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Costanzo Physiology (Chapter 9B) Endocrine Physiology: Hypothalamus/Pituitary axis || Study This!

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hello and welcome to the second part of

the endocrine physiology chapter of

costanzo's physiology textbook

in this video we are going to go over

the hypothalamic pituitary axis

which is essentially the mastermind

that's able to control the majority of

our endocrine systems

it consists of the hypothalamus which is

clearly up in the brain which we covered

in the neurology portion

and then also the pituitary gland that

kind of sits just underneath it

the pituitary gland is made up of two

separate glands

or two separate lobes the posterior lobe

which is called

also the neural hypothesis mainly

because it's made out of neuron cells

and secretes neuropeptides and then we

have the anterior lobe

which is also called the adeno

hypothesis which is actually made out of

endocrine cells

themselves so you can see it over here

figure 9.9 here

where we have the posterior lobe made

out of neurons and you can see that the

cell body

of the neuron is actually located within

the hypothalamus

and then also the anterior lobe made out

of endocrine cells

which is connected with the hypothalamus

with a bloodstream its own hypothalamic

hypophyseal portal vessels so this is

essentially the venous system

to the hypothalamus so then the anterior

lobe of the pituitary gland receives

high concentrations

of the hormones from the hypothalamus

that does not enter the systemic

circulation

and that directs which hormones should

be released from

the anterior pituitary gland once either

the posterior or anterior pituitary

gland is stimulated to release a certain

type of hormone

that just gets released into the

systemic circulation

now the posterior pituitary gland only

secretes

two neuropeptide hormones adh

and oxytocin adh is primarily associated

with the supraoptic nuclei within the

hypothalamus

whereas oxytocin is primarily associated

with the paraventricular nuclei in the

hypothalamus

so how this works is that the hormone is

actually synthesized in the cell body of

the neuron within the hypothalamus

and then actually gets transported to

then sit in vesicles

right at the end of the neuron and the

dendrites waiting to be stimulated to be

released when told so

by the hypothalamus whether that's adh

or oxytocin we'll go into more details

about those two different hormones

later on in this video and to start with

we'll talk about the

anterior pituitary gland hormones

because we have six

major hormones here and each are

secreted by their own

cell type ending in troph for example

we have thyroid stimulating hormone or

tsh released from

thyrotropes we have acth

released from corticotropes we've got

growth hormone released from

somatotropes

prolactin from the lactotrophs and then

lastly follicular stimulating hormone

and luteinizing hormone

fsh and lh secreted by gonadotrophs so

these

tropes a particular endocrine cells

within the anterior pituitary gland that

secretes its own endocrine hormone

when stimulated too from the release of

a releasing hormone from the

hypothalamus

so hypothalamus secretes a releasing

hormone in response to a stimuli that

releasing hormone

tells the stimulating hormones from the

pituitary gland to be released which

then get released into the systemic

circulation

and then these stimulating hormones go

to their target endocrine glands within

the body

to then stimulate the release of the

hormone that they want to release

so for instance when it comes to thyroid

hormone which we'll go in in another

video

the hypothalamus releases thyroid

releasing hormone which then tells the

anterior pituitary gland to release

thyroid stimulating hormone and the

thyroid stimulating hormone tells the

thyroid gland to release

thyroid hormone so that's the basics

behind the

hypothalamic territory axis so going

through

some of the particular hormones released

from the anterior pituitary gland

specifically now

just briefly tsh fsh and lh are all

glycoproteins it goes into a little bit

of detail about their actual molecular

structure which i don't think is as

important but essentially they are all a

similar type of protein a glycoprotein

tsh we will go into more details in the

thyroid hormone video which will be

coming up shortly

and then fsh and lh will be in the

reproductive tract is

acth or adrenocorticotrophy hormone

is released from the anterior pituitary

gland to

increase the secretion of our adrenal

cortical hormones from the adrenal gland

we will go into much more details about

that actually in the adrenal video

coming up i know

this seems ridiculous that we're going

to go over these in more detail later

but these are the major hormones that we

will be covering in much more detail

in a later video so acth is slightly

different to these other ones and how it

is formed within the anterior pituitary

gland you can see that

ac th actually comes from originally

this molecule called pomc

or pro opio melanocortin the main point

here

is that although we get acth getting

produced we do have these

other and the fragments of acth that can

also have a minor effect and more

importantly if we have a high production

of acth we will get increased of these

other fragments

and more important clinically is the

production of

the melanocytes stimulating hormones the

msh hormones

so these hormones will actually cause

skin pigmentation so then that will

cause

clinical signs in the presence of

excessive acth or end up with

increased skin pigmentation so we'll go

into growth hormone in more detail

now so growth hormone is also released

from the anterior pituitary remember

from the somatotropes

the growth hormone as the name implies

is important for growth

so it does that by altering our protein

carbohydrate and fat metabolism

it gets stimulated to be released from

the anterior pituitary gland

due to growth hormone releasing hormone

from the

hypothalamus and that occurs in a

pulsatile way every

roughly two hours and also has some

other stimulatory

factors as well all noted in table 9.4

here

in addition to its inhibitory factors

the best way to think about this

is that anything that will be inhibiting

growth so let's say you don't have

enough nutrients

then your growth hormone will be

stimulated to increase those nutrients

in your body

so growth hormone is trying to provide

an environment for you to grow

so if you have decreased glucose

decreased free fatty acids

you're fasting or you're exercising

you're under stress then you're going to

release growth hormones to try and

provide an environment for you to

actually grow

obviously when you're going through

puberty you have higher growth hormone

during those times as well growth

hormone will then steadily decrease as

you get older now our inhibitory factors

are going to be the opposite of those so

if we have high glucose high free fatty

acids then we already

kind of have an environment for growth

so you don't need to release your growth

hormone

obesity reduces it some metastatin

remember that's our stop hormone from

our gi chapter somatostatin

also plays a role with inhibiting our

growth hormone effects as well

growth hormone itself actually inhibits

itself there are negative feedback

mechanism and then circling back to

somatostatin

this is an example of a gi protein

coupled receptor remember we talked

about the gs

protein receptors which cause an

increase in cyclic amp

gi proteins are inhibitory g proteins

they reduce the level of

cyclic amp by inhibiting the admiral

cyclase enzyme

so somatostatin the stopping hormone

which inhibits growth hormone does so

by interacting with a gi protein

as a receptor so figure 9.11 here

tells us how growth hormone has a

negative feedback on itself

the first thing to point out here is

that when growth hormone actually has

its effect on the target tissue

it gets broken down into these

somatometers or igf's

these igfs then actually have an

inhibitory role

on the release of further growth hormone

by having a direct effect on

inhibiting our anterior pituitary gland

but then also

by having a stimulatory effect on the

hypothalamus to release somatostatin

remember somatostatin our stopping

hormone inhibits also the anterior

pituitary gland

so that's one way the growth hormone has

negative feedback on itself

when it's broken down the byproducts

have an inhibitory effect growth hormone

itself

also has an inhibitory effect on itself

increasing the release of somatostatin

from the hypothalamus so

increased growth hormone will actually

self-regulate itself

and the last mechanism out of the three

growth hormone releasing hormone

actually having an inhibitory effect

on the hypothalamus itself so although

it's released from the hypothalamus as

soon as that increases in concentration

it's going to tell itself to stop

secreting itself

essentially so the growth hormone that

negative feedback mechanism has these

three different

feedback systems somatometers growth

hormone and growth hormone releasing

hormone

so how does growth hormone actually have

an effect

on the body we know it's used to promote

growth but what is it actually doing

well we have three main effects here to

remember number one

is being diabetogenic or having an

insulin resistant

effect it blocks the effects of insulin

which is trying to reduce your glucose

levels in your body or in your blood

so by blocking or making insulin

resistant you increase the amount of

glucose in your bloodstream

and then it also increases lipolysis and

adipose tissues

basically what this is doing is

increasing our energy stores and our

plasma

so then our body has a lot of energy to

be able to grow

so we're increasing energy availability

by antagonizing insulin in an effect for

an easy way to think about that first

effect our second effect

is increasing growth by stimulating

protein synthesis and organ growth so

we're increasing the uptake of amino

acids into

our cells and we're increasing the

stimulation of protein development this

will increase

lean body mass and organ size our third

effect

is an increased in linear growth so

before puberty before your growth

plates have used it will increase the

production of bone within your growth

plate so then you're able to grow you

know this is why during your growth

spurt your

high growth hormone but then if you're

already finished your growth it will

actually

increase our periosteal bone growth so

kind of the

edges of our bones so we have this

influence on bone growth

more dramatic obviously before puberty

that brings

us to when we have an issue with our

growth hormone

if we have deficiency then that's going

to lead into dwarfism which is treated

with

growth hormone with excess what you're

going to see depends on when this occurs

if it's before puberty

then you end up with gigantism because

you're actually

increasing your long bone growth after

puberty

when linear growth is complete then you

end up with just

larger features so larger facial

features larger hands

increased organ size insulin resistance

glucose intolerance etc from that

excessive growth hormone so that is

growth hormone in a nutshell

next up is prolactin now prolactin is

responsible for milk

production so producing milk not letting

it down that's oxytocin

but milk production and the development

of the breasts

so obviously we're going to have an

increased secretion of prolactin during

pregnancy and lactation

now the thing with prolactin secretion

from the anterior pituitary gland which

works on the breasts

is that on the day-to-day it's getting

inhibited from dopamine release from the

hypothalamus

up until pregnancy or lactation that's

when that gets overridden and we

start to increase trh release trh

stimulates the release of prolactin and

prolactin nature has an

inhibitory effect on itself for its own

negative feedback by increasing the

level of dopamine

so the stimuli for prolactin release

is suckling that's the main stimulation

obviously that's a need for lactation

after pregnancy

then you're going to increase milk

production there is also another time

for

prolactin release which is that puberty

for breast development but otherwise

it only gets released during lactation

in order to produce milk for the baby

any pathophysiology of prolactin

includes deficiency where obviously you

fail to lactate and then

excess which can occur due to some kind

of prolactin producing tumor which can

lead to infertility because prolactin

does inhibit ovulation and also

galactoria or excessive milk production

so moving on to

our posterior lobe hormones now remember

we talked about adhd and oxytocin

as our two posterior pituitary gland

hormones produced

and synthesized by the cells within the

hypothalamus in the neuron

but then that neuron extends all the way

down into that posterior pituitary gland

where it sits waiting to be

stimulated to be released so adh

is the first one that we'll focus on

here this gets secreted

whenever we have a depolarization of

that nerve

that the adh is sitting in that

stimulates calcium and to enter the

terminal and causes exocytosis

of the adh and also the oxytocin when we

get to talking about oxytocin

now we've already talked about adh in

our renal chapter remember adh is

involved with controlling our oils

predominantly and then also an influence

on controlling our blood pressure

now our hypothalamus will sense if our

osmolarity will change

if there is an increase in osmolarity

then that stimulates increased

adh secretion adh goes to the kidneys

and then tells the kidneys to increase

the reabsorption of water

it's able to do that by actually

interacting with a v2 receptor which is

a gs

protein to increase cyclic amp in the

principal cell of the

late distal tubule and cortical tubules

that will ultimately end up with the

phosphorylation of

aquaporin two proteins that insert

themselves into the membranes

aquaporin ii results in increased

permeability of those principal cells to

water so now that terminal nephron can

actually absorb water when it was

previously impermeable

so the absorbing of water from the

nephron reduces the osmolarity in our

plasma

and helps to restore our osmolarity now

if we also need to increase the water

reabsorption from our kidneys because of

hypotension

then that will occur because our dairy

receptors within our carotid artery and

aortic arch

will sense a low blood pressure that

will transmit a signal via the vagus

nerve to the hypothalamus

and then that will tell the hypothalamus

to stimulate the release of adh to

increase water reabsorption to help to

increase our blood volume again

and blood pressure now adh also has

another influence to help with blood

pressure

through contraction of our vascular

smooth muscle via the v1 receptor so v1

for vascular smooth muscle contraction

v2 for aquaporin 2

and increasing water reabsorption from

the kidneys

now interestingly the v1 receptor for

the vascular smooth muscle

actually utilizes the ip3 calcium

secondary messenger system

versus the v2 receptor which utilizes

the cyclic amp

secondary messenger system so when it

comes to disorders of

adh we have central diabetes insipidus

and nephrogenic diabetes

insipidus diabetes insipidus just means

very watery urine or very dilute urine

now

that occurs because we have an

inappropriate response to adh either

because we don't have

enough adh such as in central diabetes

insipidus where there is no secretion of

adh

from the posterior pituitary gland at

all which needs to be treated by

giving an adh analogue like ddavp or

nephrogenic diabetes insipidus where the

principal cells are actually

unresponsive to adh altogether

now these will not respond to adh

analogues and will actually require a

different type of treatment like

thiazide diuretics to help to reduce our

sodium reabsorption to increase our

osmolarity of our urine and also reduce

the gfr to reduce the amount of water

that's getting excreted so diabetes

insipidus means dilute

urine due to inappropriate adh either

due to

reduced secretion and low levels in

central

or not responding to adh in the kidneys

which is nephrogenic

diabetes insipidus we do have syndrome

of inappropriate adh

siadh which means adh is getting

secreted from an anomalous site

like a cancer within the lungs this will

dilute our body fluids by

actually hyper concentrating our urine

because now adh is sucking all the water

out of our nephrons and that gets

treated by an

adh antagonist the last hormone we'll

talk about coming from the posterior

pituitary gland

is oxytocin which is the milk let down

hormone so prolactin

stimulates milk production oxytocin then

tells that milk to be let down or

ejected

so the stimulus for that is obviously

going to be suckling or we do have some

other stimulatory factors like the sight

sound or smell of an infant

and it is also released with dilation of

the cervix during pregnancy it actually

helps with uterine contractions this is

one of those positive feedback

mechanisms during pregnancy

it is inhibited from opioids but other

than that that'll conclude

our video for today in the next video

we'll go over

our thyroid hormones in our thyroid

gland feel free to drop a comment

otherwise we'll see in the next video

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YouTube Transcript:
Costanzo Physiology (Chapter 9B) Endocrine Physiology: Hypothalamus/Pituitary axis || Study This!