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Bronchial Asthma Def. Asthma is an inflammatory disease of airways that is characterized by responsiveness of the tracheobronchial tree to a multiplicity of stimuli, characterized by paroxysmal attacks of dyspnea and wheezy chest. Cause: Extrinsic asthma:(Atopic) Characterized by 1- Early childhood (early onset asthma) 2- + ve. F.H. of atopy urticaria hay ever 3- IgE ¯ Ag + IgE à mast cell ௠release of mediators à bronchospasem 4- prognosis à good due to (Natural desensitization) Types of Ag 1- Pollens 4- Dust 2- Animal dander 5- Mites 3- Drugs e.g. penicillin, Cephalosporines 6- foods Intrinsic: (mostly non allergic) Characterized by: 1- Age > 40 years 2- -ve Family History. (for atopy) 3- Ig A in some cases 4- prognosis not good. Other types of asthma: 1- Aspirin sensitive . Aspirin inhibits P.G synthesisà production of leukotrienes from arachidonic Acid, this is common in patient with nasal allergy and nasal polyps. 2- Exercise induced, asthma due to thermal changes within bronchial tree (Cooling and drying of bronchial mucosa) 3- Occupational e.g. Byssinosis, spray painting, bakers, varnishes. 4- Allergic bronchopulmonary Aspergillosis à Aspergillus Ab. in serum. 5- Cough variant asthma. 6- Chest infection due to respiratory syncytial virus. 7- Stress induced asthma. Pathogenesis of asthma (A topic) 1- Ag. - Ab. over mast cell à mediators 2- Eosinophils à release O2 radicals, and major basic protein. 3- T lymphocytes à release interleukin-5. C/P During attacks Dyspnea + wheezy chest O/E harsh vesicular, breathing. + rhonchi - signs of emphysema or hyperinflated chest In between. Attacks à free Investigation: 1- X-ray à there is no diagnostic features of asthma on the chest X ray but it may be helpful in excluding pneumothorax. 2- Blood gases (during attacks) ☺mild cases à wash of Co2 due to hyperventilation so Co2 ¯ ☺sever cases à hypoventilation so Co2 either normal or 3- skin hypersensitivity test. 4- Blood Ig E à extrinsic Ig A à intrinsic eosinophilia aspergillus Ab 5- Sputum: * Churchman’s spirals = mucous that form a cast of the small airway. * Charcot laden crystals = breakdown products of eosinophils Metacholine, histamine test indicates the presence of non specific bronchial hyper-reactivity à bronchospasm at lower dose in asthma. Cold air challenge (i.e. inhalation of cold air à bronchospasm) Treatment of Bronchsopasm during attack Inhaled beta 2 – specific sympathomimetic No response Good response ¯¯ 40-60 mg methyl continue therapy, discharge, prednisolone /6 hrs injection and arrange for follow up & ¯ treat as below No response ¯ Anticholinergic inhalers A minophyline injection Scheme for treatment of bronchospasm in patients (in between attacks) with stable disease Occasional use of inhaled short acting B2 agonist bronchodilator Treatment of bronchial asthma: à (drugs used in treatment of bronchial asthma)*Step 1 à Regular inhaled B2 agonist as required + beclomethasone inhaler 800 mcg twice daily. *Step 2 à High dose inhaler (800- 2000 mcg/d) + B2 agonist *Step 3 à As step 3+ Aminophyline oral or B2 agonist oral or anticholinergic inhaler.*Step 4 à As step 4+ oral steroids in the lowest dose that control symptom (single daily dose)*Step 5 à I- During attacks A- inhalers MDI (metered dose inhaler) Salbutamol (ventoline) = B2 agonist ¯ bronchodilator Advantages à No side effects of systemic B2 agonist Rapid action Dose: 2 puffs then, 1-2 puffs /20 m till improvement (100 ug/puff) B- Aminophylline I.V. Dose: Loading dose: 5mg/kg (very slowly) maintenance dose in acute sever asthma: 0.5 mg/kg/hr. N.B. = old age, heart disease, liver diseases௯ dose of Aminophylline = Smokers & phenytoin à dose of Aminophylline. C- Cortisone: à Hydrocortisone (rapid action) 100-300 I.V. Action: reduce airway obstruction anti - inflammatory antiallergic D- Adrenaline: the patient must be non hypertensive non cardiac patient Dose: solution (1/1000 - amp. lml) 0.5 ml. à S.C. it can be repeated after 20-30 minutes II-In between Attacks: A- Aminophylline The best is long acting preparation 200 mg/12 hr. = Quibron (Anhydrous Aminophylline) Dose: 1/3-1/2 tab. /12 hr. Advantages: Less GIT irritation, long acting. Mechanism: inhibits phosphodiasterase enzymeà action of C.A. through the level of C.A. B- B2 agonist: (bronchodilator) * Salbutamol ventoline Salbuvent * Terbutaline Bricanyl * Side effects Tremors Tachycardia (palpitation) * Dose 2-4 mg/D C- Inhalers (Disodium cromoglicate [intal]): stabilizes the membrane of mast cell ¯ ¯¯ release of mediators D- Ketotifen:(zaditen) • Like Intal but oral (mast cell stabilizer) Dose : 1 mg tab / 12 hrs Q : Mediators of bronchial asthma : Histamine, Bradykinies, P.G., leukotrienes platelets activiating factos. E- Bisolvon: dissolve secretion (tab. 1 x 3) F- Cortisone: a- Local inhalers Becotid) = BeclomethazoneDose: 2-3 puffs/d (250 ug per puff) Side Effects: oropharyngeal candidiasis, To avoid we can wash the mouth by water after use. b- Systemic steroids: à prednisolone Dose: 30- 40 mg/d à till improvement then low dose maintenance 5 - 10 mg/d III. Treatment of status asthmatics: Def. status asthmaticus Is a severe form of asthmatic attack which is prolonged & not responding to usual therapy. = (Acute severe asthma) 1- Hospitalization. 2- O2 therapy. 3- Aminophylline • loading dose 5mg/kg • maintenance 0.5 mg/kg/hr 4- Hydrocortisone à 200 mg I.V/6 hrs for 24 hrs. then prednisolone 60 mg/d orally for 2 weeks, then gradual withdrawal then we can use steroid inhaler. 5- Bisolvon à amp. I.M. à to dissolve secretions. 6- Fluids à to overcome dehydration and dissolve secretion. N.B • we can give B2 agonists by nebulizer, (5 mg/4 hrs) • We can mix B2 agonists + normal saline & inhaled over 5-15 minutes. 7- Bronchial lavage à to dislodge the viscid secretion. 8- Ventilator à indication when Co2 = bad sign (I.e. hypoventilation) 9- Ab. for infection Sedatives are contraindicated as à R.C depression with hypoventilation. Other measures in treatment of bronchial asthma 1. Anticholinergic (Ipratropium Bromide) inhaler. 2. Avoid Ag if possible. 3. systemic desensitization: by gradual S.C injection of small doses of Agàto form Ig.G (blocking Ab) so when Ag introduced once more it well be attacked by Ig G and not by Ig E. 4. Tryptizole small dose 10 mg/d. Tricyclic Antidepressant sedative anticholinergic 5. Methotrexate: low dose may be useful in management of steroids dependent asthma allowing reduction in steroid dose. Signs of severe asthmatic attacks 1- Tachycardia >120/m. 2- Exhaustion 3- Pulsus paradoxius. 4- Silent chest (No rhonchi) 5- Cyanosis, pt can’t speak 6- Dehydration due to hyperventilation 7- O2 ¯ - Co2 8- Peak expiratory flow < 60% of the expected value by peak flow meter. Source: Internal Medicine Book of Dr.Osama Mahmoud (Ain Shams University) |
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