All About Gynecological Pathology

In med school, we learn about the beauty of the human body, yet how ugly it can become at times. We learn how everything in the body fits together to work in harmony, yet how everything can fall apart at the same time. After taking pathology, I realized so many things can go wrong with the body in so many unimaginable ways. We walk around everyday living life seemingly fine, yet every body part, process or point of contact is a spot of potential vulnerability. We may be vulnerable but we are not lost. By understanding our weaknesses, we can manage them better and live stronger lives. We’ve been covering some gynecology in pathology recently. How can there be so many things that could go wrong in such a small (yet important) part of the body?


Q: What is Herpes Simplex Virus 2?
A: HSV2 causes red vesicular papules on and around the genital and buttocks area. It breaks out 3 to 7 days after sex and is very painful. If you get it the first time it could also cause fever and leukorrhea. The vesicles contain lots of virus, and so HSV is highly contagious both when it is active and latent. To diagnose, you pop one of the vesicles, scrape at the base of the ulcer, smear the sample on a glass, and stain the cells. If it is HSV, you should see multinucleated cells with ground-glass appearance with the viral inclusions. This is called a Tzanck test. HSV can be transmitted from the mother to a newborn baby during delivery, especially if it is the mother’s first time having HSV and if it is active. They get it 2-12 after birth and half of babies who get neonatal herpes infection have a systemic infection with high mortality. They get jaundice, conjunctivities, GI bleeding, among other horrible things. If you are a mother who suspects HSV, even when it is asymptomatic, please consider getting a C-section.

Q: What is Molluscum Contagiosum?
A: For both young kids and adults, a poxvirus called molluscum contagiosum lurks around. It can be spread through articles of clothing or any sort of direct contact, like sexual contact. You get domed vesicular ulcers.

Q: What are the things that cause vaginitis?
A: Candida (yeast), Trichomonas (protozoa), Gardnerella (bacteria), Mycoplasma hominis/Ureaplasma urealyticum (bacteria)

Q: What is Candida?
A: It is a yeast that is carried by 10% of women. An infection can cause leukorrhea and pruritus, and white patches on the mucosa. Although most people are asymptomatic, you got increased risk of getting a candida infection if you are immunocompromised (like if you have diabetes or pregnant) or use oral contraceptives.

Q: What is Trichomonas vaginalis?
A: It is a flagellated protozoan that is sexually transmitted. You get vaginal discharge and the cervical mucosa becomes fiery red, aka strawberry cervix.

Q: What is Gardnerella?
A: gram negative bacteria that causes vaginalis. It shows up as mixed bacteria in culture.

Q: What is Mycoplasma hominis and Ureaplasma urealyticum?
A: bacteria that causes vaginalis and PREMATURE DELIVERY.

Q: What is Pelvic Inflammatory Disease (PID)?
A: pelvic pain, fever, vaginal discharge caused by infection of anything cervix or above by either Chlamydia or Gonorrhea. You can get such an infection after spontaneous abortion or after both normal and abnormal deliveries. While for many it is asymptomatic, for others it can cause infertility or ectopic pregnancy due to the scarring. The infection starts in either the endocervical mucosa (cervix) or Bartholin gland and spreads via surfaces if it is gonococcal.

Q: What is the life cycle of Chlamydia?
A: EB goes in –> turns into RB –> RB replicates –> EB goes out.
EB = elementary body (spores)
RB = reticulate body (replication)


Q: What is a Bartholin Cyst?
A: it’s when you get an infection that obstructs the bartholin duct, causing a cyst. The cyst has squamous metaplliasa or transitional epithelium. It hurts a lot. You cut it out or open it permanently (marsupialization).

Q: What is leukoplakia?
A: it’s a general term that describes a white plaque. Since it can be either from a benign or malignant source, the word doesn’t describe much about the pathology.

Q: What is Lichen Sclerosus?
A: It’s the thinning of the vulva epithelium usually in older women (although can happen at all ages), probably due to autoimmunity. It is not precancerous but there it is associated with a slightly higher risk for carcinoma.

Q: What is Lichen Simplex Chronicus?
A: It’s the squamous thickening of the vulva epithelium due to scratching. Since the itching can be caused by many things, the term is non-specific.

Q: What is Papillary Hidradenoma?
A: It’s the vulvar equivalent of intraductal papilloma of breast, both of which are benign. Vulva (which you can think of as “ectopic breast”) and breast tissue are both derived from modified sweat glands, so they both have the same type of tumor. They are well circumscribed and have have tubular ducts lined with columnar cells and myoepithelial cells characteristic of sweat glands.

Q: What is Condyloma Acuminatum?
A: They are benign sexually-transmitted “genital warts” caused by HPV 6, 11. Under the microscope you see acanthosis, parakeratosis, hyperkaratosis, and koilocytosis, which are squamous cells that have vacuolization around the nucleus. They are benign and often regress. You can always cut it out using laser or knife, or freezing it off with liquid nitrogen (cryotherapy)

Q: What’s the most common malignancy of the vulva?
A: Squamous cell carcinoma. Vulvar carcinoma is already very rare, but of those, 85% is squamous cell carcinoma, the rest being basal cell carcinoma, melanoma, or adenocarcinoma. Basaloid or Warty squamous is due to HPV (causing VIN), whereas Keratizing squamous is due to non-HPV factors like lichen sclerosis.

Q: What is Vulvar Intraepithelial Neoplasm (VIN)?
A: It’s a malignant squamous cell carcinoma caused by HPV 16, 18 seen in women usually over 60 but also under 40 as well. It’s the carcinoma in situ (not invasive yet) or Bowen’s disease or the HSIL equivalent for the vulva. They form plaques in the vulva and are multicentric and often associated with neoplasm in vagina or cervix. There is a 10% risk of progression to an invasive form, especially if you are a smoker, diabetic, or immunocompromised.

Q: What is Extramammary Paget Disease?
A: Like we said above, vulva and breast are actually a lot a like in that they both are derived from sweat glands. Because of this, Paget Disease of the Nipple also has an equivalent in the vulva, called Extramammary Paget Disease. They both have Paget cells, which remember are large, round “halo cells” in the epithelial layer. Clinically the lesion is pruritic, red, and well circumscribed on the vulva, and your patient is usually a post-menopausal woman. The lab results will show up positive for PAS, mucopolysaccharides, CEA (carcinoembryonic antigen), and MEA. Comparing Pagets for breast vs. vulva though, there is a big difference… while the presentation of Paget Disease of the Nipple is caused by ductal breast carcinoma underneath (and therefore poor prognosis), Extramammary Paget Disease is not… there is only the surface epithelial presentation and no carcinoma underneath (therefore better prognosis).You can cut it out with a wide local excision.

Q: What is Malignant Melanoma of the Vulva?
A: Exactly how it sounds… It is rare, and looks a lot like Paget disease, except the lab tests will show up negative for CEA (carcinoemb
ryonic antigen) and mucopolysaccharides.


Q: What are Gartner Duct Cysts?
A: pretty common congenital cysts found in vagina that are derived from Wolffian ducts. They are filled with fluid.

Q: How common are vaginal carcinomas?
A: very rare… only 1% of female genital cancers. 95% of these are squamous cell carcinomas. The greatest risk factor is a previous carcinoma in the cervix or vulva. The signs include leukorrhea, urinary/rectal fistulas, bloody vagina.

Q: What is Vaginal Adenosis (or Adenocarcinoma)?
A: Back in the 1930’s to 70’s, women with high-risk pregnancies were treated with a synthetic estrogen called DES. Of these women, a small portion of their daughters subsequently got a rare tumor called Vaginal adenosis (clear cell adenocarcinoma) in which the squamous cells of the vagina become replaced with glandular cells. The average age of diagnosis was 19 and most cases were in the US.

Q: What is Embryonal Rhabdomyosarcoma (Sarcoma Botryoides)?
A: It’s a malignant vaginal tumor found in infants and young kids, derived from embryonal rhabdomyoblasts (mesenchymal cells). They look like grape clusters in the vagina (botryoides means “grape”). They grow in a cambium layer, which is a layer with crowded cells. They invade locally and can obstruct urinary tract, causing death.


Q: How do you get Chronic Cervicitis?
A: menarche –> produce estrogen –> maturation of cervical and vaginal squamous mucosa –> cells shed –> provide place for bacterial growth –> bacteria drops the pH of vagina –> this causes reserve cells in basal layer to proliferate –> columnar to squamous metaplasia –> squamous epithelium overgrows –> covers glands –> mucus accumulates and forms cysts –> PMNs and monocytes come –> inflammation –> cycle of erosion and repair called chronic cervicitis. Virtually all women have some degree of cervical inflammation, mostly asymptomatic. Infections and trauma can make it clinically more pronounced.

Q: What are endocervical polyps?
A: They are harmless inflammatory tumors that grow in the endocervix of some women. They are soft, and contain mucus-secreting glands, and possibly squamous metaplasia as well.

Q: What are the two types of Cervical Cancers?
A: Squamous Cell Carcinoma — most likely caused by HPV 16
Adenocarcinoma — most likely caused by HPV 18

Q: There are many systems in classifying Cervical pre-cancers. How do they relate?
A: Low-grade squamous intraepithelial lesions (LSIL) = CIN I, II — caused by HPV 6, 11, 16, 18
High-grade squamous intraepithelial lesions (HSIL) = CIN III — caused by HPV 16, 18
Carcinoma in situ can be CIN II, III but not vice versa.

Q: Why is Papanicolaou smear (Pap smear) so effective?
A: Because you can detect cervical precancers very early. Lots of times, precancers exist in noninvasive stage for over 20 years.

Q: What are the fates of LSIL (CIN I, II) vs. HSIL (CIN III)?
A: LSIL — 60% regress, 30% persist, 10% progress to HSIL.
HSIL — 30% regress, 60% persist, 10% progress to carcinoma

Q: What do you see under a pap smear to suspect CIN?
A: large nucleus, little cytoplasm. perinuclear halo.

Q: How do you stage Cervical Cancers?
A: Stage 1a — carcinoma in cervix only. see with microscope (1a1 — less than 3mm deep/7mm wide; 1a2 — 3-5mm deep/7mm wide)
Stage 1b — carcinoma in cervix only. see with eye
Stage 2 — carcinoma goes beyond cervix.
Stage 3 — carcinoma goes beyond pelvic wall
Stage 4 — carcinoma goes to bladder or rectum, and metastasizes.

Q: If you see abnormal Pap smear, what’s the next step?
A: Do acetowhite test (apply acetic acid on cervix.. if white patches appear those are the spots of high mitotic activity). Then visualize it by colposcopy. If you see the acetowhite with the colposcopy, then do a punch biopsy to see if it’s CIN I, II, or III. If its CIN I, do ablation therapy (scrape it off). If it is CIN II or III, you can cut it out with cryotherapy, laser, loop electrical excision procedure (LEEP), or cold-knife conization. If you got actual cervical cancer (vs. CIN precursor), then do radiation or chemotherapy.

Q: What is HPV Vaccine?
A: Intramuscular vaccine. You can give it to girls as early as 9 years old. Give 3 doses over 6 months.


Q: What are the causes of excessive uterine bleeding?
A: The most common cause of bleeding is the anovulatory cycle, or failure to ovulate, due to unexplainable reasons (or hormonal imbalances). You can also get anovulatory cycle from thyroid/adrenal/pituitary problems, ovarian tumor or polycystic ovary, or obesity/malnutrition/chronic systemic disease, etc. If you fail to ovulate, then you get prolonged estrogen stimulation, leading to prolonged proliferative phase without progestation. This leads to mild hyperplasia and dilation of glands. Normally, the stages are proliferative (follicular) phase à ovulation à secretory (luteal) phase à menstrual phase.

Q: What are the most common causes of excessive uterine bleeding by age group?
A: Prepuberty – precocious puberty
Adolescence – anovulatory cycle
Reproductive age – pregnancy complications, organic lesions, anovulatory cycle, ovulatory dysfunction
Perimenopausal – anovulatory cycle, irregular shedding, organic lesion
Postmenopausal – organic lesions, endometrial atrophy.

Q: What is Inadequate Luteal Phase?
A: It’s when you have an inadequate corpus luteum function leading to low progesterone secretion, and therefore early menses. You essentially become infertile and have bleeding and amenorrhea. If you take a biopsy during the supposed secretory phase (after ovulation), you’ll see its expected characteristics are lagging.

Q: What endometrial changes do you see in women who use oral contraceptives?
A: you see inactive glands within pregnancy-like decidua (large stroma).

Q: What do you see in the endometrium after menopause?
A: After you get anovulatory cycle, remember you have mild hyperplasia and cystic dilation of glands. At menopauase, you also get ovarian atrophy. Together, these effects are called Cystic Atrophy.

Q: What is Acute Endometritis?
A: an uncommon inflammation of the endometrium following delivery or miscarriage, due to baceteria or products of conception.

Q: What is Chronic Endometritis?
A: It’s more common than acute endometritis, usually in women with chronic Pelvic inflammatory disease (PID), or after delivery/miscarriage due to retained products of conception, or women with intrauterine contraceptive devices (IUD, which could harbor actinomyces), or women with TB. Chronic endometritis is secondary to all of these. 15% of cases have no obvious cause. You get bleeding, pain, and infertility. Under the microscope, you see plasma cells, which aren’t normally present in endometrium. Treat with antibiotics to prevent infections from spreading.

Q: What is Endometriosis?
A: When you find endometrial tissue in places outside of uterus. Most frequently, you find it in ovaries, uterine ligaments, rectovaginal septum, and others. It occurs in 10% of women and often causes infertility in 30-40% of those affected, dysmenorrhea (severe pain during menstruation), and other pelvic or abdominal pain. They are possibly caused by three reasons: 1. Regurgitation of endometrial tissue to peritoneal cavity through fallopian tube. 2. metaplastic differentiation from coelomic endothelium. 3. vascular or lymphatic disseminat
ion to places like lungs or lymph nodes. If you get endometriosis in the bladder, it can cause dysuria. If you get it in the intestines, you could have trouble defecating. Since endometriosis is endometrial tissue, you can get endometrial malignancies there as well.

Q: What is Adenomyosis?
A: When you find endometrial tissue in the myometrium (uterine wall), 3+mm from basalis layer. They are usually contiguous with the rest of the endometrium but just grow into the grooves between myometrial fascicles. You see it in 20% of uterus, so it’s not uncommon. More endometrium means more bleeding, so you get menorrhagia, which is prolonged and heavy periods, and therefore the endometrium is usually dysfunctional (but not always).

Q: What is Endometrial Polyps?
A: They are masses that protrude into the endometrial cavity. They can cause abnormal bleeding if they ulcerate or necrose. They can be made of functional endometrium or hyperplastic endometrium. They grow with increased estrogen, but not progesterone. Rarely, you see adenocarcinomas grow within the polyps. Their growth is associated with tamoxifen (antiestrogen used in treating breast cancer). The polyps grow because they have 6p21 rearrangements.Under the microscope, you see disordered endometrial tissue with thick-walled vessels in the stroma.

Q: What is Endometrial Hyperplasia (Endometrial Intraepithelial Neoplasia)?
A: It’s exactly what it sounds like. It causes endometrial bleeding. It is due to prolonged estrogen stimulation of any cause: supplemental estrogen treatment, menopause, polycystic ovarian disease, granulosa cells tumor (which remember produces estrogen). It is also caused by inactivation of PTEN tumor suppressor gene. Morphologically, they can be either low grade (simple) or high grade (atypical). Simple hyperplasia is simply a result of prolonged estrogen stimulation and has irregular gland shapes but no gland crowding (no increased gland:stroma ratio). Atypical hyperplasia is hyperplastic and has both irregular gland shape and gland crowding (increaseed gland:stroma ratio).

Q: What is Endometrial Adenocarcinoma?
A: It is the most common invasive cancer in the female genital tract, even more common than cervical cancer. It causes irregular vaginal bleeding and excessive leukorrhea. They look either polypoid or diffuse over the endometrium. They are graded 1-3, and staged I-IV. Grade 1 is most differentiated and Grade 3 is least. Stage I — carcinoma stay in corpus uteri. Stage II — carcinoma spread to cervix. Stage III — carcinoma spread outside uterus to pelvis. Stage IV — carcinoma spread outside pelvis to places like bladder or rectum. There are two types of Endometrial Adenocarcinoma:
Type I (Endometrioid) is found in perimenopausal women, is Stage 1 low grade, and have favorable prognosis. It happens most often with postmenopausal women with obesity, diabetes, hypertension, infertility, or unopposed estrogen stimulation. It starts with proliferative endometrium –> hyperplasia –> atypia –> endometrioid carcinoma. Genetics: PTEN, P1K3CA, KRAS, MSI, B-Catenin, P53. Spread via lymphatics.
Type II (Serous or Clear Cell Carcinoma) is found in postmenopausal women, is treated as Stage 3 high grade, and has bad prognosis. Type II is NOT caused by prolonged estrogen stimulation. It starts with atrophic endometrium –> endometrial intraepithelial carcinoma –> serous carcinoma. Genetics: aneuploidy, P53. Spread via intraperitoneal or lymphatics.

Q: What are the three types of stromal tumors of the endometrium?
A: Carcinosarcomas, Adenosarcomas, and Stromal tumors. They are all uncommon.

Q: What is Carcinosarcoma?
A: It is an endometrial adenocarcinoma plus malignant stromal sarcoma. It is also known as Malignant Mixed Mullerian tumor). The stroma differentiates into a variety of different types of tissue, like cartilage, muscle, or even bone (hence mixed), yet they are all derived from the same cell. It occurs in post-menopausal women with bleeding (which is abnormal), and many of them have had radiation therapy in the past. Morphologically, they look bulkier and fleshier than adenocarcinomas and has both epithelial and mesenchymal elements. They are staged the same way as adenocarcinomas and are highly malignant with poor prognosis. They spread as adenocarcinomas.

Q: What is Adenosarcoma?
A: They are polypoid growths that consist of benign endometrial glands (adeno) plus stromal sarcomas. They carcinosarcoma, they can prolapse through the cervical os where the doctor can see it. It occurs in women 30-50 (4th and 5th decades). Unlike Carcinoma which is very malignant, Adenosarcomas are low grade. They trick is to distinguish it from benign polyps, which they look a lot like. Since adenosarcomas are estrogen sensitive, to treat, you’ve got to get an oophorectomy as well as a hysterectomy, whereas for benign polyps, you don’t.

Q: What are Stromal Tumors?
A: They are neoplasms that arise in the endometrial stroma and can be either Benign Stromal Nodules (well-circumscribed, good prognosis) or Endometrial Stromal Sarcomas (diffuse infiltration, bad prognosis).

Q: What is Uterine Leiomyoma (fibroids)?
A: They are the most common tumor in humans because they are found in 75% of women of reproductive age, and each uterus has 6.5 of these. Each one is a unique clonal neoplasm, and they are pretty much all benign. Morphologically, they are well-circumscribed, round, firm, and found in the myometrium (intramural), under the endometrium (submucosal), or under the serosa (subserosal). Histologically, they are made of smooth muscle (hence leiomyoma) and have a whorled pattern. They are all benign, despite there being two rare types that can spread (although still considered benign): Benign Metastasizing Leiomyoma can migrate through vessels into lung, and Disseminated Peritoneal Leiomyomatosis can spread to peritoneum.

Q: What is Leiomyosarcoma?
A: It’s a malignant smooth muscle tumor of the myometrium. They occur in peri and postmenopausal women and they tend to recur and metastasize even after removal, and therefore has bad prognosis. They usually arise de novo (NOT from leiomyoma, which remember doesn’t become invasive). Unlike Leiomyoma, they have infiltrative borders, nuclear atypia, large cells, high mitotic activity, making them malignant. Treat with hysterectomy plus bilateral salpingo-oophorectomy (BSO) (basically remove uterus, fallopian tube, and ovaries), but good luck. Using Adjuvant therapy doesn’t improve prognosis.

Q: What is STUMP?
A: Smooth muscle Tumor of Unknown Malignant Potential — basically if you have something that looks like leiomyomas but is mitotically active and in young or pregnant women, or other scenarios where you don’t know how to classify it, then you call it a STUMP beccause you don’t know if it’s malignant or not because it doesn’t fit some category of disease we know of.


Q: What is Salpingitis?
A: It is the inflammation of the fallopian tubes. It is the most common disease of the Fallopian Tube. It can be acute or chronic, and can cause Pyosalpinx (pus in tube), Hydrosalpinx (fluid in tube), and fibrosis. It is caused by STDs ascending from lower genital tract like Chlamydia or Gonorrhea, Post-obstetrical, IUD (carrying actinomyces), or TB. Salpingitis can lead to ectopic pregnancy or infertility, chronic pain, tubal obstructions or ruptures.

Q: What is Ectopic Pregnancy?
A: It’s when the ovum implants somewhere else besides the endometrium due to PID, endometriosis, prior tubal surgery, or unknown reasons. The most common place of ectopic implantation is the Fallopia
n tube (95%). It can lead to spontaneous regression, rupture of the fallopian tube, hemorrhage, or infertility. To treat, do a salpingostomy (creating a new opening for the tube), salpingectomy (removal of the tube), or methotrexate.

Q: What is Paratubal Cyst?
A: They are the most common lesions of the fallopian tube. They are translucent cysts fillerd with serous fluid and arise from the remnants of the mullerian duct. If they are larger and found on the fimbriated end of the tube, they are called Hydatid of Morgagni. They are benign so nothing to worry about.

Q: What is Fallopian tube Adenocarcinoma?
A: Just like what it sounds like.. primary malignant glandular tumors of the fallopian tube. They are very rare (vs. metastatic tumors which are the most common malignancy of fallopian tube). Like anything above the cervix, you get pelvic pain along with bleeding. Prognosis is poor.


Q: What are Follicular Cysts?
A: They are a non-neoplastic, and most common type of cyst in the ovary. They originate from unruptured (or ruptured, then resealed so pre-ovulation) graafian follicles and are made up of granulosa and thecal cells. They are filled with serous fluid.

Q: What are Luteal Cysts?
A: Cysts formed from teh corpus luteum after ovulation (vs. pre-ovulation like follicular cysts). They are made of fibrin and filled with fluid. Usually asymptomatic, unless it becomes too large and ruptures, causing a peritoneal reaction or hemorrhage.

Q: What is Polycystic Ovary Disease (PCOD)?
A: You get lots of cystic follicles, often accompanying irregular mensees, infertility, anovulation, amenorrhea, hirsutism (50%), obesity (40%), acne, alopecia (hair loss), elevated androgen and not enough estrogen. You have an increased LH, which remember causes thecal cells to produce androgens. Morphologically, the ovaries are twice the size of normal, have tons of cysts, and thecal hyperplasia (thick cortex). You don’t see corpus luteum!

Q: What are the three derivations of ovarian neoplasms?
A: Surface Epithelium Tumors, Sex Cord (Stroma) Tumors, Germ Cell tumors

Q: What are the three types of Surface Epithelium Tumors?
A: Serous (derived from tubal epithelium), Mucinous (derived from cervical epithelium), Endometrioid (derived from endometrium epithelium) Tumors. And these can be each divided into Benign, Borderline, or Malignant. They are derived from transformation of coelomic mesothelium.

Q: What is Serous Cystadenocarcinoma?
A: It’s a malignant serous epithelium tumor (vs. serous cystadenoma), and the most common malignant ovarian tumor. It occurs bilaterally in older women. Histologically, you see Psammoma bodies, which are concentric calcifications. It has bad prognosis.

Q: What is Mucinous Cystadenocarcinoma?
A: It’s a malignant mucinous epithelium tumor (vs. mucinous cystadenoma). Unlike serous cystadenocarcinoma, it is more likely unilateral than bilateral. They are large and multilocular.

Q: What is Pseudomyxoma Peritonei?
A: It’s a type of malignant mucinous ovarian tumor that is probably derived from non-ovarian source, like appendix. If too big, it can cause intestinal obstruction and eventual death.

Q: What is Endometrioid Carcinoma of the Ovary?
A: Histologically it resembles adenocarcinoma and it often accompanies it, but they arise independently, not by metastatic spread. Sometimes it co-exist with endometriosis as well and you hae the same genetic markers on both (PTEN, KRAS, beta-catenin, p53). It has good prognosis.

Q: What is Clear Cell Adenocarcinoma?
A: It is an uncommon surface epithelial tumor characterized by large epithelial cells with lots of clear cytoplasm. They originate from mullerian duct and can be either solid or cystic in nature. Most of the time they stay in the ovary, but if htey spread, they are aggressive and will have bad prognosis.

Q: What is Cystadenofibroma?
A: It is a benign multilocular proliferation of fibrous stroma under the columnar lining epithelium of the ovary.

Q: What is Brenner Tumor?
A: It is an uncommon, benign, unilateral, and solid yellow adenofibromas. They are made of transitional cells.

Q: What is CA-125?
A: It is a biochemical marker used in detecting serous and endometrioid epithelial tumors.

Q: What is a Teratoma?
A: It is the most common ovarian germ cell tumor occurring during reproductive years. 95% of teratomas are benign, called Mature Cystic Teratoma, because they have histologically mature tissue. They may contain ectoderm, mesoderm, or endodermal cells, so you can see hair or teeth in the tumor. Ectoderm tissue is most common. They may be cystic (dermoid cyst), solid (rare), or cystic with malignant transformation. Then you have Monodermal or Specialized Teratomas in which one specialized tissue overgrows the other tissue types in the teratoma. For example, Struma ovarii is when you get thyroid tumor growing in ovary, and it can cause hyperthyroidism. Lastly, you got malignant teratomas called Immature Solid Teratoma. Their tissue resemble the fetus or embryo rather than adult. They are found in young women and can spread easily and rapidly. Good prognosis if Stage I low grade. If high grade, treat with chemotherapy.

Q: What are Dysgerminomas?
A: It is the ovarian counterpart to the seminoma of the male testicles, and the most common malignant germ cell tumor in women. Most of the tumors don’t have endocrine function, but some may. It happens in young women and is associated with Turner’s Syndrome. Although malignant, it has good prognosis with most people surviving over 5 years. It occurs unilaterally. Histologically, you see lymphocytes in the stroma.

Q: What is an Endodermal Sinus Tumor (Yolk Sac tumor)?
A: It’s a rare malignant, germ cell tumor that has alpha-fetoprotein like yolk sac. It happens in young women and girls. Histologically, you see Schiller-Duval bodies, which are blood vessels surrounded by germ cells. It grows rapidly and has poor prognosis.

Q: What is Choriocarcinoma?
A: It is a germ cell tumor that is identical to placental tumor, except it is found in the ovaries. They raise the level of human chorionic gonadotropin (B-hcg) and is very aggressive, but responds well to chemotherapy.

Q: What are Ovarian Sex Cord-Stromal Tumors?
A: They are tumors derived from undifferentiated gonadal mesenchyme, so they can differentiate into male or female structures. They can cause masculinizing or feminizing effects on the patient. There are several types: Granulosa-Theca Cell Tumors, Fibroma-Thecomas, Sertoli-Leydig Cell Tumors (Androblastomas), among other types. I will talk about these now.

Q: What are Granulosa-Theca Cell Tumors?
A: They are malignant tumors made of granulosa cells or both granulosa and theca cells in varying proportions. There is a juvenile as well as a much more common adult type. Since granulosa cells produce estrogens, you get an increase in estrogens, which remember can cause endometrial hyperplasia and endometrial carcinoma among other things. Occasionally, granulosa cell tumors can produce androgens, masculinizing the patient, making them more hairy, lose menstruation, or enlarge their clitoris. To treat, do a hysterectomy with BSO (bilateral salpingo-oophorectomy), or just effected side if you still want to have babies. Histologically, you see Call-Exner Bodies, which are glandlike structures filled with acidophilic material.

Q: What are Thecoma-Fibroma Tumors?
A: They ar
e benign tumors that arise from ovarian stroma and made of either spindle cells (thecoma) or fibroblasts (fibroma) or a mix of both. Thecomas look yellow while Fibromas look grayish-white. They can be active, producing estrogen or occasionally androgen, and are usually unilateral. You get the usual pain and pelvic mass but sometimes also ASCITES or HYDROTHORAX on the right side. Ascites + Hydrothroax + tumor = Meigs syndrome, so thecoma-Fibroma causes Meigs Syndrome.

Q: What are Sertoli-Leydig Cell Tumors (Androblastomas)?
A: They are sex-cord stromal tumors that differentiate into androgen-producing testicular cells… in the ovaries! They cause masculinization, o0r at least defminization, like amenorrhea, breast and uterus atrophy, hirsutism, clitoral hypertrophy, acne, or temporal alopecia (loss of hair). Like Thecoma-Fibromas, they are benign.

Q: What are Metastatic Tumors of the Ovary?
A: tumors from breast, GI tract, or other parts of the pelvis that spreads to the ovaries. A classic example is Krukenberg Tumor, which is a metastatic mucin-producing signet-ring carcinoma from the stomach that spreads bilaterally to both ovaries.


Q: What are the greatest risk factors for ectopic pregnancy?
A: Prior Tubal Surgery, Smoking (more than 20/day), STD (with PID).

Q: What causes Twin-Twin Transfusion?
A: Being monochorionic, or disproportionately sharing fetal circulations. The bigger twin is actually at higher risk because it has all these vesssels all over, causing edema. It can cause death to both twins.

Q: What is Placenta Previa?
A: It’s when the placenta is implanted covering the internal cervical os. It causes hemorrhage during third trimester and even death. Please do a C-section delivery if you have placenta previa.

Q: What are the TORCH organisms?
A: TOxoplasma, Rubella, CMV, HSV

Q: What is Preeclampsia?
A: It’s when pregnant women in their third trimester get hypertension, edema, proteinuria, and HEELP Syndrome (hemolysis, elevated liver enzymes, low platelets.). It is NOT associated with infections.

Q: What is Eclampsia?
A: When the mother gets seizures during pregnancy.

Q: What is Gestational Trophoblastic Disease?
A: It’s when you get a complete hydatidiform mole, grown from the DNA of two sperm, or partial hydatidiform mole, grown from the DNA of two sperm and an egg. A Partial Hydatidiform Mole is triploid, have half normal and half dilated villi, and can see fetal parts. A Complete Hydatidiform Mole is diploid, have all dilated villi, and cannot see fetal parts (because it is completely turned into a mole), and INVADES.

Q: What is Placental-Site Trophoblastic Tumor (PSTT)?
A: It is a trophoblastic tumor that grows on the placental membrane and implantation site after pregnancy. They are weakly immunoreactive to Human Placental Lactogen (hpl). Prognosis varies depending on how long after pregnancy you get diagnosed. A tenth of cases leads to metastasis and death.