W10. Diseases of femal genital system (begge pp) Flashcards
inflammatory disroders -sexual transmitted
- treponema pallidum (spirochete)–>syphilis. most common STD
₋ Neisseria gonorrheae->purulent infla
₋ Gardnerella vaginalis
₋ chlamydia trachomatis (rickettsia)->most common bacterial stf
₋ viruses - HPV (serotypes 6,11)->most common viral STD
- herpes simplex/ zoster
- CMV, HIV
inflammatory disroders -nonsexual
Nonsexual transmitted:
₋ actinomyces israelii
₋ mycobacterium tuberculosis
₋ candida albican
vuulva is what and what does it include
external female genitals
-clitoris
-flotroal hood
-outer and inner labia
- vaginal opening
-urethraø openeing
non infectious inflammatory disorders by vulvua
chronic non infectionus
Leukoplakia
-white spots bc of ^keratinization of epidermis
-weel demarcated
Kraurosis
-shrinkage bc acc of fibriotis tissue
-
hwo are the infectious infla disorders of vulva spreafing
- from vincinity
A. ant->urethra =urinary area
B. post–>anus = rectal area - vaginal discharge
-vuvlovaginitis-both vagina and the vulvua bc discahreg will affectt it
bacterial infections of vulvula
- coccus bacteria
- chlamydia
- syphilis
4.gonorhea - candidias
- herpes simplex
- granulomas inguinale/venerum
- chancroid
coccus bacteria (vuvla)
- staphylococcus
- localized infection-abscess
-purulent infection=abscess - streptococus-
-diffuse=phlegmona
chlamydia
-responsible for what
-responsible for lymphogranuloma
venerum
-one of most common STD
lymohogranuloma venerum types (chlamydia)
L1,L2,L3
- erosion /ulcer in the area where clahmydia penetarte epidermis
- paindul lymphadenititis
- abscess, fistulas(regional lymp tissue–>lymphangitis and adenitits–>IS responese–>necrosis+liquefaction–>suppurative lymphadenitits–>pus->abs-> enlarge , inf and pus filled LN–>rupture –>driang absess–>^risk of fistula eller sinus tract
-healed–>fibrosis–>stenosis pf blood and lymoh vv
syphilis -treponema pallidum
-dvelopemtn
- chancre: small,painless, ulcerated noduel+LN swell
-vagina or vulva
-glans of penis
-infla–>LN swell - 1-3 months: diffuse macopapular eruption, febrilias, lymphadenitis
-spreding–>systemic manifestation - moths(year: teritary systemic syphilis
-gummas(granulomatous localized infla)
- neurosyphilis:neurological dysfunction affecting dorsal root of SC–>lose skin senisitivyty
-cardiovascular syphilis:large vv contain masse elastin–>aneurysm of aorta–>rupture–>beøeeding–>lethal
gonorhhea
-infection of paarurethral and bartholins galnd (urethral+parauretral glad)
-secual transmitted purulent
- prurlent dischatrge
candidas
-not sexually
-normal flora-50%
-fungi in skin
-pregnancy, DM, corticotherapu
-thick curdy disharge, pruritus, pain, dyspareunia (like cheese, painful sex)
-vagina always affected
herpes simplex
-type
-pahses
-2 type is moee common
1. 3-7 days after infection
-flu like symp: febrile, headache, myalgia(muscle ache)
-vulvar erythema and edema, serous infla
-pailful burdning and stinging
- 12-48 haurs, lasting 10-12 days
- formation of blisters and bullas, erosions, purulent infl. lymphadenopathy
-antibiotics - phase: recidivas by immunosuppression, stress, UV light
- spreading along peripheral nerves
-less sever formation of painful blister:erythema irritation of skin w blisters
-NO DIFFUSING
-self limited
Granuloma inguinale /granuloma venerum
-klebsilla granulomatosis
-sexual trabsmission(fecal contact
-typical is purulent inflammation, local spread to regional LN
-chronic infla–>post infla stenoses
chancroid
-soft chancre, ulcus molles—-
-haemophylus ducreyi (Gram-streptobacilus)
-multiple painful purulent vulvar papule and ulcers
-lymphadenopathy with abscess formation
-healing by fibrotisation
-they cause purulent inflammation of the LNs and Lymphatic vessels of vulva, so they have similar manifestations
₋ healed by fibrotisation and deform vulva and destroy the lymphal drainage–>
lymphostenosis
₋ so better treated in early stages
inflammation of bartholins gland
ducts and gland prone to infalmmaiton,–>fibrosis–>obstruction of duct of gland–>acc of secrete–>purulent inflammation==>cyst of abetholion gland
bathrolin gland cyst or acute bartholinitis
mucous gland
bartholinitis is purulent inflammation
if not surgically treated, the blocked duct
(postinflammation stenosis) will keep the mucous
accumulated and form a cys
ectopic mammary tissue
-develops
-disroders
-develops form milk line crest: from clavicle–>middle of chest–>abdomen–>into inguina
disroders
-act by hormonal stimulaiton
-lactation, fibrocystic disease, tumors
Humnan papilloma virus
-most common secually infection
-Most common type: 6,11
-asymp and mininal clinical
-oncogenic: 16,18,31
bening lesions
-condylomas lata: ^prolif of epidermis–>thick
-common wart: lovcalised infection, femanl genital
-papilloma: prolif of squamos epo,
vulvular intra epi lesion (VIN)
-dysplasia
-precancerous
-caused by HPV 16,18,31
developemtn of valcular intraepi neoplasia=bowens dermatitis (Dysplasia)
- bowmans dermatitis-dysplasia of epidermis
-diff is that bowmans happen all oever skin but VIN only vulva, vagina, cervix
most common malignancy of vulva
spinocellular carcinoma of vulvula
- elederly women, 60-70y, local spred(vagina, LN)
subtypes
1. HPV associated(papilloma, bowen disease, <60 y
- chronic inflammation, >70y
sec most common malignancy of vulca is
malignant melanoma
- anywere melanocytes are: anus, femal genital, bulb of eye
-5-10% of malignanc
-disseminate
most common agents responsible for vaginitis
microbial picture of vulva-MVP
MPV 1-6
MPV I. –normal microbial flora
(lactobacillus acidofilus): chnage glycogen to lactose, respon for acidic enviroment, protect vahina
₋ MPV II. – bacterial purulent inflammation
₋ MPV III. bacterial nonpurulent inflammation
₋ MPV IV. – gonorrhoic inflammation
₋ MPV V. –trichomonad inflammation
₋ MPV VI. –candidous inflammation
vaginosis
disturbance of MOP I. by alkali environment - inflammation of vulva with rich discharge
without distinct clinical symptomatolog
bening vaginal tumors
papilloma-w or wout keratinzation
squamos papilloma-w keratinization
tubuvilous adenoma
most common maligant tumor of vagina
spinocellular carcinoma
- upper third of vagina
-silent, painless bloody discharge
-ulcerating muvosa–>bleeding
embryonal rhabdomysarcoma-maligannt of vagina
- children-90% <5 y
-botryoid: like bunch of grapes
-composed of immature cells of SM
part of uterus
exocervic:
-part of cervix exposed to vagina
-stratified SQUAMOS epi
endocervix
-single layer tall COLUMNAr/GLANDULAR mucus secreting
- channel inside cervix
squamos columnar junctuin: junctional mucosa
what happens with vaginal epi durinng growing
glandular epi extend to surface of cervical channel=ectopy
next that happens is it meet acidic enviroment and will undergo squamos metaplasia =squamos epi
so the cells are changed into the squamous
epithelium again, which block the duct of the glands
mucous accumulate in the duct and becomes cyst=NABOTHIAN CYSTS
chronic cervicitis
-common
-asymp
- all STD, inf disorder form lower genital sys
Complications
1.ascendant spread–>PID-pelvic inflammatory disease
- bacteria spred up to endometrium, ovary, fallopian tube
2. tumorigenesis
3. development of endocervical polyps
4. pregnancy:a bortion, premature delievru
5. chorioamnitis. stillbirth
6. neonatal pneumonia/seoticaemi
7.postpartum endometritis
HOV of uteri
-cervix most common site
- signs: acanthosis(thick squamos epi)+papillomatosis(prolif of epi and intrude into dermis)+mitotic activity(+kilocytosis(nuclear enlargment, irr membrane, darker, clear area around(bc acc of glycogen) nucleus, (nuclei wdeformated:wrinkled, dense and small liker aisin)
=cytopathic effect
precancerosis of uterus cervic: cervical intraepo neoplasia-CIN
development of CIN I CIN II CIN III CIS-carcinoma in situ
caharcteristic for all grades:
dysplastic nucleo w irr outline, denser chromatin, distinct nucleoli, ^mitotic activity
grade 1:eneste LOW GRADE
- 1:3 third of lower squamos
-only base of epi is dyspalstic
mild lesion, not severe
grade 2:
-moderate
-in lower 2/3
-
grade 3:
-upper third
CIS
-whole epi
- still siperficial chnages are present
risk factors of precancerosis of cervic uteri(CIN)
factors increasing the risk of HPV infection- early sexual life, multiple partners, promiscuity
of partners
long-term oral contraceptives- early first pregnancy, high parity- low socioeconomic status- other sexually transmitted disorders- smoking, diet, poor hygiene
carcinoma of cervic uteri
spincellualr carcinoma :80%
-developing countries
-3. most common female mortal cancer (after lung, breast)
-medial age 40-50 years
adenocarcinoma-10-15%
-conventional and mucinous type
risk factors+MTS :carcinoma of uterus cervic
HPV (16, 18, 31, 33, 35, 39, 45. 51, 52, 56, 58, 59, 66) => risk factors identical for HPV infection- local spread to vicinity: uterus, vagina, parametrium,
urinary system- MTS ad LU, lung, bone, ovarium
tumor of cervic uteri: symptomalogy and complicaiton+ mts
symptomatology:
-bleeding from vagina
- pain, swelling, itching
complications
-if upward spreding –<uterus: extensive uterine bleeding
- ant to urinary wall: hematuria, incontinence of urine and urinary infections
-psot to rextal wall: blood in stool, incontinence of stoll, tenesmus-painful defecation
mts:
-regional ln
-lungs
-liver
cervical conisation
excision of cone shaped sample from mucous membrane of cervix
-laser
-loop electrical excision
-surgical knife
cold knife
amputaiton
invasive cervical cancer
-^40-60y
-developing countries
-^squamocolomunar junction
-exophyattic /infiltatet growth
layers of uterus
inner: endo
middle: myo-muscular wall
external: parametrium
metrorrhagia
- irr, frquent bleeding
- not assiated with menstrual cycle
-m
menorrhagia/hypermenorrhagia
excessive(prolonged menstruatuion
menoorhagia: prolonged menstruation
hyper: menstrual blededing is stornger and more intense
1st etiology for functional disorders are disturbances of
ovulation cycle
anovulatory cycle: Graafian follicle doesn’t rupture and release egg, but still produce estrogen (hyperplasia of endometrium)(no progesterone produced)
inadequate luteal phase: Graafian follicle ruptures, but the corpus leuteum is small and weak, not strong enough to produce adequate amount of progesterone
hypoprogesteronism, so again the problem of mucosal development and cause bleeding
irregular endometrium, in the patient at one time, we can see different stages (early, middle, late) of proliferative phase, or of secretory phase
mix endometrium: combination of proliferative +
secretive endometrium
acute endometritis
-after birth, abortion, instrumentation
-basically after dilation of cervical cahnnel
chronic endometritis
-what
clincial
- consqeunce of acute
- chronic mucosal irritation
-bacterial of viral
clinical manifestation
- bloody discharge
-menorrhagia/ metrorhagia
-pelvic pain
-infertility
-asymptomatic
complications of chronic endometritis
1.PID
- tubes and ovary
2.pyometra
-uterine cavity filled with pus
3. hematometra
-uterine cavity filled with hemtoma,extensive blleding of uterus
1 %2 proone to ruptureing
adenomyosis(endometriosis interna)
-presence of endometrial mucosa in smooth muscle of uterus
-21-25% of women =1/3 of women
-hypermenorrhea, dysmenorrhea
rupture of uterus in pregnancy
micro:
-thikening of wall of uterus
-small cavities
endometrososi
-what
clinical
-occurence of endometrial mucosa outside of uterus
- 10-15% of women, mainly in reproductive age
-every part of female genital +urinary system, peritoneum, intestine, LN, peripheral nerve, muscle
metastatic theory:spreading of endometrium from uterus
* through uterine tube to peritoneum
* through lymphatic and blood vessels
* direct implantation by surgery, SC
-most common oavry or follapoan tube
- metaplastic theory – metaplasia from peritoneal lining
clincal:only inferticle women bc MC active and mucosa functional
dysmenorrhea
abdominal and pelvic pain
dyspareunia
irregular bleeding
infertility (30%)
local associated complications (intestine, peritoneum
endometrial polyp
-develops by hormonal disroder, tamoxifen therapy
-pseudotumors lesions
- not true, overprolif of endometrial mucosa
-caused by overprod of estorgen aka fertile women
-in premenopausal postmenopausal women (estrogen)
-13-17% of women, 25% causes of uterine bleeding(bc large –>compress mucosa–>atrophy or ulceration–>bleeding
endometrial hyperplasia
-precancerous lesion
-come from lon term estrogen overstimulation
categories:
1. simplex hyperpklasia
- prolif of endometrial gland and stroma
-like prolif phase of MC
-large cysts
- compelc hyperplasia
-endometrium composed mainly of clands
-less stroma - atypia
- happens in both
uterine non-neoplastic diseases
bleeding
₋ metrorrhagia
₋ menorrhagia
₋ hypermenorrhea
functional disorders
inflammation of endometrium
adenomyosis and endometriosis
endometrial polyp
endometrial hyperplasia
endometrial intraepi neoplasia-EIN
-what
-criterias
-chronic estrogen stimulation
- as complex hyperplasa w atypia
criterias
1. ratio of endo gland/stroma >50%(more glands)
2. cytological atypia: cell lingin gland not functional
3. size of lesion >1mm
endometrial carcinoma
- who
-riskfactors
-most common malignancy of female genital, 4th. female mal. – affect all ages (mainly postmenopausal women)
-risk factors: obesity, DM, hypertension, infertility, ovarian disturbances, ovarian dysgenesis, tamoxiphen
types of endometrial carcinoma
I-type – estrogen dependent– proceeded by hyperplasia
-classical risk factors
-endometroid Ca and low-grade Ca
II. II. type –estrogen independent
-Serous carcinoma, clear cell Ca high-grade –
carcinomas
-in elderly postmenopausal w.
-worse prognosis
-local spread +MTS ad lung, bone, liver, brain, skin
endometroid carcinoma
80% of all carcinomas
grades
first 2 grades=low grade, estrogen related
grade 3: high, estrogen independent
garde 1:
-only glandular structures, no solid tumorus burden
-weel diff endometrial carcinoma
grade 2: solid component make up 50% of tumor
garde 3: ore than 50
other types:estrogen independent
1. squamos differentiation: samme som endomertrial carcinoma
2. villoglandular endometroid carinoma
3. secretory tyoes
endometrial carcinoma growth
exopthitic: toward lumen
-hood bc not deep penetration
endophytic: toward wall
-MTS
endometrial carcinoma:serous and clear cell carcinoma
both estrogen independent
serous:
-aggresive
-ovary, but also endometrium
- distinct branches apperance
clear cell
-glycogen and fat
-pale
-
endometrial stroma tumors
endom, stromal nodule
- being,
-normal lloking stroma w/o atypioa and mitosis
endom.stromal sarcoma
-not well demarctaed
-stromal cells with atypia and mitrosis
mullerian carcinosarcoma-homo and heterlogues (malignant mixed mullerian tumors)
both epi and mesenchymal
-most common
homologous:
-sarcomatous components(stroma) resemble normal endometrial stromal sarcoma
hetero:
-stromal componet dont match the
mullerian adenosarcoma( (malignant mixed mullerian tumors)
-epi (glandular) component is being and stromal(mesenchumal) compnent is malignant
msot common tumor of uterine wall is
leiomyoma
leiomyoma(smooth muscle cell tumor of endometrium
-what
-who
-micro
-^bening uterine tumor of smooth muscle origin-most common in uterus, small bowel and eso
-solitary/multiple
-40%, >50y
- aymptomatc
-infertilty
-compression of surrounding structures
micro
-circumscribed, firm, nodular
-often multiple->uterus myomatosus
leiomyoma
-clinical
-structure
depends on localization
1. sub-endometrial myomas(under mucosa): pressire–>atrophy and bleeding
2. intramural: stretchin of smooth muscle–>pain bc dilation
3. sub-serous(arising form surface of uterus): asymptomato
structure
-well diff smooth muscle
-no morphological disturbances
-ususally large–>cant be supplied by normal vv–>ischemia and regressive chnages–>fibrotic degeneation, red or hdyrpic
leiomyosarcoma
-what
-looks
-who
-clinical
-growth
-mts
-true malgannt
- pleomprphic apperance
-high grade obci
-40-60th
-enlargment of uterus, bleeding
-diffuse/polypoid growth
-,ts->lungs, liver, bones, brain
STUMP-smooth mucle cell tumors of myometrium
-uncertain maligannt poteinal
-featuires of maligancy but behave bening
-severe atypical features
recurrence or MTS
3 ways of inflammation development in follapian tube
- ascendant
-form lower genital sys
-microflora of vagina destroyed–>cervical channel dilated–>spread thorug - hematogenous
- TB - parametrial vv
- infection spread form vivinty by LN or blood
consequence of this spred is acut of chronic infla of fallopian tube=salpingitis
salpingitis-acute and chronci
acute:
-ascendant bacterial spreading–>PID
chrinic:
-from acute
-adhesions-sterility, extrauterine growth): fibrotization–>adhesions–>impermapble for eggg thorugh fallopian–>infertility and extrauterine gravidity
-
salpingitis -complications
- Pyosalpinx:
- filled with pus
- plugging–>acite infla–<dilation +pus - hydrosalpinx:
-pus resolved by macrophess–>clear fluod remain - tubo-ovarian abcess
- ovarian tube or ovary
- prevent spreaf of bacteria to abd cavity (Salpinc opens into abd)–>tube attach to surface of obary–>fusion–<goblet of infected organs–<abscess - tuberculos salpingits
acute salpingitis-micro
odema
acute infla infiltarte of neutrophils
purulent exsudate w leucocytes and epi cells
chronci salpingits-chronic
lymohocytes, plasmacells, fibrosis
TBC salpingitis
secondary to focues elsewhere in the body
haematogenous route -^lungs
caseating grnulomas in tubal wall+chornic infla
PID
-what
-spreding
-agents
-clincal
-complicaitons
inflammatory disorders of small pelvic
₋ development mainly by ascendant spreading
₋ spreading of inflammation from primary focus
to vicinity
₋ most common agents: Neisseria g., chlamydias,
streptococci, staphylococci (most common
mixture of several agents)
₋ clinical manifestation:
* chronic pain in small pelvic
* dyspareunia, febrilias, discharge, bleeding, urinary symptoms
₋ complications: peritonitis, adhesions (ileus),
infertility, bacteremia (endocarditis, inf.
arthritis, meningitis)
ectopic pregnancy
-what
implants of blastocyst outside endometrium
fallopian tube (95%)
₋ up to 1% of pregnancies
₋ etiology: unknown – chronic salpingitis (88%)(bc fibrotization)
clinic: amenorrhea(absence of menstruation), uterine bleeding, abdominal pain
rupture abdominal/intraperiotneal bleeding
risk factors: PID, tubal surgery, IUD, congenitAL ANOMALIES
ovarian dysgenesis
-varibale disturbances of the content of sex chromosomes
-resut of dyspmorphic gonads–>abnormal morhplogy of genital system: loike not functionnaly secreting hormones to for their development
- gonads are afunctional->dont make mature sperm or obum–>sterile
- gonads are prone to malingant transformaiton
turners:fibr.undiff, female,
true hermaphroditis: testes+ovarium, both
ovarian inflammation
-most common ascendant inf fomr uterus
-tubes always affected->PID
-yuboovarial abscess->rupture->peritonits
-healing: fibrosis->infertility
ovarian cysts-types
- inclusion cyts:
-most common
-from superficail epi
-ovulation–>graafian follicle rupture->expelled form ovary–>fragmented surfca eof epi develop cusys
-common, asymp - follicular
- symtomatic, menstrual abnormalitis, rupture–>bleeding
- anovulatory cycle–>graafian follicle cont rupture
. hyperestrogenoism - lutein cyst
-symtomatic, menstrual abnormalitis, rupture–>bleeding
- extensive vleeding into corpus luteum
-mor eprogestrone - multicystic changed ovarial stromal hyperplasia
- small cyst can ariese
stein-leventhal syndrome -polycystc ovaries
-develoment on basis of hormonal syrregulation
-blockage of follicular development
-amenorrhea+sterility, oftened endometrial hyperplasia
steps
1. dysreg of CNS:
-disturbance f prod of FSH
-^Lh ->dysreg of normal androgen secretion to ovary->^intraovarian androgen sti instead of estroegn->foliccular atresia, atrophy and hyperandrogenesia=> masculinsm of women(hair, alopecia, acne, hirsutism) or androgens chnages into estorgen(both hyperandrogen and estorgen
Bilaterally enlarged and cystic ovaries – excessive production of androgens, low levels of female hormons
Ovarian tumors: classification
- tumors from epithelial surface (epithelial tumors)
- tumors of germ cells
(germinal tumors) - tumors from supporting cells
(“sex cord/stromal tumors”)
-cells which support the immature eggs
-cells develop form ovarian stroma
Ovarian carcinoma
-who
-riskfactors
-clincial
-asymptomatic bc plenty of place to grow
- older women 63 y
-risk factors:childless, early menarche, late menopause, endometriosis,
inflammation, weight, age
clinical:
- pelvic abdominal pain, abdominal swelling, malaise, gastrointestinal complaints
-asymptomatic
-presence of metastases, paraneoplastic signs
mts: contralt ovarium, peritoneum, LN, liver, lungs and pleura
follicular cyst
aka: >3cm, serous fluid, granulosa cells lining-flattend cells
luteal cyst/corpus luetum cyst
-> 3cm
after corpus luteum organization
-lined by luteinesed granulos cells
endometrioma
chocloate cyst
åaraovarial cyst
thin walled cysts
surface epi tumors:
-geeral
-diginity
-most common ovarian tunors
-mullerin oriigin-vagina, uteeus, uterine tube
-bilat, cystic chnaged tunmors, papillary sturcutre
dignigty
-bening-cystic: mucus inside
-malignant:
-borderline: increased gwoth but dont disrupt membrane aka dont MTS, low malignant potential
surface epi tumors-serous tumors
-50% of ovarian tumors, 90% of malignancies
₋ 60% benign, 10% borderline, 30% malignan
general
-metaplasia form surface/coelomic epi-differntiate along tubal-type(like fallopian tube) of epio
-unilat/bilat
-uniocular/mutliocular, contain serous fluid
cystadenoma, papillary cystadenoma ,cystadenocarcinoma
Surface epithelial tumors-mucinous tumir
15% ovarian Tu, 10% of malignancies
₋ intestinal/ Müllerian (cervical) type
general:
- metaplasia form surface(coelomic epi-differntiate along endocervical type/intestinal type of mucosa
-uni/bilat
-uniocular/mutli, contain mcuin
mucinous cystandenoma–>mucinous bordelrine tumor–>mmucinos cystadenocarcinoma
surface epi tumors-endometrial tumors
-3% of ovarian Tu, 15% of malignancies – 1/3 associated with endometriosis,
-15-20% with endometrial Ca
general:
-from coelomic epi-dffierantietd toward endometrial type of epi
-presence of structures resembling endometrial glands
surface epi tumors: clear cell (mesonephroid) carcinoma
-cca 5% of carcinomas
-often associated with hypercalcaemia or thromboembolic complications
Surface epithelial tumors: brenner tumors
₋ 1-2% of ovarian tumors
₋ tumor of transitional epithelium
₋ problematic assessment of dignity 90% benign)
-morphology of urotehlium
surface epi tumors-mixed malignant mullerian tumors
both epi and mesenchymal compinent
-arie in ovary
germinal tumor
affectt typically young people while epi more adult and older
-mostly bening
30% of ovarian tumors
95% of germ cell tumors are mature teratomas
malignant germ cell tumors -2% of ovarian tumors of children and young adults 60%
germinal tumors: dysgerminoma
-tumor of immature germinal cell
-50% of malingant germinal tumors
-1% of ovarian cancers
-morphology of primordial germ cells-seminoma(like testes of male)
germinal tumors-yolk sac tumors
-maligantn cells which line the embryonal sturcture called tolks sac
-20% of malignant germ cell tumor
-young women: 16-19y
-aggresive
germinal tumors: embryoncal carcinoma
-malignanty of immature cells
-more in male
-1% of ovarian germ cell Tu
₋ usually mixed with other Tu (mixed
germ cell tumors)
₋ common endocrine manifestation
(bleeding, amenorhoeae, hirsutism
germinal tumors: teratomas
-general
-one of most commontumors of ovaru
-bening, mature
-tumor composed of mature tissue of human body-tissue dont belong where it arises
-if imature->maligngat =2%
mature(bening) and dermoid cyst of teratomas
Mature (bening):
- 60% of ovarian being
-asympotmatic
-arise form germalc cells–>develop to antyhing in the body
-ectodermal component and skin
-categories
-lined by stratified aquamo s epi w adnexal structures+bronchuss, intestinal epi, cartilage, bone, tooth
1. mondermal: dervied form one germinal layer -ectoderm
2.bidermal:
3. tridermal
Dermoid cyst:
- lined by skin-hair and skin compinents
-bening
ectodermal layer
neural tissue in teratoam, neural brain tissue and their processes
endoderm layer
bronchial stissue
mesodermal layer
CT, cartilage, bone, teeth
ovarian sex cord tumors:
-from supporting cells of ovary
ovarian sec cord tumors: cell tumor
-cells which accompany the ovum
₋ 12% of sex-cord / stromal Tu
₋ low-grade malignancy bc diff to asses
₋ production of estrogen: bleeding, amenorrhea,
end. hyperplasia
₋ adult/juvenile type
-recurrence
ovarian sex cord/stromal tumors: thecofibroblastic tumros
-cell sof ovarial stroma
2a. fibroma
- apperance of normal ocvarial stroma
-tumors composed of cell whhich resemble fibroblasts
-hard white nodule
-common, fully bening
2b.thecoma
-theca cells form corpus luteum –>produce progestrone
-rare
-fucntionally active producing progestirone
-yellow appearnce like corpus luteum
- thecofibroma
-mix of corpus luteum and stromal cells
-yellow apperance
meigs syndrome
combination of fibroma pleural effusion and being ascites
metastatic tumors
-10% ovarian cancer
-usualli bilat
-hematogenous, lymohogenus route
-direct exntesion form adjecent organs(uterus, colon)
-most common: breast, genital tract, GIT, haemotopoetic system
mcirogalndular hyperplasia(cervic uteri)
Microglandular hyperplasia
Benign condition
Closely packed proliferation of
endocervical glands without
intervening stroma
Progestin stimulation
(pregnancy, postpartum period,
oral contraceptives)
CIN=
squamos intraepi lesions-SIL
adenomyosis vs adenomyoma
Abnormal distribution of histologically benign endometrial tissue within the myometrium
Circumscribed mass made up of endometrium and smooth muscle tissue
salpingitis ishemic nododsa
Multiple nodules containing spaces lined
by benign tubal epithelium
Inflammatory changes – scanty or absent
tubal pregnancy-micro
Chorionic villi and / or trophoblast in the tubal wall, bleeding
common finding med falloipian tube
paraovarian/paratubal cyst-thin walled cysts hanginf from tubal fimbriae
pseudomyxoma peritonei
mucinous ascites associated with muscinous tumors
(mucinous eoi tumor of ovary)
mondodermal teratmoia:
1.struma ovarii
2. carcinoid tumor
1.composed of thyroid tissue
granulosa theca cell tumor-sex cord stromal tumor
Locally aggressive, recurrences are common
Production of hormons → puberta praecox, / endometrial hyperplasia and carcinoma
fibroma: sex cord stromal tumor
Hormonaly inert
Meig´s syndrome – combination of fibroma
pleural effusion and benign ascites
krukenberh tumor: MTS tumpr
Distinctive bilateral tumour metastatic to the ovaries by transcoelomic spread
↑ MTS gastric carcinoma
