Gyn Pathology, Exam 3

Front 1

What kind of tissue is the uterus made up of?

Back 1

Smooth muscle tissue.
Uterus is divided into endomterial, myometrial, and perimetrial.

endo prepares for implant of ovum.
3rd lower most glands, in basalis, do not change.
upper 2/3s, upper basalis do go through changes through menstrual cycle.

Front 2

Where do changes in the endocervical canal occur?

Back 2

There are changes in the squamocolumnar junction - transition zone. This is particularly susceptible to infection such as HPV.

Front 3

Describe the endometrial changes during menstrual cycles

Back 3

1. LH spike in mid cycle that triggers ovulation.
2. corpus luteum secretes progesterone.
3. predominance of E maintains glands, and progresterone. Both support the implanted embryo.
4. Without implantation, progresterone drops and menstruation occurs.

Front 4

What is the endometrium called when it is triggered by estrogen?

Back 4

Proliferative endometrium : tubular glands with mitotic activity

Front 5

What is the endometrum called when trigered by progresterone?

Back 5

Secretory endometrium: serrated glands with luminal secretions.
Secretions occurs in the middle of the gland lumen.

Front 6

Ovary as an organ..

Back 6

Medulla - inner part with glands
cortex: all the follicles. female embryoes born with primordial follicle. at onset of cycle, it changes to primary follicle eventually to 2ndary.

Once its released from ovary, the structures are called corpus luteum and produce progetserone. After time as passed w/o fertilization corpus luteum becomes corpus albicans.

Front 7

Fallopian tube as an organ

Back 7

contain complex mucosal folds with distinct ciliated columnar
epithelium. The funnel-shaped opening called the infundibulum contains many finger-like projections called fimbriae. During ovulation, the fimbriae get close to the ovary and help to sweep the ovum that is released into the abdominal cavity.

As the tube approaches the uterus, the mucosal folds become less complex

Front 8

Pelvic Inflammatory disease (PID)
Etiology, clinical manifesations

Back 8

Etiology:
Sexually transmitted disease (gonorrhea)
Puerperal, Post-abortion, Instrumentation
2-7 days post-inoculation: acute inflammation with vaginal exudate; Ascending spread to tubo-ovarian region -> Acute suppurative salpingitis.
Days to weeks: Fimbria of fallopian tubes seal off to become adherent to ovaries
Pyosalpinx - tube that has puss in it.
Salpingo-oophoritis
Tubo-ovarian abscesses

Treatment: usually through antibiotics

Front 9

Cervical cancer epidemiology

Back 9

Most of cases are due to human papilloma virus
-cancer death in US has fallen dramatically but in the developing world is a real killer.
-pts are much more likely to be detected and cured at earlier stages. cancer related deaths have gone down due to this/

-mostly attributed to invention of Pap smears. Pap smear is a sampling of the transitional zone- want to look for ellipsoidal change if tehre is HPV infection.

Front 10

Pathogensis of cervical cancer

Back 10

HPV most infects at 20s.
-exposed area transition zone is infected by virus; HPV DNA integrates into cell and have unrestrained prolif in the cell.
-HPV has 2 variables: type of virus (low or high malignancy)

2nd variable: immune status of pt.
high risk HPV: can develop invasie cancer.

Front 11

When do most interventions occur?
CIN 1, 2 and 3

Back 11

With Pap smear, usually at earlier stages so patients can be treated early.
Normal: non keratinized squamous eptihelium
CIN1: low risk lesion, analagous to gential wart. not invasive. nuclei are larger with halos
CIN-2- more changes.
CIN-3 no maturation going on. Cells at hte top are similar to the cells on the bottom. will have cerivcal exision to hopefully excise the lesions.

Front 12

Chronic endometritis

Back 12

Chronic PID
Postpartum (retained gestational tissue)
Intrauterine device (IUD)
Tuberculosis.
Non-specific
(15%. Chlamydia)

accumulation of plasma cells. sign that patient has been chronically affected.

Front 13

Endometriosis

Back 13

Endometrial glands or stroma in abnormal locations: ovaries, uterine ligaments, rectovaginal septum, pelvic peritoneum, laparotomy scars, umbilicus, vagina, vulva, appendix
.
Infertility, dysmenorrhea, pelvic pain

Clinical manfiestations
Powder burns: endometriosis in serosal surface shows hemorrhage.
can have chocolate cysts - filled with old blood.

Endometrial glands or stroma in abnormal locations: ovaries, uterine ligaments, rectovaginal septum, pelvic peritoneum, laparotomy scars, umbilicus, vagina, vulva, appendix
.
Infertility, dysmenorrhea, pelvic pain

Front 14

Adenomyosis

Back 14

Nests of endometrial glands deep within myometrium.
15-25% of examined uteri.
Pelvic pain, dysmenorrhea, dyspareunia, menorrhagia

can cause heavy and painful periods, and pelvic pain in between menstrual periods

Front 15

Endometrial hyperplasia

Back 15

-too densely packed glands.
-precursor to tumors.

Related to abnormally high, prolonged level of estrogenic stimulation: Menopause, persistent anovulation, PCOD, functioning granulosa cell tumors, estrogen replacement therapy.
Low grade hyperplasia:
Simple cystic hyperplasia
Complex hyperplasia
High grade hyperplasia:
Atypical complex hyperplasia

Front 16

Endometrial carcinoma

Back 16

Most common GYN cancer.
Endometrioid type:
80%. Postmenopause.
Estrogen dependent.
Arises from endometrial hyperplasia

Non -endometrioid type (Serous, clear cell, high grade variants):
20%. Older postmenopause women.
Non-estrogen dependent.
High grade, more aggressive.

Endometroid: PTAN mutation
Papillary serous: p53 mutation

Front 17

Leiomyoma (fibroid)

Back 17

Mesenchymal tumor, benign.
75% of women in reproductive life.
Estrogen responsive.
Submucosal, intramural, subserosal.

-mostly asymptomatic.
-grow during pregnancy.
-can be found on surface of the wall.
-histologically, looks very normal

clinical manifestation: heavy periods, pain
Treatment: excision of uterus through hysterectomy

Front 18

Leiomyosarcoma

Back 18

malignant proliferation in wall of utuerus.
-much more infiltarted in wall.
more mitotic figures, and can metastsize to lung.

Front 19

Ovarian tumors
-epidemioloy
-risk factors
-what mutations and genes are involved?

Back 19

6% of all cancers in female.
About 80% are benign.
Risk factors: nulliparity, family history, gonadal dysgenesis..
BRCA1 and BRCA2 mutations increase susceptibility.
30% express high levels of HER2neu(ERB-1) oncogene.
Mutations in p53 are found in 50% of ovarian carcinomas.

Front 20

Ovarian tumors classification

Back 20

1. Surface epithelium (derived from coelomic epithelium or ectopic endometrial epithelium).
65-70% of tumors
2. Germ cells which migrate to the ovary form the yolk sac and are totipotential.
3. Ovarian stroma

Front 21

Ovarian tumors derived from surface epithelium
-clinical manifesattions
-tumor marker?
-histological subtypes

Back 21

All have similar clinical manifestations and mostly remain undiagnosed until they are large.pretty nonspecific complaints that dont point to this.

If tumor extension to seed the peritoneal cavity with massive ascites (diagnostic exfoliated tumor cells) and numerous tumor implants/nodules.
Tumor markers: CA-125 (glycoprotein)
Histological Subtypes Include (but not limited to) :
Papillary Serous
Mucinous
Endometrioid

Front 22

1. Papillary serous carcinoma
2. Mucinous

Back 22

High grade atypical celss.
2. filled with mucous material. histolically mucin filled cells with clear spaces as tumor grows

Front 23

Endometrioid carcinoma

Back 23

20% of ovarian tumors arising from surface epithelium.
Resemble endometrial adenocarcinoma (15-30% are associated with adenocarcinoma of the endometrium).
15% associated with endometriosis (glands locatd where they shouldn't be. If there's too much E, can develop this caricnoma).

-usually have better prognosis

Front 24

Germ cell tumors
epidemiology

Back 24

15-20% of all ovarian tumors.
Children and young adults
Teratoma(95%)
Dysgerminoma
Choriocarcinoma
Endodermal Sinus (Yolk Sac Tumor).
15-20% of all ovarian tumors.

note: germ cells are pluripotent.
form tumors that have a variety of different parts to it. can see hair, teeth, fat, thyroid. try to form different tissues in a haphazard way.

Front 25

Sex cord- stromal tumors

Back 25

Derived from ovarian stroma which derives from sex cords of the embryonic gonad (female and male gonads)
Estrogen producing (75%).
Adult and Juvenile granulosa cell tumors (precocious sexual development in prepuberal girls)
Endometrial hyperplasia, cystic disease of breast, and endometrial carcinoma in adult women.

subtype: granulosa tumor has rosettes. if not detected early, can see development of endometrial carcinoma.