Pathology of Asthma and its Symptoms Essays

Asthma itself is an inflammatory disease characterized by increased airway responsiveness due to a variety of stimulus. The inflammation causes the hyper-responsiveness than in turn causes bronchiolar smooth muscle constriction, resulting in obstruction of airflow. Some

The innate and adaptive immune response start with exposure to an antigen in the epithelium of

Asthma is the most common childhood condition in Australia (Better Health Channel, 2015). The National Institute of Health [NIH] (2014), describes asthma is a chronic long-term lung disease that causes a person’s airways to swell and become very sensitive. The airways are tubes that carry air into and out of a person’s lungs. When theses airways react to certain stimuli, the muscles around them tighten, narrowing the airways and causing less air to flow to the lungs. When this occurs, cells in the airways can also make more mucus than usual, which causes a sticky, thick liquid to be excreted and further narrows the swollen airways. This process is all caused when the person inhales certain substances that aggravate the sensitive airways.

Asthma is a chronic lung disease characterized by episodes in which the bronchioles constrict due to oversensitivity. In asthma, the airways (bronchioles) constrict making it difficult to get air in or out of the lungs. Breathlessness is the main symptom. The bronchi and bronchioles become inflamed and constricted. Asthmatics usually react to triggers. Triggers are substances and situations that would not normally trouble an asthma free person. Asthma is either extrinsic or intrinsic. Extrinsic is when the inflammation in the airway is a result of hypersensitivity reactions associated with allergy (food or pollen). Intrinsic asthma is linked to hyper responsive reactions to other forms of

Asthma is a disease of the lungs that can be influenced by different genes or alleles. When the epithelial or mucosal barrier is exposed to pollens, allergens, microbes or pollutants, these can stimulate the underlying antigen presenting cells (APC) which causes an immune response to occur.17 This can cause a cell influx into the airway that is primarily eosinophilic or neutrophilic. When the allergens present themselves, they can initiate a breakdown in the physical barriers, causing further allergic, inflammatory responses.

Etiology Preexisting compromised lung function from uncontrolled bronchitis, asthma, and emphysema can develop overtime. Environmental conditions can exacerbate the disease and hasten the progression toward COPD. One of the primary causes and leading exacerbations is viral infections. In the subzero climates of cold and flu season when rhinovirus and various forms of upper respiratory infections run rampant through many cities, patients with chronic lung issues have an increased risk for contracting infections. Viruses attach to the lower lobe of the lung via the intracellular adhesion molecule, ICAM-1, and intensify the underlying inflammation. The ICAM-1 molecule can be a target for treatment when symptoms are caused by the rhinovirus. When COPD is aggravated because of rhinovirus, plasma fibrinogen levels and molecules known to stimulate the production of plasma fibrinogen elevate and can increase the onset of myocardial infarction and stroke. These levels not only worsen COPD for patients, but put them at increased risk for cardiovascular

Inflamed bronchioles may become over sensitive to allergens or irritants. The airways may become irascible this is called hypersensitive phase of asthma. Asthmatics and allergic individuals have higher risk of bronchial hyperactivity than non-asthmatic and no allergic people. In sensitive individuals, there are 2 times more chances of airways swelling and constriction when they come in contact with triggers such as allergens, cigarette smoke and level of physical activity. In asthma patients, some may have lenient symptoms while other may have critical and drastic symptoms.

The virus attacks the respiratory system, especially the lungs and sinuses. When the virus attacks the system, it causes inflammation to the surrounding tissues leading to heavy congestion and a sticky yellow mucus. This mucus is meant to soothe the friction within the tissues and to expel the virus with drainage through the nose and also through the

The pathophysiology of Asthma includes inflammation of the airway. The way in which this works is from an irritant which can include dust, pollen, cedar, or cat hair. When a reaction occurs, the airways become inflamed and narrow. The narrowing occurs because once the inflammatory response is triggered by an irritant, histamines, immunoglobulin E antibodies, and leukotrienes are released. Because of this, mucous production occurs. Since the bronchioles are inflamed and narrow, breathing becomes difficult. Wheezing sounds can be heard due to the lack of air being able to easily move in and out of the narrowed bronchioles.

Many immune cells and mediators have been identified and the connection between them is very complex. The severity and response to treatment varies widely among individuals making asthma a heterogeneous disease in both its severity and presentation. Some common allergens that can trigger the asthmatic inflammatory response include pollen, dust mites, animal dander and fungi. Airway epithelium is normally the first line of defense against external pathogens or stimuli, but in asthmatic patients, the epithelium’s barrier function is defective due to incomplete formation of tight junctions between the epithelial cells, which allows pathogens to permeate the airways more easily (Kudo et al. 2013). Dendritic cells are the body’s next line of defense once foreign pathogens have invaded the body. Upon exposure to and inhalation of an allergen, Dendritic cells detect the antigen, bind to it and travel to the lymph nodes, where they will present the antigen to naïve T-

Human rhinovirus (HRV) infections are major risk factors for asthma and chronic obstructive pulmonary disease (COPD) [1-4]. The airway epithelial cell is the dominant site of HRV infections in vivo [5,6], and both upper and lower airway epithelial cells are infected at a similar frequency [7].

Analysis of bronchoalveolar lavage fluid and lung tissue will quantify IFNα and TH2 cytokine expression and AHR will be assessed with methacholine doses. This study will show IRF7-mediated signaling by pDC to be crucial for appropriate responses to viral infection and thus can be used as a novel therapeutic target for prevention and treatment of viral-induced asthma.

Uncomplicated GAS strains, those not displaying emm gene that encode for the M protein, have an asymptomatic initial infection but more virulent strains can lead to sudden-onset fever and inflammation of the pharynx and tonsil. Duration of a primary infection is 2-5 days irrespective of the presence of an antibiotic therapy. However, in the case of persistent symptoms it is recommended to perform a rapid antigen test and an inoculate a differential growth medium (Blood Agar) with the bacterium to detect the deadly GAS Beta hemolytic pathogen as these strains can cause systemic hemorrhage in untreated GAS pharyngeal infections. Post infectious sequelae may occur If the GAS strain of the initial infection is positive for the virulence factor M protein resulting in an antibody-mediated autoimmune inflammatory response. Certain self-antigens of the heart, synovial, skin, and brain become susceptible to this autoimmune response since they have remarkable structural and sequential homology amino acid sequence to GAS M protein. T cells recognize epitopes in these self-antigens with equal or more priority than the M protein epitopes (Repeat B Region). While B cells recognize homologous non-identical amino acid sequence and epitopes. Studies have long supported the link between Acute Rheumatic Fever as an autoimmune disease with an involvement of

Release of chemotactic and toxic mediators causes activation of macrophage and degranulation of mast cells, which can lead to an inflammatory response that is at the highest level in airway remodeling.5 It brings about subepithelial thickening, and changes of mucous glands and smooth muscles structure.5,12 In addition, there is some evidence in bronchial biopsies of the cases with acute-onset of IIA, including epithelial desquamation (denuded epithelium), significant detected number of lymphocytes (mononuclear inflammation), airway remodeling, collagen deposition in the bronchial wall (edematous mucosa).5,15,70 These types of alterations have been reported in the experiments with animal models as well.71 Furthermore, studies revealed that there are other alterations in this type of asthma, such as mucosal squamous cell metaplasia, basement membrane

The first disease is common cold, with ICD-10 Code of J00. It is also known as nasophayngitis or rhinopharyngitis, which is a viral infectious disease of upper respiratory tract that affect the nose primarily. Most commonly, it is caused by rhinovirus (30-80%). Other virus include human coronavirus (15%), influenza virus (10-15%) and adenovirus(5%). Symptoms include coughing, sore throat, sneezing, runny nose and fever which will usually resolve in 7 to 10 days.1,5