Airway obstruction in COPD type B (chronic bronchitis) is due to
hyperplasia and deformation of bronchial cartilage
loss of alveolar elastin
pulmonary edema
thick mucus, fibrosis, and smooth muscle hypertrophy
The Correct Answer is D
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.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
Choice A reason: This is the correct mechanism of action of propranolol. Propranolol is a beta blocker medication, which means that it blocks the beta receptors in the heart and blood vessels. This reduces the sympathetic stimulation in cardiac muscle, which lowers the heart rate, contractility, and oxygen demand. This also reduces the renin release from the kidneys, which lowers the blood pressure.
Choice B reason: This is not the mechanism of action of propranolol. Propranolol does not increase the diuretic response in the renal tubules. This is the effect of diuretic medications, such as furosemide or hydrochlorothiazide, which increase the urine output and decrease the blood volume and pressure.
Choice C reason: This is not the mechanism of action of propranolol. Propranolol does not inhibit the conversion of angiotensin I to angiotensin II. This is the effect of angiotensin-converting enzyme (ACE) inhibitors, such as lisinopril or enalapril, which block the formation of angiotensin II, a potent vasoconstrictor that raises the blood pressure.
Choice D reason: This is not the mechanism of action of propranolol. Propranolol does not block alpha receptors throughout the body. This is the effect of alpha blockers, such as doxazosin or prazosin, which block the alpha receptors in the blood vessels and cause vasodilation, which lowers the blood pressure.
Correct Answer is D
Explanation
Choice A reason: Hereditary decrease in IgE responsiveness is not related to airway hyper-responsiveness in extrinsic asthma. IgE is an antibody that binds to allergens and triggers the release of histamine and other inflammatory mediators from mast cells. A decrease in IgE responsiveness would reduce the allergic reaction, not increase it.
Choice B reason: Increased sympathetic nervous system response is not related to airway hyper-responsiveness in extrinsic asthma. The sympathetic nervous system is the part of the autonomic nervous system that prepares the body for fight or flight. It stimulates the bronchodilation, or the widening of the airways, by activating the beta2 receptors on the smooth muscle cells. This would improve the airflow, not obstruct it.
Choice C reason: The release of stress hormones is not related to airway hyper-responsiveness in extrinsic asthma. Stress hormones, such as cortisol and adrenaline, are secreted by the adrenal glands in response to stress. They have anti-inflammatory and bronchodilator effects, which would reduce the symptoms of asthma, not worsen them.
Choice D reason: Exposure to an allergen causing mast cell degranulation is related to airway hyper-responsiveness in extrinsic asthma. Mast cell degranulation is the process of releasing histamine and other inflammatory mediators from the granules inside the mast cells. These substances cause bronchoconstriction, or the narrowing of the airways, by stimulating the smooth muscle contraction and mucus secretion. This leads to the symptoms of asthma, such as wheezing, coughing, and dyspnea.
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