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75 Cards in this Set
- Front
- Back
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recommended daily adult iodide intake
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150 mcg; 200 mcg during pregnancy
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what occurs if iodide intale is increased
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fractional iodine uptake by thyroid is diminished
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what is the iodide transporter in the cell basement membrane
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sodium/iodide symporter (NIS)
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what can inhibit NIS
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thiocyanate (SCN-), pertechnetate (TcO4-), and perchlorate (ClO4-)
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what is the I- transporter at the apical cell membrane
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pendrin
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where else is the enzyme pendrin found
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cochlea of the inner ear
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Pendred's syndrome
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deafness and goiter when pendrin deficient
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what oxidized iodide
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thyroid peroxidase
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what can block thyroidal peroxidase
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high levels of intrathyroidal iodide transiently and persistently by thioamide drugs
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L-thyroxine
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2 molecules of DIT; T4
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ratio of T4:T3 in thyroglobulin
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~5:1
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how much T3 and T4 are in free form in plasma
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0.04% T4 and 0.4% T3
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deiodination of T4 can result in
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outer ring creates active T3 that is 3-4 times more potent than thyroxine; inner ring creates metabolically inactive rT3
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what can inhibit 5' deiodinase necessary for T4 to T3 conversion
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amiodarone, iodinated contrast material, B blockers, corticosteroids, severe illness or starvation; results in low T3 and high rT3
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what do large doses of iodide inhibit
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organification step
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Grave disease cause
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autoimmune - secretion of TSH receptor stimulating anitbody called TSI
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oral bioavailability of L-thyroxine and T3
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~80%, ~95%
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when is paternal therapy important in treating hypothyroidism
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severe myxedema with ileum
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what durgs induce hepatic microsomal enzymes and affect T3/T4 clearance
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rifampin, phenobarbital, carbamazepine, phenytoin, imatinib, protease inhibitors
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what occurs when thyroid binding sites increased (eg pregnancy)
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initial shift of hormone from free to bound and decrease in rate of elimination until normal concetration restored; total and bound hormone increases, but concentration of free and steady-state elimination remain normal
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what converts T4 to T3
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5'-deiodinase
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what does T3 bind in the nucleus
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c-erb oncogene family - alpha and beta
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what do many manifestations of thyroid hyperactivity resemble
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sympathetic nervous system overactivity, but catecholamine levels are not increased
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preparation of choice for thyroid replacement and supression therapy and why
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synthetic levothyroxine; stable, low cost, lack of allergies, easy lab measurement, long 7 day half-life
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liothyronine
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T3; shorter half-life (24 hours); should be avoided with cardiovascular disease
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what is liothyronine (t3) best used for
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short-term supression of TSH
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why not use desiccated thyroid
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protein antigenicity, prouct instability, variable concentrations, difficultly monitoring
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goitrogens
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agents that suppress secretion of T3 and T4 to subnormal levels and thereby increase TSH (produces goiter)
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commonly used antithyroid cmpds
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thioamides, iodides, and radioactive iodine
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two major thioamides used in treating thyrotoxicosis
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methimazole and propylthiouracil; methimazole is 10 times more potent
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why does the short plasma half life of methimazole and propylthiouracil have little effect on the antithyroid action
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they accumulate in the thyroid; can cross placenta and accumulate in fetus
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mechanism of thioamides
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inhibit thyroid peroxidase-catalyzed rxns and blocking iodine organification, also block coupling of iodotyrosines
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why is onset of drug action slow for thioamides
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they affect synthesis, not release; often require 3-4 weeks before stores of T4 depleted
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toxicity of thioamides
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2-12%; nausea, GI distress, maculopapular pruritic rash (4-6%)
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most dangerous complication of thioamides
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agranulocytosis (0.1-0.5%), rapidly reversible when discontinued
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why isn't switching thioamides after severe adverse rxn recommended
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propylthiouracil and methimazole have cross-sensitivity of 50%
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anion inhibitors of thyroid
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perchlorate, pertechnetate, and thiocyanate; competative inhibition of iodide transport mechanism
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what is potassium perchlorate associated with
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aplastic anemia; rarely used clinically
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iodides action on thyroid
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inhibit organification and hormone release and decrease size and vascularity of hyperplastic gland
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uses of iodides
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thyroid strom due to quick action (2-7 days), pre-operative preparation for surgery
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disadvantage of iodide therapy
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increased intraglandular storage; shouldn't be used alone since thyroid will escape iodide block in 2-8 weeks
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toxicity of iodide
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uncommon; acneiform rash, swollen salivary glands, mucous membrane ulcerations, conjunctivitis, rhinorrhea, drug fever, metallic taste…
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what is the only isotope of iodine used to treat thyrotoxicosis
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I-131; no recognized tumor/cancer increases
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B blocker most used in thyrotoxicosis
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propranolol
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Beta blocker affect on thyrotoxicosis
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clinical imporvement, but don't alter TH levels
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what does propranolol cause over 160 mg/day
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may reduce T3 levels about 20% by inhibiting peripheral conversion of T4 to T3
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most common cause of hypothyroidism in the USA
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Hashimoto's thyroiditis - immunological disorder
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most satisfactory preparation for treating hypothyroidism
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levothyroxine
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infant vs adult dosing of levothyroxine
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infant 10-15 mcg/kg/day; adults 1.7 mcg/kg/day
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how should thyroxine be administered
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on empt stomach since certain food and drugs can interfere with absorption
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how long does it take to reach steady state levels with thyroxine
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6-8 weeks; dosage changes should be made slowly
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when should thyroxine therapy be started at lower doses
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cardiac issues, older patients
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toxicity signs in children
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restlessness, insomnia, accelerated bone maturation and growth
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toxicity signs in adults
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increased nervousness, heat intolerance, episodes of palpitation and tachycardia, unexplained weight loss
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why must correction of myxedema be done cautiously in older persons
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avoid provoking arrhythmia, angina, or acute MI
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myxedma coma treatment
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IV levothyroxine 300-400 mcg initially followed by 50-100 mcg daily; have large amount of empty T3/T4 binding sites that must be filled b4 enough to affect tissue metabolism
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how much much thyroxine dosage be increased during pregnancy
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30-50%
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what antibodies are usually present in Graves' disease
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antithyroglobulin, thyroid peroxidase, and TSH-R Ab [stim]
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3 primary methods of controlling hyperthyroidism
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antithyroid drug therapy, surgical thyroidectomy, and destruction of gland with radioactive iodine
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when is drug therapy most useful in Graves
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young patients with small glands and mild disease
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incidence of relapse using drug therapy
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50-68%
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why is methimazole preferable to propylthiouracil and when would you use propylthiouracil instead
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can be administered once daily; pregnancy
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why does propylthiouracil bring down thyroid levels more quickly
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inhibits conversion of T4 to T3
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when is thyroidectomy the prefered treatment
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very large gioters or multinodular goiters
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when is radioactive iodine the preferred treatment
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most patients over 21
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how often do patients receiving radioactie iodine become hypothyroid
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~80%
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when are B-adrenoceptor blocking agents without extrinsic sympathomimetic activity extremely helpful and why
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during acute phase of thyrotoxicosis; controls tachycardia, hypertension, and atrial fibrilation
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what can be used in patients when B-blockers are contraindicated (athsma)
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Diltiazem (ca2+ channel blocker)
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how can barbituates be helpful in antithyroid therapy
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accelerate T4 breakdown (by hepatic enzyme induction), useful as sedative and lower t4 levels
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example of bile acid sequestants that can rapidly lower T4 levels via fecal excretion
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cholestyramine
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how long can infant be affected by mother's graves'disease after birth
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4-12 weeks
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subclinical hyperthyroidism
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suppressed TSH in conjunction with normal TH levels; treatment if TSH below 0.1 mIU/L
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amiodarone-induced thyrotoxicosis
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iodine-induced in people with underlying thyroid disease and inflammatory thyroiditis due to leakage of TH into circulation
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Treatment of type I and II amiodarone-induced thyrotoxicosis
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I - thioamides II-glucocorticoids
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nontoxic goiter common causes
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iodide deficiency, Hashimoto's thyroiditis, genetic
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