do a I'm going to talk to you about clinical

aspect of thyroid disease.

So you all know that the thyroid gland is a

hormonal endocrine gland based at the front part of the

neck.

There's a little diagram of how it fits, uh, compared

to the thyroid cartilage and the cricoid cartilage.

Um, and we know that the thyroid gland secretes thyroid

hormones as T4 and T3.

So predominantly the thyroid hormone secretes T4, but peripherally T4

is converted to T3.

And T3 is the hormone that has the predominant physiological

um action.

And as you know, thyroid hormone controls your metabolism.

And so you get this situation of stimulation by the

hypothalamus and the pituitary gland to induce the thyroid gland

to produce some thyroid hormone.

And that is the this this is a this is

the system, as you know.

So uh, the hypothalamus produces TR and that stimulates the

pituitary to produce TSH.

And that stimulates the thyroid gland to produce its hormones

T4 and T3.

And they act by negative feedback to control the system.

So you you know, all about negative feedback is sort

of mechanism of homeostasis.

I think it comes up to a certain extent in

GCSE and A-level biology, where one talks about maintaining the

the the temperature of the body, you you get a

set point.

Essentially there's a set point where the body kind of

wants, if you like uh, the T4 levels to be

at a certain level and if it's if it's too

low, they will stimulate more production of the hormones, and

if the levels are too high, they will inhibit the

production so that that's how the whole system is controlled

to keep the TSH and the T4 kind of in

the normal level and to keep the metabolism, you know,

on track.

So if the pituitary gland is working normally, you can

kind of imagine or you can see even a graph

of TSH versus T4.

And you get the idea that that is kind of

how the relationship would be represented.

If the I may have a pointer, I may not

I don't know if this.

Yeah.

So if you're, shall we say if your T4 levels

drop for whatever reason your body will produce more loads

more TSH to try and get the normal working pituitary

to restore things back to this area, which is the

normal range.

And if you produce extra T4, then if your pituitary

is working normally, it will essentially stop producing TSH and

silence itself because you've already got too too much T4

around so it doesn't want to.

It doesn't want to stimulate any more.

So this is this is the normal normal range for

both T4 and TSH.

Um, so that's how the system is supposed to work.

So the prob the clinical problems we would talk about

are hypothyroidism and hypothyroidism and also nodules and lumps.

All of endocrinology is having too much or too little

of hormones pretty much.

Also tumours of endocrine glands.

So that's kind of a model for a lot of

clinical endocrinology.

Um, so if we start with hypothyroidism, not having enough

thyroid hormone that has lots of clinical symptoms, it's a

slowing of your metabolic processes.

So people pretend to be tired or cold, possibly with

weight gain, thin hair, dry skin, low mood, constipation and

bradycardia.

Those are the some of the symptoms.

And there's also a diagram there that might include some

other things.

It says heavy periods and infertility on the diagram as

opposed to the list I've got there.

And it also says I think depression and forgetfulness.

So a few other features.

But but it's it's quite broad.

It affects lots of different systems.

So if you imagine a kind of case study, you

might have a lady who's 69 years old she comes

in with to hospital with confusion and exhaustion, and somebody

does blood tests showing a TSH is 84 and a

free T4 is four.

Now I realise I haven't showed you previously the normal

ranges of these hormones, but in our labs the normal

ranges are kind of given in this.

So you want your T4 to be somewhere between, shall

we say ten and 20, although actually the exact numbers

given they're a little bit different and you want your

T3 to be somewhere between 3 and 6, and you

want your TSH to be somewhere between .0.4 and five,

shall we say.

So?

I mean, you know, the exact numbers are given.

They're a bit different.

So you can see that she's hypothyroid.

Her TSH is way too high and her T4 is

very low.

So it's this is clearly primary hypothyroidism a kind of

very obvious case.

And hypothyroidism gives the symptoms we described on the previous

slide.

Um, you can get this coarsening of hair puffiness of

the face because of depositions of things called glucosamine or

glycans in the soft tissues and in the tongue and

various places.

This is quite an extreme example.

They've put on the caption gross clinical hypothyroidism.

I mean, maybe that's not the nicest way of expressing

it, but it is a severe case.

She has lots and lots.

She's very she's very puffy.

She's got, um, uh, and you can imagine that the,

the in the enlarged tongue you can't see and the

hoarseness of voice.

These are other features of we keep ticking on.

Maybe that's why we find it might.

Um.

So hypothyroidism has a variety of causes.

Um, the two commonest causes are iatrogenic.

So us doing a treatment that renders the thyroid not

working, that would be an operation to remove the whole

of the thyroid.

That's one way you end up hypothyroid.

If you give radio iodine treatment to the to for

for a for a for an overactive thyroid, you're very

likely to end up with an underactive thyroid.

So I think is the top of that list.

And the other really common reason why the thyroid becomes

underactive is a chronic autoimmune disease.

Um, so autoimmunity where the thyroid is attacked and stops

functioning.

Um, it can be atrophic where the thyroid is, you

know, uh, it essentially becomes, uh, shrunken, or it can

be Hashimoto's where it becomes nodular.

Um, so whether the thyroid is big or little doesn't

tell you so much about what's going on in terms

of function, but that those are the two most common

causes.

And and so this is an extension of the previous

slide where you've got the two common causes at the

top.

But there are a bunch of other, uh, rarer causes

of an underactive thyroid that I thought we would touch

upon.

So one is thyroiditis.

Thyroiditis is a kind of, um, a broad term.

It just means inflammation in the thyroid.

And there's lots of different types.

Um, but but a viral thyroiditis or the other types

of thyroiditis are listed there.

All types of thyroiditis can make the thyroid go underactive,

either temporarily or permanently.

And iodine has bizarre effects on the thyroid, but a

severe iodine deficiency can make your thyroid very underactive.

Actually, excess iodine can also cause the thyroid to be

stunned.

And it can be you can be hypothyroid with excess

iodine as well.

But that's a that's a detail.

But that is another cause.

And then some drugs and some diseases that infiltrate the

thyroid.

Um, so there's a list of drugs there that I

think we won't go into in great detail, but also,

um, the infiltrated disease of the thyroid, strange things like,

um, uh, sarcoidosis or lymphoma, these are quite rare, but

but, but, but but things that will, will infiltrate and

stop the thyroid from working.

So the treatment for hypothyroidism is really simple.

People get given levothyroxine, which is essentially T4.

And I mentioned to you that T4 needs to be

converted to T3 peripherally by these diagnose enzymes, but that

that is supposed to be a system that works in

the majority of people normally.

Um, I don't want to go too far into controversial

area, but some people believe that T4 isn't converted that

well to T3 in some people.

And so there is a movement, uh, afoot, um, mostly

driven by patient groups who feel that they would like

to be given T3 instead of T4, which is much

more expensive.

But that's something that that's again, that's a sort of

detail.

The the top line information about being having an underactive

thyroid is that you've given levothyroxine and you get given

about 100 micrograms a day.

Um, I put 75 to 125 on the slide.

Some people do it by weight.

They say 1.6 micrograms per kilogram.

That would tend to give you a bit more, wouldn't

it?

I mean, but but you might end up with it.

Some people would end up on a dose of 150

or more.

Um, and the way in which you check that your

thyroid is, um, adequately treated as you do blood tests

to check that the TSH is normal.

And so if your TSH is in the normal range,

you that.

And if your pituitary gland is working normally, then you're

on the right dose of levothyroxine.

That's the that's the kind of conventional mantra.

Um, so blood tests to check the TSH.

Um, you can check the T4 as well, but TSH

is a more kind of bankable, um, stable thing to

monitor.

So if we go to a second case, this is

a 25 year old patient who's tired, and so they

have a TSH that's as shown.

And a T4 and T3, uh, measured there.

And so the point about those blood tests is that

they're all in the normal range.

And so this person doesn't have a thyroid problem.

And I suppose the point I wanted to make there

is that the symptoms of hypothyroidism are incredibly non-specific.

Loads of us gain weight and we don't want to

gain weight.

Loads of us are tired.

You know, loads of people maybe have more hair thinning

than they want or have, you know, whatever those things.

So lots of people think they've got thyroid problems.

But we tend to trust the biochemistry.

And so you will I guess you just The point

is you need to do the tests to, to check.

Um, having symptoms that are potentially consistent with hypothyroidism is

really common.

So if someone says, I think I'm hypothyroid, but my

blood tests are normal, the blood tests must be wrong.

We tend to argue the other way and say no,

we actually would trust the blood test in that stage

situation, and it's not thought that you would benefit from

thyroid hormone if you're not properly hypothyroid despite symptoms.

Um, some people believe differently, but that's the conventional idea

that I think you should have taken at least as

your top line information.

Um, thyroid antibodies, um, are very common.

Uh, and they do indicate that you might have a

predisposition to become, to develop a thyroid dysfunction in the

course of your life.

But it is very common to have thyroid.

There are different types of thyroid antibody, but the most

common one is the TPO antibody.

And I get a really lot of GP's writing to

me saying, you know, this patient, they're tired, their thyroid

function is normal, but their TPO antibody is positive.

So would you like to see them in clinic because

you know you can make them better.

And I'm in a nice, positive way.

I have to be like, no, I can't make them

better.

You know, TPO antibodies are positive and 12% of the

female population of the UK and tiredness with normal thyroid

function, we don't really have a treatment for uh so

that's not not a pathology.

It's not an endocrine pathology.

Um but, but it is something that we, we, we,

we, we hear about a lot.

If the only thing that's wrong is the antibodies and

the, um, if the only thing is wrong is the

antibodies and the and there are symptoms, but the thyroid

function is normal, but that's not regarded as thyroid pathology.

Um, and all you would do there is say it's

sensible for the patient to keep having their thyroid checked

every year or so to check because they might develop

hypothyroidism, as in biochemical hypothyroidism in the future.

Okay.

So now we're going to move to an overactive thyroid.

So this is a case of a 30 year old

female patient anxious shaky pulses going along at 100.

The biochemistry shown there you can see the TSH is

suppressed.

And the T4 and T3 are both high.

So we recognise that to be hypothyroidism overactive thyroid.

We use the term thyroid toxic doses as well.

Um, I actually use the term thyroid psychosis and hypothyroidism

fairly interchangeably.

There is a technical difference, um, which maybe we won't

go into.

I mean, don't worry about it.

Uh, but, uh, but but but essentially thyroid psychosis is,

is the is the is the clinical term the correct

clinical term for having an overactive sort of having, uh,

having too much thyroid hormone and the clinical effects from

it.

Um, so, so, uh, people who are thyroid toxic will

get mood and behavioural changes.

They'll get restlessness, shaking, sweating, palpitations, breathlessness, diarrhoea, muscle weakness

sometimes.

Um, so, uh, some of the clinical signs you might

see with someone who an overactive thyroid is that you

get little attack traction because of over sympathetic stimulation to

the eyelids.

So you can see with this, uh, his left eye,

uh, you can see that you can see the white

of the eye above the iris.

Uh, one shouldn't be able to do that.

That's, uh, that's, you know, uh, lid retraction, um, lid

lag is the idea that if you have a if

you ask a patient to, um, if you move something

in an arc from high up to low down and

ask the patient to follow it with their eyes, that

their, their eyelids will, will, will be they will follow

it with their eyes, but their eyelids will remain retracted,

um, in a more pronounced way.

And so the eyelids would follow slowly.

Um, and so you can sort of see in a

dynamic way the lid retraction.

Um, so the main causes of thyroid psychosis are graves

disease and a nodule in the thyroid that's producing too

much thyroid hormone.

Not all nodules in the thyroid produce too much thyroid

hormone.

But some do.

Uh, we'll come back to thyroid nodules in a second.

Um, so graves disease is Autoimmunity.

I think there's going to be a further slide on

it.

So it's an autoimmune disease where you produce the TSH

receptor antibody and that stimulates the thyroid to be overactive.

Um a thyroid nodule.

Again we'll come back to you.

But but some nodules produce additional thyroid hormone in a

toxic in a in a in a in an autonomous

way.

Um there are some rarer causes of thyroid toxicities listed

um, uh, in black on this slide.

So if you have a pituitary tumour that's making too

much, uh, tsh, um, too much thyroid hormone, then that

will in turn make the thyroid produce too much thyroid

hormone.

And that is one reason why you might get thyroid

psychosis.

That's really rare.

So TSH is one of the rarer types of pituitary

tumour.

And pituitary tumours aren't that common anyway.

So um so that's to bear in mind.

But but you will probably not see one of those,

uh, in su to start doing a job like like

mine.

Uh, hCG stimulated hypothyroidism is the idea that pregnancy can

make your thyroid toxic because beta hCG, as you know,

is the hormone of early pregnancy.

So, um, women in the first trimester of pregnancy sometimes

are a little bit thyroid toxic, and that's normally just

settles by itself.

It's not too bad if you have a clinical stage

where you produce a lot of hCG, you can have

quite significant thyroiditis with this.

That's more common if you have a molar pregnancy or

if you have very bad hyperemesis gravidarum.

So a women who are getting lots of vomiting in

early pregnancy or with twins you get more HCG.

So anyway there there can be um hCG mediated hypothyroidism

is perhaps more of a physiological cause, but um, it's

definitely something we see if you're taking thyroid hormone and

you take too much of it, then that is a

cause of, um, uh, that was obviously a cause having

too much hormone and thyroiditis.

Um, thyroiditis.

There are several types which I think will come to,

but thyroiditis can generate extra thyroid hormone as well as

potentially making you have underactive thyroid.

Um, I said I wouldn't go into the difference between

thyroid psychosis and hypothyroidism, but since I'm on this slide,

I mean, I think the the point is that thyroid

toxicities, where is any condition where you have too much

thyroid hormone.

So everything on this slide is thyroid causes hypothyroidism is

when the thyroid gland is making the extra thyroid hormone.

Um, and so uh, so for example, if you think

about excess or excess excess thyroid hormone medication that that

is an example of your thyroid toxic.

But you don't have hypothyroidism because the, the because the

the reason your thyroid hormone is too high is not

because the thyroid hormone, the thyroid gland is making too

much.

It's just it's coming from another source.

So that's a, um, that that's a detail.

Um, but I would use the terms interchangeably.

And so if we go to somebody with graves disease,

this is somebody an example of primary hypothyroidism is grave

disease.

It's an autoimmune disease where you make an antibody.

The antibody binds to the TSH receptor and stimulates it.

Um, these patients, yes, they have an overactive thyroid.

They can also have thyroid disease.

And they can also have a swollen thyroid gland.

So this lady is, um, got, um, you can see

her little retraction.

We she we can believe she's thyroid toxic.

She looks a bit stressed.

Um, her thyroid gland looks a little bit enlarged.

Um, thyroid eye disease is only about 20% of people

who have graves disease get thyroid disease as well.

And it classically gives you itching and watering of the

eyes.

And it makes the whites of the eyes go red

and you get irritation.

Um, it can produce a bulging of the eyes, It's

the thalamus, where the eyes are further forward in the

skull than they should be.

And potentially it can give you double vision and sight

threatening.

I mean, that's quite rare.

So most people, most people with graves disease don't have

thyroiditis at all.

And those that do, they mostly get symptoms which are

very unpleasant, uh, to have itchy eyes that water and

have tearing.

So they're often very unhappy about having this illness.

But, um, the idea that, you know, but you have

to have really quite a severe case for it to

be sight threatening or cause double vision so that those

problems are rare.

But, um, but but thyroid disease itself is actually is

actually, you know, not not a nice thing to have

and takes a while to settle down.

Um, so if you have graves disease, you can have

these other manifestations.

So we've mentioned thyroid eye disease.

That's relatively common because it's about 1 in 5.

It's about 20%.

The other manifestations of graves disease that you some see

are really rare.

So you can get this thyroid, which is the is

basically like clubbing, but it's very, very rare.

But it is one of the many causes of clubbing

where it gives you this, you know, this the the

drumstick, the swelling of the, of the distal part of

the fingers.

And you can get a dermal pathy a skin disease

related to Graves's.

Again, it's very rare.

It's a sort of orange peel type appearance.

And this is one slide of it.

But you know that again, that is that is not

a common manifestation of graves.

These are rare things that we sometimes sometimes see.

Um, but the most, most people, graves disease will have

an overactive thyroid, a swollen thyroid gland.

And they may or may not have thyroid disease.

So the tests one would do would be that you

need to have, um, thyroid function, blood tests, obviously, as

we've said.

And then you check for this TSH receptor antibody.

Um, that's a different antibody to the TPO antibody I

mentioned.

T they're both antibodies for the thyroid, and they both

are markers of an autoimmunity, uh, in the thyroid.

But the TPO antibody is, um, more, more associated with

an underactive thyroid.

And it's also quite common in the population in general.

As I said, uh, the TSH receptor antibody, which we

call trap is um, is a more specific marker of

autoimmunity causing graves.

And it is basically the diagnostic tests for graves, the

tribe antibody.

Um, so if someone's overactive got an overactive thyroid, you

might check their antibody because if it's positive, they've almost

certainly got graves disease and you got your diagnosis, um,

if they don't have a positive antibody, then it's more

uncertain what's going on.

And you would in that situation do a thyroid uptake

scan, which is a nuclear medicine scan where they use

they use they can use a variety of things, but

they use technetium normally to see if the thyroid gland

itself is taking up, take the ECM or and therefore

functioning um, in the whole gland.

And so that helps you to determine if you have

a toxic nodule.

So I mentioned one of the common, uh, causes of

an overactive thyroid is that you might have a nodule

in the thyroid that is autonomous, that's producing too much

thyroid hormone.

And a thyroid uptake scan would give you that diagnosis.

Um, and the other investigation you might consider is an

ultrasound that's less specific.

I mean, an ultrasound is a good way to image

the thyroid in general.

It's not going to tell you whether you have a

nodule that's over functioning or definitively tell you you've got

graves disease or thyroiditis, but it is sometimes a useful

test to have a, a better understanding in a sort

of global sense of what's happening with the thyroid.

So those are the investigations for hypothyroidism and then treatments.

Um, yeah.

I mean, so people with hypothyroidism, thyroid psychosis are often

have lots of symptoms.

And so you might give them beta blockers because they're

going to work quickly to suppress and control the symptoms.

So beta blockers stop you being from shaky.

Uh, they make you less anxious, less tremulous, less tachycardic.

Um, and so starting beta blockers is one way to

get someone who has Start-Up psychosis to feel a bit

better today.

And that's so that's that's a good thing.

And that would be something you would use.

You're then going to use a medical treatment to make

their thyroid hormone levels come down.

Those medications are much slower.

So you might start them on carbon muscle or uracil.

Carbon muscle is the drug of choice that you use.

Um, and proper thyroid uracil is only mostly only really

used uh, in a situation of either pregnancy or anticipate,

you know, either planned pregnancy or actually being pregnant because

it's a bit safer in pregnancy.

Um, but otherwise it's not such a good drug as

carbamazepine.

Um, so those are the two medical drugs, but they

don't work straight away.

So if you see someone in clinic who's thyroid toxic

and you start them on a beta blocker, that will

help their symptoms straight away, but it won't treat the

underlying problem, you can give them carbine resolve to treat

the underlying problem, but it'll take a few weeks to

kind of fully normalised the numbers, the the thyroid hormone

levels.

Um, if those things don't work or can't be used

or whatever, what we call definitive treatment for graves disease

is you can give radio iodine.

So that's where the patients, um, they eat or they

swallow a, should we say a capsule of radio labelled

iodine.

And then because it's iodine, it finds its way to

the thyroid and because it's radio labelled it will destroy

the overactive thyroid cells.

Um, and so that would stop them being overactive with

their thyroid.

Um, or you can do surgery, you can do an

operation to remove the thyroid.

And in that situation you would remove the whole of

the thyroid normally.

Because if you're trying to treat graves disease with an

operation, you kind of need to remove the whole of

the thyroid so that the graves doesn't come back.

Um, that is the the current belief they used to

always do, like subtotal thyroid surgery to try and take

the most of the graves disease away, but leave some

thyroid tissue But now, if you're doing an operation for

graves disease, the belief is that you should probably just

remove the whole of the thyroid and kind of cure

the patient from being thyroid toxic hypothyroid.

So, um, that is supposed to be a diagram about

a toxic nodule, as I mentioned already.

But, um, it's just it's not really.

It's not it's not a diagram.

It's.

Well, it's a yeah.

So the idea is that within the thyroid, you could

have a nodule or a lump, uh, of, of thyroid

tissue, um, that could be overactive and producing too much

thyroid hormone.

So, you know, classically it might just be a centimetre

or two in size.

The way you would find that out is firstly, the

patient would have be they'd be thyroid toxic.

So they might have symptoms and their blood tests would

tell you they were hypothyroid thyroid toxic.

And then when you do an uptake scan the nuclear

medicine scan uptake scan, which I said was also known

as a technician scan, that would show you that this

area was working way too hard and that the rest

of the thyroid was perhaps not working so hard.

And that way you would know that that's a toxic

nodule, and that although you can control that with tablets

temporarily, that's going to be better treated with radio iodine

or surgery, because that's a those are those are definitive

treatments for that for this condition.

So I mentioned thyroiditis I think thyroid disease is quite

a confusing word.

Obviously it just means inflammation of the thyroid.

That's kind of obvious.

But there's loads of different types and they're not that

similar to each other.

So it's a hotchpotch of weird things, but you can

divide it into painless and painful types, which are sort

of useful.

Um, so, um, people who have a painless form of

thyroiditis will often just become hypothyroid, uh, insidiously.

So lymphocytic thyroiditis or a postpartum thyroiditis or Hashimoto's thyroiditis,

these patients will often become hypothyroid with an underactive thyroid.

They might go through a phase of being thyroid toxic

before they become hypothyroid.

Um, and which we'll see, I think on the next

slide.

And similarly, these are, these are painful forms of, uh,

thyroiditis, uh, radiation used and this, this granulomatous thyroiditis, which

we used to call declare veins thyroiditis.

So, um, uh, and when I say painful, I mean,

in the, in the thyroid.

So if you have a.

Oh, yes.

So the next slide kind of tells us the kind

of cadence of these things.

So if you have an episode of thyroiditis, you'll often

be hypothyroid for a bit.

And then you'll go through being your thyroid and then

you'll become hypothyroid.

And then sometimes.

So I guess what you ask you to look at

is the red and the blue lines, because those are

the T3 and T4 hormones, and those are the ones

that are how much thyroid hormone you actually have.

Um, and though people who have thyroiditis will often go

hypothyroid and then hypothyroid and then either go back to

normal or sometimes this diagram doesn't really show it, but

sometimes they can just remain hypothyroid.

And um I guess I just put the graph up

to, uh, to indicate to you that thyroiditis is a

bit complicated and your thyroid can be overall or underactive,

or it can be changing with thyroiditis, but it can

present with a very painful anterior neck.

Or it can be painless.

Of course, if you have a completely painless form of

thyroiditis, you may not really notice that you're you're briefly

hypothyroid.

So people with lymphocytic thyroiditis sometimes just end up hypothyroid.

Um, uh, and they sort of don't notice the, uh,

the thyroid toxic phase.

Um, but but thyroiditis is a bit confusing, but it

is a condition of inflammation of the thyroid, often where

the thyroid will go high and low and then stay

there or high and low and recover briefly.

Yeah.

So that's what I was going to say about thyroid

psychosis and hypothyroidism.

I think we should just talk about thyroid nodules, which

is the third of the three kind of clinical areas

we talked about.

So if you saw a patient who was, um, comes

and tells you they've got a nodule in their front

part of their neck that they've noticed, that's not a

particularly, you know, it's a reasonably common presentation.

Um, this is quite a quick history.

They've just noticed it in the last couple of weeks.

Um, so in that situation, you would do some thyroid

function blood tests so that you're kind of expecting them

to be normal, but you would just check because it

could be a toxic nodule, uh, an overactive nodule, which

you would see that in the thyroid function, if the

person's thyroid function is normal.

The next tests for a thyroid nodule to do an

ultrasound scan, and often for a needle to be put

in to get a sample of cells, we call that

fine needle aspiration.

So it's a bit like a biopsy, but it it's

but it gives you a cytology sample.

So it's a bit it's a bit less invasive than

a biopsy.

And also a biopsy would give you, you know, histology.

It would give you a 3D uh, structure of, of

a bit of a lump of tissue.

Whereas a final aspiration only gives you cells, it gives

you cytology.

So it's analysed slightly differently Um, so I guess the

point about thyroid nodules is 90% of them are benign.

So when people come and see us with thyroid nodules,

we try and reassure them that it's very likely to

be nothing to worry about.

But it does need to be assessed.

Some nodules are thought to be low risk, so if

they have ultrasound appearances that are benign, uh, if the

cytology is benign, these are very reassuring things.

Uh, the, the ultrasound are graded on this weird you

scale where you two is benign and you five is

malignant.

You four is I think it's malignant, but I'm not

certain you one is essentially doesn't really exist.

I guess it's to have a completely normal thyroid where

you don't even have a nodule, so that's fine.

But no one really talks about U1 because it's not

clinically relevant.

So you two is a benign nodule.

And if it's something is you 4 or 5, you're

already thinking this is probably a malignant lesion.

It's going to have to come out with an operation.

Um, the cytology, you know, when they put the needle

in for the fine needle aspiration, you may get suspicious

or diagnostic of malignancy cells.

The management of this is this surgery, and the extent

of surgery would depend a bit on how big the

nodule and how bad it looks.

If it's a small nodule, you might end up with

just the nodule being removed.

A sort of Lubeck to me, where one lobe of

the thyroid is removed.

But often you'd have a total thyroidectomy if you've got

thyroid cancer or a strong suspicion of thyroid cancer.

That's kind of how we would look at thyroid nodules

in general.

Um, so thyroid cancer is um, is a cancer that

has several different types.

Um, the vast majority is papillary thyroid cancer.

And then there are other types of follicular, medullary, anaplastic.

And sometimes you can get lymphoma in the thyroid.

Uh slightly different thing.

But but that that is another malignancy that you'd see

in the thyroid.

Um, both um papillary thyroid cancer and follicular thyroid cancer

have really good prognosis.

I mean, it's still a really big deal to be

told you have thyroid cancer and it needs to be

worked up and people have to have an operation and

they have to have follow up.

So I'm not trying to belittle the experience, but actually

the the five year, the ten year prognosis is really,

really good.

And so these people notwithstanding that it's disruptive to have

an operation and have that diagnosis, uh, you know, a

very it's not a life limiting condition or it's very,

very unusual, very rarely.

Medullary thyroid carcinoma is linked with multi endocrine neoplastic syndrome

type two.

And the tumour marker is calcitonin.

So that's a bit more it's a bit more aggressive.

It has a slightly less good prognosis.

And it has this interesting genetic link with other other

tumours for example for a chromosome as we were going

to do today.

Um anaplastic thyroid cancer is is very rare, but it's

extremely aggressive.

And it um and it, it increases in size very

fast and it is not responsive to very many treatments.

So, um, so the vast majority of thyroid cancer has

an excellent prognosis, but you have to be a little

bit careful about saying that, because of course an anaplastic

thyroid cancer has a terrible prognosis.

So that's a it's often just that's the small print.

But but one needs to be aware that there is

this spectrum.

And I've said at the bottom there that the prognosis

for papillary thyroid carcinoma is excellent, with a five year

survival of more than 89, sorry, 98%.

So, so, so, so very good compared to other types

of cancer.

So I mean, in summary from the talk we've we've

talked about hypothyroidism, underactive thyroid and hypothyroidism, uh, which is

classically graves disease.

But there are some other forms.

And then we've done we've touched upon thyroid nodules and

thyroid cancer.

Um, I had a few kind of questions just to

go through briefly to just, um, emphasise some of those

things.

So this is the question.

One is there's a Polish lady who's referred to your

clinic for an assessment of a thyroid nodule.

Uh, so it's a two centimetre thyroid nodule.

It's palpable, soft, mobile.

And she's got normal thyroid function.

So I guess one question they could ask you is

what would be the following management strategies.

Um, and so what about those are rather wordy answers

aren't they.

But I've said ultrasound is not required because it's soft

and you think it's clinically low risk.

That's not really quite right.

Uh, because you still need to assess these nodules.

The B says ultrasound should be, uh, performed with an

F and a C says you should do, um, ultrasound

and an FNA, uh, regardless of the findings.

And D says you should do an operation on the

thyroid.

Um, so actually B is correct.

I haven't really emphasised that in the talk, but if

you have, um, if you do an ultrasound, you do

put a needle in if there's any suspicion on the

ultrasound, if the ultrasound says it's completely benign, then the

guidelines say it's not a brilliant idea to put a

needle in.

Because if you do an FNA and you get cytology,

the cytology can be a bit misleading sometimes.

Uh, so, um, you kind of then start to worry

about a nodule that you weren't worried about, which which

makes everything kind of more difficult.

So you're supposed to trust your ultrasound.

If an ultrasound says it's benign.

That's the end of the matter.

If the ultrasound says there's a question to answer, a

fine needle aspiration is the next test.

So that's one example of how you'd work up a

nodule and and a question about it.

Um, the next case is a 25 year old lady

she presents with tiredness and weight gain.

She's got those, um, blood tests and TPO antibody positive.

So it just asks you for an interpretation.

So we kind of touched upon this earlier.

The point about this is that she has normal thyroid

function.

And so she's not got a thyroid pathology.

She might think she has.

But but she doesn't have a thyroid pathology, at least

not one that's kind of active at the moment.

She does have TPO antibodies that are positive, and we're

not unsympathetic to the fact that she's got tiredness and

weight gain, and I suppose she could be in the

process of developing an overactive and underactive thyroid.

So it's not unreasonable to recheck her thyroid function.

Maybe in a few months, but I think we'd have

to tell her.

At the moment, a thyroid is working normally and that

we don't really have a treatment to offer her.

And if you said, well, you anticipate her thyroid becoming

underactive in the future, couldn't you give her something to

kind of prevent that?

There isn't really a treatment that does that at the

moment in the thyroid world.

Um, if you want to prevent someone developing an autoimmune

disease, you sometimes can immunosuppressed them in in other walks

of, you know, in other and other fields of medicine.

But we wouldn't immunosuppressed someone to avoid them.

Developing hypothyroidism because hypothyroidism is quite easy to treat.

And immunosuppression is not a trivial thing.

So you don't you don't, at least not under current

medical practice.

You're going to you're going to note that the TPO

antibodies are positive, and therefore note that there might be

a predisposition to develop hypothyroidism at some future point, but

you're just going to monitor and offer her treatment, you

know, if and when it was an active issue at

some point in the future.

Um, so question three is that there's a lady who's

feeling hot with a racing heart, anxious, breathless, weight loss.

And you can see her blood test show that she's

clearly thyroid toxic, and she has a lab antibody that

is elevated.

So we've asked you just for the diagnosis.

So again that's that's relatively easy.

This is grave disease because the tribe antibody is the

is the marker of graves disease.

So it could have been any of the other as

well.

Papillary thyroid cancer doesn't really give you thyroid tox cases.

And autoimmune hypothyroidism makes you hypothyroid as the name suggests.

So that would be um, uh, those would be the.

Yeah.

So, so whereas toxic nodule and how she talks closest

are both reasonable suggestions for the clinical presentation.

But the tribe antibody makes this graves.

Um, I didn't put a question in about this.

I was going to but then.

But I think that if they were going to ask

you a question about treatment of hypothyroidism, I think that

what they might ask you and I haven't mentioned it,

but perhaps I should, is that carbon muscle has a

well-known and important side effect, not side effect, but, well,

potential side effect, which is that it can make you

pant out to panic.

What am I doing here?

I was trying to.

Yeah.

Okay.

That slide.

Yeah.

So, um, carbon is all and all but but but

these anti thyroid medicines, they can give you a side

opinion um or neutropenia shall we say.

So you can have um, uh low white cells.

And that is something that you're kind of told to

watch out for.

And I didn't put it on the slide.

But I think that if any of you ended up

in general practice and you were seeing kind of thyroid

patients and they were taking carbon muscle, when you start

someone on carbon muscle, you were expected to kind of

warn them that there is a small risk that they

develop a, uh, they develop, um, uh, leukaemia.

So low, low white cell counts.

Um, uh, when they're on carbon result, the risk is

really small.

It's quantified as three in every thousand patients that take

carbon muscle.

So it's less than 1%.

But it is quite important because the patients who develop

um, uh, what they call a granular psychosis, don't they?

But but low white cell counts, uh, on carbon muscle

can, um, you can become really sick with that because

your immune system is not functioning weirdly.

It can present with any type of infection, I suppose,

because if you're a white cells very low, you could

develop an infection.

Um, but classically it always presents with or at least

in the series of it.

When they describe like a series of 20 cases, everybody

seems to get a very, very bad pharyngitis, like a

really, really bad sore throat, uh, which is associated with

the immune suppression of their, uh, of them having, of

having a granulosa ptosis.

So patients with Covid mas all are usually warned if

they develop an extremely bad sore throat, uh, they should

have a blood test to check their white cell levels

are still okay.

And that is I think that's an important sort of

general medical point that although not in the slides, I

thought that you should know that.

And it's a rare side effect of carbon muzzle, and

it wouldn't be unreasonable to ask question about that, I

guess, although, yeah, because it is an important thing to

know.

So.

So Cuban missile can give a granular status, low white

cells.

And although that could present with any infection for some

reason, it is a very bad sore throat.

That is the kind of classic clinical presentation of this

which people are asked to look out for.

Um, and so they're asked to just make sure they

get a blood test to check their white cells are

okay.

And I think that if they were going to ask

you a question, a clinical question on the thyroid, they

might ask you about, you know, the, you know, what

should patients on Cuban missile look out for in terms

of severe side effects?

Um, so that that would be a question for if

it were written, but it's only for, um, only for

you listening, uh, because it's not on the slide.

Um, that is kind of the end of this section.