Calcium and vit d and phosperous and stuff like that

What is hydrocyapatite made up of?

Calcium and phosphate

What inhibits hydroxyapatite formation?

Pyrophosphate

What inhibits pyrophosphate

Alkaline phosphatase

What is normal serum Ca2+?

8.4-10.2 mg/dL

What percfent of Ca is ionized

50%

What percent of Ca is protein bound

40%

What percent of Ca is complexed?

10%

What types of Ca are free?

Ionized and complexed

What happens with Ca in a state of acidosis?

More of it is released ‘ionized’

What happens to Ca when there’s alkalosis

More Ca is bound

What is the average intake of Ca2+?

About 1000 mg/d

How much Ca is absorbed by the gut?

500 mg/d

How much Ca does the gut release

325 mg/d

How much Ca is excreted in total from the gut

825 mg/d

How much does the kidney excrete

175 mg/d

What is the major storage of Ca2+

Bone, about 1000g

Normal serum Pi

3.0 to 4.5

What percent of Pi is ionized

45%

What percent of Pi is protein bound

15%

What percent of Pi is complexed?

40%

what percent of percent of the Pi is ionized and complexed/free

85%

What happens to Pi in acidosis

More ionized

What happens to Pi in alkalosis

more bound

How much Pi is taken in on average?

1400 mg/d

How much Pi is aborbed by the gut

1100 mg/d

how much Pi is excreted by kidney

900 mg/d

How much Pi is released by the feces

500 mg/dl

What is the major store of Pi and how much

Bone, 600

What brings Ca in from the lumen

TRPV5/6

What brings Ca out of the cell

Ca2+ ATPase

What brings Pi in

Na/Pi

What activates calcitonin

Increased plasma Ca activates Ca2+ sensing receptors on C-cells, causing release

How is calcitonin inhibited

Decreased plasma Ca, leads to lease CaSR activation, leads to decreased calcitonin

What does calcitonin do to bone

inhibits osteoclasts, decreasing bone resorption, and decreased plasma Ca

What does calcitonin do to the kidney

increased uribary Ca2+ excretion, and minor Pi reabsorption

What can be used to treat osteoporosis

Calcitonin as a short tierm in severe hypercalcemia

How are parathyroid chief cells activated?

Low plasma Ca, less CaSR activation, increased PTH release

What does PTH bind to?

PTH1R

What doe high plasma Pi cause?

Binding of Ca, lowering free Ca, resulting in PTH increase

How is PTH inhibited?

Increased plasma Ca, Increased calcitriol, increased FGF23

What does PTH do in bone?

Increases osteoblasts, TNKL, osteoclastic bone resorption, and increased plasma Ca and Pi

What does PTH do in the kidney duct?

Ca reabsorption

What does the kidney do in the proximal tube?

Decreases Pi absorption

What does the kidney do to 1a-hydroxylase?

Increased conversion of calcidiol to calcitrol

What organs are used for calcitriol synth

skin/diet → Liver → kidney

What is made from skin/diet

cholecalciferol

What is made from the liber?

25-Hydroxycholecaliferol

What is made from the kidney?

1,25-dihydroxcholecalciferol

What activates 25 Hydroxycholecalciferol?

1a-hydroxylase

What stimulates 1-a hydroxylase

Increased PTH, decreased Pi

What inhibits 1a-Hydroxylase?

Increased Ca, Increased FGF23

How does 25 Hydroxylase inhibit production?

Feedback inhibition

Inactive form of od 25 Hydroxycholecalicerol/1,25 dihydroxycholecalciferol?

24,25 Dihydroxycholecalciferol, 1,24,25-Trihydroxycholecalciferol

What makes 24,25 Dihydroxycholecalciferol, 1,24,25-Trihydroxycholecalciferol

24 Hydroxylase

What is rickets

childhood vitamin D deficiency which leads to defective bone mineralixation

What is osteomalacia

Adult deficiency of vit D

What is hypervitaminosis D

excess vitamin D

What is the transport function of calcitriol

Circulate bound vitamin D-binding protein

What is the receptor function of Vitamin D

Vitamin D receptor, a nuclear steriod receptor

What does calcitrol do in the small intestine

Increases Ca and Pi absorption

What does calcitriol do to parathyroid

decreases PTH synth

What does calcitriol do to the osteocytes

FGF23 synth

What does calcitriol do to the bone?

Bone turnover, movilizes Ca and Pu for bone remodeling

What doe calcitriol do to the kidney

Ca reabsorption in DCT via increased Calbindin, and Pi absorption in PT

What does an increased in plasma Ca result in?

reverses inhibition of 1a-hydroxylase

What activates FGF23

increased plasma Pi, increased PTH and Calcitrol, FGFR

What decreases FGF23

decreased plasma phosphate

Actions of FGF23 in tha parathyroid

PTH synth in chief cells

Actions of FGF23 in the kidney

NPT expression in proximal tubule, increasing urinary Pi excretion, decreased 1a-hydroxylase

What does FGF23 do to the small intestine via calcitrol

Decreased NPT expression, decreasing Pi absorption

What parts of CKD results in 2nd deg hyperparathyroidism

Increased phosphate, decreased vit D, and decreased Ca+ stimulate the release of PTH,

How does CKD result in teriary hyperparathyroidism

Loss of CaSR and feedback sensitivity, and causing autonomous PTH secretion

What is decreased and increased in 2nd deg hyperparathyroidism

Vit D, Ca2+, Pi decreased, FGF23 increased

What happens in tertiary hyperparathyroidism

Increased ca2+, PTH, Pi, and decreased Vit D

Why can cause hypocalcemia?

Hypoalbuminemia, hypoparathyroidism, pseudohyparathyroidism, vitamin D deficiency or renal insufficiency

Symptoms of hypocalcemia?

Convulsions, arrythmias, tetany, trousseous sign, chvosteks sign

What is trousseau sign?

Spasm in hand with BP held above wrist

What is Chvostek’s sign?

Lip twitch upon tapping facial nerve

What causes hypercalcimia

Primary hyperparathyroidism, hypervitaminosis D, bone metastases, cancer

What are symptoms of hypercalcimia

Stones, bone pain, GI spasm abd pain nauesea, toilet due to polyuria, depression

What is pseudohypoparathyroidism

defective PTHR

What does OPG do?

Decoy receptor for Rankl, that prevents osteoclast maturation

What increases OPG?

Calcitrol, estrogen, exercise/loading, androgens

what does RANKL do

binds RANK on osteoclast to activate osteoclast precurorsor

What increases RANKL?

PTH, calcitrol, and glucocorticoids

Step one of osteolysis

PTH and vit D bind receptors on osteoblast

Step 2 osteolysis

Increase secretion of RANKL, macrophage colony stimulating factor, IL-6, and reduce OPG

Step 3 osteolysis

M-CSF diffrentiates stem cells into osteoclast precursors

Step 4 of osteolysis

reduced secretion of OPG allows RANKL to bind RANK

Step 5 of osteolysis

RANKL, VD, and IL-6 transform precuror cells into pre-osteoclasts

Step 6 of osteolysis

Pre-osteoclasts merge into a mature osteoclast, which attaches to bone

What are inhibitors of osteoclasts?

Estrogen, bisphosphonates, denosumab