kp hipertensi sekunder
DESCRIPTION
hipertensiTRANSCRIPT
-
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