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Asthma Pathology Profile The symptoms of asthma include chest pain, tightness of the chest, shortness of breath, coughing, and wheezing. These symptoms are caused by the constriction of the airways and excess mucus production.
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The pathway begins with the development of Th2 cells and their production of the cytokines IL-4, IL-5, and IL-13. These cytokines stimulate allergic and eosinophilic inflammation as well as epithelial and smooth-muscle changes that contribute to asthma pathobiology.
A case study of a patient with Asthma. This is a case of a 25-year old woman with episodic shortness of breath and chest tightness. The physical findings of chest pains, wheezing, heavy coughs, blocked sinuses, breathing difficulties, skin rashes together with presented symptoms is suggestive to Asthma infection.
Initial diagnosis of Asthma is made with differential diagnosis of chronic obstructive pulmonary disease, hyperventilation syndrome and panic attacks, congestive heart failure, foreign body aspiration, pulmonary infiltration with eosinophilia, and vocal cord dysfunction.
Defined by the National Asthma Education and Prevention Program as a "chronic inflammatory disorder of the airways" in which many cells and cellular elements play a role - in particular, mast cells, eosinophils, T lymphocytes, macrophages, neutrophils and epithelial cells
The pathophysiology of asthma is complex and involves airway inflammation, intermittent airflow obstruction, and bronchial hyperresponsiveness.
The pathologic changes include hyperplasia of mucous glands, hyperemia and edema of the mucosa, eosinophilic infiltration of the mucosa, hypertrophy of bronchiolar mus- culature, and formation of mucous plugs. The actual thickness of bronchiolar walls may be considerably increased by t,he summation of alterations.
During an asthma episode, inflamed airways react to environmental triggers such as smoke, dust, or pollen. The airways narrow and produce excess mucus, making it difficult to breathe. In essence, asthma is the result of an immune response in the bronchial airways.
To diagnose asthma, your doctor will discuss your medical history with you and perform a physical exam. You may need a lung function test and maybe other tests, such as a chest or sinus X-ray. If you or your child are having problems breathing on a regular basis, don't wait! Visit a doctor immediately.
Many basic and clinical studies suggested that airway inflammation was a central key to the disease pathophysiology. The existence of chronic airway inflammation in asthma has been recognized for over a century. The inflammation is induced by the release of potent chemical mediators from inflammatory cells.
The biochemical determinants of asthma heterogeneity are many. Examples include decreased activity of superoxide dismutases; increased activity of eosinophil peroxidase, S-nitrosoglutathione reductase, and arginases; decreased airway pH; and increased levels of asymmetric dimethyl arginine.
A FeNO test is most often used as a test to diagnose asthma. But it may be used in a specialist centre to monitor your severe eosinophilic asthma.
Testing for Asthma The most common lung function test is called spirometry. This lung function test uses a device called, a spirometer, to measure the amount and speed of the air you blow out.
A simple calculation using routine blood test results can identify eosinophilic asthma patients. Complete blood count (CBC) with differential, a standard test that enumerates different types of white cells in peripheral blood, is often performed during routine patient visits in clinics and hospitals.
Defined by the National Asthma Education and Prevention Program as a "chronic inflammatory disorder of the airways" in which many cells and cellular elements play a role - in particular, mast cells, eosinophils, T lymphocytes, macrophages, neutrophils and epithelial cells
Episodes are usually associated with widespread but variable airflow obstruction that is often reversible, either spontaneously or with treatment. Inflammation also causes an associated increase in the existing bronchial hyperresponsiveness to a variety of stimuli. Very common, affects 14 - 15 million Americans.
Allergy-induced asthma, caused by airborne contaminants such as pollen, mold spores, cockroach or skin debris, and pet-shredded, dried saliva.
Respiratory: increased breathing, chest pains, shortness of breath, wheeze, heavy cough, speaking difficulty, and chest tightness. The case study patient for this paper presented with episodic shortness of breath, and chest tightness.
The patient presented herself to the healthcare office with complaints over chest tightness and episodic shortness of breath that occurs twice or thrice a month.
Also, the disease presents dizziness, fatigue, and abdominal pains. The disease was considered based on the patient’s wheezing, smoking, congestive lungs, breath shortness, and abdominal pains, characteristics that appear in patients with smoking habits. This disease was considered based on the patient physical symptoms.
Several results indicate that children with atopic dermatitis can suffer more serious and chronic adult asthma. Differential Diagnoses. 1. Chronic obstructive pulmonary disease (COPD) This disease was considered because the patient is an adult aged 25 years, which is the age group of the case study.
Besides, those with critical Asthma are advised to keep their inhalers nearby for use in case of panic attacks or allergic reactions (“Asthma – Diagnosis and treatment – Mayo Clinic,” 2018). Moreover, Asthmatic patients avoid Asthma trigger s such as smoking, perfumes, unprescribed drugs, and irritative pets.
Risk factors for asthma can be a genetic predisposition or from environmental factors. If a patient has a family history of asthma, it increases his or her chances of developing asthma. This is an intrinsic factor that is out of the patient’s control. Environmental factors are extrinsic and can be somewhat controlled by the patient avoiding triggers. Patients that are not exposed to bacteria, and viruses early in life have an increased susceptibility to develop asthma. This reduced exposure varies the proportion of immune cells so they are more reactive in protective responses. Early onset asthma is usually a result of genetic factors, while later onset asthma is due to environmental factors (Morris). Both of these factors increase the hypersensitivity of the airways, making asthma attacks more common.
Asthma symptoms vary in each person; some may experience symptoms only while exercising, while others experience symptoms every day (Mayo Clinic Staff). Therefore, in some people asthma is a major problem that seriously impacts their life, while in others it is just a minor problem. A physician will commonly diagnose a patient with asthma by doing a spirometry test or a peak flow test and asking about the patient’s symptoms. A spirometry test measures how much air a patient can exhale and how fast he or she breathes it out. The physician will calculate a predicted value for test scores based on age, gender, height, and other factors. If the patient’s test result is 80% or more of the predicted value it is “normal” and if results are below that, it indicates lung disease or that damage has occurred to the patient’s lungs. A peak flow test measures how fast a patient can breathe out. If this number is low, it indicates that the patient’s lungs are not functioning normally (Mayo Clinic Staff).
Asthma affects 16.4 million adults and seven million children in the United States, which is approximately ten percent of the population. In the United States, the mortality rate of asthma is higher in African Americans than in Caucasians. This difference in mortality is not only due to genetics but also due to affordability of treatment. It is suspected that minorities have a higher mortality rate because they struggle more to afford treatment (Morris). Preadolescence asthma occurs more often in boys than girls. In both cases, boys and girls are likely to experience a decrease or even disappearance of symptoms by age eighteen. Therefore, most patients with asthma are diagnosed at a young age. Asthma is more commonly diagnosed in industrialized nations where there is air pollution, smoking, and environmental allergens.
In people with asthma, the immune system has a reaction to this allergen. The immune cells of the lungs create inflammation in response and that makes the airways narrower and more difficult to breathe through: this is an asthma attack (“Pathophysiology of Asthma). Eosinophils are abundant in the tissues of the lungs and release their granules when they are presented with an environmental trigger. These granules contain things like histamine and platelet activating factor which cause inflammation. The release of granules also causes the smooth muscle around the bronchioles to spasm and secrete mucus which narrows the airways even more. Substances that trigger these attacks can be air pollution, smoke, dust, mold, and pet dander (Morris). Patients with asthma have inflamed airways that are hypersensitive to allergens or triggers. Patients without asthma do not have hypersensitive airways, which is why they can inhale these allergens and have no reaction to it.
The prognosis of a patient with asthma is good if the patient treats their asthma. Even with treated asthma, a patient may miss work or school occasionally due to an attack. When children receive treatment for their asthma, it usually improves by late adolescence. Long-term with no treatment, patients can develop changes to their airways which could lead to chronic symptoms and more difficulty controlling the disease with treatment options. Over time, the airway begins to scar, and the membrane begins to thicken, which is irreversible. Patients who do not receive treatment are at a greater risk of mortality than those who receive treatment and control their asthma, although the mortality rate of asthma is low (Morris).
The pathway of asthma pathophysiology is very complicated and involves numerous cells and signaling molecules of the immune system while theories about asthma initiation are still controversial. 26 In general, it is believed that the disease is the result of complex interactions between genetic and environmental factors such as allergens, infectious agents, and pollutants. 27, 28
This peaks after about 30–60 minutes, after which spirometric measures generally return towards baseline.
3-5 ), mast cells, lymphocytes, monocytes, and neutrophils.This infiltration of inflammatory cells can vary with time, symptoms, treatments, and severity. We will review the respective roles of each of these cell types.
The late asthmatic response is delayed by hours. It is caused by a multitude of inflammatory cells continuing the inflammatory process. Of the inflammatory cells, the T cells play an important role. Antigen presenting cells may present a variety of allergenic antigens to chronically activated T helper cells.
Personalised care is an attempt to match each patient with the optimum intervention, guided by treatable traits and biomarkers. Currently, in primary care (point of care) there are limited biomarkers available with a greater range available in specialist care. Patient stratification is an element of personalised care which can be achieved in primary care, identifying those patients who remain uncontrolled in spite of structured assessment.
Macrophages. Macrophages can be seen in increased concentrations within the airway wall of asthmatic subjects, even though this level is far under what can be seen in chronic obstructive pulmonary disease (COPD) ( Fig. 3-9 ). Macrophages are mainly derived from recently migrated blood monocytes.
Mast Cells. Mast cells are leukocytes that are effectors of the inflammatory process ( Fig. 3-8). Rarely observed directly in the epithelium, they have been shown to have direct relationships with smooth muscle cells.
In association with the airway epithelium and underlingmucosa is a specialized population of antigen-presenting cells(APCs) called DCs (Holgate, 2012). As allergen sensitization, DCstake up the allergens and present small peptide from them. DCsexpress receptors of the innate immune system and process aller-gens into small peptides and then present them through the majorhistocompatibility complexes, MHC class I and MHC class II forrecognition by T cell receptors. In allergic individuals, it is pro-moted by interaction of the allergen with IgE attached to FcεRI,the high-affinity receptor for IgE (Sallmann et al., 2011). Whenindividual is born, there is no DCs in the airway. Damage to andactivation of the respiratory epithelium are the major stimuli thatinitiate the ingression of immature DCs from the bone marrow(McWilliam et al., 1994) and cause the release of C–C chemokineswhich direct DCs migration toward the epithelium and under-lying mucosa (Hammad et al., 2010). GM-CSF, which is releasedfrom epithelial cells and immune cells in the presence of IL-4 andTNF-α, leads to DCs maturation to a fully competent as APCs.During initial allergen entering to airways to sensitize, Th2 lym-phocyte differentiation from naïve T cells requires IL-4 release.The cellular source of the IL-4 is still unclear. There are somehypotheses to explain that (Holgate, 2012). Polarization to Th2cells subtype is also under epigenetic regulation. From the studywith mouse, microRNA-21 has been shown to exert a pivotal rolein setting a balance between Th1 and Th2 responses. It worksthrough binding the promoter of the gene encoding IL-12 p35and inhibiting its activation in favor of a Th2 profile. Conversely,reduced microRNA levels lead DCs to produce more IL-12, andallergen-stimulated T cells toproduce more interferon-γ(IFN-γ)and less IL-4, enhancing Th1 delayed-type hypersensitivity (Lu
The clinical phe-no type of asthma is notoriously heterogeneous. It is shown thatcellular immune process in the asthmatic airways inFigure 2.