DIABETES MELLITUS PROBLEMS AND MANAGEMENT

Eva Decroli

Problems
Increased of prevalence Cronic complications ex. Diabetic Foot Problems Prevention, primer, secunder tertier

Etiology of Insulin Resistence

Weight gain Obexisity
Circulation FFA

Lipoatrophy adipokines

Insulin Resistance
The subnormal biologic response to a given concentration of insulin

Physical inactivity

Aging

Genetica

Etiology of -Cell Dysfunction

Genetics

Lipotoxicity

Glucose toxicity

-Cell Failure
Inadequate compentation for insulin resistance and selective non-responsivoness to glucose

Loss of

-cell ?

Cytokines ?

Amyloid accumulation

The Role of Genes and the Environment

Normal

GENES

Insulin resistance

Environment

Diabetes genes insulin resistance genes -cel function genes Obesity genes

Decreased Insulin secretion

Diet Activity Toxins

Type DM

Risk Factors for Type 2 Diabetes Genetic factors -Ethnicity -Family history
Type 2 Diabetes Gastational Diabetes polycystic Ovarian syndrome, and party

Diet

Increasing age

Central obesity

Physical inactivity

Pathophysiology of DM

Hepatic glucose Production (HGP

Peripheral Glucose Uptake

Blood Glucose

Macrovascular Complication of Type 2 Diabetes

80% of people with type 2 diabetes thr from CVD ~ Coronary heart disease (CHD) - eg, angina, heart attack, heart failure - 2-to 4-fold increased risk ~ Cerebrovascular disease - eg, stroke, transient ischemic attacks - 2-to 4-foid increased risk ~ Peripheral vascular disease - eg. Intermittent claudication, gangrene, amputations

Diabetic Foot Problems

Complek interaction between

Periperal neuropaty Micro angiopathy Macro vascular disease Poor foot hygiene

Peripheral neuropathy with loss of pain sensation is the commount cause of fort ulceration, closely followed by poor higiene

Management of foot problems

Education center Metabolic control Mechamical control Wound control Microbiological control

Management of Diabetis Mellitus

Monitoring of Glucosa levels Food planning Phsical activity
Treatment of hyper glycemid Treatment of Cardiovascular risk factor

Milestones of Diabetes Management

Nutrition th/

Education

Exercise

Anti hyperglycemic ogents

PENATALAKSANAAN DM
Dr. H. Eva Decroli SpPD KEMD FINASIM

PILAR PENATALAKSANAAN DIABETES

1. Edukasi 2. Terapi gizi medis 3. Latihan jasmani 4. Intervensi farmakologis

20

EDUKASI
Kepada penderita Kepada keluarga Kepada kelompok Masyarakat beresiko

TERAPI GIZI MEDIS

Diet Diabetes Mellitus Diet berimbang Pengaturan jumlah kalori Pengaturan jadwal makan Contoh : - DD 1100 kkal - 1300 kkal - 1500 kkal - 1700 kkal

LATIHAN JASMANI
150/menit/minggu Frekuensi 3-4 kali seminggu Continue Ritmik Aerobik Teratur Terukur Progressif

INTERVENSI FARMAKOLOGIS Obat golongan insulin Golongan DPP4

inhibitor - Gliptin Golongan Insulin - Basal Insulin, Insulin Prandial Golongan Inkretin Hormon - Exenatide

sekretagou : - Sulfunil urea Golongan Biguanid - Metformin Golongan alfaglikosilase inhibitor - Akarbose Golongan PPAR - Glitazon

Algoritma pengelolaan DM tipe 2 tanpa disertai dekompensasi

25

Tahap 1
Gaya hidup +
Saat diagnosis:

Tahap 2

Tahap 3

Gaya hidup + Metformin +

Metformin +

Gaya hidup + Metformin

Well validated core therapies

Insulin basal

Insulin intensif

Gaya hidup + Metformin +

Sulfonilurea
Gaya hidup + Metformin +

Gaya hidup + Metformin +

Pioglitazon

Pioglitazon + sulfonilurea

Gaya hidup +
Less well validated core therapies

Gaya hidup + Metformin +

Metformin +

GLP-1 agonis

Basal insulin

26
Nathan DM et al, Diabetes Care 32:193203, 2009

Target Pengendalian DM

27

DIABETES MELLITUS PADA ANAK

Eka Agustia Rini

DIABETES MELLITUS
High levels of blood glucose : defects in insulin production, insulin action, or both Type 1 Diabetes cells that produce insulin are destroyed results in insulin dependence Type 2 Diabetes Lack of insulin production Insufficient insulin action (resistant cells)

Diabetes - Diagnosis

Symptoms of diabetes plus random plasma glucose >200mg/dl (11.1mmol/l) or Fasting plasma glucose >126 mg/dl (7.0 mmol/l) or 2 hour plasma glucose >200 mg/dl during an oral glucose tolerance test
American Diabetes Association Consensus Statement Type 2 Diabetes in Children and Adolescents Diabetes Care 2000;23(3) 381-389.

1.

GEJALA KLINIS
HIPERGLIKEMI

Poliuria Polidipsi Poli fagia

KOMPLIKASI -Ketoasidosis -Hipoglikemi -Mikrovaskular -Makrovaskular

Type 1 DM
What Causes Type 1 Diabetes? Autoimmune Response Genetic Abnormalities Viruses Cows milk

Etiology
80%-85% no affected family member Autoimune destruction of pancreas islet
Multiple genetic (predisposition) Enviromental factors (trigger)
viral infection, diet and toxins

or

Insulin secretion

Pathogenesis
Destruction of -cell is quite variable.
Fasting hyperglycemia can rapidly change to severe hyperglycemia or ketoacidosis (in infection or other stress). Manifestation little or no insulin secretion low or undetectable C-peptide

Pathophysiology
Insulinopenia
Utilization glucose decreased postprandial hyperglycemia Glycogenolysis and gliconeogenesis fasting hyperglycemia

Glucosuria

Loss of calorie and electrolyte, dehydration

Clinical Manifestation
Phase of type 1 DM
1. 2. 3. 4. Prediabetes Presentation of diabetes Partial remission or honeymoon Chronic phase of lifelong dependency on administrated insulin

Clinical manifestation
Polyuria or nocturia glucosuria Polydipsia Polyphagia calories lost in urine Weight loss Monilial vaginitis glucosuria

Diagnosis
Symptoms and casual plasma glucose 200 mg/dL or FPG 126 mg/dL or 2-h postload glucose 200 mg/dL Low or undetectable C-peptide ICA positive

MANAGEMENT OF T1DM
Diabetes education. Insulin replacement. Nutritional plan. Psychological adjustment Exercise Diabetes camp

Diabetes Management Principles

An effective insulin regimen Monitoring of glucose As flexible with food and activity as possible Must remember Young children need routine and rules Young children need to develop autonomy Young children need to explore and experience Young children need to begin to make decisions

The aims of DM management:

Optimal metabolic (glycaemic) control. Normal growth and development. Optimal psychosocial adjustment. An individualised plan of diabetes care incorporating the particular needs of the child or adolescent and the family.

Diabetes education
The cause of diabetes. Insulin replacement ; adjustment, storage, inj. techniques Blood glucose measurement. Exercise. Diabetes and exercise. Psychological and family adjustment. Hypoglycaemia and its management. Diabetes management during illness. Travel. Dietetic principles. Contraception. Alcohol and Drugs. Diabetes complications. Driving. Smoking.

INSULIN REPLACEMENT

Insulin types
Rapid-acting Lyspro, aspart, glulysine Short-acting Regular Insulin Intermediate - Lente, NPH Long-acting - Ultralente, Glargine, Detemir

Physiologic Insulin Therapy

Prandial Boluses

Basal Insulin BG mg/dl

0hr

24hr

Insulin management
Fixed dose regimens:
requires scheduled meals and snacks and is not flexible enough for most young children

Basal bolus regimens:

MDI
useful only if child is willing to take frequent injections

Insulin pumps (CSII)

child must be willing to wear the pump

Location of injection

On Target!

Insulin pump therapy

Based on what body does naturally
- Small amounts of insulin all the time
(basal insulin)

- Extra doses to cover each meal or snack

(bolus insulin)

Rapid or Short-Acting Insulin Precision, micro-drop insulin delivery Flexibility Considered as a treatment option Initiated and supervised by a specialised multidisciplinary

Nutrition
adequate energy and nutrients, optimal growth and development, avoid hyperglycemia or hypoglycemia. Number of recommended meal : 6/day 3 main meal (25/20, 25/30 and 20/20) and 3 snacks (10%). Caloric:
1000 cal + 100 cal / year age Ideal BW + activity (<12 year)

Emergency conditions
Diabetic ketoacidosis Hypoglycemia

Longterm complications
Cardiovascular Neuropathy, Vascular Injury, and Amputations. Eye Complications. Kidney Damage (Nephropathy). Other Complications. Specific Complications in Women. Diabetes appears to affect female hormones. Specific Complications for Adolescents.

Diabetic Ketoacidosis
Hyperglycemia Insulin secretion

Beta Cell Toxicity +

Insulin resistance 2o obesity

Relative Insulin Deficiency

Lipolysis

Free Fatty Acids

Ketonemia Ketonuria

Manifestation of ketoacisodosis
Ketoacid accumulate when low insulin levels Abdominal discomfort nausea & emesis Dehydration, but still polyuria Sign of metabolic acidosis Diminish of neurocognitiv function coma The biochemical criteria : hyperglycaemia (> 200 mg/dL), pH <7.3 and or bicarbonate < 15

Type 2 DM

Childhood Obesity
The prevalence of childhood obesity is estimated to be 25 to 30 %. type 2 diabetes is increasing in children and adolescents obesity Family history of diabetes is strongly associated with type 2 diabetes in children

Type 2 Diabetes - One End of Continuum

Genetic Predisposition Environmental Trigger Beta Cell Obesity

the

Hyperglycemia

Dysfunction
Type 2 Diabetes

Insulin Resistance

Obesity

Insulin Resistance Metabolic Syndrome

Type 2DM NASH PCOS Dyslipidemia

Hypertension

Type 2 Diabetes - Risk factors

Obesity 85% overweight or obese on diagnosis
American Diabetes Association: Type 2 diabetes in children and adolescents (Consensus Statement). Diabetes Care 23:381389, 2000).

65% of children with type 2 diabetes have first degree relative with Type 2 diabetes
Pinhas-Hamiel O, Dolan LM, Daniels SR, Standiford D, Khoury PR, Zeitler P. Increased incidence of non-insulin-dependent diabetes mellitus among adolescents. J Pediatr.1996; 128 :608 615

74%-100% have first or second degree relative with type 2 diabetes

American Diabetes Association: Type 2 diabetes in children and adolescents (Consensus Statement). Diabetes Care 23:381389, 2000).

Type 2 Diabetes Risk factors

African American, Hispanic, Asian, Native American descent
American Diabetes Association Consensus Statement Type 2 Diabetes in Children and Adolescents Diabetes Care 2000;23(3) 381-389.

Increased insulin resistance (puberty,ethnicity, inactivity,visceral fat distribution,PCOS)

American Diabetes Association Consensus Statement Type 2 Diabetes in Children and Adolescents Diabetes Care 2000;23(3) 381-389.

Female/male 1.7:1
Pinhas-Hamiel O, Dolan LM, Daniels SR, Standiford D, Khoury PR, Zeitler P. Increased incidence of non-insulin-dependent diabetes mellitus among adolescents. J Pediatr.1996; 128 :608 615

Type 2 Diabetes- Prevalence

4.1/100,000 for all 15-19 year old American Indians up to 50.9/100,000 for 15-19 yr old Pima Indian
Fagot-Campagna A, Pettitt DJ, Engelgau MM, Ros Burrows N, Geiss LS, Valdez R, et al. Type 2 diabetes among North American children and adolescents: an epidemiological review and a public health perspective. J Pediatr 2000; 136: 664-672

Estimated incidence of type 2 diabetes 7.2/100,000/yr (Ohio 1994)

10 fold increase from 1982-1994

Pinhas-Hamiel O, Dolan LM, Daniels SR, Standiford D, Khoury PR, Zeitler P. Increased incidence of non-insulin-dependent diabetes mellitus among adolescents. J Pediatr.1996; 128 :608 615

Type 2 Diabetes - Risk

Lifetime risk of diabetes for individuals born in 2000
1 in 3 for males 2 in 5 for females
Narayan KM, Boyle JP, Thompson TJ, Sorensen SW, Williamson DF: Lifetime risk for diabetes mellitus in the United States. JAMA290 :1884 1890,2003

Components of the Met Syndr in Childhood

Abnormal blood lipids (HDL cholesterol <40mg/dl or triglycerides >150mg/dl LDL>130mg/dl). Impaired glucose tolerance (fasting glucose > 100 (110) mg/dl, random glucose >200mg/dl). Obesity (BMI >95% for age and sex) Elevated blood pressure (SBP or DBP > 90% for age).

Type 2 Diabetes
Diagnosis Elevated fasting insulin and hyperglycemia. Only 20% present with polyuria, polydipsia, and weight loss. Etiology One third of new diabetics presenting between 10-19 years had NIDDM.
Pinhas-Hamiel J Pediatr 1996;128:608-615.

 Acanthosis nigricans and polycystic ovarian syndrome (PCOS), disorders associated with insulin resistance and obesity, are common in youth with type 2 diabetes

Currently, type 2 diabetes are usually diagnosed over the age of 10 years and are in middle to late puberty

Acanthosis Nigricans

Dr. George Datto

Acanthosis Nigricans
Hyperpigmentation and velvety thickening that occurs in neck, axilla, and other skin folds In pediatrics, commonly in obese children. Also seen in malignancies and other insulin resistant syndromes.

Obese pediatric + acanthosis have higher fasting insulin and lower insulin sensitivity

Screening (ADA recomendation)

1. 10 years /puberty 2. BMI > p 85, BB > 120%

Family history
Special ethnic

Insulin resistent

OGTT every 2 years

Impaired glucose tolerance

Increased incidence of impaired glucose tolerance in obesity clinic population 25% of obese children (aged 4-10yrs)
21 % of obese adolescents (aged11-18 yrs)
Sinha R, Fisch G, Teague B, Tamborlane WV, Banyas B, Allen K, Savoye M, Rieger V, Taksali S, Barbetta G, Sherwin RS, Caprio S: Prevalence of impaired glucose tolerance among children and adolescents with marked obesity. N Engl J Med 346:802810, 2002

Diagnosis criteria
Diabetes mellitus 1. Symptom DM + Glucose random > 200 mg/dl 2. Fasting blood glucose > 125 mg/dl 2. Blood glucose, 2 hr OGTT > 200 mg/dl
Prediabetes 1. Gula darah puasa terganggu (> 11O & <125) 2. Toleransi glukosa terganggu (> 140 mg/dl & < > 200 mg/dl)

Treatment of Type 2 DM
Lifestyle changes Pharmaceutical therapy Biguanides Sulfonylureas Meglitinide Thiazolidenediones Monitoring for complications Hypertension and hyperlipidemia treatment

Nutrisi treatment
Children or adolescent calori requirement
Carbohydrat : 55%-60% Protein : 10-20% Fat : 30%

dr. H. Eva Decroli, SpPD-KEMD, FINASIM

DIABETES MELLITUS GESTASIONAL

PENDAHULUAN
Indonesia : Prevalensi DM Gestasional 1.9%3.6% Ibu hamil dengan riwayat keluarga DM 5.1% Dampak DMG pada kehamilan : Makrosomia, Preeklamsia, Malformasi janin, Peningkatan mortalitas perinatal Komplikasi jangka panjang : Resiko obesitas, Gangguan toleransi glukosa, sindroma metabolik dan DMT2

KLASIFIKASI MENURUT O Sullivan-Mahan

Diabetes pada kehamilan dibagi : 1. DM yang sudah diketahui sebelumnya dan kemudian menjadi hamil DM Tipe 1 dan Tipe 2 2. DM yang baru ditemukan saat hamil DM Gestasional

DEFINISI DMG
Suatu gangguan toleransi karbohidrat (TGT, GDPT, DM) yang terjadi atau diketahui pertama kali saat kehamilan sedang berlangsung (Perkeni, 2010)

PATOFISIOLOGI
Autoimun Kelainan genetik Insulin Resisten Kronik

Resistensi insulin pada kehamilan karena 1. Peningkatan deposit lemak pada ibu 2. Peningkatan hormon-hormon kehamilan : HPL, Progesteron, Kortisol dan Prolaktin

PENAPISAN DAN DIAGNOSIS

PERKENI Pemeriksaan penyaring DMG pada semua ibu hamil saat ANC 1 dan jika hasilnya negatif diulangi pada kehamilan 2628 minggu Diagnosis berdasarkan TTGO dengan beban 75 g glukosa setelah berpuasa 8-14 jam

DIAGNOSIS
DMG ditegakkan jika Glukosa darah puasa 95 mg/dl Glukosa darah1 jam setelah beban 180 mg/dl Glukosa darah 2 jam setelah beban 155 mg/dl

PENATALAKSANAAN
1. Edukasi diabetes 2. Perencanaan makan dan aktifitas fisik Untuk mencapai normoglikemia dan menjamin pertumbuhan serta perkembangan janin yang optimal. Kebutuhan kalori ibu hamil 35 kkal/kgBB

PENATALAKSANAAN
3. Pemantauan kadar glukosa darah Sasaran kendali glikemik menurut PERKENI : - Glukosa darah puasa : < 105 mg/dl - Glukosa darah 2 jam setelah makan : < 120 mg/dl

PENATALAKSANAAN
4. FARMAKOTERAPI - Terapi Obat Hipoglikemik Oral (OHO)
Tidak direkomendasikan pada Ibu Hamil karena banyak OHO yang bisa melewati barier plasenta dan tidak cukup kuat mengendalikan Glukosa darah post pandrial

- Terapi Insulin
Dilakukan jika dengan perencanaan makan dan aktifitas fisik tidak berhasil

KOMPLIKASI AKUT DIABETES

EVA DECROLI
PERKENI CABANG PADANG
88

KETOASIDOSIS DIABETIK

89

PENDAHULUAN
Keto berasal dari kata keton, yaitu suatu zat yang dibuat oleh tubuh, akibat pemecahan lemak selama ketoasidosis. Kata asam juga dipakai, karena keton tersebut membuat darah menjadi bersifat asam.

90

GEJALA
1. Mual dan muntah : karena banyak asam dan hilangnya zat-zat tubuh yang penting 2. Nafas yang cepat dan dalam (kusmaul breathing) akibat banyaknya asam tubuh, dan tubuh berusaha mengeluarkan sebagian asam melalui paru-paru. Nafas berbau seperti buah karena adanya aseton 3. Kelelahan dan rasa kantuk yang berlebihan : kelelahan karena otak dipenuhi darah yang sangat kental, seperti sirup, dan juga kehilangan zat penting yang keluar melalui urin 4. Lemas : karena jaringan otot tidak mendaptkan bahan bakarnya, yaitu : glukosa
91

Skema Patogenesis DKA dan HHS

Defisiensi insulin (mutlak)

PATOGENESIS
Glucagon Catecolamin Cortisol GH Proteolisis Proteinsintesis Gluconeogenic substrat Glukosa Utilisasi Gluconeogenesis Hiperglikemia Defisiensi insulin (relatif)

Liposis FFA Ketogenesis Alkali reserve

Ketoasidosis

glycogenolysis

Triacil glyceral hiperlipidemia

Osmotic diuresis Kehilangan air Kehilangan elektrolit Dehidrasi hiperosmolariti Fungsi ginjal
HHS

92

DKA

Kriteria Diagnosis DKA

Hiperglikemia

Asidosis DKA

Ketosis

93

Kriteria Diagnosis DKA

DKA
Ringan > 250 > 25 - > 30 15 8 + + > 10 Alert Sedang > 250 > 724 10 < -15 + + > 12 Drawsi Berat > 250 > < 10 + + > 12 Stupor/coma

Plasma Glukosa mg/dl PH Arteri Serum bicarbonat meq/l Serum Keton Ketonuria Anion Gap Status mental

94

Skema pemberian cairan untuk pada DKA

Cairan infus

Tentukan Status Hidrasi Hipotensi Ringan Hipovolemic syok Nacl 0,9 % 1 liter / jam dan atau plasma expander

Kardiogenik Syok

Evaluasi serum Na

Monitor Hemodinamik

Na Serum Tinggi

Na Serum Normal

Na Serum Rendah

Nacl 0.45 % 4-14 ml/kgBB/jam

Nacl 0.9 % 4-14 ml/kgBB/jam

Bila gula darah 250 mg % Pasang infus Dextrose

95

Yang harus diperiksa :

Kadar glukosa darah Analisa gas darah arteri Elektrolit Fungsi ginjal ECG X Ray
96

Observasi
Klinis dan status biokimia Contoh : jam : TD Nadi, urine tiap jam : analisa gas darah 2 jam : Elektrolit khususnya K

97

Cairan & Elektrolit

Kebanyakan pasien kehilangan cairan beberapa liter (40 80 ml/kg) ditambah dengan perkiraan kehilangan cairan 24 jam kedepan dan koreksi 1/3 kebutuhan dalam 5-6 jam I, yaitu 9 NaClo gr%
K. dievaluasi tiap 2 jam
98

Insulin
Bolus IV 0-15 unit/kg netral insulin Dan infus insulin 100 mnt/1000 cc saline Jika ada siringe pump 50 unit/50 cc salin, lalu infark 0.05 0.15/kgBB sesuai dosis tergantung kadar gula darah. KAD dapat berkomplikasi berupa trombosis arteri syok, lactic asidosis dan odema otak Setelah terapi inisiasi sebaiknya rujuk kespesialis
99

HIPOGLIKEMIA

100

Risk Factors and Consequences of Hypoglycemia in Type 2 Diabetes

Risk factors13
Use of insulin secretagogues and insulin therapy Missed or irregular meals Advanced age Long duration of diabetes Impaired awareness of hypoglycemia Exercise Taking greater than the prescribed dose of medication Consequences4,5 Suboptimal glycemic control Other health effects
1. Amiel SA et al. Diabet Med. 2008;25(3):245254. 2. American Diabetes Association. Diabetes Care. 2005;28(5):12451249. 3. Miller CD et al. Arch Intern Med. 2001;161:16531659. 4. Landstedt-Hallin L et al. J Intern Med. 1999;246(3):299307. 5. Cryer PE. J Clin Invest. 2007;117(4):868870.

101

American Diabetes Association Definition of Hypoglycemia

Hypoglycemia is a condition characterized by
Neuroglycopenic and/or neurogenic symptoms Low plasma glucose level Symptom relief after administration of carbohydrates

Hypoglycemia is defined as episodes of abnormally low plasma glucose concentration (70 mg/dL) that expose the individual to potential harm
American Diabetes Association. Diabetes Care. 2005;28(5):1245 102 1249.

American Diabetes Association Classification of Hypoglycemia

Severe hypoglycemia Documented symptomatic hypoglycemia Asymptomatic hypoglycemia Probable symptomatic hypoglycemia Relative hypoglycemia

American Diabetes Association. Diabetes Care. 2005;28(5):1245 103 1249.

Symptoms of Hypoglycemia
Neurogenic1,2
Adrenergic
Palpitations

Neuroglycopenic1,2
Cognitive impairments Behavioral changes Psychomotor abnormalities Seizure Coma

Tremor Anxiety/arousal

Cholinergic
Sweating Hunger Paresthesia

1. Cryer PE. J Clin Invest. 2007;117(4):868870. Factors affecting glycemic thresholds are poorly controlled type 1 and type 2 2. Cryer PE. Diabetes . 2003;26(6):1902 1912. diabetes, tight glycemic Care control in type 1 diabetes, and older age.2,3 3. Meneilly GS et al. J Clin Endocrinol Metab. 1994;78(6):1341 104 1348.

Potential Complications of Severe and Prolonged Hypoglycemia

105

Complications and Effects of Severe Hypoglycemia

Plasma glucose level
6 110 100 5 90 80 4 70 60 3 50 40 2 30 1 20
mg/dL

Increased Risk of Cardiac Arrhythmia1

Progressive Neuroglycopenia2

Abnormal prolonged cardiac repolarization QTc and QT dispersion Sudden death

mmol/L

Cognitive impairment Unusual behavior Seizure Coma Brain death

10

1. Landstedt-Hallin L et al. J Intern Med. 1999;246:299307. 2. Cryer PE. J Clin Invest. 2007;117(4):868870.

106

Severe and Prolonged Hypoglycemia Increases Morbidity and Mortality

Glucose is necessary for metabolic function in the brain.1
The brain depends on circulating glucose because it cannot synthesize its own.1 When arterial glucose levels fall, blood-to-brain glucose transport is slowed, limiting brain metabolism and, eventually, survival.1

Hypoglycemia is the cause of 6% to 10% of deaths of 1. Cryer PE et al. Diabetes Care . 2003;26(6):1902 1912. 2,3 people with type 1 diabetes. 2. DCCT/EDIC Study Research Group. N Engl J Med. 2007;356:1842 1852. Fatal hypoglycemia is not limited to type 1 diabetes.4 3. Skrivarhaug T et al. Diabetologia. 2006;49:298305. 107 4. Cryer PE. J Clin Invest. 2006;116(6):14701473.

A History of Severe Hypoglycemia Is Associated With a Greater Risk of Dementia

Attributable risk of dementia with any hypoglycemia: 2.39% (1.72 3.01)a

7
Excess Attributable Risk Per Year, % (95% CI)

6 5 4 3
4.34

4.28

2 aAttributable 1

risk calculated as difference between rate in group and 1.64 rate in reference group (0 hypoglycemic events).n=205 n=1,002 n=258 0 bDiagnoses of hypoglycemia were 2 identified using 1 3ICD-9-CM codes Number of Severe Hypoglycemic Episodesb hypoglycemia), and 251.0 (hypoglycemic coma), 251.1 (other specified 251.2 (hypoglycemia, unspecified). 108 Whitmer RA et al. JAMA. 2009;301(15):15651572.

Severe Hypoglycemia May Cause a Prolongation of QT Interval in Patients With Type 2 Diabetes
Baseline (t=0) End of clamp (t=150 min) 450 Mean QT interval, ms P=0.0003

440
430

420
410 400 390

P=NS

NS=not significant. 380 Thirteen patients with type 2 diabetes taking combined insulin and 370 glibenclamide treatment were studied during hypoglycemia; 8 360 participated 0 in the euglycemic experiment clamped between 5.0 and Euglycemic clamp Hypoglycemic clamp (n=8) 2 weeks after 6.0 mmol/L. The aim was to achieve stable hypoglycemia between 2.5 glibenclamide withdrawal (n=13) and 3.0 mmol/L (45 and 54 mg/dL) during the last 60 minutes of the experiment. 109 Landstedt-Hallin L et al. J Intern Med. 1999;246:299307.

Significant prolongation of QT interval after hypoglycemic clamps Increased risk of arrhythmias

Nutrisi pada Diabetes Melitus dan Gestational Diabetes Melitus

Nur Indrawaty Liputo Bagian Ilmu Gizi FK - UNAND

Pilar Utama penanggulangan DM

1. 2. 3. 4. Edukasi Perencanaan Makan Latihan Jasmani Obat

Edukasi
Prinsip
Bertahap Tidak terlalu banyak Sesuaikan dengan masalah pasien Perhatiakn kondisi psikologis, jasmani, pendd Libatkan keluarga Nasihat yang besarkan hati Audio-visual aid Kompromi Diskusi hasil lab Motivasi dan penghargaan hasil

 Penyuluhan
Penyuluhan untuk pencegahan primer Penyuluhan untuk pencegahan sekunder Penyuluhan untuk pencegahan tersier

Penyuluhan primer
Sasaran
Kelompok masyarakat risiko tinggi DM Perencana kebijakan kesehatan

Tujuan:
Mencegah atau mengurangi kejadian DM

Materi
Faktor berpengaruh dan usaha mengatur DM

Penyuluhan Sekunder
Sasaran
Kelompok pasien DM

Tujuan
Mencegah komplikasi

Materi
Tingkat pertama
Apa itu DM Penatalaksanaan DM Perencanaan makan DM dan latihan jasmani Obat Pemantauan gula darah

 TINGKAT LANJUT
Komplikasi akut DM Komplikasi menahun DM Dm dan penyakit lain Makan diluar rumah DM ketika bepergian Pemeliharaan kaki Pengetahuan mutakhir DM

Penyuluhan tersier
Sasaran
Kelompok DM dg komplikasi

Tujuan
Mencegah kecacatan

 Materi
Pengobatan komplikasi DM Uapaya rehabilitasi Kesabaran dan ketaqwaan untuk menerima keadaan

Pokok bahasan
Pengetahuan umum tentang DM: gejala, diagnosis, klasifikasi, macam pengobatan Evaluasi nutrisi: interaksi obat dg mak, makanan dan kegiatan jasmani Latihan jasmani dan hipoglikemia Pemantauan glukosa darah dan keton urin Kerja insulin (atau obat oral): pemilhan insulin, teknik penyuntikan insulin

Pokok bahasan
Hipoglikemia, hiperglikemia, ketoasidosis diabetik: sebab gejala, pengoabatan Sikap biala sakit atau gawat darurat Pra konsepsi, diabetes gestasional, gula darah selama hamil, dan faktor risiko Komplikasi menahun: deteksi, cara pengobatan, pencegahan, rehabilitasi Pemeliharaan kuku, gigi, kulit Fasilitas kesehatan Startegi perubahan prilaku

Diabetes Melitus Tipe 1

Metabolisme tubuh dalam keadaan diabetes berat (tak terkontrol)
Terjadi hiperglikemia, ketoasidosis, dan hipertrigliserida

Diabetes Melitus tipe 2

Hampir sama dengan DM tipe 1 tetapi jarang atau tidak ditemukannya ketoasidosis.

Metabolisme zat gizi pada hamil normal

Selama hamil terjadi perubahan metabolisme karbohidrat dan lemak Agar memungkinkan suplai makanan terus menerus untuk janin Penurunan sensitifitas insulin Peningkatan sekresi insulin Peningkatan produksi glukosa hepatik Peningkatan penggunaan karbohidrat

 Peningkatan kadar estrogen, progesteron, insulin mencegah lipolisis akumulasi penyimpanan lemak pada tubuh ibu

Gestational Diabetes Melitus (GDM)

Manajemen GDM: memperbaiki sensitifitas insulin
Melalui diet, aktifitas, pengendalian BB

Metabolisme pada GDM

Definisi GDM: gangguan toleransi glukosa yang terjadi pada saat hamil GDM: umur, kegemukan dan genetik Faktor risiko DM Terjadi peningkatan resistensi insulin di perifer

 Terjadi peningkatan kadar trigliserida, asam lemak dan asam amino

Asam lemak ibu menyeberangi plasenta makrosemia

Diet Diabetes Melitus

Komposisi
Karbohidrat 60 70% Protein 10 15% Lemak 20 25%

Status gizi
IMT: BB/TB2
Normal wanita: 18,5-23,5 Normal pria: 22,5-25

Indeks Broca: BBI: (TB-100)-10%

BB kurang: <90% BBI BB normal: 90-110%BBI BB lebih: 110-120% Gemuk: >120% BBI

Kalori basal

Laki-laki: BBI x 30 kkal Wanita: BBI x 25 kkal

 Koreksi/penyesuaian
Umur >40 tahun: -5% x kalori basal Aktifitas ringan: +10% x kalori basal Aktifitas sedang: +20% x kalori basal Aktifitas berat: : 30% x kalori basal BB gemuk: -20% x kalori basal BB lebih: -10% x kalori basal BB kurang: +20% x kalori basal Stress metabolik: + (10-30%) x kalori basal Hamil trim I&II = +300 kkal Hamil trim III/laktasi = +500 kkal

DM dan Berat Badan

Pasien DM dan Gangguan Toleransi glukosa fat abdominal>>> insulin resistance, dislipidemia, hipertensi penurunan BB risiko PJK menurun Penurunan 1-2 kg/bln atau 2-4 kg/bln Ketergantungan insulin dapat distop dg penurunan BB

Karbohidrat
Indeks glisemik: menunjukkan kapasitas makanan menaikkan kadar gula darah yang dibanding dengan roti Untuk memilih makanan mengandung tepung Dipengaruhi: tingkat daya cerna dan absorpsi karbohidrat yang ada pada makanan,dan adanya protein, lemak, jenis serat dan metoda masak

Karbohidrat kompleks dan serat tinggi

Serat: larut dan tidak larut Serat larut: gums, gels, pectin Serat tidak larut: selulosa dan lignin Serat larut: menurunkan indeks glisemik dan membantu metabolisme lemak Serat larut: memperbaiki sensitifitas insulin Serat larut: modifiaksi aktifitas hormon cerna, fermentasi di usus besar dan pembentukan Short chain fatty acid Serat larut: menurunkan kolesterol

Pemanis
Sukrosa: tidak menaikkan GD dibanding makanan karbohidrat dengan jumlah kalori sama Sukrosa dalam dosis tinggi (1-1,5g/kgBB) dapat menaikkan trigliserida Tidak disarankan pada overweight dan hipertrigliseridemia bagian dari karbohidrat

Fruktosa
Dibanding sukrosa, fruktosa lebih tidak menaikkan GD dan meningkatkan respon insulin.
Fruktosa alamiah pada buah2an: aman untuk DM

 Nutritive sweeteners seperti madu, maltosa, alkohol: mengandung kalori harus dihitung Non nutritive sweeteners: sakarin, siklamat, aspartam, alitame, dan sucrolose dibolehkan untuk menurunkan BB Aman????

Protein
Disarankan rendah: 0,8 g/kg BB Pada pasien dengan riwayat preclinical diabetic nephropathy: 0,6 gr/kg BB Tapi protein <0,6 gr/kg BB: menyebabkan kehilangan lean body mass (otot) sekalipun kalori tinggi

Vitamin dan aktioksidan

Vitamin A dan karoten: antioksidan, mengurangi komplikasi PKV pada DM Vitamin B: tiamin, piridoksin, riboflavin, niacin sbg koenzim dalam katabolisme karbohidrat, lemak dan protein Diabetes tak terkontrol: ekskresi vit B>>> dalam urin perlu suplemen vit B

DM: ggn metabolisme vitamin C Def. vit C: risiko katarak Vitamin D: def vit D ggn sekresi insulin Vitamin E: menghambat peroksidasi vit A dan lemak Vit E: menghambat katarak Flavonoid: antioksidan mengurangi risiko PJK pada DM

Mineral
DM: rendah natrium, garam <6 gr/hari Zinc: defisiensi ggn sekresi insulin Chromium: meningkatkan ikatan insulin dalam transporasi glukosa (Glucose tolerance factor) Defisiensi Cr: meningkatkan Gula Darah

Referensi
Nancy F Butte. Carbohydrate and lipid metabolism in pregnancy: normal compared with gestational diabetes mellitus; American Journal of Clinical Nutrition, Vol. 71, No. 5, 1256S-1261s, May 2000

OBAT HYPERGLIKEMIA
Elly Usman Bagian Farmakologi dan Terapi

PROSES TERAPI

ANAMNESIS

DIAGNOSIS

TENTUKAN RENCANA TERAPI

R/ NON TERAPI

R/

BERI OBAT BERI INFO EVALUASI

INSULIN
INSULIN KERJA CEPAT INSULIN KERJA PENDEK INSULIN KERJA MENENGAH KERJA PANJANG INSULIN CAMPURAN TETAP

MEKANISME KERJA
PERMUKAAN LUAR MEMBRAN SEL SINTESIS GLIKOGEN MENINGKATKAN AMBILAN ION K DAN ION MAGNESIUM SECOND MESENGER

EFEK SAMPING
HIPOGLIKEMIA
REAKSI IMUN INSULIN RESISTENSI

HIPERTROPI
GANGUAN PENGLIHATAN

INTERAKSI
HORMON
KORTIKOSTEROID TIROID ESTEROGEN PROGESTIN GLUKAGON

ANTIBIOTIKA SALISILAT PENGHAMBAT ADRENORESEPTOR PENGHAMBAT MAO

DASAR TERAPI
INSULIN MAMPU MENIRU SEKRERSI INSULIN FISIOLOGIS DEFIIENSI INSULIN BASA, PRANDIAL ATAU KEDUANYA HIPERGLIKEMIA SUBSITUSI DIBERIKAN SECARA TUNGGAL

CARA PEMBERIAN
DIBAWAH KULIT
KEADAAN KHUSUS : IV, IM, BOLUS ATAU DRIP LOKASI PENYUNTIKAN PENYIMPANAN

OBAT HIPOGLIKEMI ORAL (OHO)

SULFONIL UREA
GENERASI I GENERASI II

BIGUANID

 PEMICU SEKRESI INSULIN

S.U GLINID

MEKANISME KERJA

PENAMBAH SENSITIVITAS THD INSULIN :

TIAZOLIDINDION

PENGHAMBAT GLUKONEOGENESIS
METFORMIN

PENGHAMBAT ABSOPSI GLUKOSA

ARCABOSE

FARMAKOKINETIK
ABSORBSI BAIK [ ] OPTIMAL DICAPAI 30 MENIT ac t 1/2 bervariasi S U generasi II 12 -24 jam semel de die METABOLISME DI HATI EKRESI MLL GINJAL : Chlorpropamid

BSO dan DOSIS

SU
BSO : TABLET DOSIS : TUNGGAL TERBAGI BEBERAPA DOIS BIGUANID BSO : TABLET DOSIS : 2 3 KALI SEHARI

EFEK SAMPING
SU
GLINID METFORMIN TIAZOLIDINDION

: HIPOGLIKEMIA
BB NAIK

: HIPOGLIKEMIA
BB NAIK

: DIARE
DISPEPSIA ACIDOSIS LAKTAT

: EDEMA

KONTRA INDIKASI
ACIDOSIS LUKA BAKAR BERAT COMA DIABETIKUM INFEKSI BERAT BEDAH MAYOR TRAUMA BERAT KONDISI TERTENTU

BIGUANID
INDIKASI
DM RINGAN # DIET SU OBESITAS TERAPI KOMBINASI DGN SU TERAPI KOMBINASI DGN INSULIN

KONTRA INDIKASI
PENDERITA PENYAKIT HATI PENDERITA PENYAKIT GINJAL DGN UREMIA PENDERITA PENYAKIT JANTUNG KONGESTIF HAMIL

TERIMA KASIH

EVA DECROLI
PERKENI CABANG PADANG
166

Definisi
American Diabetes Association (ADA) tahun 2010 suatu kelompok penyakit metabolik dengan karakteristik hiperglikemia yang terjadi karena kelainan sekresi insulin, kerja insulin, atau keduaduanya.

167

Klasifikasi etiologis :

168

169

Diagnosis DM dapat ditegakkan melalui tiga cara:

1. Jika keluhan klasik ditemukan, maka pemeriksaan glukosa plasma sewaktu >200 mg/dL sudah cukup untuk menegakkan diagnosis DM 2. Pemeriksaan glukosa plasma puasa 126 mg/dL dengan adanya keluhan klasik. 3. Tes toleransi glukosa oral (TTGO). Meskipun TTGO dengan beban 75 g glukosa lebih sensitif dan spesifik dibanding dengan pemeriksaan glukosa plasma puasa, namun pemeriksaan ini memiliki keterbatasan tersendiri. TTGO sulit untuk dilakukan berulang-ulang dan dalam praktek sangat jarang dilakukankarena membutuhkan persiapan khusus. 170

Kriteria diagnosis DM

171

172

PILAR PENATALAKSANAAN DIABETES

1. Edukasi 2. Terapi gizi medis 3. Latihan jasmani 4. Intervensi farmakologis

173

Algoritma pengelolaan DM tipe 2 tanpa disertai dekompensasi

174

Tahap 1
Gaya hidup +
Saat diagnosis:

Tahap 2

Tahap 3

Gaya hidup + Metformin +

Metformin +

Gaya hidup + Metformin

Well validated core therapies

Insulin basal

Insulin intensif

Gaya hidup + Metformin +

Sulfonilurea
Gaya hidup + Metformin +

Gaya hidup + Metformin +

Pioglitazon

Pioglitazon + sulfonilurea

Gaya hidup +
Less well validated core therapies

Gaya hidup + Metformin +

Metformin +

GLP-1 agonis

Basal insulin

175

Nathan DM et al, Diabetes Care 32:193203, 2009

Target Pengendalian DM

176

TERIMA KASIH

177