Flashcards in Calcium Metabolism (5/21) Deck (37):
Describe the normal calcium feedback mechanism
1. Decreased serum calcium is recognized by the parathyroid glands
2. PTH secretion is increased and goes to the bone and kidney
3. At the bone, PTH stimulates increased bone Ca+ and phosphate resorption. At the kidney, PTH stimulates increased renal Ca2+ resorption. At the kidney, PTH also signals for activation of 1,25-dihydroxyvitamin D3 via addition of a hydroxy group.
4. D3 causes GI Ca2+ and Pi absorption into serum
5. Increased levels of excreted phosphate and calcium are detected in the urine (calcium because the body is trying to get rid of the XS serum calcium it senses)
What is primary hyperparathyroidism?
Abnormal hypersecretion of PTH leading to hypercalcemia
What causes primary hyperparathyroidism?
Solitary adenoma (one parathy gland is enlarged +over produces)
Diffuse hyperplasia (all 4 overproductive)
Parathyroid carcinoma (very rare)
What is the most common cause of primary hyperparathyroidism?
Solitary adenoma (one of 4 parathyroid glands is enlarged)
What are the consequences of hyperparathyroidism?
-Osteitis fibrosa cystica (bony lesions)
-Increased kidney stones due to xs secretion of calcium
-Stomach ulcers, pancreatitis
-Psychosis: can feel better after treatment
What happens to bone in primary hyperparathyroidism?
-Generalized demineralization of bone, subperiosteal bone resorption and bone cysts
-Osteitis fibrosa cystica
What do most pts present with in primary hyperparathyroidism?
Elevated serum calcium only
Additional signs and symptoms:
-kidney stones, renal dysfxn, reduced bone mineral density
What kind of bone has the most reduced bone mineral density in primary hyperparathyroidism?
Where is the best place to do a dexa scan to determine primary hyperparathyroidism?
Look at 1/3 distal bone radius because the bone is 80% cortical bone there
Treatments for primary hyperparathyroidism?
-Asymptomatic with no complications: medical monitoring
-Symptomatic pt with kidney stones and fracture: Surgery
-Asymptomatic pts <50 because dis progresses. Reduced creatinine because Ca deposition messes with creatinine.
What is secondary hyperparathyroidism?
-Hyperfunctioning parathyroid glands compensate for hypocalcemia..this is actually an appropriate response
-Have increased PTH because serum calcium levels are low
How do we treat secondary hyperparathyroidism?
Treat the underlying cause:
-Vit D def
What is tertiary hyperparathyroidism?
-Parathy gland hyperfxn and hypersec due to prolonged secondary hyperparathyroidism
-Elevated serum ca
-Req surgery if severe
-Often occurs in setting of renal insufficiency. If long term low Ca, one parathyroid can become autonomous leading to elevated serum Ca levels
What is familial hypocalciuric hypercalcemia (FHH)?
-Autosomal dominant disease
-Abnormal calcium sensor shifts parathyroid setpt for calcium
What are the lab findings in FHH?
-Elevated serum Ca
-Normal or slightly elevated PTH
-Low urine calcium*: receptors are also in the kidney and will reabsorb calcium to reach the elevated setpt
Is FHH malig or benign?
Benign condition so surgery is not necessary
How do we get hypoparathyroidism?
-Post-surgery: following total thyroidectomy or radical neck dissection
-Due to infiltrative disease
-Congenitally (like DiGeorges in which it failed to dev or familial in an autosomal recessive autoimmune fashion (polyglandular type 1))
What are the dangers of hypocalcemia in hypoparathyroidism?
-Neuromuscular irritability: paresthesias around mouth, tingling of fingers and toes, tetany
What is Chvostek's sign?
Tap the facial nerve and lips turn up (tests for tetany)
What is Trousseau's sign?
Cut off circulation in arm with bp cuff and see if you get carpal spasm for 3 minutes. More specific sign. Tests for tetany.
How do we treat hypoparathyroidism?
-Oral calcium and activated D3 (1, 25-dihydroxy D3)
-Monitor serum and urinary Ca concentration
What is the goal serum Ca level in pt with hypoparathyroidism and why?
-In setting of hypoparathyroidism you have less PTH, so there is less stimulation for the kidney to reabsorb Ca2+. Thus, Ca2+ accumulates and you can get kidney stones
What is vitamin D intoxication?
-OD of Vit D that requires very large doses (10,000 units/day)
-Uncommon cause of hypercalcemia
What are the symptoms of vit D intox?
Altered mental status
Prolonged hypercalcemia (because vit D is stored in fat)
How do we treat vit D intox?
Hydration, no consumption of dietary ca
How do we get a vit D def?
-Lack of solar irradiation
-Dec intake or impaired absorption
-Metabolic defects in vit D system
What does vit D def cause?
What is the goal dietary intake of Vit D in adults <50
1,000 mg and 400-800 IU of vit D/day
What is the goal dietary intake of Vit D in adults >50
1,200 mg and 800-1000 IU of vit D/day
MilkWhat foods are enriched with vit D?
Milk, cereals, yogurt, OJ
Fatty fish, beef, liver, eggs
Added to some margarines
What is MED?
Amt of UVR exposure req to cause minimal erythema of the skin (minimal erythemal dose). Releases vit D3 into circ
What are the consequences of vit D def?
-Metabolic bone dis (rickets (kids), osteomalacia (adults)
-Widened osteoid seams and impaired mineralization
-Risk factor for osteoporosis
What process in bone remodelling req vit d?
What happens to the bones in rickets?
-Bowing of the legs
-Metaphyseal cupping and fraying in the distal radius and ulna
What is osteomalacia
Often asymptomatic vit D def with diffuse bone pain and tenderness and proximal muscle weakness
How do we treat vit D def?
-Treat underlying disorder
-Correction of hypocalcemia and vit D def