Secondary or Tertiary Hyperparathyroidism1 Flashcards
What is secondary parathyroidism?
Secondary hyperparathyroidism refers to increased PTH production due to external factors that stimulate the parathyroid glands to enlarge and secrete PTH.
What is the most common cause of secondary parathyroidism?
Chronic renal failure
What are other less common causea of secondary parathyroidism?
Gastrointestinal malabsorption, vitamin D deficiency, osteomalacia, rickets, malnutrition, osteoporosis, hypermagnesuria, and idiopathic hypercalciuria.
What is tertiary hyperparathyroidism?
Autonomous hypersecretion of PTH even after the cause of secondary HPT has been corrected (i.e., after kidney transplantation with normal renal function in patients with history of chronic renal failure), or when patients with secondary HPT develop refractory hypercalcemia.
In secondary hyperparathyroidism, what are the lab findings?
Hypocalcemia, hyperphosphatemia
What is the cause of hyperphosphatemia in secondary hyperparathyroidism and how this affect the calcium level?
Results from the kidneysﾒ inability to excrete phosphorus, retention of which potentiates hypocalcemia by lowering the levels of ionized calcium in the blood and interfering with the production of 1,25(OH)2D3.
What is the nonoperative management of secondary hyperparathyroidism?
Nonoperative treatment consists of dietary modifications and medical therapy. Dietary control entails restriction of phosphate intake to between 800 to 1000 mg/day when the serum phosphorus concentrations are elevated (>4.6 mg/dL for stages 3 and 4 and >5.5 mg/dL for stage 5), or when the PTH level is higher than the target range for the stage of renal failure (>70 pg/mL for stage 3, >110 pg/mL for stage 4, and >300 pg/mL in stage 5). Deficiencies in serum calcium and vitamin D are corrected by supplementing normal dietary intakeﾠ
What medical therapy can be used for the hyperphosphatemia in patients with secondary hyperparathyroidism?
Hemodialysis is usually effective at decreasing the blood phosphate concentrations in the majority of these patients; however, phosphate binders are added when dietary phosphorus restriction and dialysis cannot effectively control the hyperphosphatemia.
Calcium-based phosphate binders are very effective in lowering serum phosphorus concentrations, however, there is a risk of hypercalcemia and soft-tissue calcification. This risk is higher in patients on dialysis, so the use of calcium-based phosphate binders is not recommended when the serum calcium concentration is above 10.2 mg/dL, or the plasma PTH is below 150ﾠpg/mL.
Vitamin D analogs have been used to effectively prevent or improve high bone turnover in this situation. The use of calcitriol or other vitamin D analogs is recommended for patients with persistently elevated PTH (>70 pg/mL for stage 3 or >110 pg/mL for stage 4) despite adequate dietary restriction or in patients with stage 5 renal failure and PTH over 300 pg/mL.
How cinacalcet, a new calcimimetic, works?
Targets the calcium-sensing receptor on the surface of the chief cells of the parathyroid gland. It acts as an allosteric modulator of the calcium-sensing receptor and decreases PTH secretion, leading to the reduction in serum calcium and phosphorus levels.ﾠ
What are the indications for a parathyroidectomy on a patient with secondary hyperparathyroidism?
Calciphylaxis
SHPT refractory to medical therapy consistent with the following:
PTH >600 pg/mL
(Ca+2 � PO?4) >55
High-turnover bone disease
SHPT consistent with the above conditions and associated with one of the following: Subperiosteal resorption, Bone pain, Pathologic fractures, Severe pruritus, Persistent anemia, Renal osteodystrophy, Hypercalcemia, Hyperphosphatemia, Extraskeletal nonvascular calcification
What are the indications for a parathyroidectomy on a patient with tertiary hyperparathyroidism after kidney transplantation?
Subacute severe hypercalcemia (Ca+2 >12.5 mg/dL)
Persistent hypercalcemia 2 years posttransplant associated with the following: Decline in renal function, Nephrolithiasis, Acute pancreatitis, Progressive bone disease
What is renal osteodystrophy and what is the pathophysiology behind it?
Renal osteodystrophyﾠis defined as bone disease associated with renal failure. It results from a combination of phosphate retention, bone resistance to the metabolic effects of PTH, and the inability of the kidneys to hydroxylate 25-hydroxy-vitamin D to 1,25(OH)2D3. Persistent elevation of PTH produces increased osteoclast and osteoblast activity, resulting in high bone turnover and the haphazard deposition of collagen that ultimately replaces the bone marrow with fibrosis and cysts (osteitis fibrosa cystica). As a consequence, bone is severely weakened, increasing the risk of pathologic fractures.
What is calciphylaxis?
Persistent refractory hypercalcemia resulting in disseminated vascular and soft-tissue calcification can produce severe tissue ischemia and necrosis. Parathyroidectomy may slow the progression of ulcer formation and allow for proper wound healing, but calciphylaxis is associated with over a 50% mortality rate. The presence of calciphylaxis is an absolute and emergent indication for parathyroidectomy.
What is a postoperative complication of parathyroidectomy in patients with secondary or tertiary hyperparathyroidism?
Patients with SHPT and renal failure have a high risk of experiencing hungry bone syndrome postoperatively, which results from increased skeletal calcium deposition and causes severe hypocalcemia. Transient hypocalcemia occurs in as many as 85% of patients, and permanent hypocalcemia occurs in approximately 10%. To prevent symptoms of hypocalcemia, patients are placed on 4 to 6 g/day of calcium postoperatively. Calcitriol (0.5 to 4 ?g/day) is often necessary to prevent hypocalcemia.
