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
endocrinology playlist and if you haven't already please consider liking
subscribing and clicking the notification Bell to stay up to date and
support the channel and as always thank you so much for watching and I hope to
see you next time