Graves Disease - Overview (causes, pathophysiology, investigations and treatment)

hello in this video we're going to talk about Graves disease this is an overview and introduction Graves disease is the most common cause of hyperthyroidism which is essentially the thyroid gland working on overdrive producing a lot of thyroid hormones and Graves disease is a syndrome that may consist of hyperthyroidism gorta optimal path II and occasionally droppeth II which is a skin disease associated with the overactive thyroid gland in order to understand Graves disease it is important to learn or recap the anatomy and physiology of the thyroid gland and it's hormones as well as the hypothalamic pituitary thyroid axis so here is the brain important structures to note in the brain is the hypothalamus and below the hypothalamus is the pituitary gland which actually consists of two lobes the anterior and posterior lobes but here we will mainly focus on the anterior lobe here I'm drawing the circulation which is the blood and the most important organ in the story is a thyroid gland the thyroid gland sits on the trachea the tracheal rings right below the larynx and here again is a circulation the blood so the hypothalamus in the brain secretes thyroid releasing hormone or T or H which will stimulate the anterior pituitary to secrete thyroid stimulating hormone or TSH for short TSH will travel in circulation and target the thyroid gland the thyroid gland has receptors for TSH the binding of TSH to the TSH receptor on the thyroid gland will stimulate the thyroid gland to produce and secrete thyroid hormones and it will secrete thyroid hormones into circulation hormones are t3 and t4 t3 and t4 are carried in circulation in the blood via proteins thyroid binding protein an increase in t3 and t4 in circulation will have a negative feedback on the hypothalamus on the brain and the negative feedback will tell the hypothalamus to stop producing T RH and thus TSH to reduce the thyroid hormone production when we already have enough in circulation so what does t3 and t4 do well t3 and t4 are lipid soluble and so when they're at the target cell or target organ they simply detach from the thyroid binding protein and move inside the cell t4 will get converted to t3 because t3 is the more potent one you can say it's the more effective one and so t3 is actually also known as triad o'the irony but let's just call it t3 t3 will bind onto thyroid hormone receptors within the nucleus where it will stimulate transcription or it will tell the DNA to make things that will result in production of proteins enzymes all these things that will cause an increase in metabolic rate metabolic activity as well as increase sympathetic activity and growth and development Graves disease is where there is elevation of the thyroid hormones t3 and t4 an increase in t3 and t4 in circulation and the effects of these is called hyperthyroidism a Graves disease is not the only cause of hyperthyroidism there are other causes of hyperthyroidism which include pituitary adenomas which can cause more thyroid stimulating hormone TSH being produced by the anterior pituitary gland more TSH means more stimulation to the thyroid gland to secrete t3 and t4 thurid medication is also another cause meaning fired hormone analogues can of course cause hyperthyroidism iodine and amiodarone can cause or induce hyperthyroidism thyroid adenoma specifically toxic thyroid adenoma can cause more thyroid hormones being produced which then will cause hyperthyroidism similarly toxic multinodular goiter can cause hyperthyroidism it's really important to understand that the use of the word toxic really means that it's cause more things are being produced it's and thus it's more toxic so toxic in this case means more overproduction of thyroid hormones have the physiology of Graves disease again here is the brain here we have the hypothalamus and the anterior pituitary gland here is a thyroid gland and the circulation on the thyroid gland we have the receptor the TSH receptor in Graves disease there are auto antibodies being produced what I mean by OTO antibody are antibodies against our self the main auto antibodies are the antibodies which basically mimic thyroid stimulating hormone so these antibodies will target thyroid stimulating hormone receptors the binding of the thyroid stimulating hormone receptors by these Auto antibodies will actually stimulate the thyroid gland to produce more thyroid hormones t3 and t4 the increase in t3 and t4 of course will cause a negative feedback to the hypothalamus to tell it to stop making trh and TSH because we already have enough t3 and t4 but regardless of the decrease in TSH the thyroid stimulating hormone receptor Oh two antibodies will still exist and so we'll keep telling the thyroid gland to produce more thyroid hormones this means that there are a lot of thyroid hormones in circulation and so there's over activity of the thyroid hormones causing hyperthyroidism in Graves disease the main antibodies are the thyroid stimulating hormone receptor or two antibodies however there are other antibodies such as thyroglobulin or Auto antibodies and thyroid peroxidase antibodies or TPO antibodies but these are less common in Graves disease on a sidenote thyroid peroxidase antibodies are more often seen in hypothyroidism particularly Hashimoto's disease the next question to ask is where do these antibodies come from well like most autoimmune diseases there is no exact pinpoint cause rather it is postulated that many factors cause inappropriate or abnormal activation of immune cells against the thyroid gland within the lymph nodes cells called antigen presenting cells normally activate naive t-cells in situations where there is an infection or when the body is in trouble the antigen presenting cell in this scenario may present thyroid stimulating hormone receptor like antigen and this will activate the naive T cell within the lymph node the activated t cell can then activate B cells the T cells will tell the B cells to become another cell called a plasma cell and it becomes a plasma cell so that it can produce antibodies against the antigen plasma cells are the cells that secrete and produce antibodies and so in this scenario thyroid stimulating hormone receptor Auto antibodies are produced but instead of damaging the thyroid stimulating hormone receptor it actually stimulates it and acts similar to a thyroid stimulating hormone the thyroid stimulating hormone receptor Auto antibody produced are not very specific meaning that they most often bind to thyroid stimulating hormone but there are third stimulating hormone like receptors all around our body particularly the eyes and the legs and so the thyroid stimulating hormone receptor OTO antibodies can cross react with other parts of the body such as it can cross react with things in the eyes leading to up the mapa the-- or cross-react with skin causing demography pathology of Graves disease after some time there are some notable changes seen in the thyroid gland of patients with Graves disease so normally the thyroid gland are made up of follicular cells which form the inner colloid where thyroid hormones are produced in Graves disease the follicular cells become packed and squeezed together becoming tall cells this then subsequently causes a scant colloid further in Graves disease there are presence of lymphocytes so there's a lymphocytic infiltration the risk factors for Graves disease include female gender family history infection leading to thyroiditis which is inflammation of the thyroid gland stress is also risk factor as well as smoking and amiodarone now remember that Graves disease is hyperthyroidism and is characterized by increase in metabolic rate and increase in sympathetic activity and so now let us look at the signs and symptoms of Graves disease the clinical presentation can include hyperactivity irritability insomnia sweating heat intolerance fatigue weakness graves ophthalmopathy feeling thirsty dis near palpitation weightloss Allah Gherman area amenorrhea decreased libido and symptoms of Graves de mapa thei clinical examination or clinical findings can include patient being anxious and irritable presence of goiter abdullah petha hair loss presence of congestive heart failure tachycardia or atrial fibrillation patient might have a fine tremor that can be increased in bowel sounds that can be uncle Isis essentially clubbing hyperreflexia and also presence of Graves droppeth II the investigations with someone with suspected Graves disease again just recapping here's the brain the hypothalamus and the anterior pituitary gland which produces thyroid stimulating hormone or TSH the thyroid gland has the thyroid stimulating hormone receptor in Graves disease there are presence of antibodies Auto antibodies so an investigation is to check serum thyroid stimulating hormone which will show a decrease Bloods may also show presence of thyroid stimulating hormone receptor Auto antibodies another investigation is a thyroid ultrasound which can look at the thyroid architecture and structure to see any signs of other causes of hyperthyroidism such as toxic thyroid adenoma or toxic multinodular goiter the most important investigation is to check Thurid function which will show an increase in t3 and t4 levels a fire it's can such as sinter scanning is an investigation where iodine dye is injected into the bloodstream in a normal thyroid iodine is taken up by the thyroid gland and so we can see distribution of iodine uptake in the thyroid because the iodine is tagged however in Graves disease there is a big increase in iodine uptake by the thyroid gland because the thyroid gland is working on overdrive it is producing a lot of hormones management the management of Graves disease can be divided into pharmacological radio iodine therapy and surgery pharmacological or pharmaceutical therapy include the use of anti-thyroid drugs such as Co mind the mechanism of action of theö MI it basically inhibits the enzyme thyroid peroxidase which normally helps in the synthesis of t3 and t4 and so inhibiting thyroid peroxidase or TPO will decrease t3 and t4 fired hormone levels ena blockers is also another form of pharmacological management and the mechanism of action is to decrease the sympathetic activity by blocking the beta adrenergic receptors beta blockers are given because we see signs of heightened sympathetic activity in Graves disease just tachycardia radioiodine therapy is the second management for Graves disease and it is used for people who don't want to take medication or want something alternative then surgery or medication essentially in radioiodine therapy a radioactive iodine is taken either via liquid or pill the iodine taken is radioactive and so naturally decays to xenon when it decays it emits energy which theoretically destroys the surrounding thyroid tissue thus the destroyed thyroid tissue will decrease thyroid hormone production surgery is a third type of management for Graves disease and for people who do not want radioiodine therapy and where medication is not useful or is ineffective the surgery is thyroidectomy which is removal of the thyroid gland and this can be partial or total thyroidectomy complications of Graves disease include congestive heart failure atrial fibrillation decrease in bone density leading to osteoporosis graves ophthalmopathy complications include blurry vision and Graves droppeth II the complication of this in severe cases is elephantitis ramappa thee finally it is important to know the complications associated with thyroidectomy such as a laceration to the laryngeal nerves internal bleeding infection post-surgery and accidentally removing the parathyroid gland which actually sits on the thyroid gland you

Channel: Armando Hasudungan

Views: 490,575

Keywords: graves disease, hyperthyroidism, graves', graves opthalmopathy, graves disease pathophysiology, pathogenesis, mechanism of disease, pathology, thyroid disease, thyroid disorder, overactive thyroid, TSH, Thyroid stimulating hormone antibody, treatement, management, graves dermatopathy, anatomy and physiology of the thyroid gland, investigation, medicine, animation, summary, lecture, signs and symptoms of graves disease, clinical presentation, manifestation, hyper and hypothyroidism

Id: I2L1NXhZOEE

Length: 17min 9sec (1029 seconds)

Published: Fri Nov 11 2016