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Hold propranolol for an apical pulse greater than 100/min. Beta blockers are typically held for bradycardia, commonly defined as an apical pulse below 50 to 60 beats per minute, depending on institutional policy. A pulse greater than 100/min may indicate the need for the medication rather than withholding it.

Administer propranolol to increase the client’s blood pressure. Propranolol lowers blood pressure by decreasing cardiac output and inhibiting renin release. Administering it to raise blood pressure is incorrect and reflects a misunderstanding of the drug’s pharmacologic effect.

Check for hypokalemia frequently due to the risk for propranolol toxicity. Propranolol is not associated with hypokalemia. In some cases, beta blockers may slightly increase serum potassium levels by reducing cellular uptake. Routine potassium monitoring is not required specifically for propranolol toxicity.

The propranolol can produce insulin resistance. While some beta blockers may modestly affect glucose metabolism, propranolol is not primarily associated with clinically significant insulin resistance; this is not the main safety concern requiring client education.

The two drugs used together will increase the risk of ketoacidosis. Propranolol does not precipitate diabetic ketoacidosis in insulin-dependent clients. Ketoacidosis risk is related to insufficient insulin or severe hyperglycemia, not beta-blocker therapy.

Propranolol will increase insulin requirements by antagonizing the effects at the receptors. Propranolol does not directly block insulin action at receptor sites. While it may mask hypoglycemia symptoms, it does not necessitate an automatic increase in insulin dosage.

“Hyperglycemia.” Amiodarone does not typically alter glucose metabolism or produce hyperglycemia. While thyroid dysfunction secondary to amiodarone can indirectly affect metabolism, hyperglycemia is not a primary or expected adverse effect.

“Dysphagia.” Difficulty swallowing is not a recognized effect of amiodarone. Any report of dysphagia should prompt assessment for unrelated conditions, such as esophageal disorders, rather than attributing it to the medication.

“Urticaria.” Cutaneous reactions to amiodarone are generally limited to photosensitivity, blue-gray skin discoloration, or rash, not urticaria. This option misrepresents the typical dermatologic effects of the drug.

“This is an expected side effect and should go away soon.” While amiodarone has common side effects such as photosensitivity and mild skin reactions, blue-gray pigmentation is not transient and may be permanent if exposure continues. Minimizing sun exposure and consulting the provider is necessary; stating it will resolve soon is inaccurate.

“This is a harmless effect. As long as the medication is working, we’ll just monitor your skin.” Blue-gray skin discoloration is clinically significant and indicates chronic photosensitivity and drug deposition, which warrants evaluation. Passive monitoring without provider notification is unsafe because it may precede other systemic toxicity.

“How much sun exposure have you had recently?” While sun exposure can exacerbate photosensitivity, asking this alone does not address the seriousness of the skin change or prompt provider notification, which is required for appropriate management.