What is the first-line bronchodilator medication used in the treatment of an acute asthma attack?
Salmeterol
Montelukast
Ipratropium bromide
Inhaled beta-agonist bronchodilator
The Correct Answer is D
A. Salmeterol is a long-acting beta-agonist used strictly for the long-term maintenance and prophylaxis of bronchospasm in chronic asthma or COPD. It possesses a delayed onset of action and does not provide the immediate smooth muscle relaxation required during a life-threatening acute exacerbation. Using a LABA as a rescue medication is contraindicated because it cannot rapidly reverse the acute narrowing of the airways.
B. Montelukast is a leukotriene receptor antagonist that provides anti-inflammatory benefits by inhibiting the late-phase response to allergens and exercise. It is an oral maintenance medication that requires daily administration to achieve therapeutic levels in the systemic circulation. It has no direct bronchodilatory effect and is therefore entirely ineffective for the immediate management of an acute, symptomatic asthma attack in an emergency.
C. Ipratropium bromide is an anticholinergic agent that provides bronchodilation by blocking muscarinic receptors in the large airways. While it is frequently used in combination with beta-agonists for severe asthma exacerbations, it is not considered the stand-alone first-line therapy. Its onset of action is generally slower than that of beta-agonists, making it an adjunctive rather than a primary rescue medication in most clinical protocols.
D. Inhaled short-acting beta-agonists, such as albuterol, are the first-line treatment for acute asthma due to their rapid onset within minutes. These medications bind to beta-2 adrenergic receptors on pulmonary smooth muscle cells, increasing intracellular cyclic AMP and causing immediate muscle relaxation. This swift physiological reversal of bronchoconstriction is essential for increasing airflow and resolving the acute respiratory distress associated with an asthma flare.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
A. Elevated high-density lipoprotein (HDL) cholesterol levels: HDL is often referred to as "good" cholesterol because it facilitates the transport of lipids from the tissues back to the liver. High levels of HDL are generally considered cardioprotective and are not a diagnostic criterion for dyslipidemia. Dyslipidemia typically involves a decrease in HDL, which contributes to an increased risk of atherosclerosis.
B. Decreased triglyceride levels: This is not a criterion for dyslipidemia; in fact, dyslipidemia is characterized by hypertriglyceridemia, or elevated levels of triglycerides. High triglyceride levels contribute to the thickening of arterial walls and increase the risk of pancreatitis. Clinicians look for elevations in these fatty acids when diagnosing metabolic syndrome or lipid disorders.
C. Normal total cholesterol levels: By definition, dyslipidemia involves abnormal lipid levels, so normal total cholesterol would not be used to meet the diagnostic criteria for this condition. A diagnosis requires at least one component of the lipid panel, such as LDL, HDL, or triglycerides, to be outside the healthy physiological range. Normal values indicate a healthy lipid metabolism.
D. Elevated low-density lipoprotein (LDL) cholesterol levels: LDL is the primary carrier of cholesterol in the blood and is highly associated with the development of atherosclerotic plaques when present in excess. An elevated LDL level is a central component of the diagnostic criteria for dyslipidemia. Reducing these levels is a primary goal of pharmacologic and lifestyle interventions to prevent cardiovascular disease.
Correct Answer is D
Explanation
A. Thrombus leading to myocardial infarction: A thrombus is usually a terminal event resulting from the rupture of an unstable plaque, leading to acute occlusion. While it causes infarction, it is not the primary long-term mechanism that develops coronary artery disease over many years. CAD is the underlying chronic condition, whereas a thrombus represents an acute complication of the pre-existing atherosclerotic disease process.
B. Impaired coronary artery dilation due to endothelial dysfunction: Endothelial dysfunction is an early physiological change in the CAD process where the vessel loses its ability to vasodilate via nitric oxide. While this contributes to the progression of the disease, it is considered a functional precursor rather than the physical disease itself. The primary structural cause of the disease mentioned in the question is the actual lesion formation.
C. Vasospasm causing transient myocardial ischemia: This describes Prinzmetal or variant angina, where the smooth muscle of the coronary artery wall contracts abnormally. While it can cause ischemia, it is not the standard mechanism driven by hypertension, hyperlipidemia, and diabetes. Those specific metabolic risk factors are classically linked to the accumulation of lipids and fibrous tissue within the arterial wall.
D. Atherosclerosis resulting in coronary artery narrowing: This is the definitive pathophysiological process where chronic inflammation and lipid accumulation form fibrofatty plaques within the intimal layer of the arteries. Hypertension and diabetes cause endothelial injury, allowing LDL cholesterol to penetrate the vessel wall. Over time, these plaques enlarge and obstruct blood flow, directly causing the clinical manifestations of coronary artery disease.
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