hyperthyroidism

• hyperthyroidism is an elavated thyroid hormone levels(t3 and t4) and increased circulation of these hormones.
• thyroid hormones are important in fetal development and metabolism
• thyrotoxicosis refers to a clinical syndrome caused by an excess circulation of thyroid hormones(t3 and t4) irrespective of the source
• thyroid releasing hormone(TRH) from hypothalamus stimulates the synthesis and secretion of thyroid stimulating hormone(TSH) in pituitary gland
• TSH act on thyroid gland to stimulate synthesis and secretions of hormones in the thyroid by binding on the TSH receptors
• hormones in thyroid gland are triiodothyronine(t3) and thyroxine(t4)
• t3 and t4 control the secretion of TRH and TSH by negative feedback
• too much t3 and t4 will decrease levels of TRH and TSH
• parafollicular cells produce calcitonin hormone that has important role in calcium homeostasis
• when TSH binds on TSH-receptors in thyroid gland, this stimulates thyroglobulin production and stimulates opening of sodium iodide channels.
• when sodium iodide channels opens, this allow circulating iodide to enter follicular cell and become oxidized into iodine
• iodine and thyroglobulin will produce t3 and t4. then t3 and t4 will go back to circulation to increase metabolism
• causes of hyperthyroidism with normal to high radioiodine intake include: 1)Autoimmune disorder-Graves' disease where there is antibodies against TSH-receptor. 2)toxic adenoma & multinodular goiter. 3) high iodine in the bloodstream. 4)early stages of pregnancy, where HCG react with tsh receptor. 5)Pituitary adenoma,where it autonomously secrete lots of TSH levels.
• causes of hyperthyroidism where there is near absent iodine uptake include: 1)levothyroxine overdose. 2)hamburger thyrotoxicosis-eating cows' thyroid gland. 3)thyroiditis.
• thyroiditis can be caused by radiation, medication, lithium, infection and autoimmune
• Primary hyperthyroidism is associated with thyroid problems and secondary hyperthyroidism is associated with brain problems(hypothalamus and pituitary gland problems)
• primary causes of hyperthyroidism(hyperfunctioning thyroid causes) include: 1)Graves disease. 2)toxic adenoma. 3)toxic multinodular goiter. 4)Jod-basedow phenomenon-overactivation of the thyroid gland
• graves disease caused by mutation HLA-DR3 and HLA-B8
• exophthalmos(bulging eyes) is one of the signs of Graves disease
• toxic adenoma and toxic multinodular goiter increases TSH-resceptor sensitivity
• jod-basedow phenomenon is when a patient with graves disease,toxic adenoma etc.. has excess iodine
• primary causes(hyperfunction of the thyroid) lead to permanent thyrotoxicosis
• primary causes(thyroid dysfunction) lead to transient thyrotoxicosis
• primary causes(thyroid dysfunction) of hyperthyroidism include: 1)Hashimoto. 2)postpartum pregnancy. 3)Dequervains' thyroiditis
• hashimoto causes antibodies production angainst TSH-receptor. anti-TPO and anti-TG. eventually this will lead in to chronic hypothyroidism
• dequervain' thyroiditis is caused by viral upper respiratory tract infection. and this is very painful thyroid with increased ESR
• secondary causes of hyperthyroidism is pituitary microadenoma
• clinical findings of hyperthyroidism include: 1)enlargement of thyroid gland-goiter. 2)metabolic dysfunction. 3)neurological dysfunction. 4)cardiovascular dysfunction. 5)reproductive dysfunction. 6)gastrointestinal dysfunction. 7)integumentary dysfunction-skin. 8)thyroid storm.
• when a patient has tachycardia,hyperthermia,agitated delirium and sign of heart failure(pulmonary edema) think about thyroid storm
• Graves' hyperthyroidism treatment include: 1)Carbimazole, oral,20-40mg daily. duration is 12-18 months. 2)beta blocker atenolol, oral, 50mg daily. give atenolol for 2-6weeks with carbimazole until t4 normalize. 3)radioactive iodine is administered incase of failed medical therapy and incase of coexisting heart failure
• surgery in graves hyperthyroidism is considered incase of: 1)large thyroid that is causing obstructive symtoms. 2)failure of medicine therapy. 3)allergic to anti-thyroid therapy. 4)2nd trimester pregnant women
• carbimazole has risk of neutropenia or agranulocytosis
• medicine treatment for toxic multinodular goiter is radio-active iodine. incase of coexisting HF, medical therapy(carbimazole) is indicated until euthyroidism then after do raio-active iodine
• in toxic multinodular goiter,surgery is restricted in patients with obstructive symptoms
• obstructive symtoms if hyperthyroidism include: difficulty swallowing, snoring, cough, difficulty breathing and hoarseness
• single toxic nodule treatment: 1)small nodules treat with radio-active iodine, large nodules require surgery. 2)for sympathetic symptoms like palpitations=give beta-blocker,atenolol,oral,50mg daily for 2-4 weeks.
• thyrioditis is a toxic phase of hyperthyroidism that lasts up to 3 months
• thyroiditis treatment include: 1)beta-blocker,atenolol,oral,50mg daily(can adjust dose according to how the patient respond,max dose is 100mg).
• for painful subacute thyroiditis(De Quevain's) treatment include: 1)NSAID,Ibuprofen,oral, 400mg, 8hourly with meals. 2)Give corticosteroids-intermediate acting,Prednisone,oral,40mg daily
• Thyroid crisis treatment include: 1)IV fluid. 2)Carbimazole, oral,40-60mg,6hourly until crisis problem is controlled. 3)after 30min of first dose of carbimazole give Lugol's iodine, oral,put 10 drops of it in milk,8hourly. 4)Give beta-blocker,atenolol,oral,50mg. 5)for life-threatning case Add Hydrocortisone,IV,100mg,8hourly.