A staff member asks a nurse to describe foam cells. The nurse's best response is that foam cells are
lipid-laden mast cells that have a soap-like texture.
macrophages that engulf low-density lipoproteins (LDLs).
injured neutrophil clots.
deposited adipose cells.
The Correct Answer is B
Choice A reason: Lipid-laden mast cells are not foam cells. Mast cells are immune cells that release histamine and other inflammatory mediators. They do not accumulate lipids or have a soap-like texture.
Choice B reason: Macrophages that engulf low-density lipoproteins (LDLs) are foam cells. They are part of the atherosclerotic process that leads to plaque formation in the blood vessels. They are called foam cells because they have a foamy appearance under the microscope.
Choice C reason: Injured neutrophil clots are not foam cells. Neutrophils are immune cells that fight infection and form pus. They do not engulf LDLs or contribute to atherosclerosis.
Choice D reason: Deposited adipose cells are not foam cells. Adipose cells are fat cells that store energy and secrete hormones. They do not phagocytose LDLs or form plaques in the blood vessels.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
Choice A reason: Jugular vein distention is a sign of right-sided heart failure, not left-sided. It indicates increased pressure in the right atrium and vena cava.
Choice B reason: Peripheral edema is also a sign of right-sided heart failure, not left-sided. It indicates fluid retention in the lower extremities and abdomen.
Choice C reason: Decreased systemic vascular resistance is not a characteristic of left-sided heart failure. It is a compensatory mechanism that occurs in response to reduced cardiac output.
Choice D reason: Pulmonary congestion is a characteristic of left-sided heart failure. It indicates fluid accumulation in the lungs due to the inability of the left ventricle to pump blood effectively.
Correct Answer is D
Explanation
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.
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