This document discusses hypertensive disorders of pregnancy including gestational hypertension, pre-eclampsia, and eclampsia. It defines each condition and lists risk factors such as primigravidity, family history, and placental abnormalities. The pathophysiology involves endothelial dysfunction and vasospasm. Diagnosis is based on blood pressure, proteinuria, and other organ involvement. Management involves monitoring, controlling blood pressure, and timely delivery to prevent maternal and fetal complications.

2.  Gestational HTN,
 Pre-eclampsia
 Eclampsia
 Chronic HTN
 Pre-eclampsia,eclampsia superimposed on
chronic HTN

3.  Def: BP>140/90mmHg ,proteinuria after 20
wks of pregnancy in a normotensive,non-
proteinuric women
 PIH-1) Gest.HTN
2)Pre-eclampsia
3)Eclampsia
 Incidence-5-15%

4.  Primigravida
 Family history
 Placental abnormality-poor placentation,
hyperplacentosis
placental ischaemia
molar pregnancy
 genetic
 Immunological
 New paternity
 Vascular,renal disease
 thrombophilias

5.  BP>140/90
 MAP- 20mmHg over previous reading or
MAP>105mmH
 How to record BP?
 Proteinuria-24 hr urine>.3gm or> than
1gm/L in 2 random samples 4 hrs apart
 edema

7.  Endothelial dysfunction
 Intense vasospasm
 In normal pregnancy-increase prostacyclin a
vasodilator PG produced by vascular endothelium
and relative decrease in thromboxane a
vasoconstrictor and platelet aggregator produced
by platelets
 In pre –eclampsia imbalance between the two
 So in pre-eclampsia-vasospasm,platelet
activation ,activation of coagulation system

10.  In normal pregnancy –spiral arteries of
placenta invaded by cytotrophoblast in 1
trimester ,a second wave of cytotrophoblastic
invasion transforms myometrial segments of
spiral arteries into wide mouthed vessels
unresponsive to vasomotor stimuli in 2
trimester .Former is deficient and later is
absent in pre-eclampsia.
 Reduces ut placental flow causes IUGR

11.  Placenta
 Kidney-glomerular ,tubular
dysfunction,proteinuria,decrease GFR ,creatinine
clearance,ARF due to ATN (reversible)rarely
ACN(irreversible). Increase BUL,sr.creat. sr.uric
acid
 Liver-periportal thrombosis,fibrin
deposition,haemorrhages,necrosis,subcapsular
haematoma,HELLPsyndrome
 Heart
 Eyes-haemorrhages,pappiloedema,retinal
detachment.

12.  MILD-DBP<110mmHg..
 SEVERE-DBP >
 110mmHg or more 4 hrs apart
 Proteinuria>5gm in 24
 Headache ,visual disturbances,epigastric pain.
 Oliguria or urine O/P<400ml in 24 hrs
 Platelet count<1 lakh
 Increase liver enzyme
IUGR ,pul.edema
 IMPENDING or IMMINENT ECLAMPSIA.

13.  Symptoms-pedal edema,
increases to face ,abd wall,vulva
,anasarca.Alarming symptoms –
headache,disturbed sleep,diminished urine
output,epigastric pain ,blurring of
vision,complete blindness
 Signs -abnormal wt gain
,BP,oedema,pul.edema, IUGR
Oligohydramnios.

15. URINE
FUNDOSCOPY
RFT
LFT
PLATELET COUNT
TOTAL COUNT ,Haematocrit,Peripheral
smear,APTT,PT,LDH.
USG ,COLOUR DOPPLER.

16.  Maternal-eclampsia,cerebral haemorrhage
corticalblindness,pul.oedema,ARDS,HELLP,DIC
,renal failure ,hepatic rupture,abruptio
placenta,postpartum collapse
 Fetal-prematurity,IUGR,IUD.

20.  MAP
 ROLL OVER TEST
 Angiotensin sensitivity test
 Uterine artery doppler
 Raised sr B hCG at 14 to 20 wks,sr.uric
acid,sr.inhibin A level at 14 wks.
 Cold pressor test,isometric contraction test.

PREVENTION:Low dose aspirin,anti
oxidants,folic acid,high dose calcium.

21. Rest
Diet
Sedatives
Diuretics
Anti hypertensive
MONITOR PROGRESS CHART
BP controlled no PET symptoms continue pregnancy till
37 wks then deliver.
If BPpersistently high no signs of PET-If preg beyond
37 wks terminate ,If less expectant mgt till 37 wks
If B P high ,PET persists termination irrespective of
gestation,steroids may be given for lung maturity.

22.  Induction of labour
 LSCS-urgent delivery reqd but Cx
unfavourable,obst.indications,fetal distress
IUGR,failed induction.
 MONITORING LABOUR-
 Conduct of delivery-
 Post partum care
 PROGNOSIS –maternal ,fetal.