Respiratory conditions Flashcards
(5 cards)
What is the Pathophysiology of Asthma?
Asthma is a chronic inflammatory disease of the airways characterized by airway hyperresponsiveness, intermittent airflow obstruction, and bronchial inflammation. The pathophysiology involves an immune response-often triggered by allergens-where IgE antibodies activate mast cells, leading to the release of inflammatory mediators such as histamine, leukotrienes, and prostaglandins. These mediators cause bronchoconstriction (airway narrowing), increased mucus production, and airway edema. Over time, persistent inflammation leads to structural changes in the airway (remodeling), smooth muscle hypertrophy, and increased airway hyperreactivity, resulting in recurrent symptoms like wheezing, cough, and shortness of breath. Multiple immune cells-including eosinophils, T-helper (Th2) lymphocytes, and macrophages-contribute to the ongoing inflammation and tissue remodelling seen in asthma
What is the pathophysiology of COPD?
Chronic obstructive pulmonary disease (COPD) is characterized by persistent, poorly reversible airflow limitation resulting from chronic inflammation and structural changes in the lungs. The pathophysiology involves an abnormal inflammatory response to inhaled irritants-most commonly cigarette smoke-which triggers activation of neutrophils, macrophages, and other immune cells. This leads to an imbalance between proteases (enzymes that degrade connective tissue) and antiproteases, resulting in destruction of alveolar walls (emphysema), loss of elastic recoil, and narrowing and remodeling of small airways (chronic bronchitis and bronchiolitis).
Oxidative stress further amplifies tissue injury by promoting apoptosis, inactivating antiproteases, and stimulating mucus hypersecretion. The cumulative effects include increased airway resistance, air trapping, lung hyperinflation, impaired gas exchange, and, in advanced stages, pulmonary hypertension and systemic effects such as muscle wasting. These changes persist and progress even after cessation of exposure to irritants, underpinning the chronic and progressive nature of COPD
What is the Pathophysiology of a Pulmonary
Embolism?
Pulmonary embolism (PE) occurs when a blood clot-most often originating from the deep veins of the legs or pelvis-travels to and lodges in the pulmonary arteries, obstructing blood flow in the lungs. This blockage leads to a cascade of pathophysiological effects: the obstructed pulmonary vascular bed causes a mismatch between ventilation and perfusion, resulting in increased dead space, impaired gas exchange, and hypoxemia. The mechanical obstruction and subsequent hypoxic vasoconstriction increase pulmonary vascular resistance, raising pulmonary artery pressure and right ventricular afterload. As a result, the right ventricle may dilate and fail, reducing left ventricular filling and ultimately compromising cardiac output. Release of inflammatory and vasoactive mediators further exacerbates vasoconstriction and impairs surfactant function, contributing to respiratory distress and, in severe cases, cardiovascular collapse
What is the Pathophysiology of anaphylaxis?
Anaphylaxis is an acute, severe systemic hypersensitivity reaction most commonly triggered by an IgE-mediated immune response. Upon re-exposure to an allergen, antigen-specific IgE on mast cells and basophils cross-links, leading to rapid degranulation and release of mediators such as histamine, tryptase, leukotrienes, prostaglandins, and platelet-activating factor. These mediators cause widespread vasodilation, increased vascular permeability, and smooth muscle contraction, resulting in hypotension, tissue edema, bronchoconstriction, and, in severe cases, cardiovascular collapse and shock. Non-IgE-mediated mechanisms and direct mast cell activation by certain agents can also cause anaphylaxis. The cardiovascular and respiratory systems are most critically affected, with manifestations including airway narrowing, decreased cardiac output, and potential myocardial dysfunction
