Hashimoto’sthyroiditis so and 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 hashing notice I read itis is chronic autoimmune thyroiditis causing primary hypothyroidism due to cellular and humoral mediated destruction of thyroid tissue so key points to take it is an autoimmune condition that causes primary hypothyroidism.
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 so7 females for everyone 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 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 its 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 each if you actually saw 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 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 the question of well this site cigarette smoking cause this or does some kind of infection cause this is not quite known there are actually a couple of subtypes I want you to just know about these are really not that important for this lesson but the subtypes for Hashimoto’sthyroiditis 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 hypothyroid 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 estate p–Hashimoto’s so these are the two conditions I want you to think about what actually causes Hashimoto’s thyroiditis.
What is the pathophysiology in order to understand what happens in hatch motor started it is important to know the general basic endocrine signaling pathway abnormal thyroid functioning so generally in a normal thyroid or a normal patient healthy patient with 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 were going to get the 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 needmentation 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 iodide 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 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.
That’s why we’re gonna read all of these responses to the attack on the thyroid gland again low t4 and t3 a high TSH and a high th Hashimoto’sessentially presents with signs and symptoms of hypothyroidism and the thyroid gland as mentioned for produces t4 and t3 which are responsible for mental 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 metabolismthey’re gonna have a weight gain they’re gonna have an intolerance to cold they’re gonna feel cold hypothermia they’re also gonna have muscle cramping.
They’re gonna have the power they’re gonna have great cardio so reduced heart rate and they’re gonna have delayed reflex relaxation so the delayed deep tendon reflexes another 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 khalat, Rhea, because of the 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 fact we’ve already talked about it before if we see a high TSH and a low t4we 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.