Benign And Malignant Lesions Of The Female Genital Tract

Front 1

What is the most common gynecologic malignancy in the US?

Back 1

Endometrial (uterine) cancer

Front 2

What is the most common gynecological malignancy worldwide?

Back 2

Cervical cancer

Front 3

What type of cells make up the exocervix?

What type of cells make up the endocervix?

What is the junction between the two called?

Back 3

Exocervix → squamous epithelium

Endocervix → glandular/columnar epithelium

Junction → transformation zone (where dysplasia/malignancy develops)

Front 4

How is HPV usually eradicated?

Back 4

Infection is usually eradicated by the immune system

-see more aggressive disease in women with a compromised immune system → these patients need to be more aggressively treated and have closer follow up

Front 5

What is a risk of persistent HPV infection?

Back 5

Leads to increased risk for cervical dysplasia (CIN) and cervical cancer

Risk of transformation depends on type of HPV

Front 6

What types of HPV leads to condyloma (typically not a premalignant condition)?

What types of HPV lead to dysplasia/malignancy?

Back 6

Low risk types: HPV 6, 11

High risk types: HPV 16, 18, 33

Front 7

What are the characteristics of CIN (Cervical, Intraepithelial Neoplasia)?

Back 7

Koilocytic change, disordered cell maturation, nuclear atypia and increased mitotic activity within the cervical epithelium

Divided into grades based on extent of epithelial involvement by immature, dysplastic cells

CIN classically progresses in a stepwise fashion to CIS/invasive disease

The higher the grade of dysplasia, the more likely it is to progress, and the less likely it is to regress

Front 8

What is the origin of the uterine artery?

Back 8

Anterior division of the internal iliac

Front 9

What are the risk factors for cervical carcinoma?

Back 9

HPV infection → so anything that increases the risk for HPV infection (i.e. early age of sexual debut, multiple sexual partners, etc.)

Tobacco use

Front 10

What are the two techniques for HPV screening?When should screening be performed?

Back 10

PAP → cytological evaluation, not sensitive or specific but it works because it is done so frequently (disease transforms slowly enough that you catch it)

HPV testing → if HPV is present, a type can be identified

Screening begins at 21, initially performed yearly, >30 can be performed less frequently

Front 11

What types of HPV are covered by the qudrivalent and bivalent vaccines? When are these vaccines ideally administered?

Back 11

Quad: 6, 11, 16, 18

Bivalent: 16, 18

Ideally administer before sexual debut

Front 12

What hormone drives proliferation of the endometrium? What hormone prepares the endometrium for implantation?

What is a consequence of unopposed proliferation?

Back 12

Proliferation is estrogen driven

Preparation for implantation is progesterone driven

Endometrial hyperplasia/malignancy develops as a consequence of unopposed proliferation (estrogen)

Front 13

What are the features of type 1 and type 2 endometrial cancer?

Back 13

Front 14

What are the risk factors for type 1 endometrial cancer?

Back 14

Increasing age

Unopposed estrogen therapy (must add progesterone if giving HRT to a patient with a uterus)

Tamoxifen therapy (commonly prescribed for the treatment and prevention of breast cancer, estrogen antagonist in the breast but estrogen agonist in the endometrium)

Early menarche

Late menopause (after age 55)

Nulliparity

PCOS (chronic anovulaiton)

Obesity

DM

Estrogen secreting tumor

Lynch syndrome

Cowden syndrome

Family history of endometrial/ovarian/breast/colon cancer

Front 15

What is Lynch syndrome?

Back 15

Hereditary nonpolyposis colorectal cancer

An inherited cancer due to a defect in mismatch repair genes and proteins

Mismatch is recognized by the defective machinery can't repair the mismatch → incorporated into new strand → malignancy

Increased risk of type 1 endometrial cancer

Front 16

What is endometrial hyperplasia? How does it normally present?

Back 16

Proliferation of endometrial glands relative to stroma

Classically presents as postmenopausal bleeding

Classified histologically based on architectural growth pattern (simple/complex) and presence/absence of cellular atypia

Risk of progression of hyperplasia to invasive adenocarcinoma correlates with degree of hyperplasia ("penny, nickel, dime, quarter")

Front 17

What is endometrial cancer? How does it present? What dictates therapy?

Back 17

Malignant proliferation of endometrial glands

Presents as postmenopausal/abnormal uterine bleeding

Diagnosed by endometrial biopsy

Stage determines prognosis and therapy

-type 2 often requires chemotherapy after surgery

Front 18

What are two common types of type 2 endometrial cancer?

Back 18

UPSC (uterine papillary serous carcinoma → most common type of type 2)

Clear cell carcinoma

Front 19

What is a leiomyosarcoma? What are its defining histological features?

Back 19

Malignant proliferation of smooth muscle arising from the myometrium

Do not arise from leiomyomas (fibroid, most common benign proliferation of a myometrium)

Histological features (need all three): increased mitotic activity (>10 mitoses/HPF), cellular atypia, and necrosis

Often diagnosed incidentally after hysterectomy for "fibroids"

Rare

Aggressive prognosis

Front 20

If a patient has a BRCA 1 gene mutation, which of the following malignancies is she NOT at increased risk of developing?

1) breast cancer

2) ovarian cancer

3) primary peritoneal cancer

4) pancreatic cancer

5) colon cancer

Back 20

Colon cancer

Front 21

Hemorrhage into a corpus luteum can result in ____________

Degeneration of follicles results in ___________

Back 21

Hemorrhagic cyst

Follicular cysts

Front 22

What types of ovarian surface epithelium-stroma are benign and which are malignant?

Back 22

Benign or malignant: serous and mucinous

Malignant: endometrial, clear cell, transitional cell

Front 23

Germ cell tumors are all benign/malignant?

Back 23

malignant

Front 24

What gene mutation puts women at an increased risk for serous ovarian/tubular cancer?

Back 24

BRCA mutation

Front 25

What is a serous cystadenocarcinoma?

Back 25

Malignant tumor

Most common form of epithelial ovarian cancer/ovarian cancer in general

Complex cysts

Atypical serous cells form sheets

Most commonly arise in postmenopausal women

Front 26

What are the features of type 1 ovarian cancer?

Back 26

Clinically indolent

Present at an early stage

Exhibit shared lineage between benign neoplasms and corresponding carcinoma through an intermediate (borderline tumor) step

Include low grade serous, low grade endometrioid, clear cell, and mucinous carcinomas

Chemotherapy less effective (slow growing tumors)

Front 27

What are the features of type 2 ovarian cancer?

Back 27

Highly aggressive

Present at an advanced stage

Represent 75% of all ovarian cancers

Include high grade serous, endometrioid, and undifferentiated carcinomas

Originate from distal fallopian tube

Front 28

What is the result of a BRCA mutation (cellularly)?

Back 28

BRCA: tumor suppressor genes on chromosomes 17 (BRCA 1) and 13 (BRCA 2)

Most mutations result in truncated protein product

Proclivity for breast/ovarian cancer may be related to hormonal interactions

Function: repairs faulty DNA via homologous recombination

-if mutated → tumorgenesis due to genomic instability

Mutations in BRCA1 more prevalent than mutations in BRCA2

Front 29

What are some strategies for risk reduction of cancer development in patients with known BRCA mutations?

Back 29

Screening - least effective

Chemoprevention - OCP really lowers risk of developing ovarian cancer

Surgery - main thing that can lower risk, standard is removing both ovaries and fallopian tubes (starting to offer just removal of fallopian tubes)

Front 30

What is the most reliable predictor of epithelial ovarian cancer?

Back 30

Internal mass architecture

-surgical intervention is recommended for suspicious masses (don't usually do biopsies)

Front 31

What is a reliable symptom in predicting epithelial ovarian cancer?

Back 31

Changes in bladder habits

Front 32

What are the three most common metastatic tumors to the ovary?

Back 32

Breast

Colon

Endometrium

Front 33

A patient presents with new onset abdominal bleeding. CT scan reveals a pelvic mass. Serum LDH, AFP, and hCG are all in the normal range. What is the most likely diangosis?

Back 33

Immature teratoma

Front 34

What are the three reliable markers for germ cell tumors?

Back 34

LDH

AFP

b-hCG

Front 35

What is a mature cystic teratoma ("dermoid")? Presence of what type of tissue indicates malignancy?

Back 35

Most common GCT

Cystic tumor composed of fetal tissue derived from 2 or 3 embryologic layers (skin, hair, bone, cartilage, thyroid)

Benign

Presence of immature tissue (i.e. neural) indicates malignany → immature teratoma

Front 36

What is dysgerminoma?

Back 36

Most common malignant GCT

Tumor composed of large cells with clear cytoplasm and central nuclei

Serum LDH may be elevated

Front 37

What are the serum markers for the following germ cell and sex cord stromal tumors:

a) Dysgerminoma

b) Choriocarcinoma

c) Endodermal sinus (i.e. yolk sac tumor)

d) Immature teratoma

e) granulosa cell (sex cord-stromal tumors)

Back 37

a) LDH

b) hCG

c) AFP

d) none (don't normally have elevated tumor markers)

e) Inhibin

Front 38

An 8 year old female presents with an ovarian mass and recent history of development of breast buds and menses. What is the most likely diagnosis?

Back 38

Granulosa cell tumor

Front 39

What is a granulosa cell tumor? What is the characteristic histological finding in these tumors?

Back 39

Neoplastic proliferation of granulosa and theca cells

Often produces estrogen and presents with signs of estrogen excess

Call-Exner bodies are identified by their rosette appearance

Malignant; treatment = surgery + chemo

Prognosis is more favorable than epithelial ovarian cancer

Front 40

Biopsy of a vulvar lesion showing S-100(+) cells is a sign of....

Back 40

Vulvar melanoma (the second most common type of vulvar tumor)

Front 41

What is a condyloma? What commonly causes them? What characterizes them histologically?

Back 41

Warty neoplasm of vulvar skin, often large

Most commonly due to HPV 6 and 11

Benign process

Characterized by koilocytes (hallmark of HPV infected cells)

-koilocytes = nuclear enlargement and peri-nuclear halos

Rarely progress to invasive cancer

Front 42

What is lichen sclerosis?

Back 42

Thinning of epidermis and fibrosis of the epidermis

Presents as a white patch with parchment like skin

Must be biopsied to confirm diagnosis (and make sure there's not squamous cell carcinoma in the lesion)

Most common in postmenopausal women

Autoimmune etiology

Benign; slightly increased risk for SCC

Treatment = topical steroids

Front 43

What is Paget's disease?

Back 43

Malignant epithelial cells in epidermis of vulva

Erythematous, pruritic vulvar skin

Represents CIS (carcinoma in situ) usually with no underlying carcinoma

Occasionally associated with adenocarcinoma

Treatment = wide local excision

Front 44

What is vulvar carcinoma?

Back 44

Etiology may be HPV or non-HPV related (50/50)

Arises from VIN (vulvar intraepithelial neoplasm), a dysplastic pre-cursor lesion

Generally seen in elderly women (HPV related variant can be seen in younger women, i.e. 30s)

Diagnosed by biopsy

Treatment = radical vulvectomy + groin LND

Front 45

What is a hydatidiform mole?

Back 45

Abnormal conception characterized by swollen and edematous villi with proliferation of trophoblasts

Uterus expands as if normal pregnancy is present → but uterus is much larger and beta-hCG is much higher than expected for date of gestation

Classified as partial or complete

Classic gray and white "snowstorm appearance" on ultrasound

Treatment is suction curettage

Front 46

What are the features of partial and complete moles?

Back 46