Chronic Kidney Disease

Which scenario describes a drug-related risk for patients with kidney disease?

What happens to P04 levels in patients with kidney disease?

What effect does reduced kidney function have on calcium reabsorption?

How does high P04 and low Ca levels affect the release of PTH in patients with healthy kidneys?

What is the maximal action time for the serum potassium level to start trending down after insulin and glucose administration?

What is the recommended dose of albuterol via nebulizer for shifting potassium into cells?

What are the most common side effects of beta-agonists?

What is the recommended bolus of insulin with glucose for hyperglycemic patients to avoid worsening of hyperkalemia?

What is the effect of beta-agonists and insulin together in lowering potassium level?

What is the usual duration of the effect of insulin and glucose administration on serum potassium level?

What is the main reason for the ineffectiveness of inhaled beta-agonists in some patients?

In which patients is the use of bicarbonate therapy controversial?

Which type of phosphate binder is rarely used due to the risk of aluminum accumulation?

Which type of phosphate binder can lead to hypercalcemia, especially with concomitant use of vitamin D?

Which phosphate binder has no aluminum accumulation and less hypercalcemia but may cause other side effects?

Phosphate binders should be administered separately from which type of medication?

What is primarily used to treat elevations in parathyroid hormone (PTH) after controlling hyperphosphatemia?

Which medication mimics the actions of calcium on the parathyroid gland and reduces PTH?

What is primarily responsible for anemia in chronic kidney disease (CKD)?

What worsens bone disease and increases the risk of cardiovascular disease in CKD patients?

Which supplementation may be necessary, especially in early CKD stages?

What is the primary cause of anemia in CKD?

Which medication is used to reduce PTH and can cause hypocalcemia in dialysis patients?

Which mineral deficiency may worsen bone disease in CKD patients?

Which statement about anemia in chronic kidney disease is correct?

What is a risk associated with ESAs like epoetin alfa and darbepoetin alfa?

At what hemoglobin level should ESAs be discontinued?

What is essential for ESAs to be effective in treating anemia of CKD?

How is hyperkalemia defined?

What can increase the risk of hyperkalemia?

What are symptoms of hyperkalemia?

Which of the following drugs can raise potassium levels?

What is used to cause potassium to shift into cells in the treatment of severe hyperkalemia?

What is the role of calcium therapy in severe hyperkalemia?

What does insulin do in the treatment of severe hyperkalemia?

When should calcium therapy be administered in patients taking digitalis?

Patients with healthy kidneys do not experience bone demineralization and increased fractures due to increased release of PTH

In CKD, the kidneys can activate vitamin D to increase dietary calcium absorption

In CKD, drug accumulation may be unsafe due to increased risk of bleeding with some anticoagulants

In CKD, the kidneys can effectively increase calcium reabsorption in response to high P04 and low Ca levels

Insulin alone can be given to hyperglycemic patients to avoid worsening of hyperkalemia by hyperosmolar state

The recommended dose of albuterol via nebulizer for shifting potassium into cells is 10–20 mg

Sodium bicarbonate is recommended for patients without metabolic acidosis to reduce potassium levels

The effect of beta-agonists and insulin together is not additive in lowering potassium level

Bicarbonate therapy may cause hypernatremia, hypocalcemia, metabolic alkalosis, and hypervolemic state

Inhaled beta-agonists are usually ineffective in patients taking beta-blockers

The effect of beta-agonists and insulin together is generally ineffective in 30%–40% of patients for unknown reasons

Insulin and glucose administration has a maximal action on serum potassium level within 30–40 min

Phosphate binders are primarily used to increase the absorption of dietary phosphate in the intestine.

Aluminum-based phosphate binders are rarely used due to the risk of aluminum accumulation, which can cause toxicity.

Calcium-based phosphate binders can lead to hypercalcemia, especially with concomitant use of vitamin D.

Aluminum-free and calcium-free phosphate binders have no aluminum accumulation and less hypercalcemia.

Phosphate binders are known to have minimal drug interactions.

After controlling hyperphosphatemia, elevations in PTH are primarily treated with iron supplements.

Cinacalcet, a calcimimetic, is used in dialysis patients and can cause hypocalcemia.

Anemia in CKD is primarily due to a lack of erythropoietin (EPO) produced by the kidneys.

Vitamin D deficiency worsens bone disease and increases the risk of cardiovascular disease in CKD patients.

Supplementation with oral ergocalciferol or cholecalciferol may not be necessary in early CKD stages.

Phosphate binders are primarily used to block the absorption of dietary phosphate in the intestine.

Phosphate binders should be administered separately from certain medications such as levothyroxine and antibiotics.

Anemia of chronic kidney disease is also known as anemia of chronic disease

ESAs like epoetin alfa and darbepoetin alfa can prevent the need for blood transfusions without any risks

ESAs should only be used when hemoglobin is < 10 g/dL and discontinued if it exceeds 11 g/dL

High dietary potassium intake or use of drugs like ACE inhibitors cannot increase the risk of hyperkalemia

Insulin is effective in causing potassium to shift into cells by increasing Na–K-ATPase activity

Calcium therapy is used to prevent potential lethal arrhythmias in severe hyperkalemia, and it should be administered cautiously in patients taking digitalis

Adequate iron is not essential for ESAs to be effective in treating anemia of CKD

Hyperkalemia is defined as potassium level > 5.3 or > 5.5 mEq/L; kidney failure is not the most common cause

Treatment of severe hyperkalemia involves cardiac stabilization with calcium and shifting potassium into cells with insulin and glucose

Anemia symptoms and an inflammatory state in CKD are not contributed by decreased EPO production

Drugs that can raise potassium levels include ACE inhibitors, ARBs, and potassium supplements

Symptoms of hyperkalemia include muscle weakness, bradycardia, and fatal arrhythmias; severe cases do not require urgent clinical intervention

Which medication and dosage should be given to hyperglycemic patients to avoid worsening of hyperkalemia by hyperosmolar state?

What is the usual dose of albuterol via nebulizer for the treatment of hyperkalemia?

What are the most common side effects of beta-agonists?

In patients taking beta-blockers, inhaled beta-agonists are usually ineffective due to what reason?

What are the potential adverse effects of short-term bicarbonate therapy in patients without metabolic acidosis?

Why is the use of bicarbonate therapy controversial in patients without metabolic acidosis?

What is the additive effect of beta-agonists and insulin in lowering potassium levels?

What is the duration of the maximal action of insulin and glucose administration on serum potassium level?

What are the common scenarios related to medications and kidney disease?

What are the effects of high P04 and low Ca levels on PTH release in patients with healthy kidneys?

What happens to P04 levels in patients with kidney disease?

What is the primary cause of anemia in chronic kidney disease?

What is the term for declining kidney function leading to decreased EPO production, causing anemia symptoms and contributing to an inflammatory state in CKD?

What are the risks associated with ESAs like epoetin alfa and darbepoetin alfa?

When should ESAs be used and discontinued based on hemoglobin levels?

What is essential for ESAs to be effective in treating anemia of CKD?

What is the definition of hyperkalemia?

What are the symptoms of hyperkalemia?

What are the drugs that can raise potassium levels?

What is the treatment for severe hyperkalemia involving cardiac stabilization and shifting potassium into cells?

How does insulin cause potassium to shift into cells?

What is used to prevent potential lethal arrhythmias in severe hyperkalemia?

What is the most common cause of hyperkalemia?

What is the term for anemia of CKD, also known as anemia of chronic disease?

What are the three types of phosphate binders?

Why are aluminum-based phosphate binders rarely used?

What is the primary treatment for hyperphosphatemia in chronic kidney disease?

What can calcium-based phosphate binders lead to, especially with concomitant use of vitamin D?

What is the primary cause of anemia in chronic kidney disease?

What is the primary treatment for elevations in parathyroid hormone (PTH) after controlling hyperphosphatemia?

What is the role of Cinacalcet in reducing PTH?

What may worsen bone disease and increase the risk of cardiovascular disease in CKD patients?

What supplements may be necessary, especially in early CKD stages?

What mineral deficiency worsens bone disease in CKD patients?

What should phosphate binders be administered separately from?

What is the primary cause of anemia in CKD?