Diabetes Mellitus

Oleh :
Prilian Akbaril
Farah Nishfi Ramadhani
Adinda Amaliadani
Melyana Habibie
SUPERVISOR:
dr. Laksmi Sasiarini Sp.PD

Outline
Definisi

Epidemiolo
gi

Klasifikasi

Kriteria
Diagnosis

Manifestasi
Klinis

Patofisiologi

Tata
Laksana

Prognosis

Definisi
Diabetes mellitus merupakan suatu kelompok
penyakit metabolik dengan karakteristik
hiperglikemia yang terjadi karena kelainan sekresi
insulin, kerja insulin, atau kedua-duanya
(Purnamasari D, 2009).
Diabetes mellitus merupakan suatu kelainan yang
bersifat kronis yang ditandai dengan terganggunya
metabolisme glukosa dan sumber energi lainnya
yang akan berakibat pada komplikasi vaskuler dan
neuropati (Inzucchi E.s and sherwin r.s, 2007).

Epidemiologi
21 juta penduduk amerika (7% dari seluruh penduduk
Amerika) terdiagnosis diabetes mellitus, 21% dari penduduk
tersebut adalah yang berusia lebih dari 60 tahun, dan 30%
dari mereka tidak mengetahui bahwa terkena diabetes
mellitus (Purnamasari D, 2009).

285 JUTA ORANG DI DUNIA MENDERITA DIABETES MELLITUS

PADA TAHUN 2010 (WORLD DIABETES FOUNDATION, 2010).

8,4 JUTA PENDERITA DM DAN AKAN MENCAPAI 21,3 JUTA

TAHUN 2030. INDONESIA URUTAN KE-4
(Kusumadewi, 2009).

Klasifikasi Diabetes Mellitus (ADA, 2009)

I. Diabetes Melitus tipe 1
(destruksi sel , umumnya menjurus ke defisiensi insulin absolut)
A. Melalui proses imunologik
B. Idiopatik
II. Diabetes Mellitus tipe 2
(Bervariasi mulai yang predominan resistensi insulin disertai defisiensi insulin relative
sampai yang predominan gangguan sekresi insulin bersama resistensi insulin)
III.
A.
B.
C.
D.
E.
F.
G.

Diabetes Mellitus tipe lain

Defek genetik fungsi sel
Defek genetik kerja insulin
Penyakit Eksokrin Pankreas
Endokrinopati
Karena obat/zat kimia
Infeksi
Sindroma genetik lain

IV. Diabetes kehamilan

TYPE 1 DIABETES MELLITUS

Patofisiologi

Clinical Manifestations
Classically, symptoms appear abruptly (i.e., during days or

weeks) in previously healthy, nonobese children or young

adults who may have close relatives with the disease but more
commonly do not
Most type 1 diabetic patients are ill and symptomatic, most
commonly presenting with polyuria, polydipsia, polyphagia,
and weight loss; such patients may also present with
ketoacidosis
Type 1 diabetes is believed to have a prolonged asymptomatic
preclinical phase (often lasting years), during which
pancreatic cells are gradually destroyed by an autoimmune
attack influenced by HLA and other genetic factors as well as
by the environment

Kriteria diagnosis
Gejala klasik DM + GDS 200
mg/dL
Gejala klasik DM + GDP 126
mg/dL
Glukosa 2 jam PP pada TTGO
200 mg/dL

Tata laksana

Life style

Diet
Exercise

Insulin
Farmakolog Oral glucose-lowering
i
drugs

LIFESTYLE MODIFICATIONS FOR PATIENTS WITH DIABETES

DIETARY PRESCRIPTION
Weight reduction, gain, or maintenance to achieve and to maintain ideal
body weight

Restriction of saturated fat to less than 10% of total calories, to be

replaced in the diet by carbohydrates and monounsaturated fats; if low-density
lipoprotein reduction is also desired, saturated fats should be further restricted to
less than 7% of daily calorie intake

Decreased cholesterol intake to less than 300 mg/day; if low-density

lipoprotein reduction is also desired, cholesterol intake should be further
restricted to less than 200 mg/day

Sodium restriction (<2.4 g/day) in patients with hypertension; with overt

nephropathy, sodium intake should be further restricted to less than 2.0 g/day

Protein restriction to less than 20% of total calories; with nephropathy,

protein intake should be further restricted to less than 0.8 mg/kg/day or to about
10% of daily calorie intake

EXERCISE PRESCRIPTION
A combination of aerobic exercise and resistance training is preferred. Avoid heavy lifting,
straining, and Valsalva maneuvers, which can raise blood pressure and may aggravate proliferative
diabetic retinopathy.

Intensity: Increase heart rate moderately to at least 55% of maximal heart rate (220 minus
age in years), with adjustments based on the patient's cardiovascular fitness. Patients with
improved cardiovascular fitness can proceed to harder activities, achieving heart rates exceeding
70% of maximum.

Duration: 30 minutes, preceded and followed by stretching and flexibility exercises for a
minimum of 5 to 10 minutes.

Frequency: at least 3 days per week. Results are best if exercise occurs nearly every day.

Avoid strenuous exercise if fasting glucose levels are 250 mg/dL or higher. Avoid all forms of
exercise if glucose levels are 300 mg/dL or higher or ketosis is present.

Monitor blood glucose level before, during, and after exercise to learn responses to different
exercise conditions and to identify when changes in insulin or food intake are necessary.

Consume added foods as needed to avoid hypoglycemia. A rapidly absorbed carbohydrate

source should be readily available during exercise and for up to 8 hours after exercise is completed.

THERAPEUTIC TARGETS FOR NONPREGNANT DIABETIC PATIENTS

Parameters
Normal
Preprandial plasma glucose
<100
(mg/dL)
2-hour postprandial glucose
<140
(mg/dL)
Bedtime plasma glucose (mg/dL)
<120
Hemoglobin A1c (%)[]
<6
LDL cholesterol (mg/dL)
<130
HDL cholesterol (mg/dL)
>40 (m), >50 (w)
Fasting triglycerides (mg/dL)
<150
Blood pressure (mm Hg)
<140/90

Target[*]
90130
<160180
110150
<7
<100
>45 (m), >55 (w)
<150
<130/85

HDL = high-density lipoprotein; LDL = low-density lipoprotein; m = men; w = women.

INSULIN PREPARATIONS: EFFECT ONSET, PEAK, AND

DURATION AFTER SUBCUTANEOUS ADMINISTRATION
Duration
Preparatio Onset of
Peak
of Action
Class
n
Effect
Effect (hr)
(hr)
Rapid
Lispro,
1015 min 12
34
acting
aspart, or
glulisine
Short acting Regular (R) 30 min
24
58
Intermediat NPH (N) or 24 hours 612
1624
e acting
Lente
Long acting Ultralente 46 hours 816
24
(U)
Glargine
24 hours No peak
>30
Detemir
1 hour
No peak
Up to 24

Several intensive insulin regimens commonly used in the treatment of diabetes. Each is designed to
provide a continuous supply of insulin around-the-clock and to make extra insulin available at the
time of meals, thereby simulating more closely the normal physiologic pattern of insulin secretion

A summary of the results of the Diabetes

Control and Complications Trial (DCCT).

Prognosis

TYPE 2 DIABETES MELLITUS

Epidemiology

INTERNATIONAL DIABETES FEDERATION

Predisposition Factor
Age greater than 45 years
Overweight
Family history of type 2 diabetes in a first-degree relative (eg, parent or

sibling)
Hispanic, Native American, African American, Asian American, or Pacific
Islander descent
History of previous impaired glucose tolerance (IGT) or impaired fasting
glucose (IFG)
Hypertension (>140/90 mm Hg) or dyslipidemia (HDL cholesterol level < 40
mg/dL or triglyceride level >150 mg/dL)
History of gestational diabetes mellitus or of delivering a baby with a birth
weight of over 9 lb
Polycystic ovarian syndrome (which results in insulin resistance)

Pathophysiology

DIABETES TYPE 2
Type 2 diabetes- Results from insulin resistance (a
condition in which the body fails to properly use insulin),
combined with relative insulin deficiency. Approximately
90-95% (16 million) have type 2 diabetes.

(American Diabetes Association, ADA)

Clinical manifestation
Asymptomatic
Classic symptoms : polyuria, polydipsia, polyphagia and

weight loss
Other symptoms: blurred vision, lower extremity
paresthesias and yeast infection

Diagnosis
TheAmerican Diabetes Association(ADA) criteria for the diagnosis

of diabetes are any of the following[3]:

An HbA1c level of 6.5% or higher additional or optional criteriaor
A fasting plasma glucose (FPG) level of 126 mg/dL (7.0 mmol/L) or
higher; fasting is defined as no caloric intake for at least 8 hours,or
A 2-hour plasma glucose level of 200 mg/dL (11.1 mmol/L) or higher
during a 75-g oral glucose tolerance test (OGTT),or
A random plasma glucose of 200 mg/dL (11.1 mmol/L) or higher in a
patient with classic symptoms of hyperglycemia (ie, polyuria,
polydipsia, polyphagia, weight loss) or hyperglycemic crisis

Prognosis
Individualized-varies

Hipoglikemia

Definisi
kadar
glukosa
darah

Dibawah
< 55
level
mg/dl
normal

Penurunan
Tanda
kesadaran
dan
Stimulasi saraf
gejala
simpatis

Epidemiologi

The Diabetes control and complication trial

DM tipe 1 60 pasien/ tahun pada pasien yang
mendapat
terapi insulin intensif
20 pasien/tahun pada pasien
yang mendapat
terapi konvensional
The Dusseldorf
DM tipe 1 28 pasien pertahun pada pasien
yang
mendapat terapi insulin intensif
17 pasien/tahun pada pasien
yang mendapat
terapi konvensional
The United Kingdom prospective diabetes

Klasifikasi
Ringan

Dapat diatasi sendiri, tidak mengganggu aktivitas seharihari

Penurunan glukosa saraf simpatis perspirasi,
tremor, takikardia, palpitasi, gelisah
Penurunan glukosa saraf parasimpatis lapar, mual,
tekanan darah turun
Dapat diatasi sendiri, mengganggu aktivitas sehari-hari
Otak mulai kekurangan glukosa gangguan SSP
headache, vertigo, gg. Konsentrasi, penurunan daya
ingat, perubahan emosi, double vision
Karena gangguan kognitif pasien tidak mampu
mengatasi sendiri
1. Membutuhkan pihak ketiga tetapi tidak membutuhkan
terapi parenteral
2. Membutuhkan terapi parenteral (glucagon
intramuscular atau glukosa intravena)

Secara Klinis
Sedang

Berat

Penyebab

Insulin

Penyebab
fasting hypoglycaemia
Ex

Exogenous drugs

Penyebab
Post-Prandial Hypoglycaemia
Gastric surgery

Proteksi Fisiologis melawan

hipoglikemia

Source : Fauci AS, Kasper DL, Harrisons principles of Internal

Tanda dan Gejala

Keluhan dan gejala hipoglikemia akut yang

sering dijumpai pada pasien Diabetes
Otonomik
Berkeringat
Jantung Berdebar
Tremor
Lapar

Neuroglikopenik Malaise
Bingung
Mual
(confussion)
Sakit kepala
Mengantuk
Sulit berbicara
Inkoordinasi
Perilaku yang
berbeda
Gangguan Visual
Parestesi

Glukosa

Terapi

Tablet glukosa dengan

initial dose 20g atau
cairan yang
mengandung glukosa;
permen, makanan
manis
Glukosa intravena 25
cc dilanjutkan dengan
pemberian glukosa
infus diikuti dengan
pemeriksaan kadar
glukosa darah berkala.

Glukagon 1 mg pada
dewasa

Thankyou