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The thyroid secretory organ varies in size from individual to individual but it has an highly high blood supply along with a assortment of cardinal maps within the organic structure ( Martini – 2006 ) . The maps of the thyroid secretory organ are carried out through procedures affecting the endocrines T3 and T4 that it synthesises ( Marshall – 1995 ) . Cardinal maps include control of ATP production and glycolysis hence commanding radical metabolic rate. Diseases that affect the thyroid may merely impact one secretory organ but can evidently bring forth systemic symptoms/ complications. An illustration of this can be seen in Graves disease.

Graves disease is an autoimmune disease with a female to male prevalence of 7:1 ( Benjamini – 2000 ) where the organic structures own immune system produces antibodies against the thyroid exciting endocrine receptor ( TSHr ) . This consequences in the antibodies adhering to the TSHr but alternatively of demobilizing the receptor, the binding produces effects similar to that of TSH binding ( Benjamini – 2000 ) .

Discussed in this paper shall be the mechanism of this disease, symptoms, diagnosing and intervention of Graves disease.

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Mechanism of the Disease

In order for a patient to hold Graves disease, their organic structure must foremost be synthesizing the auto-antibodies which act against the TSHr. There are different influences which may do this to happen. Generally it is believed that infiltration of the thyroid by lymph cells causes the self-generated production of the auto-antibodies ( Weetman – 1994 ) . However a familial constituent to the disease has besides been identified. Reveille ( 2006 ) found that familial mutants of the HLA-DRB1*0301, DQA1*0501, DQB1*0201 part gave rise to increased incidence of the production of the specific auto-antibodies against the TSHr. The produced antibodies have the ability to adhere to the TSHr, making so produces stimulatory signals to the thyroid secretory organ in the same manner that TSH itself does. This procedure is illustrated in image 1 below.

Due to the antibody adhering holding a stimulatory consequence, the overall consequence is the production of the endocrines T3 and T4 from the thyroid secretory organ. Problems begin from two attacks, these endocrines are being produced without simulation from TSH and the half life of the antibody is longer than that of TSH ( Roitt – 2001 ) significance that the simulation is happening over a longer period of clip than that of TSH stimulation. These two procedures together result in overly high degrees of thyroid endocrine within the patients blood supply. The high degree of these endocrines consequences in systemic effects every bit good as localized effects in some parts. By and large the thyroid hormones act on cell receptors signalling them to increase ATP production and glycolysis. This consequences in high energy production and high alimentary use every bit good as extra bodily heat produced.

Other jobs associated with Graves disease include Graves ophthalmopathy. Graves ophthalmopathy is a status caused by Graves disease where by redness of the oculus occurs ( Khoo – 2007 ) . It is thought that this occurs due to look of the TSHr on the cell membranes of the cells of the oculus. As a consequence of this, the auto-antibodies besides bind to these receptors which stimulates local adipogenesis. Due to the increased adipose volume within the tissues and the enlisting and activation of T-cells, inflammatory cytokines are released by the T-cells bring forthing the redness of the tissue ( Khoo – 2007 ) . This produces redness of the oculus perchance doing it to pouch from the socket and or compact the ocular nervus impacting signal transmittal ( Khoo – 2007 ) .


Due to Sculpt disease bring forthing over stimulation of the thyroid, typical patient presentations are by and large the same as that of thyrotoxicosis. The list of symptoms is rather extended but the most outstanding symptoms include weight loss, increased appetite, weariness and increased organic structure heat production, rapid bosom beats at remainder, extra perspiration and general muscular failing. These are all due to the greatly increased metamorphosis from the complete activation of the thyroid. Dependent upon the phase of the disease, most patients will besides show with a perceptibly enlarged thyroid know as a goiter. Due to the associated Graves ophthalmopathy, symptoms related to this may include bulging of the oculus from the socket and inability to to the full shut the oculus palpebras. In more advanced instances, marked diminution in oculus sight public presentation may be seen due to compaction of the ocular nervus due to the redness ( Khoo – 2007 ) .


Initially an rating of the patients clinical presentation will supply sufficient grounds to propose some sort of thyrotoxicosis. This can be chiefly confirmed by mensurating the serum concentration of free T3 and T4. Highly raised degrees will corroborate a signifier of thyrotoxicosis. Another simple trial to transport out would be the serum degree of TSH which in the presence of high degrees of T3 and T4 should be low due to the negative feedback ( Roitt – 2001 ) . Ultimately the best diagnostic method would be to prove the patient serum for the auto-antibodies against the TSHr. This can be done utilizing an ELISA check. Second, an iodine uptake trial can be done ( Roitt – 2001 ) where by radioactive I is injected into the patients blood watercourse. Time is allowed for the tyroid to uptake the I so the thyroid is visualised for radiation, in Gravess disease the thyroid will demo a diffuse even radiation across the whole of the secretory organ, other conditions may demo more focal concentrations of I ( Roitt – 2001 ) .

Making these trials would give an un-doubtable diagnosing of Graves disease caused by auto-antibodies.


The intervention of Graves disease is the same as that of thyrotoxicosis and usage of each will from patient to patient.

Antithyroid drugs such as methimazole or propylthiouracil work by suppressing the exzyme thyroperoxidase which usually catalyses the add-on of the I groups to the base constituents of T3 and T4 ( Nakamura – 2007 ) . Suppressing the enzyme lowers the sum of endocrine released by the thyroid despite still being stimulated by the antibodies ( Nakamura – 2007 ) . Common side effects include

O roseolas

O febrility

O articulation hurting.

Rare but still noted side affects include:

O Decreased white blood cell count giving possible susceptibleness to infection.

O Thrombocytopenia giving possible susceptibleness to shed blooding

O Liver harm

A radioactive isotope of I may besides be used as intervention. Due to the thyroid necessitating I for its production of T3 and T4, the thyroid will uptake the radioactive isotope and due to its radiation, the endocrine synthesizing cells will be destroyed. This will once more take down the sum of endocrine secreted by the thyroid due to reduced production.

Possible side effects include

O Swollen thoat

O Mild sickness

O In some instances inflamed salivary secretory organs.

Most patients treated by this method will develop hypothyroidism as a consequence of over devastation of the thyroid. This is easy remedied by administrating exogenic thyroid endocrine.

A concluding intervention that may be used if the thyrotoxicosis is peculiarly unmanageable by the old two intervention methods is surgery. Removal of part/the whole of the thyroid secretory organ will evidently halt production of thyroid endocrine ( Miccoli – 1996 ) but will necessarily make a province of hypothyroidism that will once more necessitate to be treated by exogenic thyroid endocrine.


Overall it can be said that Graves disease is an autoimmune disease that produces comparatively manageable symptoms and is the patient is diagnosed early, intervention is normally straightforward with by and large a really good forecast.


Benjamini – 2000 — Immunology: A Short Course, Fourth edition, By Eli Benjamini, Richard Coico and Geoffrey Sunshine, Published by Wiley Liss, 2000

Breedlove – 2008 — Image 1: Interaction of Anti-TSHr Antibodies with the TSHr, By Mellisa Breedlove, Davidson College, 2008, Content accessed via hypertext transfer protocol: // mmunology/Students/Spring2003/Breedlove/GravesDisease.html, Last accessed 8th December 2009

Coleman – 1992 — Fundamental Immunology, Second edition, By Robert Coleman, Mary Lombard and Raymond Sicard, Published by WCB Publishers, 1992

Khoo – 2007 — Pathogenesis of Graves ‘ Ophthalmopathy: The Role of Autoantibodies, By Teck Kim Khoo and Rebecca S. Bahn, Thyroid, October 2007, 17 ( 10 ) : Pages 1013-1018

Marshall – 1995 — Clinical Biochemistry: Metabolic and Clinical Aspects, By William Marshall and Stephen Bangert, Published by Pearson Professional Limited, 1995

Martini – 2006 — Fundamentalss of Anatomy and Physiology, By Fredrick H Martini, Seventh edition, Published by Daryl Fox, 2006

Miccoli – 1996 — Surgical intervention of Graves ‘ disease: Subtotal or entire thyroidectomy, By Paolo Miccoli, Paolo Vitti, Teresa Rago, Pietro Iacconi, Luigi Bartalena, Fausto Bogazzi, Emilio Fiore, Rocco Valeriano,

Luca Chiovato, Roberto Rocchi, and Aldo Pinchera, Journal of Surgery, 1996, Volume 120, Number 6

Nakamura – 2007 — Comparison of Methimazole and Propylthiouracil in Patients with Hyperthyroidism Caused by Graves ‘ Disease, By Hirotoshi Nakamura, Jaeduk Yoshimura Noh, Koichi Itoh, Shuji Fukata, Akira Miyauchi, Journal of Clinical Endocrinology, Jun 2007 ; 92: 2157 – 2162.

Reveille – 2006 — The familial footing of autoantibody production, By John D. Reveille, Autoimmunity Reviews 5, 2006, Pages 389–398

Roitt – 2001 — Essential Immunology, By Ivan Roitt and Peter Delves, Tenth edition, Published by Blackwell Science Ltd, 2001

Weetman – 1994 — Extrathyroidal sites of autoantibody synthesis in Graves ‘ disease, By A. P. Weetman, A. M. McGregor, M. H. Wheeler and R. Hall, Clinical Experimental Immunology, 1994, Volume 56, Pages 330-336

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