Test 2 Endocrine Control Of Calcium

Front 1

calcium is involved in

Back 1

bone/neuromuscular excitability, cardiac conduction, muscle contraction, secretion, coagulation, intercellular mediation, cellular adhenison 2nd messenger

Front 2

control over calcium is tight/loose?

Back 2

tight

Front 3

phosphate roles

Back 3

bone, membrane, nrg metab, nucleic acid polymerizaiton, maintenance of cell excitability and viabiltiy by ATP hydrolysis for ion pumping, extracellular buffering, regulation of cellffunction (proteing phosphyrlation/ getp hydrolysis0)

Front 4

99% of bodiy's calcium is in

Back 4

bone

Front 5

extracellular vs intracellular calcium

Back 5

intracellular 4 orders of magnitude less

Front 6

what keeps intracellular ca low

Back 6

na ca exchange and atp dependent ca 2+

Front 7

bone remodeling

Back 7

ostoclasts precursors activated by osteoblasts…. Recruited to sites in bone to diffentiate and fomre osteoclasts… resorb bone… preosteoblasts arrive, differntaite, osteoblast secrete osteoid collagen matrix; osteoblasts then secrete ca and p which are deposidted

Front 8

osteoclast differentiate from

Back 8

macrophage-monocyte lineatge

Front 9

preosteoclasts hav ewhat kind of nucleus

Back 9

mono- they fuse and form multi-nucleate osteoclasts and acquisition of secretory activity

Front 10

RANKL

Back 10

activates Rank

Front 11

RANKL

Back 11

receptor activator of NFKB

Front 12

where is RANK L

Back 12

surface protein of osteoblasts/stromal cells while rank is on osteoclast

Front 13

MCSF

Back 13

macrophage colony stimulating facort promotes osteoclast

Front 14

rank l is induced by

Back 14

pth and vitamin d during resorption

Front 15

opg osteoprotegenir

Back 15

on osteoblast

Front 16

M-CSF is on

Back 16

osteoblast stims osteoclast progenitor

Front 17

PTH, 1,25 D; PGE2; IL1

Back 17

all stimulate RANKL and OPG

Front 18

the osteo clast bind to bone via

Back 18

matrix integrins and then folrm a membrane

Front 19

what passes through the osteoclased ruffled membrane

Back 19

Cland H+ is pumped in.. Mobilizing bone

Front 20

Cathepsin K

Back 20

degrades demineralized protein component of bone… it's a lysososma protease

Front 21

the deradation producst are processed how

Back 21

endocytosed, transported to and released from the aniresorptive surface

Front 22

BMP

Back 22

bone morphogenic protein… most notable frowth factor for osteoblast

Front 23

which step of osteoblast differntiation is stimulated by PTH and vitamin D?

Back 23

both

Front 24

how much Ca2+ circulating is active

Back 24

50% the ionized form is the physiologic active form

Front 25

what decreases protein bound calcium

Back 25

cirrosis total drops but free same

Front 26

what decreases diffusable calcium

Back 26

citrate, phosphate komplex… usually is 7%

Front 27

majro regulators of ca and PO4

Back 27

claclitriol and PTH

Front 28

minor regulator of Ca nd PO4

Back 28

calcintonin

Front 29

how to correct total plasma

Back 29

correct total plasma ca by adding .8mg/dl for every mg/dl reduciton in serum albumin below normal

Front 30

how does hypocalcemia cause excitability

Back 30

remember the Ca+ lineed up outside the membrane, so it depolarizes when low

Front 31

hypercalcemia symptoms

Back 31

lethargy, drowsiness, coma, neuromsucular fatige and weakness, HTN brady cardia, arrythmias, nausea vomiting constipation, nephropathy, ectopic calcification

Front 32

hypocalcemia symptoms

Back 32

increased neuromuscular excitability; paraestheis, muscle cramps, tentany and convulsions… prolonged asphygiation due to laryngospasm

Front 33

excessive sulights

Back 33

degrade previtamin d3 and vitamin d3 into inactive photoproducts

Front 34

25OHD3

Back 34

calciferol

Front 35

skin vit d rxn

Back 35

7dehydrocholestorl to

Front 36

pre d3 goes to

Back 36

cholecalciferal (same that's absorbed

Front 37

vitamin D2 and D3 transport from diet

Back 37

chylomicrons transported by lymphatic into vensous

Front 38

where is D2 or D3 stored

Back 38

fat cells

Front 39

how is vitamin d ciruclated

Back 39

citamin d binding protedin

Front 40

the major circulating forma f vitmaind

Back 40

25(OH)D

Front 41

vD-25 hydoxylase

Back 41

converts vitamin d (D3, to 25OH3 (what's measured)

Front 42

FGF-23 and vit amind D

Back 42

FGF-23 decreases 1,25 (OH)2D synthessis as does 1,25 9OH)2D itself

Front 43

what promotes 1,25 synthesis

Back 43

low phosphate or low Ca2+

Front 44

D-1 alpha hydroxylase

Back 44

converts 25(OH)D to 1,25 (OH)2 D

Front 45

vitamind d is a ligand for

Back 45

VDR vitamin d receptor

Front 46

Steroids and vitamin D

Back 46

VDR is a transcription factor in the steroid-hromone superfacmilty of nuclrear transcriptional regulators

Front 47

VDR distribution

Back 47

wide

Front 48

vit amind d and cell differentiation

Back 48

has the potential to promote

Front 49

the main stimulus for secterionof PTH

Back 49

hypocalcemia

Front 50

in familial hypercalcmin hypocalcurir what must happen

Back 50

ca must rise to a higher level before inhibitn pth secertion

Front 51

normal pth but high Ca

Back 51

Familiaal hypercalcemic hypoclcuria

Front 52

TRPV6

Back 52

transcellular Ca pathway apical channel

Front 53

Calbinding

Back 53

intracellualr transcellular pathway

Front 54

Ca?na exchanger

Back 54

last step in intenstial transcellular pathway

Front 55

what transcellular ca steps are stimulated by calcitriool

Back 55

ll 3 , trpv5, ca/na xchg; calbindidn

Front 56

major ca absorption route

Back 56

not transcellular

Front 57

calcitrio effects on bone

Back 57

enhances phosphate mobilization directly, but indirectly (stimulates osteoblast differentiation) aids in bonode formation and by maintianng proper ca 2+ it aids in ineralization

Front 58

calcitiorl effects on kidne

Back 58

decreases excretion of clacium and phosphate

Front 59

PTH1R recognizes

Back 59

both PTH and PTHrP

Front 60

PTH1R in

Back 60

bone, kidney and proximal tubles

Front 61

PTH1R is what type of receptr

Back 61

G proteing

Front 62

PTH or PTHrP binding to PTH1r indcuses

Back 62

two g proteins Gs (PKA) and Gq (PKC)

Front 63

intracellular messenter for PTH action in bone

Back 63

cAMP in bone (Gs PKA cAMP)in kidney it's both PKA and PKS

Front 64

PTH2R

Back 64

recognizes only PTH, uncertain role

Front 65

Calcitonin MOA

Back 65

stimulate cAMP produint in bone and kidney however a requirement for cAMP in CT effects is not established

Front 66

Calcitonin effects

Back 66

direct inhibition of bone resorption and calcium and phosphatel 2. increases excretion of calcium and phosphate by the kidney

Front 67

does calcitonin effect intestinal absorption?

Back 67

no not of calcium or phosphate

Front 68

calcitonin secreted

Back 68

inresponse to hypercalcemia