Obgyn - Path Of Fallopian Tube, Ovary, Placenta

Front 1

Salpingitis
- what is?
- cause?
- results of CHRONIC salpingitis?
- results of ACUTE?

Back 1

= inflammation of the fallopian tube
- usually caused by ascending infection - e.g., gon, chlam, e. coli, mycoplasma

CHRONIC
- plasma cells and lymphocytes
- leads to tubular distortion and impaired function... infertility and ectopic pregnancy might occur

ACUTE
- tube lumen might become blocked... purulent exudate (pyosalpinx = neutrophils) or serous fluid (hydrosalpinx) might accumulate
- could lead to PID if organisms gain access to peritoneum... can lead to adhesions and abscesses in adnexa and cause infertility

Front 2

What is Pyosalpinx?

Back 2

Purulent fluid that accumulates in lumen of fallopian tubes - due to salpingitis

Front 3

What is Hydrosalpinx?

Back 3

Serous fluid that accumulates in lumen of fallopian tubes - due to salpingitis

Front 4

Ectopic Pregnancy
- where do most cases (%??) occur?
- causes
- MOA
- when does rupture occur?

Back 4

- >95% in fallopian tube
- often due to PID, endometriosis
- MOA: bc tube is much thinner than uterus, trophoblasts can penetrate into (placenta increta) or through (placenta percreta) the muscular wall of the tube
- Rupture - usually by 12th week of gestation --> assoc'd with life-threatening intraabdominal hemorrhage

Front 5

Placenta Increta?

Back 5

when the trophoblasts penetrates into the wall of the fallopian tube during ectopic pregnancy

Front 6

Placenta Percreta?

Back 6

when the trophoblasts penetrates through the wall of the fallopian tube during ectopic pregnancy

Front 7

Non-neoplastic Ovarian Cysts - what are the different varieties?
- descrip?
- size?
- cause?
- clinical sx?

Back 7

FOLLICLE CYSTS
- thin-walled, <5 cm diameter
- may develop at menopause- due to abnorms in release of pituitary gonadotropins
- histo: lined by granulosa cells with underlying layer of theca cells
- Clinical sx: associated with precocious puberty in kids, menstrual irregularities, rupture with intraperitoneal bleeding

CORPUS LUTEUM CYSTS
- due to delayed involution of corpus luteum - central bleeding and cyst formation
- yellow wall surrounding the area of hemorrhage
- Prolonged progesterone synthesis --> menstrual irregularities

THECA LUTEIN CYSTS
- often multiple and bilateral
- due to high circulating gonadotropin/HCG levels -e.g., pregnancy, hydatidiform mole, choriocarcinoma - causing exaggerated stim of theca interna
- occasional rupture and intraabdominal hemorrhage

Front 8

Polycystic Ovarian Syndrome
- aka
- pathogenesis
- typical age?
- symptoms/signs
- tx?
- gross appearance of ovary?
- histo appearance of ovary?

Back 8

- aka: Stein-Leventhal Syndrome

- due to abnormal regulation of 17 alpha- hydroxylase --> increased ovarian production of androgens
- androgens inhibit follicle maturation in ovary --> mult follicles at various stages of development - premature follicular atresia --> anovulation
- in adiopose tissue, androgens converted to estrogen --> increases pituitary secretion of LH; negative feedback on FSH --> LH stims theca cells of ovary to increase androgen production...
- hyperinsulinemia --> increase GnRH pulse freq (but LH >>> FSH) and increase androgens

- age: usually in young 20s

- persistent anovulation
- obesity (assoc'd with hyperinsulinemia and increased adipose tissue)
- sx of excess androgen secretion - e.g., hirsutism, acne, male-pattern alopecia
- marked insulin resistance --> further increases androgen synth and LH release
- infertility due to anovulation
- increased incidence of endometrial hyperplasia and adenocarcinoma due to unopposed estrogen

- Gross: ovary appears enlarged and smooth, but contains numerous small cortical cysts within
- Histo: follicle cysts in early stages of development and increased ovarian stroma

- Tx: hormonal tx to reduce androgen production

Front 9

Ovarian Carcinoma
- frequency?
- diagnosis/prognosis?
- cause?

Back 9

= 2nd-most common gyn. malignancy (endometrial cancer = #1)

- higher mortality than all other gyn cancers bc late-stage diagnosis

- can arise from:
1. surface eptihelium (90%)
2. germ cells
3. stromal cells
4. metastasis from other cancers - e.g., krukenberg tumor comes from GI tract

Front 10

Krukenberg Tumor

Back 10

- secondary ovarian cancer -- comes from GI cancer that metastasizes to ovary (usually both)

Front 11

Epithelial Ovarian Tumors
- frequency?
- pathogenesis?
- genetic?
- benign or malignant?
- histo?

Back 11

- most frequent (90%) ovarian tumor

Path:
- repeated disruption and repair of surface epithelium
... more common in nulliparous women
... less common in women who have been pregnant or used OC

GENETICS
- increased incidence if first-degree relative had ovarian cancer
- BRCA-1 gene implicated

TYPES:
- benign cystic adenomas
- solid, malignant invasive carcinoma
- borderline group - cytologic atypia and some malignant potential, but no frank invasion

HISTO - all cellular forms of mullerian differentiation
* serous (fallopian tube)
* mucinous (endocervix)
- endometriod (endometrium)
- clear cell (glycogen-rich endometrium from pregnancy)
- transitional cell (bladder)

***serous and mucinous are most common

Front 12

Benign Ovarian Cystadenomas
- types
- histo
- size?

Back 12

- serous or mucinous differentiation

- can grow to large size
- unilocular (serous) or multilocular (mucinous)

Histo:
- serous - lined by single layer of well-differentiated ciliated columnar epithelium
- mucinous - lined by mucin-producing glandular epithelium

*another type benign: Brenner Tumor - solid (not cystic) - contains nests of transitional type epithelium in dense fibrous stroma

Front 13

What is a Brenner Tumor?

Back 13

Type of Benign Ovarian Tumor
- solid (not cystic)
- contains nests of transitional type epithelium in dense fibrous stroma

Front 14

Borderline Ovarian Tumors
- what are?
- differentiation from benign?
- tx?
- prognosis?

Back 14

= tumors of low malignant potential
- generally cystic
- usually either serous or mucinous

Distinction from Benign:
- presence of epithelial atypia
- increased mitotic activity
- architectural complexity (e.g., papillary structures)

- NO INVASION of underlying ovarian tissue
- slight potential to metastasize into peritoneal cavity or regional lymph nodes

Tx: surgical removal
Prognosis: excellent following surgical removal

Front 15

Invasive Adenocarcinoma of the Ovary
- differentiation?
- most common?
- gross?
- histo?
- sx?
- metastasis - where? how?
- tx?
- prognosis?

Back 15

= Cystadenocarcinoma

- any type of differentiation - serous, mucinous, endometrioid, clear cell, transitional
- Serous = most common - often both cystic and solid areas

- Histo: often papillary growth and frank invasion; psammoma bodies (focal calcifications) within invasive epithelial nests

** Sx often only after achieved large size or metastasized

Metastasis:
- Intraperitoneal Seeding (pseudomyxoma peritonei) may occur
- Lymph Spread - usually paraaortic or external iliac nodes

Tx: surgical removal and chemo
Recurrance not uncommon...

Prognosis:
- depends on surgical staging
- overall 5-year survival = 35%

Front 16

Pseudomyxoma Peritonei

Back 16

Massive intraperitoneal seeding of ovarian cancer

Front 17

Germ Cell Tumors of the Ovary
- types?
- population?

Back 17

- analygous to those seen in testis

Include:
- dysgermanoma
- teratoma
- yolk sac tumors
- choriocarcinoma

**Tend to occur in YOUNGER women when compared to epithelial malignancies; may be seen in children/infants

Front 18

Dysgerminoma
- what is?
- frequency?
- gross appearance?
- histo?

Back 18

= malignant transformation of germ cells with NO histologic differentiation
= ovarian counterpart to seminoma (but much more rarely)
- only 2% of ovarian cancers
- gross: homogenous tan appearance
- histo: sheets of uniform clear cells with surrounding lymphocytic infiltrate

Front 19

Psammoma Bodies

Back 19

focal calcifications found in ovarian cystadenocarcinomes; found within nests of invasive epithelial cells

Front 20

Teratoma
- what is?
Types?

Back 20

= germ cell tumor with evidence of somatic differentiation- usually along all 3 embryonic layers

Front 21

Struma Ovarii

Back 21

type of teratoma composed of only thyroid tissue
- rarely associated with hyperthyroidism

Front 22

Mature Cystic Teratoma
- aka?
- frequency?
- pathogenesis?
- description?
- malignancy?

Back 22

- aka: dermoid cysts
- 25% all ovarian tumors

PATH:
- parthenogenesis (autofertilization of haploid ova --> female diploid tumor cells)

Descrip:
- may contain skin, sebacious glands, hair (90% of time - hence dermoid)
- may contain any epithelium (GI, repir, etc.), mesenchymal cells (bone, cart), neural tissue (glia), teeth
- Struma Ovarii - all thyroid tissue

- 1% undergo malignant transform - usually to SCC

Front 23

Immature Teratoma
- what is?
- malignancy?
- prognosis?

Back 23

- contain elements from all 3 germ layers, but may have an embryonal appearance
- malignant
- prognosis correlates with amt embryonal tissue present

Front 24

Yolk Sac Tumors
- what are?
- population?
- gross?
- histo?
- malignant?
- how do you monitor them?

Back 24

= germ cell tumors
- highly malignant!
- younger women <30

- gross: identical to testicular lesions - areas of hemorrhage and necrosis
- histo: presence of Schiller-Duval Bodies

- monitor: HIGH alpha- fetoprotein levels... monitor effectiveness of tx and disease recurrence

Front 25

Choriocarcinoma
- what is?
- population?
- gross?
- histo?
- monitor?

Back 25

= germ cell tumor that mimics epithelial components of placental chorionic villi - i.e., cytotrophoblasts and syncytiotrophoblasts

- occur in young girls - may cause precocious puberty and menstrual irregularities
- in older women, usually represents metastasis from intrauterine tumor

- gross: extensive hemorrhage
- histo: malignant cyto- and syncytiotrophoblasts

- monitor: tumor cells make HCG - diagnose, monitor, etc

Front 26

Benign Fibromas
- what are?
- gross?
- histo?
- associated problem?

Back 26

= most common type of ovarian stroma tumor

- gross: solid, white, firm
- histo: well-differentiated fibroblasts and collagen, uniform spindle cells

Meigs Syndrome - association of ovarian fibroma with ascites and pleural effusions

Front 27

Meigs Syndrome

Back 27

association of ovarian fibroma with ascites and sometimes pleural effusion

Front 28

Thecomas
- what are?
- population?
- gross?
- histo?
- associated problem?

Back 28

= benign estrogen-producing tumors
- post-menopausal women

- gross: solid, yellow
- histo: lipid-laden theca cells

- increased estrogen level can lead to endometrial hyperplasia or adenocarcinoma

Front 29

Granulosa Cell Tumors
- pop?
- cause?
- gross?
- histo?
- associated with?
- metastasis?

Back 29

- post-menopausal women
- estrogen-producing

- development related to loss of oocytes, which normally regulate granulosa cell proliferation

- gross: partially cystic; contain hemorrhagic areas
- histo: sheets of uniform cells with grooved nuclei - form Call-Exner Bodies (follicular-like lesions)

- increased estrogen may cause endometrial hyperplasia or adenocarcinoma
- 10% metastasize

Front 30

Sertoli-Leydig Tumors

Back 30

= similar to testicular lesions
- may produce androgens - associated with virilization and hirsutism

Front 31

Gonadoblastoma
- what is?
- frequency?
- cause?

Back 31

- rare ovarian tumor
- due to gonadal dysgenesis
- contains both germ cell and primitive sex cord elements

Front 32

Granulosa Cell Tumors
- pop?
- cause?
- gross?
- histo?
- associated with?
- metastasis?

Back 32

- post-menopausal women
- estrogen-producing

- development related to loss of oocytes, which normally regulate granulosa cell proliferation

- gross: partially cystic; contain hemorrhagic areas
- histo: sheets of uniform cells with grooved nuclei - form Call-Exner Bodies (follicular-like lesions with granulosa cells in a rosette pattern)

- increased estrogen may cause endometrial hyperplasia or adenocarcinoma
- 10% metastasize

Front 33

Sertoli-Leydig Tumors

Back 33

= similar to testicular lesions
- may produce androgens - associated with virilization and hirsutism

Front 34

Gonadoblastoma
- what is?
- frequency?
- cause?

Back 34

= contains both germ cell and stromal elements
- rare ovarian tumor
- due to gonadal dysgenesis

Front 35

Call-Exner Body

Back 35

= histology of granulosa cell tumors in ovary
- follicular-like lesions with granulosa cells (with grooved nuclei) in a rosette pattern

Front 36

Chorioamnionitis
- what is?
- cause?
- gross?
- histo?
- result of acute chorioamnionitis?

Back 36

= Inflammation of placental membranes
- due to ascending bacterial infection - esp in setting of premature rupture!

- gross: membranes and cord appear dusky, opaque and edematous
- histo: neutrophilic infiltrate

** umbilical cord may become secondarily involved

ACUTE - might result in premature labor, fetal infections, intrauterine hypoxia

Front 37

Villitis
- what is?
- cause?

Back 37

= inflammation of the placental villi
- due to complication of underlying endometritis or hematogenous spread of maternal infection

Front 38

Preeclampsia
- what is?
- when does it occur?
- cause?
- can lead to...?
- tx?

Back 38

= hypertension associated with proteinuria and edema
- during third trimester
- often in first pregnancy

- eclampsia = seizure

= type of trophoblastic disease - bc occurs with mole

Path:
- improper invasion by trophoblasts into spiral arteries --> impaired dilation of spiral arteries --> placental blood flow markedly diminished
... leads to endothelial cell injury an DIC - involves rbain, kidneys, liver
... can lead to placental infarction

- tx: delivery and removal of placenta

Front 39

Gestational Trophoblastic Disease
- types?

Back 39

= spectrum of conditions that demonstrate abnodmal proliferation and maturation of trophoblasts

- includes complete/partial hydatidiform mole; choriocarcinoma

Front 40

Complete Hydatidiform Mole
- what is?
- cause?
- chromosomes?
- risk factors?
- gross?
- histo?
- clinical sx?
- can lead to...?

Back 40

= placenta containing swollen chorionic villi (resembles a bunch of grapes) with trophoblastic proliferation, but no demonstrable embryo

- due to fertilization of an empty ovum by sperm --> then duplication of paternal chromosomes = usually 46,XX

Risk Factors:
- pregnancy when <15 y.o. or >40 y.o.
- Asian
- previous molar pregnancy

- gross: uterine cavity completely filled with edematous villi
- histo: atypical trophoblasic hyperplasia

Sx:
- excessive uterine enlaregement
- abnormal uterine bleeding
- serum HCG rises RAPIDLY - becomes markedly elevated

- ~2% patient develop choriocarcinoma following uterine evacuation

Front 41

Partial Hydatiform Mole
- cause?
- chromosomes?
- gross?
- consequences?

Back 41

- due to fertilization of an ovum with 2 sperm OR 1 diploid spem (has not yet undergone meiosis)
= triploid karyotype

- some chorionic villi appear normal; others enlarged and edematous
- mild, focal trophoblastic proliferation

- fetus usually aborted after 10 wks gestation - fetal parts recognizable
- no risk of choriocarcinoma

Front 42

Invasive Hydatidiform Mole
- what is?`
- metastasis?
- distinguish from choriocarcinoma?

Back 42

- villi invade into/through uterine wall (can cause perforation)
--> may enter dilated uterine blood vessels and spread distantly in body (e.g., to lungs), but does not invade other structures

- difficult to distinguish from choriocarcinoma, but the latter does NOT have chorionic villi

Front 43

Choriocarcinoma
- what is?
- malignant?
- gross?
- histo?
- metastasis?
- monitor?

Back 43

= fully malignant neoplasm derived from trophoblasts

Risk Factors:
(same for complete mole)
- pregnancy at <15 y.o. or > 40 y.o.
- Asian
- previous molar pregnancy

- gross: foci within placenta can be small or extensive; hemorrhage and necrosis
- histo: prolif of atypical cytotrophoblasts and syncytiotrophoblasts BUT NO TRUE FORMATION OF CHORIONIC VILLI!!! (differentiates from invasive mole)

- may metastasize widely - sometimes not for many years after preg

- elevated serum HCG - can monitor