3.2.4.2Hipertensi sekunder
Syaiful Azmi
1. Hypertension in pregnancy
H P
morbidity and mortality
10% with complication
15 % maternal mortality
Prevalence 5-8%
Indonesia 2,1%
Perubahan hemodinamik
Trimester I
Tekanan darah sama dengan sebelum hamil
Trimester II
Tekanan darah 10mmHg
Vasodilatasi pembuluh darah
Trimester III
Tekanan darah
Volume plasma dan cairan ektra sel
CLassification of HP (NHBPEP 2000)
BP 140/90 mmHg first time during pregnancy
No proteinuria
BP return normal < 12 weeks post partum
Final diagnosis made only post partum
1. Gestational Hypertension
2. Chronic Hypertension BP 140/90 mmHg before pregnancy or < 20
weeks gestation
BP persistence after 12 weeks post partum
3. Preeclampsia
BP 140/90 mmHg
Proteinuria 300 mg/24 hours
4. Eclampsia
PE with seizures that cannot other causes
5. Superimposed PE (On chronic Hypertension )
BP 140/90 mmHg < 20 weeks gestation with
Proteinuria > 300 mg/24 hours before 20 weeks gestation
Or
Sudden increase BP
Platelet count
HIPERTENSI KHRONIK
Sering tidak terdeteksi pada awalkehamilan
Menetap setelah melahirkan
Obat hipertensi sebelum hamilditukar apabila kontra indikasi dengan kehamilan
Terapi
1 Modifikasi gaya hidup
Istirahat / exercise dibatasi
Penurunan BB tidak dianjurkan
Batasi garam
Kendalikan faktor risiko hipertensi
Terapi2. Obat
Methyldopa
Anti hipertensi yang bekerja sentral
Lini pertama
Tidak mengganggu hemodinamik janin
CCB (Nifedipin), Hidralazin, Labetalol
Lini kedua
Slow release (Nifedipin)
Diuretik tidak dianjurkan
ACE I dan ARB kontra indikasi
OAH dimulai bila TD 150/100 mmHg
Penurunan TD hati-hati dan pelan pelan
Target TD < 140/90 mmHg
2. HIPERTENSI PADA PENYAKIT GINJAL
a. Hipertensi pada Glomerulonephritis
b. Hipertensi pada Penyakit Ginjal Kronik
Patogenesis
Yg paling berperan adalah RAAS
Angiotensinogen
Angiotensin I
Angiotensin II
Ellis ML, et al. Pharmacotherapy 1996;16:849-860;
Carey RM, et al. Hypertension 2000;35:155-163
AT1 AT2 Vasoconstriction
Aldosterone secretion
Catecholamine release
Proliferation
Hypertrophy
Vasodilation
Inhibition of cell growth
Cell differentiation
Injury response
Apoptosis
BP
(-)
Renin-angiotensin-aldosterone system
Renin
Angiotensin-
converting
enzyme
Bradykinin
Inactive kinins
BP, blood pressure
Pengobatan
ACE-I / ARB (=Compelling Indication)
Inhibition of the RAAS by ACE inhibitors
Angiotensinogen
Angiotensin I
Angiotensin II
Bradykinin
Inactive kinins
AT1 AT2 Vasoconstriction
Aldosterone secretion
Catecholamine release
Proliferation
Hypertrophy
Vasodilation
Inhibition of cell growth
Cell differentiation
Injury response
Apoptosis
BP
(-)
Non-
reninNon-
ACE
Renin
Angiotensin-
converting
enzyme
ACE
inhibitor
Ellis ML, et al. Pharmacotherapy 1996;16:849-860;
Carey RM, et al. Hypertension 2000;35:155-163
RAAS, renin-angiotensin-aldosterone system; ACE, angiotensin-converting enzyme; BP, blood pressure
Inhibition of the RAAS by ARBs
ARB
Angiotensinogen
Angiotensin I
Angiotensin II
AT1 AT2
Renin
BP
Bradykinin
Inactive kinins
Angiotensin-
converting
enzyme
Ellis ML et al. Pharmacotherapy 1996;16:849-860;
Carey RM et al. Hypertension 2000;35:155-163;
Mizuno M et al. Eur J Pharmacol 1995;285:181-188
RAAS, renin-angiotensin-aldosterone system; ARB, angiotensin II receptor blocker; BP, blood pressure
2. FEOKROMOSITOMA
- Tumor kelenjer adrenal- 90% jinak
- Hipertensi karena peningkatan ketokolamin
Gejala
Trias : Takikardi
Berdebar-debar
Berkeringat
Pemeriksaan fisis
Teraba masa tumor di abd
Terapi
Operasi
bloker
3. HIPERTENSI RENOVASKULER
Menurun aliran darah ke ginjal yang disebabkan karena kerusakan pada a renalis
Etiologi : - stenosis a renalis
- arteritis a renalis
PatogenesisIskemi Ginjal
Renin me
Angiotensin I
Angitensin II me
Vasokonstriksi resistensi
Gejala Klinis
Onset < 30 tahun
RPK
Hipertensi sukar dikendalikan
Atropi ginjal yang iskemi
Hipokalemia
Pem. penunjang
USG
Angiografi
TerapiOperasi