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