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group_5_presentation_3_-_asthma [2016/04/01 23:29] dmellonr |
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| There are several factors that make one more prone to this disease: | There are several factors that make one more prone to this disease: | ||
| - | * Heredity:A toddler has an 80 - 90% chance of contracting this illness if both parents are asthmatic, however, if one parent has the disease, then the toddler would be 30 - 40% at risk of contracting the illness (Duffy, 1997). There are several studies that looked at monozygotic and dizygotic twins and found that monozygotic twins have a 19% chance of presenting with the same disease, whereas dizygotic twins only have a 4.8% chance of presenting with the same disease (Edfors-Lubs, 1971). An individual with a family history of this disease is four times as likely of getting the disease (Ronmark et al., 1971). | + | * Heredity: A toddler has an 80 - 90% chance of contracting this illness if both parents are asthmatic, however, if one parent has the disease, then the toddler would be 30 - 40% at risk of contracting the illness (Duffy, 1997). There are several studies that looked at monozygotic and dizygotic twins and found that monozygotic twins have a 19% chance of presenting with the same disease, whereas dizygotic twins only have a 4.8% chance of presenting with the same disease (Edfors-Lubs, 1971). An individual with a family history of this disease is four times as likely of getting the disease (Ronmark et al., 1971). |
| * Fetal environment: Studies have found a relationship between the fetal environment and the development of the atopic disease later in life (Keller, 2002). It is more likely for the child to contract the disease if the mother has the disease as opposed to the father having it(Keller, 2002). The risk for a child to develop asthma in later life has been correlated with a mother’s exposure to allergins in the first 22 weeks of gestation (Warner et al., 2000). Bronchial hyperresponsiveness has been shown to be more commonly found in infants with lower birthweight as opposed to infants with a higher birthweight (Keller, 2002). Moreover, It has been found that mothers who smoke and are younger than 20 years, were more likely to have a child who suffers from asthma (Keller, 2002). Moreover, maternal prenatal stress has also shown to be a possible risk factor for developing asthma (Sears, 2014). Research also has looked at the relationship between different modes of delivery and the likelihood of developing asthma. It was found that mothers who had undergone a caesarean section, were 10% to 20% more likely at risk to have an asthmatic child (Sears, 2014). | * Fetal environment: Studies have found a relationship between the fetal environment and the development of the atopic disease later in life (Keller, 2002). It is more likely for the child to contract the disease if the mother has the disease as opposed to the father having it(Keller, 2002). The risk for a child to develop asthma in later life has been correlated with a mother’s exposure to allergins in the first 22 weeks of gestation (Warner et al., 2000). Bronchial hyperresponsiveness has been shown to be more commonly found in infants with lower birthweight as opposed to infants with a higher birthweight (Keller, 2002). Moreover, It has been found that mothers who smoke and are younger than 20 years, were more likely to have a child who suffers from asthma (Keller, 2002). Moreover, maternal prenatal stress has also shown to be a possible risk factor for developing asthma (Sears, 2014). Research also has looked at the relationship between different modes of delivery and the likelihood of developing asthma. It was found that mothers who had undergone a caesarean section, were 10% to 20% more likely at risk to have an asthmatic child (Sears, 2014). | ||
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| {{:ji.png|thumb|left|alt=A}} | {{:ji.png|thumb|left|alt=A}} | ||
| - | Figure 1: Asthma Risk Factors | + | **Figure 1**: Asthma Risk Factors |
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| - | Figure 2: Difference between normal and pathophysiological bronchiole. Shows tightened muscles which constrict airway, mucus accumulation, thickened airway wall. As a result, there’s a narrow airway and limited airflow. | + | **Figure 2**: Difference between normal and pathophysiological bronchiole. Shows tightened muscles which constrict airway, mucus accumulation, thickened airway wall. As a result, there’s a narrow airway and limited airflow. |
| ==== The Normal Physiological Response ==== | ==== The Normal Physiological Response ==== | ||
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| {{:image6.png?550}} | {{:image6.png?550}} | ||
| - | Figure 3 : Flat-end arrows show the inhibitory effect of T-reg cells on B cells, dendritic cells, mast cells, basophils, eosinophils and mucus secretion during the normal response to allergens. | + | **Figure 3**: Flat-end arrows show the inhibitory effect of T-reg cells on B cells, dendritic cells, mast cells, basophils, eosinophils and mucus secretion during the normal response to allergens. |
| ==== The Pathophysiological Asthmatic Response ==== | ==== The Pathophysiological Asthmatic Response ==== | ||
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| 6. Macrophages: These are the most numerous cells in the airway and can be activated by allergens through low affinity IgE receptors to release pro-inflammatory mediator and cytokines (National Heart, Lung, and Blood Institute 2007). | 6. Macrophages: These are the most numerous cells in the airway and can be activated by allergens through low affinity IgE receptors to release pro-inflammatory mediator and cytokines (National Heart, Lung, and Blood Institute 2007). | ||
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| 1. Chemokines: important in the recruitment of inflammatory cells into airways, expressed mainly in airway epithelial cells. Eotaxin is selective for eosinophils. Thymus and activation-regulated chemokine (TARCs) and macrophage derived chemokine (MDCs) recruit T helper 2 cells (National Heart, Lung, and Blood Institute 2007). | 1. Chemokines: important in the recruitment of inflammatory cells into airways, expressed mainly in airway epithelial cells. Eotaxin is selective for eosinophils. Thymus and activation-regulated chemokine (TARCs) and macrophage derived chemokine (MDCs) recruit T helper 2 cells (National Heart, Lung, and Blood Institute 2007). | ||
| - | 2.Cytokines: direct, modify and determine the severity of the inflammatory response in asthma. Th2 derived cytokines include interleukin 5 which is needed for eosinophil differentiation and survival, interleukin 4 which is important for Th2 cell differentiation and interleukin 13 which is important for IgE formation. Other key cytokines include IL-1-beta and tumour necrosis factor-alpha which increase the inflammatory response, and granulocyte-macrophage colony-stimulating factor (GM-CSF) which prolongs the survival of eosinophils in airways. | + | 2. Cytokines: direct, modify and determine the severity of the inflammatory response in asthma. Th2 derived cytokines include interleukin 5 which is needed for eosinophil differentiation and survival, interleukin 4 which is important for Th2 cell differentiation and interleukin 13 which is important for IgE formation. Other key cytokines include IL-1-beta and tumour necrosis factor-alpha which increase the inflammatory response, and granulocyte-macrophage colony-stimulating factor (GM-CSF) which prolongs the survival of eosinophils in airways. |
| - | 3.. Cysteinyl-leukotrienes: potent bronchoconstrictors that are derived from mast cells. Inhibition of this mediator has been linked with an improvement in lung function and asthma symptomology (National Heart, Lung, and Blood Institute 2007). Also, studies have shown leukotriene B4 to contribute to the inflammatory response by recruiting neutrophils (National Heart, Lung, and Blood Institute 2007). | + | 3. Cysteinyl-leukotrienes: potent bronchoconstrictors that are derived from mast cells. Inhibition of this mediator has been linked with an improvement in lung function and asthma symptomology (National Heart, Lung, and Blood Institute 2007). Also, studies have shown leukotriene B4 to contribute to the inflammatory response by recruiting neutrophils (National Heart, Lung, and Blood Institute 2007). |
| IgE: important for allergic diseases and the development and persistence of inflammation. It attaches to a cell surface via a high affinity receptor. The mast cell has large numbers of IgE receptors and when activated after interacting with an antigen, there’s a release of mediators to initiate acute bronchospasm and the release of pro-inflammatory cytokines to induce airway inflammation (National Heart, Lung, and Blood Institute 2007). Other cells such as basophils, dendritic cells and lymphocytes also have high affinity IgE receptors. The development of antibodies against IgE has proved that reducing IgE is effective in treating asthma (National Heart, Lung, and Blood Institute 2007). | IgE: important for allergic diseases and the development and persistence of inflammation. It attaches to a cell surface via a high affinity receptor. The mast cell has large numbers of IgE receptors and when activated after interacting with an antigen, there’s a release of mediators to initiate acute bronchospasm and the release of pro-inflammatory cytokines to induce airway inflammation (National Heart, Lung, and Blood Institute 2007). Other cells such as basophils, dendritic cells and lymphocytes also have high affinity IgE receptors. The development of antibodies against IgE has proved that reducing IgE is effective in treating asthma (National Heart, Lung, and Blood Institute 2007). | ||
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| - | Figure: Difference between no disease condition. In particular, there is no mucociliary clearance and increase of T helper 2 cells in asthmatic conditions. | + | **Figure 4**: Difference between no disease condition. In particular, there is no mucociliary clearance and increase of T helper 2 cells in asthmatic conditions. |
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| + | ==== TREATMENTS ==== | ||
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| + | At its current state, there has yet to be an established permanent cure to individuals suffering from asthma. Fortunately, various management techniques are available and can be implemented in order to help alleviate the various symptoms associated with the disease. The primary suggestion asthmatic patients are recommended to do is to avoid any of the mentioned irritants involved in triggering an inflammatory response of the airway. In addition to avoiding any potential allergens, medication is available for both short-term and long-term relief. While short-term medication can provide immediate relief to counteract the constriction of the airway, long-term medication can be taken in the form of a daily supplement to aid in controlling against any future aggravation (Kuna & Kuprys, 2002). | ||
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| + | A common short-term therapeutic can be found in the form of bronchodilators such as Ventolin. Bronchodilators are classified as beta-agonists, which seek target beta-adrenergic G-protein coupled receptors (GPCRs) of the bronchial smooth muscle (Kuna & Kuprys, 2002). Upon binding to these membrane-bound receptors, surrounding adenyl cyclase and ATP interact, leading to the production of cyclic-AMP (cAMP) and a subsequent cascading release into the cell. With the function of cAMP being a secondary messenger for enzyme-catalyzed processes within the cell, the relaxation of the smooth muscle cells acts further downstream in this reaction pathway (Kuna & Kuprys, 2002). Normally requiring epinephrine to produce smooth muscle relaxation, Ventolin acts as mimic to adrenaline due to both its conformation and structure, allowing it to produce the same intended result when taken by an asthmatic patient (Kuna & Kuprys, 2002). Another alternative to Ventolin is another inhaler known as Formoterol, which is better known for its more long-term viability. Taking advantage of a mechanism similar to Ventolin, the active ingredients in Formoterol allow the drug to remain at the level of the cell-membrane for an extended period of time (Pauwels et al., 1997). In addition to allowing the bronchodilation of the patient, Formoterol is also able to bind to beta2-adrenergic receptors located on the membrane of mast cells. With the binding of Formoterol to beta2-adrenergic receptors, the release of histamine, an inflammatory agent released by cells in response to any allergic response, is negatively inhibited (Pauwels et al., 1997). With the inhalation of Formoterol on a regular basis, individuals suffering from asthma will be able to relieve themselves of both bronchoconstriction and a hypersensitive response due to any irritants over a long term period. | ||
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| + | {{:group5asthma1.jpg|}} | ||
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| + | **Figure 5**: Ventolin, a bronchodilator used in providing short-term relief from symptoms of asthma | ||
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| + | A different type of medication used to treat asthma is anti-inflammatory medication. These anti-inflammatory drugs are corticosteroids such as Budesonide and alike bronchodilators, this form of drug is taken by inhalation. Budesonide reaches the target cells within one minute of inhalation and closes vascular micro leaks via vasoconstriction of the bronchi. Relaxation of the bronchial smooth muscles is experienced after 2-3 hours due to the activation of transcription factors, which increases the number of accessible beta-2 receptors (Pauwels et al., 1997). A new type of therapeutic being tested is a combination therapy involving both bronchodilators and anti-inflammatory pathways. Symbicort is a prime example of this combination medication and its use displayed that the two mechanisms have synergistic effects. Since budesonide leads to an increased number of expressed beta-2 adrenergic receptors, there are more total receptors for formoterol to bind to. In addition to this, the binding of formoterol to these beta-2 receptors increases the activity of budesonide, leading to an increased amount of anti-inflammation (Bryan et al., 2000). | ||
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| + | {{:group5asthma2.jpg|}} | ||
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| + | **Figure 6**: Symbicort, used in combination drug therapy, is efficient due to the synergistic effects provided when using both bronchodilators and anti-inflammatory medication in tandem. | ||
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| Bacharier, L. B., Boner, A., Carlsen, K. H., Eigenmann, P. A., Frischer, T., Götz, M., ... & Platts‐Mills, T. (2008). Diagnosis and treatment of asthma in childhood: a PRACTALL consensus report. Allergy, 63(1), 5-34. | Bacharier, L. B., Boner, A., Carlsen, K. H., Eigenmann, P. A., Frischer, T., Götz, M., ... & Platts‐Mills, T. (2008). Diagnosis and treatment of asthma in childhood: a PRACTALL consensus report. Allergy, 63(1), 5-34. | ||
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| + | Bryan, S. A., Leckie, M. J., Hansel, T. T., & Barnes, P. J. (2000). Novel therapy for asthma. Expert opinion on investigational drugs, 9(1), 25-42. | ||
| Chiang, L. C., Ma, W. F., Huang, J. L., Tseng, L. F., & Hsueh, K. C. (2009). Effect of relaxation-breathing training on anxiety and asthma signs/symptoms of children with moderate-to-severe asthma: a randomized controlled trial.International Journal of Nursing Studies, 46(8), 1061-1070. | Chiang, L. C., Ma, W. F., Huang, J. L., Tseng, L. F., & Hsueh, K. C. (2009). Effect of relaxation-breathing training on anxiety and asthma signs/symptoms of children with moderate-to-severe asthma: a randomized controlled trial.International Journal of Nursing Studies, 46(8), 1061-1070. | ||
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| Keller, M., Lowenstein, S. (2002). Epidemiology of Asthma. Seminars in Respiratory and Critical Care Medicine, 23(4). 317-329. | Keller, M., Lowenstein, S. (2002). Epidemiology of Asthma. Seminars in Respiratory and Critical Care Medicine, 23(4). 317-329. | ||
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| + | Kuna, P., & Kuprys, I. (2002). Symbicort Turbuhaler: a new concept in asthma management. International journal of clinical practice, 56(10), 797-803. | ||
| Lambrecht, B., Hammad, H. (2015). The Immunology of Asthma. Nature Immunology, 16(1), 45-56. | Lambrecht, B., Hammad, H. (2015). The Immunology of Asthma. Nature Immunology, 16(1), 45-56. | ||
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| - | National Asthma Education and Prevention Program, Third Expert Panel on the Diagnosis and Management of Asthma. Expert Panel (Report 3): Guidelines for the Diagnosis and Management of Asthma, Bethesda (MD): National Heart, Lung, and Blood Institute (US); 2007 Aug. Section 2, Definition, Pathophysiology and Pathogenesis of Asthma and Natural History of Asthma. Available from: http://www.ncbi.nlm.nih.gov/books/NBK7223/ | ||
| Pauwels, R. A., Löfdahl, C. G., Postma, D. S., Tattersfield, A. E., O'Byrne, P., Barnes, P. J., & Ullman, A. (1997). Effect of inhaled formoterol and budesonide on exacerbations of asthma. New England Journal of Medicine, 337(20), 1405-1411. | Pauwels, R. A., Löfdahl, C. G., Postma, D. S., Tattersfield, A. E., O'Byrne, P., Barnes, P. J., & Ullman, A. (1997). Effect of inhaled formoterol and budesonide on exacerbations of asthma. New England Journal of Medicine, 337(20), 1405-1411. | ||
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| Potter, P. C. (2010). Current guidelines for the management of asthma in young children. Allergy, asthma & immunology research, 2(1), 1-13. | Potter, P. C. (2010). Current guidelines for the management of asthma in young children. Allergy, asthma & immunology research, 2(1), 1-13. | ||
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| - | Ronmark E, Lundback B, Jonsson EA, et al. (1997). Incidence of asthma in adults—report from the Obstructive Lung Disease in Northern Sweden study. Allergy, 52:1071–1081. | ||
| Reed, C. (2006). The natural history of asthma. Journal of Allergy and Clinical Immunology, 118( 3), 549-550. | Reed, C. (2006). The natural history of asthma. Journal of Allergy and Clinical Immunology, 118( 3), 549-550. | ||
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| + | Ronmark E, Lundback B, Jonsson EA, et al. (1997). Incidence of asthma in adults—report from the Obstructive Lung Disease in Northern Sweden study. Allergy, 52:1071–1081. | ||
| Sears, M. (2014). Trends in the Prevalence of Asthma. Chest, 145(2), 219-225. | Sears, M. (2014). Trends in the Prevalence of Asthma. Chest, 145(2), 219-225. | ||
