Summary

This document provides an introduction to asthma, covering causes, symptoms, and epidemiology. It explores potential triggers and factors influencing the condition's development and prevalence.

Full Transcript

Asthma Case Mariam Al-Saef is a 17-year-old girl who presents to her pulmonologist for follow-up and evaluation regarding her asthma. During her visit, she reports having a wheeze, being short of breath and having to use her salbutamol MDI approximately three to...

Asthma Case Mariam Al-Saef is a 17-year-old girl who presents to her pulmonologist for follow-up and evaluation regarding her asthma. During her visit, she reports having a wheeze, being short of breath and having to use her salbutamol MDI approximately three to four times per week over the past 2 months, but over the past week she admits to using salbutamol once daily. She reports being awakened In especially becomes short of breath when she exercises, t iI a by a cough three times over the past month. She states that she Larampalthough she admits that her shortness of breath is not always brought on by exercise and sometimes occurs when she is not actively exercising. In the last week, her headaches have been getting worse needing the use of extra pain Notalways killers. somepainkillers.ae Ds forSOMEpts not all asthmaticpts imp staff p asneeded usedtotreatasthma hon In addition to her MDI, which she uses PRN, she also has a fluticasone MDI, which she uses ALEJI pan "most days of the week." She indicates that her morning peak flows have been running around 300 L/min (personal best = 400 L/min) over the past several weeks. Eat thebest 4 inflammatory Chronic Asthma is a condition in which your airways narrow and swell and may Definition of Asthma produce extra mucus Asthma is characterized by variable symptoms of: 1. wheeze it 2. shortness of breath 3. chest tightness 4. and sometimes cough Pitt but that are caused mainly by variable expiratory airflow limitation. Both symptoms and airflow La limitation characteristically vary over time and in intensity. This variation in symptoms/intensity is mainly due to trigger factors such as exercise, allergen or irritant exposure, change in weather, or viral respiratory infections. Epidemiology of Asthma prevelancedifferse Asthma is a common, chronic respiratory disease affecting 1-18% of the population in different countries. The overall prevalence of current asthma symptoms in GAN Phase I was 9.1% for children, 11.0% for adolescents, and 6.6% for adults. This differed by country income level with lower prevalence across all three age groups in low to lower-middle-income countries and highest prevalence in high-income countries. Generally, in industrialized countries, the prevalence of asthma is higher because people there tend to spend more time indoors, which can trigger asthma. pediatricdsse Industrialization increases the prevalence of asthma, while less industrialization decreases it 5 Causes of Asthma 1. Genetics and Family history 3 6 If you have a parent with asthma, you are three to six times more likely to develop it IEiiiitiie ii 2. asthma than someone who does not have a parent with asthma. Allergens m their tEm f Indoor: House dust mites, cockroach allergen, fungal molds, furred animals (dogs, cats, mice). Outdoor: Pollens – plants, grass or tree pollen, also molds 3. ha Occupationalaexposures Exposure to certain elements in the workplace can cause asthma symptoms. For some people, exposure to certain dusts (industrial or wood dusts), chemical fumes and vapors, and molds can cause asthma to develop for the very first time. 4. Viral respiratory infections Childrenhaveto majority exposed Respiratory problems during infancy and childhood can cause wheezing. Some children beless toprevent who experience viral respiratory infections go on to develop chronic asthma. toviruses developing it 5. Smoking Smokers have a high risk of asthma. Those whose mothers smoked during pregnancy or who were exposed to secondhand smoke are also more likely to have asthma. 6. Air Pollution Exposure to the main component of smog (ozone) raises the risk for asthma. Those who grew up or live in urban areas have a higher risk for asthma. 7. Obesity Children and adults who are overweight or obese are at a greater risk of asthma. Although the reasons are unclear, some experts point to low-grade inflammation in the body that occurs with extra weight. Obese patients often use more medications, suffer worse symptoms and are less able to control their asthma than patients in a healthy weight range. 6 majority are children Asthma Phenotypes Asthma is a heterogeneous disease, with differing causes, onset of disease, underlying disease processes and even response to therapy. Recognizable clusters of demographic, clinical and/or pathophysiological characteristics are often called 'asthma phenotypes'. Many clinical phenotypes of asthma have been identified and some of the most common are: 1. Allergic asthma: this is the most common and easily recognized asthma phenotype, which often commences in childhood and is associated with a past and/or family history of allergic disease such as eczema, allergic rhinitis, or food or drug allergy. Examination of the induced sputum/blood of these patients before treatment often reveals high IgE and or/ eosinophilic airway inflammation. Patients with this asthma phenotype usually respond well to inhaled corticosteroid (ICS) treatment. 2. Non-allergic asthma: some patients have asthma that is not associated with allergy. The cellular profile of the sputum of these patients may be neutrophilic, eosinophilic or contain only a few inflammatory cells. Patients with non-allergic asthma often demonstrate less short-term response to ICS 3. Adult-onset (late-onset) asthma: some adults, particularly women, present with asthma for the first time in adult life. These patients tend to be non-allergic, and often require higher doses of ICS or are relatively refractory to corticosteroid treatment. Occupational asthma (i.e. asthma due to exposures at work) should be ruled out in patients presenting with adult-onset asthma. 4. Asthma with obesity: some obese patients with asthma have prominent respiratory symptoms and little eosinophilic airway inflammation. Iea mainlyinadults 20 30ns dontrespondwell same 7 antthoodast oa ossaesarean.mn EE.imid Diagnosis Diagnosis of asthma in a patient not on controller treatment, is based on identifying: 1. A characteristic pattern of respiratory symptoms such as wheezing, shortness of breath (dyspnea), chest tightness or cough. (The pattern of symptoms is important, as respiratory symptoms may be due to acute or chronic conditions other than asthma.) 2. Variable expiratory airflow limitation. Patients (especially adults) experience more than one of these characteristics of symptoms. a. Symptoms are often worse at night or in the early morning. c b. Symptoms vary over time and in intensity. c. Symptoms are triggered by viral infections (colds), exercise, allergen exposure, changes in weather, laughter, or irritants such as car exhaust fumes, smoke or strong smells. The following features decrease the probability that respiratory symptoms are due to asthma: a. Isolated cough with no other respiratory symptoms b. Chronic production of sputum c. Shortness of breath associated with dizziness, light-headedness or peripheral tingling (paresthesia) d. Chest pain e. Exercise-induced dyspnea with noisy inspiration. Lung Function and Spirometer 5 FVC = 5L s Volume, liters 4 FEV1 = 4L FEV1/FVC = 0.8 Normal Ratio 3 3 2 1 1 2 3 4 5 6 FEV YMÉra f 80 Time, sec 8 Mild 80 FEV Moderate 6080 Diagnosis Sever460 The current asthma guidelines use FEV1 in judging asthma severity. Patients with mild persistent asthma are said to have FEV1 values of more than 80% of predicted, patients with moderate persistent asthma have values of 60 to 80% of predicted, whereas those with severe persistent asthma have values of less than 60% of predicted. In asthma the degree in decrease in the FEV1 is the same as in FVC Confirmation of expiratory airflow limitation and its variability 1. Positive bronchodilator (BD) BI Measure FEV1 and see it if is reduced and measure its reversibility (response to b2 therapy). Bagonist no So, you first measure FEV1 and again 10-15 minutes after 200-400 mcg Asthma is diagnosed if in: Adults: increase in FEV1 of >12% and >200 mL or equivalent. Children: increase in FEV1 of >12% predicted steroids 2. Responsiveness to anti-inflammatory treatment (steroids) Significant increase in lung function after 4 weeks of anti-inflammatory treatment. Asthma is diagnosed if in Adults: increase in FEV1 of >12% and >200 mL Children: increase in FEV1 of >12% predicted 3. Positive bronchial challenge test Methacholine, hypertonic saline challenge test 9 Mla Asthma Triggers Exposure to various irritants and substances that trigger allergies can trigger signs and symptoms of asthma. Asthma triggers are different from person to person and can include: 1. Airborne allergens, such as pollen, house dust mite, mold spores, pet dander or particles of cockroach waste 2. Respiratory infections, such as the common cold 3. Physical activity 4. Cold air 5. Air pollutants and irritants, such as smoke antagonist 6. Certain medications, including beta blockers, aspirin, and nonsteroidal anti-inflammatory drugs, such as ibuprofen and naproxen sodium 7. Strong emotions and stress 8. Sulfites and preservatives added to some types of foods and beverages, including shrimp, dried fruit, processed potatoes. 9. Gastroesophageal reflux disease (GERD), a condition in which stomach acids back 10 Pathogenesis Asthma is a chronic inflammatory disease driven by pro-inflammatory cells and pro- inflammatory mediators edu ammator 8ea sweat ttEs Inflammatory Cells in Asthmatic Airways  T-lymphocytes: a. (Th2) cells release specific cytokines including IL-4, IL-5, IL-9, and IL-13, that orchestrate allergic airway inflammation supressestokines b. B lymphocytes are important in that they mature into plasma cell under the influence of IL-4, and then produce IgE Piggy p Antiser FAB binds to FC binds to F  Mast cells: a. These airway resident cells are activated by allergens through high-affinity IgE receptors. niting b. Activated mucosal mast cells release bronchoconstrictor mediators (histamine, cysteinyl leukotrienes LTC4, LTD4 and LTE4) and are responsible for the early airway response.  Eosinophils: neurotoxin a. Contains many cytotoxic proteins – MBP, ECP and EDN b. Release of these proteins damages airway epithelial cells and allow more allergen to enter deep into the sub mucosa which perpetuates the inflammation. 11 Airway Nerves and Asthma coldair a. Sensory nerves in the airways may be activated to result in reflex responses (efferent – cholinergic) such as bronchoconstriction, edema, mucus hypersecretion and cough and can be activated to locally release inflammatory neuropeptides (SP, NKA and NKB) which also result in bronchoconstriction, edema, mucus hypersecretion b. Cholinergic nerves may be activated (to release Ach) as a reflex response to afferent nerve activation and also in response to many stimuli (inflammatory mediators) and result in responses in the airways such as bronchoconstriction and mucus secretion.) ◦ Cholinergic nerves play a role in severe asthma and in exacerbation of asthma Important Inflammatory Mediators a. Cytokines: 1. Cytokines play a critical role in asthma because of their ability to direct/organize the inflammatory response in asthma and likely determine its duration and severity, e.g. IL-4, IL-5, IL-9, IL-13 etc. b. Chemokines: 1. Chemokines are mediators that are important in recruitment of inflammatory cells into the site of tissue injury (airway). Some chemokines are cytokines:  RANTES, IL-8 (cytokines)  LTB4, and PAF (Lipid mediators) 12 c. Cysteinyl-leukotrienes: 1. Cysteinyl-leukotrienes (LTC4, LTD4 and LTE4) are potent bronchoconstrictors derived mainly from mast cells but other cells as well. 2. They induce bronchoconstriction, airway edema and cell recruitment and hence result in symptoms such as breathlessness and cough. 3. They are currently the only lipid mediators whose inhibition/antagonism is a therapeutic target in the treatment of asthma. d. Immunoglobulin E 1. IgE antibody responsible for activation of allergic reactions and is important to the pathogenesis of allergic diseases and the development/persistence of inflammation. 2. IgE attaches to cell surfaces via a specific high-affinity receptor. 3. The mast cell has a large number of IgE receptors 4. Many inflammatory cells can be activated via IgE such as eosinophils, neutrophils, macrophages, epithelial cells etc. 5. When cells are activated through interactions with antigen, they release a wide variety of mediators to initiate acute bronchospasm and also to release pro-inflammatory cytokines and other mediators to perpetuate the underlying inflammation. 13 basicprotein Major Eeosnit imp 2. Released cytokines induce hematopoiesis 6. Inflammation 1.Bronchoconstriction 5. 3.Release chemokines 4. Recruit inflammatory cells into the airways 14 Asthma is a chronic inflammatory disease of the airways. However, superimposed on this chronic inflammation can be acute inflammatory changes. The ACUTE changes in the asthmatic airways ACUTE Mechanisms of Airway obstruction A. Bronchoconstriction (ASM contraction) 1. Can be fast developing (with a few minutes of exposure) 2. Results from a variety of mediators acting on their receptor on ASM 3. Drugs can also induce this effect. B. Airway wall thickening 1. Edema (Airway edema is due to increased microvascular leakage in response to inflammatory mediators. This may be particularly important during acute asthma C. Mucus hypersecretion 1. Mucus hypersecretion is a product of increased mucus secretion by goblet cells and sub-mucosal glands and may lead to ‘mucus plugging” 15 These changes contribute to the acute airway obstruction and it is important to realize that most of the changes are reversible which can be demonstrated by measuring the FEV1 Changes in lung function during a classical asthma attack Early airway response (bronchoconstriction) usually within 5 min and lasts up to 2h and is predominately a bronchospasm. Mediators involved: Histamine, leukotrienes and PGD2 Late airway response (airway obstruction due to bronchoconstriction and airway obstruction edema + mucus secretion) begins within 2-3h and can last for 24h. It is a result of an intense cellular influx and release of mediators which include leukotrienes, PAF, neurokinins, bradykinin, free-radicals etc. 16 Chronic Mechanisms of Airway Narrowing (remodeling, not fully reversible) Airway smooth muscle hypertrophy and hyperplasia Sub-epithelial fibrosis (due to excess collagen deposition) Sub-mucosal and goblet cell hyperplasia and hypertrophy Angiogenesis 17

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