ENDOKRINOLOGI

Zulkhah noor
Endocrine vs. Nervous System
 Major communication systems in the
body
 Integrate stimuli and responses to
changes in external and internal
environment
 Both are crucial to coordinated
functions of highly differentiated cells,
tissues and organs
 Unlike the nervous system, the
endocrine system is anatomically
discontinuous.
Nervous system

•The nervous system exerts

point-to-point control through
nerves, similar to sending
messages by conventional
telephone. Nervous control is
electrical in nature and fast.
Hormones travel via the
bloodstream to target cells
•The endocrine system broadcasts its
hormonal messages to essentially all
cells by secretion into blood and
extracellular fluid. Like a radio
broadcast, it requires a receiver to get
the message - in the case of endocrine
messages, cells must bear a receptor
for the hormone being broadcast in
order to respond.
 A cell is a target because is has a specific
receptor for the hormone

Most hormones circulate in blood, coming into contact with essentially

all cells. However, a given hormone usually affects only a limited
number of cells, which are called target cells. A target cell responds
to a hormone because it bears receptors for the hormone.
Principal functions of the
endocrine system
 Maintenance of the internal environment in
the body (maintaining the optimum
biochemical environment).
 Integration and regulation of growth and
development.
 Control, maintenance and instigation of
sexual reproduction, including
gametogenesis, coitus, fertilization, fetal
growth and development and nourishment of
the newborn.
CLASSIFICATION OF
CHEMICAL MESSENGER
 Endocrine/hormone
 Neuroendocrine

 Neurotransmitter

 Paracrine

 Outocrine

 disebut FIRST MESSENGER

7
8
 STRUKTUR HORMON
GLIKOPRO PEPTIDA AMINE STEROID
TEIN
FSH GH TIROKSIN KORTISOL
LH ACTH TRIIODOTIRO- ALDOSTERON
TSH NIN ESTRADIOL
INSULIN
HCG EPINEFRIN PROGESTERON
GLUKAGON
NOREPINE- TESTOSTERON
PROLAKTIN FRIN VITAMIN D
GASTRIN
KOLESISTOKI-
NIN, DLL

EICOSANOID : PROSTAGLANDIN, TROMBOKSAN

LEUKOTRIEN
9
 SINTESIS HORMON

 Berbeda sesuai struktur hormon

 Peptida dan Glikoprotein :mRNA 
Retikulum endoplasma:  Preprohormon
 Prohormon  Aparatus golgi:
Prohormon  hormon dalam vesikel
(disimpan)

10
Peptide/protein hormone synthesis
Amine hormones
There are two groups of hormones derived
from the amino acid tyrosine
Thyroid hormones and Catecholamines
Thyroid Hormone
 Thyroid hormones are basically a "double" tyrosine
with the critical incorporation of 3 or 4 iodine atoms.
 Thyroid hormone is produced by the thyroid gland

and is lipid soluble

 Thyroid hormones are produced by modification of a
tyrosine residue contained in thyroglobulin, post-
translationally modified to bind iodine, then
proteolytically cleaved and released as T4 and T3.
T3 and T4 then bind to thyroxin binding globulin for
transport in the blood
Thyroid hormones
Catecholamine hormones
 Catecholamines are both neurohormones
and neurotransmitters.
 These include epinephrine, and

norepinephrine
 Epinephrine and norepinephrine are
produced by the adrenal medulla both are
water soluble
 Secreted like peptide hormones
Synthesis of catecholamines
Amine Hormones
 Two other amino acids are used for
synthesis of hormones:
 Tryptophan is the precursor to
serotonin and the pineal hormone
melatonin
 Glutamic acid is converted to
histamine
Steroid hormones
 All steroid hormones are derived from
cholesterol and differ only in the ring
structure and side chains attached to it.
 All steroid hormones are lipid soluble
Types of steroid hormones
 Glucocorticoids; cortisol is the major
representative in most mammals
 Mineralocorticoids; aldosterone being
most prominent
 Androgens such as testosterone
 Estrogens, including estradiol and
estrone
 Progestogens (also known a
progestins) such as progesterone
Steroid hormones
 Are not packaged, but synthesized and
immediately released
 Are all derived from the same parent
compound: Cholesterol
 Enzymes which produce steroid hormones
from cholesterol are located in mitochondria
and smooth ER
 Steroids are lipid soluble and thus are freely
permeable to membranes so are not stored in
cells
Steroid hormones
 Steroid hormones are not water soluble so
have to be carried in the blood complexed to
specific binding globulins.
 Corticosteroid binding globulin carries cortisol
 Sex steroid binding globulin carries
testosterone and estradiol
 In some cases a steroid is secreted by one
cell and is converted to the active steroid by
the target cell: an example is androgen which
secreted by the gonad and converted into
estrogen in the brain
 Extracellular
lipoprotein LH
Cholesterol
acetate pool
ATP

cholestero cAMP
l PKA+

Pregnenolone
3bHSD
Progesterone
P450c17
Androstenedione
17bHSD
TESTOSTERONE
 Steroidogenic Enzymes
Common name "Old" name Current name

Side-chain cleavage enzyme; P450SCC CYP11A1

desmolase

3 beta-hydroxysteroid 3 beta-HSD 3 beta-HSD

dehydrogenase
17 alpha-hydroxylase/17,20 lyase P450C17 CYP17

21-hydroxylase P450C21 CYP21A2

11 beta-hydroxylase P450C11 CYP11B1

Aldosterone synthase P450C11AS CYP11B2

Aromatase P450aro CYP19

 Fatty Acid Derivatives -
Eicosanoids
 Eicosanoids are a large group of
molecules derived from polyunsaturated
fatty acids.
 The principal groups of hormones of this
class are prostaglandins, prostacyclins,
leukotrienes and thromboxanes.
SEKRESI HORMON
 Hormon akan disekresi jika ada
rangsang:
-Hormon
-Saraf
-nutrisi: glukosa, a.amino,mineral,dsb
-Obat

26
Mekanisme Kerja Hormon
 Berbeda sesuai struktur hormon
 Hormon diterima oleh Reseptor
membran luar (ektraseluler):
Hormon Glikoprotein , polipeptida,
epinefrin dan norepinefrin 
menbentuk second messenger
intraseluler ( cAMP, DAG, Ca 2+,
Tirosin kinase) untuk aktivitas sel.

27
 Hormones and their receptors
Hormone Class of Location
hormone

Amine Water-soluble Cell surface

(epinephrine)

Amine (thyroid Lipid soluble Intracellular

hormone)

Peptide/protein Water soluble Cell surface

Steroids and Lipid Soluble Intracellular

Vitamin D
Second messenger systems
 Receptors for the water soluble
hormones are found on the surface of
the target cell, on the plasma
membrane. These types of receptors
are coupled to various second
messenger systems which mediate the
action of the hormone in the target cell
Second messengers for cell-
surface receptors
 Second messenger systems include:
 Adenylate cyclase which catalyzes the conversion
of ATP to cyclic AMP;
 Guanylate cyclase which catalyzes the conversion
of GMP to cyclic GMP (cyclic AMP and cyclic GMP
are known collectively as cyclic nucleotides);
 Calcium and calmodulin; phospholipase C which
catalyzes phosphoinositide turnover producing
inositol phosphates and diacyl glycerol.
Types of receptors
Second messenger systems
 Each of these second messenger systems
activates a specific protein kinase enzyme.
 These include cyclic nucleotide-dependent protein
kinases
 Calcium/calmodulin-dependent protein kinase, and
protein kinase C which depends on diacyl glycerol
binding for activation.
 Protein kinase C activity is further increased by calcium
which is released by the action of inositol phosphates.
Second messenger systems
 The generation of second messengers and
activation of specific protein kinases results in
changes in the activity of the target cell which
characterizes the response that the hormone
evokes.
 Changes evoked by the actions of second
messengers are usually rapid
 Signal transduction
mechanisms of hormones
Activation of Inhibition of Increased Tyrosine
adenylate adenylate phospho- kinase
cyclase cyclase inositide activation
turnover
b-adrenergic a2-adrenergic a1-adgrenergic Insulin

LH, FSH, TSH, Opioid Angiotensin II Growth factors

hCG (PDGF, EGF,
FGF, IGF-1
Glucagon Muscarinic Muscarinic Growth
cholinergic – cholinergic – hormone
M2 M3
Vasopressin- Vasopressin – Prolactin
V2 V1
ACTH
Protein Hormone Mechanism of Action - cAMP second messenger
35
Protein Hormone Mechanism of Action -
calcium second messenger

36
 Hormon diterima langsung oleh
Reseptor Intraseluler (sitoplasma,
terutama inti) : T3, T4, steroid
terikat reseptor  aktivitas inti
untuk sintesis protein

37
38
39
40
41
Steriod Hormone Mechanism of Action

42
 SECOND MESSENGER INTRASELULER
cAMP Ca++ , DAG Tirosin kinase
Meningkat: Asetilkolin Insulin
ACTH’FSH,LH, Alfa- IGF-1
TSH, ADH, Beta- adrenergik- Epidermal GF
adrenergik- katekolamin
katakolamin Angiotensin
glukagon Oksitosin
Menurun: TRH
somatostatin GnRH,dll
Alfa-adrenergik-
katekolamin,dll

43
HIPOTALAMUS-HIPOFISIS

44
 Hormon Target Efek fisiologis
organ
GH Hati, jar.adiposa Meningkatkan pertumbuhan ,
kontrol metabolisme protein,
lipid dan karbohidrat
Hipofisis TSH tiroid Merangsang sistesis dan
Anterior sekresi hormon tiroid
ACTH Korteks adrenal Merangsang sintesis dan
sekresi glukokortikoid
Prolaktin Kel.mamae Produksi susu
FSH Ovari, testis Kontrol fungsi reproduksi
LH Ovari, testis Kontrol fungsi reproduksi
Hipofisis ADH ginjal Penghematan air
Posterior
Oksitosin Uterus, Kontraksi uterus, milk
kel,mamae ejection

45
FEEDBACK CONTROL DALAM
PRODUKSI HORMON
 FEEDBACK CIRCIUT (sirkuit umpan
balik) adalah dasar dari sistem kontrol
pada berbagai mekanisme fisiologi,
 FEEDBACK LOOP digunakan secara
ekstensif dalam sekresi hormon pada
AKSIS HIPOTALAMUS-HIPOSISIS
 Tanda + (=merangsang sekresi),
tanda – (=menghambat sekresi)

46
AKSIS HIPOTALAMO-HIPOFISIS-SEL TARGET

Contoh:

47
48
49
50
51
TIROID DAN
PARATIROID
folikel

Sel para folikel 52

 TSH DALAM PRODUKSI HORMON
TIROID
 TSH cAMP  FUNGSI SEL
TIROID:
1. Mengumpulkan dan mentransport I 
koloid
2. Sintesis tiroglobulin  koloid
3. Sintesis dan sekresi hormon tiroid
(T3,T4) dari tiroglobulin (koloid) 
sirkulasi

53
STRUKTUR KIMIA HORMON
TIROID

54
 T3,T4  T3  efek sel target
1.Jantung: reseptor beta-adrenergik dan respon
katekolamin
2. Jarangan adiposa : lipolisis
3. Otot:  pemecahan protein
4. Tulang: pertumbuhan normal
5. Saraf: pertumbuhan normal
6. Usus:  absorbsi
7. Lipoprotein:  reseptor LDL
8. Umum (mitokondria):  konsumsi O2,
metabolisme
9. Hematopoietin : normal
10. Pertumbuhan fetus
55
56
57
58
Apa Penyebab hipotoroid dan
hipertiroid?

59
 Metabolisme Ca dan PO4
TULANG GINJAL USUS

PTH - PELEPASAN Ca2+ -  REABSORSI Ca2+

DAN PO4 - REABSORBSI PO4
-  KONVERSI
25 -OHD31,25-(OH)2
- RESORBSI HCO3-

CT -  PELEPASAN Ca2+ -  REABSORBSI Ca2+

DAN PO4 DAN PO4

VIT - MENJAGA SIST. - REABSORBSI - ABSORBSI

D TRANSPORT Ca2+ Ca2+ DAN PO4
Ca2+

60
HORMON PARATIROID

61
Vitamin
D

62
 PANKREAS

SEL PANKREAS:
1. Sel A (alfa): mensekresi
glukagon
2. Sel B (beta) mensekresi
insulin
3. Sel D (delta) mensekresi
somatostatin

63
 INSULIN
- Polipeptida 51 asam amino, BM :5808,
- Sekresi : dewasa,normal : 40–50 U/hari ;
puasa (basal) : 10  U/ml ;
setelah makan : 100  U/ml ;
- Kadar insulin mulai naik 8 – 10 menit
setelah makan, puncaknya pada 35 – 45
menit, dan kembali semula pada 90 – 120
menit.
- Second messenger : inositol monofosfat,
glukosamin, diasil gliserol (DAG) Protein
kinase C fosforilasi

64
 PENGATURAN SEKRESI
INSULIN
1 STIMULAN
- glukosa, mannosa
- stimulasi vagal
- Obat : sulfonilurea
2 PENGHAMBAT
- Neural : stimilasi a-adrenergik
- Hormon : somatostatin
- obat : Phenitoin
65
66
67
68
69
 EFEK INSULIN
I. Efek parakrin : menghambat sekresi
glukagon oleh sel A
II. Efek endokrin :
A. HATI
*Anabolik : glikogenesis, sintesis trigliserida,
kolesterol, VLDL, protein, dan glikolisis
*Antikatabolik : menghambat glikogenolisis,
ketogenesis, dan glukoneogenesis

70
B. OTOT
1.  transport asam amino,stimulasi ribosom
 sintesis protein
2.  transport glukosa dan aktivitas glikogen
sintase serta menghambat aktivitas glikogen
fosforilase  sintesis glikogen
C. LEMAK
Meningkatkan simpanan trigliserida melalui :
1. induksi lipoprotein lipase absorbsi asam
lemak ke sel adiposa
2. peningkatan transport glukosa di sel adiposa
3. menghambat lipolisis intraseluler

71
 GLUKAGON
 Polipeptida rantai tunggal, 29 asam amino,
BM : 3485
 KONTROL SEKRESI
-dihambat oleh: glukosa (efek parakrin)
- ditingkatkan oleh :katekolamin,
kolesistokinin, gastrin, glukokortikoid,
neuron (stimulasi vagal)
 Second messenger : cAMP 
protein kinase A  enzim fosforilasi

72
Glukagon
 TARGET ORGAN : hati (terutama), otot
sel adiposa

 EFEK: berlawanan dengan insulin

(counterregulatory hormon) 
mempertahankan kadar glukosa darah
melalui :glikogenolisis,glukoneogenesis,
oksidasi asam lemak, pengambilan
asam amino oleh hati.

73
Insulin dan Glukagon dalam
homeostasis glukosa

74
 DIABETES MELITUS
I. Tipe Insulin Dependent (IDDM), TIPE I,
JOUVENIL
II. Tipe Non-insulin Dependent (NIDDM),
TIPE II, MATUR
a. Non obese
b. Obese
III. Malnutrition-related diabetes melitus
(MRDM), Pancreatic Diabetes
IV. Peningkatan hormon counterregulatory
insulin, karena berbagai sebab.

75
 PATOFISIOLOGI
Kadar rendah insulin menyebabkan :
1. Pemakaian glukosa berkurang
(glukosa sedikit masuk ke dalam sel),
konsentrasi glukosa darah meningkat,
GLUKOSURIA, DEHIDRASI,
KEHILANGAN ELEKTROLIT. Nilai
ambang glukosa darah 180 mg/dl.
2. Mobilisasi lemak dari jaringan adiposa
meningkatmetabolisme lemak secara
abnormal, deposisi lemak pada dinding
pembuluh darahATEROSKLEROSIS

76
Selain itu, kadar asam aseto-
asetat,asam beta hidroksibutirat
(badan keton) meningkat  pH
menurun
3. Pemecahan protein sel/jaringan
DEGENERASI  kelemahan/rentan
penyakit
4. GEJALA 3 P (poliuria, polidipsia,
polifagia), Berat badan menurun,
astenia (kurang tenaga)

77
Hiperinsulinemia
- kadar insulin yang tinggi 
kadar glukosa darah menjadi
rendah otak kekurangan
glukosapeningkatan aktivitas
listrik sarafhalusinasi, nervous,
gemetar, kejang klonik, hilang
kesadaran

78
ADRENAL

79
 HORMON ADRENAL
PENGATUR ANATOMI PRODUK

Renin-Angiotensin Z. glomerulosa Aldosteron

Cortikotropin (ACTH) (Minerarokortikoid )

Cortikotropin (ACTH) Z. fasciculata Kortisol (glukokor-

CRH hipotalamus tikoid),H. seks

Cortikotropin (A Z. retikularis Hormon seks,

CRH hipotalamus kortisol

Serabut preganglioner Medula Katekolamin ;

saraf simpatis (Epinefrin, norepinefrin)

80
 Kontrol sekresi CRH dan ACTH :
1. sekresi episodik/ritme diurnal/irama
sirkadian
2. stres
3. feed back negatif kortisal
Pola episodik berubah jika : perubahan waktu tidur,
paparan sinar (gelap/terang), stres fisik dan
fisiologis, intake makanan (puasa), sakit,
pembedahan,kelainan SSP-hipotalamus-hipofisis-
adrenal, penyakit hati, dan lain-lain yang
berpengaruh terhadap metabolisme kortisol, gagal
ginjal kronik, alkoholosme, obat antiserotonergik
(seperti cycloheptadin), preparat kortisol eksogen.
81
MEKANISME KERJA
*Stres , emosional (rasa takut,
kawatir, gelisah), perlukaan (injury)
badan (pembedahan), hipoglikemia 
memacu sekresi CRH  ACTH 
cAMP aktivasi enzim-enzim
perubahan kolesterol menjadi
steroid.

82
Hypothalamopituitary adrenal (HPA) axis: Negative
Immune
Stress Feedback system:
Circadian altered
rhythm Hypothalamus
Muscle:
CRH Net loss of amino
Posterior Acids (glucose)
Anterior Pituitary Gland
Pituitary Gland Liver:
(-) Deamination of
proteins into amino
ACTH acids,
gluconeogenesis
Glucocorticoids,
Adrenals Catecholamines, (glucose)
etc.. Fat Cells:
Free fatty
acid
Kidney mobilization

Heart rate:
Increased
Corticosteroids are Gene-Active
 GLUKOKORTIKOID (kortisol,
kortikosteron)

 Preparat sintetik : Kortison,

prednison, metilprednison,
deksametason
 Mekanisme kerja : Kompleks
hormon(steroid)- reseptor di
sitosolintitranskripsi DNAsintesis
protein (enzim & protein yang
memerantai respon glukokorticoid
87
 Efek fisiologis :
1. Hati : Sintetik : meningkatkan
glukoneogenesis, sintesis glikogen &
penyimpanan, aktivitas glukosa-6 fosfatase,
kadar glukosa darah
2.Otot : Katabolik : menghambat pengambilan
glukosa dan metabolisme, penurunan sintesis
protein, meningkatkan pelepasan asam amino,
asam laktat
3.Lemak : Lipolitik : memacu lipolisis,
meningkatkan pelepasan FFA dan gliserol
4. Sistem imun: supresan lekosit, anti inflamasi,
88
5.Kardiovasculer : meningkatkan
cardiac output dan tonus pembuluh
darah perifer.
6.Ginjal : Meningkatkan filtrasi
glomerulus, menjaga keseimbangan air
& elektrolit.
7.Lain-lain : antagonis terhadap insulin
(meningkatkan glukosa darah),
meningkatkan ketahanan terhadap
stres

89
Stress and The Adrenal Glands
Actions: Carbohydrate and protein
metabolism
Negative nitrogen balance and hyperglycemia

 Gluconeogenesis
 Peripheral actions (mobilize aas and glucose and
glycogen)
 Hepatic actions

 Peripheral utilization of glucose

 Glycogen deposition in liver

(activation of hepatic glycogen synthase)
Actions: Lipid metabolism

 Redistribution of Fat
 Buffalo hump
 Moon face

 Promote adipokinetic agents

activity
(glucagon, growth hormone, adrenaline,
thyroxine)
Actions: Electrolyte and water balance
 Aldosterone is more important
 Act on DT and CD of kidney
 Na+ reabsorption
 Urinary excretion of K+ and H+
 Addison’s disease ??
• Na+ loss
• Shrinkage of ECF
• Cellular hydration
• Hypodynamic state of CVS
• Circulatory collapse,
renal failure, death
Actions: Cardiovascular system

 Restrict capillary permeability

 Maintain tone of arterioles
 Myocardial contractility

Mineralocorticoid induced hypertension ??

Na+ sensitize blood vessels to the action of

catecholamines & angiotensin
Actions: Skeletal Muscles
Needed for maintaining the normal function of Skeletal
muscle

Addison's disease: weakness and fatigue is due

to inadequacy of circulatory system

Prolonged use: Steroid myopathy

 Actions: CNS

 Direct:
 Mood
 Behaviour
 Brain excitability
 Indirect:
 maintain glucose, circulation and electrolyte
balance

ICP (pseudotumor cerebri) - Rare

Pseudotumor cerebri
(Intracranial hypertension)

 Glucocorticoids
 Mineralocorticoids
 Amiodarone
 Vitamin A
 Oral contraceptives
 Tetracyclines

From Harrison. 15th edition, volume 1, page 435

Actions: Stomach

Aggravate peptic ulcer. May be due

to:

 Acid and pepsin secretion

 immune response to H.Pylori

Actions: Blood

RBC: Hb and RBC content

(erythrophagocytosis )

WBC: Lymphocytes, eosinophils,

monocytes, basophils
Polymorphonucleocytes
Actions: Anti-inflammatory
 Recruitment of WBC and monocyte-
macrophage into affected area &
elaboration of chemotactic substances
 Lipocortin
 ELAM1 and ICAM-1 in endothelial cells
 TNF from phagocytic cells
 IL1 from monocyte-macrophage
 Formation of Plasminogen Activator
 Action of MIF and fibroblastic activity
 Expression of COX II
 Corticosteroids

Lipocortin
Phospholipids

Phospholipase A2

Arachidonic acids

lipoxygenase Cycylooxygenase

Prostaglandins,
Leukotriene Thromboxane
PAF by Prostacyclins
lipocortin
Anti-inflammatory actions of corticosteroids

Corticosteroid inhibitory effect

Immunosuppressive and anti-allergic
actions

 Suppresses all types of hypersensitivity

and allergic phenomenon
 At High dose: Interfere with all steps of
immunological response
 Causes greater suppression of Cell-
mediated immunity (graft rejection and
delayed hypersensitivity)
 Transplant rejection: antigen expression from
grafted tissues, delay revascularization,
sensitisation of T lymphocytes etc.
 Actions: Growth and Cell
division

 Inhibit cell division or synthesis of

DNA
 Delay the process of healing
 Retard the growth of children
Actions: Calcium metabolism

 Intestinal absorption

 Renal excretion

 Excessive loss of calcium from spongy

bones (e.g., vertebrae, ribs, etc)
 Actions: Respiratory system

 Not bronchodilators
 Most potent and most effective anti-inflammatory
 Effects not seen immediately (delay 6 or more hrs)
 Inhaled corticosteroids are used for long term
control
 MINERALOKORTIKOID
Aldosteron (utama), deoksikortikosteron
1. Renin-Angiotensin sistem
Sekresi renin dikontrol oleh ritme sirkadian (meningkat
pada pagi hari) dan oleh penurunan volume darah
(hipovolemia) , dehidrasi, hiperosmotik.
2. ACTH
Efek ACTH terhadap sekresi aldosteron bersifat
sementara
3. Kadar elektrolit plasma
Na + rendah / K+ tinggi  merangsang zona
glomerularis sekresi aldosteron  Na + tinggi / K+
rendah  sekresi aldosteron dihambat (feed back
negatif)
109
Mekanisme kerja
aldosteron :
 Steroid-Reseptor kompleks  inti
 transkripsi DNA  produksi
mRNA  memacu sintesis protein
oleh ribosom  protein enzim
untuk transport aktif Na + /K+
(Na + /K+ATPase)

110
Target Organ
 Di ginjal retensi Na + diganti dengan
K+ dan H +
 Di kolon, duodenum, kel. saliva, kel.
keringat meningkatkan reabsorbsi Na
+

 Di Otot dan Otak : meningkatkan K

+ dan menutunkan Na + intrasel.

111
 MEDULA ADRENAL
 Secara embriologi sel medula adrenal merupakan
derivat sel saraf.
 90 % sel mensekresi epinefrin dan 10 %
mensekresi norepinefrin, dan sedikit
mensekresi dopamin.
 Dalam kondisi normal,hanya sedikit epinefrin
dan norepinefrin disekresi oleh medula adrenal.
Jumlah yang banyak disekresi sebagai respon
terhadap rangsangan yang menyebabkan
kenaikan emosional (seperti marah).
 Sekresi terjadi mengikuti pelepasan
asetilkolin dari saraf preganglioner yang
menginervasi medula adrenal.
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 PATOFISIOLOGI ADRENAL
A. Kelebihan produksi glukokortikoid
(hiperadrenocortikalism, hiperkortisolism,
Cushing’s sindrom).
B. Insufisiensi Adrenokortikal (Addison’s
disease)
C. Kelebihan mineralokortikoid/
Hiperaldosteronisme (Conn’s disease)
D. Kelainan medula adrenal
1. Pheochromositoma adalah neoplasma sel-sel
chomafin medula adrenal
2. Hipofungsi medula adrenal

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HORMON SEKS
PRIA (UTAMA)
1. FSH
2. LH
3. Testosteron
WANITA (UTAMA)
1. FSH
2. LH
3. Estrogen (estrin, estron, estradiol)
4. Progesteron
5. Relaksin
HORMON LAIN yang ikut berperan:
hCG, prolaktin, GH, inhibin, tiroksin, dll.
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 GONADOTROPIN
GnRH(hipotalamus)  FSH dan LH
(hipofisis anterior)
- Pada laki-laki disekresikan secara tonik
(kontinyu), pada perempuan disekresikan
secara siklik sehingga ada siklus menstruasi.
- Masing-masing adalah glikoprotein terdiri dari
sub unit a dan b
- Second messenger adalah cAMP protein
kinase C respon seluler

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SIKLUS MENSTRUASI

116
 Fungsi FSH dan LH
FSH :merangsang sel sertoli untuk
memproduksi androgen-binding protein dan
spermatogenesis, serta pertumbuhan awal
folikel ovari dan sekresi estrogen
LH : bersifat tropik, merangsang sel-sel Leydig
tumbuh dan sekresi testosteron, berperan
dalam pematangan akhir folikel ovarium dan
sekresi estrogen dari folikel , berperan dalam
ovulasi, pembentukan korpus luteum, dan
sekresi progesteron.
Hormon-lain yang berperan dalam
pengaturan fungsi gonad antara lain adalah
hCG, prolaktin, GH, hormon seks (testosteron,
estrogen, progesteron, inhibin) 117
 ANDROGEN
(Testosteron, dihidrotestosteron)
 EFEK Umum :pertumbuhan dan pematangan
permatogenesis ,Anabolik : peningkatan sistesis
protein (terutama protein kontraktil otot),
penurunan pemecahan protein
 Fetus : diferensiasi dan perkembangan genitalia
internal & eksternal
 Pubertas :perkembangan karakteristik seks
sekunder, meliputi genitalia ekterna & interna,
laring, rambut, muskuloskeletal, kulit/gland.
sebacea, mental.
 Dewasa : untuk fungsi reproduksi.
 Lain-lain : merangsang eritropoiesis. 118
 FUNGSI ESTROGEN:
1.Perkembangan karakteristik seks
sekunder normal pada anak
perempuan menjadi dewasa,
meliputi genitalia interna ( vagina,
uterus, ovarium), dan genitalia
eksterna.rambut, kulit, distribusi lemak
tubuh (akumulasi di pinggul dan
payudara) sehingga membentuk kontur
tubuh khas perempuan.

119
2. Metabolisme:
- Antagonis paratiroid hormon
- menjaga struktur mormal kulit dan pembuluh
darah
- mengurangi motilitas saluran cerna, sehingga
meningkatkan absorbsi
- Dihati : meningkatkan sintesis protein.
3. Faktor pembeku darah : meningkatkan faktor II,
VII, IX, X. , menurunkan daya lekat trombosit.
4. Meningkatkan kadar HDL, menurunkan LDL dan
kolesterol.
5. Menimbulkan libido.

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FUNGSI PROGESTERON

1. Perkembangan gland. mamae dan

endometrium, hingga mampu sekresi.
2. Sangat penting dalam proses kehamilan ,
meliputi peningkatan metabolisme , penurunan
potensial istirahat otot terutama miometrium,
mencegah sekresi prostaglandin, menghambat
pembentukan reseptor oksitosin
3. Mengatur siklus menstruasi.

121