Until rupture occurs, an ectopic pregnancy may be indistinguishable from a normal pregnancy, with cessation of menstruation and elevation of serum and urinary placental hormones. Under the influence of these hormones, the endometrium (in approximately 50% of cases) undergoes the characteristic hypersecretory and decidual changes of pregnancy. The absence of elevated gonadotropin levels does not exclude the diagnosis because poor attachment and necrosis of the ectopic placenta are common. Rupture of an ectopic pregnancy may be catastrophic, with the sudden onset of intense abdominal pain and signs of an acute abdomen, often followed by shock. Prompt surgical intervention is necessary.
http://ebooksmedicine.net
Ectopicpregnancyisdefinedasimplantationofthefertilizedovumoutsideoftheuterinecorpus.Approximately1%ofpregnanciesimplantectopically;themostcommonsiteisthefallopiantube.
Chronicsalpingitiswithscarringisamajorriskfactorfortubalectopicpregnancy.
Ruptureofanectopicpregnancyisamedicalemergencythat,ifleftuntreated,mayresultinexsanguinationanddeath.
Gestational trophoblastic disease refers to an abnormal proliferation of fetal trophoblast cells. The World Health Organization broadly divides these diseases into two categories: molar lesions and nonmolar lesions. The molar lesions are further divided into partial, complete, and invasive hydatidiform moles. The nonmolar category consists of choriocarcinoma and other more uncommon types of trophoblast-derived malignancies. All elaborate human chorionic gonadotropins (hCG), which is detected in the blood and urine at levels considerably higher than those found during normal pregnancy. In addition to aiding diagnosis, hCG levels in the blood or urine can be used to monitor treatment efficacy. Clinicians prefer the umbrella term gestational trophoblastic disease because the response to therapy, as judged by the hormone levels, is significantly more important than pathologic subtyping of lesions. However, the genetics, pathology, and natural history of these disorders are sufficiently distinct to merit discussion of each.
HydatidiformMole:CompleteandPartial
The typical hydatidiform mole is a voluminous mass of swollen, sometimes cystically dilated, chorionic villi, appearing grossly as grapelike structures. Varying amounts of normal to highly atypical chorionic epithelium cover the swollen villi. There are two distinctive subtypes of hydatidiform moles: complete and partial. Complete hydatidiform moles are not compatible with embryogenesis and rarely contain fetal parts. All of the chorionic villi are abnormal, and the chorionic epithelial cells are diploid (46,XX or, uncommonly, 46,XY). The partial hydatidiform mole is compatible with early embryo formation and therefore may contain fetal parts, has some normal chorionic villi, and is almost always triploid (e.g., 69,XXY) ( 19.5 ). Both types result from abnormal fertilization with an excess of paternal genetic material. In a complete mole the entire genetic content is supplied by two spermatozoa (or a diploid sperm), yielding diploid cells containing only paternal chromosomes, whereas in a partial mole a normal egg is fertilized by two spermatozoa (or a diploid sperm), resulting in a triploid karyotype with a preponderance of paternal genes.
Table19.5FeaturesofCompleteandPartialHydatidiformMole
Karyotype46,XX(46,XY)Triploid(69,XXY) hCG,Humanchorionicgonadotropin.