My Female Path

Front 1

HPV infects what body parts?

Back 1

the lower genital tract
-vulva
-vaginal canal
-cervix

Front 2

condyloma

Back 2

-commonly due to HPV types 6 or 11

Front 3

HPV infections have what histological look?

Back 3

Koilocytic change = the nucleus crinkled like a raisen

Front 4

how are the risks of HPV classified?

Back 4

high and low risks based on DNA sequencing = risk is how likely to develop carcinoma

LR = 6, 11

HR = 16, 18, 31, 33
(16, 18 MOST common)

Front 5

common pathology for HPV LR and HR

Back 5

LR (6,11) = Condyloma (warty neoplasm of vulvar skin)

HR(16,18) = dysplasia --> Carcinoma

Front 6

Condyloma?

Back 6

warty neoplasm of vulvar skin
-HPV 6 or 11
-Low risk to progress to carcinoma

Front 7

carcinomas stain + for what?

Back 7

keratin +

Front 8

lower 2/3 of vagina derives from?

in development
Upper 1/3 derives from?


histology of each part? (type of tissue)
what happens during development?

Back 8

lower 2/3 (squamous) = Urogenital sinus (UGS)

upper 1/3 (columnar cells) = mullerian duct

-lower squamous cells take over columnar cells and replace them completely

Front 9

adenosis?

Back 9

persistance of columnar epithelium in upper 1/3 of vagina

-inc incidence in females exposed to DES in utero
-inc risk for clear cell adenocarcinoma

Front 10

Vaginal carcinoma
-arises from?
-etiology

Back 10

carcinoma arising form squamous epithelium lining the vaginal mucosa

-related to high-risk HPV
-precursor lesion is Vaginal Intraepithelial Neoplasia (VIN)

Front 11

Clear cell adenocarcinoma

Back 11

malignant proliferation of glands with clear cytoplasm
-due to DES associated vaginal adenosis

Front 12

Embryonal rhabdomyosarcoma
-origin

Back 12

malignant mesenchymal proliferation of immature skeletal muscle
(rare)

Front 13

Embryonal rhabdomyosarcoma
-presentation

Back 13

bleeding grape-like mass protruding from vagina or penis is child (<5)

Front 14

lower 2/3 of vagina derives from?

Back 14

urogenital sinus

Front 15

upper 1/3 of vagina derives from?

Back 15

mullerian duct (but then is replaced by ?)

Front 16

cancer from lower 2/3 of vagina goes to what lymph nodes?

Back 16

inguinal lymph nodes

Front 17

cancer from upper 1/3 of vagina goes to what lymph nodes?

Back 17

iliac lymph nodes

Front 18

Squamous hyper plasia -lichen simplex chronicus?
-etiology

Back 18

-hyperplasia of vulvar squamous epithelium
-leukoplakia with thickening of the vulvar skin (leather like)
-benign
-opposite of lichen sclerosis

Front 19

lichen sclerosis
-presentation

Back 19

thinning of epidermis (parchment-like = paper-like skin) and fibrosis of dermis

leukoplakia- white plaques on skin
-normally benign

Front 20

common infections of female reproductive path (3) and the organism that causes it

Back 20

Herpes virus (HSV-2) = vulvar cancers

Molluscum contagiosum = molluscum lesions

HPV = genital warts, cervical dysplasia

Front 21

HPV causes?

Back 21

genital warts, cervical dysplasia

Front 22

Molluscum contagiosum causes?

Back 22

molluscum lesions

Front 23

Herpes virus (HSV-2) causes?

Back 23

= vulvar cancers

Front 24

Squamous hyperplasia
-presentation

Back 24

-plaques
-hyperkeratosis
-thickened epithelium
-chronic inflammation
slight inc risk for squamous cancer

Front 25

Condyloma acuminatum
-etiology

Back 25

venereal warts (benign tumors)
-HPV-induced (types 6 and 11)
-Koilocytes (raisen)
-perinuclear clearing

Front 26

vulvar tumors?

Back 26

Condyloma

Front 27

Extra-mammary Paget’s disease

Back 27

Labial red crusted lesions
-Similar to disease in breast

Front 28

melanoma of vulva

Back 28

Similar to melanomas elsewhere, S100+
-older women

Front 29

Melanoma

Back 29

Melanoma is a malignant tumor of melanocytes.[2] Melanocytes are cells that produce the dark pigment, melanin,

Front 30

vaginal squamous cell carcinoma
-etiology
-risks

Back 30

malignant neoplasm
-HPV associated
-previous cervical cancer

Front 31

vaginal adenocarcinoma
-etiology
-risks
-histology

Back 31

-DES treated in utero
Risk = vaginal adenosis
-Clear cell adenocarcinoma

Front 32

Embryonal rhabomysarcoma
-Clinical features
-Morphology

Back 32

Infants and children <5 yoa
-polypoid bulging mass, protrudes from orifice

Front 33

list the vaginal malignant neoplasms-

Back 33

-squamous cell carcinoma
-adenocarcinoma
-embryonal rhabomysarcoma

Front 34

cervix tissue demaracated into?
-what type of tissue is each
-name of area where it changes?

Back 34

exocervix - non-keratinized stratified squamous epithelial

endocervix - columnar epithelial

-Transformation zone

Front 35

most common region HPV infects?

Back 35

transformation zone, most common of all the lower genital tract (uterus, cervix, vagina)

Front 36

CIN?

Back 36

cervical intraepithelial neoplasia

Front 37

when does HPV infection lead to CIN risk?

Back 37

persistant infection leads to inc. risk for cervical intra-epithelial infection (CIN)
(90% of time infection is cleared by immune system)

Front 38

Risks of CIN depend on?

Back 38

HPV tpyes

16, 18 = HR

6, 11 = LR

Front 39

HR HPV...what makes them high risk?

Back 39

HR HPV (16, 18) makes E6 & E7 protein
E6- destroys p53
E7- destroys Rb

Front 40

p53 can?

Back 40

-inhibit dna synthesis and allow DNA repair
or
-if there is too much DNA damage, activate Bax and cause apoptosis

Front 41

CIN
-characterization
-

Back 41

-Koilocytic change
-nuclear atypic
-inc mitosis

Front 42

gradation of CIN
-based on

Back 42

based on number of cells showing dysplasia

I, II, III, CIS
(Carcinoma in situ)

higher grade means more dysplasia seen in the stratified squamous epithelia

Front 43

gradation of CIN
-prognosis

Back 43

I & II are reversible 66% and 33% respectively (III rarely reverses)

III & CIS, carcinomas will become malignant, and become a "invasive squamous cell carcinoma"

Front 44

what is the difference between dysplasia and carcinoma (in context of the CIN gradation)

Back 44

dysplasia can reverse, but carcinomas are unable to reverse differentiation

Front 45

steps in CIN progression

Back 45

CIN I --> CIN II --> CIN III => CIS --> invasive cervical carcinoma

(may regress)

Front 46

Cervical carcinoma
-define
-onset?

Back 46

end malignant stage of CIN progression (invasive cervical carcinoma)
-onset is usually 40-50, takes time 25-30 yrs after HPV virus infection for progression through the CIN stages

Front 47

what is the difference between CIS and cervical carcinoma

Back 47

CIS is NOT invasive
-cervical carcinoma is invasive, it can be called invasive cervical carcinoma

Front 48

Cervical carcinoma
-presents as?

Back 48

vaginal bleeding

Front 49

important risk factors for cervical carcinoma?

Back 49

1) HR HPV (16,18)
2) smoking
3) immunodeficiency

Front 50

common subtypes of cervical carcinoma?

Back 50

1) squamous cell
2) adenocarcinoma

(both are HPV related)

Front 51

goal of cervical screening?
-golden standard?
-effective in detecting?

Back 51

catch dysplasia before it develops into carcinoma

-pap smear, only effective for detecting the squamous cell subtype NOT the adenocarcinoma arising from the endocervix

Front 52

what does the HPV vaccine cover against?

Back 52

Quadrivalent, HPV subtypes 6,11, 16, 18

(only protects for 5 years)

Front 53

ectocervix
-histo

Back 53

non-keratinizing squamous mucosa
in continuity with vaginal mucosa)

Front 54

transformation zone

Back 54

zone squamo-columnar junction

Front 55

endocervix
-histo

Back 55

single layer of mucous-secreting columnar epithelium with invaginating glands (this is why it gives rise to adenomas)

Front 56

endometrium

Back 56

complex glandular mucosa, hormonally-regulate

Front 57

myometrium

Back 57

thick smooth muscle wall

Front 58

Cyst

Back 58

an epithelial lined sac, containing fluid or mucus

Front 59

Cervical neoplasia
-risk factors

Back 59

Early age at first intercourse
MULTIPLE SEXUAL PARTNERS
Male partner with multiple previous sex partners (HPV)

Front 60

Cervical neoplasia
-length of progression
- How screened?
-How Dx

Back 60

Slow progression (up to 20 yrs), not all lesions progress to cancer

- PAP smears detect pre-Ca and cancer (a screening tool)

- BX is required for DX

Front 61

what type of nucleotides does HPV have?

Back 61

DNA

Front 62

HPV
-common symptoms?

Back 62

common skin warts to condylomas to invasive cancers

Front 63

LGSIL (LSIL) HGSIL vs. CIN 1/2

Back 63

- Low Grade Squamous Intraepitheliel Lesion
-grades used for pap smear

CIN1,2,3 is for biopsies

Front 64

what happens to the cells of the cervical epithelium when neoplasia/dysplasia occurs/worsens?

Back 64

The nucleus shrivels (koilocyte), the nucleus becomes large
-the density of cells inc.

Front 65

Glandular neoplasms of the cervix?

Back 65

Adenocarcinoma in situ (AIS) --> Invasive adenocarcinoma-
major morphologic subtypes
endocervical*

Front 66

growth of endometrium is dependent on?
shedding of the endometrium lining depends on?

Back 66

estrogen

-removal of progesterone (this maintains the endometrium)

Front 67

estrogen and progesterone, cause which phases of the endometrium?

Back 67

estrogen = proliferative (grows)

progesterone = secretory (prepares for implantation)

Front 68

asherman syndrome
-symptoms
-pathophys
-etiology

Back 68

-secondary amenorrhrea due to loss of the basalis (regenerative layer of the endometrium)

-due to overaggressive Dilation and curettage (D&C) procedure

Front 69

Curettage

Back 69

is the use of a curette (French, meaning scoop[1]) to remove tissue by scraping or scooping

Front 70

Anovulatory cycle
-pathophys

Back 70

presence of estrogen proliferative phase without progesterone driven secretory phase
-Thus there is endometriual growth without removal of progesterone and thus no endometrial wall shedding each cycle, and every cycle the endometrium grows, leading to abnormal blood vessel development

Front 71

Acute endometritis
-symptoms
-etiology

Back 71

fever, abnormal uterine bleeding, pelvic pain

-caused by bacterial infection of endometrium
-usually due to retained products of conception

Front 72

Chronic endometritis
-histo
-causes

Back 72

chronic inflammation of endometrium
-characterized by plasma cells
-caused by retained products of conception, chronic PID (from STD), IUD

Front 73

endometrial polyps

Back 73

-hyperplastic protrustion of endometrium
-present as abnormal uterine bleeding
-can arise by side effects of tamoxifen ( antagonist of estrogen receptor at breast, but agonist in endometrium)

Front 74

PID

Back 74

Pelvic inflammatory disease
(can lead to chronic endometritis)

Front 75

Inflammations of endometrium?

Back 75

acute and chronic endometritis

Front 76

Chronic endometritis
-hisopath?
-cause?

Back 76

PMN’s, lymphs and plasma cells

- Chronic PID
Retained elements of pregnancy
Intrauterine devices (IUD)

Front 77

order of progression of histological cellular features of endometrium

Back 77

-proliferative
-secretory
-predecidual
-PMN
-Menses

Front 78

2 broad categories of dysfunctional uterine bleeding?

Back 78

1) hormonally associate (progesterone/secretory phase)
2) other = fibroids and endometrial/endocervical polyps

Front 79

Anovulatory cycles

Back 79

Most common
Prolonged estrogen phase
Hyperplasia and breakdown

Front 80

main causes of dysfunctional uterine bleeding

Back 80

-Anovulatory cycles
-Inadequate luteal phase
-Oral contraceptives
-Menopause

Front 81

Inadequate luteal phase

Back 81

-Inadequate progesterone
-Infertility

Front 82

Acute endometritis:
-caused by?

Back 82

Miscarriage or post-partum

Front 83

Endometriosis
-define

Back 83

-abnormal placement of endometrial glands and stroma outside the uterine endometrial lining

Front 84

Endometriosis
-symptoms
-pathophys

Back 84

-dysmenorrhea (pain during menstruation), pelvic pain, infertility
-b/c abnormally place endometrial glands will also cycle during the menstrual cycle

Front 85

Endometriosis
-cause?

Back 85

1) Regurgitation -retrograde menstruation theory- (most popular)
2) metaplastic -endometrial metaplasia (differentiation from precursor tissue)
3) vascular/ lymphatics spread (lungs)

Front 86

what are the characteristics of endometriosis?

Back 86

hemorrhagic (chocolate) cysts (usually ovary)
-Stroma with “decidual” change and hemosiderin

Front 87

common sites of endometriosis occurrence?

Back 87

“Seeding pattern” (descending order)
Ovaries (chocolate cyst)> uterine ligaments > rectovaginal segment >
peritoneum > abdominal scars > umbilicus etc

Front 88

endometrial hyperplasia
-etiology

Back 88

**Prolonged estrogen stimulation**

-decreased progesterone- i.e., hormonal imbalance
-Menopause, tumors, hormone replacement therapy

Front 89

endometrial hyperplasia
-histology changes?

Back 89

-more glands (circles)

low grade - architectural changes (simple & complex)

High grade - architectural changes with cellular atypia

Front 90

what causes endometrial hyperplasia?
-how does it normally present

Back 90

-too much unopposed estrogen
-postmenopausal uterine bleeding (they have lost progesterone --> no shedding)
and they have estrogen still released not from ovaries but from adipocytes (aromatase) likely in a obese patient

Front 91

most important predictor for progression to carcinoma is?

Back 91

Cellular atypia

Front 92

Most common invasive gynecologic tumor?

Back 92

Endometrial carcinoma

Front 93

Endometrial carcinoma
-etiology?

Back 93

Prolonged estrogen stimulation and hyperplasia
(endometrial hyperplasia --> carcinoma)

Front 94

Endometrial carcinoma
-gross

Back 94

-Local polypoid mass or involving entire endometrial surface

Front 95

Endometrial carcinoma
-histopath

Back 95

Adenocarcinomas (85%)
Stratified columnar epithelium (normal is simple columnar)

Front 96

two pathways (types) to develop endometrial carcinoma?

Back 96

1) hyperplastic pathway leading to endometriod type
2) sporadic pathway leading to serous type

Front 97

endometriod endometrial carcinoma
-histopath

Back 97

Adenocarcinomas
-Stratified columnar epithelium

Front 98

Endometrial carcinoma, serous type
-histopath

Back 98

-serous looking
High grade with complex papillary features--> can form psamomma bodies
-Marked nuclear atypia
hypechromasia
atypical mitoses
prominent nucleoli

Front 99

Endometrial carcinoma, serous type
-associations?

Back 99

p53 mutations drives this pathway (early event)

Front 100

psamoma bodies?

Back 100

arise from concentric layers of calcification, from death of papillae that necrose and calcify

Front 101

key differences of Leiomyoma vs Leiomyosarcoma

Back 101

Leiomyoma = multiple masses

Leiomyosarcoma = single mass
= has necrosis
= seen in postmenopause (70-80 age)


-----> Leiomyoma does NOT become Leiomyosarcoma

Front 102

does Leiomyoma become Leiomyosarcoma?

Back 102

NO NO NO

Front 103

Leiomyosarcoma
-define
-etiology
-presentation
-histo

Back 103

malignant proliferation of smooth muscle from myometrium
-arises de novo
-seen in postmenopausal women
-single lesion with necrosis/hemorrhage
-necrosis, mitotic activity, cellular atypia

Front 104

Leiomyosarcoma
-histo

Back 104

necrosis/hemorrhage
-necrosis, mitotic activity, cellular atypia

Front 105

Leiomyosarcoma vs Leiomyoma
-lesions?

Back 105

sarcoma = single lesion (with necrosis mitotic activity)
myoma = multiple lesions

Front 106

Leiomyomas aka?

Back 106

(fibroids)

Front 107

Leiomyomas
-define path
-incidence
-presentation

Back 107

smooth muscle tumor of the uterine wall
-25% of ALL reproductive age women; higher in African
American
-clinical feature = asymptomatic

Front 108

Leiomyomas
-gross and histo

Back 108

multiple Whorled smooth muscle bundles ~ myometrium
-firm, round, gray-white masses. range in size, small to large

Front 109

Leiomyoma
-clinical features

Back 109

Asymptomatic,
Hormonally responsive (related to estrogen exposure)
-multiple well defined white whorled masses
-BENIGN

Front 110

Leiomyoma -

Back 110

leio means smooth
myoma means muscle

Front 111

age of Leiomyoma vs Leiomyosarcoma?

Back 111

Leiomyoma - premenopausal women (caused by estrogen)

Leiomyosarcoma- post menopausal

Front 112

Leiomyosarcoma
-gross and histo features?

Back 112

single lesion with necros, inc mitosis,and cellular atypia

Front 113

Leiomyosarcoma
-gross and histo features?

Back 113

single lesion with necros, inc mitosis,and cellular atypia