Book of Medical Disorders in Pregnancy - Tintash
Book of Medical Disorders in Pregnancy - Tintash
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