A nurse is preparing to administer Lactated Ringer's 1000 mL IV to infuse over 6 hours. The drop factor of the manual IV tubing is 10 gtt/mL. What is the flow rate in gtt/min? (Round to the nearest whole number & fill in the blank with the numerical value only)

A. Cardiotoxicity: While NSAIDs can contribute to cardiovascular risks such as hypertension and fluid retention, nephrotoxicity is the more direct explanation for the elevated kidney function tests and potassium level. Cardiotoxicity typically presents with symptoms like heart failure or arrhythmias rather than kidney-related lab abnormalities.
B. Nephrotoxicity: NSAIDs inhibit prostaglandin synthesis, which plays a key role in maintaining renal blood flow, especially in older adults or those with preexisting renal impairment. Chronic NSAID use can reduce glomerular filtration, leading to elevated creatinine, hyperkalemia, and worsening blood pressure control, all of which are evident in this patient.
C. Neurotoxicity: Neurotoxic effects are not commonly associated with NSAID use. Symptoms of neurotoxicity include confusion or seizures, which are not relevant to the clinical findings in this scenario.
D. Hepatotoxicity: NSAID-induced liver injury is rare and would typically present with elevated liver enzymes (AST, ALT), not elevated creatinine or potassium. The current lab findings and blood pressure changes are more consistent with kidney involvement.

• Losartan: As an angiotensin II receptor blocker (ARB), losartan reduces aldosterone secretion, leading to decreased potassium excretion and potential hyperkalemia, especially in patients with renal impairment or those on potassium supplements.

• Furosemide: This loop diuretic promotes the excretion of sodium and potassium in the urine, commonly resulting in hypokalemia. Patients on furosemide often require potassium monitoring or supplementation.
• Spironolactone: A potassium-sparing diuretic and aldosterone antagonist, spironolactone reduces potassium excretion in the distal nephron. This can lead to hyperkalemia, particularly when used with other potassium-elevating drugs.
• Lisinopril: An ACE inhibitor that blocks the conversion of angiotensin I to II, reducing aldosterone levels and thereby decreasing potassium excretion. This places patients at risk for hyperkalemia.
• Digoxin: This cardiac glycoside may cause hypokalemia indirectly by increasing sensitivity to potassium shifts. Additionally, low potassium levels enhance digoxin toxicity, so maintaining normal potassium is critical during therapy.