A nurse is preparing to teach the staff about asthma. Which information should the nurse include? Airway hyper-responsiveness in extrinsic asthma is related to:

Choice A reason: Hyperplasia and deformation of bronchial cartilage are not the causes of airway obstruction in COPD type B. Bronchial cartilage is the rigid structure that supports the bronchi, the large airways that branch from the trachea. Hyperplasia is an increase in the number of cells, and deformation is a change in the shape or structure of the cells. These processes can affect the bronchial cartilage, but they do not directly obstruct the airway.

Choice B reason: Loss of alveolar elastin is not the cause of airway obstruction in COPD type B. Alveolar elastin is the elastic fiber that allows the alveoli, the tiny air sacs at the end of the bronchioles, to expand and recoil during breathing. Loss of alveolar elastin is a characteristic of COPD type A (emphysema), which causes the alveoli to lose their shape and collapse. This reduces the surface area for gas exchange, but it does not obstruct the airway.

Choice C reason: Pulmonary edema is not the cause of airway obstruction in COPD type B. Pulmonary edema is the accumulation of fluid in the lungs, usually due to heart failure or lung injury. It causes shortness of breath, coughing, and crackles in the lungs. It can impair gas exchange and oxygenation, but it does not obstruct the airway.

Choice D reason: Thick mucus, fibrosis, and smooth muscle hypertrophy are the causes of airway obstruction in COPD type B. Thick mucus is the result of chronic inflammation and infection of the bronchi, which stimulates the mucus glands to produce more and thicker mucus. Fibrosis is the formation of scar tissue in the bronchial walls, which narrows the airway and reduces its elasticity. Smooth muscle hypertrophy is the enlargement of the smooth muscle cells that surround the bronchi, which increases the airway resistance and causes bronchospasm. These processes combine to obstruct the airway and cause chronic cough, wheezing, and dyspnea.

Choice A reason: Vasodilators are not the preferred agents for the initial treatment of heart failure. They are used as adjunctive therapy to reduce the afterload and preload on the heart. However, they do not address the fluid overload that is the main cause of heart failure symptoms.

Choice B reason: Diuretics are the preferred agents for the initial treatment of heart failure. They help to reduce the fluid overload and congestion in the lungs and peripheral tissues. They also lower the blood pressure and improve the cardiac output and renal function.

Choice C reason: Calcium channel blockers are not the preferred agents for the initial treatment of heart failure. They are contraindicated in most cases of heart failure because they can worsen the cardiac function and increase the mortality. They can also cause peripheral edema and hypotension.

Choice D reason: Direct renin inhibitors are not the preferred agents for the initial treatment of heart failure. They are a newer class of drugs that block the renin-angiotensin-aldosterone system (RAAS), which is involved in the pathophysiology of heart failure. However, they have not shown any significant benefit over the existing RAAS inhibitors, such as angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). They can also cause hyperkalemia and renal impairment.