female Pathology Flashcards
infections that cause vulvitis
HPV, HSV, gonococcal, syphilis, candida
candida vulvitis, risk factor
pregnant ladies, diabetes mellitus
most common vulvitis infectious agent
HPV
HSV vulvitis presentation
vesicular eruption could be perioral or paranasal
valvulitis complications
Bartholin glands ducts obstruction
cyst and abscess
Unilateral & painful dilation of the glands
Lichen Sclerosis:
Fibrotic disorder & Presents as leukoplakia
Lichen Sclerosis etiology
20% family history of AIDS or lichen sclerosis
Lichen Sclerosis association
40% vulvar carcinoma
1%-5% SCC
Lichen Sclerosis presention
pruritus, introital stenosis
Lichen Sclerosis pathology
loss of rete ridges, thin epithelium, ecchymosis
Lichen Sclerosis therapy
tropical testosterone or progesterone
Lichen Simplex Chronicus
Thickening of the epithelium, Presents also as leukoplakia.
Lichen Simplex Chronicus clinical presentation
pruritus, Thick gray white skin
Lichen Simplex Chronicus pathology
Acanthosis & hyperkeratosis
Lichen Simplex Chronicus treatment
Topical corticosteroids
Leukopenia etiology
Nneds, vitiligo, inflammatory dermansses, cis, pager disease, invasive carcinoma
HPV related to which cancers
Vulvar, vagina, cervical, head, neck & laryngeal
HPV pathoognomonic
Koilocyres
HPV low-risk
6 & 11
HPV low risk association
Dm, pregnancy & immunosuppression
HPV high risk
16, 18, 31, 45
HPV high risk proteins
E6 & E7
Low risk HPV may involve
Perineum, vulva, vagina, cervix, gnus
VIN1
limited to the lower 1/3 of the epithelium
VIN2
limited to the lower 2/3, Mitoses are often seen
VIN3
beyond the lower 2/3 (whole thickness: CIS)
Vulvar malignant tumors incidence
Very rare: less than 1% of all tumors & 3% of FGT tumors
Vulvar malignant tumors median age
older than 60
high grade VIN if younger
Vulvar malignant tumors cancers
95%: SCC, 2% melanoma (Pigments), AdenoCA, Basal CC
Vulvar malignant tumor’s symptoms
pruritis, infections, bleeding, masses
frequent SCC type
older women (77), no HPV, well differentiated
frequent SCC associations
NNED (lichen Sclerosis), cigarette smoking & DM
less frequent SCC
younger (55), poorly differentiated, HPV
less frequent SCC associations
HPV 16, CIN, VIN & cigarette smoking.
SCC survival
less than 2cm 90% 5 years
larger 20% 10 years
Extra-mammary Paget’s disease
Intraepidermal adeno CA in vulva
Extra-mammary Paget’s disease association
underlying adeno CA in 1/3 of cases
Extra-mammary Paget’s disease origin
multipotential epidermal cells.
Extra-mammary Paget’s disease manifestion
red scaly crusted plaque, may mimic appearance of inflammatory dermatitis.
Congenital vaginal anomalies
uncommon
Total absence of vagina (vaginal agenesis)
Septate or double vagina
Vaginitis
common, transit
atrophic Vaginitis
postmenopausal women
vaginitis infectious agents
Gonorrhoeal, candida albicans, trichomonas vaginalis, STD
Vaginal tumors
Adenocarcinoma, melanoma, sarcoma & SCC (95%)
Most common vaginal tumor
SCC
Highly malignant vaginal tumor
Sarcoma
Comments vaginal childhood umm
Sarcoma, (below 5 average 3)
Embryonal rhabdomyosarcoma is seen in
sarcoma
Embryonal rhabdomyosarcoma
mimics skeletal MC rhabdomyoblasts
cambium
condensation of malignant cells under mucosal surface
Sarcoma grossly
polypoid grape like mass protrude out of the vagina.
Exocervix epithelium
Non kertanized stratified squamous
Endocervix epithelium
Columnar
Cervicitis
Common condition with purulent vaginal discharge
Pop smear reduced mortality by
99 %
LSIL
Koiolocytosis
CIN 1
Mild dysplasia, (lower1/3 of epithelium): LSIL
CIN2
Moder dysplasia (lower2/3):HSIL
CIN3
more than 2/3 or totally involved, sever dysplasia or carcinoma, HSIL
can be detected in ____ of precancerous lesions & invasive malignancies.
85-90%
pathogensis of latent HPV
Integrates its DNA → Intranuclear replication or episomal
pathogensis of chromosomal HPV
E6 inhibits P53
E7 inhibirs RB
endocervix CA it is an ____ CA unlike the Exocervix Which is _____ ca.
adeno, sc
most effective method of cancer prevention
Detection of precursor lesions by cytological examination & their eradication
(?) of the population might be exposed to HPV
75%
(?) exposed to high risk HPV
50%
(?) exposed to HPV-induced CIN
10%
microinvasive Cervical Carcinoma
<3mm
invasive Cervical Carcinoma
exophytic (papillary), ulcerative (infiltrative),, nodular
cervical carcinoma SCC: ___ Adenoca: ___
80%, 10%
cervical carcinoma complications
Hydronephrosis (causes obstruction), pyelonephritis
Renal failure.
Lymphatic spread to regional pelvic nodes.
Vascular to lungs and liver
Endometritis
inflammation of the uterus endometrium
acute Endometritis etiology
N. gonorrhea or C. trachomatis after delivery or miscarriages.
acute Endometritis symptoms
Higher grade fever, intense abdominal pain, menstrual abnormalities, ectopic pregnancy, infertility
Chronic endometritis etiology
Chronic gonorrheal pelvic disease
Tuberculosis
Postpartal or postabortal endometrial cavities
IUCDs: considered foreign bodies producing infection Spontaneously in 15% of patients.
Chronic endometritis symptoms
Lower grade fever & vague abdominal or pelvic pain
Chronic endometritis pathognomonic
plasma cells
Adenomyosis
Growth of basal cell layer of endometrium down into the myometrium (No cyclical bleeding).
Adenomyosis symptoms
Menorrhagia (interfere with vascularity), dysmenorrhea, pelvic pain before onset of menstruation
Adenomyosis complications
Reactive hypertrophy of myometriumm leading to thickened uterine wall (detected by US image).
Endometriosis
Presence of endo. tissue (functional: respond to cyclical changes) in remote sites:
where does Endometriosis occur
Ovaries (More common), Ovarian cyst might appear
Douglas pouch, uterine ligaments
tubes, peritoneal cavity, umbilicus
Uncommonly in LN, lungs, heart, & bone
Endometriosis: clinical symptoms
Pain on defecation / Infertility / Dyspareunia & Dysuria (pain induced by cyclical changes), severe dysmenorrhea, pelvic pain (In almost all cases) & Abdominal discomfort.
The favored theory
regurgitation of menstrual blood flow to fallopian tubes and ovaries.
Benign mets theory
that endometrium spread to different sites via blood vessels of lymphatics
Metaplastic theory
endometrium differentiation of coelomic epithelium is the real source
Extrautarine, extrapelvic theory
circulating stem cells from BM, differentiate into endometrial tissue.
Endometriosis grossly
Red blue to yellow brown implants, discoloration.
Variability in size & Chocolate cyst, as the blood ages, it turns brown.
Fibrosis, leading to adherence of pelvic structures, sealing of tubal fimbiriated ends (Infertility)
The most common problem for which women seek medical attention
Dysfunctional uterine bleeding:
Menorrhagia
profuse or prolonged bleeding at time of period
Metrorrhagia
irregular bleeding between the periods.
abnormal uterine bleeding common causes
polyps, leiomyomas, endometrial carcinoma, endometrial hyperplasia, and endometritis.
abnormal bleeding in the absence of organic uterine lesion
DUB
DUB causes
Anovulatory cycles (failure to ovulate) → excess of estrogen.
Inadequate luteal phase → delayed or underdevelopment of secretory phase.
Endomyometrial disorders; chronic endometritis, endometrial polyps, submucosal fibroids.
OCP
DUB causes in Prepuberty
Precocious puberty (hypothalamic, pituitary, or ovarian origin)
DUB causes in Adolescence
Abnormality within hormones – Anovulatory cycle
DUB causes in Postmenopause
Endometrial atrophy (hormone loss), but should role
out Organic lesions first (carcinoma, hyperplasia, polyps).
DUB causes in Reproductive age
Complications of pregnancy (abortion, trophoblastic disease, ectopic pregnancy)
Organic lesions (leiomyoma, adenomyosis, polyps, endometrial hyperplasia, carcinoma)
Anovulatory cycles and Ovulatory dysfunctional bleeding (inadequate luteal phase)
you must role out _____ first to consider DUB in Reproductive age group
pregnancy
DUB causes in Perimenopause
might have Anovulatory cycle, irregular shedding or organic (CA, HP, polyps).
Endometrial hyperplasia etiology
Excess unopposed estrogen
Excess unopposed estrogen seen in
Anovulatory cycles, Polycystic ovarian disease
Prolonged administration of estrogenic steroids.
Estrogen producing tumors (granulosa-theca cell
tumors, cortical stromal hyperplasia)
Obesity.
Endometrial hyperplasia classified according to what
presence of atypia
incident of Endometrial hyperplasia with atypia
20%-50%
The most frequent CA of FGT
Endometrial adenocarcinoma
Endometrial adenocarcinoma median age
55-65 (menopausal and postmenopausal women)
Endometrial adenocarcinoma predisposing factors
estrogen stimulation due
endometrial hyperplasia, obesity, Infertility (single & nulliparous), late menopause, diabetes, HTN.
Endometrial adenocarcinoma types
Endometroid, Serous, clear cell, adenosquamous
common Endometrial adenocarcinoma
Endometroid
Endometrial adenocarcinoma Estrogen related, Associated with hyperplasia
endometroid
endometroid younger or older women
younger perimenpause
Microsatellite instability & PTEN gene mutations
endometroid
Endometrial adenocarcinoma Unrelated to estrogen, not associated with hyperplasia
Serous, clear cell, adenosquamous
Serous, clear cell, adenosquamous younger or older women
older
Endometrial adenocarcinoma mutation TP53
seros
Endometrial adenocarcinoma most aggressive type
adenosquamos
syndromes have increased risk to develop endometrium CANCERS
Cowden’s syndrome, HNPCC
HNPCC
Inherited genetic defect in DNA mismatch repair gene
Clinical course of endometrial adenocarcinoma
Irregular bleeding & marked leukorrhea (vaginal secretion) , Enlarged uterus & palpable, fixation to surroundings.
endometrial adenocarcinoma survival rate
stage 1 carcinoma has 90% 5 YSR
Stage 3 & 4 have less than 20% 5 YSR.
Most common benign tumor arising from uterine smooth muscle in females
Leiomyoma
Found in 30%-50% of women of reproductive age
leiomyoma
Leiomyoma common in which race
black
Leiomyoma grossly
Well circumscribed, round, often multiple, firm to hard, gray-white.
Monoclonal T with nonrandom chromosomal abnormalities in 40% of tumors
leiomyoma
leiomyoma symptoms
asymptomatic, menorrhagia &infertility
Leiomyoma shape
Sharply demarcated, Whorled cut surfaces (wrinkled), Single or multiple, Variably sized.
Leiomyosarcoma etilogy
denovo
Smooth muscle tumors of uncertain malignant potential
Leiomyosarcoma
Leiomyosarcoma features
tumor necrosis, cytologic atypia, mitotic activity.
Leiomyosarcoma survival rate
40% 5 years
most common disease; component of PID.
Salpingitis
Salpingitis symptoms
Fever, lower abdominal pain, or pelvic pain.
Pelvic mass, adherence leading to tubo-ovarian abscess.
Salpingitis complications
Increase risk of tubal pregnancy (Permanent sterility) – Dysfunctional cilia.
Acute Salpingitis etiology
MO: NG, C.trachomatis, Mycoplasma hominis, U.urealyticum
Sources of infections: VTD from the LGT.
Puerperal or post abortive, especially after IU instrumentation.
Intra-abdominal infections following peritonitis.
Hematogenous as in TB.
Primary adenocarcinoma origin
Papillary serous (derived from epithelium), or endometrioid (Mimic Endometrial Gland)
Primary adenocarcinoma common site
fimbria
Primary adenocarcinoma mutation
BRCA
Primary adenocarcinoma presention
advanced stage, with involvement of the peritoneal cavity.
Ovarian cysts origin
unruptured graffian follicles
Ovarian cysts placement
immediately subjacent to serosal covering
Ovarian cyst’s symptoms
Small, clear serous fluid, Pelvic pain, acute abdominal symptoms
Polycystic ovaries etiology
Oligomenorrhea, hirsutism, infertility, obesity.
Polycystic ovaries presention
Excessive estrogens & andorgens & some insulin resistant (Ovary twice the normal size).
Thickened fibrotic outer tunica, numerous cysts lined by granulosa
cells with hypertrophic and hyperplastic lutenized theca interna.
Absence of corpora lutea.
Polycystic ovaries
5th common CA in US & 5th leading cause of CA death in women.
Ovarian Tumors
Familial cases of ovarian tumors
Breast ovary syndrome related to BRCA 1
Ovary, endometrium and colon (Lynch II): DNA mismatch repair gene mutation
overian tumor rf
↑ risk: Nulliparity (1.5-3.2 folds), Drugs (induce ovulation but have not become pregnant)
OCP ↓ risk by 1/2
Surface epithelial stromal tumors origin
multipotential coelomic covering epithelium
Surface epithelial stromal tumors malignant or benign
90% malignant
recapitulate the components of the Mullerian ducts.
Surface epithelial stromal tumors
Serous Tumors median age
30-40
Serous Tumors incident
60% benign (25% are bilateral), 15% malignant, 25% LMP.
LMP & M serous account for 60% of all ovarian CAs.
most common malignant & bilateral tumour of the ovary
Serous cystadenocarcinoma
Psammoma bodies
Serous Tumors
Serous Tumors growth pattern
papillary
Serous Tumors size
large, 30-40cm
Serous Tumors borderline
Delicate papillary projections, Milder atypia, No or little stromal invasion.
Serous Tumors carcinoma
Large bulky tumor mass, Anaplasia & stromal invasion.
Mucinous Tumors median age
30-40
Mucinous Tumors incident
80% benign (5% bilateral), 10% malignant (20% bilateral), 10% LMP.
pseudomyxoma peritonei
Mucinous Tumors met to git
Mucinous Tumors met or rupture
pseudomyxoma peritonei
Krukenberg
mets of mucinous T of GIT
Krukenberg presention
bilateral, glands infiltrating ovarian stroma, dirty necrosis.
Teratomas incidence of ovarian tumors
15%-20%
Teratomas age group
first two decades
Teratomas incidence
> 90% benign
90% unilateral
Commonest germ cell tumor in women
Mature cystic teratoma
Mature cystic teratoma differentiation
somatic
dermoid cysts found in
Mature cystic teratoma
placental infections predisposing conditions
Premature rupture of membranes (>18 hours),
placental infections mo
Mycoplasma, candida, vaginal flora
placental infection’s complications
congenital pneumonia, gastroenteritis, otitis media, meningitis.
placental infection’s pathogensis
ascending and hematogenous
Acute villitis etiology
maternal sepsis, Syphilis, TB, listeriosis, toxoplasmosis., viruses.
where does Ectopic pregnancy occure
ovaries (90%) , abdominal cavity, IU portion of the oviduct (interstitial pregnancy).
Ectopic pregnancy etiology
chronic inflammatory changes, IU tumors, or endometriosis.
50%; no anatomic cause identified.
Ectopic pregnancy complications
Hematosalpinx; intratubal hematoma.
Intense abdominal pain, can lead to shock.
trophoblastic diseases etiology
Empty (NO M.dna) ovum fertilized by either 2 sperms or one diploid sperm.
trophoblastic diseases histology
Large avascular villi with central edema & circumferential trophoblasts proliferation.
mass of grape like vesicles.
trophoblastic diseases
Choriocarcinoma age group
<20 & 40<
Choriocarcinoma etiology
50% follow complete mole, 25% follow abortions.
24% follow normal pregnancy, 1% follow ectopic pregnanc
Choriocarcinoma clinical
Very high titers of bhCG, Vaginal bleeding and discharge.
Hemorrhagic tumor with anaplasic sycytio and cytotrophoblasts, NO chorionic villi seen.
Choriocarcinoma met
lungs (50%), vagina (30-40%), brain, liver, kidneys.