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112 Cards in this Set
- Front
- Back
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what gland secretes:
PTH Calcitonin Vit D (1,25dihydroxycholecalciferol) |
Parathyroid
Thyroid Kidney |
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what is important for:
NM Fx NM excitation Excitation Contraction coiupling Stim/secretion coupling MAINTAINICE of TJ homeostasis and clotting of blood cardiac mechs membrane/enzyme fx metabolism component of teeth/bone |
CALCUIM
**calcium is SUPER importnant in many dif things, that why we have like 3 hormones to keep it in tight regulation |
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what can happen if Calcium levels are messed up
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1. CNS irritability
2. NM irritability 3. Numbness 4. Tetnus 5. Spasms 6. decreased neurotransmission 7. mm weakness 8. impaired mentation 9. lethargy 10 coma |
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where is calcium in the body?
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MOST is in the bones and teeth
The rest is distributed in teh soft tissue and plasma Most in soft Tissue (ER, mito, membranes) Small amt is in the plasma: of this half is bound and half is free and biologically available |
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what are the top 3 places to find Ca in the body
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1. Bone/Teeth
2. Soft Tissue 3. Plasma: half bound to PO4, Albumin, bicarb and the rest is FREE and bioavailable |
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about what % of plasma calcium is availbe to do stuff
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half, the rest is complexed with albumin, PO4 or bicarb
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what happens to Ca levels in acidosis
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Increase! hypercalcemia
H and Ca are both + and will compete for binding areas on albumin, when there is lots of H+ around it kicks Ca out |
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what happens to Ca levels with alkalosis
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decrease! hypocalcemia
**Low H means more Ca will be bound to albumin and less Ca is free |
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what are the 2 differnet stores of calcium we have in bone
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1. Stable: long term, hydroxyapatite, mineralized bone, SLOW exchange via bone resprption
2. Labile Pool: bone fluid, Amorphous crystals, FAST exchange of Ca/PO4 via asteolytic osteolysis |
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bone resorption liberates Ca from where, is it fast or slow
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hydroxyapatitie crystals in the stable bone pool of mineralized bone
SLOW exchange |
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when we steal Ca from bone and its SLOW where do we get it from?
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the Stable pool of mature mineralized bone
Bone Resorption |
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when we have osteolytic osteolysis what pool are we taking from? what about resorption
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Labile Pool, bone fluid, fast
Stable Pool: mineralized bone, slow |
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what is the labile Pool
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its a store of Ca and PO4 in bone fluid
**its easily assessible for Osteolytic Osteolysis *Ca in amorphous crystals |
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if we need calcium fast from the bone where to we take from, whats the process called
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the labile pool,
made of "bone fluid" amorphous crystals *osteolytic osteolysis |
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whats the definition of bone resorption
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SLOW breakdown of bone (hydroxyapatite crystals) to free Ca nad PO4 into plasma
**taken from the stable pool of Ca |
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whats the definition of osteolytic osteolysis
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FAST breakdown of bone (amorphous crystals) to release Ca and PO4 into the plasma
**taken from bone fluid, labile pool of calcium found in bone |
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whats the definition of bone remodelig
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cycle of bone resorption and formation
**does even when we are in Ca balance |
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so when we drink milk what are hte fates of the Calcium?
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1. it can pass through GI unabs and pooed out
2. Vit D can help abs Ca and it can enter ECF 3. From ECF it can go to the kidney for filtration and be abs or excreted OR 5. OR from ECF into the bone |
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what will help us abs Ca from diet
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Vit D
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what will cause bone resorption
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bone resorption is BREAKdown of bone!
**PTH **Vit D **Calcitonin antagonizes these hormones |
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wht does calcitonin do to bone resporption
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resorption is the breakdown of bone
*calcitonin INHIBITS this |
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what hormones affect bone resporption and how
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PTH and Vit D activate bone resorption to increase plasma Ca
Calcitonin inhibits it |
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wahts bone resportion, formation
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resporption is breaking down bone to liberate ca and PO4 in the plasma (+ PHT, + Vit D, - Calcitonin)
**the combination of the 2 leads to bone remodeling formation is making new bone |
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what types of things are phosphate impotant for?
consequences of depletion |
metabolic paths
NAD+ 2 messengers **depletion leads to: sk mm weakness *cardiac/respiratory arrest *RBC integrity dies |
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so ____ is important as 2 messengers adn NAD+, what happens in causes of severe depletion
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PO4
**cardiac/respiratory arrest **Loss of RBC integrity **sk mm weakness |
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where does most of the PO4 stay in the body
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Bones/Teeth!
*the rest is in mm, cytoplasm and ECF |
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what were the numbers of that Ca homeostatis graph? 1000 mg taken in
Abs/Secretion from GI filtration/Reabs/Secretion of Kidney |
Abs 350
Secreted 150 NET ABS: 200 We then see that 200 was excreted from the kidney and 800 was excreted from GI for a total loss of 1000= input |
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does PO4 participate in bone remodeling/
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yep
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compared to calcium, how much dietary PO4 is abs
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lots! it can abs 65%
Ca only did 20% |
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what are the 3 hormones that regulation Ca and PO4?
what are the 3 otgan systems that help regulate Ca and PO4 |
PTH, Calcitonin, Vit D
Kidney, GI, Bone |
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that things does PTH regulate
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Ca
PO4 **released from parathyroid gland |
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what cell secretes Calcitonin
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the clear or Parafollicular cells of the thyroid
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what cell makes PTH? how is it made?
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Cheof Cells of the parathyroid
*made as a PreProPTH |
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How is PTH given the signal for release?
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it has Ca R, with Ca bound no PTH is released
WHen Ca is NOT bound it releases PTH so that Ca will be liberated from teh bone to increase levels of Ca and its signal is turned off |
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PTH is released when blood calcium does what? what organs does it act on?
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drop in blood Ca, this causes an increase in blood Ca via:
1. Bone: resoprtion 2. Kidney: blocks PO4 reuptake, increase Ca reuptake 3. GI: influences it to make Vit D for increasd Ca resorb fromGI |
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how os the PTH signal shut off
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its clever,
low Ca stim PTH release bc there is no Ca bound to the R on cheif cells and so PTH is released. PTH works really super hard to increase Ca levels and in doing so there will be Ca that can then bind to teh Ca R on the cheif cell and this then inhibits PTH secretion |
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is the increase in blood Ca due to PTH associated with the bone resportion alone?
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nope, this frees BOTH Ca and PO4, we just want Ca and PO4 can cause it to ppt out in blood
*we also need the kidney. PTH acts on the kidney to increase Ca reabs and decrease PO4 reuptake so that we pee out PO4 and cAMP |
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if we have cAMP in the urine what can we infere about Ca and PO4 uptake in the kidney
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Ca is beind reabs
PO4 is being excreted out |
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how does the kidney respond to PTH
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1. Increase Ca reabs
2. Decrease PO4 reabs. Inhibits co uptake of Na abd PO4 in the PCT **net effect, increase Ca reabs, PO4 is peed out |
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what does PTH do to Ca abs in the GI? HOW
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increase abs indirectly via Vit D
PTH stimulated 1ahydroxylase which turns vit D into its active form (25 hidroxycalciferol ---> 1,25 dihydroxycalciferol) |
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what the mech of action of PTH onthe bone
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increase Ca reabs!
**it actually binds to osteoblasts first, (initial bone formation) they then secrete things to make the osteoclats active **we need some kind of check adn balance b4 we just start breaking down bone **can be fast or slow |
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the osteocytic osteoblastic bone membrane seperates what
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mineralized bone and labile bone
"seperates the bone itself from the plasma within the canals" has a HUGE SA, just a small amt of activity can have a huge flux of Ca |
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does PTH act on bone to do fast or slow exchange of Ca/PO4
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BOTH
Fast: osteolytic osteolysis from labile pool, rapid exchange btwn bone and ECF Slow: this is bone resorption, Ca and PO4 are released from stable pool |
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bc hte osteolytic osteoblastic membrane is such a large SA a small movemnt of Ca across is actually a large flux of Ca, where is Ca moveing bten
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bone fluid and plasma
**it is made of interconnections of osteocytes nad osteoblasts, when you take Ca across this membrane its "fast" labile pool stuff |
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how is Fast Ca exchange done with PTH at the bone
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Ca is take from labile pool across the osteolytic osteoblastic membrain into the plasma
**done by activating PTH activated Ca pumps lovated on the membrain |
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how is SLOW ca exchange done at the bone?
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still PTH mediated
this is when we ahve Ca being taken from the mature mineralized bone. this when we have PTH binding to blasts and blasts talking to clasts **more long term way to regulate calcium |
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oh so when PTH is used to release Ca into plasma via SLOW mature bone pool what is the mechanism?
role of osteooblasts/clats modulators |
1. PTH binds osteoBLAST
2. Blasts control Clast activity via OPG and OPGL (osterprotegrin and ligand) 3. Whn PTH binds blast it causes OPGL to be released 4. OPGL on clast stimulates bone resorption and Ca/PO4 are liberated into blood |
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what are the 2 things released from blasts to modulate clast activity in SLOW (mineralized bone) resorption
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1. OPG
2. OPGL (osteoprotegrin) **PTH causes the release of OPGL from the blast, this makes the clast be resporptive **If something causes blast to release OPG AND OPGL bone fromation is favored |
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release of what from blasts makes clasts havor bone formation, resorption
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1 formation: OPG and OPGL
2. Resorption: OPGL only |
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will hypo or hyper calcemia cause PTH release
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hypo
**Calcium is a PTH secretagogue |
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sp PTH causes release of BOTH Ca and PO4. we know Ca is important and PO4 is important to make NAD and 2 messengers and things. do we keep both of these useful molecules around
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nope! the kidney makes us pee out PO4 and reabs Ca (vascular calcification)
**this prevents PPT of CaPO4 crystals in the blood **plus if Ca was bound to PO4 its not like we'd have an free bioavailable Ca |
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the product of the Ca and PO4 conc must be below what
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60-70 mg/dl
**this prevents them from ppt nad contributing to vascular calcification |
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what hormoen is responsible for the phoshaturic effect of the kidney
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PTH
**makes you pee out PO4 so that it wont bind to Ca this is good bc Ca is free and bioavailable and CaPO4 crystals can lead to vascular calcificaiton |
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the net effect due to PTH on kidney is what/
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decreased plasma PO4, increased urinary PO4 (blocks reuptake by blocking Na/PO4 cotransport)
increased Ca plasma increased cAMP in urine |
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how can we measure the PTH status in the body
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by measuring cAMP in the urine
**when we have lots of cAMP we have lots of PTH **this is the mech that decreases PO4 reabs, blocks Na/PO4 cotransport with cAMP |
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how is PTH used to increase abs of Ca from GI
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acts of KIDNEY!
**PTH acts in kidney to increase a1hydroxylase, an enzymed needed to make active Vit D. (1 hydroxy --> 1,25 dihydroxy, the active vit D) **vit D then increases abs in the gut |
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where is PTH used to stim 1ahydroxylase to make good Vit D
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done in the kidney
Vit D acts ont eh gut, by stim calbindin synthesis, this means more Ca can bind for abs |
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activated vit D does what?
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stim calbindin synthesis so you can increase Ca abs
**PTH can stim vit D |
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what things can stim PTH release (4)? (inhibit 1)
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1. Low Ca (MAIN)
2. High PO4 3. Low Mg 4. Glucocorticoids inhibited by vit D *stim of PTH causes Ca mobilization from bone, Ca reabs from kidney, Ca abs from GI |
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what does Mg do to PTH
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increases PTH release
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glucocorticoids have what effect on PTH?
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stim release of PTH, can have long term effects on bone resorption leading to osteoperosis and bone fracture
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what does high PO4 do to PTH
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increase secretion!
PTH acts to lower plasma PO4 |
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what effect does Vit D have on PTH
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inhibits its release
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what is the TF RunX2 for
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it differentiates stromal cells into osteoblasts
**when its broken we have a disorder called cleidocranial dysplasia |
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what is cleidocranial dysplasia
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its a disorder when RunX2 is deleted and we cant make osteoblasts,
*blasts regulate clasts so that they can liberate calcium **your shoulders are narrow and have dental problems |
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how are osteoblasts made and what do they do?
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the are made from stromal cells under the influence of RnuX2
**M CSF differntiates them into osteoclasts *tblasts then secrete OPGL (RANKL, same thing) to act on the clast to release bone |
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what is another word for OPGL. what does it do
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RANKL
**when secreted from osteoblasts it acts on clasts to resorb bone |
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if you dont have RunX2 what happens?
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you cant make osteoblasts
**cleidocranial dysplasia, malformed shoulders and teeth issues |
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does PTH monitor Ca levels on a minute to minute basis? does Calcitonin
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yep
Nope |
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what is releases whan plasma Ca is high? Low?
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High: calcitonin
PTH: low |
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what is the stimulus for calcitonin secretion
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high plasma Ca
**inhibits osteiclast bone resorption |
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if we remove the thyroid do we have calitonin problems
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nope, not a huge regulator on Ca levels but when Ca is high it is released to decrease osteoclasts
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where is calcitonin made?
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thyroid
**parathyroid (C) cells **made as a pre pro hormone and hten stored as calcitonin **ready for release when blood Ca is high **inhibits clast activity **ANTI PTH |
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what organs doe Calcitonin act on
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1. Bone: inhibits resorption via clasts so plasma Ca and PO4 decreases
2. Kidney: stim Ca AND PO4 excretion 3. GI: NONE |
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what hormone causes us to excrete Ca nad PO4
What hormone causes us to secrete PO4 only |
calcitonin
PTH |
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what are the total effects of Calcitonin (what is the signal for release, what does it act on, what does htis organ do?
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1. Releases with high Ca
2. Act on Bone to inhibit resportion by clasts, this decreases Ca ADN PO4 3. At the kidney is causes Ca AND PO4 to be excreted 4. Ca nad PO4 plasma levels decrease |
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does calcitonin act on PO4
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yep decreases it
**less PO4 liberated by clasts *more excreteion by kindey **net decrease in PO4 in the plasma |
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what hormone is the one where if we have too much or too little nothing really changes
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calcitonin
1. deficiency of calcitonin doesnt lead to hypercalcemia 2, excess doesnt lead to hypocalcemia 3. May prevent hypercalcemia after a mean 4. may protect against excess bone resorption when Ca demand increases in pregnancy or growth |
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what observations made us know that calcitone wasnt a huge regulatory thing?
what do they think it might be for? |
1. excess or less wont cause a messy Ca balance!
they think it may prevent hypercalcemia after a mean **or protect against excess bone resorption in growth or pregnancy (increased Ca needs) |
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a decreased plasma Ca stim what and inhibits what
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stim PTH
inhibits thyroid C cells calcitonin |
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an increase in plasma Ca stim what, inhibits what
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Calcitonin from thyrpoid C cells
PTH from parathyroid |
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whats the goal of Vit D
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increase Ca and PO4 in plasma so it can be used to make new bone
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what hormones is all about wanting to make new bone
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Vit D
*actions increase plasma Ca and PO4 so that new bone can be laid down |
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what is the active Vit D, what is inactive
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1,25 dihydroxycalciferol
1.24 dihydroxtcalciferol |
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where do we get vit D from ? how is it activated
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1. dietary
2. skin **inactive in either case adn gets OH on in the liver (25) and the kidney (1, stim by PTH) |
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what does Vit D do to Ca and PO4 abs
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increased
**increase plasma levels so new bone can be made |
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how is vit D activated? inactivated
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1. made in skin
2. Goes to liver for Oh at 25 3. Goes to kidney, when Ca is low, PTH is high and PO4 is low we add the 2 OH to the 1 position and made ACTIVE 4. When Ca is high, PO4 is high and PTH is low we add an OH to 24 and INACTIVATE vit D |
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how does the kidney know where to put the last Oh on Vit D (ie why would it make inactive or active Vit D)
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1. when Ca is high, inactive is made
2. when Ca is low, Active form is made so Ca plasma levels will increase |
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what organs does Vit D act on/.
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all
1. Bone: REMODELING, helps PTH to respob bone and free Ca so tht new bone can be made 2. Kidney: promotes Ca AND PO4 reabs (antagonizes PTH with PO4) 3. GI: icnrease calbindin so we can increase Ca abs, induces basolateral Ca/ATPase |
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what hormone increase reabs of BOTH PO4 and Ca in the kidney
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Vit D
**Just Ca reabs is PTH **excretion of both is Calcitonin |
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what is the "anti PTH' action tht Vit D has
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PTH makes PO4 leave in pee
Vit D causes reabs of PO4 in teh kidney |
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what is calbindin? who makes it, what does it do? how does it work
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synthesis is stim by Vit D, acts in GI to increase Ca reabs
**Ca enters the GI cell, Ca binds to calbindin, then the basolateral Ca ATPase sends to Ca into the blood **VITAMIN D DEPENDENT |
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what does Vit D do in GI, how
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stim Ca abs
**makes calbindin *Ca enters GI cells, binds Calbindin, then a basolateral Ca ATP ase sends Ca into the blood **Vit D dependent increase in abs to inrease Plasma Ca levels |
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what causes the activation of Vit D itseld
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PTH, stim the kidney to add on that last OH to make active Vit D
**vit D then acts on bone, kidney, and GI to increase PO4, Ca and make new bone |
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what diesase is "bones, stoans, and groans"
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hyperpatathyrpodism
Increased PTH secretion Causes: hypercalcemia/phoHYPOsphatemia osteroperosis osteomalacia kidney stones (increase Ca/PO4 in plasma) mm weakness, decreased excitability |
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the excess PTH seen in hyperparathyroidism causes what
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increased Ca PO4 makes kidney stones
(but we know a relative increase of PO4 in urine, increased cAMP in urine) hypercalcemia/HYPOphostatemia (constipation) decreased mm excitability. mm weakness Osteoperosis **Bones, stones, groans |
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what does a + trousseaus sign mean
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hypoparathyroidism, decreased PTH
**with a BP cuff on the hand spasms **decreased Plasma Ca **hyper phosphatemia *increased mm excitability **cramps and spasms |
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what disease gives increased mm excitability
decreased |
hypoparathyroidism
hyperparathyroidism |
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in what disease is there lots of cramp like spasms of the body
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poyoparathyroid
**decreased PTH hypocalcemia, hyperphosphatemia |
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what are the 2 types of pseudohypoparathyroidism
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1. Autosomal Dominant disorder
2. Biologically inactive PTH **increased PTH, hypocalcemia, and hyperphosphatemia **weird 4th finger, albrights hereditary osteodystrophy |
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in what disease is PTH high, Ca is low, and Po4 is high
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PTH high should increase Ca and decrease PO4 but this is not hte case
**its PseudoHYPOparathyroidism can be genetic or an inactive PTH molecule |
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why is pseudohypoparathydoidism called such
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we have effects as if PTH was low, BUT its actually high
Low PTH: low ca, high PO4 **get those weird short fingers, albrights hereditary osteodystrophy |
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what is Rickets
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vit D deficiency (Vit D acts on ALL systems to increase PO4 and Ca in plasma)
No vit D means no bone remodling We have decreased Ca, and increased PTH |
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what happens to Ca nad PTH in rickets
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ca is low
PTH is high **we are killing our bones, get growth deformities |
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what leads to osteoperosis
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osteomalacia
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what is osteomalacia
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Vit D deficiency in ADULT, rickts is vit D deficit in children
**caused by decreased dietary intake, or bowel resection **hypocalcemia **painful bones, lots of fractures |
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what is the Vit D deficiency in adults
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osteomalacia
**dietary deficit **bowel sirgery **soft weak bones, fractures lots, painful **low Ca **tx with vit D |
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what is the disease that is characterized by brittle bones tht fracture lots
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osteoperosis
**seen in menopause/female athlete triad: estrogen is bone protective |
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what does estrogen do to bone health, what aout deficiency
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increased bone health
with less estrogen we increase IL4 and IL6, this stim clast activity adn mskes bones weak |
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who is susceptible to osteoperosis
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old
menopausal women female athletes w/.o periods smokers drinkers asthamtics |
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how is osteoperosis tx
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estrogen
exercise flouride biosulfinates (increase hydroxyapatite to strenghten bones, this is the mineralized pool) |
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what IL stim osteoclast activity when there is a decrease in estrogen, what disease
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IL4 IL6
*osteoperosis |
