Hyperthyroidism resident survival guide
Hyperthyroidism and thyroid storm are disease states that result from thyroid hormone-induced hypermetabolism. The excess thyroid hormone is released from the thyroid gland as a result of excess thyroid hormone production, or by processes that disrupt the follicular structure of the gland with subsequent release of stored hormone . Most patients with severe hyperthyroidism present with a dramatic symptom constellation. Hyperthyroidism's typical symptoms include palpitations,heat intolerance, increased bowel movement frequency tremor, anxiety, weight loss despite normal or increased appetite and shortness of breath.Goiter is commonly found on physical examination.
Specific organ systems
|Cardiovascular||Heart rate is increased,Systolic hypertension ,pulse pressure is widened, congestive heart failure, Atrial fibrillation|
|Neuropsychiatric||Anxiety, tremor, restlessness, irritability,insomnia,psychosis, agitation,depression, seizures|
|Respiratory||Dyspnea, tracheal obstruction, exacerbate underlying asthma,Pulmonary arterial systolic pressure is increased|
|Gastrointestinal||Weight loss,hyperphagia,hyperdefecation and malabsorption|
|Skin||Sweating,Onycholysis,Hyperpigmentation,Thinning of the hair|
|Eyes||Stare and lid lag, ophthalmopathy.|
|Genitourinary||Urinary frequency and nocturia|
|Hematologic||Normochromic, normocytic anemia|
|Bone||Osteoporosis and an increased fracture risk|
Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
- Drug-induced thyroiditis: Overproduction of thyroid hormones (amiodarone-induced thyrotoxicosis type 1) or release of preformed thyroid hormones (amiodarone-induced thyrotoxicosis type 2, interferon alfa, interleukin-2, or lithium)
- Factitious thyrotoxicosis: Surreptitious ingestion of thyroid hormones
- Hyperemesis gravidarum ; High level of β-hCG stimulates TSH receptors
- Graves’ disease:Autoimmune process in which antibodies stimulate the TSH receptor leading to overproduction of thyroid hormones
- Painless or transient (silent) thyroiditis: Autoimmune destruction of thyroid tissue leading to a release of preformed thyroid hormones
- Postpartum thyroiditis: Variant of painless thyroiditis with the same mechanism, occurring after delivery
- Struma ovarii: Ectopic thyroid tissue in ovarian dermoid tumor produces thyroid hormones
- Subacute granulomatous (de Quervain) thyroiditis: Painful inflammation of the thyroid gland caused by viral infection, often with fever, triggering a release of preformed thyroid hormones
- TSH-secreting pituitary adenoma: Tumor secreting large quantities of TSH, and not responding to thyroxine and triiodothyronine feedback
- Toxic adenoma (Plummer disease): Somatic mutation in TSH receptor or Gs alpha gene in a thyroid nodule
- Toxic multinodular goiter:Expansion of clonogenic cells with an activating TSH receptor mutation 
Serum TSH measurement has the highest sensitivity and specificity of any single blood test used in the evaluation of suspected thyrotoxicosis and should be used as an ini-tial screening test . However, when thyrotoxicosis is strongly suspected, diagnostic accuracy improves when aserum TSH, free T4, and total T3 are assessed at the initial evaluation. Serum TSH levels are considerably more sensitive than direct thyroid hormone measurements for assessing thyroid hormone excess. In overt hyperthyroidism, serum free T4,T3,or both are elevated, and serum TSH is subnormal (usually<0.01mU/L ina third-generation assay). In mild hyperthyroidism, serum T4 and free T4 can be normal, only serum T3 may be elevated, and serum TSH will be low or undetectable. The diagnosis of a thyrotoxic crisis is made entirely on the clinical findings. Most importantly, there is no difference in thyroid hormone levels between patients with "uncomplicated" thyrotoxicosis and those undergoing a thyroid storm.
|Check TSH level|
|High TSH||Low TSH|
|High Free T4||High Free T4||Normal Free T4|
|Secondary hyperthyroidism||Primary hyperthyroidism||Subclinical hyperthyroidism|
Thyroid storm may lead to irreversible cardiovascular collapse and death if proper treatment is not initiated in the Emergency Department. For patients with clinical features of thyroid storm,we start immediate treatment with a beta blocker And then either 200 mg of propylthiouracil (PTU) every four hours or methimazole (orally 20 mg every four to six hours). PTU is preferred over methimazole due to the effect of PTU to decrease the conversion from T4 to T3. Iodine administration should be postponed for at least one hour after administration of thionamide to prevent the iodine from being used as a substrate for new hormone synthesis. We also administer glucocorticoids (hydrocortisone, 100 mg intravenously every eight hours) in patients with thyroid storm clinical features.Supporting therapy and the detection and treatment of any precipitating factors ( e.g. infection) in addition to specific thyroid therapy can be vital to the eventual outcome.The infection needs to be detected and treated, and the aggressive correction of hyperpyrexia is required. Acetaminophen should be used instead of aspirin, as the latter will increase concentrations of serum-free T4 and T3 by interfering with protein binding.
Once clinical improvement is shown, iodine therapy may be discontinued and glucocorticoids may be tapered and discontinued.Beta blockers can be stopped but only after the tests on thyroid function have returned to normal.To maintain the euthyroidism, the dosage of thionamides should be titrated. PTU should be changed to methimazole due to the improved safety profile of methimazole and higher compliance rates. Patients who fail medical therapy should be treated with therapeutic plasma exchange or thyroidectomy. The mortality of thyroid storm is currently reported at 10%.
|Drug||Initial daily dose||Mechanisim of action|
|Beta blocker||Propranolol 60 to 80 mg orally every four to six hours,||Control the symptoms and signs|
|Thionamide||PTU 200 mg every four hours or methimazole,20 mg orally every four to six hours||Block new hormone synthesis|
|Iodine||(Lugol's) solution, 10 drops (6.25 mg iodide/iodine per drop [0.05 mL]) three times daily||Block the release of thyroid hormone|
|Glucocorticoids||Hydrocortisone, 100 mg intravenously every eight hours||Reduce T4-to-T3 conversion, promote vasomotor stability, possibly reduce the autoimmune process in Graves' disease, and possibly treat an associated relative adrenal insufficiency|
|An iodinated radiocontrast agent||0.5 to 1 g once daily.||inhibit the peripheral conversion of T4 to T3|
|Bile acid sequestrants||Cholestyramine,4 g orally four times daily||Decrease enterohepatic recycling of thyroid hormones|
- Start immediate treatment with a beta blocker
- Acetaminophen should be used instead of aspirin
- Iodine administration should be postponed for at least one hour after administration of thionamide
- Propranolol, PTU, and methimazole can be administered through a nasogastric tube
- The content in this section is in bullet points.
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