DIABETES MELITUS

KAD,HHS

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 DEFINISI
Suatu kumpulan gejala yang timbul pada
seseorang akibat adanya peningkatan
kadar glukosa darah akibat kekurangan
insulin baik absolut maupun relatif

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 PATOFISIOLOGI
 Badan memerlukan bahan bentuk sel baru &
mengganti sel rusak
 Badan memerlukan energi agar sel berfungsi
dengan baik (KH, Prot & Lemak)
 Dalam usus :KH  gula,
Protein  as.amino,
Lemak  as. Lemak
 Masuk pemb. darah  masuk ke sel
 Insulin (hormon pankreas) memasukkan glukosa
ke dalam sel agar dapat diolah sebagai energi
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 IMPORTANT
 Healthy pancreas have: 100 000
Langerhans island and every Langerhans:
100 ß cells (insulin production) 
10.000.000
 Insulin and insulin receptors like key and
the door

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 Pankreas
 Suatu kelenjar di belakang lambung
 Berisi sekitar 100.000 pulau Langerhans yang berisi
setiap pulau sekitar 100 sel beta10.000.000 sel
beta/insulin
 Sel alfa  glukagon (meningkatkan KGD)
 Sel delta  somatostatin,menghambat hormon
pertumbuhan

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Associated Structures of the Gall
Bladder and Pancreas

Pancreas
• The pancreas is unique in that it has an endocrine and exocrine
function. The endocrine pancreas secretes insulin, glucagon,
somatostatin and pancreatic polypeptide.
• The exocrine pancreas is composed /d ubah of acini and
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networks of ducts that secrete digestive enzymes that hydrolyze
proteins, carbohydrates and fats.
 KERJA INSULIN
 Insulin sebagai anak kunci  membuka
pintu sel untuk memasukkan glukosa
 Bila insulin tak ada glukosa tak dapat
masuk sel & glukosa tetap dalam
pembuluh darah  KGD naik
(badan lemah karena kurang energi)  ini
disebut DM tipe 1 atau IDDM

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 DM tipe 1 (IDDM)
 Adanya peradangan pada sel beta (insulitis) 
reaksi otoimun  antibodi terhadap sel beta (ICA:
islet cell antibody)
 Reaksi antigen (pankreas) & antibodi (ICA) 
hancurnya sel beta
 Insulitis akibat cocksakie virus, rubella, CMV,
herpes dll
 Insulitis hanya menyerang sel beta, sedangkan
sel alfa & sel delta utuh

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 DM tipe 2 (NIDDM)
 Tipe ini jumlah insulin normal/meningkat
tetapi jumlah reseptor kurang (lubang kunci pintu)
KGD tetap tinggi
 Sama dengan DM tipe 1 (KGD tinggi, kurang insulin
relatif/absolut )

PENYEBAB:
 Obesitas sentral
 Diet tinggi lemak rendah KH
 Kurang gerak badan (olah raga)
 Faktor keturunan (herediter)

Pada DM tipe 1 atau 2: KGD tinggi melewati batas

ambang ginjal glukosuria  kencing manis
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Progression to Type2 Diabetes
Normal
Acquired
Obesity
Genes Insulin Resistance Sedentary Lifestyle
Aging

Hyperinsulinemia

Compensated Insulin Resistance

Normal Glucose Tolerance/dpat mnrima

Impaired Glucose Tolerance

 - Cell “Failure” Genes

Type 2 Diabetes 10
brtambah

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 Diabetes: What It Is and How It Develops

Copyright © 2010 Pearson Education, Inc.

Diabetes: What It Is and How It Develops (cont.)

Copyright © 2010 Pearson Education, Inc.

Diabetes: What It Is and How It Develops (cont.)

Copyright © 2010 Pearson Education, Inc.

 Perbandingan DM tipe 1 & tipe 2
Perbedaan DM tipe 1 DM tipe 2

Nama lain IDDM NIDDM

Nama lama DM Juvenil DM dewasa
Umur Biasa <40 th Biasa >40 th
Klinis saat Dx Berat Ringan
Kadar insulin Tak ada insulin Cukup/tinggi
Berat badan Biasanya kurus Gemuk/normal
Insulin, Diet, OR(o
Pengobatan raga)
Diet, OR, OHO,
insulin

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DIAGNOSIS DM
• Gejala klinis banyak makan, banyak
minum, banyak kencing (3P)/50% &
penurunan BB, disertai KGD yang
tinggi merupakan gejala khas DM
• KGD puasa > 126 mg/dL (7mmol)
2x Px
• KGD 2jPP > 200 mg/dL (11,1mmol)
• KGD acak > 200 mg/dL + gejala khas

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 KLASIFIKASI DM
 Tipe 1: destruksi sel beta  defisiensi insulin
absolut (Otoimun & Idiopatik)
 Tipe 2: resistensi insulin dg def. insulin
defek sekresi dg resistensi insulin
 Tipe lain: defek genetik sel beta
defek genetik kerja insulin
penyakit eksokrin pankreas
endokrinopati
karena obat atau zat kimia
infeksi
sebab imunologi yang jarang
Sindrom genetik lain yang berkaitan dg DM
 Diabetes gestational 19
 I. DM tipe 1
• Ada 2 kelompok:
Dekstruksi sel beta
Defisiensi insulin absolut (insulinopenia)
Dalam klinik dimediasi 2 bentuk:
otoimun dan idiopatik
Mudah jatuh dalam keadaan gawat darurat
medis (KAD) bila tidak dapat insulin
karena itu disebut DMTI/DM Tergantung
Ins. (IDDM)

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 II. DM tipe 2
• Predominan resistensi insulin dengan
defisiensi insulin relatif
• Predominan gangguan sekresi insulin
bersama resistensi insulin
• Disebut pula DMTTI (NIDDM) karena bila
tidak diberi insulin tidak jatuh dalam KAD
• Resistensi insulin umumnya karena
obesitas

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 Resistensi Insulin

Defek utama pada sebagian besar Diabetes Melitus tipe 2

Definisi :

Terganggunya respon terhadap efek fisiologis Insulin,

termasuk pula metabolisme glukosa, lemak, protein
dan fungsi endotelial pembuluh darah
 III.DM tipe lain
1. Defek genetik fungsi sel beta:
Kromosom12, HNF-1 alfa
Kromosom 7, glukokinase
DNA mitokondria
2. Defek genetik kerja insulin
3. Penyakit eksokrin pankreas: pankreatitis,
trauma/pankreatektomi, neoplasma,

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 III. DM tipe lain(lanjut)
4. Endokrinopati: akromegali
sindroma Cushing
feokromositoma
Hipertiroidisme
5. Karena obat/zat kimia:
glukokortikoid, hormon tiroid, tiazid,
dilantin, interferon alfa
6. Infeksi: rubella kongenital & CMV
7. Imunologi (jarang): antibodi anti reseptor insulin

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 IV. DM Gestasional
• DMG berbagai derajat yang ditemukan
pertama kali pada saat hamil, tanpa
dibedakan perlu insulin tidak.
• Walaupun ringan, Dx DMG harus
ditegakkan karena dapat menyebabkan
faktor penyulit bagi ibu & janin
• Angka kesakitan/kematian ibu & janin
meningkat seiring dengan meningkatnya
KGD ibu, dan ibu DMG risiko terjadi DM

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TATALAKSANA DM

1. EDUKASI
2. LATIHAN JASMANI
(EXERCISE)
3. DIET (PENGATURAN
MAKANAN)
4. FARMAKOLOGI

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 Education
Very important, included:
 Pathophysiology of DM
 Targets of DM management
 Management of nutrition and diet
 Phamacologik intervention
 Exercise and physical activity
 Self monitoring blood glucose (SMBG)
 Prevent and manage of acute and chronic
complication
 Psychosocial aspect
 Management of Stress
 Health care system
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 Excersice
Minimal 30 minutes (fat burning), 150
minutes/weeks
CRIPE:
 Continous
 Rhythmic
 Interval (Sa’i)
 Progresive
 Endurance  maximum PULSE=80%
(220-age in year) 28
 NUTRITION and DIET
Ideal body weight:
Normoweight: 90-110% (Ideal BW) or BMI 18,5
– 23
 30 calories/KgBW/day
Underweight: <90% (Ideal BW) or BMI < 18,5
 40 calories/Kg BW/day
Overweight: >110% (Ideal BW) or BMI >23
 20 calories/Kg BW/day

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FARMAKOLOGI

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 Indikasi pemberian OHO
 Diabetes sesudah usia 40 tahun
 Diabetes diderita kurang dari 5 tahun
 Jika memakai insulin dosisnya <40
unit/hari
 Diberikan pada penderita diabetes dengan
berat badan normal atau lebih

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 Sulfonilurea:
Aksi utama sulfonilurea menutup ATP-K+ Chanel
pada membran sel β pankreas  influks Ca+ 
pengeluaran insulin
Efek ekstrapankreatik melalui peningkatan jumlah
dan ikatan reseptor terhadap insulin
Efek hipoglikemik yang kuat, terutama generasi
kedua (glicazid, glipizid & glibenklamid)
terutama pada lansia
Diminum 30’-15’ sebelum makan
SU menurunkan HbA1c 1-2% dan KGD (level 1A)

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 Efek samping:
 Rash sering pada generasi pertama (tolbutamid &
khlorpropamid)
 Dispepsia & mual
 BB naik (efek anabolik karena peningkatan sirkulasi
insulin)
 Hipoglikemia (terutama pada lansia, berat o.k.
khorpropamid & glibenklamid  10% angka
kematian)
 Ikterik kolestatik (gangguan fungsi hati) &
penekanan sumsum tulang (jarang)
 Hati-hati pada pasien IHD (menutup ATP-K+
channel jantung  prekondisi iskhemik). 33
 BIGUANID
Penformin (1950) –X asidosis laktat
 Metformin banyak dipakai sampai kini HbA1c
turun 1-2% (level 1A)
 Meningkatkan sensitifitas insulin
 Menekan produksi glukosa hati (GDP ↓)
 Meningkatkan insulin memasukkan glukosa
pada otot
 Sedikit menurunkan GD PP o.k. insulin dalam
sirkulasi tidak meningkat
 BB tidak ↑ & tidak hipoglikemia
 Dosis 500-2000mg/hari (2-3X dosis)
 Diminum kapan saja tidak berhubungan makan
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INSULIN

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 Indication of Insulin therapy:
 Type 1 DM
 Type 2 DM Uncontrolled with diet, exercise
and OHA (included allergy and contra-
indication).
 Gestasional DM
 Severe hepatic and kidney failure.
 Acute Infection(cellulitis, gangren), severe
tuberculosis, critical illness (stroke/AMI)
 DKA/Diab.Keto Acidosis & HHS (HONK)
 Mayor surgical and fracture of bones
 Underweight, DM related malnutrition
 Grave’s disease
 Carcinomas
 Corticosteroid teraphy 36
 Type of Human Insulin
Type Begining Peaks Duration
Short action
15-30 mnt 2-4hr 6-8hr
Actrapid
Humulin R
Premixed
15-30mnt 1-8hr 14-15 hr
Humulin 30/70
Mixtard 30/70
Intermediate actian /NPH
2-4hr 1-8hr 14-15 hr
Humulin N
Insulatard

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 Type of Analogue insulin
Type begining peaks duration
Rapid action
Lyspro (Humalog)
Aspart (Novo Rapid) 5-15 mnt 2 hr 4-6hr
Gluisine (Apidra)

Premixed
5-15mnt 2-4hr 12-14 hr
Humalog 25/75
Novomix 30/70
Long action
No peaks 24 hr
Lantus
Levemir

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Sistem NovoLet®

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 Tempat Penyuntikan
Ideal untuk insulin aksi pendek atau campuran pagi
hari:
• Perut dibawah pusar
Ideal untuk insulin aksi menengah, aksi panjang atau
campuran malam hari:
• Lengan atas bagian luar
• Glutea
• Paha atas bagian luar
Sebaiknya berpindah tempat untuk mencegah insulin
lipodistrofi atau jaringan sikatrik yang luas
Regio satu berpindah ke regio lain sekitar 2 minggu
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 Sites of INSULIN injection
(move every 2 weeks)
-

75-90 1-15

61-75 16-30
45-60 31-45

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 Dosis Insulin
Pertama kali diberikan dengan dosis
yang kecil, biasanya dimulai insulin
aksi pendek 3X2n/hari (n=angka
ratusan KGD)
Dinaikkan 2-4 unit setiap sekitar 3
hari bila KGD target belum tercapai
Dosis Insulin jangka menengah 75-
80% jumlah insulin jangka pendek
perhari, dapat diberikan 2 dosis pagi
dan malam (dosis malam<pagi
nocturnal cicardian) 42
KEGAWATAN DIABETES
MELLITUS

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 DKA
Occurs when muscle cells become so
starved for energy that body takes
emergency measures & breaks down
fat  toxic acids as ketones
Most common type 1 DM
insufficient insulin to
adjust/mengatur  raise of blood
sugar
Cause by extreme stress or illness
Infection  body produce adrenalin
 works against insulin
Forget to take insulin 44
 Sign & symptom of DKA
Deep, rapid breathing
Sweet, fruity smell on breath
Loss of appetite
Nausea • Fatigue
Vomiting • Weakness
Fever • Confusion
Stomach pain • Drowsiness
Weight loss
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 Clinical presentation
Lost more than 5% body weight
More than 35 breaths a minute
Can’t control blood sugar
Become confused
Nausea and vomiting

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 What should you do?

Check ketones  if feeling especially

stressed or blood sugar persistently
above 240mg/dL
High ketones in blood  ketones
excreted in urine.
High ketones in urine must
treatment & stay in hospital
DKA can lead into coma and posibly
death. 47
 Treatment
Replenishing/mengisi lost fluids
through i.v. line
Insulin combined with glucose,
injected into iv  stop making
ketones
Gradually blood sugar level back to
normal, if quickly can produce
swelling in the Brain
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 HHS
Blood sugar reaches such a high level that
blood become thick and syrupy (level >600
mg/dL)
Cells can’t absorb much blood sugar, the
sugar passed from blood to urine  draws
tremendous/hebat amounts of fluid from
body and produces dehydration
Common in type 2 DM, especially who don’t
monitor blood sugar and who don’t know
have DM
Trigger factors: high-dose steroid, diuretics,
infection, illness, stress or drinking 49

excessive alcohol
 HHS, sign & symptom

Excesive thirst
Increased urination
Weakness
Leg cramps
Confusion
Rapid pulse
Convulsions
Coma 50
 What should you do?
Check blood sugar level (>
600mg/dL)
Emergency treatment can correct the
problem within hours
Give intravenous fluids to restore
water to the tissue
Short acting insulin to help cells can
absorb glucose
Without prompt treatment  can be 51

fatal
 Hypoglycemia
 Blood sugar level <60mg/dL
 Basssically from too much insulin and too
little glucose in blood
 Most common among people taking insulin
or oral medication to release or action of
insulin
Reasons:

 Exercising longer or more strenuously than

normal
 Not adjusting your medication to
accommodate changes in blood sugar
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 Sign & symptom of Hypoglycemia
Blood sugar level 40-55mg/dL:
 Sweating
 Visual disturbances
 Weakness
 Hunger
 Dizziness
 Nervousness
 Headache
 Fast heartbeat
 Irritability
 Cold, clammy skin

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 Sign & symptom of Hypoglycemia
Later symptomp (BG < 40mg/dL)
 Slurred speech/bicara kacau
 Drunkenlike/spt mabuk behavior
 Drowsiness/kantuk
 Confusion
Emergency symptoms (BG <20
mg/dL)
 Convulsions
 Unconsiousness, wich can be fatal
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 What should you do?
As soon realize blood sugar is low,
eat or drink something raise BG
level quickly. Example:
Hard candy, equal to about five live
saving
A regular (not diet) soft drink
Half a cup of fruit juice
Glucose tablets, nonprescription
sugar pills made especially for
treating low blood sugar 55
 What should you do?
If after 15 minutes continue to experience
symptoms, repeat the treatment. If they
still, contact the doctor.
If lose consiousness or for some other
reason are unable to swallow, the treatmen
of choice is an injection D 40% or glucagon
injection

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 CHRONIC
COMPLICATION
Of
DIABETES MELLITUS

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 Chronic complications
Development of other diseases
Long-term DM complications are
those that develop gradually and
that may become disabling or live-
threatening. They include nerve,
kidney, eye, heart and blood vessel
disease

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 Type 2 diabetes is NOT a mild disease
Stroke
Diabetic 2 to 4 fold increase in
cardiovascular mortality
Retinopathy and stroke3
Leading cause
of blindness
in working age Cardiovascular
adults1
Disease
8/10 diabetic patients
die from CV events4

Diabetic
Nephropathy Diabetic
Leading cause of
Neuropathy
end-stage renal disease2 Leading cause of non-
traumatic lower
extremity amputations5

1 Fong DS, et al. Diabetes Care 2003; 26 (Suppl. 1):S99–S102. 2Molitch ME, et al. Diabetes Care 2003; 26 (Suppl. 1):S94–S98.
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3 Kannel WB, et al. Am Heart J 1990; 120:672–676. 4Gray RP & Yudkin JS. In Textbook of Diabetes 1997.
5Mayfield JA, et al. Diabetes Care 2003; 26 (Suppl. 1):S78–S79.
CHRONIC COMPLICATION
MACROVASCULAR
CHD RISK
2–4x
DEATH  60 %
CEREBROVASCULAR
STROKE : 4x
PERIPHERAL VD
40 – 50 % NON-TRAUMATIC AMPUTATION
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 IMPOTENCE in DM
 Refers: inability an erection of the penis
or inability an erection long enough
for sexual intercourse
 Physical: excess blood sugar can damage the
nerves & blood vessel  no longer
communication nerves to small blood vessel &
large blood vessel narrowed or blocked  not
enough blood to erection (common in DM)
 Psychological: anxiety, stress or depression
impaired Brain and Hormones respond
 Medication: drugs for hypertension, anxiety &
depression
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 MEDICATION of IMPOTENCE
I. Sildenafil (Viagra, Androz, Edegra,Silagra)  isn’t
effective for everyone
1hour before activity  effective 4 hours
II. Alprostadil (synthetic of prostaglandin E-1)
not a pill  self intraurethral (a grain rice)
or self injection therapy (5-20 minutes before and 1
hour erection)
III. Vacuum device
IV. Penile implant
a. semirigid, benabled rod (permanent erection)
b. inflantable (with pump in scrotum produce an
erection only when you want)
V. Counseling (if psychologycal factors) 64
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