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CHILDREN
A S R I P U R WA N T I
DIVISION OF ENDOCRINOLOGY
D E PA R T M E N T O F P E D I AT R I C
DIPONEGORO UNIVERSITY
D R . K A R I A D I H O S P I TA L
SEMARANG
CURRICULLUM VITAE
Nama Lengkap
Tempat/TanggalLahir
S1
Sp.1
S2
Sp.2
S3
1
2
3
4
Yogyakarta, 06-11-1955
RIWAYAT PENDIDIKAN
FK Universitas Diponegoro (S1)
Spesialis Anak FK UNDIP
Magister Bimbingan Konseling Universitas Negeri Semarang
Kolegium Kesehatan Anak Indonesia /
Pediatric Endocrinologi Konsultan (Sp2)
S3 univesitas Negeri Semarang
1982 Kedokteran
1994 Ilmu Kesehatan Anak
2002
2007
SpA(K)
2014 DR
Pendidikan Lanjutan Klinik di Klinik Tumbuh Kembang Khusus dan Genetika 1995
Klinis (dismorfologi) RSAB Harapan Kita Tempat di Jakarta
Kursus Genetika Klinis NUH Singapore Tempat di Singapore
1996
Orientasi di Sub Bidang Endokrinologi Anak FKUI Tempat di Jakarta
2005
Fellowship APPES Pediatric Endocrinologi Tempat di Wuhan, Cina
2005
No
Dari
1 Mendiknas
2 Presiden RI
3 Presiden RI
Penghargaan
Mahasiswa Teladan Universitas Diponegoro
Satya Lencana KARYA SATYA 20 tahun
Satya Lencana KARYA SATYA 30 tahun
Tahun
1981
2004
2013
CURRICULLUM VITAE
Tahun
2 Januari 1996
1996- Sekarang
2008- Sekarang
2008 - sekarang
2005- sekarang
2005 - sekarang
2002- Sekarang
1996-1999
1999-2002
2002-sekarang
1998-2001
2002- sekarang
2008-sekarang
2009-sekarang
2008-sekarang
1997-sekarang
1997-sekarang
2008-sekarang
Riwayat Pekerjaan
Dokter Spesialis Anak di RS dr. Kariadi
SK Pengajar Luar Biasa FK UNDIP di Bagian Ilmu Kesehatan Anak
SK Pengajar S2 Biomedik FK UNDIP
SK pengajar S2 Genetik Konseling / Biomedik
SK Pengajar SP.1 PPDS.1.Kesehatan Anak. FK UNDIP RSDK
SK pengajar S2 (MKIA) Magister Kesehatan Ibu dan Anak UNDIP
Ketua POKJA KIPI JATENG
Sekretaris IDAI JATENG
Wakil ketua IDAI JATENG
Anggota IDAI JATENG
Seksi Organisasi IDI cab Semarang
Anggota Satgas Imunisasi Nasional
Anggota MKEK IDI Jateng
Sekertaris SMF Bagian Anak FK UNDIP / RSUP. Dr Kariadi
SEmarang
Tim GAKI FK UNDIP
Tim Pelayanan Genetik RS Kariadi FK UNDIP
Tim DSD (Disosder of sexual Development)/
Tim Penyesuaian Kelamin RS Kariadi FK UNDIP
Tim Stem cell RS Kariadi FK UNDIP
OUTLINE PRESENTATION
Epidemiology
Classification
Diagnosis
Etiology
Patogenesis
Clinical Manifestation
Complication
EPIDEMIOLOGY
In 2007, the total child population of the world
(014 yr) was estimated to be 1.8 billion, of whom
0.02% had diabetes. (ISPAD 2014)
Every years the type 1 DM occurs in 80 000
children (Craig et al. 2014)
Every year increasing type 1 DM in adults in 3%
and in 4.8% in children (EURODIAB)
Type 2 DM is becoming higher prevalence In
geographical areas where T1DM occurs with
Lower incidence, there is a higher rate of diabetic
ketoacidosis (DKA)
ETIOLOGIC CLASSIFICATION
I. Type 1 diabetes
(b-cell destruction, usually leading to absolute insulin deficiency)
A. Immune mediated
B. Idiopathic
DIAGNOSIS OF DIABETES
Diabetes in children --. Most characteristic symptoms
polyuria, polydipsia, blurring of vision, and weight loss, in
association with glycosuria and ketonuria.
most severe form, ketoacidosis, or rarely a non-ketotic
hyperosmolar state, stupor, coma, death.
hyperglycaemia incidentally-or under conditions of acute
infective, traumatic, circulatory, or other stress may be
transitory and should not in itself be regarded as diagnostic
of diabetes.
A1C 5.76.4%
*For all three tests, risk is continuous, extending below the lower
limit of a range and becoming disproportionately greater at higher
ends of the range.
ADA. 2. Classification and Diagnosis. Diabetes Care
2015;38(suppl 1):S10; Table 2.3
GENETICS:
Several alleles of HLA-DQB1 are
associated with an increased risk of
developing type 1 diabetes.
The locus also has the genetic name IDDM1
as it is the highest genetic risk for type 1
diabetes.
The strongest gene, IDDM1, is located in
the HLA Class II region on chromosome
6, at staining region 6p21.
Certain variants of this gene increase the
risk for decreased histocompatibility
characteristic of type 1.
Such variants include DRB1 0401, DRB1
0402 etc.
Race.
White people have a
greater risk for
developing type 1
diabetes than black,
Asian, or Hispanic
people.
PRECLINICAL DIABETES
Preclinical diabetes (stages 13) refers to the months
or years preceding the clinical presentation of type
1 diabetes when islet antibodies can be detected as
markers of -cell autoimmunity :
Exercise
Metabolic
control
Education
Diet
GOAL OF TREATMENT
Optimal metabolic control
Optimal growth and development
Prevent short and long term complication
Normal physchosocial function
Self management depends on their development
24
Intermediate-acting insulin
Long-acting insulin
Appearance
Onset (hr)
Peak (hr)
Duration (hr)
Insulin lispro
Clear
0.2-0.3
1-1.5
3-5
Insulin aspart
Clear
0.2-0.3
1-1.5
3-5
Insulin glulisin
Clear
0.2-0.4
1-2
3-5
Clear
0.5-1
2-3
6-8
Cloudy
1-2
8-10
20-24
NPH or isophane
Insulin
Cloudy
1-2
8-10
20-24
Clear
Glargine: 2-4
Detemir: 1-4
RAPID ACTING
SHORT ACTING
Regular (soluble)
insulin
INTERMEDIATE
ACTING
LONG ACTING
Insulin glargine and
Insulin detemir
_
_
Glargine: 24
Detemir: 20-24
6 8
10 12
Hours
14
16
18
20 22 24
27
INSULIN REGIMEN
MDI (multiple daily injection) Basal Bolus
CSII ( continouos subcutaneous insulin
infusion) Pump insulin
Premixed Insulin
1. INSULIN
Type of Insulin
Dose of insulin : Total daily dose in children at initial
treatment approximately 0,5-1unit/kg
Regimen of insulin
Injection site
INJECTION SITE
MONITORING
Metabolic
target
Preprandial
Postpandrial
Urine
reduction
HbA1c
Very good
Good
Moderate
Poor
< 120
mg/dl
< 140
< 140
< 180
>180
< 200
< 240
>240
+-
>+
<7%
7 -7,9
%
8-9%
>10%
2. TARGET METABOLIK
Age
Target A1C
<8.0%
6 to 12 years of age
7.5%
Adolescents
7.0%
Lipohypertrophy
Obesity
Insulin allergy
Insulin antibodies
Insulin induced edema
MONITORING KOMPLIKASI
3. NUTRITION
4. EXERCISE
Tailor insulin regimen to activity
Discuss the percentage reductions in insulin
before exercise
Any exercise is dangerous and should be
avoided if pre-exercise blood glucose levels
are high (> 14 mmol/L, 250 mg/dL)
with ketonuria / ketonemia (> 0.5 mmol/L).
EDUCATION
At the diagnosis : overview diabeter for family
Including :
- hyperglycaemia, hypoglycaemia
- the dos and donts life with diabetes
SELF-CARE
Patients should be educated to practice self-care. This allows the
patient to assume responsibility and control of his / her own
diabetes management. Self-care should include:
FUTURE PROMISES
Proportion (%)
Asymptomatic
35%
Acanthosis nigricans
73%
Obesity
95%
Ketosis
44%
Diabetic ketoacidosis
10%
PCOS
12.1%
Dyslipidemia
44.8%
Hypertension
28.3%
22.2%
Micro-/macroalbuminuria
14.2%
GOAL OF MANAGEMENT T2 DM
Education for diabetes self-management
Normalization of glycemia
Weight loss
Reduction in carbohydrate and calorie intake
Increase in exercise capacity
Exercise
Metabolic
control
Education
Diet
INITIAL TREATMENT
Lifestyle change should be initiated at the time of
diagnosis of T2D .
Initial pharmacologic treatment of youth with T2D
should include metformin and insulin alone or in
combination
Initial treatment is determined by symptoms, severity
of hyperglycemia, and presence or absence of
ketosis/ketoacidosis.
Zeitler et al 2014
GLP
RECOMMENDATION MANAGEMENT
In children with type 2 diabetes and an A1C 9.0%,
and in those with severe metabolic decompensation
(e.g. DKA), insulin therapy should be initiated, but
may be successfully weaned once glycemic targets
are achieved, particularly if lifestyle changes are
effectively adopted [Grade D, Level 4].
Weight Gain
COMPLICATIONS OF DIABETES
Acute:
Diabetic keto acidosis (DKA)
Hypoglycemia
Late-onset:
Retinopathy
Neuropathy
Nephropathy
Ischemic heart disease & stroke
COMPLICATIONS OF DIABETES
Microvascular1,2
Cognitive impairment3
Diabetic retinopathy
Macrovascular1,2
Cerebrovascular disease
Coronary disease
Coronary heart disease
Diabetic nephropathy
Diabetic neuropathy
Cardiac autonomic
neuropathy
Atherosclerosis
Skin infection
Gastro-intestinal and
bladder dysfunction
Peripheral vascular
disease
Sexual dysfunction
Peripheral sensory
dysfunction
Diabetic foot
Adapted from: 1. International Diabetes Foundation. Time to Act: Type 2 diabetes, the metabolic
syndrome and cardiovascular disease in Europe. 2006. 2. International Diabetes Federation. Time to Act.
2001. 3. Seaguist ER. Diabetes. 2010;59:4-6.
21%
Deaths related
to diabetes *
37%
Microvascular
complications e.g.
kidney disease and
blindness *
14%
Heart attack *
43%
Amputation or fatal
peripheral blood
vessel disease *
HbA1c
1%
* p<0.0001
** p=0.035
12%
Stratton IM et al. UKPDS 35. BMJ 2000; 321: 405412
Stroke **