Hormonal regulation of minerals Flashcards
What is the active form of Vitamin D
Calcitriol
What converts inactive vitamin D into active
Liver takes dietary vitamin D into calcidiol then the kidney with 1a-hydroxylase transforms it into calcitriol
What species do not have renal 1a-hydroxylase
equines
Need high dietary intake
What is the short term control of Ca
PTH, vitamin D controls the day to day levels instead of hour to hour
Major organs targeted by vitamin D
Intestine first then kidney and bone
Effects of vitamin D on intestines
Stimulates production of luminal Ca transporters, calbindins, and basolateral ATP dependent Ca pumps to increase Ca
Increase transcellular and paracellular P absorption
Effects of vitamin D on Kidneys
Increase calbindins in DCT and increase fCa
Effects of vitamin D on bone
Facilitates action of PTH on osteoblasts
Stimulus for increased Vitamin D production
-PTH
-Decreased fCa
-Decreased phosphate
-Growth hormone
Inhibitors of vitamin D production
-Vitamin D
-Increased fCa and Pi
Causes of hypovitaminosis D
-Dietary deficiency
-Gastrointestinal diseases: malabsorptive or pancreatic insufficiency
-Kidney disease: acute or chronic kidney disease or protein losing nephropathies
Causes of Hypervitaminosis D
-Exogenous vitamin D (Cholecalciferol rodenticides, drugs, cholecalciferol plants)
-Endogenous vitamin D (Neoplasia, granulomatous disease)
Primary hypoparathyroidism
Intrinsic. May be immune mediated destruction or iatrogenic.
Leads to decreased PTH and hypocalcemia and hyperphosphatemia
Clinical signs of hypoparathyroidism
Asymptomatic (common)
Tetany and seizures
Primary hyperparathyroidism
Intrinsic.
Increased PTH secretion due to autonomous secretion of PTH. Leads to persistent hypercalcemia and hypophosphatemia. Often due to neoplasia or hyperplasia
Clinical signs of primary hyperparathyroidism
-Weakness
-PU/PD
-UTI
-Lethargy
-Inappetence
Secondary hyperparathyroidism
Extrinsic. From a Ca-P imbalance
-Nutritional- increased PTH from too little Ca and too much P
-Renal: renal disease decreased reabsorption or GFR
Nutritional secondary hyperparathyroidism
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
Pathophysiology of Nutritional HyperPTH
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
Lab findings for nutritional HyperPTH
Serum Ca WRI usually
Mild to moderate hyperphosphatemia
Clinical signs Renal Hyper PTH
Increased PTH from CKD
-CKD signs
-Rubber jaw
-Facial fibrous osteodystrophy
Lab findings for Renal HyperPTH
Abnormalities of CKD
Variable serum Ca
Mild to severe hyperphosphatemia
Calcitonin
Released by parafollicular cells in thyroid
Decreases fCa and P
Most useful for limiting post meal rise in Ca
PTHrp
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
Main hormone for hypercalcemia of malignancy
PTHrp
Mimics PTH and see produced by tumors
Tumors that secreate PTHrp
-Apocrine gland adenocarcinoma
-T cell lymphoma
-Certain carcinomas
