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q#19 - drtaher
#1
A 38-year-old woman is in her first pregnancy, which has been uneventful until the 34th week, when she
develops swelling of feet and hands. An obstetric check-up reveals that she also has
hypertension and proteinuria. Laboratory analysis shows elevated aspartate aminotransferase
(AST) and alanine aminotransferase (ALT) and slightly decreased platelets. The initial event in
the pathogenesis of her condition is thought to be which of the following?
A. Chorioamnionitis
B. Disseminated intravascular coagulation
C. Maternal hypertension
D. Maternal renal ischemia
E. Placental ischemia
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#2
EEEEEeee
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#3
eclampsia .. but maybe eee
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#4
bbbbbbbbbb
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#5
e...
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#6
C?
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#7
The correct answer is E. This patient's condition is a classic third trimester complication
referred to as toxemia of pregnancy, or preeclampsia. It occurs in 6% of all pregnancies but is
more frequent in primiparas. Although the pathogenesis is still unclear, the first event
appears to be placental ischemia, probably due to abnormalities in the trophoblast and
alterations in the maturation of placental vessels. The trophoblast of invading placental
vessels fails to acquire the characteristics of normal endothelial cells, with subsequent
alterations in blood flow. Placental ischemia then triggers the release of thromboplastic
substances, increases renin synthesis, and reduces prostaglandin E levels.
Chorioamnionitis (choice A) is an infection of chorioamnionic membranes due to bacteria that
ascend through the vaginal canal. This is an important cause of spontaneous abortion in the
second and third trimester, but it plays no role in the pathogenesis of toxemia of pregnancy.
The release of thromboplastic substances may cause disseminated intravascular coagulation (DIC)
(choice B).
Increased renin and reduced prostaglandin E mediate increased sensitivity to angiotensin,
leading to maternal hypertension (choice C).
Ischemic damage to maternal organs, including brain, liver, and kidneys (choice D), results
from thrombotic occlusion of arterioles and capillaries as a consequence of DIC.
Overall, the clinical picture of toxemia is due to DIC-mediated ischemic damage to brain
(changes in mental status and convulsions), liver (elevated liver enzymes), and kidneys
(proteinuria, leading to peripheral edema). A manifestation of toxemia is HELLP syndrome, which
stands for hemolysis, elevated liver enzymes, and low platelets.
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