Thyroid Function Tests Tost Use Comments “Thyroid stimulating hormone (TSH) Total thyroxine (Ta) and ‘modotnyronine (13) “Thyrod bang globuin (736) 1, resin uptake (T3RU) Free thyroxine index (FT) Free Ts (To) ‘Produced by pitutary; cumulates thyroid to produce “Ty and T, (Which feed back on pituitary) 1 Suggests Fypothyrcicism 1 Suggests rypertnyrotatimn Heiptul to quantitate the degree of hormone “dericiency of excess Ty is active form in tssuos Ty's converted (0 Ts in tiyroid and peripherally 3999 bound to TG Free fraction (<19%) determines biologic action sands T, and 7, ‘An indirect measure of the binding capacity of patient's serum proteins (measutes unoccupied Te-binding sites) Used in conjunction with serum T, Product of serum T, and T; resin uptake ‘Corrects for changes In binding protein concentration Direct measurement of free hormone; bypasses Intertening eflacts of alsease or drugs on TEG eves ‘Very senate; normal TSH enectvely excludes ‘isease n asymptomatic patien’s Exceptions Patents wih severe nonthyroidal ness (NT), patents on Gopamnine or high dose ccocoricovds Si willbe normal or bw in central typotiyroidn Routine assays measure the (otal level need to ‘ake inte account TAG status (Causes of | Te Drugs (estrogen, oral contraceptives, tamoxifen, heroin, methadone, Sflucrouraci) ‘cite nepauts ‘Congenital ‘Acute inerritert porphya ‘causes of! TEC Drugs (androgens, glucocorticoids, slow- reas nicotinic a0) Severe ness oF matnutrtion Chronic tver disease Protein-osing sates (eg, nepitic synccme) Congental 1 T,RU: Hypertyroidsm, low TRC sates UTRU: Hypothyroidism, righ TEC states Highly correlated with ee T, Preferable over FTITres eithess of yronine binding global SUE ers lncrened tala f yo hormene‘Serum TSH level Low Normal High | | Eu Mh Normal) High Low Normal [ac] ! | Cental ‘suciicl Primary Sibdrical | | TsH-saceting Iypothyiism | |hypertyridsm | Thyoioxicoss| | hypothyroidism | | hypothyoiésm | | turar orNT OT, tonioosis| FIGURE 38-1 Sequential thyroid function testing using the serum thyroid-stimulating hormone (TSH) as a starting point. Ths strategy is ‘useful in asymptomatic individuals. f symptoms are present, both the free thyroxine (T,) and TSH should be assessed, (NTI, nonthyrcidal illness; T,, triodothyronine)Mengukur TSH ae ae al Meningkat Normal 1 Mengukur Ta bebas jduga kelainan hipofise f 1 Normal Rendeh Ya Bukan_) l = 1 ” Hipotiroid | Hipotirid trig | _MengulurT4 bebas cS came reese | TPOAbs, TPoAb+ TPOAD Rendah) (Normal a tak ada géjala) L = Hipotiroid Lakukan_ Tak ada | Otomn | | pemeriksaan untuk tes I menyampingkan Lakukan Terapi Evaluasi tiap Terapi penyebab pemeriksaan untuk dengan 74| L_ tahun dere 4] | hosts yang xin ‘menyampin efek obat, sick euthyroid syndrome selanjutnya evaliasi fungsi hipofise anteriorSuspected Hypothyroidism Check TSH and free T, ] {TSH {TSH Normal / [TSH ‘Normal TSH Free Ts Normal free Ta J Free Ts Normal free Ta Mild or subclinical * Central hypothyroidism Normal hypothyroidism hyroidal linesNodul tiroid —<—oe [ste rena | [nets oe rst eo LTSHs normal atau ingsi_| = TL . | Jaan Evaluasi klinik la | 1-131; alternatif, ole oan Sonia ethan taser Diagnostik cor [sinak | tunturan USS "92" tentian ues [ bocan] | Atomaut onsen Bedah i bedah, terapi, levotiroksin, ngnostk | i Non-diagnostik | suntikan ethanol, laserDiscover a =1-1.5 am nodule Perform history, physical exam SoumTs4, ‘utasound = ES =e Tatas) | are = esrauee ae co lam ea) (eat Ba Es 1 aa Fa i Suse tearing a | Se Se | ears Sang] [Roper] [Sapo | [Sapam] | [Mpa Bicicte| |Baceeson| [inuoasy eee | |Porreser meus | |_Sncn Sone] [Roe] [ey] [ios ] [a cerue | [mets] [ea] [URGE | [oyrttony mes] tnitony| [my sny ro aaa NA or lobectomyCauses of Thyrotoxicosis Etlology Mechanism Thyrold Examination —_—_—Radllolodiine Uptake Graves disease Stimulatoy anti-TSH receptor antibodies Dituse goiter 1 May be induced by interferon alfa Toxic multinodular goiter Activating gene mutations Nodules), usually>3cm_ 1 or sotary nocule Thyroiditis Follicular destruction causing release of stored Tender goiter in subacute; hormone; viral (¥ubacut), autoimmune nontender goiter in “silent” (“slent” or postpartum), of crugeinauced (amiodarone) lodnenduced ‘odine surpus (V dye or amicdarone.induced Nodular or diffuse goiter =| thyrotoxicosis type 1) Choriocarcinoma Secretes hCG, a thyroid stimulator Minimal goiter t Ptitary tumor TSH overproduction Minimal goiter 1 Struma ova Ectopic thyroid tssue in ovarian tumor Normal 4 (over thyroid) Exogenous thyrotoxicosis ‘Normal in both 1 Iatrogenic Oversupplementation of thyroxine Factitious Surepttious ingestion of thyroxine HCG, human chorionic gonadotropin, Iv, intravencus; TSH, tytoid-stimuating hormone,ae et ed Organ System ‘Constitutional ‘Cardiovascular Respiratory ‘Gastrointestinal Musculoskeletal Neuropsychiatric Endocrine Hematologic ‘Ophthalmologic Dermatologic Clinical Manifestations of Thyrotoxicosis Symptoms and Signs Weight loss, heat intolerance Palpitations, atrial arrhythmias, congestive heart failure, systolic hypertension: Dyspnea Hyperdefecation, increased appetite, nausea Proximal muscle weakness, osteopenia, hypercalciuria, hypercalcemia, extraocular muscle weakness,~ myasthenia gravis~ Nervousness, anxiety, tre insomnia, impaired mentation, delirium, psychosis Hypomenorrhea, amenorrhea, ‘gynecomastia, decreased libido: Splenomegaly,~ enlarged thymus,~ lymphadenopathy, neutropenia” Stare, lid lag,* proptosis,~ diplopia,~ visual loss™ Warm, moist, velvety skin; palmar ‘erythema, onycholysis, thinning hair, pruritus, hives, pretibial myxedema,” vitiligo,~ thyroid acropachy™ *Denotes findings only seen in Graves disease.BLE 233-6 FRACTIONAL 24-HOUR RADIOIODINE ETIOLOGY UPTAKE (%) THYROID SCAN APPEARANCE Graves’ disease 35-95 ‘Diffuse increased from isthmus Toxic adenoma 20-60 Solitary focus of intense uptake; suppression of uptake in remainder of thyroid Toxic multinodular goiter 20-60 Patchy heterogeneous foci of increased uptake interspersed with regions of diminished uptake Subacute thyroiditis 0-2 ‘Minimal to absent uptake Autoimmune thyroiditis 0-2 Minimal to absent uptake; patchy heterogeneous uptake recovery Todine-induced 0-2 ‘Minimal to absent uptake a ve Exogenous thyroid 0-2 Minimal to absent uptake hormone intoxication. Metastatic differentiated 0-5 Focal uptake in metastases ‘thyroid cancer ‘TSH-secreting pituitary 30-80 ‘Diffuse increased homogeneous adenoma uptake