Which of the following clients is at a higher risk of developing osteoarthritis?
A client who has hypertension and is taking amlodipine
A client who has COPD and has been on frequent courses of prednisone
A client with atrial fibrillation who is taking warfarin
A client who is Caucasian and has had multiple child
The Correct Answer is B
A. Amlodipine is a calcium channel blocker used to manage hypertension. It is not associated with an increased risk of osteoarthritis. While hypertension itself is a health concern, amlodipine does not directly contribute to the development of OA.
B. Prednisone is a corticosteroid that can lead to various side effects, including bone loss and osteoporosis with long-term use. Although osteoporosis and OA are different conditions, long-term use of corticosteroids can potentially increase the risk of joint issues and contribute to the development or exacerbation of OA due to the impact on joint cartilage and bone density.
C. Warfarin is an anticoagulant used to prevent blood clots in atrial fibrillation. It is not directly associated with an increased risk of osteoarthritis. The primary concerns with warfarin involve bleeding risks rather than joint health.
D. Being Caucasian and having multiple children do not directly contribute to an increased risk of osteoarthritis.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
A. Otitis media is an infection or inflammation of the middle ear. This condition primarily affects the middle ear structures and can cause conductive hearing loss, which is due to problems with sound transmission through the outer or middle ear.
B. An injury to the eardrum, such as a perforation, can lead to conductive hearing loss. This occurs because the eardrum (tympanic membrane) is crucial for transmitting sound waves from the outer ear to the middle ear. While an eardrum injury affects sound transmission, it does not directly damage the inner ear or auditory nerve, so it does not typically cause sensorineural hearing loss.
C. Exposure to loud noise is a common cause of sensorineural hearing loss. Prolonged or intense noise exposure can damage the sensory hair cells in the cochlea or the auditory nerve pathways, leading to permanent hearing loss. This type of hearing loss is due to damage in the inner ear or auditory nerve rather than the outer or middle ear structures.
D. Impacted earwax can cause conductive hearing loss by blocking sound transmission through the ear canal. This type of hearing loss is due to a blockage and is usually reversible once the wax is removed. It does not cause sensorineural hearing loss, which involves damage to the inner ear or auditory nerve.
Correct Answer is A
Explanation
A. The late-phase response in asthma is characterized by a delayed and prolonged inflammatory reaction that can occur 4 to 6 hours after exposure to a trigger. It involves the recruitment of additional inflammatory cells, such as eosinophils and T cells, which contribute to ongoing airway inflammation, increased mucus production, and bronchoconstriction. This phase often leads to a return of symptoms or worsening of symptoms after the initial relief provided by a rescue inhaler.
B. The late-phase response does not typically respond as well to rescue inhalers (such as albuterol) as the early-phase response does. Rescue inhalers are primarily effective for the immediate, bronchospastic component of asthma (early-phase response).
C. The late-phase response occurs as part of the natural progression of asthma inflammation and is not necessarily related to improper use of a rescue inhaler. Even with proper use of a rescue inhaler, the late-phase response can still occur due to the underlying inflammatory processes.
D. The late-phase response can occur even if the trigger is no longer present. It is related to the ongoing inflammatory process rather than continued exposure to the trigger. Although continued exposure to triggers can exacerbate symptoms, the late-phase response can still occur independently of further exposure.
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