Essay On Asthma

Lungs – Mucus plugging, chronic bacterial infections, pronounced inflammatory response, damaged airways leading to respiratory insufficiency, progressive decline in pulmonary function.

Bronchitis is the inflammation of the mucous membranes of the bronchi, the airways that carry airflow from the trachea into the lungs. The thin mucus lining of these airways can become irritated and swollen; the cells that make up the lining may leak fluids in response to the inflammation. Bronchitis most often occurs during the cold and flu season usually coupled with an upper respiratory infection. Bronchitis can be divided into two categories: acute or chronic each of which has distinct etiologies, pathologies, and therapies. I chose this condition because it seemed like an interesting topic to research on, and I am also interested in learning more

The presence of fluid in the alveolar space could potentially cause the lung capacity to be effected as well.

Discuss the roles of medications, ICS for long term anti-inflammatory effect and Beta adrenergic for immediate bronchial dilation.

According to the National Heart, Lung, and Blood Institute, Asthma is a chronic lung disease that affects the airways, which is comprised of tubes that carry air in and out of the lungs. People who experience difficulties breathing have inflamed airways. The inflammation causes the tubes to swell and become sensitive, especially when inhaling strong substances. As a result, the airways tighten and the muscles around the tubes become swollen and narrower. In addition, cells in the airways might produce more mucus. This sticky and thick mucus makes it even more difficult for air to pass into the lungs.

The bronchi and bronchiole tubes are loosely wrapped with muscle. During regular breathing, the muscles around these airways are relaxed (5). This allows air to flow freely through these passageways to the alveoli. However, during an asthma attack, air has trouble reaching the alveoli, which prevents the body from receiving oxygen. This is because the airways become smaller. Firstly, the muscles around the airways spasm and contract. This then causes inflammation of the bronchioles and bronchi themselves, which causes a mucus to be produced.

movement of water in tissues and maintain the fluidity of mucus and other secretions [3].

When the respiratory tissue damaged, the body’s inflammatory responses cause the lining of the airways to become swollen and thickened as a result of constant irritation that leads to an excessive mucus secretion in effort to protect the lungs from inhaled irritants such as cigarette smoking, air pollution, passive smoking, occupational dusts and chemicals (Currie 2009).

The World Health Organization (WHO) (2006A) defines COPD as a disease state characterized by airflow limitation that is not wholly reversible. The airflow limitation is usually both progressive and associated with abnormal inflammatory response of the lungs to noxious particles or gases. John's chronic bronchitis is defined, clinically, as the presence of a chronic productive cough for 3 months in each of 2 successive years, provided other causes of chronic cough have been ruled out. (Mannino, 2003). The British lung Foundation (BLF) (2005) announces that chronic bronchitis is the inflammation and eventual scarring of the lining of the bronchial tubes which is the explanation for John's dyspnea. The BLF (2005) believe that when the bronchi become inflamed less air is able to flow to and from the lungs and once the bronchial tubes have been irritated over a long period of time, excessive mucus is produced. This increased sputum results from an increase in the size and number of goblet cells (Jeffery, 2001) resulting in John's excessive mucus production. The lining of the bronchial tubes becomes thickened and an irritating cough develops, (Waugh & Grant 2004) which is an additional symptoms that john is experiencing.

Necrosis of the cells in the small, lower airways occurs, and mucous secretions are increased (Conquest, Cremonesini, & Neill, 2013). Because of the ciliary damage in the infants’ lungs, it is almost impossible for the secretions to be cleared. Bronchiolar level obstruction is caused by these mucosusal secretions, as is desquamation of the dead skin cells and edema (Conquest, Cremonesini, & Neill, 2013). Plugs of soughed, necrotic epithelium and fibrin in the airways will cause partial or total obstruction to airflow, making it very difficult for he infant to exhale which will consequently result in air becoming trapped and will reduce gaseous exchange (Conquest, Cremonesini, & Neill, 2013).

Until recently, it was thought that stimulation of lower airway rapidly adapting receptors (RARs) elicited cough 18. However, it has been shown that another population of airway sensory receptors that is found primarily in the larger airways is most likely responsible for cough 19. These sensory receptors are specifically termed cough receptors. Slowly adapting receptors have a permissive role in the production of tracheobronchial cough and a facilitatory role in laryngeal cough 20,21. The exact role of pulmonary C-fibers in the production of cough is more controversial, with some groups supporting an excitatory role 22 and others supporting an inhibitory role 23. Sensory information from these pulmonary afferents is processed in the brainstem, where the basic central elements responsible for the production of cough are located 11,12,14,16,24-27. Pulmonary vagal afferent information is processed by second order interneurons located near to and in various subnuclei of the NTS 28,29. These interneurons include pump cells, so called because their respiratory modulation is derived from lung SAR activity 30, laryngeal second-order relay neurons 31,32, and relay neurons mediating pulmonary C-fiber reflexes 32. Second order RAR interneurons are located in the commissural subnucleus of the NTS 28, but the role of RARs in regulating cough is currently

When someone sneezes, swallows or yawns their eustachian tube opens which allows the air to flow in and out of the passageway. If this passageway

In conclusion, the airway hyperresponsiveness, odema of bronchial mucosa, increase mucus secretion, bronchospam will lead to airway obstruction hence it will result in patient having wheezes and dyspnoea.

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.

Bronchitis is an inflammation and swelling of the respiratory tubes between the nose, throat and the lungs. These tubes include the trachea, the bronchi, and the bronchioles. Chronic Bronchitis is a serious long-term lung disease that can be caused by a long-term exposure to inhaled irritants such as cigarettes. Chronic Bronchitis is one of the conditions that correlates with Chronic Obstructive Pulmonary Disease (COPD). As the study shows M.K is noted to have a history of smoking for 22 years. Smoking is known to be the predominant cause associated with chronic bronchitis. Risk factors commonly lead to acute exacerbation and estimates suggest that cigarette smoking account for 85-90% of bronchitis and chronic obstructive pulmonary disease. Smoking impairs the ciliary movement, which obstructs the function of alveolar macrophages. M. K is also exhibiting chronic cough with severe sputum mainly in the morning. Chronic bronchitis is associated with excessive tracheobronchial mucus production sufficient to cause coughing. The alveolar epithelium is both the target and the initiator of inflammation because the airway epithelial cells release inflammatory mediators in response to toxic, infectious, and inflammatory stimuli which decrease the release of regular products such as angiotensin-converting enzyme or neutral endopeptidase. As the patient experiences sputum production, the sputum becomes purulent because of the presence of neutrophils increases the quantity of sputum