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Glossary of Terms Frequently Asked Questions How to arrange a consultation What is Perinatal Pathology?

 

Acute Inflammation

Cardiovascular Risk Factors

Chronic Inflammation

Coagulation Related Pathology

Introduction to IVF

Perinatal Pathology

Recurrent Obstetric Compromise

Uteroplacental Vascular Pathology

Uteroplacental Vascular Pathology Case Reports

Coagulation Related Pathology

Coagulation is a principal defense mechanism of organisms against invading microorganisms. It plays a central role in both the damage and repair stages of tissue or cell injury or death. Coagulopathy has been implicated in the pathogenesis of certain types of obstetric compromise, including antiphospholipid antibody-related death and preeclampsia. The potential targets for pathologic coagulation include the maternal vasculature, the basal plate, the intervillous space, the villous (syncytiotrophoblast) surface and the fetoplacental vascualture.

The deposition of a fibrinoid layer at the maternal-placental interface is a standard process of normal pregnancy. This layer of Nitabuch's fibrin is progressively laid down throughout gestation, leading to, at term, a smooth plane of cleavage for the delivery of the placenta. Fibrin/fibrinoid deposition in the basal plate has been proposed to be a by-product of maternal-placental immunologic interactions; increased basal plate coagulation has been identified in cases of pregnancy compromise believed to be of immunologic origin. Increased basal coagulation results in a thick band of basal plate fibrin/fibrinoid replacing the normal zone of extravillous cytotrophoblasts and may even extend to involve several layers of entrapped and necrotic basal villi. Chronic anchoring villitis can often be seen in the "surviving" villi, perched atop the pile of necrotic and fibrinoid material. As in the extraplacental membranes, this material may contribute to the "immune barrier," but may not be the barrier to maternal lymphocytes it appears to be at the extraplacental choriodecidual interface.

The uterine vascualture is particularly susceptible to thrombosis (because its endothelium is normally eroded and the basement membranes and decidual stromal collagen are normally exposed to circulating maternal platelets) for up to 24 weeks.

Coagulation Related Case Reports (coming soon)

 


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