Thyroid Malfunction

what precipitates myxedema coma? what is the disease course?

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what are the skin and finger findings of Graves' disease?

dermopathy clubbed fingertips - deposition seen on X-ray clubbed fingertips in lung disease do not have deposition - plain X-ray

causes of 2o and 3o hypothyroidism

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how is subclinical hyperthyroidism diagnosed (what has to happen on 2 occasions)?

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how is subclinical hypothyroidism diagnosed and treated?

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what 2 kinds of thyroid nodules can be found?

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what are some symptoms of hy*PER*thryoidism? weight ______; _________appetite _____ intolerance ______(heart _______) _____bowel movements _____hair _____cardia _____skin _____(anxiety or lethargy) hand______

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what are the classifications of hyperthyroidism based on process?

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what are the symptoms and physical exam findings of hy*po*thyroidism? _____cardia weight______; _____appetite _____skin ____hair hy___reflexia (lethargy or anxiety) (constipation or diarrhea) _______intolerance _________ edema ___________ on tongue

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what causes hypothyroidism in pregnancy? what will the effects if untreated?

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when does subacute thyroiditis occur? is the thyroid tender or non-tender?

(rarely - 15% of cases) may progress to hyPOthyroidism, pretty much does NOT

what is consumptive hyPOthyroidism?

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*what are the T3/T4 and TSH levels in:* secondary hy*per*thyroidism primary hy*per*thyroidism

*High target gland hormone* + *low trophic* hormone level = autonomous secretion of target hormone Primary hy*PER*thyroidism: ex - graves's *High target gland hormone* + *high trophic* hormone level = autonomous secretion of trophic hormone or trophic gland resistance Secondary hyPERthyroidism: ex - TSH adenoma

what is Hashimoto's thyroiditis? what is the infiltrate? what are the associated antibodies? what is the effect on TPO?

*TPO works less*, less production of thyroid hormone anti-TPO and anti-thyroglobulins heterogeneous gland or gland w/ decreased overall echogenicity on ultrasound

what is hyPERthyroidism? what is thyrotoxicosis?

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what is schmidt's syndrome? how is it treated?

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what is the last option in treating Graves' disease?

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other causes of hypothyroidism what is Reidel's thyroiditis? what is the thyroid like in this disease?

. Thyroid replaced by fibrous tissue with inflammatory infiltrate D . Fibrosis may extend to local structures (eg, trachea, esophagus), mimicking anaplastic carcinoma. 1 ⁄3 are hypothyroid. Considered a manifestation of IgG4 -related systemic disease (eg, autoimmune pancreatitis, retroperitoneal fibrosis, noninfectious aortitis). Findings: fixed, hard (rock-like), painless goiter.

what are the side effects of thionamides? when should they ever by stopped?

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what are some physical exam findings of hyPERthyroidism? _________ heart rate hand ________ hy___reflexia ______ skin eyelid _____ ____ fingernails

detached fingernails

dessicated porine thyroid and thyrolarare used for:

DESSICATED THYROID GLAND (ARMOUR THYROID, NATURE-THROID): "natural" preparations of T4 and T3 derived from dessicated porcine thyroid glands; *hypothyroidism*; PO T4 + T3 (THYROLAR): synthetic combination of T4 and T3; *hypothyroidism*; PO

what is the treatment for Graves' disease if thyroid storm is concern?

IODINE (Thyro-Block, Lugol's Solution, SSKI): iodine is a key thyroid hormone constituent; rapidly inhibits thyroid gland function and decreases thyroid gland vascularity; thyroid storm; also added to some foods to prevent iodine deficiency; PO. LITHIUM: inhibits thyroid hormone secretion by an unclear mechanism; hyperthyroidism G. DEXAMETHASONE, PREDNISONE: useful for their anti-inflammatory properties; hyperthyroidism such as that due to subacute thyroiditis

what are levothyroxin and liothyronine?

LEVOTHYROXINE: T4; hypothyroidism, hormone replacement therapy; PO, IV. LIOTHYRONINE: T3; hypothyroidism; PO.

what are the treatment options for: toxic adenomas or toxin MNG subacute thyroiditis graves' opthalmopathy

NSAIDS such as Ibuprofen: useful for their anti-inflammtory, analgesic properties; subacute thyroiditis LITHIUM: inhibits thyroid hormone secretion by an unclear mechanism; hyperthyroidism G. DEXAMETHASONE, PREDNISONE: useful for their anti-inflammatory properties; hyperthyroidism such as that due to subacute thyroiditis

what are the thionamides that are used in treatment of Graves' disease? what do they inhibit? what is the dosage? which is used in pregnancy? which is used for all other patients?

PROPYLTHIOURACIL (PTU): Thyroid peroxidase inhibitor; hyperthyroidism; PO. METHIMAZOLE (Tapazole; MMI): Thyroid peroxidase inhibitor; hyperthyroidism; PO

what is the most effective therapy for Graves' disease? what are the side effects?

SODIUM IODIDE [I 131]; Radioactive iodine: Thyroid hormone constituent; radiation destroys thyroid gland, hyperthyroidism; PO. Hypothyroidism is easier to treat

what medications and tumors can cause thyrotoxicosis?

TSH adenoma = secondary hyperthyroidism

what is the most common cause of hyPERthyroidism? what is the pathophysiology of this cause? what is the Ig called? how is the thyroid in this condition?

TSI (thyroid stimulating immunoglobulin) is elevated in Graves disease Antibodies will cause the continual release of thyroid hormone (*elevated T3/T4*). the T3/T4 has negative feedback on the hypothalamus and pituitary causing *low levels of TSH*, but T3/T4 will continue to be overproduced and oversecreted b/c the Ig's activates the TSHRs. Ig's have NO neg. feedback regulation. thyroid autoantibodies (anti-TPO, anti-thyroglobulin) may or may not be elevated

what is thyroiditis? what does it release? how long does the hyperthyroidism last? what are the 4 types of thyroiditis?

elevated T3/T4 low TSH because pituitary can still respond to its negative feedback primary hyPERthyroidism

what sxs of hyperthyroidism do beta blockers ameliorate? when should it be started? what does it not interfere? (Advantage) what are the 3 beta blockers that have *once* daily dosing?

ameliorate the palpitations, tachycardia, anxiety, heat intolerance beta blockers *decrease* the adrenergic tone PROPRANOLOL, *ATENOLOL, METOPROLOL, NADOLOL*: β-adrenergic blocker; symptomatic treatment of hyperthyroidism; PO, IV

Graves' Disease may be associated with all the following EXCEPT: A. Elevated TSH leading to elevated free T4 B. Uniformly enlarged thyroid gland on physical exam C. Diffusely increased uptake of 123I on thyroid uptake and scan D. Palpitations, tremors and hyperreflexia E. Elevated Free T3

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what are 7 eye findings in Graves' disease? proptosis = ___________ lid____ dryness leads to ____ing ____ ___ movements color is ___ do they occur concurrently with hyperthyroidism?

i. Fibroblasts behind the orbit and overlying the shin express the TSH receptor. ii. TSH activation results in glycosaminoglycan (chondroitin sulfate and hyaluronic acid) buildup, inflammation, fibrosis, and edema leading to exophthalmos and pretibial myxedema.

what does the thyroid scan and uptake look like in: graves' toxic adenoma toxic multinodular goiter

i. Graves': uniform in distribution ii. Toxic adenoma: single nodule uptake with remainder of gland with reduced uptake iii. Toxic multinodular goiter: regional uptake

Which of the following statements about levothyroxine (LT4) is FALSE: A. Most hypothyroid woman require increased amounts of levothyroxine during pregnancy to treat the hypothyroidism effectively B. The half-life (T1/2) of levothyroxine is relatively short (7 hours), thus causing it to have a relatively quick onset and offset of action C. Levothyroxine is a good method of treating hypothyroidism resulting either from Hashimoto's thyroiditis or following surgical removal of the thyroid gland D. Levothyroxine has relatively few side effects unless a person is given too much of it

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We can expect all of the following to occur during the course of subacute thyroiditis EXCEPT: A. Improvement in symptoms of palpitations and anxiety with administration of beta blockers B. Reduced uptake of 123I on thyroid scan and uptake C. Full eventual recovery to euthyroid state by nearly all individuals affected by 3 months D. Development of hypothyroid state following initial period of thyrotoxicosis

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what are the T3/T4 and TSH levels in: tertiary hypothyroidism secondary hypothyroidism primary hypothyroidism

primary hyPOthyroidism = low target gland hormone (*low T3/low T4*) + high trophic hormone (*high TSH*) = *primary failure of the TARGET gland* secondary hyPOthyroidism = low target gland hormone (*low T3/low T4*) + *low trophic* hormone (*low TSH*) = *secondary failure of the TROPHIC gland*

what occurs in the thyroid storm?

serious complication that occurs when hyperthyroidism is untreated and then significantly worsens in the setting of acute stress such as infection, trauma, surgery. Presents with *vomiting, hypovolemic shock, hyPERthermia and tachyarrhythmia (cause of death)*. Treat with the 4 P's : β -blockers (eg, P ropranolol), P ropylthiouracil, corticosteroids (eg, P rednisolone), P otassium iodide

what are 2 interesting causes of thyrotoxicosis factitia?

thyroglobulin may be undetectable in thyrotoxicosis factitia

what is: postpartum thyroiditis sporadic silent thyroiditis infectious thyroiditis

thyroid autoantibodies (anti-TPO, anti-thyroglobulin) may be elevated

what imaging studies can be used to diagnose a cause of hyperthyroidism?

ultrasound is not best