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Costanzo Physiology (Chapter 9F) Endocrine Physiology: Calcium Regulation || Study This!

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hello and welcome to the final portion

of the endocrine physiology chapter of

costanzo's physiology textbook

in this video we're going to go over the

regulation of calcium and phosphate

mainly going over the actions of pth

or parathyroid hormone if you enjoyed

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otherwise let's jump straight into

talking about

calcium and how it's moved around in the

blood starting off with the calcium

that's actually bound to plasma proteins

about 40 of the total calcium within our

blood

is bound to proteins the rest is ultra

filtratable meaning that it can actually

go into our nephron because remember

proteins don't cross that glomerular

membrane

out of that 60 that gets ultra filtrated

50 is ionized so the majority of that 60

is ionized calcium the remaining 10 is

complex to anions like phosphate

now this ionized portion this 50 percent

this is what is metabolically active and

this is what the parathyroid hormone is

regulating it's trying to regulate the

ionized calcium

if we are hypocalcemic or hypercalcemic

to the point of causing clinical signs

it's because of a change in our ionized

calcium

we may get a change in our total calcium

due to a change in our protein levels

within our bloodstream

but it's important to focus on the level

of the ionized calcium

so we do have some factors that once

again alter our total calcium so plasma

proteins alter it

anion concentration alter it so if we

have increased phosphate within our

system within our bloodstream

and that's going to increase the amount

that's complex to iron ions

so then our ionized calcium is going to

decrease relatively

and then our acid-base abnormalities can

change things in

acidemia albumin actually binds to more

of those hydrogen

ions so it displaces the calcium bound

to plasma proteins

so then our ionized calcium is actually

going to increase

and vice versa for alkalemia so you may

actually notice some clinical signs of

hypocalcemia

during an alkalotic state now the

clinical signs associated with

calcium abnormalities hypocalcemia we

end up with

excitability of tissues and cells that's

because we actually

lower the threshold potential basically

we make those

sodium channels more twitchy to open so

now it's going to

open much more readily and therefore we

need a lower stimulus

for an action potential to be fired so

hypocalcemia

results in increased action potential

firing in cells

and basically causes twitches and

excitability

hypercalcemia on the other end so high

calcium

is going to cause the opposite and slow

things down so we end up with

constipation we end up with hyporeflexia

lethargy coma potentially even death we

also end up with polyuria and diptyo

with hypercalcemia because we're

increasing the amount of calcium going

into our

urine which takes with it water so

getting to overall calcium homeostasis

this figure down the bottom here depicts

it nicely we have our extracellular

fluid concentration so our plasma

calcium level

and you can see we have three organ

systems contributing to it we've got our

intestine

our kidney and our bone our bone is

constantly remodeling so our osteoblasts

are constantly adding bone to bone and

our osteoclasts are constantly removing

old bone so we're constantly recycling

old bone for new bone

and that can be altered to increase

resorption to increase our calcium

levels within our blood

or increase deposition to reduce our

calcium levels within our blood we'll

get to the hormones that are able to do

that shortly when it comes to the

intestine

we can increase our absorption of

calcium from our intestine but we can't

alter

secreting additional so mainly in the

intestine we're trying to absorb more

calcium during hypocalcemic states

in the kidney we're able to reabsorb

more calcium as well

so we are able to increase the amount of

calcium getting reabsorbed

from the nephron so we lose less in the

urine so that's able to also

increase our calcium during hypocalcemic

states

so you'll also see these little plus

signs which mean that they are

activating and you'll see that pth and

125

dihydroxycholine calciferol which is a

mouthful

we're going to call this just activated

vitamin d they

activate the reabsorption of calcium

from each of these

organs so that increases calcium when we

have low body calcium levels

you'll notice that the only other

hormone here is calcitonin which we'll

touch on right at the end

this is an inhibitory effect on boner's

absorption so that's

actually going to be secreted when we

have high calcium levels within the

bloodstream

but we're not going to focus on that one

too much because this chapter is mainly

about the parathyroid hormone

so a parathyroid hormone gets released

whenever we have changes

and now ionized calcium and you'll see

in this graph here that we have the

sigmoidal

shape to pth secretion compared to our

total plasma calcium

so this shows that calcium wants to be

maintained right

in the middle here and one minor change

of calcium in either direction

will result in a dramatic change in our

pth secretion

if we slightly reduce our ionized

calcium we get a remarkable change with

increase in pth secretion instantly if

we slightly increase our calcium then we

get instantly a reduction in our pth

secretion

so we finely tune our calcium level and

try to keep it as constant as possible

parathyroid hormone is actually released

from the chief

cells within the parathyroid glands it's

called parathyroid because there are

these four

tiny little glands right next to the

thyroid gland itself

if we have chronic hypocalcemia so low

calcium levels

then we're going to get a constant

stimulus to produce pth

and the actual cells themselves the

chief cells

will be told to transcribe more of that

gene

that's going to synthesize pth so you

actually see hypertrophy of your

parathyroid glands

and a hyperparathyroid state with

chronic hypocalcemia

and that's called secondary

hyperparathyroidism it's a little teaser

for what we're going to be talking about

later on in this video now it does touch

very briefly on magnesium basically

magnesium

has similar effects to calcium or pth

secretion so if we have hypomagnesemia

then we'll have some pth

secretion as well it's not really the

focus of this

video or this chapter but just a little

side note there

so the actions of parathyroid hormone

it mainly works through the adenylyl

cyclase secondary messenger system by

increasing cyclic amp

and by doing that we increase the

resorption of bone and we increase the

reabsorption of calcium within the

kidney it also works on the intestines

in an indirect manner by

activating vitamin d active vitamin d

then actually increases the reabsorption

of calcium from the intestines

so pth works on those three organs but

in an

indirect manner works on that intestine

so in bone

the first thing pth does is actually

interestingly this is going to be

confusing

it actually increases the activity of

the osteoblasts so it actually slightly

increases the deposition of bone

initially but the long-term effects

through the increased production of

cytokines from the osteoblasts

it's actually going to be a marked

increase in the osteoclastic activity to

reabsorb bone

so really the net effect is a resorption

of both

calcium and phosphorus from the bone

into your

extracellular fluid space in the kidney

remember we talked about pth

in the kidney how it inhibits phosphate

reabsorption from that proximal

convoluted tubule so we increase the

amount of phosphorus

excretion in the kidney resulting in

phosphateuria but not only that

it increases the reabsorption of calcium

within the kidney

and this is important because since the

parathyroid hormone has increased the

resorption of both calcium and phosphate

from bone

if it keeps reabsorbing both of these

together then calcium will just get

complexed with phosphate and our ionized

calcium wouldn't increase as much

so it needs to actually excrete some

phosphate and just

increase the amount of ionized calcium

within the bloodstream because that's

what it's trying to maintain that is the

metabolically active form of calcium

so in the kidney it increases phosphate

secretion or excretion

and also increases calcium reabsorption

from that distal convoluted tubule in

the small intestine once again

it works indirectly via activated

vitamin d

to increase the absorption of calcium

from the intestine and we'll get into

more details and exactly how it's able

activate vitamin d in the kidney but at

least for now just remember

small intestine is going to increase the

calcium absorption

in the presence of pth indirectly due to

activated vitamin d now how about some

issues of parathyroid hormone

we've got a couple conditions here

number one primary hyperparathyroidism

think about this logically

primary means that the issue is the

parathyroid gland itself so the

parathyroid gland

is increasing the secretion of pth this

is going to occur due to a tumor that's

producing pth

if we have excessive pth that means

we're going to reabsorb a lot of calcium

and excrete a lot of

phosphorus from the kidneys so we're

going to have hypercalcemia

and hypophosphatemia our bones are going

to also become very very weak because we

are

absorbing a lot of those minerals so you

end up

with the saying of stones bones and

groans

stones because you start to produce

calcium stones within your urine

although there's increased reabsorption

in your kidneys there's still so much

calcium in the bloodstream

that there's a high filtered load so you

still end up technically with more

calcium being

in the urine along with that phosphorus

so you end up with calcium stones within

the urine

your bones become weakened because

they're getting resolved

and groans because of the constipation

from hypercalcemia

the treatment for this is

parathyroidectomy secondary

hyperparathyroidism means that there is

a hypocalcemic state that is chronic

that's causing the parathyroid gland to

increase its secretion

so something is causing calcium

deficiency

and that occurs due to vitamin d

deficiency so we're unable to reabsorb

enough calcium from our intestines and

we have a reduced response

with bone resorption because our

activated vitamin d helps to resolve

calcium from the bones or from chronic

renal failure so we're just excreting a

lot of calcium we're unable to reabsorb

that calcium from the kidneys so

secondary hyperparathyroidism

means that we have high pth due to a

chronic

low calcium hypoparathyroidism

is exactly as it says we have low

parathyroid hormone

either due to autoimmune destruction

surgery removing the thyroid gland also

indirectly

removing the parathyroid glands or

congenital hypoparathyroidism

if we have low pth levels that means

we're going to have

low calcium within our bloodstream

because we are unable to resolve our

bones

unable to reabsorb calcium as

effectively from the kidneys and unable

to absorb more calcium from our

intestines

so we are able to treat this with a

combination of oral calcium supplement

with activated vitamin d so then we are

able to absorb more calcium from our

intestines

pseudo pseudohypoparathyroidism is named

this way because we have what seems to

be hypoparathyroidism with hypocalcemia

and hyper

phosphatemia however circulating levels

of pth are actually increased and the

reason behind that

is because of a defective receptor

within the kidney and the bone so we

can't actually reabsorb

that calcium so pth is trying to do its

work but it's just not binding to its

receptor

last thing we'll mention here when it

comes to calcium is humeral

hypercalcemia of malignancy

this is when tumors start to release

parathyroid hormone related peptide

so this is like a pth analog and it does

the same

actions as pth to increase our calcium

levels within our bloodstream and reduce

our phosphorus levels this means that

regular pth is going to be chronically

low

because it's not going to be secreted in

the presence of high calcium

and you treat this by giving furosemide

to reduce our calcium absorption from

our kidneys and by giving medications

that

inhibit bone resorption so talking about

calcitonin very briefly here we don't

talk about this much because it seems

like it's probably got a pretty minor

role

it gets released from cells or

c cells within the thyroid gland so not

the parathyroid gland within the thyroid

gland itself and it gets released

whenever we have

high calcium levels within our

bloodstream now works on

osteoclasts by inhibiting them so then

we stop

resorption of bone and that's trying to

reduce the amount of calcium entering

the blood

because of bone resorption it doesn't

seem to have that much

role in the minute to minute regulation

of plasma calcium but we do mention here

with our calcium homeostatic mechanisms

now vitamin d

plays a role in calcium homeostasis but

it's important to distinguish how it's

different to pth

pth is role is to maintain a normal

plasma calcium level

vitamin d's role however is to promote

the mineralization of new bone so it's

trying to increase the amount of both

calcium

and phosphorus within the bloodstream so

then that's available for bone to be

able to be

deposited now if you're a student you're

able to pick up

initially this issue of well i thought

activated vitamin d

actually resolved our bone you would be

correct and i'll touch on that right now

just to avoid that confusion

activated vitamin d although its role is

to mineralize new bone

it does increase bone resorption but the

key point is that it's

increasing the resorption of old bone so

it's trying to shuttle the

old calcium and phosphorus away from the

old bone

and make it available for deposition of

new bone so that is important

vitamin d's role is to increase the

environment for the mineralization of

new bone by increasing calcium and

phosphorus whereas our

parathyroid hormone is only concerned

about our calcium levels

so it's trying to regulate calcium at

the expense of phosphorus

so talking about vitamin d its form is

cholecalciferol and it's either obtained

from your diet

or is converted from cholesterol via uv

light on your skin

polycalciferol then gets metabolized in

the liver

and then finally in the kidneys by one

alpha hydroxylase

into our activated vitamin d now this

one alpha hydroxylase is what gets

manipulated by parathyroid hormone to

increase the levels of activated vitamin

d but this is also going to be activated

by reduced calcium all together and then

also reduce

phosphorus because if we've reduced

phosphorus then we do not have an

environment for new bone formation so

one alpha hydroxylase gets activated to

produce more activated vitamin d

so then activated vitamin d once it is

produced

it goes to the intestines the kidneys

and the bone to

increase the reabsorption of both

calcium and

phosphorus so in the intestine it does

that via this figure 9.4 here

by increasing this protein called

calbindin it's not quite clear what this

does

whether it's buffering our calcium so

then the calcium levels seem

low in the cell so then we increase the

electrochemical gradient from calcium to

enter the cell

or whether it's acting like a shuttle to

shadow it all the way out into the blood

but we increase calcium and phosphorous

reabsorption within our intestine via

this mechanism

in the kidneys we increase the

reabsorption of both calcium and

phosphate

and then in the bone we increase the

resolution of

old bone so then calcium and phosphorus

is available

for new bone formation so then that gets

us to the pathophysiology of vitamin d

if we have low vitamin d what's going to

occur our bones are clearly going to

become weak and not grow appropriately

so if you're a child then you're going

to get rickets and rickets is

characterized by a failure of growth and

particularly some skeletal deformities

as well

in adults that results in osteomalacia

which is basically

really weak or poorly mineralized bones

because you're unable to mineralize new

bone so that is our calcium homeostasis

we do have this portion here of a

summary

which i have highlighted if you want the

key points of this chapter

otherwise we do also have the chapter

questions feel free to pause it at this

point if you want to get these summaries

and then also we have another page of

the questions too over here

the answers of these questions are going

to be supplied in the description

once again if you haven't subscribed

please consider doing so as it does help

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otherwise i hope you enjoyed it feel

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YouTube Transcript:
Costanzo Physiology (Chapter 9F) Endocrine Physiology: Calcium Regulation || Study This!