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    Ati lpn medical surgical proctored exam

    A nurse is reinforcing teaching for a client who has fibrocystic breasts about the use of acetaminophen. Which of the following statements should be included in the teaching?

    Explanation & Rationale

    Brief Introduction: Fibrocystic breast changes involve benign architectural alterations in glandular and stromal tissue, often characterized by fluid-filled cysts and fibrous nodules. Pathogenesis is linked to estrogen dominance or progesterone deficiency during the luteal phase, causing ductal proliferation and mastalgia. Acetaminophen is utilized as a first-line analgesic to manage the cyclical discomfort associated with these glandular fluctuations. Rationale: A. Acetaminophen is not a gastric irritant and does not require concomitant ingestion with food to prevent mucosal injury. Unlike nonsteroidal anti-inflammatory drugs, it does not inhibit protective prostaglandins in the stomach lining. It is rapidly absorbed in the small intestine regardless of the presence of a bolus within the gastric lumen. B. This medication is a standard pharmacological intervention for managing the somatic pain associated with breast tenderness. Clinical guidelines support the use of simple analgesics to mitigate the cyclical mastalgia that occurs during the menstrual cycle. It provides a safe and effective option for symptom control when used within the recommended therapeutic dosage. C. Many over-the-counter preparations for cough, cold, and sleep contain hidden acetaminophen, increasing the risk of accidental supratherapeutic ingestion. Chronic excessive intake can lead to fulminant hepatic failure through the accumulation of toxic metabolites like NAPQI. Patients must verify all ingredient labels to ensure the total daily dose remains below 4000 mg. D. Acetaminophen is an antipyretic and analgesic agent but lacks significant anti-inflammatory properties. It does not inhibit peripheral cyclooxygenase enzymes effectively enough to reduce interstitial edema or tissue swelling. Its primary mechanism involves elevating the pain threshold within the central nervous system rather than reducing localized physical mass or fluid retention.

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