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Early Path Medical Consultation Services Pathology Services Working for Safer Pregnancies Placental Pathology
- Medical Student Lecture 2001 CONTENTS
The embryonic period is the time in which the cells the embryo newly makes are primarily organized into the specific organ systems of the human. By 8 weeks, the major internal organs (except for genital tracts) should all be in their proper positions, and in their adult form. However, functional maturation is not achieved until weeks, months (or years!) later. By 9-12 weeks, the head is about one half the crown-rump length ('sitting height') of the fetus. By the end of 12 weeks, the crown rump length will double from its measurement at 9 weeks. Growth of the head slows down, but the head is still disproportionately large compared to the rest of the body. By the end of the 12th week, primary centers of ossification have appeared in the skull and long bones. External genitalia of males and females appear similar until the end of the 9th week, and their mature external form is not established until the 12th week. Between 13 and 16 weeks, growth remains rapid. Limb movements, first detectable by ultrasound at 8 weeks, become coordinated, but remain too weak to be felt by the mother. Between 17 and 20 weeks, growth rate begins to slow, but the crown rump length still increases by 50 mm during these 3 weeks. Fetal movements ("quickening") are generally first felt during this period. After 24 weeks, a baby can survive (with some reservations) outside the mother's body, but is still very immature. For example, eyelids are normally fused until week 26. Growth curves vary with ethnicity, and altitude, as well as the risk factors (smoking, poor maternal nutrition and multiple gestation) cited. The plateauing of fetal growth likely reflects the effects of the change in fetal- placental weight ratio. By term, 6.5-7 grams of baby are supported by each gram of placenta, while at 26 weeks, the ratio is closer to 3:1. While placenta functional efficiency increases in the third trimester, there is likely a limit to fetal growth imposed by the placenta. Fetal growth restriction is generally not considered normal, but it is often very difficult to sort out a baby whose small size reflects its accurate "genetic potential" from a baby whose growth has been constrained by its environment. Reduced growth can be thought of as a way for the fetus to conserve its nutrients in the face of scarcity. This is therefore a way for the fetus to "compensate" for problems in its environment. If protracted and severe, nutrient deprivation may end in fetal de-compensation, fetal distress and even fetal death. That any timing of onset of growth restriction can be tied to a particular pattern of growth measures has been called into question, and probably the use of patterns of growth restriction to time onset of fetal compensation should be applied with caution, and on a case by case basis. Abnormal increased fetal growth is most commonly a reflection of maternal "overnutrition", or abnormal glucose homeostasis (including gestational diabetes). Recently, an increased appreciation of a role for non-diabetic insulin resistance in obstetric complications has developed, extending from ovarian dysfunction to unexplained prematurity.
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