A 22 year old woman present with a unilateral painful lesion at the lower vestibule adjacent to the vaginal canal. What is the most likely cause of her condition?
Bartholin cyst. This is a cystic dilation of the Bartholin gland that arises due to inflammation and obstruction of the gland; commonly in women of reproductive age.
A 34 year old woman presents with a large warty lesion of the vulvar skin. Biopsy of the lesion is shown below. What is causing her condition?
Condylomas are most commonly due to HPV 6 or 11. They are characterized by koilocytic change (crinkled or raisinoid nucleus) on biopsy. Note that these rarely progress to carcinoma because HPV 6 and 11 are low risk infections.
Typical areas affected by HPV 6 or 11 in females
Vulvar, vaginal canal and cervical (lower genital tract) condylomas
How do you know whether a woman is infected with high risk or low risk HPV infection?
DNA sequencing (because HPV is a DNA virus). Low risk are serotypes 6 and 11. High risk are serotypes 16, 18, 31 and 33
Typical areas affected by HPV 16, 18, 31 and 33 in females
Dysplasia over time that can eventually become carcinoma in the cervix, vagina and vulva.
A 60 year old post-menopausal woman presents with parchment-like (very thin) leukoplakia on the vulvar skin. What is likely causing her condition?
Lichen sclerosis. This is a thinning of the epidermis and fibrosis of the underlying dermis. This is a benign lesion but has a SLIGHT increased risk of squamous cell carcinoma.
A 60 year old post-menopausal woman presents with thick leathery leukoplakia on the vulvar skin. What is likely causing her condition?
Lichen simplex chronicus. This is hyperplasia of vulvar squamous epithelium due to chronic irritation and scratching. Note that these are benign and have NO increased risk of squamous cell carcinoma as Lichen Sclerosis does.
A patient presents with leukoplakia on the vulvar skin. Biopsy shows cancer. What is the most likely diagnosis?
Vulvar carcinoma. This arises from the squamous epithelium lining the vulva. Note that it is rare and accounts for a very small percentage of female genital cancers.
What are the two etiologies of vulvar carcinoma?
HPV-related (40-50 year old patient has high risk HPV which results in vulvar intraepithelial neoplasia that progresses to carcinoma) and non-HPV-related (elderly patient has long-standing lichen sclerosis, chronic inflammation and irritation leads to carcinoma).
A patient presents with erythematous, pruritic and ulcerated skin around the nipple and vulva. The biopsy is shown below. How would you narrow your diagnosis?
Paget Disease of the nipple and vulva (carcinoma) or malignant melanoma. Note the malignant epithelial cells present in the epidermis of the vulva. If the cells were PAS+, keratin+ and S100- it is Paget Disease of the nipple and vulva (carcinoma) If it is PAS-, keratin- and S100+, it is melanoma. Note that this represents carcinoma in situ, with no underlying carcinoma in the vulva.
Why are you more concerned about a patient with Paget Disease of the nipple vs a patient with Paget Disease of the vulva?
Nipple usually means there is underlying cancer in the breast. Vulva usually means no underlying carcinoma.
Where does the lower 1/3 of the vagina originate from? The upper 2/3?
Lower 1/3 = Urogenital sinus. Upper 2/3 = Mullerian duct.
What drug can cause a woman to have this vaginal biopsy?
She has adenosis. Normally, the stratified squamous epithelium from the lower 1/3 of the vaginal canal proliferates and replaces the columnar epithelium in the upper 2/3 of the vagina. Adenosis is a focal persistence of columnar epithelium in the upper vagina, with increased incidence in females exposed to DES in utero. Note the two glands persisting with columnar epithelium.
Why is exposure to DES in utero such a big deal that people stopped using it?
A rare complication of DES-associated vaginal adenosis is clear cell adenocarcinoma.
Aside from adenosis and/or clear cell adenocarcinoma, what other complications may arise from DES?
Abnormal smooth muscle formation in the uterine tube carries a complication of ectopic pregnancy and infertility. Mothers who took DES is related to increased estrogen and increased risk for breast cancer.
A <5 year old girl presents with bleeding and a grape-like mass protruding from the vagina. What is the most likely diagnosis?
This is embryonal rhabdomyosarcoma. This is a malignant mesenchymal proliferation of immature skeletal muscle and is rare.
A <5 year old girl presents with bleeding and a grape-like mass protruding from the vagina. What is the key cell in this lesion? How do you distinguish them?
Rhabdomyoblasts are the key cells in defining rhabdomyosarcoma. These cells have cytoplasmic cross-striations and will stain positive for desmin (intermediate filament in muscle cells) and myogenin (nuclear transcription factor in immature muscle cells) with immunohistochemistry.
What is a patient at risk for if they have vaginal intraepithelial neoplasia?
Vaginal carcinoma. This arises from squamous epithelium lining the vaginal mucosa. It is related to high-risk HPV and the precursor lesion is vaginal intraepithelial neoplasia (VAIN).
Lower 1/3 vaginal carcinoma spreads to what nodes? Upper 2/3 vaginal carcinoma spreads to what nodes?
Lower 1/3 = inguinal. Upper 2/3 = regional iliacs.
What defines the boundary between the exocervix and the endocervix?
Exocervix = squamous epithelium. Endocervix = columnar epithelium. This division is called the zone of transition.
HPV’s favorite place to infect in the lower genital tract. What happens in the 1% of time that persistent infection occurs?
Zone of transition. With persistent infection, cervical intraepithelial neoplasia occurs and can transform to carcinoma.
What is it about HPV 16, 18, 31 and 33 that make them high risk?
They make pro-oncotic proteins: E6 increases destruction of p53 (normally promotes DNA repair & apoptotic mechanisms) and E7 increases destruction of Rb (normally inhibits E2F so transcription does not go rampant)
What checkpoint is regulated by p53?
G1 -> S phase transition via checking for DNA damage, repairing it and inducing apoptosis if repair is not possible.
What checkpoint is regulated by Rb?
G1 -> S phase transition via suppression of E2F.
How would you stage this cervical biopsy?
Note the koilocytic change, nuclear atypia and increased mitotic activity. Note that the cells no longer loose their nuclei and turn pink as the go superficial. This is characteristic of cervical intraepithelial neoplasia (CIN) III and CIS (Carcinoma in situ).
How is CIN staged? How likely is each stage to reverse?
Dysplasia of 1st 1/3 of cells = CIN I w/ 66% chance of reversal. 1st 2/3 of cells = CIN II w/ 33% chance of reversal. Most of epithelium = CIN III w/ little chance of reversal. Entire thickness of epithelium = CIS (Carcinoma in situ).
What is the key feature that differentiates CIN from CIS?
CIN has the potential to reverse. CIS cannot reverse and the next step is invasion and squamous cell carcinoma.
A 40 year old woman presents with vaginal and post-coital bleeding. She has a history of HPV infection about 20 years ago. What are secondary risk factors she may have?
Smoking and immunodeficiency increase risk of cervical carcinoma. Note that immunodeficiency results in an inability to clear the HPV infection, allowing it to become chronic and cause cervical carcinoma.
Why is cervical carcinoma an AIDS defining illness?
The body has become so immunodeficient that it cannot clear the HPV infection and allows for progression to cervical cancer.
What are the most common types of cervical carcinoma?
Squamous cell carcinoma and adenocarcinoma. Note that squamous cell is most common, but BOTH are driven by HPV.
What is a classic late finding of an advanced cervical carcinoma?
Hydronephrosis. The tumor metastasizes late but invaded through the anterior uterine wall into the bladder and causes urinary obstruction. Note that one of the most common causes of death in people with cervical cancer is renal failure, post-hydronephrosis.
Goal of screening for cervical carcinoma
Catch dysplasia before it develops into carcinoma.
How do you do a pap smear?
Scrape cells off of the zone of transition, put them under the microscope and look for atypical cells (dark nuclei, high N:C ratios).
What is your diagnosis of this pap smear?
Note the normal squamous cell on the left. Note the atypical cells with a high N:C ratio on the right, which are malignant cells and features you would expect to see in dysplasia.
What is the confirmatory test done after an abnormal pap smear?
Colposcopy. A magnifying glass is placed near the cervix, acid is placed around the cervix and areas of abnormality are biopsied.
What are limitations of a pap smear?
Inadequate sampling of the transformation zone results in a false negative screening test. Also there is limited efficacy in screening for adenocarcinoma (it doesn’t go through same progression of dysplasia that squamous cell carcinoma does).
What immunizations are available for HPV? How long does it last?
Quadrivalent vaccine against HPV 6/11 (protects against condyloma), 16/18 (protects against VIN, VAIN and CIN). Protection lasts 5 years and pap smears are still necessary because there are other high-risk serotypes of HPV that can cause dysplasia.
What are the uterine divisions shown below?
The glandular mucosa of the endometrium and the muscular myometrium.
What drives the uterine proliferative phase?
What drives the uterine secretory phase in preparation for implantation?
A 34 year old woman had to come in for a D&C (dilation and curettage) because of a miscarriage at 15 weeks gestation. She now complains of amenorrhea. What is likely causing her condition?
Asherman Syndrome from overaggressive D&C. This is due to loss of the endometrial basalis, where the stem cells are. This results in inability to regenerate the functionalis, scarring and secondary amenorrhea.
When do you typically see dysfunctional uterine bleeding due to anovulatory cycles?
Menarche and menopause. Lack of progesterone-driven secretory phase causes estrogen uterine proliferation to double on top of one another. This causes proliferating cells to outgrow their blood supply, shed and cause dysfunctional uterine bleeding.
A mother of a newborn baby presents with fever, abnormal uterine bleeding and pelvic pain 2 days after giving birth. The resident informs you that the entire placenta was not delivered after the child came out. What is causing her condition?
Acute endometritis. This is a bacterial infection of the endometrium usually due to retained products of conception.
A woman presents with abnormal uterine bleeding, pelvic pain and infertility. What might you see if a patient has retained products of conception, PID, IUD or Tb?
Chronic endometritis and plasma cells in the endometrium. She would have granulomas if she had Tb.
A 35 year old woman presents with abnormal uterine bleeding. Uterine biopsy is shown below. She has been on tamoxifen for its anti-estrogen effects due to previous breast cancer. What is the likely cause?
Endometrial polyp, a hyperplastic protrusion of the endometrium. Note that although tamoxifen is anti-estrogenic on the breast, it is pro-estrogenic on the uterus promotes uterine proliferation and formation of endometrial polyps.
A 20 year old woman presents with dysmenorrhea, pelvic pain, pain with defecation, pain with urination and abdominal pain. You are worried that her current condition may cause infertility. What is likely causing her condition?
She has endometriosis. This is misplacement of endometrial glands AND stroma outside of the endometrial lining. In her case pelvic pain is caused by involvement of uterine ligaments, defecation pain from pouch of Douglas involvement, urinary pain from bladder wall involvement and abdominal pain from involvement of the bowel serosa. She is at risk for infertility due to fallopian tube scarring.
3 theories of the cause of endometriosis
1) Retrograde menstruation through fallopian tubes into peritoneal cavity 2) Endometrial metaplasia from Mullerian duct 3) Spread through the lymphatics
Most common site of endometriosis
Ovary - chocolate cyst (menstrual product accumulation from growing and shedding of tissue as the endometriosis cycles)
How does endometriosis affect soft tissues grossly?
It produces small, brown, hemorrhagic areas called gunpowder lesions.
What is it called when endometriosis affects the myometrium?
Adenomyosis (endometrial glands in the myometrium).
Why is it imperative that you resolve endometriosis that involves the ovary?
Risk of carcinoma in an ovary affected by endometriosis is significantly increased.
A fat postmenopausal woman presents with uterine bleeding. Endometrial biopsy shows increased density of endometrial glands relative to endometrial stroma. What is causing her condition?
She has endometrial hyperplasia as a consequence of unopposed estrogen proliferative effects that cause endometrial gland hyperplasia and overgrowth eventually causes shedding and bleeding. Post-menopause is a risk because progesterone secretion is gone due to lack of ovulation. Being fat is a risk because androgen gets converted to estrone by aromatase in the fat.
How do you classify endometrial hyperplasia?
By architecture (simple and complex) and by nuclear atypia (with or without).
The most important predictor for endometrial hyperplasia progression to carcinoma is what?
Cellular atypia predicts the risk of hyperplasia progressing to carcinoma.
A 50 year old postmenopausal woman presents with bleeding. Gross image of her uterus is shown below. What are the two ways this type of carcinoma can arise?
Endometrial Carcinoma, note the growth from the normal smooth endometrium. This is a malignant proliferation of endometrial glands that can arise via two distinct pathways: hyperplasia (unopposed estrogen -> hyperplasia -> carcinoma) and sporadic (arises in atrophic endometrium with no evident precursor lesion).
Classic histology of endometrial carcinoma that arises via the hyperplasia pathway. What age typically gets this type of carcinoma?
Endometriod, looks like normal endometrium (more disorganized and piled up on itself with minimal stroma). 60+.
Classic histology of endometrial carcinoma that arises via the sporadic pathway. What age typically gets this type of carcinoma? What type of mutations drive proliferation?
Serous w/fibrovascular cores (also called papillary serous that may sometimes calcify, die and form psammoma bodies). 70+. p53 mutations.
What other tumors present with calcification of papillary tumors?
Thyroid papillary carcinoma, meningioma, papillary serous carcinoma (ovary & endometrium) and mesothelioma can form Psammoma bodies.
A 30 year old woman presents with abnormal uterine bleeding, infertility and a pelvic mass. Gross image is shown below. What is your diagnosis?
Leiomyoma, note the multiple well-defined white whorled masses. This is a benign proliferation of smooth muscle in the myometrium related to estrogen exposure (enlarge during pregnancy and shrink during menopause).
Why are the characteristic white, whorled mass important with leiomyoma?
It differentiates it from the malignant variant leiomyosarcoma (single, necrotic and hemorrhagic grossly, also seen more often in post-menopausal women).
Most common clinical finding of a leiomyoma?
A 70 year old woman presents with a single necrotic and hemorrhagic lesion in the myometrium. What would you likely see on histological examination of this lesion?
Leiomyosarcoma. These arise de novo (LEIOMYOMAS DO NOT BECOME LEIOMYOSARCOMA) and are malignant proliferations of smooth muscle in the myometrium. Histologically you would see necrosis, mitotic activity and cellular atypia.
Cells that make up the ovarian follicle? What gonadotropins control these cells?
Oocyte (bathed in estradiol during maturation), granulosa cells (FSH controlled conversion of androgen to estradiol) and theca cells (LH controlled androgen production)
What does this structure do? How might this present as a mass?
Note the yellow color sitting on top of the ovary. The cells in the corpus luteum secrete progesterone that prepares the uterus for implantation and maintains the pregnancy. It can present as a hemorrhagic luteal cysts if blood fills the cavity of the corpus luteum.
A 34 year old young obese woman presents with infertility, hirsutism and oligomenorrhea. She was recently diagnosed with type II diabetes mellitus. What is likely causing her condition?
Most women will have 1-3 follicular cysts due to normal degeneration of follicles not selected for ovulation. When there are multiple follicular cysts you consider polycystic ovarian disease due to hormonal imbalance (LH:FSH >2). Increased LH -> stimulates thecal cell androgen production -> hirstuism -> androgen goes to estrone in fat -> estrone feedback inhibits FSH -> granulosa cells don’t make estradiol -> follicular degenerates and becomes cystic.
What other conditions are women with polycystic ovarian disease at risk for?
Type II DM (increased insulin resistance) and endometrial carcinoma (lots of circulating estrone from fat conversion of androgen to estrone)
What tumors can arise in the ovary? What is their origin?
Germ cell tumors (oocyte origin), Sex cord stromal tumors (granulosa cell, theca cell, fibroblast origin), surface epithelial tumors (coelomic epithelium origin) and metastasis.
Most common type of ovarian tumor?
Surface epithelial tumors. Cystic serous tumors and cystic mucinous tumors are the most common subtypes. You can also see endometriod and Brenner tumors.
Type of ovarian tumor that most commonly arises in premenopausal women? What would you see grossly?
Benign cystadenoma. Grossly you would see a single cyst and histologically you would see a simple flat lining of epithelial cells.
A 70 year old woman presents with a large ovarian mass. Biopsy reveals a complex cyst with a thick, shaggy lining. What is the most likely diagnosis? How would you confirm this?
Malignant cystadenocarcinoma, commonly seen in post-menopausal women. You would confirm this by seeing invading cells through the connective tissue wall on histology.
What type of surface epithelial tumor would you hope you had if it were not a cystadenoma?
Borderline tumor with features between benign cystadenoma and malignant cystadenocarcinoma. Although it carries malignant potential the prognosis is better that cystadenocarcinoma.
Why might a patient with breast cancer be at higher risk for serous carcinoma of the ovary and fallopian tubes?
BRCA1 mutation carriers. They are at risk for breast cancer, serous cystadenocarcinoma in the ovary and serous carcinoma of the fallopian tubes. This is why these carriers may have prophylactic mastectomy and salpingo-oophorectomy.
Ovarian cancer associated with endometriosis
Endometriod surface epithelial tumors. These are malignant and have a histological appearance similar to that of the ovary.
Where should you look if a patient has endometriod carcinoma of the ovary?
15% of patients will have an additional endometriod carcinoma in the endometrium.
Ovarian tumor that resembles urothelium
Surface epithelial Brenner tumors.
Why to patients with surface epithelial ovarian tumors (cystadenomas, cystadenocarcinomas, endometriod and Brenner tumors) typically present with vague abdominal symptoms (pain, fullness) and urinary frequency?
There is a lot of space for surface epithelial tumors to grow and they present late, this is why they have a poor prognosis. Note that they also tend to spread locally and involve the peritoneum.
Tumor marker used to monitor treatment response and recurrence of surface epithelial ovarian cancer.
2nd most common ovarian tumor
15% of all ovarian tumors are germ cell tumors.
What ovarian tumors typically present in women ages 15-30? 35-40? 60-70?
15-30: germ cell tumor. 35-40: benign surface epithelial tumor. 60-70: malignant surface epithelial tumor.
What are the 5 subtypes of the ovarian germ cell tumors?
The key is to remember that the subtypes mimic tissues normally made by germ cells. Cystic teratoma w/skin, teeth, bone, hair from 2-3 embryologic layers. Embryonal carcinoma w/primitive cells. Yolk sac tumor. Dysgerminoma: mass of germ cells. Choriocarcinoma: placental tissue.
Most common germ cell tumor in females? How does it typically present?
Cystic teratoma. 10% of cases will be bilateral.
Most cystic teratomas are benign, but what do you need to rule out to confirm this?
Presence of immature tissue = immature cystic teratoma which is malignant. It is also possible that the tissue in the teratoma can contain cancer (skin w/carcinoma) = somatic malignancy.
What’s the most common somatic malignancy that arises in cystic teratomas of the ovary?
Squamous cell carcinoma
What is the most common type of immature tissue that arises in cystic teratomas of the ovary?
Cystic teratoma of the ovary composed primarily of thyroid tissue. How will patients present?
Struma ovarii. A young woman with hyperthyroidism and a mass in the ovary increases suspicion for this condition.
A patient presents with an ovarian mass. On biopsy you see nests of large cells with clear cytoplasm and central nuclei (shown below). Serum LDH levels are elevated. What is the diagnosis and what is the prognosis?
Dysgerminoma. This is the most common malignant her cell tumor, with the male counterpart seminoma. This has a good prognosis and responds to radiotherapy.
A 5 year old girl presents with an ovarian mass. Labs reveal elevated serum AFP. What would you likely see on histology?
Endodermal sinus tumors mimic the yolk sac and are the most common germ cell tumor in children. You would see Schiller-Duval bodies on histology (glomeruloid structure with blood vessel in the center with cells organizing around it).
A 17 year old girl presents with widespread tumors throughout the entire body and a small hemorrhagic tumor in the ovary. Serum beta-hGC is elevated. What would you likely see on histology of the ovarian mass? What is the prognosis?
Choriocarcinoma is a malignant proliferation of placental-like tissue (villi w/cytotrophoblasts, syncytiotrophoblasts and a fibrovascular core). Note that there is a malignant proliferation of the trophoblast w/o the villi in choriocarcinoma. Prognosis is poor because chemotherapy is not very effective.
What is the prognosis for a patient diagnosed with an ovarian tumor with large primitive cells?
Embryonal carcinoma is aggressive with early metastasis.
How do granulosa-theca cell tumors present in young children, middle-aged women and older adults?
Children = precocious puberty. Middle-age adult: heavy menstrual bleeding, bleeding outside of menstrual cycle. Older adult: post-menopausal bleeding. These are all symptoms due to estrogen excess.
What symptoms would a woman present with if she had an ovarian mass and Reinke crystals on biopsy?
Sertoli-Leydig cell tumors produce androgen and are associated with hirsutism or virilization in women.
A woman presents with pleural effusion, ascites and an ovarian mass. Gross biopsy of the ovarian mass is shown below. What is causing her condition?
Meigs syndrome. This is a condition associated with pleural effusion, ascites and fibroma (note the solid tumor w/white bands of fibrosis on gross specimen) of the ovary.
What are common metastatic cancer that seed in the ovary?
Kruckenberg tumor (mucinous carcinoma from diffuse gastric carcinoma w/signet ring cells, lobular breast carcinoma, colon cancer) and pseudomyxoma pertionei (“jelly belly” from mucinous fluid in abdomen produced by mucinous carcinoma of the appendix).
Typical cells seen in metastatic Kruckenberg tumors?
Signet ring cells (cell full of mucus and mucus displaces nucleus to edge of cell) are characteristic of diffuse gastric carcinoma that metastasized to the ovaries.
How do you distinguish a metastatic mucinous ovarian tumor vs. a surface epithelial mucinous cystadenoma?
Surface epithelial = unilateral. Kruckenberg = bilateral.
Most common site of ectopic pregnancy? Key risk factor?
Lumen of fallopian. Key risk factor is scarring from PID, endometriosis etc.
A 26 year old woman presents with vaginal bleeding, cramp-like pain and passage of fetal tissue. She was 16 weeks pregnant. What is the most common cause of this?
Note that spontaneous abortion occurs in up to 1/4 of recognizable pregnancies. It is most often due to chromosomal anomalies. It can also be caused by hypercoaguable states (Lupus), congenital infection and exposure to teratogens.
Teratogen exposure in 1st 2 weeks? Weeks 3-8? Months 3-9?
1st 2 weeks = spontaneous abortion. 3-8: organ malformation. Months 3-9 = organ hypoplasia.
Teratogen most commonly associated with mental retardation. Also causes facial abnormalities and microcephaly?
Teratogen that retards intrauterine growth and can cause placental abruption?
Teratogen that causes limb defects
Teratogen that causes intrauterine growth retardation
Teratogen that causes spontaneous abortion, hearing and visual impairment
Teratogen that causes discolored teeth
Teratogen that causes fetal bleeding
Teratogen that causes digit hypoplasia and cleft lip/palate
A mother presents with 3rd trimester bleeding. You can feel the placenta near the cervix and must deliver the fetus by C-section. What causes this condition?
Placenta previa is implantation of the placenta in the lower uterine segment around the cervical os. The child must be delivered by C-section to avoid compression of the fetal blood supply in the placenta.
A mother presents in her 3rd trimester with bleeding. The child delivered still born. What is a common cause of still birth consistent with her history?
Placental abruption happens when the placenta separates from the decidua prior to delivery and causes fetal insufficiency from loss of blood source.
What would you see grossly after you deliver the placenta of a mother who had placental abruption?
Blood on the maternal surface of the placenta with clots.
A mother presents with difficult delivery of the placenta and postpartum bleeding. How do you treat her?
Placenta accreta happens when the placenta improperly implants into the myometrium with no intervening decidua. This requires hysterectomy because the placenta cannot be removed and you need to stop blood loss.
A 3rd trimester expecting mother presents with new severe hypertension, headaches, visual abnormalities and proteinuria. Physical exam reveals edema. What causes her condition?
Preeclampsia is due to abnormality of maternal-fetal vascular interface in the placenta.
What effect does preeclampsia have on the vessels of the placenta?
A 3rd trimester expecting mother presents with new severe hypertension, headaches, visual abnormalities and proteinuria. Physical exam reveals edema. What happens if she develops a seizure?
This defines eclampsia and the placenta must be delivered.
A 3rd trimester expecting mother presents with new severe hypertension, headaches, visual abnormalities and proteinuria. Physical exam reveals edema. Labs show hemolysis, elevated AST/ALT and low platelets. What is causing her condition?
HELLP (Hemolysis, Elevated Liver enzymes and Low Platelets). This is a result of thrombotic microangiopathy involving the liver. Platelet thrombus formation in the liver -> shearing of RBCs, hepatocyte ischemic damage and low platelets due to thrombi formation.
Age range for SIDS. Risk factors for SIDS.
1 month to 1 year. Sleeping on the stomach, smoking in the household and prematurity are all risk factors for SIDS.
A 30 year old woman comes to you excited because she is pregnant. On physical exam her uterus is larger than you would expect for her timeline of gestation. beta-hCG is also inappropriately elevated for her time of gestation. Ultrasound at 20 weeks shows a “snow-storm” appearance and fetal heart sounds are absents. What is causing her condition?
Hydatidiform mole pregnancy occurs when abnormal conception does not grow a baby, but instead grows swollen, edematous villi w/proliferation of trophoblasts around the villi.
What will a pregnant woman pass if she has a hydatidiform mole pregnancy with no prenatal care?
Grape-like masses pass through the vaginal canal in the early second trimester. These “grape-like” masses are large, edematous abnormal villi surrounded by syncytiotrophoblasts.
How do you classify molar pregnancies?
Complete or partial. Complete mole occurs as a result of two sperm entering an empty ovum. (46 chromosomes). Complete moles have 0 fetal tissue. Villi will be completely edematous w/complete proliferation of trophoblasts all along villous. In complete mole beta-hCG is higher because there are more syncytiotrophoblasts. The complete mole has the higher risk for choriocarcinoma (2-3%). Partial mole occurs as a result of two sperm fertilizing a normal egg (69 chromosomes). This results in presence of fetal tissue, partial villous edema, partial trophoblast proliferation and partial risk for choriocarcinoma.
What does a biopsy of a molar pregnancy look like? How do you treat it?
Massive, edematous villi with proliferation of trophoblasts. Treated with D&C, monitor beta-hCG to ensure adequate removal of the mole and screen for choriocarcinoma development for 1 year after removal.
A woman presents with a uterine mass. Biopsy reveals proliferation of cytotrophoblasts and syncytiotrophoblasts without any villi. When will this tumor respond well to chemotherapy?
Choriocarcinoma can arise as a complication of gestation (normal pregnancy, spontaneous abortion or molar pregnancy) or as spontaneous germ cell tumor. Gestation pathway responds well to chemotherapy, but the spontaneous germ cell tumor does not.