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Similar a Hosanna W Asfaw Presentation on Asthma Definition, Epidemiology, Pathogenesis, Diagnosis and Treatment (39
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Hosanna W Asfaw Presentation on Asthma Definition, Epidemiology, Pathogenesis, Diagnosis and Treatment (39
- 1. Presentor: Hosanna W Asfaw
- 2. Asthma definition Epidemiology Risk factors Pathogenesis Clinical features Diagnosis Status asthmaticus Treatment
- 3. “a heterogeneous disease, usually characterized by airway inflammation. It is defined by the presence of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflow limitation.”
- 4. affects approximately 300 million people worldwide (Harrisons 19E) can present at any age, with a peak age of 3 years. In childhood, M:F ration is 2: 1 By adulthood the sex ratio has equalized
- 7. Atopy allergic rhinitis (80%) atopic dermatitis (eczema) Genetic predisposition Determines severity, is polygenic Novel genes: ADAM-33, and DPP-10 Infections Atypical bacteria, such as Mycoplasma and Chlamydophila
- 8. Obesity BMI> 30 kg/m2 more difficult to control Others Air pollution Cold air In utero exposure to environmental tobacco smoke Pharmacologic agents (ẞ blockers)
- 10. GINA
- 11. >1 sx (wheeze, shortness of breath, cough, chest tightness) Symptoms often worse at night or in the early morning Symptoms vary over time and in intensity Symptoms are triggered by viral infections (colds), exercise, allergen exposure, changes in weather, laughter, or irritants
- 12. Isolated cough Chronic production of sputum SOB associated with dizziness, light- headedness or peripheral tingling (paresthesia) Chest pain Exercise-induced dyspnea with noisy inspiration.
- 16. Allergic asthma: starts in past and/or family history of allergic disease such as eczema, allergic rhinitis, or food or drug allergy. Examination of the induced sputum reveals eosinophilic airway inflammation Respond well (ICS) treatment. Non-allergic asthma: Sputum neutrophilic, eosinophilic or contain only a few inflammatory cells Respond less well to ICS.
- 17. Late-onset asthma particularly women non-allergic require higher doses of ICS or are refractory to corticosteroid treatment. Asthma with fixed airflow limitation: some patients with long-standing asthma develop fixed airflow limitation that is thought to be due to airway wall remodeling. Asthma with obesity: obese patients have prominent respiratory symptoms little eosinophilic airway inflammation.
- 19. • classically present with a history of episodes of coughing, chest tightness, shortness of breath, and wheezing onset of symptoms with specific triggers Family history Social history home characteristics, smoking, workplace or school characteristics, educational level, social support, non-adherence of asthma medications, and illicit drug use.
- 20. Prodromal symptoms may precede an attack Itching under the chin discomfort b/n scapula unexplained fear.
- 21. Hyperexpansion of the thorax Wheezing during normal breathing Prolonged phase of forced exhalation Increased nasal secretion, mucosal swelling, and/or nasal polyps Atopic dermatitis/eczema
- 22. Lung function tests Spirometry ▪ forced expiratory volume in 1 second (FEV1) ▪ FEV1/FVC <0.7 generally defines obstruction. ▪ peak expiratory flow (PEF) ▪ Reversibility ▪ increase in FEV1 of ≥12% or >200 mL after inhalation of a short- acting bronchodilator Flow volume loop
- 24. Provocation studies airway hyperresponsiveness Metacholine/ histamine challenge A 20 % reduction in FEV1 Exhaled NO – to measure air way inflammation Total serum IgE and specific IgE to inhaled allergens Skin prick test to common inhalant allergens
- 25. Airway Hyperresponsiveness Methacholine or histamine challenge Laboratory tests: not usually helpful Blood eosinophilia Sputum eosinophilia Serum IgE levels Chest X-ray: usually normal, may show hyperinflated lungs Exhaled nitric oxide (FENO) Allergy skin testing
- 26. Upper airway obstruction flow-volume loop Endobronchial obstruction Vocal cord dysfunction COPD Congestive heart failure Pulmonary embolism Pulmonary infiltration with eosinophilia Cough secondary to drugs (e.g.,ACE inhibitors)
- 27. Condition Characteristics COPD Airway obstruction is less reversible; typically seen in older patients with smoking history Vocal cord dysfunction Abrupt onset and end of symptoms; monophonic wheeze; more common in younger patients; confirm with laryngoscopy or flow- volume loop Heart failure Dyspnea and often wheezing; crackles on auscultation; limited response to asthma therapy; cardiomegaly; edema Bronchiectasis Cough productive of large amount of purulent sputum; rhonchi and crackles are common; may have wheezing and clubbing; confirmed by CT imaging ABPA Recurrent infiltrates on chest radiograph; eosinophilia; positive skin testing to Aspergillus antigens, high IgE levels Mechanical obstruction More localized wheezing; if central in location, flow-volume loop may provide a clue Eosinophilic granulomatosis with polyangiitis Autoimmune small-vessel vasculitis presents with peripheral eosinophilia, lung symptoms similar to asthma
- 31. ẞ2-Agonists Relax airway smooth-muscle cells No effects on inflammatory cells SABAs: 3–6 h Salbutamole- useful in preventing EIA if taken prior to exercise LABAs: >12h salmeterol and formoterol (Important to use ICS when LABAs are given Anticholinergics prevent cholinergic nerve-induced bronchoconstriction and mucus secretion. once- daily tiotropium bromide Theophylline- Side Effects
- 32. Inhaled corticosteroids (ICSs) Most effective controllers for asthma Anti-inflammatory ↑expression of β2-receptors Reduce AHR First-line therapy for patients with persistent asthma Local side effects hoarseness (dysphonia) oral candidiasis Antileukotrienes, Cromones, Anti-IgE
- 33. Intermittent Persistent Components of Severity Mild Moderate Severe Symptoms ≤2 days/week >2 days/week but not daily Daily Throughout the day Nighttime awakenings ≤2 ×/month 3-4 ×/month >1 ×/week but not nightly Often 7 ×/week SABA use for symptom control ≤2 days/week >2 days/week but not more than 1 ×/d Daily Several times a day Lung function FEV1 ≥80% of predicted FEV1/FVC normal FEV1 ≥80% of predicted FEV1/FVC normal FEV1 ≥60% but <80% of predicted FEV1 <60% of predicted Exacerbations 0-1/year >2/year >2/year >2/year
- 35. Also known as STATUS ASTHMATICUS
- 36. Formerly known as status asthmaticus Acute exacerbation of asthma that does not respond to standard treatment (Bronchodilators, inhalers, steroids) Medical emergency
- 37. 50% due to URTIs Non adherence NSAID exposure in ASA-allergic patients Allergen exposure Irritant inhalation
- 38. Chest tightness, wheezing, use of accessory muscles and dyspnea that are often not or poorly relieved by their usual reliever inhaler breathless that they are unable to complete sentences cyanotic
- 39. General appearance: alteration of consciousness fatigue upright posture diaphoresis Respiratory system tachypnea (>30min) use of accessory muscles for breathing reduced respiratory excursion diffuse expiratory wheezing Cyanotic
- 40. Cardiovascular system Tachycardia (>120/min) pulsus paradoxus SPIROMETRY PEFR< 120L/MIN FEV1< 1L Arterial blood gas analysis hypercapnia or normal CXR: over inflated lung
- 41. Cardiac arrest Respiratory failure or arrest Hypoxemia with hypoxic ischemic central nervous system (CNS) injury Pneumothorax or pneumomediastinum Toxicity from medications
- 42. Good prognosis if appropriate therapy is administered. …unless a complicating illness such as CHF COPDis present A delay in initiating treatment is probably the worst prognostic factor
- 44. High concentration of oxygen + High doses of SABA Severely ill patients with impending respiratory failure, IV β2-agonists Nebulized anticholinergic- if unsatisfactory response to β2-agonists patients who are refractory to inhaled therapies, a slow infusion of aminophylline Magnesium sulfate given intravenously or by nebulizer with inhaled β2-agonists Prophylactic intubation for impending respiratory failure, when the PCO2 is normal or rises. Patients with respiratory failure necessary to intubate
- 45. These patients may benefit from an anesthetic such as halothane if they have not responded to conventional bronchodilators. Sedatives are C/I depress ventilation. Antibiotics not required unless there are signs of pneumonia.
- 46. Thank you for your attention
- 47. Harrison’s principles of internal medicine 19th e/o Global asthma initiative for asthma Review article Chapter 14: Acute severe asthma(status asthmaticus) Review article [Status asthmaticus]
Notas del editor
- A rise in asthma mortality seen in several countries during the 1960s was associated with increased use of short-acting inhaled β2-adrenergic agonists (as rescue therapy), but there is now compelling evidence that the more widespread use of inhaled corticosteroids (ICS) in patients with persis- tent asthma is responsible for the decrease in mortality in recent years. Major risk factors for asthma deaths are poorly controlled disease with frequent use of bronchodilator inhalers, lack of or poor compliance with ICS therapy, and previous admissions to hospital with near-fatal asthma.
- AHR is the characteristic physiologic abnormality of asthma and describes the excessive bronchoconstrictor response to multiple inhaled triggers that would have no effect on nor- mal airways.
- Atopy refers to the genetic tendency to develop allergic diseases such as allergic rhinitis, asthma and atopic dermatitis (eczema). Atopy is typically associated with heightened immune responses to common allergens, especially inhaled allergens and food allergens.
- Genetic screens with classical linkage analysis and single-nucleotide polymorphisms of various candidate genes indicate that asthma is polygenic, with each gene identified having a small effect that is often not replicated in different populations. This observation suggests that the interaction of many genes is important, and these may differ in different populations. The most consistent findings have been associa- tions with polymorphisms of genes on chromosome 5q, including the T helper 2 (TH2) cells interleukin (IL)-4, IL-5, IL-9, and IL-13, which are associated with atopy.
- exposure to microbial diversity appears to protect against asthma by shifting Th cells to a Th1 instead of a predominantly Th2 phenotype Th1 cells tend to generate responses against intracellular parasites such as bacteria and viruses, Th2 cells produce immune responses against helminths and other extracellular parasites
- Dendritic cells are specialized macrophage-like cells in the airway epithelium, which are the major antigen-presenting cells. Dendritic cells take up allergens, process them to peptides, and migrate to local lymph nodes where they pres- ent the allergenic peptides to uncommitted T lymphocytes to program the production of allergen-specific T cells. Immature dendritic cells in the respiratory tract promote TH2 cell differentiation and require cyto- kines, such as IL-12 and tumor necrosis factor α (TNF-α), to promote the normally preponderant TH1 response. Allergen inhalation results in a marked increase in activated eosinophils in the airways at the time of the late reaction. Eosinophils are linked to the development of AHR through the release of basic proteins and oxygen-derived free radicals. Smooth muscle Inflammatory media- tors may modulate the ion channels that serve to regulate the resting membrane potential of airway smooth-muscle cells, thus altering the level of excitability of these cells. VAsculAr resPonses There is increased airway mucosal blood flow in asthma, which may contribute to airway narrowing. There is an increase in the number of blood vessels in asthmatic airways as a result of angiogenesis in response to growth factors, particularly vascular endothelial growth factor. Microvascular leakage from postcapillary venules in response to inflammatory mediators is observed in asthma, resulting in airway edema and plasma exudation into the airway lumen. mucus hyPersecretion Increased mucus secretion contributes to the viscid mucous plugs that occlude asthmatic airways, particularly in fatal asthma. There is hyperplasia of submucosal glands that are con- fined to large airways and of increased numbers of epithelial goblet cells. IL-13 induces mucus hypersecretion in experimental models of asthma. fibrosis In all asthmatic patients, the basement membrane is appar- ently thickened due to subepithelial fibrosis with deposition of types III and V collagen below the true basement membrane and is associated with eosinophil infiltration, presumably through the release of profibrotic mediators such as transforming growth factor-β.
- Non-allergic asthma: Sputum neutrophilic, eosinophilic or contain only a few inflammatory cells (paucigranulocytic). Patients with non-allergic asthma often respond less well to ICS.
- Between attacks and exacerbations, spirometry can be normal in patients with suspected asthma Flow-volume loops show reduced peak flow and reduced maximum expiratory flow. Further lung function tests are rarely necessary, but whole-body plethysmog- raphy shows increased airway resistance and may show increased total lung capacity and residual volume. Gas diffusion is usually normal, but there may be a small increase in gas transfer in some patients.
- Spirometry and flow-volume loop in asthmatic compared to nor- mal subject. There is a reduction in forced expiratory volume in 1 second (FEV1) but less reduction in forced vital capacity (FVC), giving a reduced FEV1/FVC ratio (<70%). The flow-volume loop shows reduced peak expiratory flow and a typical scalloped appearance indicating widespread airflow obstruction.
- Inflammatory cells express small numbers of β2- receptors, but these are rapidly downregulated with β2-agonist acti- vation so that, in contrast to corticosteroids, there are no effects on inflammatory cells in the airways and there is no reduction in AHR. Increased use of SABA indicates that asthma is not controlled. They are also useful in preventing EIA if taken prior to exercise. SABAs are used in high doses by nebulizer or via a metered- dose inhaler with a spacer. Long-acting β2-agonists (LABAs) include salmeterol and formoterol, both of which have a duration of action over 12 h and are given twice daily by inhalation; indacaterol is given once daily. LABAs have replaced the regular use of SABAs, but LABAs should not be given in the absence of ICS therapy because they do not control the underlying inflammation. They do, however, improve asthma control and reduce exacerbations when added to ICS, which allows asthma to be controlled at lower doses of corticosteroids. This observation has led to the widespread use of fixed-combination inhalers that contain a corticosteroid and a LABA, which have proved to be highly effective in the control of asthma.
- Stepwise approach to asthma therapy according to the severity of asthma and ability to control symptoms. ICS, inhaled corticosteroids; LABA, long-acting β2-agonist; OCS, oral corti- costeroid.
- A high concentration of oxygen should be given by face mask to achieve oxygen saturation of >90%. The mainstay of treatment are high doses of SABA given either by nebulizer or via a metered-dose inhaler with a spacer. In severely ill patients with impending respira- tory failure, IV β2-agonists may be given. A nebulized anticholinergic may be added if there is not a satisfactory response to β2-agonists alone, as there are additive effects. In patients who are refractory to inhaled therapies, a slow infusion of aminophylline may be effec- tive, but it is important to monitor blood levels, especially if patients have already been treated with oral theophylline. Magnesium sulfate given intravenously or by nebulizer is effective when added to inhaled β2-agonists, and is relatively well tolerated but is not routinely recommended. Prophylactic intubation may be indicated for impending respiratory failure, when the PCO2 is normal or rises. For patients with respiratory failure, it is necessary to intubate and institute ventilation. These patients may benefit from an anesthetic such as halothane if they have not responded to conventional bronchodilators. Sedatives should never be given because they may depress ventilation. Antibiotics should not be used routinely unless there are signs of pneumonia.