Hormonal regulation of minerals

Question 1

What is the active form of Vitamin D

Answer 1

Calcitriol

Question 2

What converts inactive vitamin D into active

Answer 2

Liver takes dietary vitamin D into calcidiol then the kidney with 1a-hydroxylase transforms it into calcitriol

Question 3

What species do not have renal 1a-hydroxylase

Answer 3

equines
Need high dietary intake

Question 4

What is the short term control of Ca

Answer 4

PTH, vitamin D controls the day to day levels instead of hour to hour

Question 5

Major organs targeted by vitamin D

Answer 5

Intestine first then kidney and bone

Question 6

Effects of vitamin D on intestines

Answer 6

Stimulates production of luminal Ca transporters, calbindins, and basolateral ATP dependent Ca pumps to increase Ca
Increase transcellular and paracellular P absorption

Question 7

Effects of vitamin D on Kidneys

Answer 7

Increase calbindins in DCT and increase fCa

Question 8

Effects of vitamin D on bone

Answer 8

Facilitates action of PTH on osteoblasts

Question 9

Stimulus for increased Vitamin D production

Answer 9

-PTH
-Decreased fCa
-Decreased phosphate
-Growth hormone

Question 10

Inhibitors of vitamin D production

Answer 10

-Vitamin D
-Increased fCa and Pi

Question 11

Causes of hypovitaminosis D

Answer 11

-Dietary deficiency
-Gastrointestinal diseases: malabsorptive or pancreatic insufficiency
-Kidney disease: acute or chronic kidney disease or protein losing nephropathies

Question 12

Causes of Hypervitaminosis D

Answer 12

-Exogenous vitamin D (Cholecalciferol rodenticides, drugs, cholecalciferol plants)
-Endogenous vitamin D (Neoplasia, granulomatous disease)

Question 13

Primary hypoparathyroidism

Answer 13

Intrinsic. May be immune mediated destruction or iatrogenic.
Leads to decreased PTH and hypocalcemia and hyperphosphatemia

Question 14

Clinical signs of hypoparathyroidism

Answer 14

Asymptomatic (common)
Tetany and seizures

Question 15

Primary hyperparathyroidism

Answer 15

Intrinsic.
Increased PTH secretion due to autonomous secretion of PTH. Leads to persistent hypercalcemia and hypophosphatemia. Often due to neoplasia or hyperplasia

Question 16

Clinical signs of primary hyperparathyroidism

Answer 16

-Weakness
-PU/PD
-UTI
-Lethargy
-Inappetence

Question 17

Secondary hyperparathyroidism

Answer 17

Extrinsic. From a Ca-P imbalance
-Nutritional- increased PTH from too little Ca and too much P
-Renal: renal disease decreased reabsorption or GFR

Question 18

Nutritional secondary hyperparathyroidism

Answer 18

Most common in horses and exotics.
Insufficient Ca or too much P.
Can see from raw food diets, excessive grain, pastures with oxalate-containing plants.
See skeletal abnormalities

Question 19

Pathophysiology of Nutritional HyperPTH

Answer 19

Increased dietary P or decreased dietary Ca causes decreased serum Ca-> stimulates PTH-> kidney increased Ca reabsorption and bone increases Ca and P resorption and there is osteoclastic bone resorption and replacement by fibrous CT

Question 20

Lab findings for nutritional HyperPTH

Answer 20

Serum Ca WRI usually
Mild to moderate hyperphosphatemia

Question 21

Clinical signs Renal Hyper PTH

Answer 21

Increased PTH from CKD
-CKD signs
-Rubber jaw
-Facial fibrous osteodystrophy

Question 22

Lab findings for Renal HyperPTH

Answer 22

Abnormalities of CKD
Variable serum Ca
Mild to severe hyperphosphatemia

Question 23

Calcitonin

Answer 23

Released by parafollicular cells in thyroid
Decreases fCa and P
Most useful for limiting post meal rise in Ca

Question 24

PTHrp

Answer 24

Produced by numerous cell types
Exact role unknown: possibly to transport Ca in neonates
Can bind and stimulate PTH receptors and have similar effects if high concentrations

Question 25

Main hormone for hypercalcemia of malignancy

Answer 25

PTHrp
Mimics PTH and see produced by tumors

Question 26

Tumors that secreate PTHrp

Answer 26

-Apocrine gland adenocarcinoma
-T cell lymphoma
-Certain carcinomas