1. Ectopic Pregnancy and Gestational Trophoblastic Disease (GTD)
Mark A. Fischione, M.D.
Reproduction Module
Arizona School of Dentistry and Oral Health

2. Objectives Understand the pathogenesis of ectopic pregnancies.
Know the pathology and clinical of ectopic pregnancies.
Identify the complications of ectopic pregnancies
Understand the pathogenesis of Gestational Trophoblastic Disease.
Distinguish between an incomplete vs. a complete hydatidiform mole
Illustrate the gross pathology of molar pregnancies
Determine the clinical features of molar pregnancies
Define association between choriocarcinoma and GTD's.
Summarize the clinical behavior, pathology and complications of Choriocarcinomas

3. Ectopic Pregnancy
Implantation of the fetus in any other site than the normal uterine location, most common places are the ovary, abdominal cavity, and the fallopian tubes (95%).
One in every 150 pregnancies.
The most common pathologic condition leading to ectopics is chronic salpingitis. Other factors include peritubal adhesions as from endo-metriosis, previous surgeries, and leiomyomas.

4. Sites of Ectopic Pregnancies

5. Ectopic Pregnancy
The intratubal adhesions forms a barrier to normal passage of the zygote, so it implants at the site of obstruction.
The entire fertile zygote undergoes its normal development with the formation of placental tissue, and amniotic sac. The placenta is poorly attached to the wall of the tube, weakens it with the possibility of rupture and intraperitoneal hemorrhage. (the usual fate, 2-6 wks after pregnancy).

6. Ectopic Pregnancy Inside Open F. Tube

7. Ectopic Pregnancy with Dilated Fallopian Tube

8. Ectopic Pregnancy with Twin Pregnancy

9. Ectopic Pregnancy
Clinically, there is onset of severe abdominal pain with rupture and the possibility of shock, with signs and symptoms of an acute abdomen.
Pregnancy tests are positive.
Aspiration of fresh blood from the pouch of Douglas (posterior fornix) denotes rupture.
An endometrial biopsy is helpful in diagnosis.

10. Ectopic Pregnancy
The absence of chorionic villi is consistent with an ectopic pregnancy, because the villi are in the tube.
All the biopsy will show is a decidual reaction of the endometrium.
U/S will show dilation of the fallopian tube.
Rupture is a medical emergency since 1 in 400 of these patients dies before hemorrhage can be controlled.

11. Ectopic Pregnancy with Chorionic Villi and Decidua

12. Ectopic Tubal Pregnancy with Chorionic Villi and Hemorrhage

13. Transvaginal Ultrasound Ectopic Pregnancy in Dilated Tube

14. Gestational Trophoblastic Disease
GTD is a disease that involves the trophoblastic epithelium and includes a spectrum of proliferative lesions, from the benign Incomplete and Complete Hydatidiform Mole, with limited and full proliferation of the trophoblast, respectively, to the highly malignant Choriocarcinoma.

15. Hydatidiform Mole
A placental abnormality marked by trophoblastic proliferation and hydropic degeneration of the chorionic villi.
The most common form is the complete mole, where the fetus cannot be identified in the amniotic sac. Results from abnormal fertilization, where all of the chromosomes are paternal in origin due to a loss of maternal chromosomes from the zygote at the time of fertilization.

16. Complete Hydatidiform Mole
The paternal 23,X set of chromosomes reduplicates, bringing the number of chromosomes to 46. This process is called Androgenesis.
Without the maternal chromosomes, the embryo cannot develop, and the placenta undergoes hydropic degeneration.

17. Complete Hydatidiform Mole

18. Complete Hydatidiform Mole

19. Swollen Hydropic Villi

20. Complete Hydatidiform Mole

21. Molar Pregnancy with Trophoblast

22. Incomplete Hydatidiform Mole
Evolve from oocytes fertilized with two spermatozoa, therefore, the cells have 69 chromosomes, one set from the mother, and two sets from the father. This combination is also lethal, but the embryo does not die immediately, so parts of the embryo are found encased among the hydropically altered placental villi and normal placental tissue.

23. Incomplete Hydatidiform Mole with Scattered Grape-Like Villi

24. Incomplete Hydatidiform Mole

25. Incomplete Hydatidiform Mole with Scattered Normal and Swollen Villi

26. Hydatidiform Moles in General
In the U.S., H. moles are rare, about 1 in 2000 pregnancies.
The diagnosis is based on an enlarged uterus for the corresponding, calculated duration of the pregnancy, without any signs of fetal movement.
U/S is the best method for early detection (Snowstorm pattern) with no fetal heartbeat or movement.

27. Snowstorm Pattern of Hydatidiform Mole on U/S

28. Hydatidiform Mole
High serum and urine levels of hCG are also typically found. They are aborted spontaneously in mid-pregnancy. It is important to remove all parts of the abnormal placenta because the remaining trophoblastic cells could give rise to malignant tumors (Chorio). Grossly, the placenta is transformed into numerous grape-like clear vesicles that are filled with fluid and covered with hyperplastic trophoblastic epithelium.

29. Choriocarcinoma
A malignant tumors composed of trophoblstic cells. In 50% of cases it arises from a preexisting complete mole. In 25% , it arises from placental tissue retained after abortion, and in the last 25%, it arises from normal placenta after completion of a normal pregnancy.
Highly invasive tumors and secrete hCG which is a good marker for the disease and monitors tumor recurrence after chemotherapy.

30. Choriocarcinoma
Forms bulky hemorrhagic nodules in the placental bed that invades through the wall of the uterus and often implants in the vagina.
By invading veins, it metastasizes to the lung, liver, and the brain.
The tumor responds well to chemo with Methotrexate, and cure rates of % have been achieved, but only in those patients who do not have metastases.

31. Solid and Cystic Choriocarcinoma in Uterus with Extension into Pelvis-CT

32. Choriocarcinoma in Fundus of Uterus*

33. Choriocarcinoma

34. Choriocarcinoma

35. Choriocarcinoma

37. Property of M.A. Fischione, M.D.
The End
Property of M.A. Fischione, M.D.