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DIABETES MELLITUSPROBLEMS AND MANAGEMENT
Eva Decroli
Problems
• Increased of prevalence
• Cronic complications
ex. Diabetic Foot Problems
• Prevention, primer, secunder tertier
Etiology of Insulin Resistence
Weight gainObexisity
Circulation FFA Lipoatrophyadipokines
Insulin ResistanceThe subnormal biologic response to
a given concentration of insulin
Physicalinactivity Aging Genetica
Etiology of -Cell Dysfunction
Genetics Lipotoxicity Glucose toxicity
-Cell FailureInadequate 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 EnvironmentInsulinresistance
Diabetes genes insulin resistance genes-cel function genesObesity genes
Decreased Insulinsecretion
Type DM
Diet Activity Toxins
Risk Factors for Type 2 Diabetes
Genetic factors-Ethnicity-Family history
GastationalDiabetes polycystic Ovarian syndrome, and party
Type 2Diabetes
Increasing age Central
obesity
Physicalinactivity
Diet
Pathophysiology of DM
Hepatic glucoseProduction (HGP
Peripheral GlucoseUptake
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
Complek interaction between
• Periperal neuropaty
• Micro angiopathy
• Macro vascular disease
• Poor foot hygiene
Diabetic Foot Problems
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 hypergly-cemic ogents
Dr. H. Eva Decroli SpPD KEMD Dr. H. Eva Decroli SpPD KEMD FINASIMFINASIM
PENATALAKSANAAN DM
PILAR PENATALAKSANAANDIABETES
• 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
- dst
LATIHAN JASMANI
• 150/menit/minggu• Frekuensi 3-4 kali seminggu• Continue • Ritmik• Aerobik• Teratur • Terukur • Progressif• Endurance
INTERVENSI FARMAKOLOGIS
Algoritma pengelolaan DM tipe 2 tanpa disertai dekompensasi
25
Saat diagnosis:
Gaya hidup
+
Metformin
Gaya hidup +
Metformin +
Insulin basal
Gaya hidup +
Metformin +
Sulfonilurea
Gaya hidup +
Metformin +
Insulin intensif
Gaya hidup +
Metformin +
Pioglitazon
Gaya hidup +
Metformin +
GLP-1 agonis
Gaya hidup +
Metformin +
Pioglitazon + sulfonilurea
Gaya hidup +
Metformin +
Basal insulin
Well validated core therapies
Less well validated core therapies
Tahap 1 Tahap 2 Tahap 3
Nathan DM et al, Diabetes Care 32:193–203, 2009
26
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
PoliuriaPolidipsiPoli 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
Insulin secretionor ≠
Pathogenesis
• Destruction of β-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
Utilization glucose decreased postprandial hyperglycemia
Glycogenolysis and gliconeogenesis fasting hyperglycemia
Glucosuria
Loss of calorie and electrolyte, dehydration
Insulinopenia
Clinical Manifestation
• Phase of type 1 DM1. Prediabetes
2. Presentation of diabetes
3. Partial remission or honeymoon
4. Chronic phase of lifelong dependency on administrated insulin
Clinical manifestation
• Polyuria Polyuria or nocturia glucosuria
• PolydipsiaPolydipsia
• Polyphagia calories lost in urine
• Weight lossWeight loss
• Monilial vaginitisvaginitis 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-peptideLow or undetectable C-peptide
• ICA positiveICA 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
Basal Insulin
Prandial BolusesIn
suli
n
0hr 24hr
BG
mg/
dlPhysiologicPhysiologic Insulin TherapyInsulin Therapy
• 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
Insulin management
On Target!On Target!Location of injection
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 conditionsEmergency conditions– Diabetic ketoacidosis
– Hypoglycemia
Longterm complicationsLongterm 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 Beta Cell Toxicity
Insulin secretion +Insulin resistance 2o
obesity
Relative Insulin Deficiency
LipolysisFree
Fatty AcidsKetonemia
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 the Continuum
Genetic Predisposition
Environmental Trigger
Obesity
Insulin Resistance
Beta
Hyperglycemia
Type 2 Diabetes
Dysfunction
Cell
Insulin Resistance
Obesity
Metabolic SyndromeType 2DM
NASH
PCOSDyslipidemia
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 23:381–389, 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 23:381–389, 2000).
1.
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, Ríos 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 lipidsAbnormal blood lipids (HDL cholesterol <40mg/dl or triglycerides >150mg/dl LDL>130mg/dl).
• Impaired glucose toleranceImpaired glucose tolerance (fasting glucose > 100 (110) mg/dl, random glucose >200mg/dl).
• ObesityObesity (BMI >95% for age and sex)• Elevated blood pressureElevated 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)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 346:802–810, 2002
Diagnosis criteria
Diabetes mellitusDiabetes mellitus1. Symptom DM + Glucose random > 200 mg/dl2. Fasting blood glucose > 125 mg/dl2. Blood glucose, 2 hr OGTT > 200 mg/dl
PrediabetesPrediabetes1. 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%
DIABETES MELLITUS GESTASIONAL
dr. H. Eva Decroli, SpPD-KEMD, FINASIM
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
Resistensi insulin pada kehamilan karena 1. Peningkatan deposit lemak pada ibu2. 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 26-28 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
PENATALAKSANAAN4. 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 InsulinDilakukan jika dengan perencanaan makan dan aktifitas
fisik tidak berhasil
KOMPLIKASI AKUT DIABETES
EVA DECROLIPERKENI CABANG
PADANG88
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
GEJALA1. Mual dan muntah : karena banyak asam dan
hilangnya zat-zat tubuh yang penting2. 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
PATOGENESIS
Defisiensi insulin(mutlak)
Defisiensi insulin(relatif)
KetoasidosisGlukosaUtilisasi
Gluconeogenesis glycogenolysis
Hiperglikemia
Glucagon Catecolamin Cortisol GH
Liposis FFA Ketogenesis Alkali reserve
Proteolisis Proteinsintesis Gluconeogenic substrat
Triacil glyceral
hiperlipidemia
Osmotic diuresis
Kehilangan airKehilangan elektrolit
Dehidrasi hiperosmolariti
Fungsi ginjal
HHS
DKA
Skema Patogenesis DKA dan HHS
92
Kriteria Diagnosis DKA
Ketosis
Hiperglikemia Asidosis
DKA
93
Kriteria Diagnosis DKA
DKADKA
Plasma Glukosa mg/dlPlasma Glukosa mg/dl
PH ArteriPH Arteri
Serum bicarbonat meq/lSerum bicarbonat meq/l
Serum KetonSerum Keton
KetonuriaKetonuria
Anion GapAnion Gap
Status mentalStatus mental
RinganRingan
> 250> 250
> 25 - > 30> 25 - > 30
15 – 815 – 8
++
++
> 10> 10
AlertAlert
SedangSedang
> 250> 250
> 724> 724
10 < -1510 < -15
++
++
> 12> 12
DrawsiDrawsi
BeratBerat
> 250> 250
>>
< 10< 10
++
++
> 12> 12
Stupor/comaStupor/coma
94
Cairan infus
Tentukan Status Hidrasi
Nacl 0.45 %4-14 ml/kgBB/jam
Nacl 0.9 %4-14 ml/kgBB/jam
Bila gula darah 250 mg %Pasang infus Dextrose
Hipovolemic syok Nacl 0,9 %1 liter / jamdan atau plasma expander
Hipotensi Ringan
Evaluasi serum Na
Kardiogenik Syok
Monitor Hemodinamik
Na Serum Tinggi Na Serum Normal Na Serum Rendah
Skema pemberian cairan untuk pada DKA
95
Yang harus diperiksa :
- Kadar glukosa darah
- Analisa gas darah arteri
- Elektrolit
- Fungsi ginjal
- ECG
- X Ray
96
Observasi
Klinis dan status biokimia
Contoh :
½ 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 factors1–3
– 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):245–254.2. American Diabetes Association. Diabetes Care. 2005;28(5):1245–1249.3. Miller CD et al. Arch Intern Med. 2001;161:1653–1659.4. Landstedt-Hallin L et al. J Intern Med. 1999;246(3):299–307.5. Cryer PE. J Clin Invest. 2007;117(4):868–870.
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):1245–1249. 102
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):1245–1249. 103
Symptoms of Hypoglycemia
Neurogenic1,2 Neuroglycopenic1,2
AdrenergicPalpitations
Tremor
Anxiety/arousal
CholinergicSweating
Hunger
Paresthesia
Cognitive impairments Behavioral changes Psychomotor abnormalities Seizure Coma
Factors affecting glycemic thresholds are poorly controlled type 1 and type 2 diabetes, tight glycemic control in type 1 diabetes, and older age.2,3
1. Cryer PE. J Clin Invest. 2007;117(4):868–870.2. Cryer PE. Diabetes Care. 2003;26(6):1902–1912.3. Meneilly GS et al. J Clin Endocrinol Metab. 1994;78(6):1341–1348. 104
Potential Complications of Severe and Prolonged Hypoglycemia
105
Complications and Effects of Severe Hypoglycemia
Plasma glucose level
10
20
30
40
50
60
70
80
90
100
110
1
2
3
4
5
6
mg/dL
mmol/L
1. Landstedt-Hallin L et al. J Intern Med. 1999;246:299–307.2. Cryer PE. J Clin Invest. 2007;117(4):868–870.
Increased Risk of Cardiac Arrhythmia1
Progressive Neuroglycopenia2
Abnormal prolonged cardiac repolarization—↑ QTc and QT dispersion
Sudden death
Cognitive impairment Unusual behavior Seizure Coma Brain death
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 people with type 1 diabetes.2,3
• Fatal hypoglycemia is not limited to type 1 diabetes.4
1. Cryer PE et al. Diabetes Care. 2003;26(6):1902–1912.2. DCCT/EDIC Study Research Group. N Engl J Med.
2007;356:1842–1852.3. Skrivarhaug T et al. Diabetologia. 2006;49:298–305.4. Cryer PE. J Clin Invest. 2006;116(6):1470–1473. 107
0
1
2
3
4
5
6
7
1 2 ≥3Number of Severe Hypoglycemic Episodesb
Exce
ss A
ttrib
utab
le R
isk
Per Y
ear,
% (9
5% C
I)ª
A History of Severe Hypoglycemia Is Associated With a Greater Risk of Dementia
aAttributable risk calculated as difference between rate in group and rate in reference group (0 hypoglycemic events).bDiagnoses of hypoglycemia were identified using ICD-9-CM codes 251.0 (hypoglycemic coma), 251.1 (other specified hypoglycemia), and 251.2 (hypoglycemia, unspecified).Whitmer RA et al. JAMA. 2009;301(15):1565–1572.
Attributable risk of dementia with any hypoglycemia: 2.39% (1.72–3.01)a
n=1,002 n=258 n=205
1.64
4.34 4.28
108
Severe Hypoglycemia May Cause a Prolongationof QT Interval in Patients With Type 2 Diabetes
P=NS
P=0.0003
NS=not significant.Thirteen patients with type 2 diabetes taking combined insulin and glibenclamide treatment were studied during hypoglycemia; 8 participated in the euglycemic experiment clamped between 5.0 and 6.0 mmol/L. The aim was to achieve stable hypoglycemia between 2.5 and 3.0 mmol/L (45 and 54 mg/dL) during the last 60 minutes of the experiment.Landstedt-Hallin L et al. J Intern Med. 1999;246:299–307.
Euglycemic clamp(n=8)
Hypoglycemic clamp2 weeks after
glibenclamide withdrawal(n=13)
Significant prolongationof QT interval after hypoglycemic clamps– Increased risk of
arrhythmias
0
360
370
380
390
400
410
420
430
440
450
Mea
n Q
T in
terv
al, m
s
Baseline (t=0)End of clamp (t=150 min)
109
Nutrisi pada Diabetes Melitus dan Gestational Diabetes Melitus
Nur Indrawaty LiputoBagian Ilmu GiziFK - UNAND
Pilar Utama penanggulangan DM
1. Edukasi
2. Perencanaan Makan
3. Latihan Jasmani
4. 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
NON TERAPIBERI OBATBERI INFOEVALUASI
R/ R/
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 RESISTENSI INSULIN
• HIPERTROPI
• GANGUAN PENGLIHATAN
INTERAKSI
• HORMON• KORTIKOSTEROID
• TIROID
• ESTEROGEN
• PROGESTIN
• GLUKAGON
• ANTIBIOTIKA• SALISILAT• PENGHAMBAT ADRENORESEPTOR β• 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
MEKANISME KERJA• PEMICU SEKRESI INSULIN
– S.U
– GLINID
• 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
• S U : HIPOGLIKEMIA
BB NAIK
• GLINID : HIPOGLIKEMIA
BB NAIK
• METFORMIN : DIARE
DISPEPSIA
ACIDOSIS LAKTAT
• TIAZOLIDINDION : 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 DECROLIPERKENI 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 kedua-duanya.
167
Klasifikasi etiologis :
168
169
Diagnosis DM dapat ditegakkan melalui tiga cara:
1. Jika keluhan klasik ditemukan, maka pemeriksaan glukosaplasma sewaktu >200 mg/dL sudah cukup untuk menegakkandiagnosis DM2. Pemeriksaan glukosa plasma puasa ≥ 126 mg/dL denganadanya keluhan klasik.3. Tes toleransi glukosa oral (TTGO). Meskipun TTGO
denganbeban 75 g glukosa lebih sensitif dan spesifik dibandingdengan pemeriksaan glukosa plasma puasa, namunpemeriksaan ini memiliki keterbatasan tersendiri. TTGO sulituntuk dilakukan berulang-ulang dan dalam praktek sangatjarang dilakukankarena membutuhkan persiapan khusus. 170
Kriteria diagnosis DM
171
172
PILAR PENATALAKSANAANDIABETES
• 1. Edukasi
• 2. Terapi gizi medis
• 3. Latihan jasmani
• 4. Intervensi farmakologis
173
Algoritma pengelolaan DM tipe 2 tanpa disertai dekompensasi
174
Saat diagnosis:
Gaya hidup
+
Metformin
Gaya hidup +
Metformin +
Insulin basal
Gaya hidup +
Metformin +
Sulfonilurea
Gaya hidup +
Metformin +
Insulin intensif
Gaya hidup +
Metformin +
Pioglitazon
Gaya hidup +
Metformin +
GLP-1 agonis
Gaya hidup +
Metformin +
Pioglitazon + sulfonilurea
Gaya hidup +
Metformin +
Basal insulin
Well validated core therapies
Less well validated core therapies
Tahap 1 Tahap 2 Tahap 3
Nathan DM et al, Diabetes Care 32:193–203, 2009
175
Target Pengendalian DM
176
TERIMA KASIH
177