gland suprarenalis
DESCRIPTION
kelenjar suprarenalisTRANSCRIPT
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KEL DREN L
KONTROL SEKRESI D N
STEROIDOGENESIS
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KELENJAR ENDOKRIN PADA MANUSIA
dan HORMON YANG DIHASILKAN
•
hipofise : tropik hormon(ACTH, GH, FSH, LH,TSH, prolaktin)
• hipotalamus : Releasehrmon, Inhibiting hormon,
vasopresin, oksitosin• Tiroid : T3, T4
• Adrenal : mineralo &glukokortikoid, katekolamin
•Paratiroid : PTH
• Gonade : Seks hormon(estrogen, progestero,testosteron)
• pankreas : insulin,glukagon, somatostatin
• JANTUNG : ANP
• GINJAL : 1,25
dihidrokolekalsiferol,eritropoitin dan renin
• HATI : 25
hidrokolekalsiferol,
somatomedin
• kel pineal : melatonin
• KULIT : calciferol (vit D)
• GIT : CCK, Gastrin,
Skretin, VIP
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OTAK DAN HIPOTALAMUS
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Aksis
hipotalamo
hipofise
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Hypophysiotropic hormones
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Aksis hipotalamo-hipofise-target
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Anterior pituitary
• Growth hormone (GH, somatotropin)
Growth, mainly via secretion of IGF-I; protein,
carbohydrate, and lipid metabolism
• Thyroid-stimulating hormone (TSH,thyrotropin)
Thyroid gland stimulations
• Adrenocorticotropic hormone (ACTH,
corticotropin)
Adrenal cortex stimulations
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Anterior pituitary
• ProlactinBreast growth and milk synthesis; may be
permissive for certain reproductive
functions in the male• Gonadotropic hormones: Follicle-
stimulating hormone (FSH)
Luteinizing hormone (LH)Gonads (gamete production and sexhormone secretion)
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INPUTS TH T CONTROL
HORMONE SECRETIONS
The secretion of a hormone maycontroled by
1. the plasma concentratios of anion and nutrient that hormoneregulates,
2. neural input to endocrine cells,
3. one or more hormones
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INPUTS THAT
CONTROL HORMONE
SECRETIONS
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The Plasma concentrations of
Mineral ions or organic nutritions
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Reflexes a reductions in plasma calcium concentrations and the
actions of parathiroid hormone
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INPUTS TH T CONTROL
HORMONE SECRETIONS
• The autonomic nervous system is
the neural input controlling many
hormones,
•but the hypothalamic and
posterior pituitary hormonescontrloled by neurons in the brain
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Control By Neurons
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SHORT
LOOP
AND
LONG
LOOP
NEGATI
V FEED
BACKS
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Negative feed backs that control
the secretion of growth hormone
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UMPAN BALIK
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FAKTOR YANG
MEMPENGARUHI KADARHORMON DALAM DARAH
•Mekanisme umpan balik
•Variasi siklik
•Kecepatan metabolisme
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UMPAN BALIK NEGATIF
• Hormon berfluktuasi sesuai kebutuhan
• Mencegah sekresi dan aktivitas hormon
yang berlebihan• Ditentukan oleh keadaan atau produk yang
dihasilkan oleh kerja hormon di jaringan
target
• Efek umpan balik negatif dapat berupa
penurunan jumlah hormon atau penurunan
aktivitas hormon
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UMPAN BALIK POSITIF
• Menebabkan lonjakan kadar
hormon dalam darah
• Berasal dari kerja biologis dari
hormon tertentu : efek estrogen
pada hipofise anteriormeningkatkan sekresi LH
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METABOLISME
HORMON
•Penghancuran metabolik olehjaringan target
•Pengikatan oleh jaringan target•Sekresi oleh hati
•Ekskresi oleh ginjal
Sangat tergantung dari transporthormon dalam darah
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GL NDUL
SUPR REN LIS
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STEROIDOGENESIS
•Sisntesis hormon steroid (dari
kolesterol)
•Di glandula suprarenalis dan
gonade
•Terjadi dalam mitokondria
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Sintesis hormon kortek adrenal
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Gland suprarenalis
• T.a : kortek dan medula
• Medula :
- embriologis : sel neuroblas --- neuronposganglioner otonom
- morfologis : sel kromafin (feukromasit)dengan granula kromafin (katekolamin :epineprin (80%) dan norepineprin (20%)
adrenalin plasma : hampir seluruhnya berasal dari
medula adrenal.noradrenalin plasma : berasal dari : medula adrenal,serabut posganglioner simpatis, hipotalamus
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Medula adrenal
kortisol ACTH
• Sintesis :
Fenilalanin tirosin dopa dopamin
Fenilalanin hidroksilase tirosin hidroksilase dopa dekaboksilase
HEPAR MED.ADRENAL
norepineprin
epineprin
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Sekresi epineprin meningkat pada
• 3F(flight, fight,fright)
• Kondsi emergensi : cemas, nyeri, trauma,perdarahan, kerjakeras, hipotensi,
hpoglikemi, cuaca terlalu panas/dingin,perubahan pH darah.
• Kadar dlm plasma : basal 25-50pg/ml
hipoglikemi : 230pg/ml
diabetik ketoasidosis: 500pg/mlhipoglikemi berat : 1500pg/ml
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Fisiologi adrenalin/epineprin
•Sistem kardiovaskuler
•Sistem pernafasan
•Otot rangka
•metabolisme
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Glukosa darah adrenalin
• Adrenalin plasma
- glikogenolisis otot danhati
-glukoneogenesis di hati-lilpolisis di jaringanadiposa.
- glukosa, as lemak dan
gliserol plasmameningkat
• Memacu sekresiglukagon
• Menghambat sekresi
insulin
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Metabolisme KH
• Meningkatkan glukosa darah (fisiologis)
• “hiperglikemi” pada “feokromasitoma”
• Glikogenolisis di hati : hambat glikogen
sintetase dan sekresi insulin dari pankreas
aktivasi glikogen fosforilase dan glukagon
• Glikogenolisis di otot
• Glukoneogenesis• Stimulasi ACTH
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Kortek adrenal
• Glukokortikoid (kortisol,
kortikosteron) : mengatur
metabolisme karbohidrat, protein
dan lemak
• Mineralokortikoid (aldosteron) :
mengatur kadar Na dan K dalam
darah
• Seks hormon (dalam jumlah kecil)
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Zona kel suprarenalis dan hormonnya
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Kontrol sekresiglukokortikoid
• Irama diurnal (berlaku untuksemua steroid)
- siang–
malam- gelap – terang
• Aksis hipotalamo-hipofise-adrenal
• Umpan balik glukokortikoidperifer
•
Respon terhadap stres
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Kontrol sekresi glukokortikoid
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HPA AXIS
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ANDOGEN KORTEKS
ADRENAL
• DHEA (dihidroepiandrosteron)
• Efek lemah pada pria, tertutup oleh
testosteron testis• Memiliki efek kuat pada wanita (tdk
memiliki androgen lain)
• Berperan dalam maskulinisasi pada
wanita
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MINERALOKORTIKOID
(ALDOSTERON)
• Konservasi (vol dan konsentrasi) CES
• Target : sel epitel tubulus distal dan
koligent• Meningkatkan retensi natrium dan
sekresi kalium
• Reabs H2O (secara tdk langsung)
• Regulasi jangka panjang tek darah
•Hormon “esensial untuk hidup”
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RANGSANG SEKRESI
ALDOSTERON
• Pengaktifan sistem renin-
angiotensin-aldosteron
(penurunan Na dan tek darah)• Rangsang langsung pada
tubulus ginjal akibat kenaikan
kadar K plasma• Sekresi ldosteron tdk
tergantung pada CTH
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Mechanism of action of glucocorticid
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fek fisiologis glukokortikoid
• Efek metabolik• Efek anti inflamasi dan imunosupresan
• Respon tehadap stres
• Efek lain (samping) :- ginjal
- lambung
- psikoneuronal- anti pertumbuhan- tekanan darah- osteoporosis
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fek metabolik
•Metabolisme Karbohidrat
- meningkatkan kadar glukosa darah :lipolisis dan proteolisisglukoneogenesis
- anti insulin
- adrenal diabetes•Sekresi meningkat hanya pada
keadaan puasa (kadar glukosa darahturun)
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Efek metabolik
• Metabolisme protein
- proteolitik
- otot
atropi otot)
- tulang
osteoporosis)
• Metabolisme lemak
- lipolitik
ketosis)
- hambat sintesis jaringan lemak
- redistribusi lemak tdk merata
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Efek metabolik glukokortikoid
Metabolic pathways of the absoeptive state
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Metabolic pathways of the absoeptive state
M b li h f h b i
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Metabolic pathways of the post absoeptive state
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Hubungan beberapa hormon dalam metabolisme lemak
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Efek metabolik
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Glucocorticoid induce osteoporosis :hambat fs. Osteoblas, memacu resorbsi tulang,
hambat penyerapan ion Ca, hambat kerja gonadotropin
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Efek lain glukokortikoid
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fek antiinflamasi dan
imunosupresi
• Stabilisasi membranlisosom
• Menurunkan permebilitaskapiler
• Menurunkan jumlah lekosit(kec. Netrofil)
• Infolusi limfonodi---menurunkan produksiantibodi
•
Hambat motilitasmakrofag, netrofil dansistem komplemen
• Hambat ekspresi sel NK
• Hambat fungsi limfosit (limfositT)—hambat clonal expansion
• Hambat produksi IL-1 dari makrofag
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Penurunan jumlah lekosit
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• STRES : setiap perubahan lingkungan yangharus diadaptasi oleh tubuh.
• STRES : psikis/psikologis/emosional dan
fisik• STRES psikis merupakan pemicu yang
sangat kuat sekresi glukokortikoid
• STRES ACTH KORTISOL ADRENALIN
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