There are a few factors in solving sarcoidosis pain naturally. One resource I discovered that succeeds in merging these is the Remission Crusher Tactic (check it out on google) without a doubt the best plan that I've seen. Check out the interesting info .
I think its worth mentioning phosphate doesn't need Vitamin D for uptake from the diet. This is part of the reason why in chronic kidney disease, you have low serum calcium but high serum phosphate. The kidney can't make Vitamin D if its diseased, so calcium uptake is not enough, but phosphate can still get across from the intestines into the blood. Cheers Armando you rock by the way : )
CKD - Decreased GFR, Kidney cannot excrete enough phosphate, phosphate increases FGF-23 which blocks 1-alpha-hydoxylase. Decrease Calcitriol, decrease intestinal absorption of ca and phosphate, yet kidney cannot excrete enough phosphate so phosphate remains high and binds free calcium. Decreased calcium stimulates increase in PTH, PTH increases bone turnover, leads to metabolic bone disease, pt over time has bone pain, fractures. PTH normally stimulates kidney to lose phosphate, but decreased GFR and kidney injury causes phosphate to not be excreted.
If you're looking for a few extra steps and more in-dept: The precursers of vit D comes from foods (like oily fish; D3), plants (D2) and the sun D3. In the skin the suns UV-rays converts 7-dehydrocholesterol into cholecalciferol D3 (done non-enzymatically by heat). Cholecalciferol then moves into the liver (transported from the skin by vitamin D-binding-protein (DBP), and by cholemicrons from the diet) for the first part of its activation. Here it is converted by the enzyme (cytochrome P-450-based enzyme) into 25-hydroxy vit D3 (25-OH-D) (calcidiol) the step is called 25-hydroxylation, it then moves to the kidney for its second and last activation. Here the 25-OH-D/DBP complex is taken up at the surface by renal proximal cells by a specific mechanism involving cell surface receptors; megalin and cubulin. In the kidney 25-OH-D is converted to 1,25 dihydroxy vit D (1,25-(OH)2D) (calcitriol) by renal-1α-hydroxylase - this activation is called 1α-hydroxylation (patients with renal failure therefore cannot perform this step). The 1α-hydroxylase comprises 3 proteins: Cyt P-450, a ferredoxin and a ferredoxin reductase for activity. 1α-hydroxylase is strongly downregulated by 1,25-(OH)2D (calcitriol) and strongly upregulated by PTH as a calcium homeostatic loop.
You forgot to mention that PTH reduces the reabsorption of phosphate from the proximal tubule of the kidney, which means more phosphate is excreted through the urine!
Adnan Bashi that's the fosfaturic action of PTH, exactly!! On the other hand, calcitriol does not do that treating equally calcium and phosphate (reabsobring both of them, PTH only reabsorbed calcium) and so, if there's an excess of calcitriol (vit D), they can precipitate.
not true i have both high phosphate and pth with low low t4 wich i take meds for but nothing i can do for my pth issues so im fct, this condition was missed for years now i have perment bone and liver problems now and heart racing issues.
you are such a lifesaver. this was so clear. cleared a lot of confusion I had on the main hormone that controls bone growth and remodeling. keep up the great work! looking forward to more of your work.
I thought PTH decreases re-absorption of phosphate ( increases excretion ) and increases re-absorption of Ca+ ( decreases excretion ) in the kidney > ?
yes you are right! PTH increases the secretion of phosphate in the kidney and also increases retention of Ca2+ in the kidney. So Ca2+ lvls will rise and phosphate lvls will decrease, because otherwise they would form again a complex in which Ca2+ is not free so not excessable for the body needs. But be careful! PTH is just a short time response, long time regulation is the role of Vit. D3 and calcitonin. Hope that helped.
All this indicates that PTH increases serum phosphate, when in fact it lowers it. You need to make sure to be a little more complete in your explanation here.
You've got some wonderful content in here!!! I discovered this channel a few weeks ago and my whole study game has changed ever since! Thank you so much @armandohasudungan
Possible Correction: I may be wrong about this but after some researching, I found that C-FMS you mentioned on osteoclast is actually the gene that encodes CSFR-1 which is the receptor on osteoclast. If someone else could also research and confirm or deny this, that would be great! Thanks! Your videos are awesome!
they basically happen at the same time ie. PTH stimulates bones to reabsorb calcium AND phosphate back into the bloodstream, same goes for the initial GI absorption and its upregulation as per PTH. I believe the same happens in the kidneys as well. i also believe that slightly more phosphate is released by the bones than calcium, such that kidney compensates by reabsorbing slightly less phosphate to maintain pH homeostasis, but this info is from memory rather than sourced, so could be wrong.
As much as I appreciate the information, it is a major pain for the non-Anglo world to decipher Latin- or Greek-based terminology pronounced consistently wrong: calci-trial (cal-citri-ol), lie-gand (liggand), oxi-daze (oxi-dah-sey), endo-cry-nology (endocreenology, 'i' as in FIT). 'Armando Hasadungan' sounds of 'Phili-pine' origin, thus, having once been a Spanish colony, could we have a Spanish based pronunciation, PLEASE?
Calcitonin has a very limited role to play in calcium homeostasis in adults. Its mostly prevalent in infants and children. In adults the "surface calcium-sensing recepters" located on the parathyroid gland sense changes in plasma calcium levels and inhibit PTH as you describe. This is the main major adjustement, calcitonin action is very very limited.
i had an eyegasm while watching this, also your accent is so good!! tysm for this, i search everywhere for a good video about calcium homeostasis and here i am. tysm for explaining it this way. also, the drawings, i loved them!! thank you thank you
I've just been diagnosed with parathyroid disease. I have been working on my thyroid issues (Autoimmune Hashimoto's) My PTH is too high. My Vitamin D 3 is currently 82. I am peeing 8-10 times per night, and I am exhausted all the time. I am trying to get an appt with an endo to dig deeper into this issue and look for a treatment plan. I also am experiencing gut issues and am wondering if this is related?
Ok so doctor said my D levels are toxic at 157. We are thinking it's from the supplements i was taking which were 50,000 iud. But could it be from my thyroid nodules? i have cyst and nodules on it.
does calcitriol always stimulate bone breakdown for Ca++? or only when Ca++ serum levels are low? in other words, can it just work with the GI and kidneys to stimulate reabsorption without hurting the bones?
Hello Armando, I came here because I needed to understand how do interact Calcium levels, vitamin D and PTH, because I have multiple sclerosis and I’m following a therapy called Coimbra Protocol, which is based in a few pillars: - Ultra high Dosis of vitamin D3 (50.000 units in my case to set my immune system back to “default”) - Very low calcium diet (to avoid to much calcium to filter) - More than 2,5 L of liquids per day (to avoid high concentration in Urine) - Regular sport (to build bone tissue up) - Avoid stress and unhealthy food My question is, why, when a low level of Calcium in blood stimulates the production, did my PTH level increased from 21 pg/ml to 31? The second time I checked this value, it only increased from 19,5 to 21 in the same time frame. I ate a bit more calcium-rich food in this time, so my body should have absorbed way more calcium. I just don’t get it A video about the coimbra protocol, how it works and what are its dangers, would be really nice :)
Doesn't PTH decrease phosphate level not increase it ? calcitonin decreases both phosphate and calcium, vitamin d3 increases both minerals, PTH increases calcium and deceases phosphate
in renal faliure, if patients are unable to convert calcidiol to calcitriol why we are giving the suppliments of cholecalciferol (vit D3)to ckd patients.
Mr. Armando im having trouble grasping some of the functions of activated vitamin d3. While i do understand vitamin d3 main role is to absorb calcium and phosphate from the small intestines and acts similarly to pth in osteoblast proliferation and maturation I dont understand how it helps in calcium reabsorption from the proximal convoluted tubules. This is because from what i can understand all of calcium reabsorption in the proximal convoluted tubules occurs in a paracellular meaning it does not enter cells but passes between cells and it does not depend on hormonal action therefore activated vitamin does nothing in PCT, it is only by concentration gradients of Calcium and phosphate. and in your video you put that vitamin d regulates the PCT calcium phosphate absorption. Help me understand, thank you.
Thank You! Finally a good explanation of the calcium system. I wonder why it is often claimed that one cannot feel when bone is decreasing or osteoporosis sets in. The acid that "eats" the bone due to the osteoclast activity must be painful. Acid/nerves=pain.
God bless Dr.Igudia on UA-cam, all my life will keep thanking you for the great help and for your product which actually works in eradicating HSV2 out of my body system
Why my GFR dropped down to 60 . I had a surgery few months ago, my BP went up to 16/90, I'm post menopausal. Taking vit D, magnesium zinc sometimes potassium....and vit B complex .
question: normal calcium levels from BMP, low phosphate (as Phosphorus), and very low D3. How do you treat very low d3? you can't prescribe calcitriol bc that will increase the patient's calcium level and might lead to hypercalcemia. Both Phosphate and D3 can be treated individually as supplements but is that the only way? why can't an increase in D3 increase phosphate too? -med student who got an exam question wrong
This video is amazing...i mean i was about to spend 3 hrs on this metabolism now with this video in just 20 min i gain all concept regarding ca metabolism ...thanks...thanks alot
there is a mistake here!! PTH stimulate (PCT )to form vit D3 and then PTH together with 1,25 dihydroxy cholecalciferol stimulate (DCT ) NOT the reverse
facing possible parathyroidectomy after years of hyperparathyroidism (maybe my lifetime) and this is the FIRST explanation of the why of the many attempts over the years for the various 'treatments' tried to little avail. I've doubled my D3 intake, for starters, now that I understand its role.
Does 1,25 dihydorxy vit D enhance the reabsorption of only phosphate or both phosphate and calcium from the proximal convoluted tubules of the kidney??
I have one little critic point, I wonder because I found out that calcitriol doesn't effect the proximal but the distal tubules in the same manner as PTH. It leads to an increased synthesis & incorporation of EcaC-Ca2+ channels into the DCT which then take up the Ca2+ into the cells leading to increased Ca2+ reabsorption. EcaC channels are not part of PCT and I learned that regulation only takes place in the DCT. Please consider & if possible disprove my critics.
One thing that doesnt make sense to me, when talking about phosphorus, is the actions of PTH. On one hand PTH stimulates calcium and phosphorus absorption in the small bowel and increases bone resorption leading to increased serum phosphorus. But my textbook also says that a primary action of PTH is to lower serum phosphorus levels by lowering the renal phosphorus threshold, thereby decreasing renal phosphorus reabsorption, and increasing urinary phosphorus excretion. So PTH both increases and decreases serum phosphorus? This makes no sense.
So, PTH basically increase phosphate excretion by urine, and it also cause an increase in phosphate levels by the action of the osteoclasts, yet, the overall effect of this hormone is "decrease' in levels of phosphate... how come? I'm kinda confused and I hope I didn't get it totally wrong
pls clear one doubt, as PTH is stimulating both osteoblast n clast so it must be in equilibrium bcz anyways osteoclasts are also getting activated by osteoblast but you started this bone cell discussion with the context that PTH increases ca and phosphate in the blood... so how is it justificable that pth is increasing these levels in blood through osteoclasts bcz osteoblast are equally involved in bome mineralization
what conditions cause high phosphate with high pth low thyroid hormone bone liver and conective tessue desase with heart racing and diarrhea and unbreaking down of certain vegitibles . dockter does not understand why liver and phaspates and pth are high without kidney desaese.... maybe someone can help with a diagnoses because if i dont get to the bottom of it im gona die i feel my self dieing, and ive allmost dies a few times with heart puputaions
brother pls guide us regarding... the effects of levels of calcium and vitamin in blood on bone. and the related disorder like ricket, osteomalacia and osteoporosis
![[UA] NAVI проти G2 Esports | Blast Premier Fall Final](http://i.ytimg.com/vi/QWlIm4FGESQ/mqdefault.jpg)
This video just taught me more in 11 minutes than my lecturer has in like 235 powerpoint slides :))))))) ur the best
Exactly 👌🏻
Asweer chale 😂
U dey UG?
@@kingbobbie5196 ye
Oh nice... which year?
what would i do in med school without your videos
Zeynep Ece Arslan Tra
There are a few factors in solving sarcoidosis pain naturally. One resource I discovered that succeeds in merging these is the Remission Crusher Tactic (check it out on google) without a doubt the best plan that I've seen. Check out the interesting info .
trueee
go vegan and work it out for yourself
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I think its worth mentioning phosphate doesn't need Vitamin D for uptake from the diet. This is part of the reason why in chronic kidney disease, you have low serum calcium but high serum phosphate. The kidney can't make Vitamin D if its diseased, so calcium uptake is not enough, but phosphate can still get across from the intestines into the blood. Cheers Armando you rock by the way : )
CKD - Decreased GFR, Kidney cannot excrete enough phosphate, phosphate increases FGF-23 which blocks 1-alpha-hydoxylase. Decrease Calcitriol, decrease intestinal absorption of ca and phosphate, yet kidney cannot excrete enough phosphate so phosphate remains high and binds free calcium. Decreased calcium stimulates increase in PTH, PTH increases bone turnover, leads to metabolic bone disease, pt over time has bone pain, fractures. PTH normally stimulates kidney to lose phosphate, but decreased GFR and kidney injury causes phosphate to not be excreted.
I was looking for this. Thank you so much.
Anything apart from kidney disease that causes low serum calcium and high serum phosphate?
ahh thank you!
@@samuelbenson1 saved my life thank you!
If you're looking for a few extra steps and more in-dept:
The precursers of vit D comes from foods (like oily fish; D3), plants (D2) and the sun D3. In the skin the suns UV-rays converts 7-dehydrocholesterol into cholecalciferol D3 (done non-enzymatically by heat). Cholecalciferol then moves into the liver (transported from the skin by vitamin D-binding-protein (DBP), and by cholemicrons from the diet) for the first part of its activation. Here it is converted by the enzyme (cytochrome P-450-based enzyme) into 25-hydroxy vit D3 (25-OH-D) (calcidiol) the step is called 25-hydroxylation, it then moves to the kidney for its second and last activation. Here the 25-OH-D/DBP complex is taken up at the surface by renal proximal cells by a specific mechanism involving cell surface receptors; megalin and cubulin. In the kidney 25-OH-D is converted to 1,25 dihydroxy vit D (1,25-(OH)2D) (calcitriol) by renal-1α-hydroxylase - this activation is called 1α-hydroxylation (patients with renal failure therefore cannot perform this step). The 1α-hydroxylase comprises 3 proteins: Cyt P-450, a ferredoxin and a ferredoxin reductase for activity. 1α-hydroxylase is strongly downregulated by 1,25-(OH)2D (calcitriol) and strongly upregulated by PTH as a calcium homeostatic loop.
You forgot to mention that PTH reduces the reabsorption of phosphate from the proximal tubule of the kidney, which means more phosphate is excreted through the urine!
Adnan Bashi I think he included that in one of his older videos which is the "bonehomeostasis (calcium phosphate) hormones" video :D
exactly what i was confused about okay so i did understand the concept
Thanks adnan
Adnan Bashi that's the fosfaturic action of PTH, exactly!! On the other hand, calcitriol does not do that treating equally calcium and phosphate (reabsobring both of them, PTH only reabsorbed calcium) and so, if there's an excess of calcitriol (vit D), they can precipitate.
not true i have both high phosphate and pth with low low t4 wich i take meds for but nothing i can do for my pth issues so im fct, this condition was missed for years now i have perment bone and liver problems now and heart racing issues.
videos like this in youtube became my teachers in online class.. I shouldn't enroll in school 😂.. I should enroll in youtube😂
Can you post the final diagram on your website? It would be nice to have the final diagram for reference.
Hannah Helton hi
screenshot parts and redraw it
I'm studying this stuff and it's great to see it in easy to see pictures and descriptions/words. And you have pretty impressive hand skills!
this is truly an amazing explanation in a short amount of time compared to long complicated lectures ! thank you so much sir
you are such a lifesaver. this was so clear. cleared a lot of confusion I had on the main hormone that controls bone growth and remodeling. keep up the great work! looking forward to more of your work.
pituitary gland lowkey thick
facts
🤣😂😂
Lmaoo
are you still alive ?
I thought PTH decreases re-absorption of phosphate ( increases excretion ) and increases re-absorption of Ca+ ( decreases excretion ) in the kidney > ?
yes you are right! PTH increases the secretion of phosphate in the kidney and also increases retention of Ca2+ in the kidney. So Ca2+ lvls will rise and phosphate lvls will decrease, because otherwise they would form again a complex in which Ca2+ is not free so not excessable for the body needs.
But be careful! PTH is just a short time response, long time regulation is the role of Vit. D3 and calcitonin.
Hope that helped.
Thank u !
Freakzzz strong med 😉
There are mistakes in this.
I just love this guys handwriting. It's so regular and consistent.
yes he is great writer and draws beatifully
Truuuuuuuu
All this indicates that PTH increases serum phosphate, when in fact it lowers it. You need to make sure to be a little more complete in your explanation here.
Yes that is right, as pth increases the phosphate excretion in the urine
Thank you so much! Clear and easy to understand - I really loved it!
although my studies are in French but this explanation was very helpful.. Thank U Mr. Armando /big hi from Algeria :)/
You've got some wonderful content in here!!! I discovered this channel a few weeks ago and my whole study game has changed ever since! Thank you so much @armandohasudungan
your endocrinology videos are second to none, great job!
Which means over secretion of parathyroid hormone weakens our bones....... wright?
Thank you for this video😭🙏🏻
This is to complicated to me. What does it mean if you have lupus but i was just told my phosphate level to high and something in bloodstream
This is so amazing, I don't know why I couldn't find it before, but it's really very helpful , Thank you 😊😊
amazingly well explained, thank you!
1 to 2 hours lecture in just 11 minutes...
Thanx a lot....🥰
Possible Correction: I may be wrong about this but after some researching, I found that C-FMS you mentioned on osteoclast is actually the gene that encodes CSFR-1 which is the receptor on osteoclast. If someone else could also research and confirm or deny this, that would be great! Thanks! Your videos are awesome!
What about bone mineralization? I know it is done by osteoblasts, but, what factors increase the activity of osteoblast?
Quick question, if calcium in the blood serum is increased does that mean calcium in the bone is decreased?
You have a gift of teaching! Your videos are so clear and easy to comprehend! THANK YOU!!!!!!!!
It could not be explained better than this 👏🏻
Did I miss the part where he talks about phosphate? seems all about calcium
they basically happen at the same time ie. PTH stimulates bones to reabsorb calcium AND phosphate back into the bloodstream, same goes for the initial GI absorption and its upregulation as per PTH. I believe the same happens in the kidneys as well. i also believe that slightly more phosphate is released by the bones than calcium, such that kidney compensates by reabsorbing slightly less phosphate to maintain pH homeostasis, but this info is from memory rather than sourced, so could be wrong.
As much as I appreciate the information, it is a major pain for the non-Anglo world to decipher Latin- or Greek-based terminology pronounced consistently wrong: calci-trial (cal-citri-ol), lie-gand (liggand), oxi-daze (oxi-dah-sey), endo-cry-nology (endocreenology, 'i' as in FIT). 'Armando Hasadungan' sounds of 'Phili-pine' origin, thus, having once been a Spanish colony, could we have a Spanish based pronunciation, PLEASE?
I thought he was going to include the effect of FGF23 in your explanation.
Calcitonin has a very limited role to play in calcium homeostasis in adults. Its mostly prevalent in infants and children. In adults the "surface calcium-sensing recepters" located on the parathyroid gland sense changes in plasma calcium levels and inhibit PTH as you describe. This is the main major adjustement, calcitonin action is very very limited.
i had an eyegasm while watching this, also your accent is so good!! tysm for this, i search everywhere for a good video about calcium homeostasis and here i am. tysm for explaining it this way. also, the drawings, i loved them!! thank you thank you
definitely very helpful for my upcoming nutritional physiology exam!
naturaly extracted products are always best to use ...best branded product like PATANJALI & EARTHYBOON are best source of natural items
I've just been diagnosed with parathyroid disease. I have been working on my thyroid issues (Autoimmune Hashimoto's) My PTH is too high. My Vitamin D 3 is currently 82. I am peeing 8-10 times per night, and I am exhausted all the time. I am trying to get an appt with an endo to dig deeper into this issue and look for a treatment plan. I also am experiencing gut issues and am wondering if this is related?
thank you very much
how would i Be Studying microbiology without your Videos<
Make More..
Ok so doctor said my D levels are toxic at 157. We are thinking it's from the supplements i was taking which were 50,000 iud. But could it be from my thyroid nodules? i have cyst and nodules on it.
Thank you thank you thank youuu!!!!💜💜💜💜😭😭😭😭😭😭
when he is more of an artist and a scientist combined in one human entity... Respect Boss...
Screenshot at 11:14
does calcitriol always stimulate bone breakdown for Ca++? or only when Ca++ serum levels are low? in other words, can it just work with the GI and kidneys to stimulate reabsorption without hurting the bones?
go for EARTHYBOON & patanjali products for natural remedy
Hello Armando, I came here because I needed to understand how do interact Calcium levels, vitamin D and PTH, because I have multiple sclerosis and I’m following a therapy called Coimbra Protocol, which is based in a few pillars:
- Ultra high Dosis of vitamin D3 (50.000 units in my case to set my immune system back to “default”)
- Very low calcium diet (to avoid to much calcium to filter)
- More than 2,5 L of liquids per day (to avoid high concentration in Urine)
- Regular sport (to build bone tissue up)
- Avoid stress and unhealthy food
My question is, why, when a low level of Calcium in blood stimulates the production, did my PTH level increased from 21 pg/ml to 31? The second time I checked this value, it only increased from 19,5 to 21 in the same time frame.
I ate a bit more calcium-rich food in this time, so my body should have absorbed way more calcium.
I just don’t get it
A video about the coimbra protocol, how it works and what are its dangers, would be really nice :)
Porque lo que tienes es un tumor en las glándulas paratiroideas. O varios tumores. Hay que sacarlos y ya no te enfermas
Doesn't PTH decrease phosphate level not increase it ? calcitonin decreases both phosphate and calcium, vitamin d3 increases both minerals, PTH increases calcium and deceases phosphate
in renal faliure, if patients are unable to convert calcidiol to calcitriol why we are giving the suppliments of cholecalciferol (vit D3)to ckd patients.
if vitamin D3 stimulates bone to break down and relise Ca, why do we use vitamin D3 in richets, osteoporosis....?
Thank you sir
Hi this s priya I have 4 years girl child .she s suffered from hypoparathyroidism . Past 3 years we followed medicine please help me anybody
Tksss i just found that my pth is a little high and already cause some
Issue to my bones 😞,, Im still wondering what happens
EARTHYBOON &PATANJALI products are best
I have reading in hypoPTH cause hyperphosphatemia. Can u explain that reason ?
Brief, clear, and knowledgeable.
Keep up the good work.
I have adoubt ...if vit d cause osteoclast activity why is that the deficiency of vit d causes rickets ..please explain
thank you man !
your videos are really helpful for us med students
keep up the good work 😁😁
A lot of Love from Kenya♥️🇰🇪
Vit D cause Bone to release Ca. İsnt it bad for mineralization of Bone Shoulndt it cause bone diseases ?
Great! :) Please explain rapid and slow action of calcium homeostasis as well
Brilliant, that's very helpful. I appreciate you
I had a doute here I learned that calcitriol helps in mineralisation of bone but u are saying that it helps in deminaralizaton
Mr. Armando im having trouble grasping some of the functions of activated vitamin d3. While i do understand vitamin d3 main role is to absorb calcium and phosphate from the small intestines and acts similarly to pth in osteoblast proliferation and maturation I dont understand how it helps in calcium reabsorption from the proximal convoluted tubules. This is because from what i can understand all of calcium reabsorption in the proximal convoluted tubules occurs in a paracellular meaning it does not enter cells but passes between cells and it does not depend on hormonal action therefore activated vitamin does nothing in PCT, it is only by concentration gradients of Calcium and phosphate. and in your video you put that vitamin d regulates the PCT calcium phosphate absorption. Help me understand, thank you.
Why you don't mention the effect of PTH and Vit D on phosphate on the kidney?
what about FGF23 for phosphate metabolism?
Thank You! Finally a good explanation of the calcium system. I wonder why it is often claimed that one cannot feel when bone is decreasing or osteoporosis sets in. The acid that "eats" the bone due to the osteoclast activity must be painful. Acid/nerves=pain.
You are smart! And gifted! :D
Nicely Drawing and Nice Class❣️
Why don't you talk about FGF-23?
FGF23 , je pense qu'il inhibe la réabsorption tubulaire des phosphates et la synthèse de la calcitriol .
Hope it help ( its frensh )
Which cells of kidney release 1- hydroxylase???
Is the calcitonin has a receptors in osteoclasts cells
Please reply
Continue ur great work sir 🙂👍ur the best
God bless Dr.Igudia on UA-cam, all my life will keep thanking you for the great help and for your product which actually works in eradicating HSV2 out of my body system
Came here for Rank Ligand actvt and did a quick review of The 3 hormones!! Thanks a lot! ✊
Why my GFR dropped down to 60 . I had a surgery few months ago, my BP went up to 16/90, I'm post menopausal.
Taking vit D, magnesium zinc sometimes potassium....and vit B complex .
Thanks for helping my lazy ass who bunked the classes of endocrinology with this simple kickass explanation. 👁️👄👁️
Hi Armando, you drew the pituitary gland, but did not mention anything about it. Thanks again for your videos
question: normal calcium levels from BMP, low phosphate (as Phosphorus), and very low D3. How do you treat very low d3? you can't prescribe calcitriol bc that will increase the patient's calcium level and might lead to hypercalcemia. Both Phosphate and D3 can be treated individually as supplements but is that the only way? why can't an increase in D3 increase phosphate too?
-med student who got an exam question wrong
This video is amazing...i mean i was about to spend 3 hrs on this metabolism now with this video in just 20 min i gain all concept regarding ca metabolism ...thanks...thanks alot
there is a mistake here!! PTH stimulate (PCT )to form vit D3
and then PTH together with 1,25 dihydroxy cholecalciferol stimulate (DCT ) NOT the reverse
facing possible parathyroidectomy after years of hyperparathyroidism (maybe my lifetime) and this is the FIRST explanation of the why of the many attempts over the years for the various 'treatments' tried to little avail. I've doubled my D3 intake, for starters, now that I understand its role.
calcitonin , calcidiol , calcitriol , cholecalciferol
Does 1,25 dihydorxy vit D enhance the reabsorption of only phosphate or both phosphate and calcium from the proximal convoluted tubules of the kidney??
I have one little critic point, I wonder because I found out that calcitriol doesn't effect the proximal but the distal tubules in the same manner as PTH. It leads to an increased synthesis & incorporation of EcaC-Ca2+ channels into the DCT which then take up the Ca2+ into the cells leading to increased Ca2+ reabsorption. EcaC channels are not part of PCT and I learned that regulation only takes place in the DCT.
Please consider & if possible disprove my critics.
One thing that doesnt make sense to me, when talking about phosphorus, is the actions of PTH. On one hand PTH stimulates calcium and phosphorus absorption in the small bowel and increases bone resorption leading to increased serum phosphorus.
But my textbook also says that a primary action of PTH is to lower serum phosphorus levels by lowering the renal phosphorus threshold, thereby decreasing renal phosphorus reabsorption, and increasing urinary phosphorus excretion. So PTH both increases and decreases serum phosphorus? This makes no sense.
Absolutely fantastic! I get it!
Big thanks from Ireland ☘️👍🏻☘️
So, PTH basically increase phosphate excretion by urine, and it also cause an increase in phosphate levels by the action of the osteoclasts, yet, the overall effect of this hormone is "decrease' in levels of phosphate... how come? I'm kinda confused and I hope I didn't get it totally wrong
Honestly thought this was animated till looking closer, props to ur drawings and hard work
What about vitamin K2-7 ?
This video is a great way to recap physiology of Ca2+. Pictures help alot. Thanks!
Mind-blowing explanation.:))
thanks soo much,am realy enjoyed
Pleasssse pleeeease I want this diagram ):):
I was born 7 days before this video came out. After 17 years and 9 days, here I am studying for this for my exam in 2 days hahaha.
pls clear one doubt, as PTH is stimulating both osteoblast n clast so it must be in equilibrium bcz anyways osteoclasts are also getting activated by osteoblast but you started this bone cell discussion with the context that PTH increases ca and phosphate in the blood... so how is it justificable that pth is increasing these levels in blood through osteoclasts bcz osteoblast are equally involved in bome mineralization
Is there any association between hyperparathyroidism & thyroid stimulating hormone??
Thank you..i understand it even better than reading books or in class😅...Gracias❤
Man, this dude can fucking draw!
what conditions cause high phosphate with high pth low thyroid hormone bone liver and conective tessue desase with heart racing and diarrhea and unbreaking down of certain vegitibles . dockter does not understand why liver and phaspates and pth are high without kidney desaese.... maybe someone can help with a diagnoses because if i dont get to the bottom of it im gona die i feel my self dieing, and ive allmost dies a few times with heart puputaions
brother pls guide us regarding... the effects of levels of calcium and vitamin in blood on bone. and the related disorder like ricket, osteomalacia and osteoporosis