A. Notify the healthcare provider if anorexia occurs: Anorexia can be a side effect of exenatide, but it is generally mild and often transient. While persistent or severe anorexia should be reported, it is not the most immediate or dangerous concern compared to the risk of hypoglycemia when combining exenatide with a sulfonylurea like glimepiride.

B. Consume additional sources of potassium: Exenatide is not known to cause significant potassium depletion. Hypokalemia is not a common complication with either exenatide or glimepiride therapy, so there is no specific need to focus on increasing potassium intake.

C. Watch for signs of jitteriness or diaphoresis: Combining exenatide with glimepiride significantly increases the risk of hypoglycemia. Symptoms like jitteriness, diaphoresis, shakiness, and confusion are hallmark signs of low blood sugar, making it crucial to educate the client to recognize and manage hypoglycemia promptly.

D. Administer subcutaneously after meals: Exenatide should be administered subcutaneously, but it must be given before meals, typically within 60 minutes prior to eating. Administering it after meals would decrease its effectiveness in controlling postprandial blood glucose spikes.

• Pure opioid agonist: Morphine is classified as a pure opioid agonist because it fully binds and activates opioid receptors, particularly mu receptors, producing maximum analgesic effects for moderate to severe pain management.
• Mixed opioid antagonist: Mixed opioid antagonists, like nalbuphine, both activate and block opioid receptors depending on the site. Morphine does not block opioid activity; it purely stimulates, making this choice incorrect.
• Non-opioid analgesic: Non-opioid analgesics, such as acetaminophen and NSAIDs, relieve mild to moderate pain without acting on opioid receptors. Morphine’s mechanism and use are specific to the opioid class.
• Partial opioid agonist: Partial agonists, such as buprenorphine, activate opioid receptors but produce a weaker response compared to pure agonists. Morphine elicits a full receptor response, differentiating it from partial agonists.
• Mu: Mu receptors are the primary opioid receptors activated by morphine, leading to effects such as analgesia, euphoria, respiratory depression, and decreased gastrointestinal motility.
• Beta: Beta receptors are adrenergic receptors involved in cardiovascular responses, not pain modulation. Morphine does not interact with beta receptors.
• Alpha: Alpha receptors are also part of the adrenergic system and regulate vascular tone and blood pressure. Morphine’s action is not through alpha receptor activation.
• Severe pain: Morphine is most commonly used to treat moderate to severe acute or chronic pain, especially postoperative pain, cancer pain, and trauma-related injuries requiring strong opioid therapy.
• Hypertension: Morphine is not indicated for treating hypertension. While it may indirectly lower blood pressure due to vasodilation and reduced sympathetic tone, it is not a therapeutic antihypertensive agent.
• Depression: Morphine is not used for managing depression. Although it can induce feelings of euphoria, its clinical use is strictly for pain relief, not mood disorders.

A. Have a manual resuscitation bag at the bedside: Because morphine can cause respiratory depression, it is critical to have emergency resuscitation equipment readily available in case the client requires assisted ventilation during an adverse reaction.

B. Suction the client to clear the airway: Routine suctioning is not necessary unless the client has secretions impairing airway patency. It is not a standard precaution for clients receiving IV morphine without signs of airway obstruction.

C. Ask the client about other medications she takes: Morphine can interact dangerously with other medications, particularly sedatives, benzodiazepines, and other central nervous system depressants. Knowing the client’s full medication list helps prevent additive respiratory depression.

D. Perform a 12-lead electrocardiogram: A 12-lead ECG is not a standard requirement when starting morphine therapy unless there are cardiac symptoms. Continuous cardiorespiratory monitoring is already ordered, and that level of cardiac surveillance is sufficient unless new cardiac concerns arise.

E. Restrain the client with soft restraints: Restraints are not appropriate unless the client becomes a danger to herself or others. Administering morphine does not justify the prophylactic use of restraints and would violate ethical care standards.

F. Take an initial respiratory rate: An initial baseline respiratory rate is critical before starting or continuing morphine, as the drug’s main risk is respiratory depression. Ongoing respiratory assessments will be essential during PCA therapy.

A. Propofol: Propofol is a powerful sedative used mainly for anesthesia or sedation during mechanical ventilation. It is not appropriate or expected for routine postoperative pain management with morphine on a surgical floor.

B. Methadone: Methadone is another opioid used for chronic pain management or opioid dependency, not typically prescribed alongside morphine for acute postoperative pain because combining opioids increases the risk of respiratory depression.

C. Docusate sodium: Docusate sodium is a stool softener often prescribed with opioids like morphine to prevent constipation, a common opioid side effect. Promoting bowel movements is an important preventative measure in postoperative patients.

D. Ibuprofen: Ibuprofen, a nonsteroidal anti-inflammatory drug (NSAID), may be prescribed to provide additional pain relief through a different mechanism and reduce inflammation. This combination allows lower opioid doses, improving pain management while minimizing opioid side effects.

E. Naloxone: Naloxone is an opioid antagonist kept available as a safety measure in case of opioid-induced respiratory depression. Having naloxone ordered and readily accessible is a critical precaution during opioid therapy.

F. Senna: Senna is a stimulant laxative that can be prescribed along with docusate to prevent or treat opioid-induced constipation by actively stimulating bowel movements, making it a commonly expected medication alongside opioids.

A. Nausea: Morphine commonly causes nausea, which can lead to dizziness and unsteadiness when standing or moving. This increases the client’s risk of falls, especially when transitioning from bed to chair or ambulating postoperatively.

B. Euphoria: While morphine may cause a sensation of euphoria, this emotional effect alone does not directly contribute to physical instability or fall risk in the immediate postoperative period.

C. Itching: Itching is a common side effect of opioids but does not impair balance or mobility directly, so it is not a significant contributor to fall risk.

D. Orthostatic hypotension: Morphine can cause vasodilation, leading to drops in blood pressure when moving from lying to sitting or standing. Orthostatic hypotension can result in lightheadedness or fainting, sharply increasing the risk of falls.

E. Seizures: Seizures are rare side effects of morphine, typically associated with very high doses or toxicity. They are not in standard therapeutic use to be considered a primary fall risk factor.

F. Urinary retention: Urinary retention is a side effect of morphine but does not directly cause instability or contribute to falls unless it leads to urgency and hurried movement, which is less typical.

G. Sedation: Sedation is one of the most significant opioid side effects contributing to falls. Reduced alertness and slower reflexes make it much harder for clients to safely ambulate or protect themselves from falls.

A. Print an electrocardiogram strip: While cardiac monitoring is important, printing an ECG strip does not immediately address the critical issue of respiratory depression and unresponsiveness. Priority actions must focus on airway and breathing first.

B. Call for rapid response: The client is critically unstable with severe respiratory depression and unresponsiveness, meeting criteria for a rapid response or even a code blue if the situation deteriorates further. Immediate expert team support is crucial.

C. Perform chest compressions: Chest compressions are only indicated if the client is pulseless. In this case, the client has a heart rate of 92 beats/minute, meaning compressions are not appropriate at this moment.

D. Apply oxygen via nasal cannula: A nasal cannula would not deliver high enough oxygen concentrations for someone with a respiratory rate of 5 breaths/minute and oxygen saturation of 54%. Higher oxygen delivery methods and ventilatory support are urgently needed.

E. Give naloxone 2 mg intravenous push: Naloxone is indicated immediately to reverse opioid-induced respiratory depression. Giving the prescribed naloxone IV push can rapidly counteract the morphine overdose and improve the client’s respiratory effort.

F. Provide rescue breaths with a manual ventilation bag: Because the client’s respirations are critically low, rescue breathing with a manual resuscitation bag is necessary to maintain oxygenation and ventilation until naloxone takes effect or more advanced airway management is available.

Understanding:

• "You can give naloxone intravenously, intramuscularly, or subcutaneously."
• "If the first dose does not work, you can give as many doses as needed to reverse respiratory depression."
• "Naloxone works best on pure agonist opioids."

No Understanding:

• "Naloxone will not affect the client's level of pain."
• "When given IV, naloxone starts working immediately and can last several hours."

Rationale:

• "Naloxone will not affect the client's level of pain. This shows no understanding because naloxone blocks all opioid receptors, including those responsible for analgesia. Once naloxone is administered, the client's opioid-induced pain relief is lost, and pain will likely intensify unless managed separately.
• "You can give naloxone intravenously, intramuscularly, or subcutaneously." This shows understanding because naloxone is approved for IV, IM, and SC administration. IV is preferred for rapid effect in emergencies, while IM or SC may be used when IV access is delayed or unavailable.
• "When given IV, naloxone starts working immediately and can last several hours." This shows no understanding because naloxone’s onset is rapid when given IV (within 1–2 minutes), but its duration is short, generally lasting 30–90 minutes. It often requires repeated dosing to sustain reversal effects.
• "If the first dose does not work, you can give as many doses as needed to reverse respiratory depression." This shows understanding because multiple doses of naloxone may be necessary depending on the opioid’s half-life and the severity of respiratory depression. Repeated dosing ensures that ventilation is supported adequately.
• "Naloxone works best on pure agonist opioids." This shows understanding because naloxone is most effective against pure opioid agonists like morphine, heroin, and fentanyl. It competitively displaces these substances from opioid receptors, reversing their full agonist effects.

Rationale:
A. High triglyceride levels: Elevated triglycerides are a major risk factor for pancreatitis because they can cause pancreatic inflammation by leading to the accumulation of free fatty acids that injure pancreatic tissue. Clients with uncontrolled lipid levels require close monitoring while on medications like liraglutide.

B. Chronic alcohol use: Long-term alcohol consumption damages the pancreas directly by promoting inflammation and fibrosis, significantly increasing the risk of pancreatitis. Chronic use compounds the pancreatitis risk when the client is also taking medications like liraglutide that carry a pancreatic warning.

C. Gallstones: Gallstones can obstruct the pancreatic duct, leading to the backflow of digestive enzymes and resulting in pancreatic inflammation. A history of gallstones makes the client particularly vulnerable to developing pancreatitis while on incretin-based therapies like liraglutide.

D. Moderate daily alcohol use: Moderate alcohol intake is less strongly associated with pancreatitis compared to heavy or chronic use. Although any alcohol use can pose some risk, moderate consumption alone is generally not considered a primary risk factor for drug-induced pancreatitis.

E. Pancreatitis: A personal history of pancreatitis indicates previous pancreatic injury, making the pancreas more susceptible to future episodes. Starting liraglutide in someone with a history of pancreatitis requires extreme caution due to the increased likelihood of recurrence.

A. Promotes excretion of uric acid in the urine: Probenecid works by inhibiting the reabsorption of uric acid in the renal tubules, leading to increased urinary excretion of uric acid. This action helps lower serum uric acid levels, making it effective in the management of chronic gout and hyperuricemia.

B. Prevents the formation of kidney stones: Although lowering uric acid levels can indirectly reduce the risk of uric acid kidney stones, probenecid's primary mechanism is to promote uric acid excretion rather than directly preventing stone formation. Additional measures like hydration are typically emphasized for stone prevention.

C. Decreases pain and burning during urination: Pain and burning during urination are usually related to infections or inflammatory processes, not elevated uric acid. Probenecid does not have antimicrobial or analgesic effects and is not used to treat dysuria symptoms.

D. Increases the strength of the urine stream: Weak urine flow is commonly associated with bladder outlet obstruction or prostate issues. Probenecid does not act on the urinary tract muscles or prostate and has no role in improving the strength or flow of urination.

A. Observe the client for the presence of pain behaviors before the next analgesic dose is due: In a nonverbal client, observing for pain behaviors such as grimacing, restlessness, moaning, or changes in vital signs is crucial. If these behaviors increase before the next scheduled dose, it may suggest that the current analgesic regimen is becoming less effective, indicating tolerance.

B. Review the client's laboratory values for a change in the peak and trough levels of the analgesic: Peak and trough levels are useful for monitoring therapeutic ranges for certain medications but are not reliable indicators of analgesic tolerance. Tolerance is a clinical observation based on pain behavior, not solely on drug concentration measurements.

C. Prolong the interval between analgesic medication doses and monitor the client's vital signs: Extending the interval between doses risks undertreating the client’s pain and causing unnecessary suffering. Tolerance assessment should focus on evaluating pain control, not withholding medication to observe physiological responses.

D. Ask family members to report behaviors suggesting that the client's pain has returned: While family members can provide valuable insight, their observations should supplement, not replace, the nurse's direct clinical assessment. Family members may miss subtle signs of pain or misinterpret behaviors unrelated to pain.