OBESITAS

DISLIPIDEMIA
SINDROMA METABOLIK
Mahatma
FKUMS
Presentation Point of View
 Pendahuluan
- I,4 milyard Diantara 7 milyard penduduk dunia
Obese atau over weight

- Prevalensi Obesitas di Indonesia sekitar 15 persen

- Dislipidemia terjadi pada orang Obese, Berat

Badan normal, kurus

- Sindrome metabolik adalah kumpulan gejala

Faktor resiko penyakit jantung koroner

- Sindrome metabolik meliputi , kenaikan tekanan

darah, dislipidemia, intoleransi glukosa
Metabolism of Fat
 Metabolisme
LDL HDL
Atherogenicity
small dense
LDL
Inhibits oxidation Inhibits endothelial
of LDLs HDL adhesion molecules

Inhibits Stimulates
tissue factor endothelial NO
production

Enhances reverse
cholesterol transport

Opposes atherothrombosis

Potential mechanisms by which HDLs oppose atherothrombosis.

(Barter. EMCNA (2004):398)
Presentation Point of View
 Definition
Obesity is caused by imbalance of high
Food intake and or low energy expenditure
Klasifikasi dan Patogenesa
Eropa Asia
BMI > 30 kg/m2 > 25 kg/m2
Waist ♀ > 90 ♀ > 80 cm
Circumference ♂ > 102 ♂ > 90 cm
Faktor genetik :
BMI Classification
 Gen penyebab :
- Leptin
<18.5 Underweight
- Melanocortin receptor – 4
18.5-24.9 Normal weight
- Alpha-melanocyte stimulating
25-29.9 Overweight hormone
30-34.9 Obesity Class I - Prohormone convertase – 1
35-39.9 Obesity Class II Faktor Lingkungan :
40-49.9 Obesity Class III - Nutrisional - Medikasi
> 50 Super Obesity - Aktifitas fisik - Sosial ekonomi
Mengapa Orang Jadi Gemuk ?

Makanan yang
Di konsumsi

Banyak gerak Hidup santai

25 tahun 50 tahun
 Macam Obesitas

Android/ sentral Ginekoid/ trunkal

Gemuk tidak sehat Gemuk “sehat”
“Overweight and Obesity widespread, serious
But treatable”

SURGERY BYPASS

LIPO SUCTION

LIPOTRIPSY
AKUPUNKTUR

LIPOTRIPSY
 Obat Penurun Berat Badan

10/31/2018
Surgery : - Roux-Y gastric Bypass ( RYBG )
- Laparascopy Adjustable Gastric Banding (LABG )
- Vertical Banded Gastroplasty ( VBG )

Indikasi Roux-Y
gastric Bypass :
- BMI > 40
- >35 dg 2 komorbid
- Gagal non bedah
 Complications of Obesity
Pulmonary disease
abnormal function Stroke
obstructive sleep apnea
hypoventilation syndrome
Cataracts
Non Alcoholic fatty liver disease CHD
steatosis DM
steatohepatitis Dyslipidemia
cirrhosis Hypertension
Gall stone disease
Severe pancreatitis
Gynecologic abnormalities Cancer
abnormal menses breast, uterus, cervix
infertility colon, esophagus, pancreas
PCOS Osteoarthritis kidney, prostate
Phlebitis
Gout venous stasis
Presentation Point of View
 Dislipidemia
Kelainan metabolisme lipid, ditandai
dengan peningkatan serta penurunan
fraksi lipid plasma
Normal
TRIAD LIPID
 Kol-total/ kol-LDL
Gemuk

 Trigliserid (TG)

Kurus
 Kol-HDL.
DISLIPIDEMI BISA TERJADI PADA.......
Klasifikasi Dislipidemia

- Dislipidemia primer :
Kelainan Enzym, genetik
- Dislipidemia sekunder :
Pathological states : Drugs :
- Diabetes – Oral estrogens, Progestins
- Hypothyroidism
– Anabolic steroids
- Cushing’s syndrome
– Corticosteroids
- Nephrotic syndrome
- Chronic renal failure – Retinoids, such as isotretinoin
- Monoclonal gammapathy – Sertraline hydrochloride
– ARV – protease inhibitors
Lifestyle habits :
– Non-selective -adrenergic inhibitor
- Obesity, Alcohol
– Cyclosporine, Thiazide diuretics
- Stress, Merokok
 Dyslipidemia
Major of Atherogenicity
Non modifiable risk factors : Age, gender, family
DM, Merokok Rongga Pembuluh Darah
Agregasi trombosit
LDL MONOSIT
tissue factor + PAI-1
S S S i i i i i

ENDOTEL
PLAQUE
PLAQUE
LDL
kecil

Radikal LDL ox SEL BUSA

bebas.
AGEs

INTIMA Makrofag Migrasi

Sitokin+ f. pertumbuhan Proliferasi

MEDIA
SEL OTOT POLOS
PENATALAKSANAAN DISLIPIDEMIA

Non-farmakologik :
Life style ,Terapi nutrisi, Batasi minuman beralkohol, Hindari merokok
Farmakologik : Obat hipolipidemik
1. Penghambat HMG-CoA reduktase (statin)
2. Sequestran asam empedu (resin)
3. Asam fibrat
4. Asam nikotinat (niacin)
5. Penghambat absorbsi kolesterol (ezetimibe)
6. Probucol

Obat baru :
- NIACIN extended release (NIASPAN)
- Fix kombinasi NIACIN ER + LOVASTATIN (advicor)
Obat masa depan:
- Penghambat cholesteryl ester transfer protein (CETP)--> HDL 

- Penghambat microsomal transfer protein (MTP)

- Penghambat intestinal bile-acid transporter. (IBAT)

 Terapi Farmakologi untuk koreksi profil Lipid
KELOMPOK
NAMA OBAT EFEK THD LIPOPROTEIN KONTRA INDIKASI
PREPARAT
Statin Lovastatin 10mg-20 mg LDL  18-55% Gangguan fungsi hepar
Pravastatin 10mg-20 mg HDL  5-30% akut atau kronik
Simvastatin 10mg- 20 mg Trigliserid  7-30%
Fluvastatin 20mg- 80mg
Atorvastatin 20mg- 80mg
Rosuvastatin 20mg- 40mg
Ezetimibe LDL  15-20% Bila dikombinasi dgn
HDL  1-4% statin, kontra indikasi
Trigliserid  5-10% utk ggn fungsi hepar
akut atau kronik
Bile acid Cholestyramin LDL  15-30% Disbetaliproteinemia
squestrants Colestipol HDL  3-5% Trigliserid > 400 mg/dl
Colesevalam Trigliserid sqa
Nicotinic LDL  5-25% Gangguan hepar kronik
acid HDL  15-35% gout
Trigliserid  20-50%
Fibric acid Gemfibrozil LDL  5-20% (mgk  pd Gangguan fungsi hepar
derivatives Fenofibrat kasus2 dgn trigliserid tinggi) berat
200 mg 3 x sehari HDL  10-20% Gangguan fungsi ginjal
100 mg 3 x sehari Trigliserid  20-50% berat
Intensive LDL-C Goals for High-Risk Patients
Recommended LDL-C treatment goals

2004 ATP III AHA/ACC guidelines 2006

Update 2004 Update
Update 20041 <100 mg/dL:
Goal for all
<100 mg/dL :
patients with CHD risk
Patients with <100 mg/dL
- CHD
- CHD risk <70 mg/dL:
equivalents A reasonable
(10-year risk>20%)1 goal for all patients
1% <70 mg/dL with CHD†,2
- very
decrease And
1%
high-risk patients1 Very High Risk
in LDL-C increase
Patients
reduces in HDL-C
CHD risk reduces
by 1%1 Lower LDL-C goals; wider target population CHD risk
need for more effective therapies by 3%2-5

Very high risk: established CVD plus: major risk factors

especially diabetes, poorly controlled cigarette smoking, TG
≥200 mg/dL + LDL ≥130 mg/dL with HDL-C <40 mg/dL
 Pleiotropic effects of statins
 RhoA

 TXA2  t-PA  Macrophage growth  Rac1  RhoA  ET-1

 PAI-1  AT1 receptor
 MMPS  hs-CRP
 TF  Adhesion molecules  ROS  NO

Θ Θ Θ  Θ Θ Θ Θ Θ Θ
Platelet Thrombotic Plaque Vascular SMC Endothelial SMC
Vasoconstriction
activation effect stability inflammation hypertrophy dysfunction proliferation

 Atherosclerosis  Hypertension

CVD/ CVA Θ

Takemoto MArterioscler. Thromb Vasc Biol. 2001; 21:1712-1719

Presentation Point of View
 JARANG OLAHRAGA
PENUAAN
OBAT OBATAN
SEBAB LAIN PRE SAKIT
STROKE

DIABETES MELLITUS
HIPERTENSI
Insulin resistance P C O S dan NAFLD
HIPERURICEMIA
DISLIPIDEMIA
- Glycemic disorders ATHEROSCLEROSIS
( Prediabetes ) ACANTHOSIS NIGRICANS
- << HDL , >> LDL
- Hypertriglyceridemia
- Hypertension
- Endothel Disfunction
- Hiperuricemia
- Microalbuminuria
CHD
- Inflammation (hsCRP)
- Impaired thrombolysis
-  PAI-1

Central Obesity
ATHEROSCLEROSIS +++
 Autocrine
Endocrine
Paracrine

PAI-1 Leptin

TGF-β ?TNFα
?IL-6
TF
Adipsin/ASP Sex steroids
Glucocorticoids
?TNF-α /IL-6/Leptin
?Angiotensin
Renin-Angiotensin
system ?PAI-1

Steroid hormones ?Adiponectin

Adipose tissue
?AdipoQ

1. ESTROGEN  and PAI-1

CARDIO
Factors FFA, TNF 16. VISFATIN
can 31. RBPtissues
affect peripheral
PROTECTIVE 17. HSL 32. APO-E
2. Adiponectin 18. LIPOTRANSIN 33. ICAL
3. AGOUTI RELATED PROTEIN 19. PERILIPINS 34. LPL

Resistensi Insulin

Resistensi Insulin
TNF α FFAs CETP

Aterosklerosis
4. 20. 35.

Aterosklerosis
5. IL1B 21. TGF-β 36. PLTP
Resistensi Insulin

6. IL-6 22. VEGF 37. NO

Aterosklerosis

7. ANGITENSINOGEN 23. IGF-1 38. PC-1

8. ASP 24. PGE2 39. AQUAPORINS
9. ADIPSIN 25. PGI1 40. FIAF
10. FACTORS B,C3 26. GLUCOCORTICOID 41. LACTATE
11. ADHESIVE PROTEIN 27. 11βHSD 42. MONOBUTYRIN
12. PAI-1 28. AROMATASE 43. GALACTIN-12
13. TF 29. METALLOTHIONIEN 44. ESM-1
14. RESISTIN 30. MIF 45. APELIN
15. Leptin
 Components of Metabolic Syndrome
ATP III that related to CVD (2006)
1. Abdominal obesity
( Waist circumference :
♂ ≥ 90 Cm / ♀ ≥ 80 Cm )
♂ ≥ 102 Cm / ♀ ≥ 88 Cm )

2. Atherogenic dyslipidemia
HDL-Chol.( ♂ < 40 / ♀ < 50 mg/dl )
TRIGLYCERIDE ( > 150 mg/dl)

? 3. Raised blood pressure

130- 140 mmHg / 85 - 90 mmHg

4. Glucose intolerance
Fasting blood sugar 100 mg/dl – 126 mg/dl

5. Proinflammatory state
(Elevated of CRP)

6. Prothrombotic state
Central Obesity (Elevated of PAI-1)
Adipose tissue in Central Obese

ADIPOCYTE
WEIGHT GAIN WEIGHT GAIN
IR

JNK
NFB
TNF-
Leptin
VEGF
Endothelial IL-6
Cell IL-1
Angiogenesis
TNF-
Physical stress/oxidative
damage to endothelium?
MCP-1
PREADIPOCYTE
FFA MCP-1
MACROPHAGE
RECRUITMENT
MACROPHAGE – PREADIPOCYTE MACROPHAGE
RECRUITMENT

NORMAL ADIPOCYTE ADIPOCYTE DYSFUNCTION

ASK-DNC INFLAMED ADIPOSE TISSUE
Cardiometabolic Risk (CMR)
Definitions of the metabolic syndrome
(Bloomgarden 2004, 1st Conggress on Insulin Resistance Syndrome)

ATP III WHO AACE (IRS) EGIR (IRS)

IGT/HOMA-IR, One of ** Fasting hyperin-
IFG/DM and sulinemia( highest
2 of 4 below quartile) and
At least 3 of 5 And 2 of 4 2 of 4
Uirinary alb exc > 20 g / m
WHR male 90 in men
female 85 in women
Waist CF male >102 cm  94 cm
female > 88 cm  80 cm
Triglycerides  150 mg/dl 150 mg/dl or 150 mg/dl or 2.0 mmol/l or
HDL chol male 40 mg/dl 35 mg/dl 40 mg/dl  1.0 mmol/l
female 50 mg/dl 39 mg/dl 50 mg/dl
Blood pressure 130/8 5mmHg  140/90 mmHg 130/85 mmHg 140/90 mmHg or
treated for Hyp.
Blood glucose  110 mg/dl FBG 110-125 or FPG 6,1 mmol/l
2hpc 140-200 (exc.DM)

** CVD, hypertension, PCOS, NAFLD, family history of T2DM / hypertension / CVD, history of

Classification for Metabolic Syndrome

gestational diabetes, non Caucasian, sedentary lifestyle, BMI>125 or WC>40 male, >35 female,
age>40yrs
 Indonesian classification for Metabolic Syndrome
WC ( male ≥90cm / female ≥80 cm)
plus
2 of the 4 factors

1. Fasting Glucose 3. Triglyceride

100 mg/dl – 126 mg/dl > 150 mg/dl

4. HDL-Chol
2. Blood Pressure
male < 40 mg/dl
> 130/85 mmHg female< 50 mg/dl

WC
male ≥ 90 cm
female ≥80 cm
Lose weight Losing as little as 5 to 10% of your body weight can reduce insulin levels thus reducing M S
Exercise Walking just 30 minutes a day can help prevent the serious diseases associated with MS.
Stop smoking Cigarettes increases insulin resistance and worsens health consequences with MS.
Eat fiber Whole grains, beans, fruits and vegetables, important to lower insulin levels.

Weight loss Sibutramine (Meridia) and Orlistat (Xenical).

drugs
Insulin
sensitizers Thiazolidinediones and Metformin

Aspirin Aspirin is often prescribed to help reduce the risk for a heart attack.
Medications to
Major types of medications angiotensin-converting enzymes (ACE)
lower blood
pressure inhibitors, calcium channel blockers and beta blockers.
Medications to
regulate
statins ( Pleitropic effect )
cholesterol
 Metformin
Improved Reduced
Insulin sensitivity Hypertriglyceridaemia
Fibrinolysis AGE formation
Nutritive capillary flow Cross-linked fibrin
Haemorrheology Neovascularisation
Post ischaemic flow Oxidative stress

Reduced cardiovascular risk

Vascular benefits of metformin
Presentation Point of View
 Definisi Dx Terapi Komplikasi
Exercise - Cancer, C H D
Akumulasi FAT Diet - Hipertensi, S N H
di Orlistat - Dislipidemia
O B E S ITAS
Obesitas Jaringan Lemak BMI Sibutramine - OsteoArthritis
berlebihan, baik - D M, PCOS
Besar dan Akupunktur
Lipotripsy - Sleep Apneu
jumlahnya
Liposuction - Obesity H S
Surgery - Gout, Gallstone

Exercise
TG - Aterosklerosis
DISLIPIDEMI
Kelainan Diet
Dislipidemia Metabolisme C H -CHD
LDL Statin
LIPID -SNH
HDL Fibrat

WC -CHD
CH Exercise - Hipertensi
KUMPULAN GEJALA
LDL - Dislipidemia
SINDROMA YANG DISEBABKAN Diet -DM
OLEH KARENA HDL
Sindrom Metabolik RESISTENSI INSULIN. Metformin -SNH
METABOLIK DAN........... TG
( Pre Sakit ) RESISTENSI INSULIN
KARENA AU Glitazone - PCOS, Gout
- Gallstone
( pre sakit ) OBESITAS SENTRAL GDP Statin - NAFL
Alb - Acanthosis
Tensi nigricans
Closing Remark

Exercise

Diet

Orlistat

Sibutramine

Statin

Metformin The NEJM, Vol. 342 : 145-153, Jan

2000
41
 _
PENGERTIAN HORMON
Berasal dari bahasaYunani

“Hormaen”
Menggerakan

Organ yang berperan dalam sekresi hormon

Kelenjar
endokrin /
kelenjar buntu

“Hormon adalah zat kimia dalam bentuk senyawa

organik yang dihasilkan oleh kelenjar endokrin”
 Definisi
• Apa yang disebut hormon?
Hormon merupakan zat kimiawi organik
dihasilkan oleh sel endokrin yang bertindak
sebagai pembawa pesan kimiawi dan dialirkan
kedalam darah. Hormon mengatur,
mengintegrasi dan mengendalikan fungsi
fisiologik

Silverthorn, Human Physiology, 3rd

edition Figure 6-1&2
 FUNGSI HORMON
Mengatur aktifitas :
Perkembangan
Pertumbuhan

Reproduksi

Metabolisme
TARGET HORMON
Sistem Endokrin dan Sistem Syaraf
Sistem Endokrin
Komunikasi: pembawa pesan
kimiawi atau hormon
Transmisi: melalui aliran darah
Target organ menerima pesan
Transmisi: relatif lambat
Efek: tersebar luas
Respon: lambat
Respon berjangka panjang
Efek: permanen & irreversible
Sistem Syaraf
Komunikasi: melalui impuls
syaraf
Transmisi: melalui serabut syaraf
Efektor menerima pesan
Transmisi: sangat cepat
Efek: stempat
Respon: cepat
Respon berjangka pendek
Efek: temporer dan reversible
 I

II

CalcItrIol
CALCITRIOL 48
III PTH
KELENJAR HIPOTALAMUS
•Terletak dibawah otak besar
•Berperan dalam koordinasi sistem saraf
dan sistem endokrin tubuh
•Hipotalamus menghasilkan beberapa jenis
hormon yang disekresikan langsung ke
hipofisis.
 GnRF (Gonadotropin Releasing Factor)
 CrF (Corticotropin releasing Factor)
 TrF (Tirotropin Releasing Factor)

Beberapa jenis hormon yang disekresikan oleh hipofisis,

dihasilkan oleh sel-sel hipotalamus :
 ADH
 TSH
 Oksitosin
 KELENJAR HIPOFISIS
Kelenjar hipofisis atau pituitari adalah kelenjar yang
paling banyak menghasilkan hormon
Letaknya ada didasar otak (dibawah hipotalamus)

Kelenjar
intermediet
hipofisi

Kelenjar posterior hipofisis

Kelenjar anterior hipofisis

KELENJAR ANTERIOR Hormon prolaktin
HIPOFISIS
Hormon Somatotrof

Hormon Tiroid

Luiteinizing hormon

Folicle Stimulating

hormon Hormon

Adrenokortikotropik
KELENJAR POSTERIOR
HIPOFISIS Hormon
Oksitosin

Hormon
ADH
KELENJAR INTERMEDIET
HIPOFISIS
Melanocyte
2 Stimulating
1 Hormone
(MSH)
 KELENJAR TIROID
Merupakan kelenjar yang terdiri dari
folikel-folikel dan terdapat di depan
trakea

Hormon yang dihasilkan:

Hormon Tiroksin
Hormon Triodontironin
Hormon Kalsitonin
KELENJAR PARATIROID

Merupakan kelenjar hasil penimbunan

hormon somatotrof atau hormon
pertumbuhan.

Hormon yang dihasilkan:

 Hormon Parathormon
 Homeostasis calcium dan pembentukan Tulang

Bone Resorption : Osteoclast Bone formation : osteoblast.

-Paratiroid hormon
Calcium -Estrogen -Estrogen
-Steroid
-I G F I -Calcitriol
-Tiroid Hormon
-Calcitonin
-Insulin,growth hormon

Calcitriol

Catatan :Bone Remodelling Adalah bone formation dan bone Absorption. 57

Bone Turn Over Adalah kecepatan Bone formation dan Bone Absorption
 Mekanisme Osteodistrofi Ginjal

Penyakit Ginjal
Penurunan fungsi ginjal Gangguan metabolisme
Ekskresi PO4  1.25(OH)2 cholecalciferol

Kadar PO4  Absorsi Ca dari usus 

Kadar Ca 
Rangsangan
menyebabkan
pembesaran
kel.paratiroid
Resorbsi tulang  ,
mekanisme
 PTH meningkatkan kadar
Ca++
KELENJAR PANKREAS

Merupakan sekelompok sel yang terletak pada

pankreas, sehingga dikenal dengan pulau –
pulau Langerhans.

Hormon yang dihasilkan:

Hormon Insulin
Hormon Glukogen
HORMON GINJAL & ADRENAL

Terdiri atas dua jaringan aktif penghasil

hormon yang secara struktur dan
fungsinya berbeda, yaitu:

– adrenal korteks
– adrenal medulla.
Erythropoetin
 Erythropoetin Pada Gagal Ginjal Kronis
GAGAL GINJAL Kekurangan
Uremia
KRONIS Masa Ginjal

Osteodistrofi
Ginjal
Inhibitor Kecenderungan
Eritropoiesis
KEHILANGAN DARAH Berdarah

Fibrosis  Disfungsi trombosit

sum-sum tulang Eritropoietin   Prosedur hemodialisis

(Berbagai Colony-forming units

“Stem cell”  Tahap) Erythroid (CFU-E)

Malnutrisi
Hemolisis
Keracunan Al,
Def. B12
Def asam folat Eritrosit 
PTH 
PERDARAHAN KRONIS  DEFISIENSI Fe
Kehilangan Fe : 2 mg/hari, kebutuhan : 375-750 mg
 KELENJAR ADRENAL
KORTEKS

menghasilkan hormon :

1. mineralocoticoids, contoh: aldosteron, fungsi:

mempertahankan kesetimbangan kadar Na dan K.
Dengan cara meningkatkan kadar Na dan air darah
dan menurunkan kadar K dlm darah.DIABETES
INSIPIDUS
2. Glukocorticoids, contoh: khususnya cortisol.
Fungsi: regulasi metabolisme glukosa dan molekul
organic lainnya, resistensi terhadap stress dan
counter respon inflamasi.ADISSON DAN CUSHING
SYNDROME
3. Gonadocorticoids: menghasilkan sex steroid
(androgen) dalam jumlah yang tidak signifnifikan.
 Stabilitas
vaskular
Menghambat
Akumulasi
lekosit
Imunoglobulin
Menghambat & komplemen
Fungsi
lekosit ANTI Lekositopeni
INFLAMASI & monositopeni
Monositopeni
& eosinopeni
Imuno Menekan
Menekan histamin Fungsi
Supresif Limfosit
Mediated Reaction
& monosit
Komponen
komplemen
Menghambat
Kompleks Imun
Melewati
Membrana basalis
 KELENJAR ADRENAL
MEDULA

 Menghasilkan hormon epinephrine dan norepinephrine.

 Hormon epinephrine dan norepinephrine distimulasi langsung oleh saraf

simphatetik.

 Produksi meningkat pada saat terjadi stress dengan cara:

1. meningkatkan debar jantung
2. kontriksi pembuluh darah pada kulit
3. Kontraksi lympha (spleen)
4. Merubah glikogen menjadi glukosa.
5. menurunkan produksi enzim pada organ pencernaan
6. Berkeringat

FEOCHROMOSITOMA
CUSHING SYNDROME
 Kegawatan adrenal
Penyakit Addison
Akut : muntah, shock, dehidrasi, hipotensi berat.

Kronik : Signs and symptoms Percent

Weakness and fatigability 74-100
Weight loss 56-100
Hyperpigmentation 92- 96
Hypotension 59-88
Hyponatremia 88-96
Hyperkalemia 52-64
Gastrointestinal symptoms 56
Postural dizziness 12
Adrenal calcification 9-33
Hypercalcemia 6-41
Muscle and joint pains 6
Vitiligo 4
Insuff. Kronik

Krisis ADRENAL

Infeksi akut & berat Trauma

Perdarahan

• Panas 
• Kesadaran   (koma)
• Gelisah Substitusi  Cortisol injeksi  drip
• Kolaps sirkulasi
• Kejang-kejang Shock  Infus cairan + elektrolit

Infeksi  injeksi antibiotika

TERAPI
Hipoglikemia  Inj. Glucose  drip
Frequency of sign and symptoms in adrenal insufficiency

SIGN PERCENT
or SYMPTOM of PATIENTS
Weakness 99

Pigmentation of skin 98

Weight loss 97

Anorexia, nausea, vomiting 90

Hypotension (< 110/70) 87

Pigmentation of mocus membranes 82

Abdominal pain 34

Salt craving 22

Diarrhea 20

Constipation 19

Syncope 16

Vitiligo 9
 Laboratory
 No demonstrable
 Early phase abnormalities
 Adrenal reserve   Basal
steroid output
maybe normal

 Subnormal increase
after stress
 More advanced SERUM
 Sodium  Subnormal increase
 Chloride after ACTH stimulation
 Bicarbonate
 Normocytic  Potassium
anemia

 Relative
lymphocytosis

 Moderate
eosinophylia
Steroid therapy schedule
for adrenal with adrenal insufficiency undergoing surgery

Hydrocortisone
Hydrocortisone Fludrocortisone
Infusion, continous,
(orally) (orally)
mg/h
8 a.m 4 p.m 8 a.m
Routine daily medication 20 10 0.1
Day before operation 20 10 0.1
Day of operation 10
Day 1 5 – 7.5
Day 2 2.5 – 5
Day 3 2.5 – 5 40 20 0.1
Day 4 2.5 – 5 40 20 0.1
Day 5 40 20 0.1
Day 6 20 20 0.1
Day 7 20 10 0.1

All steroid doses are given in milligram. An alternative approach is give 100 mg hydrocortisone as
an intravenous bolus injection every 8 h on the day of the operation
PHEOCHROMOCYTOMA

Prepared by: Roxanne Mae E. Birador S.N.

 phaios "dark“
PHEOCHROMOCYTOMA
A neuroendocrine tumor of chroma "color“
the medulla of the adrenal
glands (originating in the chromaffin
cells) and secretes high amounts kyto s "cell“
of catecholamines, mostly epinephrine,
plus norepinephrine to a lesser extent.
-oma "tumor“
 "Five Hs"
Hypertension
Headache
Hyperhidrosis
Hypermetabolis
m
Hyperglycemia
Skin sensations
Flank pain Elevated heart rate Palpitations
Anxiety often resembling that of a panic
attack Weight loss
 The diagnosis can be established by measuring
catecholamines and metanephrines in plasma (blood) or
through a 24-hour urine collection

Laboratory tests (Blood Test)

One diagnostic test used in the past for

a pheochromocytoma is to administer clonidine,
a centrally-acting alpha-2 agonist used to treat high
blood pressure. Clonidine mimics catecholamines in the
brain, causing it to reduce the activity of the
sympathetic nerves controlling the adrenal medulla. A
healthy adrenal medulla will respond to the clonidine
suppression test by reducing catecholamine
production; the lack of a response is
evidence of pheochromocytoma.
KELENJAR KELAMIN

Terbagi atas dua kelenjar, yaitu:

– Kelenjar ovarium
– Kelenjar testis
 KELENJAR OVARIUM

 Menghasilkan Hormon estrogen, progesteron, relaxin dan inhibin.

 Estrogen dan progesteron berfungsi: membangun dan mempertahankan
karakteristik kelamin wanita: siklus mentruasi, kehamilan dan
perkembangan kelenjar mamae.

 Relaxin: membantu dilatasi uterus pada akhir kehamilan.

 Inhibin: Menghambat sekresi FSH pada akhir siklus menstruasi.

 Homeostasis
Patofisiologi Patofisiologi
calcium
osteoporosis post osteoporosis
dan pembentukan
menopause/ Post
Tulang
Primer tipe I

Bone Resorption : Osteoclast

-Paratiroid hormon Bone formation : osteoblast.
Calcium -Estrogen : R e ndah -Estrogen :R endah
-Steroid
-I G F I
-Tiroid Hormon
-Calcitriol
-Calcitonin
-Insulin,growth hormon

CALCITRIOL

78
 Normal Osteoporosis

Pada thn awal menopause kehilangan massa tulang

dapat mencapai 15% dari
MASSA PUNCAK TULANG
dan pada
10 thn sampai 15 thn post menopause dapat mencapai
30-40%
79