Calcium Homeostasis and Hormonal Regulation

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Most prevalent metabolic bone disease in adults:

Osteoporosis

Familial Hypocalciuric Hypercalcemia:

-Benign condition -Germline mutation of CSR -Stable, mild hypercalcemia from birth -Hypocalciuria

Vitamin D:

-A hormone, not actually a vitamin -Shares striking similarities in origin with steroid hormones: it is a metabolic product of cholesterol synthetic pathway -Synthesis begins in skin, where 7- dehydrocholesterol is transformed to vitamin D3 by action of ultraviolet light. -Can also be obtained from dietary sources: fortified milk, multivitamins, cod liver oil

Medications That Affect Calcium Metabolism:

-Antiresorptive agents -Medications that stimulate bone resorption -Lithium -Thiazide diuretics -Recombinant human parathyroid hormone

Functions of Parathyroid Hormone (PTH):

* All functions raise blood calcium & are mediated via a specific PTH receptor. •Stimulates bone resorption release of calcium into blood •Acts on kidney to increase fractional reabsorption of renal tubular calcium & drive production of active metabolite •Promotes intestinal absorption of calcium

Osteoporosis

*Most prevalent metabolic bone disease in adults *Affects estimated 20-25 million Americans, with 4:1 female:male predominance

Signs and symptoms of hypercalcemia:

-CNS:lethargy, decreased alertness, depression, confusion, forgetfulness, coma -GI:anorexia, constipation, nausea & vomiting -Renal:impairs kidney's ability to concentrate urine, leading to dehydration, increased risk of kidney stones -Skeletal:increased bone resorption, increased bone demineralization & risk of fracture -Cardiovascular:causes or exacerbates hypertension

Treatment of osteoporosis:

-Directed at primary consequence of disease: fracture -Modification of preventable risk factors, such as smoking & alcohol consumption -Evaluation of fall risk -Consideration of walkers, hand rails, night lights, hip pads -Adequate dietary calcium & vitamin D -Prevention for those with family history: minimize bone loss, increase bone density, & prevent fracture -Medication

Role of Kidneys in Calcium Metabolism:

-Diseased kidney impairs calcium metabolism. -PHPT, calcium kidney stones

GI Physiology and Calcium Metabolism:

-Factors required for calcium absorption •Normal intestinal function (short bowel syndrome & genetic or physiologic defects may have negative effect) •Adequate dietary calcium intake •Normal vitamin D availability & metabolism

Endocrine Causes of Hypocalcemia:

-Hypoparathyroidism as a result of: •Neck surgery •Autoimmune destruction of parathyroid tissue •Mutations in PTH gene •Abnormal deposition of copper/aluminum in parathyroids •Magnesium deficiency -Pseudohypoparathyroidism (lack of responsiveness to PTH) -Hypovitaminosis D -Tertiary hyperparathyroidism

Organ System Causes of Hypocalcemia:

-Intestinal disorders resulting in inadequate calcium or vitamin D absorption •Short bowel syndrome, dumping syndrome, celiac sprue •Threaten hypocalcemia, increased PTH secretion -Renal insufficiency/failure •As a result of hyperphosphatemia & defective metabolism of vitamin D -Genetic defects resulting in impaired ability to recover filtered calcium from tubular fluid

Organ System Causes of Hypercalcemia:

-Milk-alkali syndrome (Burnett's syndrome) -Renal failure

Signs and symptoms of hypocalcemia:

-Neuromuscular: tetany in hands, feet, legs, back; numbness & tingling in face, hands, & feet -CNS:irritability, seizures, personality changes, impaired intellectual functioning -Cardiovascular:QT prolongation, electromechanical dissociation

Causes of hypercalcemia:

-PHPT—most common -Secondary and tertiary hyperparathyroidism -CSR (calcium sensing receptor) abnormalities -Other endocrine disorders -Cancer-mediated hypercalcemia -Granulomatous diseases -Medications -Renal disease, others -Hyperthyroidism -Addison's disease, Addisonian crisis

Medications That Can Cause Hypercalcemia:

-Thiazide diuretics •Used to treat hypertension •Causes retention of glomerularly filtered calcium -Lithium •Used to treat bipolar affective disorder •Appears to shift "set point" at calcium- sensing receptor -Vitamin A •Believed to activate osteoclasts & enhance bone resorption, elevating blood calcium; PTH & 1,25(OH)2D are suppressed

Causes of hypocalcemia:

-Parathyroid glands, when functioning properly, will not only correct falling blood calcium but also prevent it by increasing PTH secretion. -Compensatory rise in PTH secretion is known as secondary hyperparathyroidism.

Endocrine Causes of Hypercalcemia:

-Primary hyperparathyroidism -Hypervitaminosis D -Cancers (PTHrP), tumors

Parathyroid Hormone (PTH):

-Secreted from 4 parathyroid glands near thyroid -Parathyroid glands have calcium-sensing receptors that respond to calcium levels by increasing or decreasing PTH secretion.

Adult human body contains _________ of calcium

1000 g

Diagnosis of Osteoporosis:

Based on clinical characteristics and/or a DEXA scan

Vitamin A:

Believed to activate osteoclasts & enhance bone resorption, elevating blood calcium; PTH & 1,25(OH)2D are suppressed

Hypercalcemia:

Blood calcium levels above expected normal range •Binding of calcium to other substances must be taken into account when considering total calcium levels.

Cancers (PTHrP), tumors:

Cause release of hormones or hormone-like substances

Rickets and Osteomalacia:

Caused by abnormal bone mineralization & vitamin D deficiency

Hypervitaminosis D:

Caused by excessive intake of vitamin D or aberrant production of 1,25(OH)2D

Bone turnover (remodeling):

Coupled process of simultaneous bone formation & breakdown occurring throughout life

What is the most common cause of hypercalcemia in outpatient setting?

PHPT = primary hyperparathyroidism

What is the only source of calcium?

The diet

What is the only "out" of calcium?

Urine output

Trabecular bone:

axial skeleton (vertebrae); has many cross-hair type connections (trabeculae), providing strength & elasticity

When resorption exceeds formation, bone mass _____________ and causes an increased risk of fracture.

decreases

Fragility fracture:

fracture occurring at an inappropriate degree of trauma

Tissues Vitamin D affects:

gut, bone, parathyroids

Patient with _____ serum albumin would be expected to have _____ total calcium & ___________ ionized calcium.

low low normal

Bone formation is mediated by:

osteoblasts

Bone breakdown (resorption) is mediated by:

osteoclasts

Cortical bone:

primary type in long bones (femur); strong, rigid

Tissues involved in synthesis of Vitamin D:

skin, liver, kidneys

Milk-alkali syndrome (Burnett's syndrome):

•From ingestion of large amounts of calcium together with an absorbable alkali •PTH level is low

-Primary hyperparathyroidism

•Most common cause of hypercalcemia in outpatient setting •Physiologic defect in parathyroid glands Results from adenoma(s) or hyperplasia of parathyroid glands

Osteomalacia:

•Occurs in bone in adults (after closure of epiphyseal plates) •No bony deformities

Rickets:

•Occurs in growing bone (in children) •Bony deformities from bending of long bones due to gravity

Features that distinguish secondary hyperparathyroidism from primary:

•Parathyroids are functioning properly; increased PTH is appropriate mechanism. •Treatment involves identifying & correcting process threatening hypocalcemia, not removal of parathyroid(s).

Renal failure as a cause hypercalcemia:

•Renal excretion of both calcium & phosphate is severely impaired. •Production of active form of vitamin D is limited. •PTH secretion is stimulated

Calcium Homeostasis:

•Serum calcium maintains at a constant level •Cellular & tissue effects of calcium depend on blood calcium maintenance within a specific range •Adult human body contains 1,000 g of calcium -99% as hydroxyapatite salt -1% in extra-cellular fluids -Diet is only source of calcium-Urine is only significant "way out"

Hypocalcemia:

•State of blood calcium levels below expected range •Best measured by ionized calcium

Lithium:

•Used to treat bipolar affective disorder •Appears to shift "set point" at calcium- sensing receptor

Thiazide diuretics:

•Used to treat hypertension •Causes retention of glomerularly filtered calcium


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