Disorders of the Fallopian Tubes and Ovaries Flashcards
Where do the primordial germ cells come from and end up?
They migrate up the midline of the yolk sac through the dorsal mesentery of the hindgut until they reach the gonadal ridge, an outpouching of mesoderm on the posterior abdominal wall
What happens once the germ cells arrive at the gonadal ridge?
They are surrounded by three mesodermally-derived structures:
- Primitive sex cords - surround the germ cells -> will become granulosa cells
- Stroma -> surrounds the follicles, will become fibroblasts and theca cells
- Surface coelomic epithelium -> still derived from mesoderm, will become the mesothelium which covers the ovary
What causes streak or absent gonads?
When the germ cells do not migrate to the gonadal ridges properly -> as in Turner syndrome
-> ovaries are replaced by useless connective tissue with no follicles
How can abnormal migration cause ovaries with premature menopause?
If sex cords are not formed properly around germ cells, then the germ cells are not protected.
Protection from granulosa cells (primitive sex cord derived) is required to protect follicles
Where are the paramesonephric ducts located in development, and where do they fuse / not fuse?
Located lateral to the mesonephric duct in the outpuching called the “lateral urogenital ridge”
The ridges will come to fuse with eachother anterior to the hindgut. They fuse inferiorly, but remain slightly apart superiorly
What do the superior and inferior parts of the paramesonephric duct become?
Superior - unfused - Fallopian tubes
Inferior - fused - uterus, cervix, and upper 2/3 of vagina
Where does the urogenital sinus come from?
From the ventral portion of the distal endodermal tube, with a small contribution (mesodermal patch) from the mesonephric ducts which forms the trigone of the bladder.
What happens in the formation of the epithelium of the vagina?
Lower 1/3: From UG sinus - ectodermal origin - SSNK
Upper 2/3: From paramesonephric ducts - mesodermal origin - columnar epithelial cells
Lower 1/3 SSNK epithelium should spread to cover entire vagina and ectocervix
What is it called if there is persistence of columnar epithelium in the upper vagina? What increases your risk of this? What is the consequence?
Adenosis
Risk increased with in utero diethylstilbestrol
Increased risk of clear cell adenocarcinoma of the vagina
What does the mesonephric duct become in males?
SEED Seminal vesicles Epididymis Ejaculatory Duct Ductus deferens
What does the mesonephric duct become in females, even pathologically?
Epoophoron and paroophoron are remnants in the broad ligament
Can become Gartner duct cysts in the lateral vaginal wall if more distal portions of the duct do not involute
What is the order of areas in the Fallopian tube from the ovary to the uterus in females? Where does fertilization occur?
Fimbrae -> infundibulum -> ampulla -> isthmus -> ostium of uterus
Fertilization typically occursin the ampulla
What is the histological structure of the Fallopian tube wall?
Papillary structure filled with “mucosal plicae” lined with columnar cells
-> ciliated and move the egg down, most developed around time of ovulation
What do corpus lutea look like grossly in a female of reproductive age?
They look like large cystic structures with a hemorrhagic interior (lots of blood) which become progressive fibrotic.
Surrounded on outside by yellowish, luteinized (lipid-filled) granulosa and theca interna cells
What are corpora albicantia vs atretic follicles?
Corpora albicantia (sing. corpus albicans) - scars resulting from regressing corpus lutea
Atretic follicles - small, wavy, hyaline scars -> obliterative fibrosis. These are due to secondary follicles that never got selected for.
What would you expect to see in the ovaries of a young child vs post-menopausal women?
Young child - numerous primordial and early primary follicles, with many atretic follicles (never enough FSH to induce ovulation)
Postmenopause - atretic follicles and corpora albicantia (assuming she had been ovulating throughout her life)
What is the definition of endometriosis and the most common spot for it? Does the myometrium count?
Endometrial tissue, including both stroma and glands, outside the uterus
Most common spot is the ovary
->involvement of the myometrium is called adenomyosis, and does NOT count as a form of endometriosis
What are the theories of pathogenesis of endometriosis and how does this relate to endometriosis being found in the following locations: Ovarian cavity Abdominal cavity Abdominal scars Lungs Lymph Nodes Occurring in men
- Metastatic theory:
Retrograde menstrual flow through Fallopian tubes -> explains ovarian and abdominal cavity spreading.
Hematogenous / lymphatic dissemination -> endometriosis appears in lungs / lymph nodes
Iatrogenic - surgeon moves it there accidentally -> explains abdominal laparotomy scars with it
- Metaplastic theory - multipotent stem cells become endometrium -> explains occurrence rarely in men
How can endometriosis appear grossly in the ovaries, serosa of pelvis / abdomen, and intestines?
Ovaries - “chocolate cysts” - blood-filled endometrioma
Serosa - “powder burns” - black spots on serosa
Intestines - induce fibrosis leading to adhesions and even mural-thickening of smooth muscle (Crohn’s like presentation)
How does endometriosis appear different than adenocarcinoma histologically?
There is proliferation of both the glands and the stroma
In endometrial adenocarcinoma -> Just the glands are proliferating
What symptoms can endometriosis present with?
Cyclic pelvic pain and dysmenorrhea, dyspareunia, dyschezia (pain with defecation, if colon involved), and even infertility
What is the cause of pelvic inflammatory disease?
Infection of fallopian tubes and ovaries, usually by gonorrhea or chlamydia. Other bacteria can do it.
-> vaginal or cervical infection alone won’t do it
What are the initial acute manifestations of PID?
- Acute suppurative salpingitis - acute inflammation of fallopian tube with epithelial injury
- Salpingo-oophoritis - extension to involve ovary
What are the later possible acute manifestations of PID?
- Pyosalpinx - fallopian tube gets filled with purulent exudate if it gets clogged at both ends
- Tubo-ovarian abscess - extensive mass involving both the Fallopian tubes and ovaries
What are the acute complications of PID? What complications could occur later because of these?
Peritonitis and bacteremia
-> the infection can spread to the body
-> may result in intestinal obstruction due adhesions formed by peritoneum
After the infection has been eradicated in PID, what are the possible sequellae? What complications can occur because of this?
- Chronic salpingitis -> chronic inflammation and fibrosis of fallopian tubes, with fusion of plicae
- > can lead to infertility and increased risk of ectopic pregnancy - Hydrosalpinx -> occur following pyosalpinx -> fimbriae fuse and accumulate tubal secretions making a large mass
What are the classical signs and symptoms of PID?
Pelvic pain / dysmenorrhea,
leukorrhea (purulent vaginal discharge), possible acute abdomen
Chandelier sign - cervical motion tenderness on pelvic exam -> patient jumps as if trying to touch a chandelier
Where does ectopic pregnancy usually occur and what are the risk factors?
Usually occurs in ampulla of Fallopian tube
Risk factors: Previous pelvic surgery History of PID Peritubal adhesions due to endometriosis or appendicitis Tubal diverticula (plicae form holes) IUD use.
