Bartholin's cyst

seen in reproductive age (18-45)

can be infected and turn into an abscess
u/l lesion on a lower vestibule (cystic dilatation)and painful
usually an anatomy type of question.
----------------------------------------------------------------------------------------------------------------------------------------Condyloma
Warty neoplasm of vulvar skin,often large
MCC-HPV types 6 and 11
Seen in vulvar skin,in the cervix or the vaginal canal.
Key features: Koilocytic change on histology
what is koilocytic change? raisin like nucleus (raisinoid nucleus)
rarely progresses to carcinoma but it can. (not 0% risk)
HPV 2 types
High risk type (to develop carcinoma b/c HPV has ability to generate carcinogene
sis)
Types 16,18,31,33
this type is based on dna sequencing. This allows us to determine if it
is a high or low risk. This also reminds us that HPV is a DNA virus.
Can go to dysplasia and eventually carcinoma (names change based on location)
Low risk type
Types 6 and 11
classic lesion is condyloma.
----------------------------------------------------------------------------------------------------------------------------------------------------------------------------Lichen sclerosis
thining of the epidermis and fibrosis of the underlying dermis.
Parchment like (super thin paper like) vulvar skin
in POST MENOPAUSAL women.
It is benign but slightly increased risk of squamous cell carcinoma.
Lichen Simplex chronicus
thick leather like vulvar skin
Benign, no risk of squamous cell carcinoma.
Hyperplasia because of irritation and scratching.
----------------------------------------------------------------------------------------------------------------------------------------------------------------------Vulvar carcinoma
Presents as leukoplakia. (once you see leukoplakia start to question is this
lichen scelosis? is this lichen simplex chronicus? is this vulvar carcinoma?)
So you do biopsy to differentiate.
Pathogenesis:
HPV related or Non-HPV related
HPV related VIN (dysplasia q/w types 16 and 18)
seen in age 40-50years
Non- HPV related
cause is long standing lichen scleorosis.(because slightly increased risk of
squamous cell carcinoma.)

chronic inflammation and irritation eventually will lead to carcinoma.

Post menopausal women, usually greater than 65 years of age.
--------------------------------------------------------------------------------------------------------------------------------------------------------------Extra mammary Paget's disease
Malignant epithelial cells in the epidermis of the vulva.
Presents as erythematous,pruritic,ulcerated skin.
Represents carcinoma in situ,usually no underlying carcinoma.
Differential diagnosis
Melanoma vs Carcinoma
(One of the locations of melanoma is the vulva)
Do stains to distinguish them
Paget cells: PAS +ve, Keratin +ve,S100 -ve
Melanoma:
PAS -ve, Keratin -ve,S100 +ve
when the patient has paget's disease in the nipple it means she has cancer some
where in the breast. But when the patient has paget's disease of the vulva then
there is no underyling cancer.
------------------------------------------------------------------------------------------------------------------------------------------------------------------Vaginal canal
Non keratinizing squamous epithelium
Adenosis
Focal persistence of columnar epithelium in upper 1/3rd of Vagina.
Increased incidence in females exposed to DES in utero, a very high yield assoc.
Vaginal devolopment
lower 2/3rd devolops from Urogenital Sinus and is squamous epithelium.
Upper 1/3rd develops from mullerian ducts and therefore is columnar.
normally squamous epithelium covers the columnar part of the upper 1/3rd.
----------------------------------------------------------------------------------------------------------------------------------------------------------------------Clear cell adenocarcinoma
Malignant proliferation of glandular epith.w/clear cytoplasm.
It occurs in the the context of DES associated vaginal adenosis.
A patient who is exposed to DES in utero, has persistence of columnar glandular
cells (Adenosis) which can turn into clear cell adenocarcinoma.
--------------------------------------------------------------------------------------------------------------------------------------------------------------------------Embryonal rhabdomyosarcoma
Malignant mesenchymal proliferation of immature skeletal muscle.
Rare

Presentation
Bleeding and grape like mass protruding from vagina
"SARCOMA BOTRY0IDES"
The malignant cells in rhadbomyosarcoma is rhabdomyoblast
Cytoplasmic cross striations in immature cells are characteristics.
Also, desmin and myoglobin +ve cells would indicate muscle cells so rhabdomyosar
coma.
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------Vaginal Carcinoma
High risk HPV ---> VaIN is predisposing factor
cancer from lower 2/3rd of vagina goes to inguinal nodes.
cancer from upper 1/3rd of the vagina goes to the iliac nodes.
so put these together to make questions.
----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------CERVIX = Neck
Divided into exocx and endocx.
very distinct demarcaion between them and different epithelium cover them.
area where demarcation occurs is called the "transformation zone"
usually when person gets HPV 90% of the time it is cleared by the immnune system
,
but when it persists and the immune system cannot fight it then it can lead to C
IN.
Risk of CIN depends on persistence of infection and also types.
VERY HIGH YIELD****
What makes high risk HPV high risk?
2proteins makes it high risk
E6 produced by the high risk HPV results in destruction of p53. (there is no cel
l
repair and therefore damaged cells go to cancer.)
E7 produced by the high risk HPV results in destruction of Rb.
p53 and Rb are tumor suppressor genes.
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------CIN
Koilocytic change,nuclear atypia,increased mitotic activity.
whats the difference between carcinoma and dysplasia?
the answer is reversibility.
CIN 1 (66% of time) and 2 (33% of time) have the potential to reverse. CIN and C
IS very rarely reverse.

CIN progresses stepwise

CIN 1 --> 2---> 3--->carcinoma in situ.
Cervical carcinoma
Invasive carcinoma,goes through the basement membrane.
usually arises in middle aged woman. (40-50 years)
they have earlier infection but takes time to progress in the dysplasia carcinom
a
sequence.
They have VAGINAL BLEEDING**** (post coital bleeding)
secondary risk factors are smoking and immunodeficiency.
smoking is important risk factor for cervical and pancreatic carcinoma.
squamous cell carcinoma and adenocarcinoma BOTH are related to HPV infection.
It doesn't metastasize until very very late. It goes through anterior uterine wa
ll into bladder.
mcc of death is post renal failure with hydronephrosis.
grows locally first.
Goal of screening.
PAP SMEAR IS THE GOLD STANDARD FOR SCREENING!!!****
high nucleus/cytoplasmic ratio.
confirmatory test is colposcopy and biopsy.
PAP smear is not good for adenocarcinoma or its precursor lesions.
immunization protection lasts for about 5 years.
pap smears are still necessary for protection form 31 and 33. immunization is on
ly good
for types 16 and 18 and 6 and 11.
------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------Endometrium and Myometrium
Endometrium is the mucosal lining of the uterince cavity but the myometrium is
the smooth muscle layer underlying the endometrium.
Endometrium is hormonally sensitive.
Grows--->Prepared--->Shed.
estrogen progesterone
--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------Ashermann Syndrome
Secondary Amenorrhea due to loss of basalis (regenerative) scarring.
Result of overaggressive dilatation and curettage.
Loss of basalis is lack of regenerative capacity to regenerate --> no menstruati
on.
What would be the cause of ashermann syndrome?
overaggressive d&c when they accidentally knock out basalis.
-------------------------------------------------------------------------------------------------------Anovulatory cycle

Once ovulation occurs the phase changes to secretory phase mediated by progester
one
in order to prepare the endometrium for implantation.
Lack of ovulation---> lack of secretory phase --->eventually pt. presents with b
leeding.
Results in estrogen driven proliferative phase without progesterone mediated
secretory phase.
Common cause of dysfuntional uterine bleeding, seen in menarche and menopause.
------------------------------------------------------------------------------------------------------Acute endometritis
Bacterial infection of endometrium.
Usually related to retained products of conception.
Presents with fever,abnormal uterine bleeding, and pelvic pain.
Chronic endometritis
chronic inflammation = lymphocytes are present but HAVE TO SEE A PLASMA CELL
IN ORDER TO CALL IT A CHRONIC ENDOMETRITIS.***
mcc- tb,pid,iud.
presents w/ infertility,abnormal uterine bleeding and pelvic pain.
infertility and chronic endometritis look for plasma cells.'
-----------------------------------------------------------------------------------------------Endometrial polyp
Hyperplastic protrusion of endometrium.
presents as abnormal uterine bleeding.
****CAN ARISE AS A SIDE EFFECT ON TAMOXIFEN*** b/c of pro estrogenic effect on u
terus.
-------------------------------------------------------------------------------------------------Endometriosis
Endometrial glands and stroma, are misplaced in another location thats called en
dometriosis outiside
the endometrial lining.
presens w/ dysmenorrhea and pelvic pain may cause infertility.pain and dysmenorr
hea b/c even though they are
displaced they still undergo the menstrual cycle.
What causes endometriosis?
1.Retrograde menstruation
2.metaplastic theory- mullerian duct has the ability to develop into multiple di
fferent epithelium (cx,endometrial,etc.)
3.lymphatic dissemination theory - endometrioisis goes thru the lymphatics and d
evelop in elsewhere sites.
mcc site of involvement is the ovaries. = chocolate cysts.
uterine ligament - pelvic pain
pouch of douglas - defecating probs
bladder wall- pain wih urination.
bowel serosa-abdominal pain and adhesions.
fallopian tube mucosa - scarring.
small hemorrhagic areas called as gunpowder lesions!!!

Involvement of the uterine myometrium is called adenomyosis.

presence of endometriosis within the endometrial glands.
complications of endometriosis is the increased risk of carcinoma at the site of
endometriosis especially in
ovaries!!!!*******
----------------------------------------------------------------------------------------------------------------------------endometrial hyperplasia
hyperplasia of endometrial glands relative to stroma.
consequence of unopposed estrogen.**
presents as postmenopausal uterine bleeding.
obesity androgen gets converted to estrone!!!!!!**** that peripheral conversion
to estrone will stimulate endometrium
causing it to become hyperplastic.!!!****
grow grow and grow ----> bleed!!!!*****
based on architectural growth and cellular atypia.
Most important predictor for progression to carcinoma is cellular atypia.
simple or complex hyperplasia.
****MOST IMPORTANT PREDICTOR OF PROGRESSION TO CANCER IS CELLULAR ATYPIA***
---------------------------------------------------------------------------------------------------------------------------------Endometrial carcinoma
malignant proliferation of endometrial gland.
there are 2 pathways of ca.
1. Hyperplasia pathway- unopposed esstrogen --->endometrium grows and grows -->h
yperplasia --->ca. (endometrioid appearance specific for hyperplastic pathway.
can occur in women in 50's or 60's.
2.sporadic pathway--> you dont have hyperplasia.you get cacner from an atrophic
endometrium.histology is serous (papillary serous) usually occurs in elderly.
sporadic pathway is driven by a p53 mutation. can get psammoma bodies. very aggr
essive tumor.
leiomyoma premenopausal women
asymptomatic but if they do have symptoms- abnormal uterine bleeding,infertility
,and pelvic mass.
sarcoma in postmenopausal women.arises denovo.
sarcoma single lesion but leiomyoma usually multipple.

persist