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Costanzo Physiology (Chapter 9C) Endocrine Physiology: Thyroid Hormone || Study This!

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hello and welcome to the next portion of

the endocrine physiology chapter

going over the thyroid hormones in the

thyroid gland

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so going over our thyroid hormones this

is produced by the

follicular epithelial cells within the

thyroid gland itself

we have two types of thyroid hormones

we've got t4 and t3

t3 is the metabolically active

hormone within the actual cell itself

but

t4 is more abundant in the plasma so

it's almost

stored as t4 and the plasma goes into

the cell and it gets converted to t3

within the cell

to then have its actions the difference

between

t3 and t4 is just the amount of iodine

within the molecule

so t4 means that there's four iodine

molecules within

that hormone whereas t3 has three iodine

molecules so that's the major difference

between the two

so going into how the thyroid hormone

gets produced within the thyroid gland

first we should look at the anatomy of

the thyroid gland within the thyroid

gland we have these thyroid follicles

which is essentially a ring of

follicular epithelial cells

which secrete colloid into the lumen

this colloid contains thyroid hormone

attached to a molecule called

thyroglobulin

when the gland gets stimulated to

secrete thyroid hormone

that thyroid hormone within the colloid

then gets endocytosed into the cell

and then excreted via the follicular

cells into

the blood vessels so now we should talk

about how thyroid hormone actually gets

produced within the follicular

epithelial cell that's shown here in

figure 9.18 here and all the specific

steps

so the first step is actually getting

iodine into the cell since that's the

major component of thyroid hormone

interestingly the thyroid gland is the

only gland that actually uses iodine so

all your dietary iodine

goes to your thyroid gland to get

incorporated

into thyroid hormone so via the sodium

co-transporter here

iodine gets transported into the

follicular epithelial cell

and this transporter actually gets

upregulated if we have iodine deficiency

to help shuttle even more iodine into

the cell

this is against its concentration and

electrical gradient so

it's quite a push it requires a lot of

energy to actually get the iodine into

the cell

clearly if there is a severe iodine

deficiency then we will have a lack of

iodine going into the cell

and then a reduced production of our

thyroid hormone but this

transporter tries to combat it initially

by up regulating in the presence of mild

deficiency

now once iodine enters the cell it then

gets oxidized

into an i2 molecule via what's called a

thyroid peroxidase this thyroid

peroxidase is going to come

up a couple times but you'll see that

within the follicular lumen now we have

our oxidized iodine as i2 now this i2

will then

bind with a thyroglobulin molecule which

comes from the cell

being synthesized from a tyrosine

molecule so the combination of iodine

with thyroglobulin

is called organification and then that

creates this molecule which is

thyroglobulin with either an

mit or dit mit stands for

mono iodine tyrosine and then dit stands

for diado tyrosine basically

mit means there's one iodine with that

tyrosine molecule on the thyroglobulin

dit means there's two iodines so at this

stage we then have another peroxidase

reaction

which will combine these molecules to

create t4 and t3

so if we combine two dits then we're

going to end up with t4

if we combine the dit with an mit then

we're going to end up with t3

because that's simple maths we're just

adding on iodine together so then we end

up with four iodines in the case of t4

and then three iodines in the case of t3

there is also some residual mit and dit

molecules

left on this thyroglobulin so this is

the kind of final product that sits

within the follicular lumen

which is this thyroglobulin with

attached t4

and then some mit and dit so this just

sits in the follicular lumen

waiting for the stimuli to secrete t4

so once that stimulus occurs which

predominantly is the secretion of

thyroid stimulating hormone from that

anterior pituitary gland

then this thyroglobulin complex is going

to get endocytosed

into the follicular cell and then it's

going to release

its t4 and t3 into circulation

that thyroglobulin tyrosine molecule is

going to get recycled

so is the mit and dit releasing its

iodine to then get recycled back

into this equation again so that is the

entire production

of thyroid hormone remember t4 is the

most prevalent molecule in the plasma

but then t3 is the more metabolically

active so once

in the circulation these thyroid

hormones actually bind to something

called

thyroxine binding globulin so the

majority of our thyroid hormone is

actually

bound to proteins within the plasma and

that means that it's almost

stored in the plasma for the cells the

free

hormones are the only physiologically

active hormones

so if we have less of this globulin

molecule that means more of the thyroid

within the plasma is going to be in the

free active

form so we may have less globulin and

hepatic failure which is the organ that

actually produces these globulins which

means we have more of the active t4 t3

in the plasma

that actually gets sensed by the

anterior pituitary gland

which means that we secrete less thyroid

stimulating hormone as a negative

feedback mechanism

so we actually reduce the amount of

thyroid gland secretion in that

situation

whereas if we have an increased level of

globulins so then it's actually

holding more of that thyroid hormone in

the plasma as

non-active or protein-bound thyroid

hormone which is going to happen let's

say in pregnancy which inhibits hepatic

breakdown of this globulin

that means that there is less active t43

that is free within the blood the

anterior pituitary gland senses that and

thinks that we have

a relative thyroid deficiency so then

it's going to release

more tsh to increase the secretion of

thyroid hormone

once the thyroid hormone actually enters

the cell remember predominantly

it's going to be t4 that enters the cell

since that is more abundant

in our plasma the target tissue will

then convert that t4

into active thyroid hormone as in t3

using the enzyme 5-ironase now that will

also produce some of this reverse

t3 which is inactive but the active

component is

t3 now during starvation when you don't

have many nutrients and you are not

producing that much energy

and you need to reduce your metabolic

rate then you will inhibit

this five iodine enzyme to reduce your

metabolic rate

by reducing the amount of active thyroid

hormone in your target cells

because thyroid hormone the whole thing

about it is that it actually

increases our metabolic rate so if

you're in the starvation

state you need to conserve energy you're

going to produce

less active thyroid hormone so then your

cell is going to have a lower basal

metabolic rate that gets us to the

regulation of hormone secretion we've

already talked about the globulin levels

so if you have

increased globulin levels then you're

going to increase the secretion of your

thyroid hormone because there's less

free hormones and vice versa thyroid

stimulating hormone is clearly the main

stimulation for secretion from the

thyroid glands and then thyroid

stimulating immunoglobulins

is another molecule which basically acts

like tsh at the receptor of the thyroid

gland

and that's actually a cause for

hyperthyroidism called graves disease

which is just

excessive production of this thyroid

stimulating immunoglobulin

which tells the thyroid gland to produce

a lot of

thyroid hormone so you end up in a

hyperthyroid state

in terms of inhibitory factors obviously

if you have severe iodine deficiency you

don't have enough iodine to incorporate

into your thyroid hormones you could

have deficiency of that drnas

which releases t4 and t3 from your

thyroglobulin ironically excessive

iodine intake actually

inhibits the organification of iodine to

a thyroglobulin

which is also an inhibitory factor and

then lastly any medications that's going

to inhibit

the movement of iodine into the cell or

inhibit those peroxidase enzymes which

create the thyroid hormone themselves

so next up we're going to talk about the

actual actions of thyroid hormones

the easiest way to think about this is

that thyroid hormone gets into the cell

activates the nuclear receptor via t3

and then that causes the increased

synthesis of new proteins via

transcription and translation

so thyroid hormone will get into the

cells

and increase the metabolism of that cell

so whatever that cell may be

it's just going to increase the

metabolic rate of that cell so it's

going to cause growth

of our organs it's going to cause bone

maturity

it's going to cause maturation of our

central nervous system

in our cardiovascular system it's going

to increase our cardiac output because

it gets into the myocardial cells

basically increases the enzymes or

calcium recycling

increases our contractions increases the

beta receptors on the cells so then

they're more likely to get stimulated by

the sympathetic nervous system

and increase cardiac output it increases

metabolism just because it increases the

cycling of glucose we're increasing the

protein production to increase glucose

absorption

to produce glucose increase lipolysis

increase protein synthesis and

degradation ultimately it actually

has a net catabolic effect on protein

degradation because your entire body

is basically just churning through its

metabolic processes it's just trying to

work as hard as possible

it increases our basal metabolic rate by

increasing the production of our sodium

potassium atpase

transporters which just increases the

amount of

oxygen consumption because we need to

produce a lot of atp

to now feed these increased sodium

potassium atpases

so oxygen consumption goes up a lot of

energy gets used

we increase our heat production due to

that increased use of

energy and then our basal metabolic rate

increases

so the typical clinical signs of someone

with excessive

thyroid hormone which is up regulating

all of these cells basal metabolic rate

is going to be an increased hunger but

yet weight loss because you're just

chewing through all that extra energy

and excitability or irritability

obviously the opposite is also true if

you don't have enough thyroid hormone

then your basal metabolic rate is going

to reduce everything's going to reduce

so you're going to become lethargic

sluggish and gain

weight now it does go into some of the

causes of hyperthyroidism and

hypothyroidism

for people the main cause of

hyperthyroidism so high thyroid gland is

that graves disease remember we

increase the level of our thyroid

stimulating immunoglobulins

if you have high of those that means

that you're going to produce a lot of t4

and t3 that's going to have a negative

feedback

on your anterior pituitary gland so your

tsh is going to be low and that's the

same if you have a thyroid gland

neoplasia that's producing excessive

thyroid

hormone so you can sometimes use thyroid

stimulating hormone levels as a

telltale to see what's going on

obviously if you've got something that's

increasing t43 production

independent of tsh that's going to have

a negative feedback on tsh

and you'll have low tsh levels obviously

if you have hyperthyroidism however due

increased tsh levels then your tsh is

going to be high in addition to your

thyroid hormones but that happens much

less commonly when it comes to

hypothyroidism the most common reason is

immune disruption of our thyroid glands

or thyroiditis

so that's going to reduce your t4 and t3

levels which via negative feedback is

going to increase your tsh levels

because tsh is going to say why aren't

we producing any t4 and t3

so tsh is going to be high t4 t3 is

going to be low

another clinical sign associated with

hypothyroidism is

mixed edema which is increased

filtration of fluid

out of your capillaries causing edema of

the subcutaneous tissues

because of increased osmotically active

muco-polysaccharides within your

interstitial fluid

when it comes to treatment it's rather

self-explanatory for hypothyroidism

you're just going to do hormone

replacement therapy by giving thyroid

hormone

for the treatment of hyperthyroidism

high thyroid hormone

then there's three real options

medications to inhibit the synthesis of

thyroid hormones

surgical removal of the thyroid gland or

radioactive

ablation that's when you give

radioactive iodine since the thyroid

gland is the only gland that uses iodine

then you just only have radioactivity

within the thyroid gland which kills off

only the thyroid gland so those are our

treatment options

now the last thing we'll talk about here

is goiter goiter just

means that the thyroid gland has

enlarged

and that's going to occur whenever we

have high levels of

trophic hormones which includes tsh

and also thyroid stimulating

immunoglobulin

so any thyroid abnormality where we have

increased tsh

or increased thyroid stimulating

immunoglobulin is going to stimulate the

growth of the thyroid gland

usually we have increased tsh either

because of a tumor

in the anterior pituitary gland which is

uncommon

or because we have low t4 tsh levels

with very low negative feedback to our

interior pituitary gland

so that's going to be the end of this

video for today i hope you enjoyed it

feel free to join in for the next one

where we are going to talk about our

adrenal glands feel free to drop a

comment otherwise we'll see in the next

one

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YouTube Transcript:Costanzo Physiology (Chapter 9C) Endocrine Physiology: Thyroid Hormone || Study This!

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YouTube Transcript:
Costanzo Physiology (Chapter 9C) Endocrine Physiology: Thyroid Hormone || Study This!