So when we talk about pituitary medicine, we're talking about

an important glandular structure that is responsible for governing The

physiology of many hormones in the human body.

The pituitary gland exists in mammals and it produces hormones.

Hormones are chemical messengers, our bioactive messenger molecules that are

secreted from a cell.

So here the hormones being secreted from the cell, entering

the vascular space and travelling to a distant target cell.

So endocrinology describes the production of hormones acting on target

cells.

And this is a good example of an endocrine axis

where one cell secretes the product.

And the product acts in an endocrine fashion on a

target cell by binding to a receptor.

That receptor can be within the cell membrane, as is

the case shown here, or it can be intra nuclear,

as is the case with many steroid hormones.

For instance.

Hormones produced by a secreting cell can act on an

adjacent cell.

That's sometimes called a paragraph.

An action has a meaning.

Beside are the hormone that is produced can actually act

on the cell that has produced it in its first

place.

And that is an autocrat in action.

So you'll hear about auto crime, peregrine and endocrine actions

of hormones.

But importantly, hormones exert an action on a target or

distal cell.

So what do they do?

Well, hormones can stimulate cell function so they can encourage

the cell to perform an action.

A good example would be growth hormone releasing hormone secreted

by the hypothalamus, which encourages the somatic cells of the

anterior pituitary to make growth hormone.

So growth is a stimulatory hormone.

Some hormones inhibit cell function and a good example of

that would be insulin, for instance, secreted by the pancreas.

You will think of insulin as something that regulates blood

sugar.

That's absolutely right.

But the other thing that insulin might do is inhibit

lipolysis.

So it will go to the adipocyte and inhibit the

release of, uh, fatty acids and glycerol.

Some hormones are responsible for the maintenance of a physiological

state.

A good example would be calcium homeostasis.

So serum calcium is very tightly regulated in the human

body because it's a positively charged ion.

And we need to keep electrically active particles in really

tight physiology.

So the serum calcium concentration in the human is 2.2

to 2 point 6mg/l.

And that is very tightly regulated by the parathyroid glands

which make parathyroid hormone.

So parathyroid hormone really good example of maintaining physiological status.

our homeostasis.

Some cell hormones stimulate or inhibit cell growth or differentiation.

And this has become really important within cancer biology.

So IGF one insulin like growth factor one will stimulate

differentiation of cells and overgrowth.

A good example would be a contribution of growth hormone

to longitudinal growth in a child.

Our IGF one to the development of certain malignancies.

To complicate matters, hormones are produced in a very tightly

regulated mechanism so that we constantly are applying either a

stimulus or a brake, or a simultaneous stimulus and brake

to very tightly regulate hormone production.

And generally, there is a hierarchy of hormone action.

And the pituitary gland and the hypothalamus or the hypothalamus

pituitary unit is the really best example of this.

So I'm showing simply here here's an end organ.

Let's think of this as a tissue in which the

hormone is ultimately going to act.

So that's the target hormone acting on the target tissue.

But that target hormone is governed by the production of

other substances which might arise in this case from the

pituitary gland.

And those target hormones can feed back to the pituitary

gland to say, there is plenty of me in the

system so the pituitary can be suppressed or inhibited.

And above the pituitary gland is the hypothalamus, which is

where much of this hierarchy commences.

So a good example of exploiting this hierarchy would be

using the oral contraceptive, the combined oral contraceptive pill in

females.

So if a woman takes an oestrogen containing pill, the

target hormone oestrogen is present at high concentration in the

circulation.

The hypothalamic hypothalamus pituitary unit recognises that and says actually

there is no requirement to produce further oestrogen because it's

already present at supra physiological levels.

So the hypothalamic hormone GnRH is suppressed, as are the

pituitary hormones LH and FSH, which govern ovarian function, including

ovarian, and governed ovulation.

So by taking a combined oral contraceptive preparation with the

target hormone oestrogen, we can suppress gonadotropin production, which is

a really effective contraceptive.

So I've taken the thyroid is a good example here.

Here is the thyroid gland in the anterior neck producing

the thyroid hormones which are the target hormones thyroxine, sometimes

called T4 because it contains four molecules of iodine, and

T3, which is aoda theanine, which is actually the bioactive

molecule.

So when the human thyroid secretes thyroxine, we convert T4

to T3 through di ordination, and T3 is the bioactive

hormone which works on the target cell.

In this case, the heart stimulating cardiac contractility and heart

rate.

But the thyroid doesn't act alone.

It's controlled by the pituitary gland, which makes the hormone

thyroid stimulating hormone.

So normally what happens is the brain acting through the

hypothalamus says, come on, thyroid makes some thyroid hormone by

making thyroid growth and releasing hormone, which gets the thyroid

site in the pituitary gland to make thyroid stimulating hormone,

which gets the thyroid to make T3 and T4.

In turn, the T3 and T4 feed all the way

back to the hypothalamic pituitary unit and control themselves.

Why does nature have such complicated mechanisms?

Well, probably because as we were evolving as mammals, There

were times that we needed to have fairly fast metabolism

hunting and gathering, and there were other times when we

would not have adequate shelter or nutrition.

And we need to down regulate and literally hibernate by

cooling down and stop using energy sources for metabolism.

So we could switch off centrally, inhibiting thyroid hormone production,

slowing down metabolic rate.

Surviving a long, cold winter and certain species still rely

on this mechanism.

There are birds, for instance, that are only fertile when

their thyroid is producing enough thyroid hormone.

The hypothalamus produces TRH, which is where the axis commences.

In rare cases, the T3 and T4 is being produced

very normally, but doesn't work at a cellular level because

there is a problem with cell action or cell responsiveness

to the end product or target hormone, and that happens

when there is thyroid hormone resistance, usually due to mutations

in the thyroid hormone receptor.

So although the hormone is produced, it can't bind and

activate the receptor in the conventional way.

And another example of nature would be when there is

androgen insensitivity.

So individuals who have an XXY chromosomal pattern have testicles

make testosterone.

But because the androgen receptor doesn't respond, that individual doesn't

undergo normal differentiation and change from a Malaysian system to

a Wolfson system.

So was born with the appearance of being female.

So that is a hormone resistance syndrome, which is relatively

rare.

So there are releasing factors from the hypothalamus.

Trophic hormones from the pituitary gland target hormones from the

the end organ target tissue.

And then there is action on the distal tissue.

And these are those just to remind you.

Now when there is deficiency we can label depending on

where that deficiency occurs as primary, secondary or tertiary.

And far and away, the commonest cause of thyroid hormone

deficiency in the developed world is an autoimmune condition called

Hashimoto's thyroiditis, where the immune system attacks the thyroid.

It gets infiltrated with lymphocytes, cytotoxic T cells, and the

thyroid is destroyed, so the individual develops primary thyroid issues,

our deficiency of hormone.

The same consequence can happen if there's a normal thyroid

gland, but it doesn't receive stimulation from the pituitary gland.

So in the setting of absent TSH but with an

intact thyroid, there is thyroid hormone deficiency due to lack

of trophic stimulation.

And that's called secondary hypothyroidism.

And rarely we have problems with production of TR.

That's most common after, uh, the presence of either a

hypothalamic tumour or a defect in trait synthesis genetically determined.

And that's called tertiary hypothyroidism.

And as I've said, if all of the system is

working but the target hormone cannot activate its receptor, there

is a resistance syndrome.

Right.

So let's get on to a pituitary case.

And this is a pretty bog standard case.

45 year old man has a head injury.

He's unconscious.

He's brought to A&E.

The team there feel obliged to do a CT scan

when he wakes up, just to make sure he doesn't

have intracranial haemorrhage.

And he's able to answer questions and pretty well.

And ultimately, he is discharged from hospital the same day.

But he had a CT scan, and the CT scan

showed what the radiologist labelled as a seller and super

seller mass, and that prompted the admitting casualty doctor to

go back and examine him again.

And the junior doctor said that he had a bi

temporal field defect.

So let's ask ourselves the questions.

What is the seller and super seller mass?

Where is the pituitary fossa?

What's a bi temporal field effect?

And can we put all this together.

So this is what's called a sagittal view.

It's a side on view.

It's a cartoon schematic.

But it's useful because you can see the nose, the

back of the head here.

This is the brain.

So frontal lobe.

Parietal lobe, occipital lobe.

This is the cerebellum.

The medulla brainstem with the pons going down into the

spinal cord.

So it's a midline slice.

We can see the corpus callosum.

And now we're seeing shaded in in red the hypothalamic

area which is at the base of the brain.

So this area is sometimes called the skull base.

And hanging on the hypothalamus is this infant column or

pituitary stalk connecting the pea sized pituitary gland to the

hypothalamus?

If we look at the skull, you can see the

foramen magnum where the brainstem exits becoming the spinal cord.

And this is where the pituitary is located within this

structure here which is called the cellar tasca.

So it's a bony cavity which has the configuration of

a Turkish saddle.

So this again is a sagittal view where we're looking

at the front of the pituitary on this side, the

back of the pituitary on this side.

This structure is the optic chiasm.

And it's quite important.

And it's related to this bi temporal field effect which

I'm going to tell you about.

So we can see now this is the floor of

the third ventricle in the hypothalamus.

And the pituitary gland is connected to the hypothalamus via

the pituitary stalk called the infant fibula, and the pituitary

comprises of two distinct anatomic areas the anterior pituitary.

The adeno hypothesis, and the posterior pituitary are the neural

hypothesis.

Now the shaded differently here.

And actually they're really functionally very different.

And they're embryological derived in a different manner.

So the normal pituitary gland is formed by an upward

growth from oral ectoderm meeting a downward growth from the

primitive brain structure.

The notochord.

And these two bits come together.

The bit of oral ectoderm breaks off and fuses with

the neural hypothesis as it comes down.

And that forms the pituitary gland.

So you can see how the anatomic differences and maybe

this one of the next slides will show it a

bit more.

This is called a coronal section.

Again, it's a cartoon obviously, and we're looking at now

from directly in front of the patient.

So this is the right hand side.

This is the left hand side.

And what we can see is the pituitary gland sits

with the configuration of a kidney bean.

It's about the size of a little fingernail.

It's hanging on a stalk.

And above and in front of the pituitary gland is

a structure called the optic chiasm.

And I'll say a bit more about that in a

second.

Lateral to the pituitary gland is the cavernous sinus, cavernous

sinus on the right, cavernous sinus on the left.

And the cavernous sinus is important because it contains a

number of important structures, including the intra cavernous carotid artery

going through a siphon, and then a number of the

cranial nerves.

The third, the fourth, two branches of the fifth and

the sixth.

So you can see if something is going on in

the cavernous sinus.

It can interfere with eye movement because these nerves are

ocular motor nerves, with the exception of the fifth.

Beneath the pituitary gland is this sphenoid sinus.

So here's a normal pituitary gland just using the same

schematic.

This is the brain.

It's a coronal view.

This is post gadolinium enhancement.

It's a T1 weighted image.

I can tell that because CSF is black on this

sequence.

So is there.

This is the sphenoid sinus containing air.

We have sinuses.

So our skull is not too heavy to lift.

And above the sphenoid sinus is the pituitary gland.

Here enhancing very symmetrically uniformly with a stalk that is

beautifully down the midline and the optical zoom above.

And similarly on the sagittal view we can see the

nose here.

This is the tongue midbrain spinal cord cerebellum corpus callosum.

Optimism.

Third floor of the floor of the third ventricle with

the hypothalamus.

Infantile.

Anterior pituitary.

And we can see this bright area behind.

This bright area is the posterior.

Pituitary.

And the posterior pituitary contains these neuro secretory granules, which

tend to be bright on a T1 weighted image.

And we look for that because the posterior pituitary produces

a number of hormones.

This is this guys scan.

So here's the normal one.

And instead he's got a large pituitary mass lesion symmetrically

enhancing and just stretched above the top of this is

the optimism.

So this tumour has arisen in the pituitary fossa.

It's made the floor of the fossa bigger than it

should be.

So there's an expanded bony cella.

MRI scan was introduced in the UK in 1991, and

CT was introduced in about 1981.

So imagine trying to be a neurosurgeon in the 60s

and 70s when you didn't have any imaging to look

at other than playing x rays.

So in the early days of of pituitary medicine, people

would have a lateral skull X-ray to see if there

was asymmetry from one side of the floor to the

other to see if there was a hint of a

pituitary tumour.

Mr..

Has really transformed our ability to to characterise pituitary tumours.

So this is now located within the cellar.

So it's the cellar and it's super cellar because it's

extending into this space here above the normal pituitary gland

which is called the super cellar cistern.

There's a diaphragmatic cellar coming across here which the stork

penetrates.

And as the tumour gets bigger, it's difficult for it

to grow downwards through bone.

So it grows upwards and it spills out into the

super cellar cistern.

And it begins to indent and subsequently distort and compress

the optic asm.

So cellar and super cellar mass lesion with cosmo compression.

So if you cover your left eye and you just

look through the screen, you will see that you've got

a nasal field and your right eye, you've got a

blind spot within your temporal field, and we've got a

midline.

So this is the field of vision that you can

see out of your right eye.

Now, I've told you that this guy has a bi

temporal field effect.

So the pupil is in the centre.

This is the nasal field and this is the temporal

field.

And he's going to be missing his temporal field.

This is his perimeter.

We use a variety of techniques to look at visual

field function.

But if you've been to the high street optician, they'll

get you to click a clicker when you're looking at

a TV screen, when you see a flash and they're

mapping out a visual field.

So that's an automated field.

It's quicken and very accessible, mostly used for glaucoma.

This is called Humphrey Primary.

It's better at looking at that full 180 degree panorama.

And the bits that are shaded dark are bits where

this guy could not see the field of vision.

So you can see he has got a severe bi

temporal hemi and opia, which is really respecting the midline.

Now the reason this happens is as follows.

So if he's looking out in the front here, you

can see this is his right eye.

This is his left eye.

And there's the pupil.

So the light falls through the pupil depending on where

the object is located.

So here's the object.

He's looking at it here.

And you can see that the object falls onto the

nasal retina here and the temporal retina here.

But the nasal retinal fibres cross over in the midline,

crossing over in the optic chasm before they go into

the optic radiation where light is perceived.

On the other hand, the temporal fibres coming from the

temporal retina.

So this would perceive the nasal field object.

But the temporal side of the retina don't cross over.

They stay lateral.

When there is a pituitary tumour, there is compression of

the Shi'ism, which distorts the function of the nerves that

are crossing over in the midline.

So they are the nerves that arise from the nasal

retina which perceive the temporal field.

So you can now see how when there's an object

that's compressing the chiasm, we lose vision within the light

that is perceived within the nasal component of our retina,

which is responsible for seeing objects in the temporal field.

So putting that together, he's got a stellar and super

stellar mass lesion, which is giving rise to a very

classic bi temporal field effect.

So he was sent to the endocrine clinic and the

registrar who saw him asked him some questions, performing a

clinical assessment, and it was fairly clear that this 45

year old had become quite hypogonadism and he felt fatigued.

He said that he'd gained weight, particularly around the middle.

He'd lost muscularity.

He was needing to rest more.

He'd had to make changes at work.

He'd lost his sex drive completely, and he was shaving

much less frequently.

So when we assess symptoms and signs of endocrine disease,

we try to use clinical cues to understand what is

happening in the hormones.

And principally when there's a pituitary mass lesion, we're looking

for two things.

We're looking to see if there is interference or absence

of certain hormones.

And the corollary is we're looking to see if the

mass lesion is over producing certain hormones.

So the patient can have hypo pituitary ism or can

have endocrine hormone excess.

And these are the hormones of the pituitary gland.

So here's the hypothalamus.

And the hypothalamus has these neuro secretory cells making the

releasing factors that I've described earlier.

They are passed down through the portal system into the

anterior pituitary where the releasing factors act on the trophic

hormone producing cells.

So we've got lactate troughs which make prolactin, some autotrophs

which make growth hormone gonadotropin, which make FSH and LH,

cortical troughs, which make Acth, and thyroid troughs, which make

TSH the posterior cells of the pituitary.

Here in green, make two substances oxytocin, which is important

for urine contraction during delivery, and an important hormone called

ADH, antidiuretic hormone, which is responsible for water balance.

So when we see an anterior pituitary hormone tumour, we're

asking ourselves Is this individual failing to produce these trophic

hormones?

Or conversely, are they produced in excess?

So if there is deficiency of TSH, there is hypothyroidism,

Acth, there is hyperrealism, hypogonadism, growth hormone deficiency and prolactin

deficiency doesn't cause clinical symptoms unless somebody is trying to

breastfeed.

It is extremely common to see excess prolactin.

So of all of the cell types within the anterior

pituitary that want to overproduce hormones, hyper prolactin are prolactin

secreting.

Tumours are the commonest.

We rarely see gonadotropin producing tumours.

We rarely see thyroid trough producing tumours, but it's reasonably

common to see acromegaly, a condition where there's growth hormone

excess, and it's reasonably common to see Acth excess, causing

excess cortisol or Cushing's disease.

So you can see that TSH governs thyroxine production, controlling

metabolism, and metabolic rate.

Acth is responsible for the production of cortisol.

So Acth deficiency we become quite unwell because we're cortisol

deficient too much Acth.

We develop Cushing's syndrome, too much growth hormone, we develop

excess IGF one.

And the consequences a condition called acromegaly.

Gonadotropin excess is rare, but deficiency is extremely common, and

hyper prolactin anaemia leads to stimulation of the mammary gland

in both genders.

So women tend to present with galactose milk production outside

of pregnancy and menstrual irregularity.

Men, when they have prolactin excess, tend to have features

of gonadotropin deficiency or hypogonadism.

So there are several aspects to the evaluation of the

patient with a pituitary lesion.

The first is what is the actual tumour doing itself?

Is it causing headache?

Is it interfering with visual field function or acuity, and

has it extended into the cavernous sinuses to interfere with.

Eye movement by interfering with the ocular motor nerves?

That usually only happens if there's a very aggressive malignant

type pituitary tumour, or if there's been a lot of

haemorrhage acutely into a pituitary tumour, a condition called pituitary

apoplexy in perpetuity.

There's fatigue and lethargy.

There tends to be weight gain because of reduced metabolic

rate.

The sexual function is compromised, as is the sex drive

or libido.

And in a younger female, we can ask about menstrual

periods.

And that's a really good biologic guide to health.

And when we examine the patient, we look at mood,

behaviour, animation.

We look at the colour of the skin.

Somebody who has no Acth tends to be very pale.

Somebody who has excess HGH tends to develop hyperpigmentation.

We examine ocular motor function and visual acuity.

We look at fat distribution, the strength of the proximal

musculature which is compromised when there's cortisol excess.

And we look for features of acromegaly.

And we examine testicular volume.

The reason that hyperthyroidism occurs is because as the pituitary

tumour gets bigger, it compromises the connections through the infant

column of these trophic hormones, so that the releasing hormones

from the hypothalamus prevent the trophic hormones being produced from

the anterior pituitary.

Okay, so this man had hypoparathyroidism as well as a

visual field effect.

He had elevated prolactin, and we did a test to

assess how well he could produce cortisol and growth hormone.

And he failed that test.

He had low testosterone, though his thyroxine was preserved.

So how do we assess endocrine function in the pituitary

disease?

And what test do we do?

Well, when we perform baseline biochemistry, we look at T4

or free T4 and free T3, as well as TSH.

We measure prolactin, LH and FSH.

We always measure simultaneous with the sex hormone that is

appropriate for gender.

We measure growth hormone and IGF one and act in

cortisol.

If there's any doubt about the functioning of the hypothalamus

pituitary adrenal, our growth axis, we can do more sophisticated

so-called dynamic tests where we try to stimulate the pituitary

gland, are stimulate the adrenal gland to produce its hormones.

So there's a very commonly performed test in endocrinology called

the short acting test, where we give synthetic Acth to

stimulate the adrenal gland to see how well it responds.

And that is a good test for adrenal insufficiency.

If we really want to look at the function of

the pituitary gland, the gold standard test is called the

insulin stress test.

Insulin stimulation test.

Our insulin tolerance test.

All of these are the same entity where we administer

intravenous insulin to make the individual hypoglycaemic.

And so we try to make the blood glucose go

less than 2.2mm/l, which is significant hypoglycaemia.

And that makes the patient feel unwell.

They get an adrenergic response where they make counter regulatory

hormones.

There are four counter regulatory hormones adrenaline or catecholamines, glucagon,

which is produced by the pancreas, cortisol and growth hormone.

So these hormones are produced when the sugar goes low.

So the principle is if the pituitary is being tested

to see if it can function.

If we've got clear definitions of what is a normal

response, and we make the individual hypoglycaemic and they don't

make the right amount of hormone, then they are underactive.

So as a rule, measure the pituitary hormone which is

in this case TSH with free T4 and free T3,

because it's not uncommon to see a TSH that just

gets into the normal range, but the T4 is actually

low.

So in our evaluation, we've done a clinical assessment of

hormone excesses or deficiencies.

We've confirmed what is happening, the hormones by measuring the

basal values and performing some dynamic testing.

We try to work out at which level of the

axis there might be deficiency.

So if the thyroxine is low, is it low because

the TSH is not responding?

Or is it a thyroid problem with a high TSH?

And then we try to identify the pathology.

So here's our example of the thyroid.

So this patient has low thyroxine.

But he's also got low TSH.

So that tells us that actually the problem isn't with

the thyroid gland.

It's going to be with the pituitary gland.

And then we do a pituitary scan.

So in primary thyroid disease the thyroxine is low but

the TSH is high because the pituitary is saying come

on thyroid.

Why are you not making thyroxine.

In secondary hypothyroidism the thyroxine is low but so is

the TSH.

So this man had an elevated prolactin.

He was making enough TSH to keep the free T4

in the normal range.

But he failed the insulin stress test and was missing

by that virtue, Acth.

He had low testosterone, gonadotropin were low, and he failed

to produce growth hormone in response to hypoglycaemia, so he

was missing some of his anterior pituitary function, so-called partial

hypoparathyroidism.

Why is the prolactin high here?

Is he overproducing prolactin?

I've told you that prolactin producing tumours are common, and

certainly that's a possibility.

But actually this man has only a modestly elevated prolactin.

And the reason it's modestly elevated is because if we

go back to our imaging.

And look at the pituitary stalk.

Normally what happens is the pituitary gland makes prolactin, but

there's an inhibition of prolactin production via dopamine, which is

released from the hypothalamus, transfers itself to the anterior pituitary

via the pituitary stalk and inhibits prolactin production.

When there is a pituitary tumour, we inhibit.

Dopamine, the ability to switch off prolactin production, Reduction.

So by loss of the hypothalamus pituitary connection, we lose

dopaminergic inhibitory tone and the prolactin rises modestly.

So he's got a jittery tumour with superscalar extension.

And it's compromising vision.

So we need to operate to decompress the optimism.

And this man had what's called transfer needle surgery.

Meaning we've instrumented the nose, traversed the sphenoid sinus, open

the floor of the fossa and taken out the tumour.

We then stain the tumour with immunostaining to try and

determine which cell type is responsible for the tumour development

or growth, because it can be any of the cell

types.

And he had what was called a non-functioning pituitary tumour.

So what types of pituitary tumour are there and how

do we treat them?

Well, here are two important definitions.

Try and remember these for the rest of your career.

So a micro adenoma is less than ten millimetres and

a macro adenoma is ten millimetres are bigger micro and

macro.

And then we define functioning or non-functioning functioning tumours overproduce

hormones non-functioning are associated with normal hormone production our low

levels of hormones.

So we had a macro adenoma because it was more

than ten millimetres but it was non-functioning.

If we have a look at the breakdown, the majority

of tumours we see in South London are indeed non-functioning

pituitary adenomas.

These often present through incidental presentations.

Guys had a CT scan or an MRI for another

reason, or because somebody's been to the ophthalmologist, and the

ophthalmologist has noted a field defect.

So almost half the patients we see have non-functioning tumours

of the other half.

TSH secreting tumours are very rare.

Prolactin normal.

Going to theatre is fairly rare, but prolactin is the

commonest functioning pituitary tumour, and acromegaly makes up about a

quarter of the patients who've ended up having surgery.

In our cohort, when there's too much growth hormone, the

body undergoes stimulatory growth, leading to the clinical condition acromegaly,

acros and megas, meaning enlargement of the extremities.

When there's too much Acth, the patient has too much

cortisol and Cushing's syndrome.

High prolactin gives rise to galactose and hypogonadism, and too

much TSH stimulates the normal thyroid gland to produce too

much thyroxine and produces an overactive thyroid state.

So this is how pituitary tumour is present.

They can be incidental.

Like this guy.

The patient may present with real clinical symptoms.

The GP does some blood tests and says you're hypothyroid,

but surprisingly, your TSH is not elevated.

You might have a pituitary problem or the testosterone is

very low.

Ah, the woman has stopped having menstrual periods or can't

get pregnant.

And there is hyper patriotism.

There can be mass effect.

So somebody might be sitting in front of the ophthalmologist,

and the ophthalmologist says, I think your fields are abnormal.

There can be a hyper functioning tumour.

So somebody might spot somebody on the tube and say,

you've got acromegaly, go and see somebody, or there can

be an acute presentation if there's rupture and haemorrhage into

a very vascular gland called apoplexy.

This is how we instrument the nose to get at

the senators traversing the sinus, taking out the pituitary tumour

through the nose.

We can watch some tumours.

If they're not so big, we can treat some medically.

We irradiate a small number, and the majority that are

large end up having surgery, the ones that respond best

to medical therapy.

I've told you that dopamine inhibits prolactin production.

We can use a dopamine agonist like bromo krypton or

how to treat prolactin secreting tumours?

And that has two effects.

It switches off the prolactin production and it shrinks the

tumour.

Similarly, we can use the metastatic analogue injections for acromegaly.

Radiotherapy is used as a second line treatment.

When there is deficiency, we have to replace the deficiency

with the appropriate physiological level of hormones.

So the hierarchy of importance is if there is Acth

deficiency, we must manage it.

Because hyperrealism is a life threatening disorder, replacing TSH deficiency

is necessary for normalisation of function and quality of life.

Hypogonadism can be treated with sex hormones, but that doesn't

restore fertility.

If we want to restore fertility, we need to give

gonadotropin, which can be given by injection, and we can

replace growth hormone deficiency by subcutaneous injection.

So the principles of endocrine replacement is to replace the

hormone that nature intended to produce And we also want

to try and do so in a physiological way.

And some of our hormones testosterone, but particularly cortisol is

produced in a circadian or Americans call it a diurnal

rhythm.

So this man has been put on hydrocortisone growth hormone

and testosterone.

And this is an example of what happens.

Somebody with normal function of the hypothalamic pituitary adrenal axis

cortisol concentrations.

You can see these are a range of individuals who

have had measurements.

And the dark line is the average of the group.

You can see cortisol peaks some stage early in the

morning.

Values fall throughout the day progressively and are really low.

During the early hours of the night, they begin to

rise about 4 a.m. again with individuals following a normal

circadian or diurnal rhythm.

So if we're giving this man who's presented with his

head injury but incidental hyperthyroidism hydrocortisone.

We want to try and mimic this curve.

So individuals very often take tablets multiple times a day

to try and get a physiological value, um, which is

beset with problems.

So there are lots of products in development to try

and make pituitary hormone replacement more effective, particularly the hydrocortisone

component.

So this man presented with an incidental finding that's a

common pituitary presentation.

He had a visual field effect which was by temporal

because of optimism compression.

He was partially a hypo pituitary.

The tumour was non-functioning.

It wasn't secreting hormones to excess.

And he was treated with surgery and hormone replacement.

The surgery was very effective at removing the entirety of

the tumour.

Had it not been and the tumour developed regrowth, he

could have had a second operation or he could have

had radiotherapy to try and prevent tumour recurrence.

And I'll stop there, come and find me.