NURS 6501: Week 6 Midterm Exam Question 10 / NURS-6501N Advanced Pathophysiology
  NURS 6501: MIDTERM EXAM: Please contact Assignment Samurai for help with NURS 6501: Midterm Exam or any other assignment. Email: assignmentsamurai@gmail.com   Which of the following best describes the pathophysiological mechanism of secondary hyperparathyroidism due to chronic kidney disease (CKD)? Group of answer choices
  • Decreased parathyroid hormone (PTH) secretion leading to hypercalcemia
  • Decreased renal activation of vitamin D leading to hypocalcemia and hyperphosphatemia
  • Increased renal phosphate excretion leading to hypophosphatemia
  • Increased calcium absorption in the gastrointestinal tract leading to hypercalcemia
  The correct answer is Decreased renal activation of vitamin D leading to hypocalcemia and hyperphosphatemia. Explanation: In chronic kidney disease (CKD), the kidneys lose their ability to properly activate vitamin D (specifically, the conversion of 25-hydroxyvitamin D to its active form, 1,25-dihydroxyvitamin D), which is crucial for calcium absorption in the intestines. This leads to hypocalcemia (low calcium levels) because less calcium is absorbed from the digestive tract. In response to hypocalcemia, the parathyroid glands secrete more parathyroid hormone (PTH), a condition known as secondary hyperparathyroidism. Additionally, impaired kidney function leads to an inability to properly excrete phosphate, leading to hyperphosphatemia (high phosphate levels). Why the other options are incorrect:
  • Decreased parathyroid hormone (PTH) secretion leading to hypercalcemia: In CKD, there is increased secretion of PTH, not decreased. The increased PTH is an adaptive response to low calcium levels and is associated with secondary hyperparathyroidism.
  • Increased renal phosphate excretion leading to hypophosphatemia: In CKD, the kidneys cannot adequately excrete phosphate, leading to hyperphosphatemia, not hypophosphatemia.
  • Increased calcium absorption in the gastrointestinal tract leading to hypercalcemia: In CKD, the impaired activation of vitamin D leads to decreased calcium absorption, not increased absorption. This contributes to hypocalcemia rather than hypercalcemia.
Conclusion: The pathophysiological mechanism of secondary hyperparathyroidism in CKD primarily involves decreased renal activation of vitamin D, which leads to hypocalcemia and hyperphosphatemia, stimulating increased PTH secretion as an adaptive response.