Calcium and Parathyroid

Question 1

What do calcium sensing receptors do?

Answer 1

Sense low calcium and then stimulate production of PTH

Question 2

On which organs does PTH act?

Answer 2

Bone: Stimulates Ca resorption
Kidney: Stimulates Ca reabsorption
Gut: Via raising 1,25 (OH)VitD, stimulates Ca absorption

Question 3

What is main result of hyperparathyroidism?

Answer 3

Hypercalcemia

Question 4

What are leading causes of primary hypercalcemia?

Answer 4

Solitary adenoma: 85%
Diffuse hyperplasia: 15%
Parathyroid carcinoma:

Question 5

What is net result of PTH on phosphate?

Answer 5

Lowers phosphate– although it raises phosphate resorption from bone, this is “trumped” by increased phosphate excretion in kidney

Question 6

What are signs of hyperparathyroidism in following areas:

GI (3)
CVS (1)
Bone (2)
Brain (2)

Answer 6

GI: pancreatitis, stomach ulcers, kidney stones
CVS: High BP
Bone: osteitis fibrosa cystica, low BMD in cortical bone
Brain: Depression/psychosis

Question 7

What criteria constitute a “symptomatic patient” for hyperparathyroidism? (2) What is treatment mainstay?

Answer 7

Symptomatic patient displays kidney stones or a fracture

Treatment would be surgical

Question 8

What are criteria for asymptomatic hyperparathyroid patient that requires surgery? (4)

Answer 8

Age 1 above upper limit of lab value
Low creatinine levels
Osteoporosis

Question 9

Describe histologic appearance of parathyroid adenoma

Answer 9

Lots of normal-looking parathyroid cells in well-encapsulated adenoma

Question 10

Describe secondary hyperparathyroidism. What are underlying causes? (3)

Answer 10

In secondary hyper functioning parathyroid glands compensate for hypoglycemia

Treatment is to address underlying cause:
Renal insufficiency (no 1,25(OH)VitD)
Calcium malabsorption
Vitamin D Deficiency

Question 11

What is tertiary hyperparathyroidism? What is the treatment?

Answer 11

Hyperfunctioning parathyroid gland and hyper secretion due to prolonged secondary hyperparathyroidism.

Treat with surgery if severe.

Question 12

What is familial hypocalciuric hypercalcemia?

What are the lab findings?

Answer 12

Autosomal dominant mutation in Calcium-Sensing receptor leading to shift in parathyroid set point for calcium.

Lab findings: Elevated serum Ca with low urine calcium and normal PTH

Question 13

What is treatment for familial hypocalciuric hypercalcemia?

Answer 13

Nah it’s benign

Question 14

What are three categories of hypoparathyroidism causes?

Name an example of each.

Answer 14

Post-surgical (thyroidectomy)
Infiltrative disease: hemochromatosis, wilson’s disease
Congenital: DiGeorge syndrome, autosomal polyglandular syndrome type 1

Question 15

What are symptoms of hypoparathyroidism?

What are big signs?

Answer 15

Cardiac arrhythmia
Neuromuscular irritability: perioral, tingling of fingers/toes, tetany
Signs: Chvostek’s sign (ipsilateral lip twitch on tapping), Trousseau’s sign (carpal spasm)

Question 16

What is treatment for hypoparathyroidism? What do you monitor?

Answer 16

Rx: Oral calcium and 1,25 (OH)VitD
Monitor: Serum/urine calcium levels

Question 17

What is goal serum calcium level for hypoparathyroidism? Why?

Answer 17

Low normal– if too much calcium most will be excreted by kidneys, but this runs risk of kidney stone

Question 18

Vitamin D intoxication: What are symptoms (4)and lab sign?

Answer 18

VitaminD intoxification requires large doses– it results in nausea, vomiting, weakness and altered mental status.

It results in prolonged hypercalcemia

Question 19

What is the treatment for Vitamin D intoxication? (2)

Answer 19

Hydration, no dietary calcium

Question 20

What is the etiology of vitamin D deficiency? (3)

What does it lead to?

Answer 20

Lack of solar irradiation
Decreased intake or impaired absorption
Metabolic defects in VitD hormone system– inadequate activation in liver/kidney, abnormalities of VitD-receptor

Leads to secondary hyperparathyroidism

Question 21

How is vitamin D deficiency treated?

Answer 21

Vitamin D intake

Vitamin D enriched foods– milk, cheese, fish, eggs

Question 22

What are metabolic bone diseases associated with vitamin D deficiency? (2) In which populations are they most common

Answer 22

Rickets in children

Osteomalacia in adults

Question 23

What is the main result of rickets in relation to bone? What are some signs? (2)

Answer 23

Lack of mineralization of bones.

Bowing of legs and metaphyseal cupping/fraying

Question 24

What is the clinical presentation of osteomalacia?

Answer 24

Usually asymptomatic

Symptoms: diffuse pain and tenderness, proximal muscle weakness

Question 25

What is treatment for vitamin D deficiency?

Answer 25

Treat underlying disorder

Correct hypoglycemia and vitamin D deficiency