Topic 81-86: Female Genital tract vagina, endometrium, tumors

Question 1

Diseases of the vulva (4 main categories with a few subcategories). describe generally

Answer 1

• Vulvitis: associated with HPV, HSV-2, syphilis, candida albicans, gonorrhea
• Contact dermatitis
• non-neoplastic epithelial disorders: thinning or thickening.
• -Lichen sclerosus - thinning of the epidermis, perhaps autoimmune.
• -Lichen simplex chronicus - thickening of the epithelium, looks like leukoplakia, no predisposition to cancer
• tumors:
• -condyloma and low grade VIN: anogenital warts, either condyloma lata from syphilis or condyloma acuminata with koilocytes from HPV
• -High grade VIN: 90% are squamous cell carcinomas, either HPV associated (16,11) or non-HPV associated (years of non-neoplastic epithelial changes such as lichen sclerosis)
• -extramammary paget - adenocarcinoma, a form of intraepithelial carcinoma
• -bartholin cyst - block of gland causing a cyst

Question 2

what are the disease of the vagina?

Answer 2

• vaginitis - caused by infections such as candida or trichomonas vaginalis
• vaginal intraepithelial neoplasia and squamous cell carcinoma - very rare, associated with HPV
• vaginal clear cell adenocarcinoma - appear in young women whose mothers took diethyl-stilbesterol during pregnancy.

Question 3

list the 3 types of pathologies of the cervix:

Answer 3

• congenital anomilies of the cervix - absense of viagin, double vagina
• cervicitis - can be infectious or not, with chlamydia being the most common
• tumors/neoplasia (next card)

Question 4

what are the 3 types of neoplasia of the cervix? What is the precursor for the most important type of cervical cancer? How is this detected? what are the stages of these grading systems?

Answer 4

three types of cervical cancer:

• squamous (75%)
• adenocarcinoma/adenosquamous carcinoma (20%)
• small cell neuroendocrine carcinoma (5%)

the precursor of squamous cell carcinoma is cervical intraepithelial neoplasia (CIN)

• CIN is detected by liquid based cytology or by pap smear.
• CIN grading system is based on either CIN 1-3 or the bethesda scale of High vs low SIL

Question 5

what is the definition of the CIN stages and HSIL and LSIL?

Answer 5

CIN I - mild dysplasia on the bottom 1/3 of epithelium with koilocytosis
CIN II - moderate dysplasia in bottom 2/3 or all of epithelium
CIN III - severe dysplasia and carcinoma with diffuse atypia and loss of maturation

LSIL = CIN 1

HSIL = between CIN I and II

Question 6

what are the most common causes of endometritis? what kind of cells are necessary to diagnose acute or chronic endometritis?

Answer 6

inflammation of the endometrium can be due to

• previous miscarriage or delivery with retained tissue that acts as a nest for infection
• foreign body or IUD (same reason)
• acute is seen as a predominance in neutrophilic infiltration
• chronic is seen as a lymphocyte infiltration with plasma cells

Question 7

endometrial hyperplasia is what? how does it occur? what are the risks of hyperplasia?

Answer 7

proliferation of endometrial cells that can be due to a high estrogen/progesterone ratio due to failure to ovulate (menopause), estrogenic steroids, tumors, or obesity

-hyperplasia can lead to crowding and atypia of cells, giving rise to neoplasia. hyperplasia can eventually lead to cells that no longer need estrogen to proliferate (autonomous proliferation)

Question 8

endometriosis is what condition? how common is it?what are the 3 theories of occurrence?

Answer 8

condition in which endometrial glands and stroma appear outside the endometrium. frequently multifocal and may involve pelvic tissue (ovaries, douglas pouch) or even remote locations like lungs, bone, lymph nodes.

-occurs in 10% of women, 50% of infertile women.

• regurgitation theory - menstrual backflow into fallopian tubes/ovaries
• metaplastic theory - endometrial differentiation of coelomic epithelium thus endometrial tissue arises in douglas pouch, etc
• vascular or lymphatic dissemination - suggested for lymph node involvement

Question 9

what are the three major tumors of the endo and mesometrium?

Answer 9

• endometrial polyps
• endometrial carcinoma
• smooth muscle tumors

Question 10

endometrial polyps: morphology? how are they defined (neoplastic or not)? why? when do they commonly develop?

Answer 10

• sessile (without stalk), projecting into the uterine cavity with dilated glands
• all cells are monoclonal and they have cytogenetic rearrangement of 6p21, thus defining them as neoplastic
• post-menopause is a common time to develop

Question 11

endometrial carcinoma is how common? what are the 2 routes in which it typically occurs? what is the morphology of endometrial and serous carcinoma?

Answer 11

endometrial carcinoma typically occurs in older women 55-65, and are relatively common.

• premenopausal women with estrogen excess (obesity, diabetes, hypertension). all are also risk factors for endometrial hyperplasia!
• –familial background of hereditary nonpolyposis coli or cowden’s syndrome (mult hamartomas) show increased risk of endometrial carcinoma

-older women with endometrial atrophy leading to SEROUS carcinoma. sometimes with a polyp in the background

morphology

• endometrial carcinoma: looks like normal endometrium, originate in the mucosa and infiltrate deeper
• serous carcinoma: small tufts and papillae with cell atypia. more aggressive!

Question 12

what are the two types of smooth muscle tumor in the uterus? how common are they? how do they appear/morphology? prognosis?

Answer 12

• –leiomyomas are benign smooth muscle tumors that occur in about 30-50% of women and almost never become malignant.
• they are clearly monoclonal with chromosomal abnormalities, but rarely transform.
• appear in multiple, tumor has a whorled cut surface that appear intramural, submucosal or subserosal
• –leiomyosarcoma -appear de-novo (not from preexisting leiomyomas) that appear singly.
• they may metastasize, typically to the lung and recur after surgical removal.

Question 13

what are the non-neoplastic disease of the ovary and fallopian tubes?

Answer 13

ovary:

• follicle and luteal cysts
• polycystic ovarian disease

fallopian tubes

• salpingitis
• ectopic pregnancy
• endometriosis
• primary adenocarcinoma of the fallopian tubes

Question 14

what is the difference between follicle cysts and polycystic ovarian disease?

Answer 14

• follicular cysts are very very common, harmless when unruptured, appear in multiples and develop under the serosal covering of the ovary.
• PCO occurs in 5-10% of women and is associated with subfertility. multiple cysts occur under a dense fibrous capsule and they always occur secondary to excessive estrogen production (high LH, low FSH, and high androgens

Question 15

generally describe salpingitis, ectopic pregnancies and primary adenocarcinomas of the fallopian tubes.

Answer 15

• salpingitis - always part of Pelvic inflam disease, mostly microbial in origin. when the inflammation causes adhesion of the ovaries and fallopian tubes to the uterus, it is called the tubo-ovarian complex
• ectopic pregnancy - implantation in the fallopian tubes, mostly in the ampullary section, can also occur in the isthmus and fimbriae end but less frequently.
• adenocarcinoma of the fallopian tubes is common in women with the BRCA mutation

Question 16

How common are ovarian tumors? what are the 4 types? what are some mutation can can increase the risk of ovarian tumors?

Answer 16

ovarian tumors are the 5th cause of death in women, in age 20-40 they are mostly benign and after they seems to mostly be carcinomas.

• Surface epithelium (65%)
• germ cell (15%)
• sex-cord stroma (10%)
• metastases (5%)

-mutations in BRCA (majority), K-Ras, and HER2 increase the risk

Question 17

Surface epithelium tumors have 4 types (technically 6). what are they? these tumors arise from where?

Answer 17

-serous
-mucinous
-endometrioid
-brenner
(clear cell and cystadenofibroma, neither are listed?)

arise from mesothelium of the ovary due to repeated ovulations and scarring, the epithelium is pulled into the cortex and it forms a small cyst. this cyst eventually undergoes metaplasia and transforms into a tumor

Question 18

serous and mucinous ovarian tumors have a lot in common. what are the commonalities and differences? Frequency? tumor prognosis? morphologies?

Answer 18

serous is the most common ovarian tumor.

• both serous and mucinous tumors are 70% benign, 10% low-malignant/borderline, 10-25% malignant.
• both have either cystadenoma, borderline tumors or cystadenocarcinoma.
• malignant type tumors are typically more solid, benign are more cyst like
• malignant tumors both have stromal invasion to differentiate from borderline tumors

differences

• they obviously arie from different cells
• mucinous tumors are typically unilateral, serous are more bilateral

Question 19

endometrioid tumors and brenner tumors:morphology, general characteristics

Answer 19

• endometrioid tumors: the second most common malignant tumor of the ovary, can be solid or cystic with glandular cells that resembles the endometrium. 30% are bilateral, some association with endometrial cancer
• brenner tumor: rare, solid, unilateral. the cells look like transitional epithelium and the tumor is encapsulated

Question 20

what is a germ cell tumor? what are the two types? when are they normally found? what do they arise from?

Answer 20

teratomas are crazy tumors that have teeth and hair
-can be a benign mature teratoma or a immature malignant teratoma

• benign mature- differentiate from ectoderm, endoderm, and mesoderm
• good prognosis, typically discovered by accident around 20 years old

-immature malignant teratomas - discovered around the same time (20 yo) but they are bulky with central necrosis and sometimes foci of neuroepithelium that aggressively metastasize

Question 21

sex cord stromal tumors are how common? differentiate from which cells? general prognosis?

Answer 21

5% of ovarian neoplasms, they are from the ovarian stroma (embryonic gonadal sex cords)

• 75% occur in women with hyperestrogenism
• more than 90% survival but they tend to recur and the malignancy can’t be predicted from histology