Analisis Klinis

Diabetes Melitus,
Sindrom Cushing, dan
Pheochromocytoma

Diabetes Melitus
Penyakit sindrom metabolik, dengan
karakteristik hiperglikemia kronis yang
diakibatkan oleh gangguan sekresi
insulin dari sel pankreas
dan atau gangguan aksi insulin sehingga
glukosa darah menjadi tidak dapat
ditransfer masuk ke dalam jaringan
melalui pentransfernya yaitu GLUT
(glukosa transporter)

Hormon-hormon terlibat dalam

metabolisme glukosa
Hormon
Insulin
Insulin
Increase
Glukagon
(table)

Principal actions

Cellular glucose uptake

Glycogen synthesis
Fatty acid and
triglyceride synthesis
Decrease Gluconeogenesis
Glycogenolysis
Lipolysis

Glucago Increase
n
M : Otot
L : Liver
A : Adiposa

Gluconeogenesis
Glycogenolysis
Lipolysis

M,A
L,M
L,A
L
L,M
A
L
L
A

Tipe Diabetes Melitus

Diabetes Melitus Tipe 1
Diabetes Melitus Tipe 2
Diabetes Melitus Gestasional

Diabetes Melitus Tipe 1

Etiologi
Destruksi sel pankreas akibat
otoimun
Idiopatik

Diabetes Melitus 2
Etiologi
Aging
Obesitas
life style

Resistensi

Diabetes Melitus
Gestational
Etiologi :
Hormon-hormon pada saat kehamilan
Human placental lactogen(hPL) atau
human chorionic
somatomammotropin(HCS)
Progesteron

HPL

Progesteron

Sensitivitas
insulin
Glukosa
darah

Keadaan Normal

Sel
Makanan
Insulin

Glikogen
Pembuluh darah

Glukosa

Jaringan adiposa

Jaringan otot

Keadaan Normal
Glukosa

Glikogenolisis

+
Glukagon

+
hepar

Jar. adiposa

Glukoneogenesis
Glukosa

otot

Glikogen glukosa

Glukosa

Patofisiologi DM tipe 2

DIABETES MELLITUS
Laboratory Test (marker)
HbA1C
Fasting Plasma Glucose Level (FPG)
2-hour Plasma Glucose Level
Random Plasma Glucose

HbA1c
Hemoglobin

Glukosa

HbA1C
Glikosilasi
2-3 bulan

Keadaan
puasa
Normal
+

Sel

Glukosa
glikogenolisis

+
+
Glukagon

glukoneogenesis

+
glukoneogenesis

Keadaan
puasa

Sel

glikogen

+
+
Insulin

Glukosa
Glukosa
normal

Keadaan
puasa
DM
+

Sel

Glukosa
glikogenolisis

+
+
Glukagon

glukoneogenesis

+
glukoneogenesis

Keadaan
puasa pd DM

Glukosa
Glukosa
glikogen

Insulin

2H PLASMA GLUCOSE
LEVEL
Makanan

Setelah 2 jam
DIABETES MELLITUS

Glukosa

Hasil Interpretasi
Marker

Clinically Significant Interpretas

Level
i

FPG
2h OGTT (75g)
RPG
HbA1c level

126 mg/dL
200 mg/dL
200 mg/dL
6,5%

Diabetes

FPG
2h OGTT (75g)
RPG
HbA1c level

100-125 mg/dL
140-199 mg/dL
180-199mg/dL
5,7%-6,4%

Increased
risk for
diabetes

Marker

Clinically
Significant
Level

Interpretasi

FPG
1h
2h

92 mg/dL
180 mg/dL
153 mg/dL

Gestational
diabetes

FPG
2h OGTT (75g)
RPG
HbA1c level

100 mg/dL
140 mg/dL
140mg/dL
5.7%

Keadaan normal

(COOPERATIVE, DIABETES, 1

Sindrom Cushing

Corte
x

Hipersekresi Cortisol

Tumor
Pituitari

Ectopic
ACTH

Tumor
Adrenal

Pengaruh
Obat
Golongan
Kortikosteroid

Hormon (cont.)
Hormon
Cortisol

M : Otot
L : Liver
A : Adiposa
T : Tissues

Principal actions
Increase

Gluconeogenesis
Proteolysis

L
M

Decrease

Tissue glucose
utilization
Antagonist Insulin

L,M,A
T

Keadaan normal
CRH
CRH
CRH

Hipotalamus
Hipofisis
ACTH ACTH
ACTHACTH
ACTH

Cortiso
Cortiso
Cortiso
l
l
l
Korteks Adrenal

Hiperglikemia pada
Sindrom Cushing
Glukoneogenesis
Corte
x

Antagonis insulin

Cortisol
Glukosa
Hiperglikemia

MARKER SINDROM CUSHING

Urinary Free Cortisol Level

Low-dose Dexamethasone
Suppresion Test
Evening Serum and Salivary
Cortisol Level

Urinary Free Cortisol Level

Cortisol

Urinary Free Cortisol

Protein Plasma
Transcortin

Urinary Free Cortisol Level

Normal

<50g/hari

Cushing syndrome

>250g/hari

Low Dose Dexamethasone

CRH
CRH
CRH

1mg
Dexamethasone
Cortisol
exogenus

Negative
feedback
Cortisol
Cortisol

Hipofisis
ACTH

Hipotalamus

ACTH

ACTH
ACTH
ACTH

Cortiso
l
Korteks Adrenal

Low dose Dexamethasone

Normal : < 50 nmol/L (1,8g/dL)
SC
: > 280nmol/L (10 g/dL)

References :
Gilbert, R., & Lim, E. (2008). An Endocrine Society Clinical
Practice Guideline. The Diagnosis of Cushings Syndrome .
McPhee, S. (2006). Disorder of The Adrenal Cortex. In S.
McPhee, & W. Ganong, Pathophysiology of Diseaase: An
Introduction Clinical Medicine (p. 607). The McGraw-Hill
Companies.

Evening Salivary Cortisol Level

Kadar Cortisol dalam Saliva
Normal: 4nmol/L
SC : >4nmol/L

References :
Newell, J. (2009). Diagonosis/ Diferential Diagnosis of Cushing
Syndrome: A Review of Best Practice.

Evening Serum Cortisol Level

Kadar Cortisol dalam Darah
Normal :
8A.M. 5-23 g/dL (138-635 nmol/L)
4P.M. 3-13 g/dL (83-359 nmol/L)
SC
: >13 g/dL (359 nmol/L)

References :
Pagana, K., & Pagana, T. (2006). Manual of Diagnostic and
Laboratory Test Third Edition. Mosby Elesevier.

Pheochromocytoma

Tumor pada Sel

Chromaffin
Hipersekresi
katekolamin
Epinephrine

Norepinephrine

Hormon (cont.)
Hormon
Adrenalin

Principal actions
Increase

Glycogenolysis
Lipolysis

L,M
A

Katekolamin

Reseptor 2
sel B

Rilis insulin

Katekolamin

Reseptor 2
sel B

+
Glikogenolisis
Di hepar & otot

Marker Pheochromocytoma
Methanephrine and
Normethanephrine Test
Catecholamine Test
Vanilylmandelic acid(VMA)

Hasil Interpretasi (urine)

Parameter

Normal

VMA

<6,8 mg/24j
(<35 mol/24j)

Metanefrin

<1,3 mg/24j
(<7 mol/24j)

Normetanefrin

15-80 g/24j
(89-473 nmol/24j)

Epinefrin

<20 g/24j
(<109 nmol/24j)

Norepinefrin

<100 g/24j
(<590 nmol/24j)

References : Pagana, K., & Pagana, T. (2006). Manual of Diagnostic and

Laboratory Test Third Edition. Mosby Elesevier.

Hasil intepretasi pada penderita pheochromocytoma

diatas batas normal.

References :
Gilbert, R., & Lim, E. (2008). An Endocrine Society
Clinical Practice Guideline. The Diagnosis of
Cushings Syndrome .
McPhee, S. (2006). Disorder of The Adrenal Cortex.
In S. McPhee, & W. Ganong, Pathophysiology of
Diseaase: An Introduction Clinical Medicine (p.
607). The McGraw-Hill Companies.
Pagana, K., & Pagana, T. (2006). Manual of
Diagnostic and Laboratory Test Third Edition.
Mosby Elesevier.
Newell, J. (2009). Diagonosis/ Diferential Diagnosis
of Cushing Syndrome: A Review of Best Practice.
Cooperative, G. H. (1996-2013). Diabetes. Type 2

Eisenhofer, Graeme, et al. 1998. Plasma

Metanephrines are
Markers of Pheochromocytoma Produced by
Cathecol-OMethyltrasferase within Tumors. USA: Journal of
Clinical
Endocrinology and Metabolism.
Ozougwu, J. C., et al. 2013. The Pathogenesis and
Patophysiology of Type 1and Type 2 Diabetes
Mellitus. Nigeria:
Academic Journals.
Pivonello, Rosario, et al. 2010. Patophysiology of
Diabetes
Mellitus in Cushings Syndrome. Italy:
Neuroendocrinology.

Frederic Castinetti, I. M.-D. (2012). disease.

Castinetti et al.
Orphanet Journal of Rare Diseases , 1-12.
Mesut Ozkaya, M. F. (2008). Incidental
pheochromocytoma
presenting with sublaboratory. BioMed Central ,
1-10.
Miriam Cnop, N. W.-C. (2005). Mechanisms of
Pancreatic-Cell
Death in Type 1 and. American Diabetes
Association. , s97s107.
NIELSEN, L. R. (2004). HbA1c Levels Are
Significantly Lower in
Early and Late Pregnancy. Diabetes Care ,

American Association of Clinical Endocrinologists. (2009).

AACE/AAES Adrenal Incidentaloma Guidelines .
American Diabetes Association. (2014). Standarts Of Medical
Care in Diabetes.
BOGDAN CATARGI, V. R.-C. (2003). The Journal of Clinical
Endocrinology & Metabolism. Occult Cushings Syndrome
in
Type-2 Diabetes .
Lynnette K. Nieman, B. M.-P. (2008). The Diagnosis of
Cushing's
Syndrome. An Endocrine Society Clinical Practice Guidline
.

Thankyou