Q1. Which patient requires tighter control of dietary potassium renal insufficiency or hemodialysis? Why? Q2. How does sodium affect the hormonal control of BP? Q3. What are acute phase reactants and how do they impact your ability to interpret lab values? Q4. What is your recommendation for a pt. with 8.8 PAB, stage 4 pressure ulcer with kidney insufficiency? defend your answer Q5. What is the significance of a lab value’s half-life? How would you use that information to assess the lab value? Q6. Which labs are adversely affected by dehydration? Q7. What are the possible causes of decreased chloride levels? Q8. What might high levels of bilirubin indicate? Q9. How does chronic renal disease effect BUN? How would you differentiate chronic renal disease from dehydration? Q10. How does low serum protein levels impact serum calcium? How would you interpret these labs? Tight Control of Dietary Potassium in Renal Insufficiency and Hemodialysis: Understanding the Difference

Hemodialysis and renal insufficiency: A tight control of dietary potassium 

Hemodialysis and patients suffering from renal insufficiency require different methods of dietary potassium control. A decrease in the glomerular filter rate (GFR), which is most commonly associated with renal insufficiency, is often responsible for hyperkalemia. Patients with renal impairment need to be careful about their potassium intake in order to avoid hyperkalemia. Patients on hemodialysis might have a normal GFR, but are not at increased risk of hyperkalemia. Due to the dialysis-related complications of intradialytic hypotension, volume overload, and high solute loads, hemodialysis patients need to be very careful with their potassium intake (Charytan, et al. 2016). Due to its impact on fluid balance and electrolyte imbalance, sodium can have a direct influence on blood pressure. Sodium intake may increase BP through an increase in intravascular volume. This can lead to increased cardiac output (SVR) and increased systemic vascular resistance. In addition, sodium also affects BP indirectly through its effect on the renin-angiotensin-aldosterone system (RAAS). The RAAS (Renin-angiotensin-aldosterone system) is an important hormone system. It is activated by decreased sodium. In turn, this causes increased aldosterone levels and vasopressin which in turn can increase BP. Cont…