faal dan disfungsi kelenjar tiroid

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FAAL DAN DISFUNGSI KELENJAR TIROID

Kelenjar TiroidKelenjar perisai = kelenjar gondokSintesis Tiroksin (T3, T4)

FOLIKEL KEL. TIROID

Kel tiroid normal sel2 folikel cuboid (kubus)Kel tiroid inaktif sel2 folikel gepeng (squamous)Kel tiroid aktif sel2 folikel silindris

BIOSINTESA DAN SEKRESI HORMON TIROID- Bahan dasar yodium

TAHAPAN SINTESIA:1. Penangkapan yodium oleh kel tiroid (iodide trapping), transport iodide iodide pump rasio yodium di dalam kel tiroid terhadap yang ada di plasma atau serum = T/S ratio2. Oksidasi yodida yodium3. Yodinasi asam amino tyrosine4. Kondensasi yiodotyrosin secara oksidasi

Untuk fungsi kel tiroid normal, orang dewasa butuh minimal intake yodium 100-150 ug/hari, di USA 500 ug/hariHormon tiroid yang disekresikan kel tiroid:- Tiroksin (T4)- Triiodothyronine (T3), juga dibuat di jaringan perifer dengan jalan deionisasi T4, lebih aktif dari T4- Sedikit reverse T3 (RT3), inaktif

Di dalam kelenjar tiroid (koloid):- MIT = 23%- DIT = 33%- T4 = 35%- T3 = 7%- RT3 dan lain-lain sedikit sekali

Sekresi Hormon Tiroid:- 80 l T4- 4 l T3- 2 l RT3

Ikatan peptida antara respon iodinasi dan thyroglobulin diputus oleh protease lysosome T3, T4, MIT dan DIT sitoplasma

DIT dan MIT dideiodinasi oleh enzyme iodotyronine dehalogenase mikrosom, sedangkan T3dan T4 sirkulasi

Yodium dan tyrosine yang bebas digunakan kembali (recycling)

Per hari (dengan cara: endocytosis exocytosisTRANSPORT HORMON TIROID

Dalam plasma:T4 = 8 l/dL; T3 = 0.15 l/dL keduanya terikat pada protein (protein bound iodine = PBI)

Plasma protein yang mengikat hormon tiroid:- Albumin thyroxine binding albumin (TBA)- Prealbumin thyroxine binding prealbumin (TBPA)- Globulin thyroxine binding globulin (TBG) mempunyai mobilitas elektroforetik antara 1 dan 2 globulin

ProteinKadar PlasmaBanyaknya hormon yang terikat (mg/dL) (%) T4 T3

TBG 2 67 46TBPA 15 20 1TBA3500 13 53

Pada penderita dengan kadar binding protein atau (terutama TBG) euthyroid

Kadar TBG pada: pemberian estrogen, kehamilan, pemberian berbagai obat- obatan

Kadar TBG pada: Pemberian glukokortikoid, androgen, antiestrogen danazol, L-asparaginase (cancer chemotherapeutic agent)

Zat yang menurunkan pengikatan T4 dan T3 pada TBG: salicylate, anticonvulsant phenytoin, cancer chemotherapeutic agent (mitotane, 5-fluorouracil)

METABOLISME HORMON TIROID

T3 dan T4 dideionasi di hati, ginjal dan banyak jaringan lainnya 1/3 dari T4 T3 45% RT3

Deaminasi di jaringan analog asam piruvat dari T3 dan T4 Decarboxylasi selanjutnya analog asam asetatDi hati T3 dan T4 dikonjugasi sulfat dan glucoronide ke kantung empedu usus hydrolysa reabsorpsi, ekskresi (feces)

EFEK HORMON TIROID

1. Kalorigenik - me konsumsi O2 me BMR- me pertumbuhan dan pendewasaan (maturation)- mengatur metabolisme lipida- me absorpsi karbohidrat dari usus- me dissosiasi O2 dai hemoglobin dengan jalan me 2,3-diphosphoglycerate (DPG) butir-butir darah merah - efek kalorigenik hormon tiroid (T3 dan T4 ) me konsumsi O2 di hampir semua jaringan yang metabolik aktif, KECUALI: otak orang dewasa, testes, uterus, kel. limfe, limpa (spleen), pars anterior hypofisis T4 menurunkan konsumsi O2 oleh pars anterior, karena T4 menurunkan sekresi TSH

2. Efek pada sistem saraf - aktivitas mental me gelisah - CSF (cerebro spinal fluid) protein me - secara tidak langsung me responsibilitas saraf terhadap catecholamine me sistem aktivasi reticularis (reticular activating system) kegelisahan - me waktu reaksi refleks achilles

3. Efek pada metabolisme karbohidrat- me absorpsi karbohidrat di usus

4. Efek pada metabolisme cholesterol- me kadar cholesterol dalam sirkulasi- me kadar cholesterol akibat dari menya pembentukan low density lipid (LDL) receptors

5. Efek terhadap pertumbuhan dan perkembangan- hormon tiroid: essential untuk pertumbuhan normal dan pematangan skelet- pada amphibia me metamorfosis

- KALORIGENIK- MORFOGENIK- KINETIK Migrasi Spawning

Mekanisme kerja hormon tiroid

Hormon tiroid masuk ke dalam sel dan T3 mengikat reseptor pada nukleus (protein non hystone dalam chromatin) bekerja pada DNA me sintesa RNA dan rRNARNA pembentukan protein di ribosome berupa enzyme yang memodifikasi fungsi sel

Kontrol sekresi hromon tiroid dengan mekanisme umpan balik negatif (negative feedback mechanism)

Aktivitas molekuler hormon tiroid

T4 mempengaruhi sintesa protein baru:1. Via efeknya pada nuclear gene transcription2. Atau mitochondrial protein sintesis3. Efek terhadap fosforilasi oksidatif di mitokondria

Kelainan fungsi kelenjar tiroid:

- hyperfungsi hyperthyroidism- hypofungsi hypothyroidism

The thyroid gland produces two related hormones, thyroxine (T4) and triiodothyronine (T3) play a critical role in cell differentiation during development and help maintain thermogenic and metabolic homeostasis in the adult. Autoimmune disorders of the thyroid gland can either stimulate the overproduction of thyroid hormones : hyperthriodism (thyrotoxicosis) or cause glandular destruction and hormone deficiency (hypothyroidism).Hyperthyroidism & ThyrotoxicosisThyrotoxicosis is the clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormones generalized acceleration of metabolic processes. In most instances, thyrotoxicosis is due to hyperactivity of the thyroid gland, or hyperthyroidism.

Occasionally, thyrotoxicosis may be due to other causes such as excessive ingestion of thyroid hormone or, very rarely, excessive secretion of thyroid hormones from an ovarian tumor (struma ovarii).

Hyperthyroidisme- Thyrotoxicosis:- Tahkikardi- nervousness (kegelisahan)- BB- Hyperphagia- Heat intolerance- pulse pressure- tremor- kulit panas dan lembek- Keringat berlebihan- Diare (peristaltik usus yang meningkat)- BMR antara +10 +100

Contoh: Graves dosease (exophthalmic goiter)- Pembesaran diffus kel. tiroid- Hyperplasia- Exophthalmia (exophthalmos)Diffuse Toxic Goiter (Graves' Disease)

Graves' disease is the most common form of thyrotoxicosis.Graves' disease is currently viewed as an autoimmune disease of unknown causeFemales are involved about five times more commonly than males.The disease may occur at any age, with a peak incidence in the 20- to 40-year. The syndrome consists of one or more of the following features: (1) thyrotoxicosis, (2) goiter, (3) ophthalmopathy (exophthalmos), and (4) dermopathy (pretibial myxedema).

Physical ExaminationExamination of the neck begins by inspecting the seated patient from the front and side and noting any surgical scars, obvious masses, or distended veins.The thyroid can be palpated with both hands from behind or while facing the patient, using the thumbs to palpate each lobe (normally the right lobe is slightly larger than the left). By asking the patient to swallow sips of water, thyroid consistency can be better appreciated as the gland moves beneath the examiner's fingers.

consists of two lobes that are connected by an isthmus. It is located anterior to the trachea between the cricoid cartilage and the suprasternal notch. The normal thyroid is 1220 g in size, highly vascular, and soft in consistency.Anatomic of the thyroid gland

PathogenesisIn Graves' disease, T lymphocytes become sensitized to antigens within the thyroid gland and stimulate B lymphocytes to synthesize antibodies to these antigens antibody is directed against the TSH receptor in the thyroid cell membrane, stimulating thyroid gland growth and function. The antibody is called a thyroid-stimulating antibody (TSAb), or TSISymptoms and SignsIn younger individuals palpitations, nervousness, easy fatigability, hyperkinesia, diarrhea, excessive sweating, intolerance to heat, and preference for cold, weight loss without loss of appetite, Thyroid enlargement, thyrotoxic eye signs, and mild tachycardia commonly occur. Muscle weakness and loss of muscle mass may be so severe that the patient cannot rise from a chair without assistance. In children, rapid growth with accelerated bone maturation occurs.In patients over age 60, cardiovascular and myopathic manifestations predominate; the most common presenting complaints are palpitations, dyspnea on exertion, tremor, nervousness, and weight loss

Treatment of Graves' Disease

Although autoimmune mechanisms are responsible for the syndrome of Graves' disease, management has been largely directed toward controlling the hyperthyroidism.

Three good methods are available: (1) antithyroid drug therapy, (2) surgery, and (3) radioactive iodine therapy.

The antithyroid drugs PTU & methimazole remission from the disease that some patients have after 12 years of treatment.

Antithyroid drug therapy is generally started with larger doses. When the patient becomes biochemically euthyroid after 412 weeks, maintenance therapy may be achieved with a lower dose

DRUGSSTART(mg/day)MAINTENANCE(mg/day)Karbimazol30 - 605 - 20Metimazol30 - 605 - 20Propiltiourasil300 - 60050 - 200

Kontrol sekresi

Hypothyroidisme:- Kretinisme (anak-anak)- Myxedema (dewasa)

Defisiensi Yodium- Iodine deficiency goiter (endemic goiter)

Zat anti tiroid (goit