hey everyone this lesson is on Hashimoto's
thyroiditis so and this that's where I'm
talking about what are some of the
causes of Hashimoto's thyroiditis who is
at risk for getting this condition we're
also going to talk about how we can
diagnose it and how we can treat it so
hashing notice I read itis is a chronic
autoimmune thyroiditis causing a primary
hypothyroidism due to a cellular and
humoral mediated destruction of thyroid
tissue so key points to take it is an
autoimmune condition that causes primary
hypo thyroidism it is in fact the most
common cause of hypothyroidism at least
in the developed world and like many
other autoimmune conditions females
outnumber males with its condition
generally the ratio is between 7 to 1 so
7 females for every one male and it is
such a common condition that it is
estimated that up to 10 percent of the
general population has this condition
and interestingly it actually increases
with increasing age so the prevalence of
Hashimoto's actually increases with age
so the older you get the more chances
you could get Hashimoto's so this is a
significant condition so how are we
going to remember that Hashimoto's
causes hypothyroidism well I want you to
think about the phrase Hashimoto's hacks
up the thyroid gland Hashimoto's hacks
up the thyroid gland and pitcher and
acts and you're essentially just
chopping up a thyroid gland and if you
have a chopped-up thyroid gland if it's
hacked up well it's not going to be
functional it's gonna be hypothyroid so
that's how you can remember that
Hashimoto's causes hypothyroidism
Hashimoto's hacks up the thyroid gland
what are some of the risk factors of
Hashimoto's thyroiditis the risk factors
include genetic conditions so it's
interesting that individuals with Down
syndrome and Turner syndrome have an
increased prevalence of Hashimoto's in
general now there's also associations
with the gene HLA dr3 because this is an
autoimmune condition and interestingly
yeah if you actually seen a family
member who has Graves diseases which is a
condition causing hyperthyroidism well
you're at more risk for actually having
Hashimoto's they're both autoimmune
conditions so they generally run
together other interesting risk factors
include having stress so increased
stress seems to be associated with the
onset of this condition again family
history this falls in line with genetic
conditions and genes gender as we
mentioned before being female is a big
risk factor in fact it's seven to one
compared to males a high iodine
consumption or high iodine diet can
actually increase your risk for having
this condition so it's been shown that
having actually a bit of a lower iodine
consumption diet so a bit on the lower
side may actually reduce the risk of
having this condition and there's also
question of well this site cigarette
smoking cause this or does some kind of
infection cause this is not quite known
so there are actually a couple subtypes
I want you to to just know about these
are really not that important for this
lesson but the subtypes for Hashimoto's
thyroiditis include a goiter as' type so
the person generally has what we
describe as a rubbery thyroid so they
have you thyroid condition that
progresses to a hypo thyroid condition
and it's due to 'the fibrotic changes
and the other condition is atrophic this
leads to hypothyroidism and is
associated with the thyroid lymphoma so
the two conditions because this is an
autoimmune attack on the thyroid gland
we're either going to have a basically
shrivel up by roid Glen like you might
see in a trophic subtype or you're gonna
have fibrotic changes scarring which is
gonna cause a rubbery goiter estai p--
Hashimoto's so these are the two
conditions I want you to think about so
what actually causes Hashimoto's
thyroiditis what is the pathophysiology
so in order to understand what happens
in hatch motor started itis it's
important to know the general basic
endocrine signaling pathway abnormal
thyroid functioning so generally in a
normal thyroid
or a normal patient healthy patient no
thyroid issues the hypothalamus releases
thyrotropin-releasing hormone trh which
acts on the anterior pituitary to
release TSH thyroid stimulating hormone
which then acts on the thyroid gland to
release t4 thyroxine and t3
triiodothyronine both of these hormones
can relay back so negative feedback
inhibition on the anterior pituitary
gland to reduce the level of TSH and
they can also feedback on the
hypothalamus to reduce the level of T
rage so in a normal functioning thyroid
we're going to get release of these
hormones in response to TSH and these
hormones are going to have a negative
feedback loop on both the anterior
pituitary and the hypothalamus to both
reduce levels of T RH and TSH that's the
normal thyroid functioning and t4 and t3
are so important because they're
responsible for the MS and the MS our
movement mentation and metabolism so we
need to metabolize we need metabolism to
survive we need to think we need
mentation and we need to move around so
these important ones are super important
so what happens in Hashimoto's well
Hashimoto's is essentially due to a
defective T cell suppressor I'm not
going to get into all the details here
but essentially you want are your body
to suppress T cells that can target its
own cells right and what happens is
there's a signaling cascade that leads
to cell needed destruction of thyroid
follicles and T cells can lead to the
activation of B cells which can lead to
the production of antibodies against a
variety of components within the thyroid
gland like thyroglobulin thyroid
peroxidase TSH receptor and the sodium
iodine in symporter so essentially
because of all these antibodies in the
cell media destruction and attack on the
thyroid gland Hashimoto's essentially
member hacks up the thyroid gland we're
gonna lose the thyroid Lane we're not
going to be able to produce t4 t3 these
hormones are going to decrease in
concentration they're going to decrease
in levels and because
we lose T4 and T3 we're gonna lose the
negative feedback regulation on the
anterior pituitary and the hypothalamus
leading to increased TSH and increased
trh and because the body sees that you
know we know why why is the thyroid
gland not in doing what it's supposed to
do it's gonna try to actually pump out
even more hormone to get it to function
so that's why we're gonna see all of
these responses to the attack on the
thyroid gland again low t4 and t3 a high
TSH and a high th Hashimoto's
essentially presents with signs and
symptoms of hypothyroidism and the
thyroid gland as mentioned for produces
t4 and t3 which are responsible for ment
a shin movement and metabolism so all of
these are going to be reduced in
function so if we were to take a broad
look at a patient with signs and
symptoms of hypothyroidism they're gonna
have hair loss you're gonna have coarse
and dry hair they're gonna have dry skin
and they're gonna have Perry or little
puffiness they're also gonna have
decreased what we call mentation right
so we're gonna have decreased mood
they're gonna be depressed they're gonna
be fatigued they're also gonna have
because they have reduced metabolism
they're gonna have a weight gain they're
gonna have intolerance to cold they're
gonna feel cold hypothermia they're also
gonna have muscle cramping they're gonna
have power they're gonna have great a
cardio so reduced heart rate and they're
gonna have delayed reflex relaxation so
the delayed deep tendon reflexes in
other sinus symptoms of hypothyroidism
include constipation so the GI system is
basically slowed down so we're gonna
there be they're gonna become
constipated they're gonna have immense
menstrual abnormalities and they're also
gonna have khalaqtu Rhea because of the
th increasing levels of product and we
didn't talk about that but that's just
an important thing to recognize now how
do we make the diagnosis and how do we
treat Hashimoto's well we basically
since we got a good understanding of the
pathophysiology of Hashimoto's and
normal thyroid functioning it's pretty
easy to diagnose this
in fact we've already talked about it
before if we see a high TSH and a low t4
we can say the patient has
hypothyroidism and if you're thinking
well maybe is it Hashim Odo's or maybe
some other cause well we can dig in a
little bit deeper to measure some of
those antibodies we talked about before
one of them that is typically assessed
is the anti-thyroid peroxidase and this
will be elevated in Hashimoto's and you
can also look for thyroglobulin
antibodies so again the diagnosis is
going to be with a high TSH and a low t4
that's essentially hypothyroidism and
then if you're thinking it's an
autoimmune condition its Hashimoto's you
want to order in anti-thyroid peroxidase
so how do we treat it well basically
it's pretty simple to treat this really
we want to replace what they've lost and
we replace that with el thyroxine or
synthroid to essentially treat their
hypothyroidism they don't have enough
thyroid hormones they don't have enough
t4 t3 we got to give it back to them so
that is how we treat it so if you want
to learn more about thyroid conditions
like Graves disease please check out my
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you so much for watching and I hope to
see you next time
