INTERNA

Dr. nidya
 ANAMNESA
1. IDENTITAS 4. RPD : HT dan DM (lamanya dan
2. KU : nyeri dada konsumsi obat apa),
3. RPS 5. RPO : alergi obat
- onset 6. RPK : HT dan DM
- Location 7. RIWAYAT SOSIO-EKONOMI-
- Duration KEBIASAAN
- Caracteristic (jenis nyeri, VAS, - Aktivitas sebelum sakit
penjalaran - Pola makan
- Associated factors (faktor yang - Merokok, narkoba, alcohol
memperberat) (durasi: 5 tahun, 1 hari 2 bungkus)
- Relieving (Yang memperingan ) - Pola tidur
- Timing (saat terjadi) dan durasi - Kondisi lingkungan tempat tinggal
berapa lama, intensitas nyeri
- Keluhan penyerta (bab dan bak)
 PEMERIKSAAN FISIK
1. Kesan umum 3. IMT (BB/TB kuadrat )
68/2,5 = 27,2
- Sakit berat : sesak hebat,
<18,5 = underweight
kejang, syok
18.5-22.9 = normal
- Sakit sedang : lemah tapi 23-24.5 = overweight
masih bisa duduk 25-29.9 = obes I
- Sakit ringan : pasien masih >30 = obes II
dapat berjalan 4. Pemeriksaan Head to Toe/ status
generalisata
2. Vital Sign - Kepala :
- TD - Mata : KA, SI, ptosis, exopthalmus,
- HR - Hidung
- RR :16-20 - Mulut
- Wajah , moon face, butterfly
- T : 36.5-37.5
- Telinga mikrotia, makrotia
- Leher : thyroid, KGB 5. Status Lokalisata
- Jantung Bagian yang menjadi
- Thorax keluhan utama di uraikan
Inspeksi, auskultasi, palpasi, disini
perkusi
- Abdomen
Inspeksi, auskultasi, palpasi,
perkusi
- Extremitas
Oedema pretibia : gagal
jantung kanan
Sianosis
Akral hangat/dingin
JVP
 JANTUNG
BATAS JANTUNG
- BATAS KANAN
- BATAS KIRI
- BATAS ATAS
- PINGGANG JANTUNG

AUSKULTASI JANTUNG
- AORTA
- PULMONAL
- MITRAL
- TRIKUSPID
PALPASI PARU
PERKUSI DAN AUSKULTASI PARU
PALPASI LIEN
PEMERIKSAAN HEPAR
Murphy sign
Mc burney
Ludwig sign
PEMERIKSAAN GINJAL
 ENDOKRIN

©Bimbel UKDI MANTAP

 MATERI
1. DM 5. SINDROMA METABOLIK
2. Kelenjar thyroid
- HIPERTIROID
(lingkar perut, Trigliserida,
- HIPOTIROID TD, HDL, gdp)
3. Kelenjar paratiroid 6. DISLIPIDEMIA (LDL, TG,
- HIPERPARATIROID (tumor dan ckd )
HDL)
- HIPOPARATIROID (post op tiroid)
4. Kelenjar Adrenal 7. DIABETES INSIPIDUS
- HIPERKORTISOL (cushing disease (HOBI PIPIS, GAGAL
dan cushing sindrom) HORMON ADH)
- HIPOKORTISOL (henti steroid tiba-
tiba, tumor supraadrenal)
 DM
Peningkatan gula darah (Hiperglikemia)
5P
POLIFAGIA
POLIDIPSI
POLIURI
POLINEUROPATI
PENINGKATAN BB
 DM
TIPE I TIPE II
• Etio : kerusakan sel beta • Etio : peningkatan resistensi
insulin dan penurunan
pancreas  insulin
sensitivitas insulin
tidak di produksi
• FR : life style, orang tua
• FR : anak <17th >17th
• PP : GDS  GD2PP • PP : GDS  GD2PP GDP +
GDP + C-PEPTIDE C-PEPTIDE (meningkat) +
(menurun) HBA1C
• th/ mutlak INSULIN • Th/ obat anti diabetes
 Perkeni 2011 Perkeni 2015 &
ADA 2016
Diagnosis DM
1. A1C ≥ 6,5%
Atau
Bahan: darah plasma vena
(DIANJURKAN), whole blood 1. Gejala klasik DM + 2. Gejala klasik DM +
vena/kapiler (kriteria diagnostik glukosa plasma sewaktu ≥ glukosa plasma sewaktu ≥
berbeda sesuai pembakuan WHO)
200 mg/dL (11,1 200 mg/dL (11,1
mmol/L) Atau mmol/L) Atau

2. Gejala klasik DM + 3. Glukosa plasma puasa ≥

Gejala khas DM: poliuri, polidipsi, Glukosa plasma puasa ≥ 126 mg/dL (7,0 mmol/L)
polifagi, dan ↓BB tanpa sebab
jelas 126 mg/dL (7,0 mmol/L) Atau
Atau

3. Glukosa plasma 2 jam 4. Glukosa plasma 2 jam

pada TTGO ≥ 200 mg/dL pada TTGO ≥ 200 mg/dL
Gejala lain: lemas, kesemutan,
(11,1 mmol/L) (11,1 mmol/L)
luka sulit sembuh, gatal, mata
kabur, disfungsi ereksi, pruritus
vulva NB: Puasa diartikan pasien tidak mendapatkan kalori
tambahan s©edBiikmibtneyl Ua K8DIjaMmANTAP
Cara pelaksanaan TTGO (WHO)

• 3 hari sebelum pemeriksaan tetap

makan seperti kebiasaan sehari-hari dan
tetap melakukan kegiatan jasmani
seperti biasa
• Berpuasa minimal 8 jam (mulai malam
hari) sebelum pemeriksaan, minum air
putih tanpa gula boleh
• Diperiksa konsentrasi gula darah puasa
• Diberikan glukosa 75 gram (orang
dewasa) atau 1,75 gram/kgBB (anak-
anak) dilarutkan dalam air 250 ml dan
diminum dalam waktu 5 menit
• Berpuasa kembali sampai pengambilan
sampel darah untuk pemeriksaan 2 jam
setelah minum larutan glukosa selesai
• Diperiksa glukosa darah 2 jam sesudah
beban glukosa
• Selama proses pemeriksaan subyek yang
diperiksa tetap istirahat dan tidak
merokok.

©Bimbel UKDI MANTAP

 Prinsip Dasar Terapi Diabetes Mellitus
1 2 3

EDUKASI TERAPI GIZI MEDIS PELATIHAN

JASMANI

4 5

INTERVENSI FARMAKOLOGIS SMBG

3 Frekuensi: jumlah olahraga perminggu sebaiknya dilakukan secara
teratur 3-5 kali per minggu

Intensitas: ringan dan sedang (60-70% Maximum Heart Rate)

Durasi: 30-60 menit

PELATIHA
Jenis: latihan jasmani endurans (aerobik) untuk meningkatkan
N kemampuan kardiorespirasi seperti jalan, jogging, berenang, dan
JASMANI bersepeda.
Untuk meningkatkan
uptake glukosa di
INTERVAL, latihan yang dilakukan
perifer sebaiknya dilaksanakan secara
CONTINOUS, latihan yang dilakukan berselang-seling, kadang cepat,
harus terns-menerus RHYTHMICAL, latihan dilakukan
secara berirama dan teratur, tidak tetapi kadang juga lambat tetapi
(berkelanjutan) selama 50-60 menit tanpa berhenti. Misalnya jalan
tanpa berhenti. asal-asalan.
cepat, kadang berlari, kemudian
jalan cepat lagi.

PROGRESSIVE, Arti dari tahap ini ENDURANCE, merupakan latihan

adalah latihan dilakukan secara ketahanan, untuk meningkatkan
bertahap dengan beban latihan kesegaran jantung dan pembuluh
ditingkatkan secara perlahan-lahan. darah penderita.

©Bimbel UKDI
 OBAT DM
1. SULFONILUREA 2. GLINID
• Tujuan : peningkatan sekresi
insulin (secretagog)
• Tujuan : peningkatan
• Cara : 15-30 menit sebelum sekresi insulin
makan • Cara : 15-30 menit
• Efek samping : HIPOGLIKEMIA +
sebelum makan
BB meningkat
• KI : kontrasepsi hormonal + CKD • ES : sama
• OBAT : • KI : sama
- GLIBENKLAMID
• OBAT :
- GLIKUIDON
- GLIMEPIRID • - repaglinid
3. Biguanid (Metformin) 5. Tiazolidindion
• Tujuan : penurunan • Tujuan : penurunan
glukoneogenesis resistensi insulin
• Cara : sesudah makan • Cara : sesudah makan
• ES : gastritis/dispepsia, ginjal
• ES : edema
• KI : hati, ginjal, jantung
• KI : jantung
• OBAT :
• OBAT : PIOGLITAZON
- Metformin

4. 5 alfa glukosidase inhibitor 6. DPP IV INHIBITOR

• Tujuan : menghambat absorpsi • Tujuan : meningkatkan
gula di usus sekresi insulin di pancreas
• Cara : saat makan • Cara : saat makan/sesudah
• ES : flatus, kembung makan
• KI : ginjal • ES : begah dan muntah
• OBAT : ACARBOSE • OBAT : sitagliptin
 Kelas Obat Mekanisme Aksi Efek Fisiologis Keuntungan Kerugian

Penutupan kanal
kalium pada ↑ sekresi - ↓ risiko - Hipoglikemia
Sulfonilurea membran sel β- mikrovaskular - ↑ berat badan
insulin
pankreas - Murah - Lini pertama pada pasien non-obese

Penutupan kanal
kalium pada ↑ sekresi
Meglitinide insulin - ↓ puncak GD2JPP - Hipoglikemia
s (Glinid) membran sel β- - Dosis fleksibel - ↑ berat badan
pankreas

- Efek samping GI (diare, nyeri perut)

- ↓ produksi - Risiko hioglikemia - Defisiensi vitamin B12
glukosa hepar minimal - Kontraindikasi: CKD, asidosis, dehidrasi,
Aktivasi AMP- - ↑ sensitivitas - ↓ risiko
Biguanides kinase hipoksia
insulin kardiovaskula - Risiko asidosis laktat
r - Lini pertama pada pasien obese
- Murah

- Risiko hipoglikemia
minimal
- ↑ kolesterol HDL - ↑ berat badan
Aktivasi nuclear - ↓ trigliserida - Retensi cairan
transcription ↑ sensitivitas - Fraktur
TZDs insulin (pioglitazone)
factor PPAR-γ - ↓ risiko - ↑ kolesterol LDL (rosiglitazone)
kardiovaskula Kontraindikasi: edema, gagal jantung
r
(pioglitazone)

Menghambat - Risio hipoglikemia - Efikasi terhadap penurunan HbA1C

enzim ɑ- Menghabat minimal tidak terlalu menonjol
ɑ-glucosidase absorbs ©Bimbel- ↓
inhibitor glucosidase puncak
UKDI GD2JPP
MANTAP - Efek samping GI (diare, flatulensi)
intestinal karbohidrat - Nonsistemik
 Kerugian
Kelas Obat Mekanisme Aksi Efek Fisiologis Keuntungan

Menghambat - Efek dermatologis terkait imun

aktivitas DPP-4 - ↑ sekresi - Risiko hioglikemia (angioedema, urtikaria, dll)
insulin minimal - Pankreatitis akut (?)
DPP-4 inhibitor →
meningkatkan - ↓ sekresi - Dapat ditoleransi
glucagon dengan baik
konsentrasi
incretin (GLP-1)

- ↑ sekresi - Efek samping GI (mual, muntah, diare)

insulin - ↑ heart rate
- ↓ sekresi - Risiko hioglikemia - Pakreatitis akut (?)
glucagon minimal - Hiperplasi sel-C tiroid
- Menghambat - ↓ berat badan - Sediaan injeksi sehingga membutuhkan
GLP-1 receptor Aktivasi reseptor pengosongan - ↓ puncak pelatihan
agonist GLP-1 labung GD2JPP
- ↑ rasa cepat - ↓ risiko
kenyang kardiovaskula
setelah makan r

- ↑ ambilan - Hipoglikemia
glukosa - ↑ berat badan
- ↓ produksi - Respon universal - Sediaan injeksi sehingga membutuhkan
Aktivasi reseptor - ↓ risiko
Insulin insulin glukosa hepar pelatihan
- Menghambat mikrovaskula
ketogenesis r

-Risiko - Infeksi Saluran Kemih

hipoglikemia - Hipotensi ortostatik
Menghambat  minimal - Dehidrasi
Sodium-Glucose reabsorbsi - Menurunkan - Fraktur
SGLT-2 Inhibitor Co-Transporter 2 glukosa pada berat badan dan - KAD
pada ginjal ginjal tekanan
©Bimbel UKDI MANTAPdarah
 Waktu Penggunaan OHO
• Sulfonilurea : 15-30 menit sebelum
makan
• Glinid : sebelum/sesaat sebelum makan
• Acarbose : bersama makan pada suapan pertama
• DPP IV inh : Sebelum /bersama makan
• Metformin : pada sebelum/saat/sesudah makan
• Tiazolidinedion : tidak bergantung pada jadwal makan

©Bimbel UKDI MANTAP

 KONSENSUS PERKENI 2011
Kadar HbA1c
<7% 7-8% 8-9% >9% 9-10% >10%
GHS GHS
+
Gaya Hidup Sehat GHS
Monoterapi
• Penurunan BB +
Met, SU, AGI,
• Mengatur diit Glinid, TZD, Kombinasi GHS
DPP-IV inh
• Latihan Jasmani 2 obat +

teratur Met, SU, AGI, Kombinasi GHS

Glinid, TZD, 3 obat +
DPP-IV inh
Met, SU, AGI, Kombinasi
Glinid, TZD, 2 obat
Catatan DPP-IV
1. Dinyatakan gagal bila dengan inh Met, SU,
terapi 2-3 bulan tidak mencapai AGI, Glinid,
target HbA1c <7% TZD
+ GHS
2. Bila tidak ada pemeriksaan
Basal +
HbA1c dapat digunakan
Insulin Insulin
pemeriksaan glukosa darah.
Rata-rata glukosa darah sehari Intensif
dikonversikan ke HbA1c menurut
kriteria ADA 2010
 KONSENSUS PERKENI 2015
MODIFIKASI GAYA HIDUP SEHAT
HbA1C < 7.5 % HbA1C ≥ 7.5 % HbA1C ≥ 9 %

Gejala (-) Gejala (+)

Dalam 3 bulan + monoterapi
HbA1C > 7 % Kombinasi 2 obat
dalam 3 bulan
Insulin + Obat Lain
HbA1C > 7 %
Kombinasi 3 obat

Monoterapi* dengan salah Kombinasi 2 obat* dengan

mekanisme kerja yang berbeda Kombinasi 3 obat
satu di bawah ini
• Metformin • Agonis GLP-1 • Agonis GLP-1 Tambahkan Insulin
• • •
Agonis GLP-1 Penghambat Penghambat atau Intensifikasi
Metformin atau obat lini

Metformin atau obat lini

• Penghambat DPP- DPP-IV DPP-IV
IV • Tiazolidinidio • Tiazolidinidio Insulin
pertama yang lain

pertama yang lain

Obat lini kedua
• Penghambat n n Keterangan
glucosidase alfa • Penghambat • Penghambat
*Obat yang terdaftar,
• Penghambat SGLT- SGLT-2** SGLT-2**
2** • Insulin Basal • Insulin Basal
pemilihan dan
• Tiazolidinidion • SU/Glinid • SU/Glinid penggunaannya disarankan
• Sulfonilurea • Kolesevelam • Kolesevelam mempertimbangkan faktor
• Glinid ** ** keuntungan, kerugian, dan
• Bromokriptin • Bromokriptin- kebersediaan sesuai tabel 11
Jika HbA1C belum -QR
Alfa QR
Glukosidase ** Penghambat SGLT-2,
mencapai sasaran Jika
• HbA1C belum
Penghambat Jika
• HbA1C belum mencapai
Penghambat
Alfa kolesevelam belum tersedia di
dalam 3 bulan, mencapai sasaran dalam 3
Glukosidase sasaran dalam 3 bulan, mulai
tambahkan obat ke 2
Indonesia dan Bromokriptin
bulan, tambahkan obat ke 3 terapiMANTAP
insulin atau intensifikasi
(kombinasi 2 obat) (kombinasi 3 obat) ©Bimbe l UKDI QR umumnya digunakan
terapi insulin
pada terapi tumor hipofisis
 INDIKASI INSULIN
Hiperglikemi
Penurunan berat Hiperglikemia berat
Ketoasidosis diabetik a
badan yang cepat yang disertai ketosis hiperosmolar
nonketotik

Kehamilan dengan
Gagal dengan Stres berat (infeksi DM/diabetes melitus
Hiperglikemia dengan
kombinasi OHO dosis sistemik, operasi besar, gestasional yang tidak
asidosis laktat terkendali denagn
optimal IMA, stroke)
perencanaan makan

Efek Samping
Gangguan fungsi ginjal Kontraindikasi dan atau • Hipoglikemia
dan hati yang berat alergi terhadap OHO. • Reaksi imunologi terhadap insulin yang
dapat menimbulkan alergi insulin atau
resistensi insulin
• Penambahan berat badan
HbA1c > 10%
• Hipokalemia
GDP > 250 mg/dl
GDS > 300 ©Bimbel UKDI MANTAP
Target : GD PP
Kerja Pendek :
30-45 menit
sebelum makan

Kerja Cepat :
5-15 menit
sebelum
makan
Target :
GD Basal
Kerja Panjang :
1x malam
sebelum tidur
ATAU
2x malam dan
pagi

©Bimbel UKDI MANTAP

©Bimbel UKDI MANTAP
Target 1 : GDP

©Bimbel UKDI MANTAP

 KRITERIA PENGENDALIAN DM
PERKENI PERKENI ADA
2011 2015 2016
IMT 18,5-<23 kg/m2 18,5-<23 kg/m2
GDP < 100 mg/dl 80-130 mg/dl 80-130 mg/dl
GD2JPP < 140 mg/dl < 180 mg/dl < 180 mg/dl
HbA1c < 7% < 7% < 7%
SBP ≤ 130 mmHg < 140 mmHg
DBP ≤ 80 mmHg < 90 mmHg
LDL < 100 mg/dl < 100 mg/dl
(< 70 mg/dl bila (< 70 mg/dl bila
dengan resiko KV) dengan resiko KV)

HDL L : >40, P : > 50

TG <150
©Bimb el UKDI MANTAP
 KOMPLIKASI KRONIK DM
Stroke
Diabetic
Makrovaskuler
retinopathy
Komplikas Mikrovaskuler Cardiovascular
disease
i DM Diabetic
Nephropathy
Makrovaskuler
Mikrovaskule
Diabetic
r
D neuropati
i Mikrovaskule
a
b r
e
t
Akut: i
c
• Ketoasidosis diabetik
F
• Hiperosmolar non ketotik o
• Hipoglikemia o
t
Kombinasi
Kronik: Vaskulopati
danvaskular
• Makroangiopati: Pembuluh koroner, vaskular perifer, neuropati
otak
• Mikroangiopati: kapiler retina, kapiler renal, Neuropati
• Cardiomyopathy (DCM-diabetic cardiomyopathy)  Lipotoxicity, glucose toxicity, ROS
• Rentan infeksi (immunocompromised)
• Disfungsi Ereksi  hiperglikemia berefek langsung menurunkan produksi NO & meningkatkan
mediator vasokonstriksi
• Diabetic foot: makro (vaskular perifer) ©+ Bmmi ikbroel(UloKDnIgMstAaNnTdAinPg peripheral
neuropathy)
 HIPOGLIKEMIA

• Keadaan dimana kadar Klasifikasi klinis Manifestasi

glukosa darah < 70 mg/dl Ringan Simtomatis, bs diatasi
sendiri, gang aktivitas -
Trias whipple untuk Sedang Simtomatis, bs diatasi
hipoglikemia secara umum: sendiri, gang aktivitas +

• 1. Gejala yang konsisten Berat Sering asimtomatik, tdk

bs mengatasi sendiri.
dengan hipoglikemia Variasi:
-Butuh org lain tp tdk
• 2. Kadar glukosa plasma perlu tx parenteral
-Perlu tx parenteral
rendah -Disertai koma atau
kejang
• 3. Gejala mereda setelah
kadar glukosa plasma
meningkat.

©Bimbel UKDI MANTAP

 ETIOLOGI GEJALA KLINIS

• Kelebihan dosis obat, • Rasa gemetar

terutama insulin atau obat
hipoglikemia oral yaitu
sulfonilurea.
• Asupan makan tidak
adekuat jumlah kalori
atau waktu makan tidak
tepat.
• Kegiatan jasmani
berlebihan.
• Perasaan lapar
• Pusing
• Keringat dingin
• Jantung berdebar
• Gelisah
• Penurunan kesadaran
bahkan sampai koma
dengan atau tanpa kejang

©Bimbel UKDI MANTAP

 TATALAKSANA HIPOGLIKEMIA TATALAKSANA HIPOGLIKEMIA
(PPK Puskesmas KMK/514/2015) (EIMED PAPDI 2009)

1. Berikan larutan dekstrose 40% sebanyak

2 flakon (=50 mL) bolus intra vena.
2. Berikan cairan dekstrose 10 % per infus 6
jam perkolf.

Periksa GDS setiap satu jam

GDS < 50 mg/dL → bolus D 40% 50 mL IV.

GDS <100 mg/dL → bolus D 40% 25 mL
IV. GDS 100–200 mg /dL → tanpa bolus D
40%.
GDS > 200 mg/dL → pertimbangan
menurunkan kecepatan drip D 10%.

• Bila GDS > 100 mg/dL sebanyak 3 kali

berturut–turut, pemantauan GDS setiap 2
jam, dengan protokol sesuai diatas, bila GDs
>200 mg/dL pertimbangkan mengganti
infus dengan dekstrosa 5 % atau NaCI 0,9 %.
• Bila GDs > 100 mg/dL sebanyak 3 kali
berturut-turut, protokol hipoglikemi
dihentikan.
©Bimbel UKDI MANTAP
TATALAKSANA HIPOGLIKEMIA
(PERKENI 2015)

©Bimbel UKDI MANTAP

 DIABETIC KETOASIDOSIS &
HIPERGLIKEMIK HIPEROSMOLAR STATE

©Bimbel UKDI MANTAP

DIABETIK KETOASIDOSIS

Trias: hiperglikemia, asidosis, ketosis

Pencetus: infeksi, AMI, stroke, pankreatitis akut, steroid,

menghentikan atau ↓dosis insulin

Gejala Klinis
Napas Kussmaul, dehidrasi, syok, Bila pasien koma, pikirkan sebab
napas bau aseton lain (uremia, trauma, alkohol)

Kriteria Diagnosis
Glukosa darah HCO3 <15 mEq/L Ketosis (Ketonuria,
pH arteri <7.3 ↑ anion gap
>250 mg/dl (rendah) Ketonemia)
©Bimbel UKDI MANTAP
HYPEROSMOLAR HYPERGLYCEMIC STATE (HHS)

Trias: hiperglikemia, hiperosmolar,

dehidrasi

KRITERIA DIAGNOSIS (ADA)

• Glukosa darah >600 mg/dl
• Osmolaritas serum efektif ≥320
mOSm/kg
• Dehidrasi hingga (8-12) L dengan
peningkatan BUN
• pH arteri ≥7.3
• HCO3 ≥15 mEq/L
• Ketonuria minimal, ketonemia (-)
• Gangguan kesadaran
©Bimbel UKDI MANTAP
Low-dose insulin infusion protocols decrease plasma glucose concentration at a rate of 50–75
mg · dl−1 · h−1. If plasma glucose does not decrease by 50–75 mg from the initial value in the
first hour, the insulin infusion should be increased every hour until a©Bimbel UKDI decline
steady glucose MANTAP is
achieved
 DIABETIK NEFROPATI
Diagnosis nefropati diabetik ditegakkan jika didapatkan
kadar albumin >30 mg dalam urin 24 jam pada 2 dari
3 kali pemeriksaan dalam kurun waktu 3- 6 bulan,
tanpa penyebab albuminuria lainnya.
Penapisan dilakukan:
• Segera setelah diagnosis DM tipe 2 ditegakkan.
• Jika albuminuria <30 mg/24 jam dilakukan evaluasi
ulang setiap tahun.

PERKENI 2011
Urin 24 jam Urin dlm waktu tertentu Urin sewaktu
(mg/24 (µg/menit) (µg/mg kreatinin)
jam)
Normal < 30 < 20 < 30
Mikroalbuminuria 30 – 299 20 – 199 30 – 299
Makroalbuminuria ≥ 300 ≥ 200 ≥ 300
PERKENI 2015
Klasifikasi nefropati diabetik tidak lagi menggunakan istilah ‘mikroalbuminuria’ dan
makroalbuminuria’ tetapi albuminuria saja. Nefropati diabetik dibagi atas albuminuria
persisten pada level 30-299mg/24 jam dan albuminuria
©Bimbel UKDI MANTAP persisten pada level ≥300mg/24 jam.
TATALAKSANA DIABETIK NEFROPATI
 Optimalisasi kontrol glukosa untuk
mengurangi resiko ataupun menurunkan
progresi nefropati.
 Optimalisasi kontrol hipertensi untuk
mengurangi resiko ataupun menurunkan
progresi nefropati.
 Pengurangan diet protein pada diet pasien
diabetes dengan penyakit ginjal kronik tidak
direkomendasikan karena tidak mengubah
kadar glikemik, resiko kejadian
kardiovaskuler, atau penurunan GFR.
 Terapi dengan penghambat ACE atau obat
penyekat reseptor angiotensin II tidak
diperlukan untuk pencegahan primer.
 Terapi Penghambat ACE atau Penyekat
Reseptor Angiotensin II diberikan pada
pasien tanpa kehamilan dengan
albuminuria sedang (30-299 mg/24 jam)
dan albuminuria berat (>300 mg/24 jam).
©Bimbel UKDI MANTTiApeP 2 di Indonesia. Perkeni. 2015
 Perlu dilakukan monitoring terhadap
kadar serum kreatinin dan kalium
serum pada pemberian penghambat
ACE, penyekat reseptor angiotensin II,
atau diuretik lain.
 Diuretik, Penyekat Kanal Kalsium, dan
Penghambat Beta dapat diberikan
sebagai terapi tambahan ataupun
pengganti pada pasien yang tidak dapat
mentoleransi penghambat ACE dan
Penyekat Reseptor Angiotensin II.
 Apabila serum kreatinin ≥2,0 mg/dL
sebaiknya ahli nefrologi ikut dilibatkan.
 Pertimbangkan konsultasi ke ahli
nefrologi apabila kesulitan dalam
menentukan etiologi, manajemen
penyakit, ataupun gagal ginjal stadium
lanjut.
Konsensus Pengelolaan dan Pencegahan Diabetes Melitus
 KAKI DIABETIK
• Kelainan tungkai kaki
bawah akibat diabetes
melitus yang tidak
terkontrol.

• Kaki diabetes dapat

disebabkan oleh:
 gangguan pembuluh
darah
(makroangiopati)
 gangguan
persarafan

(neuropati)
 infeksi

©Bimbel UKDI MANTAP

©Bimbel UKDI MANTAP
Bila terdapat gejala klaudikasio atau melemahnya
nadi dorsalis pedis → Pemeriksaan Ankle
Brachial Index (ABI)
©Bimbel UKDI MANTAP
 Kendali luka (wound control): pembuangan jaringan terinfeksi
2 dan nekrosis secara teratur. Perawatan lokal pada luka, termasuk
kontrol infeksi, dengan konsep TIME:
Metabolic o Tissue debridement (membersihkan luka dari jaringan mati)
o Inflammation and Infection Control (kontrol inflamasi dan infeksi)
Control o Moisture Balance (menjaga kelembaban)
oEpithelial edge advancement (mendekatkan tepi epitel) Kendali
3 metabolik (metabolic control): pengendalian keadaan
1 metabolik sebaik mungkin seperti pengendalian kadar glukosa
darah, lipid, albumin, hemoglobin dan sebagainya.
Wound Infection Kendali infeksi (infection control): jika terlihat tanda-tanda
Control klinis infeksi harus diberikan pengobatan infeksi secara agresif
(adanya kolonisasi pertumbuhan organisme pada hasil usap
Control namun tidak terdapat tanda klinis, bukan merupakan infeksi).
Kendali vaskular (vascular control): perbaikan asupan vaskular

Management (dengan operasi atau angioplasti), biasanya dibutuhkan pada

keadaan ulkus iskemik.

of Foot Kendali tekanan (pressure control): mengurangi tekanan pada

kaki, karena tekanan yang berulang dapat menyebabkan ulkus,

Ulcers
sehingga harus dihindari. Mengurangi tekanan merupakan hal
6 4 sangat penting dilakukan pada ulkus neuropatik. Pembuangan
kalus dan memakai sepatu dengan ukuran yang sesuai diperlukan
Education Vascular untuk mengurangi tekanan.
Penyuluhan (education control): penyuluhan yang baik.
control Control Seluruh pasien dengan diabetes perlu diberikan edukasi
mengenai perawatan kaki secara mandiri.
5
Mechanic
Control

©Bimbel UKDI MANTAP

Konsensus Pengelolaan dan Pencegahan Diabetes Melitus Tipe 2 di Indonesia. Perkeni. 2015
 DISLIPIDEMIA

kelainan metabolisme lipid yg ditandai dgn ↑kolesterol

total, LDL, TG, serta ↓HDL

Dislipidemia primer:
kelainan genetik→ dislipid moderat
ec hiperkolesterolemia poligenik
dan dislipidemia kombinasi familial

Dislipidemia sekunder:
disebabkan penyakit lain seperti
DM, hipotiroidisme, peny hati
obstruktif, SN, obat (progestin,
steroid anabolik, kortikosteroid,
beta blocker) ©Bimbel UKDI MANTAP
Pemeriksaan ATP III CLASSIFICATION
LDL Cholesterol – Primary Target of Therapy
1. skrining: dewasa >20 tahun
< 100 Optimal
2. Cara: kol total, LDL, HDL tdk perlu
100-129 Near optimal/above optimal
puasa. TG harus puasa 12-16 jam.
130-159 Borderline high
Kadar LDL dpt dihitung dengan
160-189 High
rumus Friedewald
≥190 Very high
LDL-C =
Total Cholesterol
Total Cholesterol – (HDL-C +
<200 Desirable
TG/5)
200-239 Borderline high
Rumus ini hny berlaku bila kadar ≥240 High
TG HDL Cholesterol
<400 mg/dl <40 Low
≥60 High
Triglycerides
<150 Normal
150-199 Borderline high
200-499 High
©Bimbel UKDI MANTAP
≥500 Very high
©Bimbel UKDI MANTAP
©Bimbel UKDI MANTAP
 TG ≥ 500 mg/dl

*Therapeutic Lifestyle Changes

 Lifestyle Intervention
Lifestyle Interventions aimed to:

Lower LDL-C Increase HDL-C Lower TG

Reduce dietary saturated fat

Increase dietary fiber

Reduce total amount of dietary carbohydrate

Reduce alcohol intake

Increase habitual physical activity

Reduce excessive body weight

Quit smoking

einer Z, et al. EHJ;2011:32:1769-1818

STATIN – MECHANISM OF ACTION
HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitors

Cholesterol VLDL
synthesis Apo B
LDL receptor LDL receptor–mediated
VLDLR
HMGCoA Apo E hepatic uptake of LDL
(B–E receptor)
and VLDL remnants
Intracellular synthesis Apo B Serum LDL-C
Cholesterol LDL Serum VLDL remnants
Serum IDL

Hepatocyte Systemic Circulation

1. Reduce hepatic cholesterol synthesis (HMG CoA),
2. lowering intracellular cholesterol,
3. Upregulation
Dr.Sarma
of LDL receptor → ↑ removal apo E-B containing lipoprot. from the vli er
Dr.Sarma @
4.w@ork work s
↑ the uptake
s of non-HDL from circulation.
 Intensity of Statin Therapy
High-Intensity Statin Moderate-Intensity Stain Low-Intensity Statin
Therapy Therapy Therapy

LDL–C ↓ ≥50% ; ↓ TG LDL–C ↓ 30% to <50% LDL–C ↓ <30%

Atorvastatin (40†)–80 mg Atorvastatin 10 (20) mg Simvastatin 10 mg

Rosuvastatin 20 (40) mg Rosuvastatin (5) 10 mg Pravastatin 10–20 mg
Simvastatin 20–40 mg‡ Lovastatin 20 mg
Pravastatin 40 (80) mg Fluvastatin 20–40 mg
Lovastatin 40 mg Pitavastatin 1 mg
Fluvastatin XL 80 mg
Fluvastatin 40 mg bid
Pitavastatin 2–4 mg

Lifestyle modification remains a critical component of ASCVD risk reduction, both prior to and in concert with the use of cholesterol
lowering drug therapies.

Statins/doses that were not tested in randomized controlled trials (RCTs) reviewed are listed in italics
†Evidence from 1 RCT only: down-titration if unable to tolerate atorvastatin 80 mg in IDEAL
‡Initiation of or titration to simvastatin 80 mg not recommended by the FDA due to the increased risk of myopathy, including rhabdomyolysis.

Stone NJ, et al. J Am Coll Cardiol. 2013: doi:10.1016/j.jacc.2013.11.002. Available at:

http://content.onlinejacc.org/article.aspx?articleid=1770217. Accessed November 13, 2013.
 Current Overview of Statin-
Induced Muscle Side
Effects
Classification of Muscle Adverse Events with Statins

Condition Definitions (ACC/AHA NHLBI)

Myopathy Disease of the muscles, which may be acquired or inherited
• Muscle ache or weakness without increases in creatine kinase levels
• Common complaint is muscle aches or joint pain
Myalgia • Incidence of complaints is generally reported as about 5% with statins
• Some patients have mild-to-moderate elevations of CK without muscle
complaints
• Muscle aches, soreness or weakness and associated with elevated
Myositis creatine kinase levels, generally < 10 x ULN
(may also be • Incidence - rare with statins
called Myopathy) • Most likely to occur in persons who have complex medical
problems and/or
who are taking multiple medications
• Muscle symptoms with marked CK elevations (typically substantially
greater than 10 x ULN) and with creatinine elevation (usually with
Rhabdomyolysis brown urine and urinary myoglobin)
• Incidence - very rare
• Without clinical intervention, rhabdomyolysis can be life-threatening
Pasternak Use and Safety of Statins. J AM Coll Cardiol 2002;40:567-72.
  Common side effects
 Headache, Myalgia,
Fatigue, GI intol. Flu-
like symptoms
 Myopathy occurs in 0.2 to
0.4% of patients
• Rare cases of
Rhabdomyolysis
• Who uses statins in
impaired renal
Increase in liver enzymes – serious function
problems are very rare → Occurs in • combining statins with
05. to 2.5% of cases in dose-dependent fibrates
manner  Muscle toxicity requires the
discontinuation of statin
CHOLESTEROL ABSORPTION INHIBITOR
–
MECHANISM OF ACTION
Production in liver Absorption from intestine

Bloodstream Dietary cholesterol

LDL-C
VLD Biliary cholesterol
L

Cholesterol
synthesis
Chylomicrons

Fecal sterols and neutral sterols

Ezetimibe selectively inhibits absorption of cholesterol at the brush
border membrane in the intestinal lumen.
©Bimbel UKDI MANTAP
BILE ACID SEQUESTRANT – MECHANISM OF ACTION

 Cholesterol 7- hydroxylase

 Conversion of cholesterol to BA
Gall Bladder  BA Secretion

Bile Acid
Enterohepatic Circulation Live
Terminal Ileum r
 LDL Receptors
Reabsorption of
 VLDL and LDL
bile acids removal
 BA Excretion

 LDL-C Efek samping: rasa kembung,

flatulensi, konstipasi,
menghambat absorbsi vit K

BA=Bile acid, LDL-C=Low density lipoprotein cholesterol,

VLDL=Very low density lipoprotein
 FIBRATE – MECHANISM OF ACTION

+
T
G
VLD
L Fibrate
Intestine LPL
ID
LDL- + L
R

C
C FC E
Live FC
E Nascent
r
Mature HDL HD
L Macrophage
Efek samping: miopati, peningkatan enzim hepar,
kolelithiasis CE=Cholesterol ester, FC=Free cholesterol, HDL=High density lipoprotein,
IDL=Intermediate density lipoprotein, LDL-R=Low density lipoprotein receptor,
Risiko miopati gemfibrozil + statin > fenofibrat + LPL=Lipoprotein lipase, TG=Triglyceride, VLDL=Very low density lipoprotein
statin
NICOTINIC ACID MECHANISM OF ACTION

Mobilization of FFA

Apo B
Apo B
Serum VLDL
results in reduced
VLD lipolysis to LDL
VLD
L L
TG
VLDL Serum LDL
synthesis
secretion
LDL
HDL

Hepatocyte Systemic Circulation

Decreased hepatic production of VLDL and uptake of apolipoprotein A-1 results in
reduced LDL cholesterol levels and increased HDL cholesterol levels
FFA=Free fatty acid, HDL=High density lipoprotein, LDL=Low
Efek samping: keluhan kulit (ruam, density
lipoprotein, TG=Triglyceride, VLDL=Very low density lipoprotein
pruritus, flushing), keluhan GI, DM, Source: McKenney JM. Selecting Successful Lipid-lowering Treatments presentation, 2002.
dan keluhan muskuloskeletal ©Bimbel UKDI MAAvNaTliAaPbe
l at
 Kelas Obat Senyawa Mekanisme Aksi Efek Fisiologis Keterangan

Efek samping: miopati,

HMG-CoA Menghambat enzim HMG-CoA ↓ LDL-C 18-55% peningkatan enzim
reductas Statin reductase → menurunkan sintesis ↑ HDL-C 5-15% hepar, DM onset baru,
e kolesterol hepar ↓ TG 7-30% gangguan memori
inhibitor

Menghambat absorbsi kolesterol dari

Inhibitor diet dan kolesterol dari empedu tanpa Lini kedua setelah
absorbsi ↓ LDL-C 16-18%
Ezetimibe mempengaruhi absorbsi nutrisi larut statin → kombinasi
kolestero lemak ezetimibe + statin
l

Efek samping: rasa

- Meghambat sirkulasi enterohepatic kembung, flatulensi,
Kolestiramin dari asam empedu
Bile acid ↓ LDL-C 18-25% konstipasi,
sequestran - Meningkatkan perubahan kolesterol menghambat absorbsi
Kolesevelam menjadi asam empedu di hati
t Kolestipol vit K

Efek samping: miopati,

- ↓ regulasi apoC-III → ↑ aktivitas peningkatan enzim
Gemfibrozil lipoprotein lipase → ↑ katabolisme ↓ TG 25-40% hepar, kolelithiasis
Fibrat Fenofibrat ↑ HDL-C Risiko miopati
G
T
gemfibrozil + statin >
- ↑ regulasi apoA-I dan apoA-II → fenofibrat + statin
↑
konsentrasi HDL-C
- Menghambat mobilisasi asam lemak Efek samping: keluhan
↓ TG 20-40% kulit (ruam, pruritus,
bebas dari perifer ke h e p a r → ↓ ↓ LDL-C 15-18%
Asam nikotinat Niasin sintesis TG dan VLDL flushing), keluhan GI,
↑ HDL-C 15-35% DM, dan keluhan
- ↑ produksi ap©oABi-mI dbei
muskuloskeletal
lhUeKpDaIrM→AN↑TAP HDL-C
STATINS BILE ACID RESIN
• Cholestyramin: take it with the largest
• Usually administered in the evening meal
because most hepatic cholesterol • Titrate dose slowly to avoid GI side
production occurs during the night effect
• The powder cannot be used in dry form. It
• Atorvastatin may be given any time of can be mixed with water, fruit juice, milk,
the day because of its longer half-life & with food such as thin soup or with milk
in breakfast cereal until completely
• You may take this medicine with or dissolved. The patient must drink this
mixture right away
without food
• Counsel patient to rinse the glass with
liquid to ensure ingestion of all resin
• Increase fluid intake
FIBRATE • Dose other drugs 1 hour before or 4 hours
S after resin
• Gemfibrozil should be taken twice daily 30 minutes
before meals
Patient Instructions
• Fenofibrate can be taken with food once daily & Counseling
• Monitor muscle toxicity, especially when used with
©Bimbel UKDI MANTAP
statins
 METABOLIC SYNDROME

Terkumpulnya berbagai faktor risiko metabolik pada seseorang, yang memberikan

peningkatan risiko untuk terjadinya kelainan kardiovaskular, DM tipe 2 dll.
©Bimbel UKDI MANTAP
©Bimbel UKDI MANTAP
 Pituitary
Hormones

©Bimbel UKDI MANTAP

GLANDULA
TIROID

©Bimbel UKDI MANTAP

 GOITER
Klasifikasi Goiter menurut WHO

©Bimbel UKDI MANTAP

 Goiter Toxic
Goiter
(Hyperthyroidism present)
berdasarka
Diffuse
(graves)
Nodule
n
pemeriksaa
Uninodular
(toxic adenoma)
Multinodular
(toxic multinodular
goiter)
n klinis
Endemic goiter/simple goiter
Goiter Non Toxic (defisiensi yodium) → Local Prevalence > 5-10%
(No Hyperthyroidism present)

Sporadic goiter
(faktor lingkungan/genetik)

Diffuse Nodule

Uninodular Multinodular
©Bimbel UKDI MANTAP
REGULASI NORMAL HORMON TIROID

©Bimbel UKDI MANTAP

 Primary Subclinical Secondary
Hypofunctio Hypofunction Hyperfunctio
n n

High
THYROTROPIN (TSH) LEVEL

Normal
Normal

range

Pituitary Subclinical Primary

Low

Failure Hyperfunction Hyperfunctio

n

Low Normal High

THYROID HORMONE LEVEL
 TIROTOKSIKOSIS DAN
HIPERTIROIDISME
TIROTOKSIKOSIS: PENYEBAB TIROTOKSIKOSIS
Manifestasi klinis kelebihan Hipertiroidiesm Tirotoksikosis Hipertiroidisme
hormon tiroid yg beredar dalam e primer tanpa sekunder
sirkulasi hipertiroidisme
Peny Graves Hormon tiroid TSH-secreting
HYPERTHYROIDISM: Gondok ekstrogen tumor
Tirotoksikosis yg diakibatkan oleh multinodular berlebih Tirotoksikosis
kelenjar tiroid yg hiperaktif toksik (faktisia) gestasi (trim 1)
(radioactive neck-uptake ↑) Adenoma toksik Tiroidits Resistensi
Karsinoma tiroid subakut (viral hormon tiroid
Struma ovarii atau De
Tirotoksikosis (ektopik) Quervain)
Mutasi TSHr gen Destruksi
Inflamasi Hipertiroid kelenjar:
amiodaron,
radiasi,
Ingesti adenoma, infark
©Bimbel UKDI MANTAP
SIGNS & SYMPTOMS THYROTOXICOSIS

©Bimbel UKDI MANTAP

INDEX WAYNE UNTUK HIPERTIROID

Interpretation:
> 19
toxic
hyperthyroidism

< 11
euthyroidism

11-19
equivocal.

Diagnostic
accuracy of 85%.

©Bimbel UKDI MANTAP

©Bimbel UKDI MANTAP
 GRAVES DISEASE
(Parry’s disease / Basedow’s disease)

thyroid stimulating Antibodi berikatan - Menghasilkan T3 & T4

immunoglobulin (TSI) dengan reseptor TSH - Diffuse growth
- limphosit (IgG) (TRAb)
©Bimbel UKDI MANTAP
MANIFESTASI KLINIS
1. Signs & symptoms hyperthyroid
2. Thyroid dermopathy
pretibial myxedema, indurated plak,
orange-skin appearance
3. Thyroid acropachy
manifests as clubbing finger

©Bimbel UKDI MANTAP


Proptosis may be quantitated with an
hartel exophthalmometer, an
instrument that measures the position
of the globes in relation to the lateral
orbital rim.
4. Graves ophtalmopathy
- Wide palpebral aperture
(Dalrymple’s sign)
- Lid lag (von Graefe’s sign)
- Staring or frigthened expressions
- Infrequent blinking (Stellwag’s
sign)
- Absence of forehead wringkling on
upward (Joffroy’s sign)
- Inability to keep converged
(Mobius’ sign)
- Diplopia
- Swelling of orbital contents and
puffiness of the lids
- Chemosis, corneal
injection/ulceration
- Exophthalmus
- Decreased visual acuity, retinal
edema/hemorrhages, optic nerve
damage
©Bimbel UKDI MANTAP
 THYROID EXAM
• Diffuse toxic goiter,
less symetric.
• Thrills and bruits are
important but often
absent.
• Thrills (palpable) and
bruits (audible) sign of
turbulence associated
with an increased rate
of flow through turtuos
vessel.
©Bimbel•UKPDI uMAlNsTeAP pressure 50-80
CARDIAC MANIFESTATION
• Tachycardia
• Atrial fibrillation
• LVH and strain on ECG
• Premature atrial/ventricular
contractions
• Congestive heart failure
• Angina with/without coronary
artery disease
• Myocardial infarction
• Resistance to some drug effects
(digoxin)
• Residual cardiomegaly
• Systolic BP ↑ Diastolic BP ↓
DIAGNOSIS GRAVES DISEASE
Anamnesis dan Pemeriksaan Jasmani
Pemeriksaan laboratorium
Sidik tiroid
TSH menurun
FT4 USG
Graves:
meningkat Uptake iodine
Kurang ada
BAJAH
T3 – T3 meningkat
Toksikosis (hot nodule) manfaat Tidak biasa
Tiroiditis: dilakukan
uptake (hanya kalau
rendah disertai nodul
dingin)

©Bimbel UKDI MANTAP

TREATMENT OF HYPERTHYROIDISM

Surgery

Radioacti
ve
Iodine

Anti-
thyroid
Drugs

©Bimbel UKDI MANTAP

 KELOMPOK OBAT EFEK
Thioamide • Menghambat fungsi TPO
- Propiltiuurasil (PTU) (Thyroid Peroxidase)
- Metimazol • Menurunkan oksidasi
- Karbimazol dan organifikasi iodide
• Menghambat coupling
iodotirosine
• (+) PTU menghambat
konversi T 4 → T 3 di
perifer
KETERANGAN
• Obat jangka pendek prabedah/praRAI
• Metimazol lebih disukai dari PTU karena
bekerja lebih cepat dan lebih sedikit efek
samping
• Efek samping :
- Minor : gatal, rash, demam, mual, muntah dll
- Major : Kerusakan liver (>> PTU), vasculitis
(>> PTU), agranulositosis, anemia aplastic

Beta blocker • Mengurangi dampak Obat tambahan, kdg obat tunggal pd tiroiditis
-Propranolol hormon tiroid pd
-Metoprolol jaringan
-Atenolol • Propanolol dosis tinggi
-Nadolol (>160 mg/hari)
menghambat konversi
T4→T3

Bahan mengandung iodin • Menghambat keluarnya • Persiapan tiroidektomi.

-Kalium iodida T4 dan T3 • Pd krisis tiroid.
-Sol lugol • Menghambat produksi • Bukan utk pengobatan rutin
-Na ipodat T4 dan T3 serta produksi
-Asam iopanoat T3 ekstratiroidal
-Iodine Radioactive
Therapy

©Bimbel UKDI MANTAP

Monitor terapi : T4, T3,
 PTU
• 300 mg daily in 3 divided
doses.
• Severe hyperthyroidism or very
large goiters, initial dosage may
be increased to 400 mg/day,
up to 600 to 900 mg/day.
• The maintenance dosage is 100
to 150 mg/day.
Duration of action from 12 to 24 h
PO peak serum concentrations
occurring in one hour
Side effects of are less clearly
related to dose.
MMI
• 15 to 30 mg/day as a single
dose.
• 15 mg/day for mild hyperthyroidism
• 30-40 mg/day for moderately
hyperthyroidism.
• 60 mg/day for severe
hyperthyroidism.
• The daily dose is divided into 3
doses administered every
8 hours.
• The maintenance dose is 5-15
mg/day
Duration of action even longer
Side effects are dose-related
©Bimbel UKDI MANTAP
Hyperthyroidism: Adjunctive Therapy

• Inhibits thyroid hormone • Propranolol, 40-200 mg

Iodine:
Severe Hyperthyroidism

Beta Blockers:
For palpitations, Afib with RVR
synthesis/release, dalam 4 dosis
• Decrease the vascularity • Atenolol 25-50 mg
of the thyroid gland sekali
• Should not be used for sehari
long-term therapy , Will
delay 131I
• SSKI (50 mg
iodide/drop)
• Lugol’s Solution (5-10%
KI, 8 mg iodide/drop)

©Bimbel UKDI MANTAP

 KRISIS TIROID / THYROID STORM
A clinical diagnosis at the end of a
hyperthryoid continuum

Hyperthermia

Mental status change

Cardiovascular

• colapse in hyperthyroid
Precipitatants
patients: surgery, sepsis, iodine
loads, post-partum
• Endocrine emergency
(Mortality 20-
©Bimbel UKDI MANTAP
50%)
TATALAKSANA KRISIS TIROID (PAPDI, 2009)
• rehidrasi dan koreksi elektrolit (NaCl dan cairan lain) dan kalori
UMUM (glukosa), vitamin, oksigen, obat sedasi, kompres es

• Memblok sintesis hormon baru :

PTU dosis besar loading 600-1000 mg diikuti 200 mg PTU/4 jam
dengan dosis sehari total 1000-1500 mg
KOREKSI • Memblok keluarnya hormon :
HIPERTIROIDISME sol lugol 10 gtt/6-8 jam atau SSKI (larutan kalium iodida jenuh) 5
gtt/6 jam
• Menghambat konversi perifer dari T 4 → T 3 :
propranolol, ipodat, beta blocker dan/atau kortikosteroid

HIDROKORTISON • Pemberian hidrokortison dosis stress (100 mg/8 jam) atau

DOSIS STRESS deksametason 2mg/6 jam (karena ada defisiensi steroid relatif
akibat hipermetabolisme dan menghambat konversi perifer T4).

ANTIPIRETIK • Asetaminofen, hindari aspirin

Tx Faktor Pencetus • Infeksi,

trauma©BtiimrobeildU,KoDIbMaAtNdTAlPl
HIPOTIROI
D Definition:
• Deficiency of thyroid hormone

Causes:
• Primary (TSH high) ~95%
• Secondary (TSH low) ~5%

Relatively common:
• 2% adult women, 0.2% adult men
• >60: 6% adult women; 2% adult men
• May be higher in select groups

©Bimbel UKDI MANTAP

SIGN & SYMPTOM
Pasien dengan hipotiroid bisa saja
mengalami gejala fisik dan mental
yang tidak spesifik
• Kelelahan/ mengantuk
• Mudah kedinginan
• Kram otot
• Mengalami kenaikan berat badan meskipun
diet dan berolahraga
• Depresi
• Konstipasi
• Periode menstruasi yang abnormal dan/atau
masalah kesuburan
• Rambut atau kuku yang tipis dan rapuh dan/
atau kulit kering • Onset : Usually Gradual
• Muka, tangan dan kaki bengkak • ± Goiter
• Nyeri otot • Risk Factors: Age >60, female, history of thyroid
• Libido menurun disease, history of radiotherapy to head/neck,
family history of thyroid disease, lithium or
amiodarone therapy.
©Bimbel UKDI MANTAP
Myxedem
a
The term myxedema refers to the
thickened, nonpitting edematous
changes to the soft tissues of patients
in a markedly hypothyroid state.

©Bimbel UKDI MANTAP

INDEX DIAGNOSTIK BILLEWICZ UNTUK HIPOTIROID

(Jarang dipakai)
Interpretation:
≥25: hypothyroidism
≤-30: exclude the
disease

©Bimbel UKDI MANTAP

 AUTOIMMUNE THYROIDITIS
(Hashimoto’s, Chronic Lymphocytic)
Autoimmune destruction of thyroid
tissue
– High titers of anti-thyroid antibodies
– Lymphocytic Infiltration of thyroid gland,
fibrosis

Normal Hashimoto’s Thyroiditis

©Bimbel UKDI MANTAP

TATALAKSANA HIPOTIROIDISME
Pilihan pertama, dapat dipakai
untuk Tx koma miksedema,
aman untuk ibu hamil

Monitor thyroid Dosis awal :

function tests every 50-100 mcg PO 1 x/hari
Replace with
6-8 weeks dinaikkan 25-50 mcg/3-4mgg
levo- until
steady dose is
s/d eutiroid dan kadar TSH normal

thyroxine (L- achieved; Dosis rumatan :

T4) goal is to 100-200 mcg PO 1/hr
normalize TSH in
most cases Lansia / Kardiovaskuler :
dosis awal 25-50 mcg PO 1x/hari
dinaikkan 25 mcg/4mgg
s/d eutiroid dan TSH normal

©Bimbel UKDI MANTAP

KOMA MIKSEDEMA / KRISIS MYXEDEMA

Wanita usia lanjut, infeksi, obat,

paparan lingkungan (paparan
udara dingin), keadaan terkait
metabolik.

Tanda & gejala : riwayat

hipotiroid lama, hipotermi berat
(<270C), bradikardi, gagal nafas,
penurunan kesadaran

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 PEMBERIAN PENGOBATAN TIROID PADA KOMA MIKSEDEMA

INTRAVENA ORAL

• Levothyroxine • kasus ringan

bolus awal 200-500 mkg • mulai dosis kecil dinaikkan pelan

IV/via NG, rumatan 100-200 pelan
mkg/hari IV
/ via NG
• Liothyronine (lebih cepat)
bolus 50 mkg IV pelan dilanjutkan
25 mkg IV/ 8jam sampai
membaik, kemudian 25 mkg/ 12
jam atau 5-20 mkg IV pelan/4-12
jam (umumnya 12 jam)
Pemberian IV : hati hati pada PJK . Monitor detak jantung, hentikan bila aritmia
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GLANDULA PARATIROID

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©Bimbel UKDI MANTAP
HIPERPARATIROI
D

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HIPERPARATIROID PRIMER
Primary hyperparathyroidism is one
of the most common endocrine
disorders, and it is an important
cause of hypercalcemia.
The frequency of the various
parathyroid lesions underlying the
hyperfunction is as follows:
• Adenoma 75-80%
• Primary hyperplasia (diffuse or nodular)
10-15%
• Parathyroid carcinoma < 5%
©Bimbel UKDI MANTAP
In patients with primary
hyperparathyroidism, serum PTH
levels are inappropriately elevated
for the level of serum calcium,
whereas PTH levels are low to
undetectable in hypercalcemia
because of nonparathyroid disease
Primary hyperparathyroidism is
usually a disease of adults and is
more common in women than in
men by a ratio of nearly 3:1.
The signs and symptoms of hyperparathyroidism reflect the combined effects of increased PTH
secretion and hypercalcemia.
Primary hyperparathyroidism has been traditionally associated with a constellation of symptoms
that included "painful bones, renal stones, abdominal groans, and psychic moans".

• Bone disease includes bone pain

secondary to fractures of bones
weakened by osteoporosis or osteitis
fibrosa cystica.
• Nephrolithiasis (renal stones) occurs
in 20% of newly diagnosed patients,
with attendant pain and obstructive
uropathy. Chronic renal insufficiency
and a variety of abnormalities in renal
function are found, including polyuria
and secondary polydipsia.
• Gastrointestinal

disturbances include constipation,

nausea, peptic ulcers, pancreatitis,
and gallstones.
include lethargy, and
• Central nervous system alterations
depression,
eventually seizures. abnormalities
• Neuromuscular
include complaints of weakness and
fatigue.
• Cardiac manifestations include
aortic or mitral valve calcifications (or
both).
©Bimbel UKDI MANTAP
HIPERPARATIROID SEKUNDER

Caused by any condition associated with

a chronic depression in the serum
calcium level because low serum
calcium leads to compensatory
overactivity of the parathyroid
glands.

Renal failure is by far the most

common cause of secondary
hyperparathyroidism although a number
of other diseases, including inadequate
dietary intake of calcium, steatorrhea,
and vitamin D deficiency, may also
cause this disorder.

©Bimbel UKDI MANTAP

 HIPOPARATIROI
PTH deficiency results in hypocalcemia D
- Primary hypoparathyroid:
inadequate PTH activity
Low PTH with a concomitant low
calcium level

- Secondary hypoparathyroid: a
physiologic state in which PTH levels
are low in response to a primary
process that causes hypercalcemia
Low PTH and serum calcium level is
elevated

- Pseudohypoparathyroidism: A rare
familial disorders with target tissue
resistance to PTH. PTH concentration
is elevated as a result of resistance to
PTH caused by mutations in the PTH
receptor system

©Bimbel UKDI MANTAP

MANIFESTASI KLINIS HIPOPARATIROID

The hallmark of hypocalcemia is tetany, which is

characterized by neuromuscular irritability, resulting
from decreased serum ionized calcium concentration.

These findings can range from circumoral numbness or

paresthesias (tingling) of the distal extremities and to
life-threatening laryngospasm and generalized
seizures.

The classic findings on physical examination of

patients with neuromuscular irritability
are Chvostek sign and Trousseau sign.
©Bimbel UKDI MANTAP
TATALAKSANA HIPOPARATIROID
The mainstay of treatment is a
combination of oral calcium with
pharmacological doses of vitamin
D or its potent analogues.
Phosphate restriction in diet may
also be useful with or without
aluminum hydroxide gel to lower
serum phosphate level.
©Bimbel UKDI MANTAP
Emergency Tetany
Calcium should be given
parenterally till adequate
serum calcium level is
obtained and then vitamin D
supplementation with oral
calcium should be initiated.
 EKG PADA
HIPER/HIPOKALSEMIA
Hipokalsemia Hiperkalsemia
Pemanjangan QT interval
Normal
Pemendekan QT interval

©Bimbel UKDI MANTAP

 GLANDULA
PITUITARI
POSTERIOR
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 DIABETES
Definisi: INSIPIDUS
kondisi volume urin yg
banyak (>3L/hr) karena
gangguan resorbsi air oleh
ginjal yg disebabkan :

- ↓sekresi ADH oleh

hipofisis posterior
(DI sentral) ;
atau
- gangguan respon ginjal
terhadap ADH
(DI nefrogenik)
SS: poliuria, polidipsia, dehidrasi,
gejala hipernatremia ©Bimbel UKDI MANTAP Fisiologi ADH
ETIOLOGI

Idiopatik
Kongenital: defek pada gen ADH, DIDMOAD
syndrome (resesif autosomal: DI, DM, atrofi optik, dan
tuli/Wolfram’s synd)
Inherited
Tumor: kraniofaringioma, metastasis, tumor Metabolik: ↓Kalium, ↑kalsium
hipofisis Obat: litium, demeklosiklim
Trauma: hipofisektomi, head injury CKD
Infiltrasi: histiositosis, sarkoidosis Post uropati obstruktif
Vaskular: Sheehan’s syndrome
Infeksi: meningoensefalitits

©Bimbel UKDI MANTAP

DIAGNOSIS : WATER DEPRIVATION TEST
Patient is deprived of all water intake until
1 dehydration (defined by weight loss of at least 2% of body
weight and rise in plasma osmolality above 300
mOsm/kg) is achieved. UO, BP and urine
osmolality are then measured every 2 hours.
Normally after water deprivation, a decrease in UO
(because ADH is stimulated by increased osmolality) and
an increase in urine osmolality is expected to occur. In
patients with DI, UO remains high and urine
2 diluted.

Subcutaneous injection of ADH and measurement

of urine and plasma osmolarity. Patients
nephrogenic DI lack the withability to concentrate
urine after th©eBimabedl UmKDI MinANiTAsPtration of
 INTERPRETASI WATER DEPRIVATION TEST
Normal Osmolalitas urin >600 mOsm/kg
(kemampuan mengkonsentrasi urin normal)

Polidipsia primer/psikogenik Urin terkonsentrasi, tapi kemampuan

mengkonsentrasikan urin masih kurang dr normal >400-
600 mOsm/kg
Diabetes insipidus Osmolalitas urin <400 mOsm/kg
(kemampuan mengkonsentrasi urin rendah)

DI sentral Osmolalitas urin NAIK >600 mOsm/kg

SETELAH pemberian desmopressin

DI nefrogenik Osmolalitas urin TIDAK NAIK

SETELAH pemberian desmopressin

©Bimbel UKDI MANTAP

TREATMENT

DI CENTRAL
••DI NEPHROGENIC
DESMOPRESSIN (DDAVP)
• AProvision of adequate
synthetic analog is superior
to native&AVP
fluids because :
calorie
• 1.Low
It has longer duration of
sodium diet
action (8-10 h vs 2-3 h)
• 2.Diuretic
More potent
• 3.High dose of DDAVP
Its antidiuretic activity is
3000 times greater than its
• Correction of underlying
pressor activity
• disease
• Drugs (Indomethacin,
Chlorprooramide,
Clofibrate & ©Bimbel UKDI MANTAP
GLANDULA ADRENAL

©Bimbel UKDI MANTAP

 ADRENAL CORTEX. The three
tissue layers secrete, in the same
order, the following corticosteroids:

1. Mineralocorticoids (zona glomerulosa only),

which act on the kidneys to control electrolyte
balance. The principal mineralocorticoid is
aldosterone, which promotes Na retention and K
excretion by the kidneys.

2. Glucocorticoids (mainly zona

especially
fasciculata), cortisol (hydrocortisone); 3. Sex steroids (mainly zona reticularis), including
corticosterone is a potent weak androgens and smaller amounts of
less
stimulate fatrelative.
and protein estrogens. Androgens control many aspects of
Glucocorticoids
catabolism, gluconeogenesis, and the release of male development and reproductive physiology. The
fatty acids and glucose into the blood. This helps principal adrenal androgen is
the body adapt to stress and repair damaged dehydroepiandrosterone (DHEA) (de-HY-dro-
tissues. Glucocorticoids also have an EPee- an-DROSS-tur-own). DHEA has
antiinflammatory effect and are widely used in hormonal effects in itself, but more importantly, other
weak
ointments to relieve swelling and other signs of tissues convert it to the more potent androgen,
inflammation. Long-term secretion, testosterone. This source is relatively
however, suppresses the immune system. unimportant in men because the testes produce so
much more testosterone than this. In women,
however, the adrenal glands meet about 50% of the
©Bimbel UKDI MtAoNtaTAl Pandrogen requirement.
 CUSHING
SYNDROME
• Cushing’s syndrome:
chronic glucocorticoid excess.
The commonest cause is steroid
tx. Endogenous cases are much
rarer: 85% are due to ↑ACTH, of
these a pituitary adenoma
(Cushing’s disease) is the
commonest cause.

• Cushing’s disease:
pituitary releases
gland much adrenocorticotropic
too
hormone (ACTH). Cushing's
disease is caused by a tumor or
excess growth of the pituitary
gland.
©Bimbel UKDI MANTAP
Systemic Effects of Glucocorticoids

indwiani@yahoo.co
m
©Bimbel UKDI MANTAP
 Cushing’s Syndrome
Etiology
• ACTH-dependent (↑ACTH)
– Pituitary (Cushing’s Disease)
• Microadenomas (95%)
• Macroadenomas (5%)
– Ectopic ACTH or CRH
• Small cell lung ca
• Carcinoids: lung, pancreas,
thymus
• ACTH-independent (↓ACTH due to
negative feedback)
– (Factitious): iatrogenik
– Unilateral
• Adrenal adenoma (10%)
• Adrenal carcinoma (5%)
– Bilateral
• Macronodular Hyperplasia
(AIMAH) (<2%)

• Primary pigmented Micronodular

Adrenal disease (PPNAD) (<2%)

• McCune Albright
Syndrome (<2%)

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SIGNS & SYMPTOMS

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©Bimbel UKDI MANTAP
PEMERIKSAAN
PENUNJANG

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 ADDISON’S
DISEASE
Addison disease is adrenocortical
insufficiency due to the
destruction or dysfunction of the
entire adrenal cortex.

It affects both glucocorticoid and

mineralocorticoid function.

The onset of disease usually occurs

when 90% or more of both adrenal
cortices are dysfunctional or
destroyed.

Idiopathic autoimmune Addison disease tends to be more common

in females and children.

The most common age in adults is 30-50 years, but the disease
could present earlier in patients with: polyglandular autoimmune
syndromes, congenital adrenal hyperplasia (CAH), or if onset is due to a
disorder of long-chain fatty acid metabolism.
©Bimbel UKDI MANTAP
©Bimbel UKDI MANTAP
Pemeriksaan Penunjang
Rapid ACTH stimulation test/Cosyntropin test

(1) an increase in the baseline

cortisol value of 7 mcg/dL or
more
(2) the value must rise to 20
mcg/dL or more in 30 or 60
minutes, establishing normal
adrenal
glucocorticoid function.

In patients with Addison disease,

both cortisol and aldosterone
show MINIMAL or NO CHANGE in
response to ACTH.

©Bimbel UKDI MANTAP

ADRENAL
CRISIS Sudden, severe worsening of adrenal
insufficiency symptoms is called
adrenal crisis. If the person has
Addison’s disease, this worsening can
also be called an Addisonian crisis.

SIGNS AND SYMPTOMS :

1. Fatigue, lack of energy, weight loss
2. Low blood pressure, postural
dizziness and hypotension
(≥20 mmHg drop in BP from
supine
to standing position), dizziness,
collapse, in severe cases
hypovolaemic shock
3. Abdominal pain, tenderness and
guarding, nausea, vomiting (in
particular in primary adrenal
insufficiency), history of weight loss
4. Fever
5. Confusion, somnolence, in severe
cases delirium or coma
©Bimbel UKDI MANTAP
LABORATORY STUDIES
•Serum chemistry: Abnormalities are present in
as many as 56% of patients. Hyponatremia is
common (although not diagnostic);
hyperkalemia, metabolic acidosis, and
hypoglycemia also may be present. However, the
absence of laboratory abnormalities does not
exclude the diagnosis of adrenal crisis.

•Serum cortisol: Less than 20 mcg/dL in severe

stress or after ACTH stimulation is indicative of
adrenal insufficiency.

•ACTH test (diagnostic): Determine baseline

serum cortisol, then administer ACTH 250 mcg
intravenous push (IVP), and then draw serum
cortisol 30 and 60 minutes after ACTH
administration. An increase of less than 9 mcg/dL Diagnostic measures should
is considered diagnostic of adrenal insufficiency. never delay prompt treatment of
a suspected adrenal crisis! There
•CBC: Anemia (mild and nonspecific), are no adverse consequences of initiating life-saving
lymphocytosis, and eosinophilia (highly hydrocortisone treatment and diagnosis can be safely
and formally established once the patient has
suggestive) may be present. clinically recovered
©Bimbel UKDI MANTA
P
MANAGEMENT :
1. Administer hydrocortisone: Immediate bolus injection of 100 mg
hydrocortisone intravenously or intramuscularly followed by continuous
intravenous infusion of 200 mg hydrocortisone per 24 hours (alternatively,
50 mg hydrocortisone per intravenous or intramuscular injection every 6 h)

2. Rehydrate with rapid intravenous infusion of 1000 mL of isotonic saline

infusion within the first hour, followed by further intravenous rehydration as
required (usually 4-6 L in 24 h; monitor for fluid overload in case of renal
impairment and in elderly patients)

3. Contact an endocrinologist for urgent review of the patient, advice on further

tapering of hydrocortisone, and investigation of the underlying cause of the
disease, including the diagnosis of primary versus secondary adrenal
insufficiency

3. Tapering of hydrocortisone can be started after clinical recovery guided by an

endocrinologist; in patients with primary adrenal insufficiency, mineralocorticoid
replacement must be initiated (starting dose 100 μg fludrocortisone once daily)
as soon as the daily glucocorticoid dose is below 50 mg of hydrocortisone
every 24 hours
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DISEASES OF THE ADRENAL
MEDULLA
The adrenal medulla is
developmentally, functionally,
and structurally distinct from
the adrenal cortex. It is
composed of specialized
neural crest (neuroendocrine)
cells, termed chromaffin cells,
and their supporting
(sustentacular) cells. The
adrenal medulla is the major
source of catecholamines
(epinephrine, norepinephrine)
in the body.
©Bimbel UKDI MANTAP
 PHEOCHROMOCYTOMA
Pheochromocytomas are
neoplasms composed
of chromaffin cells,
which synthesize and
release catecholamines
and in some instances
peptide
hormones. It is important to
recognize these tumors
because they are a rare
cause of surgically
correctable hypertension.
©Bimbel UKDI MANTAP
The classic history of a patient
with a pheochromocytoma
includes spells characterized
by headaches, palpitations,
and diaphoresis in association
with severe hypertension.
These 4 characteristics
together are strongly
suggestive of a
pheochromocytoma. In the
absence of these 3 symptoms
and hypertension, the
diagnosis may be excluded.