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Flashcards in Basic Science - Endocrine Deck (17):

Functions of 1,25-dihydroxyvitamin D

↑ absorption of calcium and phosphate from the intestine
↑ bone resorption of Ca2+ and phosphate


Describe the vitamin D pathway and functions


Functions of PTH

↑ serum Ca2+ and ↓ serum phosphate in response to hypocalcemia/hypomagnesemia via

↑ bone resorption of calcium and phosphate (bone is destroyed)
- PTH receptor is on the osteoblasts which secretes IL-1 to activated osteoclasts

↑ kidney resorption of calcium in distal convoluted tubule
↓ kidney resorption of phosphate
↑ 1,25-(OH)2 vitamin D production


osteomalacia labs

Hypocalcemia, hypophosphatemia, and a normal hemoglobin level


labs in HYPOparathyroidism

decreased:  PTH, calcium, 1,25 vit D, urinary Ca

increased:  phosphate

normal:  alk phos


most common cause and treatment HYPOparathyroidsm


supplement Ca and Vit D


intermittant PTH therapy

targets osteoblast

The biological activity in the clinically used recombinant PTH is in the 1-34 amino acid sequence at the N-terminus of the molecule


Name 7 conditions causing Rickets syndrome

Vitamin D-Resistant Rickets (Familial hypophosphatemic rickets

Nutritional vitamin D deficient rickets

Type I and II vitamin D dependent


Renal osteodystrophy

Hyper PTH


logic for vitamin D deficiency rickets (nutritional)

lack of vitamin D

leads to low-nl calcium → high PTH  → low phos and high alk phos


logic for vitamin D resistant rickets (familial x-linked hypophosphatemic)

defect in proximal renal tubules reabsorb phosphate

leads to elevated alk phos

So, Ca and PTH are normal

Presumed defect in 1,25 Vit D conversion because normally hypophosphemia would cause this to increase


Which rickets condition is alk phos not elevated?

ONLY hypophosphatasia


logic for Type 1 vitamin D dependent rickets

defect in conversion to 1,25 vit D

defect in renal 25-(OH)-vitamin D1 alpha-hydroxylase

→ low Ca/Phos → high PTH → high alk phos


logic for Type 2 vitamin D dependent rickets

defect in 1,25 vit D RECEPTOR

→ very high 1,25 vit D levels

→ low Ca/Phos → high PTH → high alk phos



logic for hypophosphatasia

defect in alk phos

→ alk phos activity is low

→ Ca and Phos are high (don't know why)


Renal osteodystrophy logic

defect is in phos excretion

→ PTH goes up to try to waste phos

→ high alk phos

defect is in conversion to 1,25 vit D


→ low Ca


logic for hyperparathyoidism

90% adenoma

defect is in too much PTH

causes increased bone turnover, increased alk phos, increased Ca, phos wasting


Genetics of Rickets

Type I/II vit d dependent and hypophosphatasia:AR

fam vit-D resistant rickets (hypophosphatemic): X-linked dominant