01. Diabetes Mellitus Part 1 - Prof.askandar

5/20/2018 01. Diabetes Mellitus Part 1 - Prof.askandar

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GARIS BESAR KULIAH UNTUK MAHASISWA SEMESTER-6

DIABETES MELLITUS-I

FAKULTAS KEDOKTERAN UNIVERSITAS AIRLANGGA, SURABAYA

1

2012

16-927-B

Prof. Dr. dr. Askandar Tjokroprawiro Sp.PD, K-EMD, FINASIM

SURABAYA DIABETES AND NUTRITION CENTRE - Dr. SOETOMO TEACHING HOSPITALFACULTY OF MEDICINE AIRLANGGA UNIVERSITY, SURABAYA

Division of Endocrinology and Metabolism Dept. of Internal Medicine

SURABAYA, 05 MARCH 2012

Kuliah DM-I : SLIDE 1 40

dr. Sri Murtiwi Sp.PD, K-EMD, FINASIM


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SEJARAH

1550 th SM Penyakit atau "SINDROMA DIABETES", mulai dikenal

di Mesir 1550 SM (The Egyptian Papyrus Ebers)

200 th SM ARETAEUS(Greek Physician) : DIABETES atauSIPHON = FLOW-THROUGH = RUN-THROUGH, berarti

mengalir terus. Sehabis minum banyak, diikuti kencing

banyak. MELLITUS : MADU atau MANIS.

DIABETES MELLITUS = KENCING MANIS.

2

HISTORY (Tattersall 2003) : Polyuric states resembling DIABETESMELLITUS have been described for over 3500 years. The name

DIABETES comes from the Greek word for a SYPHON; the sweet

taste of DIABETIC URINE was recognized at the beginning of the

millenium, but the adjective MELLITUS(honeyed) was only added by

John Rollo in the late 18th century.

Continued


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Th. 1909 JEAN d MEYER(Belgia) memberi nama hormon INSULIN

(Latin : Insulina = Island)

SEJARAH3

Th. 1869 PAUL LANGERHANS(Jerman) : timbunan Glukosa

dalam Hepar sebagai Glikogen, dan Hiperglikemia Akut

akibat kerusakan Medulla Oblongata (PIQRE DIABETES).

Th. 1674 THOMAS WILLIS(Inggris), merasakan rasa manis pada

Urine (Abad 5-6 rasa manis ini sudah pernah dilaporkan

oleh Dokter Indian).

Continued


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Th. 1921 FREDERIK G. BANTING(Ahli Bedah) dan CHARLES H. BEST(Asisten Student) dari Univertisy of Toronto-Canada

bekerja sama dengan JAMES B. COLLIP(Ahli Biokimia)

dan J.J.R MACLEOD(Ahli Ilmu Faal) menemukan INSULIN.

Mulai digunakan di 11 JANUARI1922, kepada pria umur

14 tahun (nama : LEONARD THOMPSON). The name

INSULIN was coined by MACLEOD

Th. 1954 - 1955

FRANKE dan FUCHS (1954) mulai menggunakan OHO

(Obat Hipoglikemik Oral)atauOAD (Obat Anti Diabetes)

pada manusia. The first oral hypoglycaemic agents

suitable for clinical use were the SULPHONYLUREAS,

developed by Auguste Loubatieres in the early 1940s.

CARBUTAMIDE was introduced in 1955 and

TOLBUTAMIDE in 1957. The biguanide PHENFORMIN

became available in 1959, and METFORMINin 1960

SEJARAH 4

Continued


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DM TYPE 2 (Tattersall 2003)

INSULIN RESISTANCE and -CELL FAILURE, the fundamental

defects of type 2 diabetes (T2D), have been investigated by many

researchers. The insulin clamp method devised by Ralph

DeFronzo was the first accurate technique for measuring insulin

action. Maturity-Onset Diabetes of the Young (MODY) was describedas a distinct variant of type 2 diabetes by Robert Tattersall in 1974.

5DIABETES MELLITUS

DM TYPE 1 (Tattersall 2003)

THE -CELL DESTRUCTION causing type 1 diabetes (T1D) was

suggested to be autoimmune by Deborah Doniach and GianFranco

Bottazzo in 1979. The significance of chronic lymphocytic infiltration

of the islets (insulitis),first observed by Eugene Opie in 1901, was

highlighted by Willy Gepts in 1965. Andrew Cudworth and John

Woodrow first described the association of type 1 diabetes with

specific HUMANLEUCOCYTE ANTIGENS (HLA).


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Data DM Di RS Pendidikan Dr. Soetomo (Hospital Data)(19642011)

JUMLAH DM TERDAFTAR DI POLI ENDOKRINOLOGI RSU Dr. SOETOMOSurabaya 19642010 (Selama 46 Tahun)

Dari 133Pasien terdaftar pada tahun 1964menjadi 35717pd th 2010(46 tahun)

meningkat 268x lipat, dengan pertambahan pasien baru rerata +110DM pertahun

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: 133 px

: 1061

: 15381: 16567

: 2914

: 22029

: 26406: 27824

: 5654

: 8222

: 10278

: 11475

: 12608

: 13818

: 19039

: 20366

: 17667 : 29394

: 31457

: 33636

: 35606

: 37704: 39875: 9150

: 42149

: 43264

: 45536

19901991

1986

1987

1988

1989

1964

1970

1975

1980

19841985

1995

19961997

1992

1993

1994

1998

1999

2000

2001

20022003

2004

2005

2006

2007

2008

2009

MANUAL

ELECTRONIC

: 33157

: 328622010 : 35717


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%0.0 10.0 20.0 30.0 40.0 50.0 60.0 70.0 80.0

Commulative Prevalence of CVD : +82%(in line with Dyslipidemia)

30 million in USA(FELDMAN, et al 1994)

Tjokroprawiro 1993 (Revised : 2002) ADA 2005-2010

CHRONIC DIABETIC COMPLICATIONS AND PROVIDED INFORMATION

DIABETIC ORAL MANIFESTATIONS : 1075%

GINGIVITIS AND PERIODONTIS ARE MOST PREVALENT

CHD : "THE WINDOW OF MACROANGIOPATHY"RETINOPATHY : "THE WINDOW OF MICROANGIOPATHY"MICROALBUMINURIA (30-299 mg/day = ACR) :IS REFERRED TO AS HAVING INCIPIENT NEPHROPATHY

MICROANGIOPATHY : RETINOPATHY, NEPHROPATHY, NEUROPATHY, MACROANGIOPATHY : CHD, STROKE, PVD

67.0Dyslipidemia

51.4Symptomatic Neuropathy50.9Erectile Dysfunction

27.2Retinopathy25.5Joint Manifestation

16.3Cataract12.8Pulmonary Tbc12.1Hypertension (WHO,1983)

10.0CHD5.7CLINICAL NEPHROPATHY

4.2Stroke3.8Cellulitis - Gangrene

3.0Symptomatic Gall Stone

Based on JNC7, 2003 : + 32%

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(McCarty & Zimmet 1994, Provided : Tjokroprawiro 1989-2012)

DIFFERENCES IN RATES (%) OF T2DM IN MAJOR ETHNIC GROUPS

LOWEST REPORTED RATES

(Hispanic) Central Mexico 5.6

(Micronesian) Rural Kiribati 4.3

(Polynesian) Rural Western Samoa 4.0

(European) Poland 3.5

(Asian Indian) Rural India 2.7(Melanesian) Rural Fiji 1.9

(Oriental) Rural Chinese 1.6

Indonesia (East Java) :

- Urban-Surabaya (Adimasta et al 1980)1.43

- Rural (Tjokroprawiro et al 1989) 1.47

Suspect MRDM : + 21% of DM in Rurals

African Rural Tanzania 1.2(Arab) Rural Tunisia 1.2

- Urban-Surabaya (Pranoto et al 2006) 6.0%

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HIGHEST REPORTED RATES

(Asian Indian) Fijian Island 22.0

(Micronesian) Urban Kiribati 14.6

(Arab) Oman 14.2

(Hispanic) US Mexican

14.1

(Oriental) Mauritian Chinese 13.1

(Polynesian) Urban Western Samoa 10.6

(African) US African American 10.3

(European) Southern Italy 10.2

(Melanesian) Urban Fiji 8.5

Prevalence Rates of Small Populations :Pima Indians 50.3% Nauru 41.3%

Manado : 8-10% Surabaya : 6.0%

Rates are age-standardized to Segi's world population for ages 30 to 64.

Prevalence rates of smaller populations such as the Pima Indians in North America (50.3),

Pacific Islanders of Nauru (41.3) & Australian Aborigin (22.5) have not been included.


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Global Diabetes Statistics(Diabetes Atlas IDF 2003, Provided : Tjokroprawiro 2004-2012)

4% Prevalence of DM, Netherlands, 2003

20% Prevalence of DM, UAE, 2003

30% Prevalence of DM, Nauru, 2003

104,800 Number of Children with TIDM, Southeast Asia, 2003

430,000 Number of Children with TIDM, Worldwide, 2003

194,000,000 Number of People with DM, 2003333,000,000 Predicted number of People with DM, 2025

314,000,000 Number of People with IGT, 2003; No Data for IFG

472,000,000 Predicted Number of People with IGT, 2025THE ROLES OF

METFORMIN

28% Proportion of DM attributable to weight gain, Southeast Asia Males, 200380% Proportion of DM attributable to weight gain, Western Europe Males, 2003

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IDF Regions and Global Projections of the Number of People with Diabetes (20-79 years) : 2011 and 2030

IDF, Diabetes Atlas 5thEdition-2011, Provided : 2012

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The 21thWorld Diabetes Congress : Dubai, 5-8 December 2011

2011 2030 INCREASEREGION MILLIONS MILLIONS %

Africa 14.7 28.0 90%

Middle East and Noth Africa 32.8 59.7 83%

South-East Asia 71.4 120.9 69%

South and Central America 25.1 39.9 59%

Western Pacific 131.9 187.9 42%

North America and Caribbean 37.7 51.2 36%

Europe 52.6 64.0 22%

World 366.2 551.8 51%


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The TOP 10 COUNTRIES of People with Diabetes (20-79 Yrs)IDF 2009(IDF Diabetes Atlas 4thEdition-2009, Illustrated : Tjokroprawiro 2012)

NO.

OFCASES(M

ILLIONS)

0

10

20

30

40

50

60

INDIA

*50.8

1

CHINA

*43.2

2

USA

*26.8

3

RUSSIAN

FEDERATION

*9.6

4

BRAZIL

*

7.6

5

GERM

*7.5

6

PKTAN

*7.1

7

JAPAN

*7.1

8

MEXICO

*6.8

10INA

9

*

7.0

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*) Number of People with Diabetes (20-79 Years): in Million

DM-by IDF

2009


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The TOP 10 COUNTRIES of People with Diabetes (20-79 Yrs)IDF 2011(IDF Diabetes Atlas 5thEdition-2011, Illustrated : Tjokroprawiro 2012)

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NO.

OFCASES(MILLIONS)

0

1020

30

40

5060

70

80

90

BRAZIL

5

*12.4**

9.72

EGYPT

9

*7.3**

15.16

RUSSIAN

FEDERATION

4

*12.6**

11.54

USA

3

*23.7

**10.94

**) Diabetes National Prevalence (%)

*) Number of People with Diabetes (20-79 Years) : in Million

INA

10

**4.73

*7.3

CHINA

1

**9.29

*90.0

INDIA

2

*61.3

**8.31

BANGLA

DESH

8

*8.4

**9.58

MEXICO

7

*10.3

**14.85

JAPAN

6

*10.7

**11.20

Germany and Pakistan : Out of the TOP TEN

Bangladesh and Egypt : Newcomers of the TOP TEN

DM-by IDF2011


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CATEGORIES OF INCREASED RISK FOR DIABETES (IRD = PREDIABETES*) : ADA 2012

(Summarized : Tjokroprawiro 2011-2012)

NORMAL : A1C < 5.7 %

1 FPG 100 mg/dl to 125 mg/dl: IFGPREDIABETES

2 2-h PG 140 mg/dl to 199 mg/dl in the 75 g OGTT: IGT PRE DIABETES

3

THE TERM PRE-DIABETESMAY BE APPLIED IF DESIRED

HbA1c5.76.4% : IRD or PREDIABETES

* For all Three tests, risk is continuous extending below the lower limit of the

range and becoming disproportionately greater at higher ends of the range

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(IRD = PREDIABETES*)

ADA = American Diabetes Association


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STANDARDS OF MEDICAL CARE IN DIABETES ADA-2012CLASSIFICATION OF DIABETES MELLITUS

(ADA-2012, Added by KONSENSUS PERKENI-2011 and SURABAYA-1986)

Drug-or CHEMICAL-INDUCED (such

Genetic Defects of -CELL FUNCTIONGenetic Defects in INSULIN ACTIONDiseases of the Exocrine Pancreas(such as Cystic Fibrosis-Related Diabetes

= CFRD)

as in-the TREATMENT of AIDS orafter ORGAN TRANSPLANTATION)

D

ABC

DM Variation : DM Type X (Tjokroprawiro et al, 1991)LADA (Tuomi et al 1993)DM 1.5 (Zimmet 1993

I TYPE 1 DIABETES* (Results from -cell destruction, usually leading to absolute insulin deficiency)

II TYPE 2 DIABETES*

III OTHER SPECIFIC TYPES OF DIABETES due to other causes, e.g. :

IV GESTATIONAL DIABETES MELLITUS (GDM) : DM diagnosed during Pregnancy

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InfectionsUncommon form of Immune-mediated Diabetes

Other Genetic Syndromes associated withDiabetes

EndocrinophathiesEF

GH

Based on PERKENI 2011 & Surabaya (E-I) :

A. Immune Mediated

B. Idiopathic

(Results from a progression Insulin Secretory Defect on the background of

Insulin Resistance)

MRDM (Surabaya 1986)I


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CRITERIA for the DIAGNOSIS of DIABETES: PERKENI 2011, ADA 2012


HbA1c> 6.5 % by NGSP Certified and Standardized to DCCT Assay

(NGSP : The National Glycohemoglobin Standardization Program)

1 HbA1c> 6.5 %

4 RANDOM PLASMA GLUCOSE > 200 mg/dl in Patients with :

CLASSIC SYMPTOMS of HYPERGLYCEMIA or HYPERGLYCEMIC CRISIS

2 FPG > 126 mg/dl FASTING means NO CALORIC INTAKE > 8 Hours

3 2-h PG > 200 mg/dl during OGTT (WHO, GLUCOSE LOADING 75g)

15

or

or

or

PERKENI 2011, ADA 2012


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Criteria for Testing for Diabetes in Asymptomatic Adult Individuals

(Standards of Medical Care in Diabetes - ADA 2012)

A Testing should be considered in all adults who are OVERWEIGHT(BMI >25 kg/m2*, Indonesia: >23 kg/m2)and WHO HAVE ONE OR MORE ADDITIONAL RISK FACTORS :

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PHYSICAL INACTIVITY1

First-degree Relative with Diabetes2

High-risk race/ethnicity (e.g., African American, Latino, Native American, Asian

American, Pacific Islander)3

WOMEN who delivered a baby weighing >9 lb or who were diagnosed with GDM4HYPERTENSION (blood pressure >140/90 mmHg or on therapy for hypertension)5

HDL CHOLESTEROL level 250 mg/dL

(2.82 mmol/L)6

WOMEN with PCOS7

A1C >5.7%, IGT, or IFG on PREVIOUS TESTING8

OTHER CLINICAL CONDITIONS associated with INSULIN RESISTANCE (e.g.,severe obesity, acanthosis nigricans)

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HISTORY of CVD10

B In the absence of the above criteria, TESTING for DIABETES SHOULD BEGIN at AGE 45 YEARS

C IF RESULTS are NORMAL, testing should be REPEATED at LEAST at 3-YEAR INTERVALS, withconsideration of more-frequent testing depending on initial results (e.g., those with prediabetes should be

tested yearly) and risk status.


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PELAKSANAAN TES TOLERANSI GLUKOSA ORAL (TTGO)(Perkeni-2006, ADA-2007, Tjokroprawiro 2006-2012)

1 3 hari sebelumnya makan karbohidrat cukup

3 Puasa semalam 10-12 jam (minimal 8 jam)

4 Diperiksa Glukosa Darah Puasa

5 Diberikan glukosa 75 gram, dilarutkan dalam air 250 ml,diminum dalam waktu 5 menit.

6 Berpuasa kembali sampai pengambilan darah untuk 2 jam

sesudah minum larutan glukosa tersebut selesai

7 Diperiksa Glukosa Darah 2 (dua) jam sesudah beban Glukosa

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Kegiatan Jasmani seperti yang biasa dilakukan2

8 Selama permeriksaan, pasien yang diperiksa tetap

istirahat dan tidak merokok; boleh minum air putih


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Langkah-langkah Diagnostik DM dan Gangguan Toleransi Glukosa

(KONSENSUS PERKENI 2011)

GDP = Glukosa Darah Puasa

GDS = Glukosa Darah Sewaktu

GDPT = IFG = Glukosa Darah Puasa Terganggu

TGT = Toleransi Glukosa Terganggu

KELUHAN KLASIK (-)KELUHAN KLASIK DIABETES (+)

KELUHAN KLINIK DIABETES

D I A B E T E S M E L L I T U S TGT GDPT NORMAL

- Evaluasi Status Gizi

- Evaluasi Penyulit DM

- Evaluasi Perencanaan Makan

Sesuai Kebutuhan

- Nasihat Umum

- Perencanaan Makan

- Latihan Jasmani

- Berat Idaman

- Belum Perlu Obat Penurun Glukosa

GDP

GDSatau

GDP

GDSatau

>126

>200

200

200

100-125

140-199

TTGO

GD 2 Jam

>200 140-199 < 140


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PRACTICAL TOOL FOR INSULIN RESISTANCE AND -CELL FUNCTION(Mathews et al 1985, Falutz et al 2002, Summarized : Tjokroprawiro 2005-2012)

HOMA-R and HOMA-BUseful in Daily Practice

:1

2 FOLLOW-UP OF TREATMENT

RATIONALE TREATMENT

HOMA-B-Cell Function

: (N: 70150%)20 x Fasting Insulin (U/ml)

FPG (mmol/l) 3.5

HOMA-RInsulin Resistance

: (N: < 4.0)Fasting Insulin (U/ml) x FPG (mmol/l)

22.5

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PREVALENCE OF IR IN SELECTED METABOLIC DISORDERS(Bonora 1998, Summarized and Illustrated : Tjokroprawiro 2006-2012)

4 HYPERTENSION

IFG & IGT2

URIC ACID 7

LOW HDL-C 6

3 The MetS

HYPER-CHOL 8

1stPhase and

IR in LiverIFG = Impaired Fasting Glucose

1stPhase and

IR in PeripheryIGT = Impaired Glucose Tolerance

IR = INSULIN RESISTANCEIR = INSULIN RESISTANCE

DISORDERS

METABOLIC

SEQUENTIALPREVALENCES OF IR

in

20

HYPERTRIGLYCERIDAEMIA

5

T2DM

1


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1. DM TIPE-1 (DMT1) : FROM -CELL DESTRUCTION TOABSOLUTE INSULIN DEFICIENCY

PROGREESSIVE INSULIN SECRETORY DEFECT ("AIR") ON THE BACKGROUND OF I.R.2. PATOFISIOLOGI DM TIPE-2 (DMT2) :

*SEKRESI INSULIN :1 FIRST PHASE (ACUTE) = "AIR" : 0-5 menit

2SECOND PHASE

GABUNGAN IR + IMPAIRED "AIR" T2DM

IR : INSULIN RESISTANCE"AIR" : ACUTE INSULIN RESPONSE (FIRST PHASE)

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MACAM DM DI PRAKTEK SEHARI-HARI(Rangkuman : Tjokroprawiro 1993-2012)

BBR 1.1

>

Dx Dugaan :Gejala mendadakInsulin DependentAnak, atau Dewasa

(


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1 DIABETES MELLITUS

2 RETINOPATI DIABETIK HARUS : POSITIF

3 PROTEINURIA yang positif tanpa penyebab lain, atau

selama 2 kali pemeriksaan dengan interval 2 minggu

apabila penyebab lain (misalnya infeksi) sudah teratasi.

(Kriteria ND 1989) : DM, Retinopati Diabetik, Kreatinin Darah

>2.5 mg/dl, Proteinuria 1 (satu) kalipemeriksaan tanpa adanya

penyebab proteinuria lain.

DIAGNOSIS DAN KLASIFIKASI NEFROPATI DIABETIK(Kriteria Surabaya 1985 dan 1989)

Atau

TIGA PERSYARATAN DIAGNOSIS NEFROPATI-DIABETIK (ND) :

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MNT : Medical Nutrition Therapy or Diet. Treatment : B2, B3, Be(Types of MNT), OAD(Oral Agents for Diabetic), INS(Insulin)

B2 & B3-Diets (Pre-HD Phase) : With Specific Composition plus Low K+

& Na+

, Protein 0.6-0.8 g/kg BW( 10% of Daily Cal.). Be-Diet (HD-Phase) : Low K+& Na+, Protein 1-1.2 g/kg BW/day, etc*) Diabetic Diets for DN are supplemented with Low Vit C, Folic Acid, Vit B6, Vit B12, GlutamineS

** THE FORMULA OF GFR MEASUREMENT RELY ON A STABLE SERUM CREATININE CONCENTRATION

B2*) 1 Micro/Macro Alb eGFR > 90 (N) B2, OAD, INS - ? -

B2*) 2 Macro Alb. eGFR 60-89 (< 2.5) B2, OAD, INS > 5 years

B2*) 3 Macro Alb. eGFR 30-59 (2.5-4) B2, OAD, INS > 2 years

5 Be, INS, HD

ESDN TransplantationBe*) Macro Alb. eGFR < 15 (> 10) 2-5 Months

4a eGFR 15-29 (4-8) B3, INS, Pre HD4b eGFR 15-29 (8-10) Be, INS, HD

B3*)Macro Alb. 4-18 Months

Be*)

(1986)Type Stage

Life ExpectancyeGFR (mL/min)**Micro/MacroAlbuminuria

MNT = DIET

OAD - INSSC (mg/dl)

eGFR ( )(mL/min.)

o (140-Age) x Body Weight (Kg)

Plasma Creatinine (mg/dl) x 72=

eGFR ( )(mL/min.)

(140-Age) x Body Weight (Kg)

Plasma Creatinine (mg/dl) x 72=+

ox 0.85

The Formula of CockroftGault : eGFR (estimated GFR); SC = Serum Creatinine

SURABAYA CLASSIFICATION OF DIABETIC NEPHROPATHY (DN)-2005Nefropati Diabetik St. 2 (Serum Kreatinin 1.5 2.5 mg/dl : Rendah Protein dan Batasi KTT)

Nefropati Diabetik St. 3 & 4 (Serum Kreatinin > 2.5 mg/dl : Rendah Protein dan Pantang KTT)

(Tjokroprawiro 2004, Yogiantoro et al 2004) KTT : Kacang, Tahu, Tempe

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STAGES OF CHRONIC KIDNEY DISEASE : CKD(National Kidney Foundation-Levey et al 2003; Position Statement ADA 2012)

STAGE DESCRIPTIONGFR (MDRD)

(mL/min/1.73 m2)

1 KIDNEY DAMAGE*)

withNORMAL or GFR >90

2KIDNEY DAMAGE*)with

MILDLY GFR60-89

5 KIDNEY FAILURE


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THE FORMULA OF COCKROFTGAULT : eGFR (estimated GFR)SC = SERUM CREATININE eGFR CREATININE CLEARANCES

eGFR ( )

(mL/min.)

o=

(140-AGE) X BODY WEIGHT(Kg)

PLASMA CREATININE(mg/dl) x 72

=(140-AGE) X BODY WEIGHT(Kg)

PLASMA CREATININE(mg/dl) x 72

eGFR ( )(mL/min.)

+o x 0.85

Other FORMULA : MDRD(Modification of Diet in Renal Disease)


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THE MDRD FORMULA (MODIFICATION OF DIET IN RENAL DISEASE)

SC = SERUM CREATININE eGFR CREATININE CLEARANCES

186 x (SC)1.154x (AGE)0.203 x (0.742) x (1.212 IF BLACK/ASIA)

eGFR (MDRD) for FEMALE

186 x (SC)1.154x (AGE)0.203x (1.212 IF BLACK/ASIA)

eGFR (MDRD) for MALE

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DEFINITION OF ABNORMALITIES IN ALBUMIN EXCRETION

(ADA 2006, Provided : Tjokroprawiro 2006 2012)

NORMAL < 30 < 20 < 30

MACRO ALBUMINURIA

CLINICAL ALBUMINURIA>300 >200 >300

ANY TWO OF THREE SPECIMENS COLLECTED WITHIN A 3-6 MONTH PERIOD

30 - 29930 - 299 20 - 199MICRO ALBUMINURIA

Eight Causesof

Elevated AER

1 Excercise within 24 h, 2 Marked Hyperglycemia, 3 Marked Hypertension,4 Infection, 5 Fever, 6 CHF

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24-h COLLECTIONTIMED COLLECTION

(mg/24 h) (g/min)CATEGORY Spot Collection : ACRg/mg Creatinine

Easiest to Carry Out


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3 LATIHAN FISIK: * PRIMER(1.02 jam sesudah makan)* SEKUNDER(Pagi dan Sore sebelum mandi)

*) SUDAH DIKERJAKAN OLEH PUSAT DIABETES DAN NUTRISI

RSUD DR. SOETOMO FK UNAIR PADA TH 1989 DAN 1991

PENTALOGI-TERAPI DIABETES MELLITUS(Askandar Tjokroprawiro 1983-2012)

1 PENYULUHAN(tentang DIABETES MELLITUS)

2 POLA MAKAN= PM(DIET ATAU TERAPI NUTRISI MEDIS = TNM)

5 CANGKOK PANKREASPusat Diabetes dan

Nutrisi(1989, 1991)

Sel Beta : pada Tikus*)

Total : pada Anjing*)

OBAT HIPOGLIKEMIK ORAL (OHO) OHO = OAD

INSULIN4

OBAT ANTI DIABETES (OAD)

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NUTRITION IN DIABETES MELLITUSClinical Experiences : Tjokroprawiro 1978-2012

DIABETIC DIETSMEDICAL NUTRITION THERAPY

(MNT) P.E.N. P-P.E.N.

PAR ENTERAL NUTRITION ( "SONDE" )

E1, E2, E3, E4, E5, E6

:08.00

:14.00:20.00

INSULIN

E1

E3E5

:11.00

:17.00:23.00

NO INSULIN

E2

E4E6

ORAL NUTRITIONSince 1978 ENTERAL NUTRITIONSince 1995

PAR ENTERAL NUTRITION = P.E.N.

Since 1993

PERIPHERAL PPAR PENTERAL ENUTRITION N

Ten Principlesof

P-P.E.N. in DM

30

21Types of Diabetic Diets

at Dr. Soetomo Hospital

From the B-Diet 1978

to

The B1-L 2004


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THE 6-E (E-1 UP TO E-6) REGIMEN OF ENTERAL NUTRITION FOR DIABETICS

("TUBE FEEDING" "SONDE")(Clinical Experiences : Tjokroprawiro 1995-2012)

Hospital Formula : E1,E3,E5 Pharm. Formula : E2, E4, E6: Sites of MUFA

ENTERAL- 1

(E-1)08.00 am

ENTERAL- 4

(E-4)05.00 pm

ENTERAL- 5

(E-5)08.00 pm

ENTERAL- 3

(E-3)02.00 pm

ENTERAL- 2

(E-2)11.00 am

ENTERAL- 6

(E-6)11.00 pm

1 6 Times/day 2 Started at 08.00 am 3 3-Hour Interval

TIMING OF INSULIN INJECTION : 30 MIN. BEFORE OR PRECISELY on E1 ,E3 ,E5

EXAMPLE : DIANERAL(D) OR HOSPITAL FORMULA

1

DIANERAL

INSULIN

6

MUFA or D

2

MUFA or D

4

MUFA or D

3

DIANERAL

INSULIN

5

DIANERAL

INSULIN

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The Diet-B 1978 (Revised TNM-2002) : The Mother - Diet

Prospective Study (1978) and Clinical Experiences (1978-2011)(Tjokroprawiro 1978-2012; TNM = Terapi Nutrisi Medik)

*) Diet-B : 68% CHO 12% Protein 20% FATs Prospective-Cross Over Design (1978)

SAFA 5% PUFA 5% PS = 1.0 MUFA 10% Chol.


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(Tjokroprawiro, Hari Witarti, Indrawati, Frieda et al, 1999-2007)

SPECIFICATIONS : 3 of 21 DIABETIC DIETS (TNMs) at Dr. SOETOMO HOSPITAL

DIET-G = Diet-H and DIET-KV

Diet-B1 plus 5 Specifications

Diet-G = Diet-H : Gangrene or HeparDiet-B plus 5 Specifications

Diet-KV : Stroke, CAD, POAD

These are able to lowerHomocysteine Level

(Chol. < 300 mg/day)

1 Arginin Content 2 Fiber 25-35 g/day

3 Folate

4 Vit B6

5 Vit B12

Diet-B (% Cal) : 68% Cbh, 20% F, 12% P

These are able to lowerHomocysteine Level

(Chol. < 300 mg/day)

1 Arginin Content 2 Fiber 25-35 g/day

3 Folate

4 Vit B6

5 Vit B12

Diet-B1 (% Cal): 60% CHO, 20% F, 20% P

ARGININ : Atheroprotective via Nitric Oxide (NO)

HOMOCYSTEINE : Oxidative Stress , ADMA

Asymmetric Di Methyl Arginine

(ADMA)

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DIET-B (1978)* : The Mother Diet

Kbh 68% kal, L 20% kal, Protein 12% kal, Kolesterol < 300 mg/hari,

SAFA 5%, PUFA 5%, MUFA 10%, Rasio PS + 1.0, Serat 25-35 g/hari

INDIKASI :

1 DIABETISI YANG TIDAK TAHAN LAPAR

3 DM LEBIH DARI 10 TAHUN

2 DISLIPIDEMIA(Salah satu atau lebih : TG , HDL , Kol. Tot. , LDL )

* Hasil Disertasi S3 (Askandar Tjokroprawiro 1978)

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(CHO plus MUFA**)

***)


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PEDOMAN DIET-B2, DIET-B3, dan DIET-BeKonsensus : Diabetologi, Nefrologi, Gizi

RSUD Dr. Soetomo - FK Unair Surabaya(Surabaya : 6 April 2002)

FASE PRA-HEMODIALISA : Diet-B2, B3)

1 PRA-HD UMUM Diet-B2Kandungan Protein : 0.6 g/kgBB/hari

2 PRA-HD KHUSUS Diet-B3

Proteinuria > 3 g/hari, atau

Kandungan Protein : 0.8 g/kgBB/hariAlbuminuria Berat (Positif 4 )

(FASE PRA-HD)

DIABETISI FASE HD : Diet-BeKandungan Protein : 1.0-1.2 g/kgBB/hari

Intensivitas MenghambatProgresivitas Gagal Ginjal

Vitamin C Maks. 100 mg,Pantang NSAID, dll

FASE HEMODIALISA : Diet-Be

(FASE HD)

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PERBANDINGAN GOLONGAN OHO(KONSENSUS PERKENI 2011)

37

Cara kerja utama Efek sampingutama

ReduksiA1C

Keuntungan Kerugian

Sulfonilurea Meningkatkan sekresiinsulin

BB naik,hipoglikemia

1,0-2,0% Sangat efektif Meningkatkan berat badan,hipoglikemia (glibenklamid dan

klorpropamid)

Glinid Meningkatkan sekresi

insulin

BB naik,

hipoglikemia

0,5-1,5% Sangat efektif Meningkatkan berat badan, pemberian

3x/hari, harganya mahal dan

Hipoglikemia

Metformin Menekan produksi

glukosa hati &menambah sensitifitas

terhadap insulin

Dispepsia, diare,

asidosis laktat

1,0-2,0% Tidak ada kaitan

dengan berat badan

Efek samping gastrointestinal,

kontraindikasi pada insufisiensi renal

Penghambat

glukosidasealfa

Menghambat absorpsi

glukosa

Flatulens, tinja

lembek

0.,5-0,8% Tidak ada kaitan

dengan berat badan

Sering menimbulkan efek

gastrointestinal, 3x/hari dan mahal

Tiazolidindion Menambah sensitifitasterhadap insulin

Edema 0,5-1,4% Memperbaiki profilLipid (pioglitazon), berpotensi

menurunkan infark miokard

(pioglitazon)

Retensi cairan, CHF, fraktur,berpotensi menimbulkan infark

miokard, dan mahal

DPP-4 inhibitor Meningkatkan sekresi

insulin, menghambat

sekresi glukagon

Sebah, muntah 0,5-0,8% Tidak ada kaitan dengan berat

badan

Penggunaan jangka panjang tidak

disarankan, mahal

Inkretin

analog/mimetik

Meningkatkan sekresi

insulin, menghambat

sekresi glukagon

Sebah, muntah 0,5-1,0% Penurunan berat badan Injeksi 2x/hari, penggunaan jangka

panjang tidak disarankan, dan mahal

Insulin Menekan produksi

glukosa hati, stimulasipemanfaatan glukosa

Hipoglikemi, BB

naik

1,5-3,5% Dosis tidak terbatas,

memperbaiki profil lipid dasangat efektif

Injeksi 1-4 kali/hari, harus dimonitor,

meningkatkan berat badan,hipoglikemia dan analognya mahal

Keterangan :


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OBAT HIPOGLIKEMIK ORAL : KONSENSUS PERKENI 2011 * Produk orisinal***** Kadar plasma efektif terpelihara selama 24 jam

Belum beredar di Indonesia38

Golongan Generik Nama Dagang Mg/tab Dosis harian Lama kerja(jam)

Frek/hari Waktu

Glibenclamid Daonil* 2,5-5 2,5-15 12-24 1-2

GlipizidMinidiab 5-10 5-20 10-16 1-2

Glucotrol-XL 5-10 5-20 12-16** 1

Gliklazid Diamicron 80 80-320 10-20 1-2Diamicron-MR 30-60 30-120 24 1Sebelum

Glikuidon Glurenom 30 30-120 6-8 2-3

makan

Glimepirid

Amaryl* 1-2-3-4 0,5-6 24 1

Gluvas 1-2-3-4 1-6 24 1Amadiab 1-2-3-4 1-6 24 1

Metrix 1-2-3-4 1-6 24 1

GlinidRepaglinid Dexanorm 1 1,5-6 - 3

Nateglinid Starlix 120 360 - 3

Tiazolidindion Tidak bergantungPioglitazon

Actos* 15-30 15-45 24 1

jadwal makanDeculin 15-30 15-45 24 1

PenghambatAcarbose

Glucobay 50-100 100-300 3 Bersama suapan

Glukosidase pertamaEclid 50-100 100-300 3

Glumin 500 500-3000 6-8 2-3

BiguanidMetformin

Glucophage 500-850 250-3000 6-8 1-3

Bersama/sesudah

makanMetformin XRGlucophage-XR* 500-750

Glumin-XR 500 500-2000 24 1

Obat Kombinasi

Tetap

Metformin +Glucovance

250/1,25 Total Glibenclamid

maksimal 20 mg/hr

12-24 1-2

Bersama/sesudah

Glibenklamid 500/2,5

makan

500/5Glimepirid + Amaryl-Met

FDC

1/250 2/500 - 2Metformin 2/500 4/1000

Pionix 15-30 15-45 18-24 1

Penghambat DPP-IV Sitagliptin Januvia 25, 50, 100 25-100 24 1

Saxagliptin Onglyza 120 5 24 1

Tidak bergantung

jadwal makan

Vildagliptin Galvus 50 50-100 12-24 1-2

MetforminPionix M

Total Pioglitazone

maksimal 45 mg/hr18-24 1

Pioglitazone + 15/50030/850

MetforminJanumet 1

Sitagliptin +50/100050/500 Total Sitagliptin

maksimal 100mg/hr

Metformin

Galvusmet

2

Vildagliptin +

50/850

50/500 Total Vildagliptin

maksimal 100mg/hr 12-2450/1000

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MEKANISME KERJA, EFEK SAMPING UTAMA, DAN A1C(KONSENSUS PERKENI 2011, Provided : Tjokroprawiro 2011-2012)

CARA KERJA UTAMA EFEK SAMPING UTAMA PENURUNAN A1C

Insulin Menekan produksi glukosa hati, Hipoglikemia, 1`.5 3.5 %stimulasi pemanfaatan glukosa BB naik

Sulfonilurea Meningkatkan sekresi insulin BB naik, 1.0 2.0 %hipoglikemia

Metformin Menekan produksi glukosa hatiMenambah sensitivitas insulin

Diare, dispepsia, 1.0 2.0 %asidosis laktat

Penghambat Menghambat absorpsi glukosa Flatulens, 0.5 0.8 %

Glukosidase Alfa tinja lembek

Tiazolidindion Menambah sensitivitas terhadap Edema 0.5 1.4 %

(Glitazon) insulin

Glinid Meningkatkan sekresi insulin 0,5-1,5%BB naik,

hipoglikemia

OAD

INSULIN

"Non" 1.13 % (6 minggu)INLACIN Novel Insulin Sensitizer (2011)

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RSUD Dr. SOETOMO

PUSAT DIABETES & NUTRISI SURABAYA (PDNS) :1986-2012 40

PDNS Lt-7

(1200 m2)

RSUD Dr. SOETOMO, 1938 2012 : Bed Capacity 1550

PDNS C St f 8 E t M b 52

Documents

01. Diabetes Mellitus Part 1 - Prof.askandar