DM DAN

PENATALAKSANAANNYA
dr. Nurhidayati, M.Kes
FK UNRAN

Diabetes Mellitus
Dasar penyakit adalah resistensi reseptor
insulin dan defisiensi insulin
Gejala klinis penyakit :
Hiperglikemia
Glikosuria
Dapat diikuti gangguan sekunder metabolisme
protein dan lemak
Dapat berakhir dengan kematian
Polifagi, poliuri, polidipsi
Penyakit ini diturunkan secara autosomal resesif
dan bersifat poligenetik

HIPERGLIKEMIA

DEFISIENSI
DEFISIENSI INSULIN
INSULIN

GLIKOSURIA
POLIURIA

POLIDIPSIA

POLIPHAGIA

Insulin
Dihasilkan oleh sel beta pankreas

Pankreas
ANATOMIS :
BAGIAN KEPALA (CAPUT)
BAGIAN BADAN (CORPUS)
BAGIAN EKOR (CAUDA)

HISTOLOGIS :
BAGIAN EKSOKRIN
BAGIAN ENDOKRIN (KULIAH
ENDOKRIN)

DUKTUS EKSRETORIS : DUKTUS WIRSUNG

PULAU-PULAU LANGERHANS

DUCTUS
BOLL

Centro acinar
cell

PULAU-PULAU
LANGERHANS
TIPE-TIPE SEL DAN SEKRESINYA
1.
2.
3.
4.
5.

SEL BETA () : INSULIN

SEL ALPHA () : GLUCAGON
SEL DELTA (): SOMATOSTATIN
SEL G
: GASTRIN
SEL PP (SEL F) : PANCREATIC
POLYPEPTIDE

Cara kerja insulin

Ada 2 teori cara kerja insulin
Teori 1 = Teori Levine :
Insulin mentransfer glukosa melalui membran sel
otot serat lintang, tetapi tidak menggangu
perpindahan glukosa melalui sel membran hati
Teori 2
Insulin diperlukan untuk fosforilasi glukosa dalam sel
glukosa 6 posfatase
Untuk pengikatan ini dibutuhkan enzim hexokinase
yang dihasilkan oleh sel hati
Kelenjar hipofisis menghasilkan zat inhibitor
hexokinase
Insulin merupakan zat antagonis terhadap
hexokinase

Glucose uptake

GLUT-2
NIMGU

ATP

Beta cell
pancreas

Gluc
ose NIMGU

Insulin-sensitive tissue
Insulin-independent tissue

Glucokinase
Glucose
G-6-P

ins
(+)

GLUT-4
ins (+)

Glucose
ins

NEFA

Glycerol
(+)

Triglyceride
(+)
ins

Adipose tissue
NIMGU

Glycogen
ins
(+)
(+)
Glucose
G-6-P

GLUT-4

Glycolysis
ins (+)

Skeletal muscle

cats
ins
(+)
Pyruvate

CO2
Lactate

TIPE 1

IDDM

RESISTENSI
RESISTENSI
INSULIN
INSULIN

RESISTENSI
RESISTENSI
INSULIN

Sel Otot

Jaringan Adipose

PATOGENESIS
DIABETES MELLITUS PRIMER

Ambilan Glukose

Pankreas

Lipolisis

Glukose Darah
Sekresi
insulin

Glukoneo
genesis

Hepar

Kepekaan Insulin Jaringan

RESISTENSI
RESISTENSI
INSULIN
INSULIN

RESISTENSI
RESISTENSI
INSULIN

Sel Otot

Jaringan Adipose

Ambilan Glukose

Pankreas

Lipolisis

Glukose Darah

Sekresi
Stimulasi
insulin

Glukoneo

Sekresigenesis
Insulin

Hepar

GLUKAGON

Sel-A

AMILIN
Sel-B

INSULIN

SOMATOSTATIN
Sel-D

GLUKAGON
KORTISOL
PANKREAS

EFEK VAGUS
GLUKOSE
GLUKOSE
ARGININ
ARGININ
LEUSIN

GASTRIN
GASTRIN
SEKRETIN
SEKRETIN
CCK
CCK
GIP
GIP

AS.
AS. AMINO
AMINO
AS.
AS. LEMAK
Hormon GIT

Rangsangan Parasimpatik
Sulfonilurea, repaglinid, nateglinid

Acanthus Insensitivitas
Endokrinopati
Jaringan
nigricans
Intoleransi
KH

Ggn Pankreas
Eksokrin

Diabetogenic
Lifestyle
Faktor
Genetik

Pregnancy
RESISTENSI
INSULIN

Medikasi

HIPERGLIKEMIA SEKUNDER

KADAR GLUKOSE DARAH

KONVERSI GLUKOSE
GLIKOGEN DI LIVER

AMBILAN GLUKOSE
OLEH JARINGAN

INSULIN

DEFESIENSI

RESISTENSI

HIPERGLIKEMIA
KADAR GLUKOSE DARAH
GEJALA
DIABETES MELLITUS
AKUT
HIPERGLIKEMIA

POLIDYPSIA

HIPERGLIKEMIA
HIPERGLIKEMIA
TRESHOLD
TRESHOLD
REABSORPSI
REABSORPSI GLUKOSE
GLUKOSE

POLIURIA
GLIKOSURIA

POLIPHAGIA

GLUKOSE

HIPERGLIKEMIA

STARVING CELL
DEFEK ENERGI
JARINGAN

Diabetes Mellitus
Symptoms
Polyuria
Polydipsia
Polyphagia
Glycosuria
Unexplained weight loss
Fatigue
Hyperglycemia

GEJALA RINGAN
DM

 Gejala pada gigi

Bercak-bercak di telapak kaki
Perubahan penglihatan
menjadi kabur
Infeksi vagina atau saluran urin
Gangguan seksual pada pria
Menstruasi tak teratur

 Menopause dini
Gatal-gatal, terutama disekitar
anus dan vagina
Kesemutan di tangan dan kaki

(Tingling)
Baal pada jari tangan
(Numbness)
Rasa kelelahan

KLASIFIKASI
DIABETES MELLITUS

BERBASIS PATOFISIOLOGIK

TIPE 1

IDDM

NIDDM

DIABETES MELLITUS
INSULIN
DEFESIENSI
KERUSAKAN
SEL -PANKREAS
INFEKSI VIRUS
AUTOALERGIK

RESISTENSI

TIPE 1

IDDM

RESISTENSI
RESISTENSI
INSULIN
INSULIN

RESISTENSI
RESISTENSI
INSULIN

Sel Otot

Jaringan Adipose

PATOGENESIS
DIABETES MELLITUS PRIMER

Ambilan Glukose

Pankreas

Lipolisis

Glukose Darah
Sekresi
insulin

Glukoneo
genesis

Hepar

Kepekaan Insulin Jaringan

RESISTENSI
RESISTENSI
INSULIN
INSULIN

RESISTENSI
RESISTENSI
INSULIN

Sel Otot

Jaringan Adipose

Ambilan Glukose

Pankreas

Lipolisis

Glukose Darah

Sekresi
Stimulasi
insulin

Glukoneo

Sekresigenesis
Insulin

Hepar

DIABETOGENIC LIFESTYLE
SEDENTARY LIFESTYLE

CALORY EXCESSIVE
INADEQUATE
CALORIC EXPENDITURE

OBESITY

TUJUAN Tx DM
Reduksi hiperglikemia kadar
gula (glukose) darah normal
Menurunkan atau menghilangkan
komplikasi kronik
Memperbaiki kualitas dan
kuantitas hidup

Correlation of A1C with average glucose

Mean plasma glucose
A1C (%)

mg/dl

mmol/l

6
7
8
9
10
11
12

126
154
183
212
240
269
298

7.0
8.6
10.2
11.8
13.4
14.9
16.5

These estimates are based on ADAG data of 2,700 glucose measurements over 3
months per A1C measurement in 507 adults with type 1, type 2, and no diabetes.
The correlation between A1C and average glucose was 0.92 (51). A calculator for
converting A1C results into estimated average glucose (eAG), in either mg/dl or
mmol/l, is available at http://professional.diabetes.org/eAG. ADA, 2011

TERAPI NON-FARMAKOLOGIK
BERAKTIVITAS FISIK

Ambilan Glukose Jaringan

TERAPI NON-FARMAKOLOGIK
PENGATURAN POLA HIDUP

Banyak
Banyak
berdoa
berdoa

Hindari
Hindari stres
stres atau
atau depresi
depresi

Melakukan kegiatan
Yang
Yang menyenangkan
menyenangkan

TERAPI
FARMAKOLOGI

TERAPI FARMAKOLOGIK

INSULIN
OAD

Oral Hypoglycemics
Insulin secretagogues:
Sulfonylureas (oldest)
Meglitinides

Insuline sensitizers:
Biguanide
Thiazolidinediones

Alpha-glucosidase inhibitors
Acrabose
Miglitol

Indications for Oral

Hypoglycemics
They are used to lower blood sugar levels
in patients that diet and exercise have
failed.
The patient must have some pancreatic
function left.
They can be used as a monotherapy or in
conjunction with other oral hypoglycemics.

Contraindications

Know drug allergy

Active hypoglycemia
Usually not used during pregnancy
Liver disease
Kidney disease
Depending on the metabolic pathways of the
medication

Sulfonylureas (Oral Hypoglycemic drugs)

First generation

Second generation

Short

Intermediate

Long

Short

Long

acting

acting

acting

acting

acting

Tolbutamide

Acetohexamide
Tolazamide

Chlorpropamide

Glipizide

Glyburide
(Glibenclamide)
Glimepiride

Sulfonylureas
Stimulate insulin secretion from the beta cells of
the pancreas, thus increasing insulin levels
Beta cell function must be present
Result: lower blood glucose levels
First-generation drugs not used as frequently
now

FIRST GENERATION SULPHONYLUREA COMPOUNDS

Tolbutami
d
shortacting

Acetohexamid Tolazamide
e
intermedia Chlorpropamid
te-acting
e
intermediateacting
long- acting

Absorptio
n

Well

Well

Slow

Well

Metabolis
m

Yes

Yes

Yes

Yes

Metabolit
es

Inactive*

Active +++ **

Active ++
**

Inactive **

Half-life

4 - 5 hrs

6 8 hrs

7 hrs

24 40 hrs

Duration
of action

Short
Intermediate
(6 8 hrs) (12 20 hrs)

Intermedia
te
(12 18
hrs)

Long
( 20 60 hrs)

Excretion

Urine

Urine

Urine

Urine

* Good for pts with renal impairment

** Patiens with renal impairment can expect long t 1/2

SECOND GENERATION SULPHONYLUREA

COMPOUNDS
Glipizide
Shortacting
Absorption
Metabolis
m
Metabolite
s
Half-life

Well
Yes

Glibenclamid Glimepirid
e
e
(Glyburide)
Longacting
Long-acting
Well
Well
Yes
Yes

Inactive

Inactive

Inactive

3 4 hrs

Less than 3
hrs
12 24 hrs

5 - 9 hrs

Duration of 10 16
action
hrs

12 24 hrs

Adverse Effects
Sulfonylureas

Hypoglycemia
hematologic effects
nausea
epigastric fullness
heartburn
many others

Interactions
Hypoglycemic effect increases when taken
with alcohol, anabolic steroids
Adrenergics (beta blockers) may mask many of
the symptoms of hypoglycemia
Hyperglycemia: corticosteroids,
phenothiazines, diuretics, oral contraceptives,
thyroid replacement hormones, phenytoin,
diazoxide and lithium.

Interactions
Allergic cross-sensitivity may occur with
loop diuretics and sulfonamide antibiotics
May interact with alcohol / OTC medication
containing alcohol)
causing a disulfiram (Antabuse) -type
reaction (facial flushing, pounding
headache, feeling of breathlessness, and
nausea)

Meglitinides
Meglitinides
repaglinide
nateglinide

Meglitinides
Action similar to sulfonylureas
Increase insulin secretion from the pancreas

Adverse Effects
Meglitinides
Headache
hypoglycemic effects
Dizziness
weight gain
joint pain
upper respiratory infection or flu-like
symptoms

Biguanides
Biguanides
metformin
Mechanism action
Increase peripheral glucose utilization
Inhibits gluconeogenesis
Impaired absorption of glucose from the gut
Decrease blool glucagon
Does not increase insulin secretion from the
pancreas (does not cause hypoglycemia)

Adverse Effects
Primarily affects GI tract: abdominal
bloating, nausea, cramping, diarrhea,
feeling of fullness
May also cause metallic taste, reduced
vitamin B12 levels
Lactic acidosis is rare but lethal if it occurs
Does not cause hypoglycemia

Thiazolidinediones
Thiazolidinediones
pioglitazone
rosiglitazone
Also known as glitazones
Mechanism action:

Decrease insulin resistance

Insulin sensitizing drugs
Increase glucose uptake and use in skeletal
muscle
Inhibit glucose and triglyceride production in
the liver

Adverse Effects
Moderate weight gain
Edema
Mild anemia
Hepatic toxicitymonitor liver function tests

Alpha-glucosidase Inhibitors
Alpha-glucosidase inhibitors
acarbose
miglitol
Mechanism action:
Reversibly inhibit the enzyme alphaglucosidase in the small intestine
Result: delayed absorption of glucose
Must be taken with meals to prevent
excessive postprandial blood glucose
elevations (with the first bite of a meal)

Adverse Effects
Flatulence
Diarrhea
abdominal pain
Do not cause hypoglycemia,
hyperinsulinemia, or weight gain

GLP-1R agonists or GLP-1

analogues
GLP-1 receptor agonists
Exendin-4
Exenatide

GLP-1 analogues
Liraglutide a long-acting
glucagon-like peptide-1 (GLP-1

DPP-4 inhibitors
Sitaglipin
Their mechanism of action is thought to
result from increased Incretin levels
(GLP-1 and GIP),which inhibit glucagon
release, increases insulin secretion and
decreases gastric emptying.

Amylin, or Islet Amyloid

Polypeptide (IAPP)
Pramlintide

Sodium-glucose transport
proteins
Gene

Location

Co-transport ratio and% of

glucose reabsorption

SGLT1

Located in the
S3 segment of
the proximal
tubule

Has a 2Na+:1Glucose co-transport

ratio and is responsible for 2% of
glucose reabsorption

SGLT2

Is
predominately
located in the
S1 and S2
segments of the
proximal tubule.

SGLT2 Is predominately located in the

S1 and S2 segments of the proximal
tubule.Has a 1Na+:1Glucose cotransport ratio and is responsible for
98% of glucose reabsorption.

Insulin

Fisiologic Insulin Response to

Constant Glucose stimulus
Level of insulin
secretion

Stimulation by
glucose
First(acut
e) Phase
on
release
Secon
d
Phase

Insulin basa

Baselin
e
Time

Diabetes Care 1984;7:491-502

Insulins
Mechanism of Action
Substitute for & same effects as endogenous
insulin
Restores the diabetic patients ability to:
Metabolize carbohydrates, fats, and proteins
Store glucose in the liver
Convert glycogen to fat stores
Most now human-derived, using recombinant DNA
technologies
Goal: tight glucose control , to reduce the

incidence of long-term complications

Indications
To treat both types of diabetes
Each patient requires careful
customization of the dosing regimen for
optimal glycemic control

Contraindications

Anyone who is hypoglycemic?????

Adverse Effects

Are all signs and symptoms of

hypoglycemia including shock and death.

Human-Based Insulins
Rapid-Acting
Most rapid onset of action
Shorter duration
Insulin

Onset
(mins)

Peak (hrs)

Duration
(hrs)

aspart (Novolog)

2-33

1-3

3-5

lispro (Humalog)

2-33

30mins 2.5

3-6.5

glulisine (Apidra)

2-33

30mins 1.5

1.-25

May be given SC or via continuous SC infusion

pump (but not IV)

Human-Based Insulins
Short-Acting
regular insulin (Humulin R, Novolin R)
Insulin

Onset (mins)

Peak
(hrs)

Duration
(hrs)

Humulin R

30 mins to 4 hrs

2.5-5

5-10

Novolin R

30

2.5-5

Onset 30 60 minutes
The only insulin product that can be given by
IV bolus, IV infusion, or even IM

Sliding-Scale Insulin Dosing

SC rapid or short-acting doses adjusted according to
blood glucose test results
Typically used in hospitalized diabetic patients
Or in patients on TPN / enteral tube feedings or receiving
steroids

Subcutaneous insulin is ordered in an amount that

increases as the blood glucose increases

Human-Based Insulins
Intermediate-Acting
isophane insulin suspension (also called NPH)
(Humulin N, Novolin N)
isophane insulin suspension & insulin injection
(Humulin 50/50 , Humulin 70/30, Novolin 70-30)
Lispro protamine suspension (Humalog 75/25, Novolog
Mix 70/30)
insulin zinc suspension (Lente, Novolin L)
Cloudy appearance
Slower in onset and more prolonged duration
than endogenous insulin

Human-Based Insulins
Intermediate-Acting
Insulin

Onset
(hrs)

Peak (hrs)

Duration
(hrs)

Humulin N

1-4

4-12

16-28

Novolin N

1-5

4-12

24

Humulin 50/50

0.5

4-8

24

Humulin 70/30

0.5

4-12

24

Novolin70/30

0.5

2-12

24

Isophane (NPH):

Isophane &
Insulin:

Human-Based Insulins
Intermediate-Acting
Insulin

Onset
(hrs)

Peak (hrs)

Duration
(hrs)

lispro protamine &

lispro:
Humalog Mix 75/25

0.25-0.5

0.5-1.5

12-24

Novolog Mix 70/30

0.2-0.33

2.4

24

Lente Iletin II

1-1.5

8-12

24

Novolin L

1-4

7-15

20-28

Insulin Zinc
Suspension:

Human-Based Insulins
Combination Insulin Products
NPH 70% and regular insulin 30% (Humulin
70/30, Novolin 70/30)
NPH 50% and regular insulin 50% (Humulin
50/50)
insulin lispro protamine suspension 75% and
insulin lispro 25% (Humalog Mix 75/25)

Human-Based Insulins
Long-Acting
Insulin

Onse
t

Peak

Duration

glargine (Lantus

No peak activity

24 (when
administered at hs)

detemir (Levemir)

6-8

6-28

Profile of Insulin Glargine vs

NPH
NPH
Glargi
ne

Injection Sites

Insulin Pumps
External

Internal

DM tipe 2
ADOLESCENT

PEDIATRI

NON - OBESE

add
add

Sulfonilurea

Glinid

Metformin

Glitazon
Insulin

INSULIN
AFINITAS
IgG
Mutasi
Reseptor Insulin

Acanthosis nigricans :
Aging
Androgenic women

HIPERGLIKEMIA SEKUNDER

RESISTENSI INSULIN EKSTRIM

AFINITAS
IgG
Mutasi
Reseptor Insulin

Acanthosis nigricans :
Aging
Androgenic women

HIPERGLIKEMIA SEKUNDER

Sulfonilurea
Substi
tusi

Glinid

Inhibitor
-Glukosidase

Insulin

Acanthosis nigricans :
Aging
Androgenic women

HIPERGLIKEMIA SEKUNDER

PANKREATITIS KHRONIS

JUMLAH
SEL-B

Pankreas

Sekresi
Insulin

HIPERGLIKEMIA SEKUNDER

INTOLERANSI KARBOHIDRAT
Output Glukose
Hepatik

Pankreas

Ekses :
Rilis
Insulin

Katekholamin
GH
Glukokortikoid
Glukagon
Somatostatin

HIPERGLIKEMIA SEKUNDER

INTOLERANSI KARBOHIDRAT
PADA
TRIMESTER II DAN III

PREGNANCY

DM GESTASIONAL

Tx. DIET

Insulin NPH

Insulin NPH + Reguler

2
:
1
Glyburide

KI : Sulfonilurea

DM GESTASIONAL

ENDOKRINOPATI
SINDROM CUSHING :
EKSES KORTISOL

INSULIN

AKROMEGALI :
EKSES GH

GLUKOSE
DARAH

SULIN COUNTERREGULATORY EXCES

Ab

Adrenokortikoid
Jar. Tiroid
Tiroglobulin
Parietal Gastrik

OTOIMUN

Penyakit Addison
Sindrom Schmidt
Gagal Poliglanduler

HIPERGLIKEMIA SEKUNDER

FAKTOR MEDIKASI

nsulin

DM tipe - 2

Kortikosteroid

Diazoksid

Fenitoin

Thiazid

Niasin

Bloker-

Interferon-

Pentamidin

Kontrasepsi oral

HIPERGLIKEMIA SEKUNDER

KOMPLIKASI
KOMPLIKASI
DIABETES MELLITUS

AKUT

KHRONIS

KOMPLIKASI AKUT
DIABETIC EMERGENCY
KETOASIDOSIS DIABETIK
HIPERGLIKEMIA HIPEROSMOLAR
HIPOGLIKEMIA

KETOASIDOSIS
GLUKOSE
JARINGAN
LEMAK

KATALISIS

ASETIL Co-A

CEPAT

SENYAWA ASETOASETAT
DAN HIDROKSIBUTIRAT

PROTEIN

KATALISIS

KETON
Fruity breath odor

KETOASIDOSIS
GLUKOSE
JARINGAN

Memperbaiki
ASETIL Co-A
KATALISIS
LEMAK
status metabolik pasien :
CEPAT

- larutan hipotonikSENYAWA
: glukose
darah

ASETOASETAT
- suplemen potassium
DAN HIDROKSIBUTIRAT
- Infus insulin konstan
PROTEIN

KATALISIS

KETON

Fruity breath odor

HIPERGLIKEMIK HIPEROSMOLAR
Usia lanjut DM tipe-2
Muda, prolong hyperglemic,
dehidrasi, ggn fs ginjal
Glukose darah > 1000 mg/dl
Mortality

Cairan hipotonik
Infus Insulin dosis rendah

Acanthus Insensitivitas
Endokrinopati
Jaringan
nigricans
KOMPLIKASI
DM KHRONIS
Intoleransi
KH

Ggn Pankreas
Eksokrin

Diabetogenic
Lifestyle
Faktor
Genetik

Pregnancy
RESISTENSI
INSULIN

Mikrovaskuler

Medikasi

Makrovaskuler

RETINOPATI

PANDANGAN KABUR
BUTA
Lensa mata kontak dengan
Kondisi hiperosmolar

Mikrovaskuler

RETINOPATI

PANDANGAN KABUR
PERBAIKAN
KADAR GLUKOSE DARAH
BUTA
Lensa mata kontak dengan
Kondisi hiperosmolar

LASER PHOTOCOAGULATION

Mikrovaskuler

NEUROPATI PERIFER

Mikrovaskuler

MUSCLE WASTING
Lemah
Mudah merasa lelah

Mikrovaskuler

Hilangnya kalium dalam tubuh

Katabolisme protein otot

KONDISI PARAH LEBIH LANJUT

Lemak Subkutan Akan Hilang Dan Otot Sulit
Digerakkan
(Muscle Wasting).

PAIN OR BURNING

Neuropati Diabetik
( Pain Or Burning )

Mikrovaskuler

Akibat Akumulasi Metabolit Glukose Aktif yang Dapat

Mempengaruhi Tekanan Osmose
Berkaitan Dengan Enzim Aldose Reduktase

PAIN OR BURNING
Neuropati
Tx DM
(KontrolDiabetik
glikemia)
( Pain Or Burning )
Antidepresan trisiklik
Akibat
Antikonvulsan
: Fenitoin,
Akumulasi
Metabolit
Glukose
Aktif Karmabazepin
yang Dapat
gabapentin,
Mempengaruhi Tekanan Osmose
Topical Capsaicin
Berkaitan
Pain medication
Dengan NSAIDs
Enzim Aldose
Reduktase

PARESTHESIA NUMBNESS
KAKI

>> TANGAN

Tx DM (Kontrol glikemia)
Antikonvulsan : Fenitoin,
gabapentin, Karmabazepin
Mikrovaskuler

NEUROPATI OTONOMIK

Mikrovaskuler

HIPOTENSI

KONDISI PARAH LEBIH LANJUT :

Poliuria menyebabkan volume
plasma
Gejala Hipotensi Pada Posisi
Berbaring (Recumbent Position)
Mikrovaskuler

HIPOTENSI

KONDISI PARAH LEBIH LANJUT :

Mandating Patient
Poliuria menyebabkan volume
Sleep in a Sitting
plasma
Or
Semirecumbent
Position
Gejala
Hipotensi Pada
Posisi

Berbaring (Recumbent Position)

Mikrovaskuler

IMPOTENSI
Hambatan Vasodilatasi
Arteria Cavernosa

IMPOTENSI
Hambatan Vasodilatasi
Arteria Cavernosa

Tx DM
SILDENAFIL
Mimba, Brototowali, Sambiloto, Daun
Sendok

GANGGUAN GI TRACT
GASTROPARESIS
Tx DM (Kontrol Glikemia)
Obat -2 slow gastric motility
dihentikan
Metoklopramid
Eritrosin
Mikrovaskuler

NEUROPATI
DM tipe 2

DIABETIC DIARHHEA

Doxycycline
Metronidazole
Octrotide

Mikrovaskuler

NEFROPATI

Kontrol Glukose darah

Kontrol Tekanan Darah :
Inhibitor ACE, Diuretik
Mikrovaskuler

NONHEALING FOOT ULCER

Stop Smoking

Revaskularisasi

Makrovaskuler
Perawatan kaki

Terapi
Hiperbarik
Antiplatelet

Kontrol Lipid

KOMPLIKASI KRONIS
DM-LIPID

STATIN : Simvastatin, Pravastatin

NIACIN
FIBRAT : Klofibrat, Benzafibrat

Makrovaskuler

KOMPLIKASI KRONIS
DM-HIPERTENSI
Tx awal

Inhibitor ACE

Tx 2nd

Diuretik Thiazid

Antagonis Kalsium :
Nifedipin,Verapamil, Diltiazem

Makrovaskuler

CORONARY HEAT DISEASE

Kontrol lipid
Kontrol hipertensi
Antiplatelet
Berhenti merokok
Blocker
ACEI : vasculer protective effect