Regulation Of Calcium And Phosphate Flashcards
Hypocalcemia Symptoms
Hyperreflexia, spontaneous twitching, muscle cramps, tingling and numbness
-Chvostek sign and Trousseau sign
Hypercalcemia symptoms
Decreased QT interval, constipation, lack of appetite, polyuria, polydipsia, muscle weakness, hyporeflexia
Acidemia vs Alkalemia
Acidemia: Free ionized Ca2+ concentration because less Ca bound
Alkalemia: Ca low because more bound
For the most part, calcium and phosphate are..
Inversely related
Regulation of PTH gene expression and Secretion
Increase in Extracellular Ca2 inhibits PTH synthesis
-Ca and 1,25 Vit D decrease PTH gene, while increasing CaSR gene
Low Calcium causes increase synthesis and storage of PTH, and hyperplasia of parathyroid gland
PTH on Bone, Kidney, Intestine
Bone: Increase bone resorption
Kidney: decrease Pi, increase Ca+, increase urinary cAMP
Intestine: activate Vit D to increase Ca2+ absorption
Vitamin D actions on Ca and Pi
Increase in both Ca2+ and Pi
-increase bone mineralization
Vitamin D Synthesis
Cholecalciferol is main enzyme from diet, but inactive
-made into 25-OH-cholecalciferol but low activity
Kidney makes active form using 1a-hydroylase
PTH receptors are located where?
On osteoblasts!
-not osteoclasts
Short Term PTH actions
Bone formation
-direct action on osteoblasts
Used to treat osteoporosis
Long Term actions of PTH
Bone resorption
-indirect action on osteoclasts
—causes increase in M-CSF cells, which are precursors for osteoclasts
Where is the RANK receptor located and what does it do?
On the osteoclasts, and is turned on by the action of RANKL
OPG Action
It is a soluble protein that inhibits RANKL/RANK interaction so that there is less bone resorption
Decreased by PTH
What is used during calcium absorption to keep calcium grandient the same?
Calbindin
-binds after TRPV6 brings calcium into cell and brings to transporter
What does Vit D do in the Kidney?
Promotes Pi reabsorption mainly
-some reabsorption of Ca2+
What does Vit D do in the Parathyroid?
Inhibits PTH gene expression and stimulates CaSR gene expression
Where are calcitonin receptors located?
Osteoclasts!
-decreases the action, thereby decreasing blood Ca and Pi by not allowing bone resorption
Estrogen and Estradiol-17-B on Ca and Pi
Stimulates reabsorption and bone formation of Ca
Cortisol action on Ca
Promote bone breakdown by osteoclasts and renal Ca wasting
Primary Hyperparathyriodism Markers
PTH: increase
Ca: increase
Pi: decrease
VitD: increase
Renal Failure (Secondary Hyperparathyroidism) Markers
PTH: increased
Ca: decreased
Pi: Increased
VitD: decreased
Vitamin D Deficiency Clinical Markers
PTH: increased
Ca: decreased
Pi: decreased (can not absorb)
VitD: decreased
Hypoparathoidism Clinical Markers
PTH: decreased
Ca: decreased
Pi: increased
VitD: decreased
Pseudohypothyroidism Cause, Phenotype, and Markers
Caused by defective Gs protein, so no AC action leading to no cAMP for T3/T4 production
Short stature and short neck with obesity
PTH: increased
Ca: decreased
Pi: increased
VitD: decreased
Humoral hypercalcemia of Malignancy
PTH: decreased
Ca: increased
Pi: decreased
VitD: decreased
Caused by a tumor that released PTHrP, which binds to same receptor as PTH
-causes T3/T4 production, leading to negative feedback to PTH
Family Hypocalciuric Hypercalcemia (FHH) Clinical Markers
Mutations that inactivate CaSR, results in decrease in amount of Ca that is urinated out; more in blood
PTH: increased/N
Ca: increased in blood, decreased in urine
Pi: N
VitD: N
Vitamin D Deficiency clinical markers
PTH: increased Ca: N/decreased Pi: decreased VitD: very low Bone: increased resorption
Rickets Type I vs Type II
Type I=low 1a-hydroxylase
Type II=low vitamin D receptor
When administering exogenous PTH, what happens in patients with pseudohypoparathyroidism?
They do not excrete increased Pi (no phosphaturic response) and no increase in urinary cAMP
