Endo-CalciumVitD Flashcards
(36 cards)
Describe the vitamin D pathway
Regardless of the method of ingestion, vitamin D3 and D2 are both inactive forms that must be hydroxylated twice before becoming active. The first occurs in the liver and converts vitamin D to 25-hydroxyvitamin D [25(OH)D], also known as calcidiol. The second occurs primarily in the kidney and forms the physiologically active 1,25-dihydroxyvitamin D [1,25(OH)2D], also known as calcitriol
What does vitamin D act on to increase calcium secretion?
Active vitamin D acts on three organ systems to achieve and maintain normal serum calcium: bone, intestine, and kidney. With adequate vitamin D, bone resorption is increased, intestinal uptake of dietary calcium is increased, and excretion of calcium through the kidney is decreased. PTH is secreted to increase the calcium in the blood in response to even the slightest degree of hypocalcemia; it acts on the kidney to increase production of active vitamin D and promote calcium reabsorption in the distal convoluted tubule and loop of Henle, and increased resorption in bones, thereby increasing release of calcium into the blood
What are the symptoms of hypercalcemia?
Classic symptoms of hypercalcemia are polyuria, polydipsia, anorexia, nausea, abdominal pain, constipation, and mental status changes; as serum calcium levels increase and/or the rate of change increases, symptoms become more severe, with profound mental status changes, obtundation, and acute kidney injury.
What is the best test for vitamin D deficiency?
25-Hydroxyvitamin D has a relatively long half-life of several weeks, is the best indicator of whole body vitamin D status, and is the recommended test for vitamin D deficiency.
If high calcium is noted… then what?
- Recheck calcium, if still high..
2. Determine if PTH dependent or independent, measure serum calcium and PTH
What is the most common cause of PTH mediated hypercalcemia?
Elevated serum calcium level, with an inappropriately normal or elevated intact PTH level
- Due to single parathyroid adenoma (most common)
- multigland hyperplasia due to ESRD or MEN syndromes
- parathyroid gland carcinoma
Once primary hyperparathyroidism is diagnosed, then what do you do?
Measure:
- serum phosphorus
- 24-hour urine calcium
- serum 25-hydroxyvitamin D levels
- serum phosphorous levels will usually be low, often normal or elevated urine calcium levels
- elevated 1, 25-vitamin D levels
What is the treatment for primary hyperparathyroidism?
SURGICAL INTERVENTION IN PTS WHO:
- Cr >1 or low creatinine clearance
- T-score on DEXA of less than -2.5
- Age 50 or younger
In patients who are not good surgical candidates, how is primary hyperparathyroidism managed?
In patients who do not meet the criteria for surgery, surveillance is recommended. Patients should have annual measurement of serum calcium and creatinine levels. A three-site dual-energy x-ray absorptiometry (DEXA) scan should be performed every 1 to 2 years to evaluate bone mineral density of the lumbar spine, hip, and distal radius. The frequency of DEXA scanning should increase to yearly when any treatment has been initiated for bone health or other medications have been added that may affect bone health (antiandrogen, antiestrogen, antiseizure medications, or glucocorticoids).
How do you manage someone with asymptomatic hyperparathyroidism?
- replete vitamin D for low levels
- Adequate physical activity to prevent bone resorption and adequate hydration to prevent kidney damage are imperative.
Describe how tertiary hyperparathyroidism happens?
Tertiary hyperparathyroidism is the result of the prolonged PTH stimulation needed to maintain normocalcemia resulting from decreased 1,25-dihydroxyvitamin D levels from kidney impairment.
This prolonged stimulation results in increased calcium levels and severe hyperparathyroid hyperplasia and elevated PTH levels that do not respond to phosphate binders and calcitriol therapy. Severe bone loss and other symptoms make surgical resection the treatment of choice.
What is normocalcemic primary hyperparathyroidism?
Normocalcemic primary hyperparathyroidism is defined as increased PTH levels in the absence of elevated calcium levels.
This is a diagnosis of exclusion used in patients being evaluated for low bone density in which all secondary causes have been ruled out, including vitamin D deficiency. Approximately 20% of these patients will develop hypercalcemia within 3 years, so they should be monitored closely.
What medications cause hypercalcemia?
Thiazide diuretics decrease the excretion of calcium by the kidney and may result in increased serum calcium levels. Primary hyperparathyroidism, however, should also be considered if the patient remains hypercalcemic despite the discontinuation of the thiazide diuretic. In these patients, the thiazide may have been masking the PTH-mediated hypercalcemia.
Lithium decreases the parathyroid glands’ sensitivity to calcium and may also reduce urine calcium excretion.
What are the two mechanisms of hypercalemia of malignancy?
There are two mechanisms of hypercalcemia of malignancy: local osteolytic and humoral.
(1) local osteolytic-lytic bone metastases are present, hypercalcemia is the result of increased mobilization of calcium from the bone
(2) humoral- less common and occurs when the tumor itself produces parathyroid-related protein (PTHrP) that binds to and activates the parathyroid receptor, raising serum calcium levels. Squamous cell carcinomas, breast cancers, and renal cell carcinomas are the tumors most commonly associated with hypercalcemia of malignancy. In multiple myeloma, the hypercalcemia is caused by the release of factors that stimulate osteoclast activity
Labwise, how can you tell if something is non parathyroid hormone-mediated hypercalcemia?
In contrast to parathyroid hormone-mediated hypercalcemia, nonparathyroid hormone-mediated hypercalcemia is associated with very low parathyroid hormone levels, typically less than 10 to 15 pg/dL (10-15 ng/L).
What is the acute treatment for hypercalcemia?
The acute treatment of hypercalcemia focuses on decreasing the serum calcium level by increasing calcium excretion with vigorous volume replacement, decreasing bone resorption with bisphosphonates.
What are the symptoms of hypocalcemia?
symptoms may develop, including paresthesias (numbness/tingling around the mouth, tingling in fingers and toes), muscle cramping (Trousseau and Chvostek signs), decreased muscle strength, electrocardiogram changes (prolonged QT interval), tetany, and seizures.
If you note hypocalcemia what do you check?
ionized calcium
then PTH… if parathyroid is responding properly and low calcium is real then PTH will be low to elevate calcium levels
What is the most common cause of hypocalcemia?
The most common cause of hypocalcemia is hypoparathyroidism, which is most often due to trauma during surgery to the neck.
What are some other causes of hypocalcemia not involving the parathyroid?
Other, less common causes of hypocalcemia include poor calcium intake, activating mutations in the CASR gene, PTH resistance, increased phosphate binding in vascular space (rhabdomyolysis or tumor lysis syndrome), increased citrate chelation with large volume blood transfusions, sepsis, vitamin D deficiency, and hypomagnesemia. Low levels of magnesium (due to alcohol abuse or malnutrition) activate G-proteins that stimulate calcium-sensing receptors and decrease PTH secretion.
How do you treat hypocalcemia from hypoparathyroidism?
If hypoparathyroidism is the cause of hypocalcemia, correction of any coexisting hypomagnesemia to serum magnesium 2 mg/dL (0.8 mmol/L) or higher is necessary.
How is osteopenia versus osteoporosis diagnosed?
The diagnosis of osteopenia is based on BMD testing. Osteoporosis, however, can be diagnosed by BMD testing or clinically in the patient with history of fragility fracture, hip fracture, or vertebral compression fracture.
What does a DEXA do?
DEXA assesses the density of the vertebral and hip bones compared with healthy young-adult sex-matched reference values.
What is the FRAX score? What does it help you decide?
In 2008, the World Health Organization (WHO) created the Fracture Risk Assessment Tool (FRAX) calculator that further defines the 10-year fracture risk for patients with osteopenia, defined as a T-score between −1.0 to −2.5 on DEXA. The FRAX score notes the probability of major osteoporotic fracture and hip fracture in the next 10 years. If the risk of major osteoporotic fracture is greater than or equal to 20% or the risk of hip fracture is greater than or equal to 3%, the patient’s benefit from therapy exceeds the risk, and treatment should be offered.
