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33 Cards in this Set
- Front
- Back
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What are villous cells, extravillous cells ?
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Villous cells contain STB and CTB and these cells do the exchange.
Extravillous are the cells present below the villous cells |
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What is vascular remodeling of the placenta ?
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In normal placentation, some of the extravillous trophoblast actually invades the endometrial blood vessel, replacing both the muscular wall and the endothelium
Increases diameter of vessels Converts to rigid tube INCAPABLE OF CONSTRICTING in response to maternal blood pressure modulations |
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How does the placenta develop ?
Should be question number 1 |
The placenta begins to develop upon implantation of the blastocyst into the maternal endometrium. The outer layer of the blastocyst becomes the trophoblast which forms the outer layer of the placenta. This outer layer is divided into two further layers; the underlying cytotrophoblast layer and the overlying syncytiotrophoblast layer. The syncytiotrophoblast is a multinucleate continuous cell layer which covers the surface of the placenta. It forms as a result of differentiation and fusion of the underlying cytotrophoblast cells, a process which continues throughout placental development. The syncytiotrophoblast (otherwise known as syncytium), thereby contributes to the barrier function of the placenta.
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Failure of what mechanisms cause pathology in the placenta ?
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Characteristics of trophoblasts associated with malignancy such as ability to invade, disseminate to distant sites and facilitate tolerance by host immune system
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Abnormal Placental Implantation
Too much trophoblast invasion ? |
Placenta accreta
Placenta increta Placenta percreta |
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Inadequate trophoblast invasion
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Toxemia (Preeclampsia)
Others |
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Placenta Accreta
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1.Failure of normal decidua to form
2.Results in failure to halt invasion of trophoblast at the normal point 3.In the absence of adequate decidualized endometrium, villi are implanted right on the myometrium without underlying decidua |
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Consequences of Accreta
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Placenta fails to separate or is incompletely delivered
May cause life-threatening hemorrhage May or may not require hysterectomy Curettage or embolization are alternative treatments Small, focal accretas may be retained in the uterus as “placental polyps” |
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Placenta Increta
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Similar failure of decidua formation and failure to block trophoblastic invasion
Deeper invasion; villous tissue actually invades into the myometrium. Hysterectomy required to remove tissue and control hemorrhage |
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Placenta Percreta
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Villous tissue penetrates the entire uterine wall
May cause uterine rupture May cause hematuria due to invasion of bladder Requires hysterectomy |
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Toxemia of pregnancy
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Occurs in ~6% of pregnancies
More common in first pregnancies, very young mothers, multiple pregnancies, molar pregnancies Clinical features : Increased blood pressure in pregnancy Proteinuria Edema Usually begins in third trimester, but onset may be earlier in patients with molar pregnancy or preexisting hypertension or kidney disease |
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Mother presents with increased blood pressure, protein in the urine and peripheral edema. What is the underlying phenomenon and what is its etiology ?
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Toxemia - abnormality of placental implantation (defective trophoblastic invasion)
Implantation is too shallow Invasion and replacement of vessels is incomplete or absent Results in reduced blood flow in placenta This decreased placental perfusion is thought to lead to increased vasoconstrictive mediators and inhibition of vasodilatory stimuli, which in turn elevate maternal blood pressure Decreased placental production of prostaglandins, which are required to reduce sensitivity of pregnant women to angiotensin |
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What changes are seen in the placenta during toxemia ?
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Decidual vasculopathy
Infarcts Abruption (sudden separation with retroplacental hemorrhage) Villous maldevelopment Decreased growth of placenta |
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Now mom starts developing infarcts of the liver, has kidney failure and has lost her speech. What are you worried about ?
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Ecclampsia with DIC
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What is decidual vasculopathy?
What does it result in ? |
Lack of physiologic conversion of vessels (failure of invasion and replacement of vascular components by trophoblast
Thrombosis Atherosis Fibrinoid necrosis These changes occur ONLY in the decidual vessels. Maternal circulation is not involved |
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In the PPT, what are the atherosis, and fibrinoid necrosis ?
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Ask someone
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Risk of clinical consequences of toxemia ?
Risk to mother? Cure ? |
IUGR
Placental abruption Potential fetal demise Eclampsia Cerebral hemorrhage DIC Seizures (HELLP syndrome (Hemolysis, Elevated Liver Enzymes, Low Platelets) Premature delivery |
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What are the types of Gestational trophoblastic diseases ?
-a heterogeneous group of diseases occurring after a fertilization event and characterized by an abnormal proliferation of trophoblast. |
Abnormal gestations, with potential for aggressive behavior and malignant transformation
Hydatidiform Mole Complete (CHM) Partial (PMH) Invasive Malignant Neoplasms Choriocarcinoma |
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Moles - abnormal gestations, not neoplasms. What is their etiology ?
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Maternal genes are necessary for embryonal development
Paternal genes are necessary for placental development So moles are gestations in which there is an abnormal fertilizations with an excess of paternal genes |
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Presenting symptoms include
rapidly enlarging uterus, vomiting, hypertension, hyperthyroidism, extreme elevation of beta-hCG, “snowstorm” on ultrasound |
Complete hydatiform Mole
Most common type of mole Presenting symptoms include rapidly enlarging uterus, vomiting, hypertension, hyperthyroidism, extreme elevation of beta-hCG, “snowstorm” on ultrasound |
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Gross findings in CHM ?
Microscopic findings ? |
Abundant tissue
Grossly identifiable, grape-like “vesicles”, up to 2 cm in diameter = hydropic villi Diffusely hydropic villi Central “cisterns”= acellular spaces Trophoblastic hyperplasia and severe atypia Circumferential (as opposed to polar) No embryo/fetus (usually) |
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What is the genetic composition of a CHM ?
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90%: homozygous 46 XX
result from: endoreduplication of a single haploid sperm 10%: heterozygous, predominantly 46 XY result from: dispermic fertilization |
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What is the clinical behavior of a CHM ?
What is the chance of a repeat mole ? Prognosis Treatment ? |
10-30% of patients will develop persistent disease
Residual tissue in uterus Invasive mole (10%) Malignant transformation (2-3%): choriocarcinoma Increased risk for repeat mole Prognosis is excellent Treatment Follow beta-hCG levels to normal 6 months to a year of contraception If beta-hCG rises, treat with chemo |
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Partial hydatiform mole
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Less common than CHM
Risk factors are similar to CHM, BUT ****MATERNAL AGE***** does not seem to have an influence Presenting symptoms include: spontaneous or missed abortion, without abnormally accelerated increase in uterine size or beta-hCG level |
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Gross findings
Microscopic findings ? |
Not as much tissue as a CHM
Normal and hydropic appearing villi May have recognizable embryo/fetus Two kinds of villi Fairly normal villi Hydropic villi Scalloped borders Trophoblastic “pseudoinclusions” (tangential cuts) Some cisterns, usually scarce ***Less trophoblastic proliferation than CHM**** |
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Genetic composition of PHM ?
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Abnormal fertilization of a normal egg by two sperm or a diploid sperm (diandric triploidy)
70% are 69 XXY 27% are 69 XXX 3% are 69 XYY Digynic triploidy is only 15-20% of triploidy cases and is NOT molar -causes triploid fetus that aborts |
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Clinical Behavior of PHM ?
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4-11% of patients will develop persistent disease
Rarely invasive Very rarely (probably never) malignant transformation Prognosis is extremely good Treatment is the same as CHM |
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Complete vs Partial Mole ?
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Histologic and clinical features
P57 immunohistochemistry is useful A paternally imprinted gene, expressed only if maternal gene is present Absent in CHM, which have only paternal genes Ploidy analysis, other genetic studies |
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Invasive Mole
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Rare
Molar villous tissue invades myometrium, blood vessels (somewhat analogous to placenta increta) Can perforate uterus Can embolize, but not true metastases Usually detected after prior diagnosis of mole by rising beta-hCG treated with chemotherapy (like CCA), without acquiring tissue |
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Choriocarcinoma
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Rare (1/ 20,000-30,000)
Usually presents within months of a known gestation, but can be years later Usually follows a molar gestation (50%), but can follow any type of normal or abnormal gestation, including ectopic (rarely) Usually is derived from the most recent gestation, but occasionally normal pregnancies have intervened (!!!) Derived from villous trophoblast NOT THE SAME AS GERM CELL TUMOR (e.g., testes or ovary) WITH SAME MORPHOLOGY |
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Gross Findings
Microscopic findings |
Variable size
Very friable (crumbly), hemorrhagic, necrotic Infiltrating borders Solid sheets of cytotrophoblast admixed with syncytiotrophoblast infiltrate myometrium Extensive vascular invasion (the cause of the hemorrhagic appearance) |
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Clinical Features
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Presenting symptoms include abnormal uterine bleeding, hemorrhage from metastases
Common sites of mets include lung, vagina, brain, liver, kidney Overall prognosis is very good, with >90% remission with current chemo regimen (unlike non-gestational CCA) |
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Conclusion
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Gestational Trophoblastic Disease and other disorders of trophoblast are
In many ways unique among human afflictions Fascinating in the extreme! Still incompletely understood, but under active investigation Better understanding of trophoblast function and dysfunction will be the key to advancing maternofetal medicine |
