Pathology Notes

Twin placenta and abnormal placentation Updated: 12/03/2018 © Jun Wang, MD, PhD Twin placenta May be monozygous Dichorionic, diamnionic : Mono or dizygotic; 2 placental plates separated or fused, NO vascular anastomoses; common membrane compose of layer of chorion between two amniotic membranes Monochorionic : Monozygotic; diamnionic (2 amniotic cavities) or monoamnionic (1 amniotic cavity), depending on timing of split; NO chorion between amniotic membrane in common membrane if presents; higher mortality due to premature labor Monoamniotic : Single amniotic cavity for both fetus; high perinatal mortality due to cord complications (twist, knot) Ectopic pregnancy Implantation outside of the uterine cavity Most common in the tubes Associated with pelvic inflammatory disease or peritubal adhesion Placenta previa Implantation in the lower uterine segment Occluding the internal os Associated with a history of D&C, Cesarean delivery and multiparity Placent

Gestational trophoblast diseases Updated: 12/03/2018 © Jun Wang, MD, PhD General feature Trophoblastic proliferation associated tumors and tumor-like lesions Poor prognostic indicators Pretreatment hCG > 40,000 Brain or liver metastases Gestational trophoblastic disease (GTD) after term gestation and failed therapy Recurrence/metastases diagnosed with serum hCG Risk factors Extremes of reproductive age, especially for complete mole History of prior mole, primigravid state Vitamin A-precursor deficiency Asian / African / Latin American origin: higher risk for complete mole White: higher risk for incomplete mole Marker Higher than normal serum hCG Classificiations Hydatidiform mole Complete Incomplete Choriocarcinoma Placental site nodule and placental site trophoblastic tumor Follow up Serum hCG Back to placenta pathology Back to female genital tract Back to contents

Placental site nodule and placental site trophoblastic tumor   Updated: 12/22/2021 © Jun Wang, MD, PhD Placental site nodule Composed of benign intermediate trophoblast cells Usually an incidental finding Remnant of implantation site that failed to involute May be identified many years after pregnancy May present with abnormal bleeding Placental site trophoblastic tumor Neoplastic transformation of implantation-site intermediate trophoblast Reproductive age women (occasionally age 50+) Present with amenorrhea or abnormal bleeding with enlarged uterus Persistently elevated serum hCG Diploid, express hCG and cytokeratin Back to placenta pathology Back to female genital tract Back to contents

Incomplete mole Updated: 12/04/2018 © Jun Wang, MD, PhD General features AKA partial mole Less common than complete mole Very low risk of choriocarcinoma ; invasive mole rare Key pathogenesis Abnormal gametogenesis and fertilization Clinical presentations Vaginal bleeding or a missed abortion Small-for-date uteri LESS marked hCG elevation Key Laboratory findings Less markedly elevated serum hCG Key morphological features Scattered small grape-like villi Mixture of edematous villi and relatively normal villi Less conspicuous central cistern formation Fetus presents Markers   hCG p53 Postive for p57 (expressed from maternal allele) Genetic abnormalities Triploid or tetraploid, some are trisomy 16 Most common: XYY Extra set of paternal chromosomes due to fertilization by two sperms or by a single diploid sperm Treatment Evacuation with curettage Back to female genital tract Back to contents

Preeclampsia and eclampsia Updated:05/10/2019 © Jun Wang, MD, PhD General feature Widespread vascular endothelial malfunction and vasospasm After 20 weeks' gestation Can present as late as 4-6 weeks post partum Preeclampsia Hypertension Proteinuria With or without pathologic edema Eclampsia New onset of grand mal seizure activity Unexplained coma during pregnancy or postpartum Background signs or symptoms of preeclampsia HELLP H emolysis E levated L iver enzymes L ow P latelets May have normal blood pressure Symptoms usually improve after delivery Risk factors Nulliparity Family history of preeclampsia, previous preeclampsia and eclampsia Poor outcome of previous pregnancy: intrauterine growth retardation, abruptio placentae, or fetal death Multifetal gestations, hydatid mole, fetal hydrops, primigravida Pregnancy in teen or those > 35, lower socioeconomic status, primigravida Others: diabetes, renal disease, etc. Patho

Complete mole Updated: 12/04/2018 © Jun Wang, MD, PhD General features Diploid paternal only genome Higher risk for invasive mole or choriocarcinoma Poor prognostic factors: Large for date uterus, ovarian enlargement due to theca-lutein cysts Key pathogenesis Abnormal gametogenesis and fertilization Invasive mole Usually complete moles Increased capacity of the trophoblast for invasion May invade parametrial tissue, broad ligament and blood vessels, but serosa is usually intact Present with uterine bleeding and elevated hCG after evacuation of a mole Differential diagnosis Choriocarcinoma : High hCG, but NO villi Placenta increta or percreta : During delivery/parturition; NO hydropic villi, NO abnormal trophoblastic proliferation Treatment: Chemotherapy Clinical presentations Vaginal bleeding or a missed abortion Passage of grape-like vesicles Disproportionately larger uterus for the stage of pregnancy Increasing serum hCG levels after the 14

Choriocarcinoma Updated: 12/04/2018 © Jun Wang, MD, PhD General features Carcinoma derived from trophoblastic Secondary to a prior pregnancy (normal or abnormal) Most commonly arising from prior moles May from prior abortions, normal pregnancies, ectopic pregnancies or teratomas More common in African American, and women older than 40 Higher incidence in India, Mexico, Paraguay and Sweden Most common metastatic sites: Lungs , vagina, brain, liver, kidney and bowel Clinical presentations Vaginal bleeding Brown, foul-smelling discharge Key Laboratory findings High serum hCG Key morphological features Fleshy, yellow-white tumor with necrosis and hemorrhage Markedly atypical cytotrophoblasts and syncytiotrophoblasts with nuclear pleomorphism, hyperchromasia and prominent nucleoli High mitotic activity Markers Positive: hCG, cytokeratin Negative: PLAP Treatment Chemotherapy Radiation therapy Surgery Monitoring with serum hCG Back to pl

Chorioamnionitis Updated: 12/03/2018 © Jun Wang, MD, PhD General feature Associated with premature rupture of membranes More frequent and severe with younger gestational age Major cause of fetal/neonatal infection, stillbirth, prematurity and perinatal morbidity and mortality Etiology Bacterial infection of amnion and chorion membranes Two paths of infection: Ascending or transplacental Commonly group B streptococci , Listeria monocytogenes and fusobacterium, mixed microbes common Clinical presentations Signs of infection: fever, leukocytosis Baseline fetal tachycardia Pathological findings Opaque membranes with yellow-green discoloration and cloudy amniotic fluid Neutrophilic infiltrate of amnions or chorionic villi Treatment Antibiotics Expedited delivery Infected neonatals may need to be treated at NICU Back to placenta pathology Back to female genital tract Back to contents

Pathology of placenta Updated: 04/16/2019 © Jun Wang, MD, PhD Anatomy/histology Fetomaternal organ Three parts Umbilical cord: 1 vein, 2 arteries, Wharton’s jelly, NO inflammatory infiltrate Fetal membrane: Amnion, chorion, decidua, NO inflammatory infiltrate in amnion Placental plate: Cotyledons, primary chorionic villi (solid outgrowth of cytotrophoblast into the syncytiotrophoblast), secondary chorionic villi (primary villi +loose connective tissue core), tertiary chorionic villi (secondary chorionic villi + blood vessel) Physiology Material and gas exchange between fetus and mother Cytotrophoblast replacing endothelial cells of uterine spiral artery to maintain sufficient blood flow to placenta Hormone production Estrogen: Converted from fetal androgen Maintain endometrium during pregnancy Suppress gonadotropin secretion Stimulate mammary gland development Inhibit prolactin secretion Promote uterine sensitivity to oxytocin Progesterone

Pathology of female genital tract   Updated: 01/23/2024 © Jun Wang, MD, PhD Key anatomic features Opened channel, pathological basis for pelvic inflammatory disease Cervix: exocervix, endocervix, transformation zone Uterus: fundus, body Fallopian tube: intramural, isthmus, ampulla, infundibulum, fimbriae Placenta: umbilical cord, fetal membrane, placenta Key histologic features Stratified squamous epithelium from vulva to exocervix Simple columnar epithelium from endocervix to fimbriae Uterine corpus Endometrium: Glands, stroma Myometrium Perimetrium: Mesothelium/peritoneum Ovaries: three components Epithelium (mesothelium) Stroma Germ cells (follicles) Placenta: Cytotrophoblast, syncytiotrophoblast, intermediate trophoblast Infectious/inflammatory diseases Diseases of vagina and vulva Molluscum contagiosum Lichen sclerosus Paget disease Sarcoma botryoides Squamous cell carcinoma Diseases of cervix Cervical intraepithelial neopla