P- Female GU System Flashcards
(39 cards)
Define the cervical transformation zone.
Where is it located?
What is the histology?
Why is it an imortant landmark?
The cervix has:
- endocervix with mucinous columnar cells
- ectocervix with non-keratinizing stratified squamous
The squamocolumnar junction is where they meet.
The transformation zone is the zone between the original [childhood] SC junction and the current [the SC junction moves up the endocervical canal in adulthood]
It is metaplastic or mature squamous epithelium OVERLYING endocervical glands
It is an important landmark bc it is where 90% of cervical cancers arise
What are the risk factors for the development of cervical carcinoma?
- > 4 sex partners
- sex before age 16
- high risk partners
- other STDs
- smoking
What are the high risk HPV serotypes for the development of cervical dysplasia and carcinoma?
16, 18, 31, 33, 35
What is cervical squamous dysplasia?
What is the etiology?
What is the long term behavior?
What is treatment?
It is a precancerous, graded squamous lesion in the transformation zone.
Almost ALL are associated with HPV [16,18,31,33,35].
Long term behavior = it can regress, stay the same or progress to carcinoma [high grade = more likely to progress]
Treatment: follow-up, cryotherapy [freezing it off] wire loop excision [LEEP] , cone biopsy
What change in histology does HPV induce in cervical cells?
How does the histology change as you progress from low grade to high grade lesions?
It changes the nuclei of squamous cells [koilocytic atypia] to look like raisins in a halo
Low grade squamous intraepithelial lesions {LGSIL} have:
- dysplastic zones - high N/C ratio, irregular nuclei
- koilocytic atypia -raisin in halo
As it progresses to high grade squamous intraepithelial lesion {HGSIL}:
- the dysplasia extends 2/3 of the epithelium
- less halo, more binucleation
- more mitotic figures near the surface
For the lowest grade dysplasia of the cervical transition zone, what terms are used for:
- dysplasia biopsy
- CIN Biopsy
- Pap Smear
- condyloma OR mild dysplasia
- condyloma OR CIN 1
- LGSIL
For high grade dysplasia of the cervical transition zone, what terms are used for:
- dysplasia biopsy
- CIN (cervical intraepithelial neoplasia) biopsy
- Pap Smear
- moderate and severe displasia [CIS]
- CIN2 and CIN 3 [mod = 2, severe =3]
- HGSIL
What cell type are 80-90% of cervical carcinomas? What age do patients tend to present? What is the spread? What is treatment? What is prognosis?
- squamous cell carcinoma.
- 40-45
- lymphatic, direct extension to pelvic side walls, liver, lungs
- surgery and/or radiotherapy
- Stage 1 = 90% 5YSR, Stage IV = 10% 5YSR
What are the 3 cancers that can form in the vagina?
What are the causes of each?
- VAIN [vaginal intraepithelial neoplasia] caused by HPV and is squamous cell carcinoma
- Clear cell adenocarcinoma - increased in women who’s mothers used DES for threatened abortions in the 50s
- Sarcoma boitryoides- embryonal rhabdomyosarcoma in children mass from the vagina
What low grade lesion in the vulva is associated with HPV 6 and 11 [low risk]?
condyloma accuminatum - white exophytic plaques associated with the viral infection
Describe VIN and vulvar squamous carcinoma.
What causes them?
What type of carcinoma are they?
VIN is vulvar intraepithelial neoplasia and is a precancerous squamous dysplastic lesion associated with high risk HPVs. 50% of patients with VIN also will have CIN
Vulvar squamous carcinoma has 2 types:
- usual type[VIN 2 and 3] = associated with HPV 16. 18
- differentiated type = older women and associated with vulvar dermatoses NOT HPV
What is PID?
What are the common presentations and sequelae?
PID is infection of the uterus, fallopian tubes or other reproductive organ that leads to lower abdominal pain, fever, menstrual abnormalities.
It is usually caused by gonorrhea or chlamydia.
Sequelae:
- ectopic pregnancy
- abscess formation
- infertility
- chronic pelvic pain
What is adenomyosis?
What is the resulting histology?
What are the clinical sequelae?
It is growth of the basal layer of endometrium down into the myometrium leading to:
- nests of benign endometrial glands and stroma deep in the myometrium between muscle bundles.
- reactive hypertrophy of myometrium –> enlarged globular uterus with thickened walls
Sequelae:
- menorrhagia - heavy bleeding
- dysmenorrhea- painful bleeding
- dysparenuria - pain during sex
What is dysfunctional uterine bleeding?
What are thought to be the causes?
It is when bleeding cycle is off due to a functional disorder and not a mass/lesion of the uterus. It is also called anovulatory bleeding because it can be spotting, frequent periods, heavy bleeding etc
Causes
- metabolic problems : obesity, anorexia
- ovarian lesion [not uterine lesions!!]
- thyroid, pituitary, adrenal problems
What is endometriosis? What is the incidence? What are common locations for it to occur? What are the three pathogenic origins? What are the clinical features?
It is when endometrial glands and stroma grow OUTSIDE of the edomyometrium.
Incidence: 10% of women 20-30 [and 1/3 of them will become infertile]
Common locations: ovaries, uterine ligament, rectovaginal septum, peritoneum [surgical scars]
Pathogenic origins:
- regurgitation through fallopian tubes
- metaplasia [peritoneum->endometrium]
- lymphovascular spread [rarely to liver, lung]
Clinical features:
- dysmenorrhea
- dysparenuria
- pelvic pain
- menstrual abnormalities
You are looking at a gross lesion and note a “chocolate cyst”. What is the likely cause?
Endometriosis
What is a uterine leiomyoma?
What is the incidence?
What is the clinical presentation?
What is the gross and histologic pathology?
What is the chance of progression to leiomyosarcoma?
It is a benign smooth muscle tumor of the uterus also called fibroid
.
It is the most common tumor in women [25%].
It presents with: abnormal bleeding, infertility
It is sharpyly circumscribed MULTIPLE nodules of benign smooth muscle cells.
Histologically: nodules of smooth muscle cells
Malignant transformation to sarcoma is EXTREMELY rare
What is the relationship between endometrial hyperplasia and endometrial carcinoma?
Endometrial hyperplasia and endometrioid carcinoma are both related to unopposed estrogen stimulation leading to overgrowth of glands.
Endometrial hyperplasia is NOT associated with high grade serous and clear cell carcinomas of the endometrium
What is endometrial hyperplasia?
What is the etiology?
What is clinical presentation?
What happens to the histology as it progresses?
It is an overgrowth of benign endometrial glands due to unopposed estrogen stimulation.
Clinical presentation: abnormal bleeding
As the lesion progresses it goes from:
- simple glandular hyperplasia
- complex hyperplasia [nests of tightly packed glands, less stroma]
- complex hyperplasia with cellular/nuclear atypia
What are the 2 basic types of endometrial carcinoma?
What is the cause of each?
Which is more common?
Which is more aggressive?
- Endometrioid carcinoma = most common and is caused by unopposed estrogen stimulation
- High grade serous or clear cell adenomcarcinoma = associated with endometrial atrophy in older patients [more aggressive]
What age group is usually affected by endometrioid carcinoma?
What are likely risk factors?
How does endometrioid carcinoma spread?
What is the prognosis?
It affects women 55-65 Risks: 1. obese 2. diabetic 3. infertile [anovulation = unopposed estrogen]
It spreads via lymph, direct spread to pelvic walls, lung, liver, bone
Prognosis: stage 1 = 90% 5YSR, stage 4 = <10
What is polycystic ovarian disease?
What is the pathology?
What is the pathogenesis?
It is a disease where numerous cystic follicles form beneath a thickened ovarian cortex which can lead to hyperestrogenism due to unbalanced and asynchronous LH secretion
What is Stein-Leventhal syndrome?
Polycystic ovarian disease with:
- oligomenorrhea - infrequent period
- anovulation
- obesity
- hirsutism
- virilism
What is the treatment for PCOs?
drugs that balance the menstrual cycle or induce ovulation
