diabetes mellitus

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Diabetes Mellitus

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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

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