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Book of Medical Disorders in Pregnancy - Tintash

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cern<strong>in</strong>g the disturbance <strong>in</strong> the Ren<strong>in</strong><br />

angio tens<strong>in</strong>g II aldosterone disruption<br />

by coupl<strong>in</strong>g it with his own theory <strong>of</strong> the<br />

role <strong>of</strong> prostagland<strong>in</strong>s. His theory postulates<br />

that an imbalance is found between<br />

the systemic vasodilatory mechanisms<br />

and the effect <strong>of</strong> Ren<strong>in</strong> and Angiotens<strong>in</strong><br />

II which produces vasoconstrictive<br />

effect.<br />

Plasma ren<strong>in</strong> levels are higher <strong>in</strong><br />

pregnant normotensive women than <strong>in</strong><br />

non pregnant normotensive women although<br />

there is some overlap <strong>in</strong> values.<br />

Angiotens<strong>in</strong>ogen levels are markedly<br />

elevated <strong>in</strong> pregnancy probably <strong>in</strong><br />

response to estrogen.<br />

The entire Ren<strong>in</strong> angiotens<strong>in</strong> aldosterone<br />

mechanism is <strong>in</strong>creased but the reason<br />

for this is not clear. It may be that the<br />

system is <strong>in</strong>creased to produce the<br />

required <strong>in</strong>crease <strong>in</strong> blood volume<br />

associated with <strong>in</strong>creased vascular<br />

capacity <strong>in</strong> pregnancy. As such the<br />

elevated aldosterone levels are not a<br />

cause <strong>of</strong> excessive sodium retention but<br />

may represent a compensatory response.<br />

The usual physiological changes<br />

affect<strong>in</strong>g renal ren<strong>in</strong>s do not affect<br />

uter<strong>in</strong>e ren<strong>in</strong>. The uter<strong>in</strong>e ren<strong>in</strong> is<br />

probably manufactured mostly <strong>in</strong> the<br />

chorion.<br />

Chronic Uter<strong>in</strong>e ischemia results <strong>in</strong><br />

hypertensive hypernatremic pro-te<strong>in</strong>uric<br />

dogs (Hodari 1976), toxemia was<br />

associated with a 40 to 60% re-duction<br />

<strong>of</strong> blood flow <strong>in</strong> the utero-placental unit.<br />

Gant (1974) has however demonstrated<br />

an <strong>in</strong>crease <strong>in</strong> Dehydro epiandrosterone<br />

Sulphate clearance early <strong>in</strong> the<br />

pregnancy <strong>of</strong> hypertensive patients,<br />

reduc<strong>in</strong>g to less than normal prior to the<br />

development <strong>of</strong> the cl<strong>in</strong>ically evident pre<br />

43<br />

eclamptic toxemia. This and other<br />

studies have suggested that there is a<br />

decl<strong>in</strong><strong>in</strong>g placental blood flow.<br />

Reduction <strong>in</strong> Uter<strong>in</strong>e blood flow results<br />

<strong>in</strong> outpour<strong>in</strong>g <strong>of</strong> ren<strong>in</strong> <strong>in</strong>to uter<strong>in</strong>e ve<strong>in</strong><br />

(<strong>in</strong> pregnant rabbits) •. Angiotens<strong>in</strong>-II<br />

<strong>in</strong>fusions acutely elevate B.P. <strong>in</strong> Rh<br />

monkeys and PgE2 <strong>in</strong> uter<strong>in</strong>e ve<strong>in</strong>s and<br />

this is associated with an <strong>in</strong>crease <strong>in</strong><br />

blood flow to the uterus. There seems to<br />

be a problem with autoregulation <strong>of</strong><br />

blood flow which produces such systemic<br />

effects.<br />

Def<strong>in</strong>itions - The def<strong>in</strong>itions presented<br />

here are those adopted by the Adhuc<br />

Committee <strong>of</strong> the American College <strong>of</strong><br />

Obstetricians and Gynecologists.<br />

Gestational edema - This is def<strong>in</strong>ed as<br />

more than one plus <strong>of</strong> edema after 12<br />

hours <strong>of</strong> bed rest or weight ga<strong>in</strong> <strong>of</strong> 5<br />

pounds or more <strong>in</strong> one week.<br />

Gestational prote<strong>in</strong>uria - This is<br />

def<strong>in</strong>ed as prote<strong>in</strong>uria <strong>in</strong> pregnancy<br />

without evidence <strong>of</strong> hypertension, renal<br />

disease (vascular or <strong>in</strong>fective) or edema.<br />

Prote<strong>in</strong>uria: This is an important sign<br />

<strong>of</strong> pre-eclampsia. Prote<strong>in</strong>uria is usually<br />

def<strong>in</strong>ed as the presence <strong>of</strong> 500 mg or<br />

more <strong>of</strong> prote<strong>in</strong> found <strong>in</strong> 24 hour ur<strong>in</strong>e<br />

collection or a prote<strong>in</strong> measurement <strong>of</strong><br />

2+ or greater <strong>in</strong> a random ur<strong>in</strong>e specimen.<br />

It is important to note that the degree <strong>of</strong><br />

prote<strong>in</strong>uria may fluctuate widely over<br />

any 24 hours period even <strong>in</strong> severe<br />

cases. Random sampl<strong>in</strong>g is thereby some<br />

what less accurate.<br />

Pre eclampsia - This is def<strong>in</strong>ed as hypertension<br />

with prote<strong>in</strong>uria and/or edema

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