Hashimoto’s thyroiditis: What Is It, Who’s At Risk and What You NEED to Know

hey everyone this lesson is on Hashimoto’sthyroiditis so and this that’s where I’m talking about what are some of thecauses of Hashimoto’s thyroiditis who is at risk for getting this circumstance we’realso going to talk about how we can diagnose it and how we can treat it sohashing notice I read itis is a chronic autoimmune thyroiditis causing a primaryhypothyroidism due to a cellular and humoral interceded slaughter of thyroidtissue so key points to take it is an autoimmune condition that reasons primaryhypo thyroidism it is in fact the most common cause of hypothyroidism at leastin the developed world and like many other autoimmune problems femalesoutnumber males with its predicament generally the fraction is between 7 to 1 so7 females for every one male and it is such a common condition that it isestimated that up to 10 percent of the general population has this conditionand interestingly it actually increases with increasing age so the prevalence ofHashimoto’s actually increases with age so the older you get the more chancesyou could get Hashimoto’s so this is a significant milieu so how are wegoing to remember that Hashimoto’s induces hypothyroidism well I miss you tothink about the utterance Hashimoto’s spoofs up the thyroid gland Hashimoto’s hacksup the thyroid gland and pitcher and behaves and you’re virtually justchopping up a thyroid gland and if you have a chopped-up thyroid gland if it’shacked up well it’s not going to be functional it’s gonna be hypothyroid sothat’s how you can remember that Hashimoto’s stimulates hypothyroidismHashimoto’s hackers up the thyroid gland what are some of the risk factors ofHashimoto’s thyroiditis the risk factors include genetic circumstances so it’sinteresting that individuals with Down syndrome and Turner syndrome have anincreased prevalence of Hashimoto’s in general now there’s also associationswith the gene HLA dr3 because this is an autoimmune condition and interestinglyyeah if you actually seen a family member who has Graves infections which is a condition causing hyperthyroidism wellyou’re at more risk for actually having Hashimoto’s they’re both autoimmuneconditions so they generally run together other interesting risk factorsinclude having stress so increased stress seems to be associated with theonset of this plight again family history this descends in line with geneticconditions and genes gender as we mentioned before being female is a bigrisk factor in fact it’s seven to one compared to males a high iodineconsumption or high-pitched iodine diet can actually increase your risk for havingthis health so it’s been shown that having actually a bit of a lower iodineconsumption diet so a bit on the lower feature may actually abbreviate the risk ofhaving this necessity and there’s also question of well this website cigarettesmoking make this or does some kind of infection cause this is not quite knownso there are actually a couple subtypes I require “youre going to” to just know about theseare really not that important for this lesson but the subtypes for Hashimoto’sthyroiditis include a goiter as’ category so the person or persons generally has what wedescribe as a rubbery thyroid so they have you thyroid condition thatprogresses to a hypo thyroid position and it’s due to’ the fibrotic changesand the other condition is atrophic this leads to hypothyroidism and isassociated with the thyroid lymphoma so the two conditions because this is anautoimmune attack on the thyroid gland we’re either going to have a basicallyshrivel up by roid Glen like you might see in a trophic subtype or you’re gonnahave fibrotic mutates disfiguring which is gonna cause a rubbery goiter estai p–Hashimoto’s so these are the two conditions I demand you to think about sowhat actually stimulates Hashimoto’s thyroiditis what is the pathophysiologyso in order to understand what happens in hatch motor started itis it’simportant to know the general basic endocrine signaling pathway abnormalthyroid functioning so generally in a ordinary thyroidor a ordinary patient healthful patient no thyroid questions the hypothalamus releasesthyrotropin-releasing hormone trh which acts on the anterior pituitary torelease TSH thyroid inducing hormone which then is acting on the thyroid gland torelease t4 thyroxine and t3 triiodothyronine both of these hormonescan relay back so negative feedback limited on the anterior pituitarygland to reduce the level of TSH and they can also feedback on thehypothalamus to reduce high levels of T violence so in a ordinary functioning thyroidwe’re going to get secrete of these hormones in response to TSH and thesehormones are going to have a negative feedback loop on both the anteriorpituitary and the hypothalamus to both abbreviate levels of T RH and TSH that’s thenormal thyroid serving and t4 and t3 are so important because they’ reresponsible for the MS and the MS our movement mentation and metabolism so weneed 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 importantso what happens in Hashimoto’s well Hashimoto’s is essentially due to adefective T cell suppressor I’m not going to get into all the details herebut basically you require are your body to suppress T cells that can target itsown cells right and what happens is there’s a signaling cascade that leadsto cadre needed extermination of thyroid follicles and T cells can lead to theactivation of B cells which can lead to the production of antibodies against avariety of components within the thyroid gland like thyroglobulin thyroidperoxidase TSH receptor and the sodium iodine in symporter so essentiallybecause of all these antibodies in the cadre media slaughter and attack on thethyroid gland Hashimoto’s essentially member hackers up the thyroid gland we’regonna lose the thyroid Lane we’re not going to be able to produce t4 t3 thesehormones are going to decrease in concentration they’re going to decreasein stages and because we lose T4 and T3 we’ re gonna lose thenegative feedback regulation on the anterior pituitary and the hypothalamusleading to increased TSH and increased trh and because the body sees that youknow we know why why is the thyroid gland not in doing what it’s supposed todo it’s gonna try to actually pump out even more hormone to get wise to functionso that’s why we’re gonna see all of these responses to the attack on thethyroid gland again low t4 and t3 a high TSH and a high th Hashimoto’sessentially presents with clues and indications of hypothyroidism and thethyroid gland as mentioned for raises t4 and t3 which are responsible for menta shin movement and metabolism so all of these are going to be reduced infunction so if we were to take a broad look at a patient with signs andsymptoms of hypothyroidism they’re gonna have hair loss you’re gonna have coarseand baked “hairs-breadth” they’re gonna have dry surface and they’re gonna have Perry or littlepuffiness they’re also gonna have decreased what we call mentation rightso we’re gonna have decreased mood they’re gonna be chilled they’re gonnabe fatigued they’re also gonna have because they have reduced metabolismthey’re gonna have a weight gain they’re gonna have intolerance to cold they’regonna feel cold hypothermia they’re likewise gonna have muscle cramping they’re gonnahave capability they’re gonna have enormous a cardio so shortened heart rate and they’regonna have delayed reflex relaxation so the delayed late tendon reflexes inother sinus manifestations of hypothyroidism include constipation so the GI system isbasically slowed down so we’re gonna there be they’re gonna becomeconstipated they’re gonna have immense menstrual aberrations and they’re alsogonna have khalaqtu Rhea because of the th increasing levels of product and wedidn’t talk about that but that’s just an important thing to recognize now howdo we oblige the diagnosis and how do we treat Hashimoto’s well we basicallysince we got a good understanding of the pathophysiology of Hashimoto’s andnormal thyroid operating it’s pretty easy to diagnose thisin fact we’ve already talked about it before if we check a high TSH and a low-spirited t4we can say the patient has hypothyroidism and if you’re thinkingwell maybe is it Hashim Odo’s or maybe some other cause well we can dig in alittle bit deeper to measure some of those antibodies we spoke beforeone of them that is typically analyse is the anti-thyroid peroxidase and thiswill be elevated in Hashimoto’s and you can also look for thyroglobulinantibodies so again the diagnosis is going to be with a high TSH and a low-spirited t4that’ s essentially hypothyroidism and then if you’re thinking it’s anautoimmune condition its Hashimoto’s you want to order in anti-thyroid peroxidaseso how do we treat it well basically it’s pretty simple to treat this reallywe want to replace what they’ve lost and we replace that with el thyroxine orsynthroid to essentially discuss their hypothyroidism they don’t have enoughthyroid hormones they don’t have enough t4 t3 we got to give it back to them sothat is how we treat it so if you want to learn more about thyroid conditionslike Graves disease please check out my endocrinology playlist and if youhaven’t already satisfy consider liking subscribing and clicking thenotification Bell to stay up to date and support the channel and as always thankyou so much for watching and I hope to see you next time