repro 3 Flashcards
lichen sclerosus
autoimmune, atrophy and fibrosis in response to inflammation
dysplasia
increase risk for VIN3 and squamous cell carcinoma
white and thick skin and wrinkled cigarette paper appearance
VIN
valve intraepithelial neoplasia
VIN of usual type - more common, HPV driven
differentiated VIN - not related to HPV, high frequency of p53 mutations, related to lichen sclerosus
vulvar SCC
more likely to metastasise if large size, deep invasion, LVSI - initially goes to nodes and eventually liver and lungs
other in situ and invasive vulva lesions
extra mammary Paget’s disease
melanoma
abnormal bleeding in prepuberty causes
precocious puberty
adolescence abnormal uterine bleeding causes
anovulatory cycles
reproductive abnormal uterine bleeding
complications of pregnancy organic lesions DUB - anovulatory cycles DUB - inadequate luteal phase iatrogenic - contraceptives, changes to the OCP, emergency contraception
postmenopausal causes of abnormal uterine bleeding
atrophy
organic lesions - polyps, leiomyoma, hyperplasia, carcinoma
DUB
dysfunctional uterine bleeding
bleeding that lacks an underlying organic cause
DUB - anovulatory cycle
common around menarche/perimenopause
also can be due to PCOS, functional ovarian tumours and metabolic/endocrine problems
anovulatory cycle
failure to ovulate
prolonged oestrogen with no progesterone
stimulation of endometrial growth
EITHER follicles eventually become atretic leading to a withdrawal bleed related to a rapid drop in oestrogen, OR follicles unable to meet the increasing oestrogen demands of the glandular proliferation leading to break through bleeding
anovulatory cycle results in
usually self resolves, if not can lead to hyperplasia than on to cancer
inadequate luteal phase
dysynchornous maturation
cause is believe to be inadequate progesterone production during the post ovulatory period
biopsy shows secretory features that lag behind those expected for that particular day of the cycle
polyps
really common, sessile masses that project into the cavity, fibrous stroma, thick walled vessels and can rarely be involved by hyperplasia or malignancy
adenomyosis
glands and stroma deep within the myometrium, can cause irregular and heavy periods
endometriosis
affects serial uterus, ovaries, peritoneum
ectopic endometrial tissue outside the uterus
cause of infertility, pelvic pain, dysmenorrhoea
macro - chocolate cyst, powder burns
micro - endometrial glands and stroma, haemorrhage
associated with endometriosis and clear cell carcinoma
2 theories for sources of endometriosis
- cells originate from shed uterine endometrium which spread either by regurgitation (retrograde flow through the tubes) or by benign metastasis (spread via blood vessels and lymphatics)
- cells originate from precursor cells either by metaplasia (endometriosis arises from mesonephric remnants or pelvic mesothelium) or extrauterine stem cells (stem cells from bone marrow differentiate into endometrial tissue
endometrial hyperplasia is due to
due to prolonged oestrogen stimulation (menopause, PCOS, ovarian stromal hyperplasia, granuloma cell tumour of the ovary, oestrogen replacement therapy, obesity)
endometrial hyperplasia pathogenesis
prolongues oestrogen causes bleeding
can lead endometroid carcinoma
microscopic appearance - increased gland to stroma ratio
divided into non-atypical hyperplasia and atypical hyperplasia
inactivation of PTEN tumour suppressor gene by deletion and/or inactivation
non atypical hyperplasia
endometrial response to persistant oestrogen stimulation
glands are crowded together with less stroma in between but normal cells
atypical hyperplasia
increased gland to stroma ration AND nuclear atypia
often need hysterectomy
some have adenocarcinoma at hysterectomy
treatment for endometrial hyperplasia
hysterectomy of progesterone therapy e.g. mirena depending on age, fertility aspiration and risk factors
endometrial endometriosis adenocarcinoma
occur in younger obese women 55-65 yr
stepwise progression of genetic alterations from hyperplasia to cancer
HNPCC/Lynch syndrome
better prognosis
endometrial serous carcinoma, clear cell carcinoma and mixed mullarian tumour
poorly differentiated worse prognosis
65-75 yr
atrophy, thin physique
endometrioid adenocarcinoma
generally well differentiated
obesity, DM, HTN, osteorgen
20% of sporadic timours show MMR defects. hereditary HNPCC/Lynch
macro-polypoid/ilfiltrative
micro - resembles endometrium but back to back, cribriform modules, with or whithout solid areas
endometrial serous carcinoma
older women, atrophic endometrium, poorly differentiated
90% p53 mutations
may see precursor serous intraepithelial carcinoma
gets out tubules, LVSI, often outside uterus at diagnosis
micro - papillary or glandular, marked cytological atypia, hyperchromasia, prominent nucleoli
CCC
clear cell carcinoma
- clear cells histologically
- poorly differentiated
MMMT
malignant mixed mullarian tumour/carcinosarcoma
- bulky large polyps can go out os
- adenocarcinoma AND sarcomatous elements - spindle cells or heterologous elements eg. muscle/cartilage/bone
- metastases usually epithelial
endometrial stroma
benign stromal nodules
endometrial stromal sarcoma - low grade look like stromal nodules but are infiltrative, high grade look like any sarcoma
adenosarcoma
myometrium
muscle wall of the uterus
benign leiomyoma
fibroid
very common
round, well circumscribed, from, white whorled cute surface
bland smooth muscle cells in bundles, low mitoses, variable cellularity/nuclear atypia/ no necrosis
