000 people die per year from the disease • It is more common in developed than developing countries • Common in both gender 6
  7. 7. Asthma Prevalence and Mortality Source: Masoli M et al. Allergy 2004 7
  8. 8. GENETICS  Higher concordance in Monozygotic twins  ↑ed incidence in primary relatives • ADAM-33 1st gene identified as Asthma susceptibility gene • 10 most common genes a/w Asthma  Innate immunity (CD-14,HLA DRB1,DQB1)  Th₂ cell signalling (IL-4,IL-13,IL-4Ra)  Cellular inflammation (TNF,FCEDR1B)  Lung development (ADAM33,ADRB2)  Genome-wide association studies (GWAS) : 17 q 21,11 p 14,5 q 23,Chr 18  Environment : Epigenetic modifications 8
  9. 9. ATOPIC ASTHMA Begins in childhood. A positive family history of atopy is common, Asthmatic attacks are often preceded by allergic rhinitis, urticaria, or eczema. The disease is triggered by environmental antigens, such as dusts, pollen, animal dander, and foods, but potentially any antigen is implicated. A skin test with the offending antigen results in an immediate wheal-and-flare reaction, a classic example of the type I IgE-mediated hypersensitivity reaction . 9
  10. 10. NON ATOPIC ASTHMA • The mechanism of bronchial inflammation and hyper- responsiveness is much less clear in individuals with non-atopic asthma. • Viral infections of the respiratory tract (most common) and inhaled air pollutants such as sulfur dioxide, ozone, and nitrogen dioxide. • In asthmatic subjects however, the bronchial response, manifested as spasm, is much more severe and sustained. • A positive family history is uncommon • Serum IgE levels are normal • There are no associated allergies • Virus-induced inflammation of the respiratory mucosa lowers the threshold of the subepithelial vagal receptors to irritants. • The ultimate humoral and cellular mediators of airway obstruction (e.g., eosinophils) are common to both atopic and non-atopic variants of asthma. 10
  11. 11. Extrinsic (Allergic) Triggers: Dust mites Mould Certain foods Animal dander Pollen Intrinsic (Non-Allergic) Triggers: Exercise Infections (cold and flu) Cold or humid air Intense emotions (ex. Stress) Medications (aspirin) Hormones Air pollution Fragrances and chemicals Occupational irritants 11
  12. 12. Pathophysiology of Asthma • Asthma is a disease characterized by airway inflammation and episodic, reversible bronchospasm. – Two characteristic features: 1) Inflammatory changes in the airway; 2) Bronchial hyperreactivity to stimuli. 12
  13. 13. Pathophysiology of Asthma • Antigens (pollen and house-dust mites) sensitize patients by eliciting the production of IgE type of antibodies, which remain either circulating in the blood or become attached to the mast cells of nasal or bronchial tissues and basophils. • On re-exposure the same antigen, the resulting antigen- antibody reaction in the early phase causes degranulation of the lung mast cells and releasing of the powerful bronchoconstrictors: histamine, 5-HT, PGD2 and cysteinyl leucotriens (LTB4, LTC4 and LTD4). 13
  14. 14. • Lung mast cells also release ILs (IL-4, IL-5 and IL-13). In the late (delayed) phase of asthma, these mediators activate additional inflammatory cells (eosinophils, basophils, and alveolar macrophages) which also release LTs and ILs. • Other mediators of inflammation, in delayed phase, are: adenosine (causing bronchconstriction), neuropeptides ( causing mucus secretion and increase in vascular permeability; neurokinin A, causing bronchoconstriction), PAF etc. •The normal tone of bronchial smooth muscle is influenced by a balance between parasympathetic, sympathetic and non-adrenergic–non-cholinergic (NANC) mediators activity. 14
  15. 15. 15
  16. 16. 16
  17. 17. 17
  18. 18. 18
  19. 19. Lung Morphology in Asthma • Bronchial inflammation • Edema, Mucousplugging • Bronchospasm • Obstruction • Over inflation
  20. 20. Lung Hyperinflation in Asthma
  21. 21. Thick bronchi with Mucous plugs
  22. 22. Airways Innervations Afferent nerves (sensory)  Irritant receptors in upper airways.  C-fiber receptors in lower airways. Stimulated by : Exogenous chemicals Physical stimuli (cold air) Endogenous inflammatory mediators 22
  23. 23. Efferent nerves (motor)  Parasympathetic supply M3 receptors in smooth muscles and glands.  No sympathetic supply but B2 receptors in smooth muscles and glands 23
  24. 24. 24
  25. 25. Aims of anti asthmatic drugs: • To relieve acute episodic attacks of asthma (bronchodilators, quick relief medications). • To reduce the frequency of attacks, and nocturnal awakenings (anti-inflammatory drugs, prophylactic or control therapy ). 25
  26. 26. Anti asthmatic drugs Bronchodilators (Quick relief medications) treat acute episodic attack of asthma • Short acting 2-agonists • Antimuscarinics • Xanthine preparations Anti-inflammatory Agents (control medications or prophylactic therapy) reduce the frequency of attacks • Corticosteroids • Mast cell stabilizers • Leukotrienes antagonists • Anti-IgE monoclonal antibody • Long acting ß2-agonists 26
  27. 27. Classification of Antiasthmatic Drugs 1. Bronchodilators • Selective β2-agonists: Clenbuterol, Salbutamol, Fenoterol, Indacaterol, Levosalbutamol, Salmeterol, Terbutaline • Nonselective β-agonists: Epinephrine, Isoprenaline, Orciprenaline; Ephedrine • M-cholinolytics: Ipratropium, Tiotropium, Oxitropium • Methyl Xanthines: Theophylline, Aminophylline, Theotard 2. Mast Cell Stabilizers: Sodium Cromoglycate, Ketotifen, Nedocromil 27
  28. 28. 3. Glucocorticosteroids (GCS) • Oral: Prednisone, Methylprednisolone • Parenteral: Methylprednisolone, Betamethasone • Inhalational: Beclomethasone, Budenoside, Fluticasone, Triamcinolone 4. Inhalational β2-agonists/Glucocorticosteroids Seretide® (fluticasone/salmeterol) Symbicort® (budenoside/formoterol) 5. Leukotriene Modulators • 5-Lipoxygenase Inhibitor: Zileuton • LTD4-antgonists: Zafirlukast, Montelukast 6. Monoclonal Anti-IgE Antibody: Omalizumab 7. Miscellaneous: NO-donors, Calcium antagonists 28
  29. 29. 29
  30. 30. Sympathomimetics - adrenoceptor agonists Mechanism of Action  direct 2 stimulation  stimulate adenyl cyclase  Increase cAMP  bronchodilation  Inhibit mediators release from mast cells.  Increase mucus clearance by (increasing ciliary activity). 30
  31. 31. Classification of  agonists  Non selective  agonists: epinephrine - isoprenaline  Selective 2 – agonists (Preferable). Salbutamol (albuterol) Terbutaline Salmeterol Formeterol 31
  32. 32. Non selective -agonists. Epinephrine • Potent bronchodilator • rapid action (maximum effect within 15 min). • S.C. or by inhalation (aerosol or nebulizer). • Has short duration of action (60-90 min) • Drug of choice for acute anaphylaxis (hypersensitivity reactions). 32
  33. 33. Disadvantages  Not effective orally.  Hyperglycemia  CVS side effects: tachycardia, arrhythmia, hypertension  Skeletal muscle tremor  Not suitable for asthmatic patients with hypertension or heart failure. Contraindication: CVS patients, diabetic patients 33
  34. 34. Selective 2 –agonists  drugs of choice for acute attack of asthma  Are mainly given by inhalation (metered dose inhaler or nebulizer).  Can be given orally, parenterally.  Short acting ß2 agonists e.g. salbutamol, terbutaline  Long acting ß2 agonists e.g. salmeterol, formeterol 34
  35. 35. • Beta agonists or adrenergic agents, can be thought of as rescue medications because they provide rapid relief of labored breathing during an asthma episode. • All of the currently available beta agonists are superior to both adrenaline and ephedrine for duration of action and less-pronounced side effects. • These potent , when inhaled, provide rapid relief of bronchial obstruction. Duration of action varies from four to six hours. An exception is salmeterol (Serevent®) which works for up to twelve hours but has a slower onset of action of about an hour. 35
  36. 36. • These agents are excellent for the prevention of wheezing triggered by exercise or cold air if taken before the activity or exposure. • Individuals may prefer one agent to another for reasons of taste, cost, or personal preference. Generic agents are now available for albuterol. • Users of generic substitutes should be aware of the potential problem of dosage variability.Side effects are mild affecting less than 10% of users. 36
  37. 37. Short acting ß2 agonists Salbutamol, inhalation, orally, i.v. Terbutaline, inhalation, orally, s.c.  Have rapid onset of action (15-30 min).  short duration of action (4-6 hr)  used for symptomatic treatment of acute episodic attack of asthma. 37
  38. 38. • Salmeterol is a bronchodilator. It works by relaxing muscles in the airways to improve breathing. • Salmeterol inhalation is used to prevent asthma attacks. It will not treat an asthma attack that has already begun. Salmeterol inhalation is also used to treat chronic obstructive pulmonary disease (COPD) including emphysema and chronic bronchitis. LONG ACTING ß2 AGONIST 38
  39. 39. Adverse Reactions of β2 agonists: 1) Skeletal muscle tremor - which results from a direct stimulation of 2-adrenoceptors in skeletal muscle. • This effect is most notable on the initiation of therapy and gradually improves on continued use. 2) Cardiac effect - 2-Agonists also cause tachycardia and palpitations in some patients. • When administered by inhalation, the 2-agonists produce only minor side effects. 3) Metabolism disturbance - ketone bodies↑, acidosis, [K+]o↓ 39
  40. 40. Theophylline • Methylxanthine derivatives. • Mechanism of Action: 1. Inhibit phosphdiesterase (PDE); 2. Block adenosine receptors; 3. Increase endogenous catecholamine (CA) releasing; 4. Interfere with receptor-operated Ca2+ channels → [Ca2+]i↓; 5. Anti-inflammatory action 40
  41. 41. • Clinical Use: 1. Asthma: maintenance treatment 2. Chronic obstructive pulmonary disease (COPD) 3. Central sleep apnea (CSA) • Adverse Reactions: – Narrow margin of safety. Toxic effects are related to its plasma concentrations. – Gastrointestinal distress, tremor, and insomnia. – Cardiac arrhythmias, convulsions → lethal. 41
  42. 42. Muscarinic Antagonists • There are M1, M2, M3 receptor subtype in the airway. • Selectively blocking M1, M3 receptor is resulted in bronchodilating effect. • Ipratropium bromide binds to all M-R subtypes (M1, M2 and M3 ), and inhibits acetylcholine-mediated bronchospasm. 42
  43. 43. • In the treatment of asthma, anticholinergic drugs are both old and new. One hundred years ago, atropine, the parent drug of this class, was smoked as a cigarette for asthma. • Its usefulness was limited by unacceptable side effects of rapid heart rate, hot skin, and dry mucous membranes. Excessive doses could even provoke delusions and irrational behavior. • Ipratropium (Atrovent®) preserves the bronchodilator effects while eliminating these adverse effects. • Atrovent® is not as potent as the sympathomimetics and is not considered a first choice medication. It has an additive effect when beta agonists are insufficient for symptom relief. It can serve as an acceptable alternate when sympathomimetics aren’t tolerated. 43
  44. 44. Anticholinergic Drugs • Atrovent® should be inhaled four times daily for maximum effectiveness. • It's available in multidose inhaler form and in unit dose ampoules for nebulizer use. • The only common side effect is dry mouth. • Combivent® is a convenient, combination product composed of albuterol and ipratropium. 44
  45. 45. 45
  46. 46. Typical Spirometric (FEV1) Tracings 1 Time (sec) 2 3 4 5 FEV1 Volume Normal Subject Asthmatic (After Bronchodilator) Asthmatic (Before Bronchodilator) Note: Each FEV1 curve represents the highest of three repeat measurements 46
  47. 47. Anti-inflammatory agents • Act at several points in this process. Cromolyn and nedocromil stabilize mast cells and nerve endings preventing initiation of the inflammatory process. • Leukotriene antagonists block the production of leukotrienes, a potent mast cell messenger chemical, or block the transmission of their message to receptor cells. • Corticosteroids stabilize blood vessels reducing vascular leakiness. They also restore sensitivity of receptor cells to beta-agonists and down-regulate the production and release of inflammatory chemicals. This results in decreased numbers of eosinophils in the airway walls. Corticosteroids have considerably greater anti- inflammatory activity than any of the other drugs. The result is a gradual resolution of the asthmatic condition. 47
  48. 48. • Since these drugs do not relax bronchial muscle, they don’t provide the immediate relief characteristic of bronchodilators. • With regular and continued use of anti-inflammatory agents however, the need for bronchodilators is gradually reduced. • Inhaled corticosteroids may trigger cough during an acute asthma attack. Oral prednisone may be substituted at such times. 48
  49. 49. Glucocorticoids (GCs) • Mechanism of Action: 1. Broad anti-inflammatory efficacy ① Block the synthesis of arachidonic acid by phospholipase A2. ② Reduce bronchial reactivity. 2. Increase the responsiveness of β-adrenoceptors in the airway. 49
  50. 50. • The anti-inflammatory actions of GCS are mediated by stimulation of synthesis of lipocortin, which inhibits pathways for production of PGs, LTs and PAF. These mediators would normally contribute to increased vascular permeability and subsequent changes including oedema, leucocyte migration, fibrin deposition. 50
  51. 51. • Glucocorticosteroids provide long-term stabilization of the symptoms due to their anti-inflammatory effects. Inhaled GCS, along with beta-2-agonists are the first choice drugs for chronic asthma. • GCS inhibit the release of PGs and LTs and thus prevent smooth muscle contraction, vascular permeability and airway mucus secretion. • GCS produce eosinopenia which prevents cytotoxic effects of the mediators released from eosinophils. • GCS enhance beta-2-adrenergic response by up-regulating the beta-2-receptors in lung cells and leuckocytes. •Several hours are required for DNA transcription and RNA translation to occur after administering GCS. 51
  52. 52. 52
  53. 53. Corticosteroids 53
  54. 54. Routes of administration  Inhalation: e.g. Budesonide & Fluticasone, beclometasone – Given by inhalation, given by metered-dose inhaler – Have first pass metabolism – Best choice in asthma, less side effects  Orally: Prednisone, methyl prednisolone  Injection: Hydrocortisone, dexamethasone 54
  55. 55. Glucocorticoids in asthma  Are not bronchodilators  Reduce bronchial inflammation  Reduce bronchial hyper-reactivity to stimuli  Have delayed onset of action (effect usually attained after 2-4 weeks).  Maximum action at 9-12 months.  Given as prophylactic medications, used alone or combined with beta-agonists.  Effective in allergic, exercise, antigen and irritant-induced asthma, 55
  56. 56. Systemic corticosteroids are reserved for: – Status asthmaticus (i.v.). Inhaled steroids should be considered for adults, children with any of the following features • using inhaled β2 agonists three times/week • symptomatic three times/ week or more; • or waking one night/week. 56
  57. 57. • Cushing’s syndrome • Osteoporosis • Tendency to hyperglycaemia • Negative nitrogen balance • Increased appetite • Increased susceptibility to infections • Obesity etc. Adverse effects of GCS Cushing’s syndrome 57
  58. 58. Side effects due to systemic corticosteroids – Adrenal suppression – Growth retardation in children – Osteoporosis – Fluid retention, weight gain, hypertension – Hyperglycemia – Susceptibility to infections – Glaucoma – Cataract – Fat distribution, wasting of the muscles – Psychosis 58
  59. 59. Inhalation has very less side effects: – Oropharyngeal candidiasis (thrush). – Dysphonia (voice hoarseness). Withdrawal – Abrupt stop of corticosteroids should be avoided and dose should be tapered (adrenal insufficiency syndrome). 59
  60. 60. Leukotrienes antagonists Leukotrienes  produced by the action of 5-lipoxygenase on arachidonic acid.  Synthesized by inflammatory cells found in the airways (eosinophils, macrophages, mast cells).  Leukotriene B4: chemotaxis of neutrophils  Cysteinyl leukotrienes C4, D4 & E4: – bronchoconstriction – increase bronchial hyper-reactivity – mucosal edema, mucus hyper-secretion 60
  61. 61. Leukotriene receptor antagonists e.g. zafirlukast, montelukast, pranlukast  are selective, reversible antagonists of cysteinyl leukotriene receptors (CysLT1receptors).  Taken orally.  Are bronchodilators  Have anti-inflammatory action  Less effective than inhaled corticosteroids  Have glucocorticoids sparing effect (potentiate corticosteroid actions). 61
  62. 62. 62
  63. 63. Uses of leukotriene receptor antagonists  Are not effective to relieve acute attack of asthma.  Prophylaxis of mild to moderate asthma.  Aspirin-induced asthma  Antigen and exercise-induced asthma  Can be combined with glucocorticoids (additive effects, low dose of glucocorticoids can be used). Side effects: Elevation of liver enzymes, headache, dyspepsia 63
  64. 64. 64
  65. 65. Mast cell stabilizers e.g. Cromolyn (cromoglycate) - Nedocromil  act by stabilization of mast cell membrane.  given by inhalation (aerosol, microfine powder, nebulizer). Have poor oral absorption (10%) 65
  66. 66. Pharmacodynamics These are Not bronchodilators. Not effective in acute attack of asthma. Prophylactic anti-inflammatory drug.  Reduce bronchial hyper-reactivity.  Effective in exercise, antigen and irritant-induced asthma.  Children respond better than adults. 66
  67. 67. Uses  Prophylactic therapy in asthma especially in children.  Allergic rhinitis.  Conjunctivitis. Side effects  Bitter taste  minor upper respiratory tract irritation (burning sensation, nasal congestion) 67
  68. 68. 68
  69. 69. Omalizumab is a monoclonal antibody directed against human IgE. prevents IgE binding with its receptors on mast cells & basophiles. ↓ release of allergic mediators. used for treatment of allergic asthma. Expensive-not first line therapy. 69
  70. 70. Summary 70
  71. 71. Antiinflammatory drugs Bronchodilators Antiinflammatory drugs 71
  72. 72. 72
  73. 73. 73
  74. 74. Medications to Treat Asthma: How to Use a Spray Inhaler The health-care provider should evaluate inhaler technique at each visit. Source: “What You and Your Family Can Do About Asthma” by the Global Initiative for Asthma Created and funded by NIH/NHLBI 74
  75. 75. Used by some (usually moderate or severe) asthma patients to monitor ongoing lung function to detect changes Also known as a “spacer” or valved holding chamber (VHC) Delivery of medication over 100% more effective 75
  76. 76. Medications to Treat Asthma: Inhalers and Spacers Spacers can help patients who have difficulty with inhaler use and can reduce potential for adverse effects from medication. 76
  77. 77. 77
  78. 78. Medications to Treat Asthma: Nebulizer • Machine produces a mist of the medication • Used for small children or for severe asthma episodes • No evidence that it is more effective than an inhaler used with a spacer 78
  79. 79. 79
  80. 80. Establishing the diagnosis Not all that wheezes is asthma • The medical history! • Pulmonary function testing with bronchodilator – Reversibility: 12% AND 200 cc change in FEV1 – Obstructive physiology on pulmonary function test (FEV1 reduced much more than FVC) • Bronchoprovocation testing – Methacholine, histamine, exercise • Exhaled nitric oxide (NO) 80
  81. 81. Methods of investigation • Objectively: Tachypnoe with prolonged expiration, wheezing, dry rales • Sputum analysis: eosinophils, Kurshman spirals (mucus from small bronchi), Sharko-Leiden crystals (enzymes of eosinophils) • General blood analysis: mild leucocytosis, eosinophilia • Spyrometry: decreased FVC, FEV1, FEV1/FVC, increased daily variability 81
  82. 82. Diagnosing Asthma: Spirometry Test lung function when diagnosing asthma 82
  83. 83. Nitric Oxide Exhaled NO • Exhaled nitric oxide is a biological marker that correlates with eosinophilic inflammation in asthma. • Exhaled NO measurement can provide diagnostic and predictive value for a corticosteroid response. • More longitudinal studies are required to clarify the clinical significance of exhaled NO in asthma. Kim et al, Curr Opin Allergy Clin Immunol 2014,14:49–5483
  84. 84. Indicators of Severe Asthma  Anxious and diaphoretic appearance, upright position  Breathlessness at rest and inability to speak in full sentences  Tachycardia (HR>120) and Tachypnoea (RR>30)  Pulse oximetry <91% (on room air)  PaCO2 normal or increased  PEFR <150 L/min or <50% predicted 84
  85. 85. controlled partly controlled uncontrolled exacerbation LEVEL OF CONTROL maintain and find lowest controlling step consider stepping up to gain control step up until controlled treat as exacerbation TREATMENT OF ACTION TREATMENT STEPS REDUCE INCREASE STEP 1 STEP 2 STEP 3 STEP 4 STEP 5 REDUCEINCREASE 85
  86. 86. 86
  87. 87. 87
  88. 88. Step-wise approach to the treatment of asthma according to recent guidelines. LTRA, leukotriene receptor antagonist; SR, slow release. The dose of inhaled corticosteroids refers to beclomethasone dipropionate 88
  89. 89. PREVENTION Primary Secondary Tertiary 89
  90. 90. Prevention: Primary • Patient awareness/education  Efficacy of patient education and parental awareness has also been shown to be effective in individual studies from India (Singh et al. 2002; Gupta et al. 1998; Ghosh et al. 1998; Lal et al. 1995). • Lifestyle Modifications: Regular balanced diet and avoidance of obesity. Short acting beta-2 agonists should be used prior to anticipated exercise, in a patient with exercise-induced Asthma, to alleviate symptoms (Consensus on Guidelines of Management of Clinical Asthma 2005). • Alternative System of Medicine: Yogic breathing exercise technique, Pranayama, was been shown to reduce in histamine reactivity (Singh et al. 1990). 90
  91. 91. Prevention: Secondary  Avoidance of precipitating factors  Avoid dusting when subject is around  Avoid using carpets, stuffed toys, open bookshelves, smoking, chemical sprays in house. Prefer mosquito nets to repellants  Food containing allergen to be avoided  Maintain record of daily symptoms *Involves avoidance of allergens and nonspecific triggers when Asthma is established. (Custovic et al. 1998; Strachan and Cook 1998; Chalmers et al. 2002; Jindal et al. 1997) 91
  92. 92. The Reality  • Asthma is not yet curable * • Under diagnosis & Under management • Therapy is still evolving Hope  • Better understanding of Pathology • New line of Promising Drugs. • Proper management  normal life. 92
  93. 93. REFRENCES • Goodman & Gilman’s - pharmacological basis of therapeutics 11th edition • Katzung - Basic & Clinical pharmacology 12th edition • K D Tripathi – Essentials of medical pharmacology 7th edition • Lippincott – modern pharmacology with clinical application • Harrison’s principles of internal medicine 18th edition • GINA guidelines 2014 93