MCQ On Pathophysiology Of Asthma

Airway remodeling refers to the structural changes that occur in the airways of individuals with asthma. These changes can include thickening of the airway walls, increased smooth muscle mass, and excessive production of mucus. These alterations contribute to the long-term progression and severity of asthma symptoms. Therefore, it is accurate to say that airway remodeling is a significant factor in the pathology of asthma.

Susceptibility for asthma is not primarily determined in adulthood. Asthma is a chronic condition that can develop at any age, including childhood. While some individuals may develop asthma later in life, it is not solely determined in adulthood. Genetic factors, environmental exposures, and other factors can contribute to the development of asthma at any age.

Airway remodeling refers to the structural changes that occur in the airways of individuals with asthma over time. These changes can include thickening of the airway walls, increased smooth muscle mass, and excessive mucus production. While airway remodeling is typically associated with long-standing and severe asthma, research has shown that even young children with asthma can exhibit signs of airway remodeling. This suggests that the structural changes in the airways can occur early in the disease process and highlights the importance of early intervention and appropriate management of asthma in children.

Reversible lower airway constriction is a characteristic of asthma. This means that the narrowing of the airways in the lungs can be reversed with appropriate treatment. This is different from irreversible lower airway constriction, which would indicate that the narrowing cannot be fully reversed. Persistent symptoms are also a characteristic of asthma, but the specific characteristic being asked for in this question is the reversible nature of the lower airway constriction. Symptoms are not the same for every person with asthma, as they can vary in severity and presentation.

The correct answer explains that inflammation in relation to asthma is associated with airway remodeling. It states that inflammation is triggered by a stimulus and causes epithelial injury, among other things. This suggests that inflammation in asthma leads to changes in the structure of the airways and can cause damage to the epithelial cells lining the airways.

Clients with asthma may experience symptoms such as dyspnea (shortness of breath) and SOB (shortness of breath), chest tightness, cough, and wheezing. These symptoms are commonly associated with asthma and can vary in severity from mild to severe. Dyspnea and SOB refer to difficulty in breathing or feeling breathless, chest tightness is a sensation of pressure or discomfort in the chest, cough can be persistent and may worsen at night or with physical activity, and wheezing is a high-pitched whistling sound produced during breathing. These symptoms can be triggered by various factors including allergens, exercise, cold air, and respiratory infections.

Asthma is a chronic inflammatory disease of the airways that is characterized by airway hyperresponsiveness, infiltration of eosinophils into the airways, and increased mucus production. IgG immunoglobulins are not typically associated with asthma. IgE immunoglobulins, on the other hand, play a significant role in the pathophysiology of asthma by triggering an allergic response and causing inflammation in the airways. Therefore, an increase in IgG immunoglobulins is not a characteristic of asthma.

During the early phase of extrinsic asthma, several physiological changes occur in the airways. These include increased vascular permeability and bronchoconstriction, which lead to inflammation and narrowing of the airways. Additionally, the allergen triggers the binding of IgE receptors on the surface of airways, activating mast cells and releasing inflammatory mediators. However, decreased mucus secretion does not occur during the early phase of extrinsic asthma. In fact, mucus production usually increases as a protective response to the inflammation and irritation in the airways.

Exposure to airborne allergens, exposure to tobacco smoke, and genetic factors are all risk factors for the development of asthma. High exposure to airborne allergens can trigger asthma symptoms in individuals who are already susceptible to the condition. Exposure to tobacco smoke can irritate the airways and increase the risk of developing asthma. Genetic factors play a role in determining an individual's susceptibility to asthma, as it can be passed down through family members. High birth weight, however, is not considered a risk factor for asthma development.

During the initial stage of an asthma attack, there is an increase in the respiratory rate, leading to hyperventilation. This causes a decrease in the concentration of carbon dioxide (CO2) in the blood, resulting in respiratory alkalosis. However, if the asthma attack persists and the person is unable to get enough oxygen (O2), the body will switch to anaerobic metabolism, leading to an increase in the concentration of CO2 in the blood. This results in respiratory acidosis.

There is actually an increase in collagen and other protein deposition.

During the late phase of an extrinsic asthma event, there is actually an increased airway responsiveness rather than a decreased one. This is because the inflammatory mediators released during this phase cause the airway smooth muscles to contract, leading to narrowing of the airways and increased resistance to airflow. This increased airway responsiveness contributes to the symptoms of asthma such as wheezing, shortness of breath, and coughing.

Lung spirometry tests are used in the initial diagnosis and to evaluate treatment, they are used with bronchial provocation tests, and they evaluate the function of the lungs. However, the statement that is false is that their red zone is less than 90% of the expected value. In spirometry tests, the red zone typically represents a value below 60% or 80% of the predicted or expected value, indicating severe impairment.

Intrinsic asthma is a type of asthma that is not caused by allergies. It is characterized by triggers such as exercise, cold air, and hormonal changes. These triggers can lead to symptoms such as wheezing, coughing, and shortness of breath. Unlike extrinsic asthma, which is caused by allergies, intrinsic asthma is not triggered by allergens. Instead, it is triggered by factors such as physical activity, exposure to cold air, and hormonal fluctuations. Therefore, the correct characteristics of intrinsic asthma are that exercise, cold air, and hormonal changes can all act as triggers for asthma symptoms.

Extrinsic asthma is characterized by two distinct phases, the early and late phases. In the early phase, an immediate allergic response occurs when the individual is exposed to an allergen. This leads to the release of inflammatory mediators, such as histamine, causing symptoms like wheezing, coughing, and shortness of breath. The late phase follows the early phase and is characterized by a prolonged inflammatory response. During this phase, additional inflammatory cells are recruited to the airways, leading to further airway narrowing and persistent symptoms.

Extrinsic asthma is characterized by airway hyperresponsiveness, which means that the airways in the lungs are easily irritated and constrict in response to certain triggers. This type of asthma is also associated with IgE hypersensitivity mediation, where the immune system overreacts to allergens, causing inflammation and narrowing of the airways. Additionally, extrinsic asthma is often triggered by allergies, such as pollen, dust mites, or pet dander, leading to symptoms such as wheezing, coughing, and shortness of breath.

On a chest x-ray of someone with asthma, hyperinflation may be seen. This refers to an abnormal increase in the size of the lungs, indicating air trapping and difficulty in exhaling. Additionally, an increase or decrease in flattening of the hemidiaphragms may be observed. The hemidiaphragms are the muscles that separate the chest cavity from the abdominal cavity, and their flattening can be a sign of increased air pressure in the lungs. These findings are characteristic of asthma and can help in diagnosing and monitoring the condition.

Adult-onset asthma is a form of asthma that develops in adulthood, typically after the age of 20. The risk factors mentioned in the answer are known to contribute to the development of adult-onset asthma. Occupational exposure to irritants, such as chemicals or dust, can trigger asthma symptoms in adults. Smoking, both active and passive, is a well-known risk factor for asthma. Obesity is also associated with an increased risk of developing asthma in adulthood. Hormonal influences, such as changes in estrogen levels, can play a role in the development of asthma. Lastly, exposure to pollutants and infectious agents can also contribute to the development of adult-onset asthma.

When mast cells degranulate, they release various inflammatory mediators. Histamine is one of the mediators released, which causes vasodilation and increased vascular permeability. Leukotrienes are also released, which are lipid mediators that promote inflammation and bronchoconstriction. Prostaglandin D2 is another mediator released, which has pro-inflammatory effects. Chemotactic chemokines are released to attract immune cells to the site of inflammation. TNFa, or tumor necrosis factor alpha, is a cytokine released by mast cells that promotes inflammation and can induce cell death.

Mast cell stabilizers and inhaled corticoid steroids are considered long-term pharmacotherapy for asthma. Mast cell stabilizers, such as cromolyn sodium, work by preventing the release of inflammatory substances from mast cells, reducing airway inflammation and preventing asthma symptoms. Inhaled corticosteroids, such as fluticasone and budesonide, are the most effective long-term control medications for asthma. They work by reducing airway inflammation and suppressing the immune response, helping to prevent asthma attacks and improve overall asthma control. Systemic corticosteroids are typically used for short-term relief of severe asthma symptoms, while anticholinergics are used as a bronchodilator to relax the airway muscles.

During an asthma attack, air becomes trapped with impaired function, and hyperinflation ensues. Alveolar hypoventilation occurs due to increasing interpleural and alveolar gas pressure. Hyperventilation is triggered. Ventilation/perfusion mismatch occurs. First alkalosis occurs due to decreased CO2 concentration in the blood, but the resulting hypoventilation eventually causes acidosis. Respiratory failure can result.

The clinical signs of asthma include wheezing heard on auscultation, vital signs such as tachypnea (rapid breathing) and decreased oxygen saturation levels, increased work of breathing observed, and the ability to maintain a conversation with the healthcare provider. These signs indicate the presence of respiratory distress and narrowing of the airways, which are characteristic of asthma. Shortness of breath and chest tightness are symptoms of asthma rather than clinical signs, as they are subjective experiences reported by the patient.

Short-acting bronchodilators, anticholinergics, and systemic corticosteroids are all considered short-acting pharmacotherapy options for asthma. Short-acting bronchodilators, such as albuterol, provide quick relief by relaxing the muscles around the airways. Anticholinergics, like ipratropium, also help relax the airway muscles and can be used as a short-term treatment for asthma symptoms. Systemic corticosteroids, such as prednisone, are used for short periods to reduce inflammation and improve asthma control. These medications are typically used in combination with long-term control medications for asthma management.