A nurse is educating a client with sinusitis about the correct use of nasal decongestants. What should the nurse emphasize?
Avoid combining decongestants with antihistamines for allergy management.
Take the medication every 4 hours, regardless of symptom relief.
Discontinue decongestant use as soon as symptoms appear to resolve completely.
Use nasal decongestants for no more than 3 to 5 days to avoid rebound congestion.
The Correct Answer is D
A. Avoid combining with antihistamines: Many allergy regimens safely combine decongestants for acute relief with antihistamines for long-term symptom control. There is no contraindication to using these two classes together to address different pathways of the allergic response. They provide additive benefits for the patient.
B. Take every 4 hours regardless of symptoms: Decongestants should be used sparingly and only when symptomatic to minimize systemic absorption and local irritation. Frequent, scheduled dosing increases the risk of side effects like tachycardia and hypertension. Using them on an "as-needed" basis is the safer clinical approach.
C. Discontinue as soon as symptoms resolve: While this is true for most symptomatic treatments, the specific instruction for decongestants must focus on the maximum duration of use. Even if symptoms persist, the patient must stop after 5 days to avoid rebound effects. The duration of therapy is more critical than the resolution of symptoms.
D. Use for no more than 3 to 5 days: Intranasal sympathomimetics provide rapid relief by constricting nasal blood vessels, but prolonged use leads to down-regulation of alpha-adrenergic receptors. This results in severe rebound vasodilation and mucosal edema when the drug is stopped. Limiting use prevents the development of rhinitis medicamentosa.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
A. Decreased alveolar surface area:Senescence involves the progressive loss of alveolar walls, leading to a reduction in the total surface area available for gas exchange. This anatomical change reduces the diffusion capacity for oxygen, particularly during periods of increased metabolic demand. It is a hallmark of the aging respiratory system.
B. Increased lung elasticity:Aging actually results in a loss of elastic recoil due to the degradation of elastin fibers within the lung parenchyma. This leads to premature airway closure during expiration and increased air trapping, rather than improved elastic function. Reduced elasticity makes the work of breathing more difficult for the elderly.
C. Thickening of capillary membranes:While some vascular changes occur, the primary age-related defect is the structural alteration of the alveoli and chest wall. Capillary membrane thickening is more characteristic of specific pathologies like pulmonary fibrosis rather than normal physiological aging. It is not the most likely contributing factor in healthy aging.
D. Enhanced mucociliary clearance:The aging process is associated with a decrease in the number and functional efficiency of cilia in the respiratory epithelium. This impaired clearance mechanism increases the risk of retained secretions and pulmonary infections. Enhanced clearance would be a protective factor rather than a cause of dyspnea.
Correct Answer is D
Explanation
A. Increased bronchial diameter: Chronic bronchitis is characterized by obstructive changes that decrease rather than increase the airway lumen. Chronic inflammation leads to wall thickening and smooth muscle hypertrophy, which increases resistance to airflow. This pathological narrowing contributes significantly to the patient’s expiratory effort and dyspnea.
B. Alveolar destruction: The breakdown of alveolar walls and loss of elastic recoil are the primary pathophysiological hallmarks of emphysema rather than chronic bronchitis. While both conditions often coexist in COPD, bronchitis specifically involves the conducting airways. Alveolar destruction leads to permanent air trapping and impaired gas exchange.
C. Overproduction of surfactant: Surfactant is a lipoprotein that reduces surface tension to prevent alveolar collapse during expiration. In chronic inflammatory lung diseases, surfactant function is often impaired or inhibited by inflammatory exudates rather than being overproduced. Overproduction is not a recognized feature of the bronchitic disease process.
D. Decreased ciliary function: Chronic inhalation of irritants causes squamous metaplasia of the epithelium and direct damage to the mucociliary escalator. This impairment prevents the effective clearance of the excess mucus produced by hypertrophied goblet cells. The resulting stasis of secretions leads to the characteristic persistent productive cough.
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