FEMALE REPRODUCTIVE SYSTEM

Oleh:
dr. Ilhami Romus,SpPA

FAKULTAS KEDOKTERAN UNIVERSITAS

RIAU
Comprise of:
1. Vulva & vagina
2. Uterine cervix
3. Uterine corpus
4. Fallopian tubes
5. Ovaries
VULVA/VAGINA

A. DEVELOPMENTAL DISORDERS
B. INFLAMMATORY
DISEASE(infeksi)
C. VULVAR DYSTROPHY(gangguan
pertumbuhan)
D. VULVAR NEOPLASIA
E. VAGINAL NEOPLASIA
A. Developmental Disorders
 Mullerian Duct Anomalies(bisa septa abnormal dan
duplikasi organ)
- Embryologic fusion anomalies  organ agenesis, abnormal
septation, organ duplication, etc.(organogenesisi masa kehamilan)
 Gardner’Duct Cyst(kista sis dari mesonefrik)
- arise in women from remnants of the degenerated
mesonephric/wolffian duct (di submukosa dinding vagina)
- Submucosa of anterolateral vaginal wall, 1-2 cm in size
 Imperforate Hymen(tidak diketahui sampai pubertas
menstruasi,tidak menstruasi perut sakit ada perdarahan di
korpus)
- May not be recognized until puberty  complain of failure to
menstruate  retain blood: hematocolpos, hematometria,(naik lagi ke
tuba darah menumpuk di tuba)
hematosalpinx
B. INFLAMMATORY DISEASE
Prone to infection: pre-pubertal period and
post-menopausal due to:
- the environment is warm and humid
- hypo-estrinism  decrease skin vascularization
 atrophy & decreased cornification  sensitive
to infection  atrophic vulvitis / vaginitis
Infection: viral or bacterial
 (infeksi diusia puberrtas dan masa post manapuse estrogen dikit waktu
pubertas yg menyebbakan vaskularisasi darah berkurang ada keratin
berkurang jadi mudah terpapar infeksi di kulit ada epitel squamosa yg ada
keratin)
GENITAL INFECTION

Infeksi biasanya ascending,bagian terluar vulva vagina jika sudh terinfeki

bisa sampai ke ovarium.bisa gonokkokus,clamia dll
Sexually Transmitted/Infectious Diseases

A. VIRAL
B. BACTERIAL
C. CHLAMYDIA
D. SYPHILIS
E. CANDIDA
F. TRICHOMONAS
Sexually Transmitted/Infectious Diseases

A. VIRAL
HERPES (Herpes simplex II virus)
 Painful red papules  group of vesicles  ulcerate
 Intraepidermal vesicles formed by acantholysis due to baloon
degeneration of infected epidermal cells
CONDYLOMA ACCUMINATA (HPV)
 Veneral warts  flat or verrucous alteration of squamous epithelia
(datar bisa veruccos(menonjol) bisa terlibat di anal,mukosa
vagina,serviks)
 Affects: skin of perianal/perineal; mucosa of vagina, cervix, others
 Verrucous condyloma(seperti bunga kol) with
hyperkeratosis(lapisan keratin berlabih tap tidak ada inti,
parakeratosis(ada inti), acanthosisI(penebalan), koilocytosis (akibat
virus)
AIDS
Virus herpes simplek 2 ada papul2 merah nyeri membentuk ada vaskuarisasi ada
vesikel intra dermal(seperti penonjolan berisi air) kalo besar bula namanya
 Lapisan tanduk
keratin

Akantolisis
hancur sel
jadi kososng
berisi air

HSV
Kantong berisi
- Painfull red papules/ vesicles
air sagat nyeri

- Intraepidermal vecicles
Condyloma acuminatum (VIN)

Numerous condylomas encircling the introitus Veruccos kayak

kembang kol ada
benjolan di
vagina (vulvaa)
 Koilositosis terinfeksi
hiperk virus stplasma
era bervakuola inti
mengkrut

pkeratosi
sis

acantholisis

Condyloma acuminatum
Acantosis, hyperkeratosis, and (VIN)
cytoplasmic vacuolization (koilocytosis)
 Koilosit
Masi normal terinfeksivirus

Condyloma acuminatum (VIN)

 B. BACTERIAL
Sexually Transmitted Infectious Diseases
1. GONORRHEA
 Initial site: Bartholin’gland, Skene’s glands,
endocervix (ifeksi akut kel.bartholine produksi
minyak terhambat dan erjadi abses)
 Acute inflammation of Bartholin’s gland  occlusion
 abscess  resolution  Bartholin’s cyst
 Cervical infection  endometrium (masuk ketuba)
purulent salpingitis  pyosalpinx 
reabsorbed(direabsorbsijika imun bagus) 
hydrosalpinx(tuba sembab dan besar) 
consequences: secondary infertility(trjadi infertilitas
sekundar)
 Can result in extragenital infectionsbisamenular lwt
eksternal)
- Pharyngitis, associated with orogenital sexual contact
- Proctitis9radang ada rektum), associated with anal intercourse(pada
LGBT)
- Purulent arthritis(menyebar melalui sendi), monoarticular, large joint,
blood-borne infection
- Gonoblenorrhoe, neonatal conjunctival infection acquired at
BARTHOLIN GLAND CYST

Kista bartholini
Sexually Transmitted/Infectious Diseases

B. BACTERIAL

2. BACTERIAL VAGINOSIS
 Etiology: gardnerella vaginalis (hemophilus
gardnerella)
 Non-specific vaginitis produces a thin, scanty,
malodorous discharge(adanya discharge atau
keputihan(vlour albus)
 The organism does not penetrate mucosa(tidak
penetrasi ke mukosa), and does not incite much
inflammatory response
Sexually Transmitted/Infectious Diseases

B. BACTERIAL

3. CHANCROID(melaui hubungan seksual)

 Etiology: Haemophilus ducreyi  genital chancre
(“soft chancre”) and regional lymphadenitis 
inguinal abscess (bubo)(adanya limfadenitis di
inguinal ada bases dan oklusi sumbatan
 Mic: lumenal occlusion and thrombosis of blood
vessel beneath the ulcer
 The organism is a gram-negative rod  sexually
transmitted disease
Sexually Transmitted/Infectious Diseases

B. BACTERIAL
4. GRANULOMA INGUINALE
 Etiology: Calymmatobacterium granulomatis
 Location: perianal or genital, as a solitary lesion
or small group of ulcers filled with granulation
tissue  peripheral extension, with dense
infiltrates of lymphocytes and macrophages,
occasional microabscess(lesi soliter ada ulkus isi
jar.granulasi )
 Intracytoplasmic inclusion bodies within
macrophage  Donovan bodies
Sexually Transmitted Infectious Diseases

C. CHLAMYDIA
(C.trachomatis)
A.Non-specific Uretritis, Cervicitis, Salpingitis
 Chlamydia is probably responsible for a majority
of the cases of salpingitis resulting in
infertility(radang pada servks,uretra,tuba paling
banyak infertil karna sumbatan tuba di
salpingitis)
B. Lymphogranuloma Venereum
 Different serotype of C.trachomatis (L1, L2, L3)
 ulcerative and papular skin lesion
 Lymphatic involvement  fibrosis, scaring(scar),
and strictures of anus and rectum
Sexually Transmitted Infectious Diseases

D. SYPHILISpada wanita
 Caused by Treponema pallidum
 Transmitted by sexual contact(sexal contact)
 Initial stage  primary syphilis  firm and
painless ulcer known as chancre (usually is not
apparent clinically)(ada ulkus tukak yg tidak
nyeri)
 Continued to secondary syphilis (condyloma lata)
 placenta(jika ibunya hamil)  lues tarda
 Tertiary syphilis: neurological and vascular
diseases
 secundary

primary

Kyk ada
sariawan Ada fibrosis
jar.parut

tertiary
 graanuloma

syphilis
Sexually Transmitted Infectious Diseases

E. CANDIDA(paling banyak)
 Caused by C. albicans  moniliasis/candidiasis
 Normal component of vaginal flora(suka yg
lembab da basah)ada divagina normal tapi kal
banyak abnormal)
 White-patch-like mucosal lesions, thick white
discharge, vulvovaginal pruritus(GATAL,bau
sepert ikan asin)
 Associated with DM, pregnancy, oral contrceptive
use, broad-spectrum antibiotic therapy,
immunosuppression (obat predinoson bisa
candida banyak)
Putih susu basi,ada bau ikan
asin

Batan
g
berca
bang

candida

spora hifa
Sexually Transmitted/Infectious Diseases

F. TRICHOMONAS
 The second most common type of
vaginitis
 Caused by T. vaginalis
 Most often transmitted by sexual contact
 Trichomonas
seperti layang2)

trichomonas
Agak kehijaun bau tidak khas
busuk aja flagella
C. VULVAR DYSTROPHY

Atrophicdystrophy
Hypertrophic dystrophy
 Estrogen berkurang
kulitnya jadi tipis

Atrophic Dystrophy:
The skin becomes pale gray andLichen
parchment-like Sclerosus
 susceptible to infection
Atrophic labia and the introitus is narrowed
(Chronic Atrophic Vulvitis)
 Epeitel menipis

-Epithelial atrophy
-Dense band of hyalin collagen
beneath the epithelium
-A band like lymphocytic
infiltration
-Mostly after menopause
- Hormonal factors ?
Lichen
Atrophic Dystrophy: Sclerosus
- predisposes to acute infection
(Chronic Atrophic Vulvitis)
LICHEN SYMPLEX CHRONICUS
 Epidermis
menipis

hialinisasi

LICHEN SYMPLEX CHRONICUS

 Hiperkeratos
is tidak
atipik

acantohos
is
-Hyperkeratosis, acanthosis
with or without atypia
-Clinically resembles atrophic
dystrophy (white plaques )
-10% potential to cancer
- unknown etiology

Hypertrophic Dystrophy:
Squamous Hyperplasia
 menipis

Menbal rentan
keganasan

Schematic composition of atrophic

and hypertrophic dystrophy
D. VULVAR NEOPLASIA
A. Granular cell tumor
B. Hydradenoma papilliferum
C. Bowen’s disease
D. Squamous cell carcinoma (SCC)
E. Extramammary Paget’s Disease
Granular cell tumor
Granular cell tumor
Tumor cell has abundant eosinophilic
and granular cytoplasm
Tuor dibatasi jar.ikat granula
Sharply circumsribed
nodule(nodulbertbatas tegas)
Mostly in labia majora/ interlabial flods
Tendency to ulcerate: Ca ??(condong
vaskularsasi)
Mic:- tubular ducts lined by single/ double
layer of nonciliated columnar cells
- flattened of myoepithelial cells

Papillary hidradenoma
 Bowen disease

Bowen disease: often in labia, sometime perianal, periclitorical

80% HPV +, 50% HSV +
precancer lesion
As a condylomatous lesion: Bisa pria isa wanita sering
Microscopic :
Diffuse cellular atypia labia di perianal,lesi prekanker
Nuclear crowding bisa tumr ganas
Pathologic mitosis
PAGET’S DISEASE of the
VULVA
( extra mammary paget’s disease )
EXTRAMAMMARY PAGET’S DISEASE

- Mucin-containing adenocarcinoma
within squamous cell epithelium
- Chronic and reccurences
-Indicative of an underlying invasive
adenocarcinoma ( 25 % ), usually
of skin adnexal origin

Ada adeno karsinma dikulit bawah

 E. VAGINAL NEOPLASIA

 SCC
 Adenocarcinoma

- Sarcoma botryoides

-
 - Predominantly affecting elderly
women
- Biasa usialanut mempengaruhi
metastase bisanya I fornix ada
keputihan
- Prognosis is determined by: size,
dept of invasion, histological grade,
presence of lymph-node metastasis

- Mostly in fornix with vaginal

discharge

- Prognosis: 5 year survival rate 20-

SQUAMOUS CELL CA
90%
 Ada mutiara
tanduk)seringusia tua

SQUAMOUS CELL CA
 Sel dgn sitoplasma

CLEAR CELL
- Arising is ADENOCA
the anterior wall of vagina
- clear cell carcinoma  DES and in young (15 – 27 yo)
 Ganas prognosisjelek Brsl dari
rhabdomio
sarkoma
kongenital

SARCOMA BOTRYIOIDES
(embryonal rhabdomyosarcoma)
- rhabdomyosarcoma, polypoid grape-like appearance
- In general the prognosis is poor
 Lapiisan kambium longar

SARCOMA BOTRYOIDES
 Sitoplasma pink

SARCOMA BOTRYOIDES
SARCOMA BOTRYOIDES
VAGINAL ADENOSIS

Klnjar banyak metaplasia

- Failure of the normal glandular epithelium that lines the embryonic

vagina to be replaced during fetal life by squamous epithelium
- Increase in the young daughters of women who had received DES
during pregnancy
- Gland in the chronically inflammed lamina propria, lined by ciliated
darkly stained cells similar to tuba or endometrial epithelium
 CERVIX

A. INFLAMMATORY DISEASE
B. POLYPS
B. CARCINOMA
 endoservix
The Development of uterine cervix
Suddut fornix

Bisa papsmear di
dkt donat yg
remaja
Ada perubahan serviks pda masa
pubrtas,vulva vagina semua ada epitel
squomos(diluar)a mulai dari servks
adaperubahan di epital klumnar

Dewasa balik lagi kyk anak2

virus
hpv nmasuk di squamos A kelenjar
junction
CERVIX Ektoservik semua

Colposcopy: dotted line is Post-menopausal cervix

transformation zone
A. INFLAMMATORY DISEASE
 Acute 9stl aborsi,melahirkan atau
kecelakaan
- Neisseria gonorrhoica: the most common etiologic
agent
- Chlamydia: more common, less symptomatic  more
difficult to diagnose
- post-abortion, post-partum, post-traumatic
 Chronic
- Follicular cervicitis
- Nabothian cyst
Etiology: bacteri,parasit, virus
FOLLICULAR CERVICITIS

folikular
Cervicitis -
metaplasia
SQUAMOUS METAPLASIA

Epitel kolumnar
ada metaplasia
squomosa ada
infeksi yg lama
 Erosi 22thn
iritasi masuk
alat di vagina
 Jar granulasi di
servks ada bintik
stroberi
servikskhas
padasitrichomon
as
Servisitislanjutan vagiinitis
Porsio( donat)
Iva (ada lesi atau tidak)
B. POLYPS (penonjolan mukosa ukan tmor
jinak
Inflammatory
5% of women
From endocervical canal – sessile or pedunculated,
fibromyxoid
Hyperplastic
Microglandular hyperplasia  consists of tightly pack
hypaerplastic endocervical glands
POLYPS

Bertgkai ada jar ikat dilapisi epitel endoserviks

C. CARCINOMA
Etiology
The bottom line risk factor:
 Early onset of sexual activity
 Increasing numbers of sexual partners
 The promiscuity of those sexual
partners
Etiologic factor:
 HPV: strain 16, 18, and 31 (high risk)
 HSV II: antibodies to HSV II antigen is
higher in women with dysplasia or
neoplasia
Knyloma infeksi hpv erucos
Condilloma
C. CARCINOMA slid dibwh infeksi

Pathogenesis
 Location: squamo-collumnar
junction
 Dysplasia (CIN)  neoplasia
Spectrum of CIN

Displasia inti mmbesar

sitoplasma sedikt (4:1)
Hanya dipitel tidak boleh
enembus membrana
basalis

Cervical Intraepithelial Neoplasia (CIN)

 Cytology: normal  CIN III
Cin 1

Epitel sqoumosa
nrmal

Cin 2 Cn 3
Squomosa
kolunar
juntion
Terpapar aibat
hub seksual
 CN 3

CIN III with micro-invasionCN

Serviks donat merah

berdempul2
C. CARCINOMA
Diagnosis (evaluation)
1. PAP Smears
- 95% reliable (5% false negative)
2. Schiller Test
- staining of the cervix with iodine and potassium
iodide
 normal-brown (glycogen content)  biopsy
3. Colposcopy
- magnification: 20X  biopsy
C. CARCINOMA

Morphology
 Grossly: infiltrative, ulcerative,
exophytic
 Mic: SCC keratinizing, non-keratinizing
 N 3 displasia berat
mmbran basalis masiutuh

CIN III
SCC, keratinized

mutiarakeratin
C. CARCINOMA

Behavior
 Depends on the spreading: bladder, ureter, rectum,
vagina
 Lymphatic: paracervical, hypogastric, external iliac
 Blood: unusual
 Grading yg nntuin pa
C. CARCINOMA Staging kinisyg nentuin kombinasi

Prognosis
 Related to grade and
stage of tumors
 Overall FYSR: 60%
Staging
 Stage 0 Carcinoma in situ
 Stage Ia Microinvasive and confined to cervix
 Stage Ib Invasive and confined to cervix
 Stage IIa Extends to upper vagina but not to para-
metrium
 Stage IIb Involve parametrium
 Stage III Extension to pelvis sidewall or lower vagina
 Stage IV Beyond the pelvis or involvement of rectal or
bladder mucosa
Bercak kecioklatan sarang endometriosis)