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Cervical and Endometrial Pathology Overview

This document summarizes the anatomy and histology of the female reproductive system. It describes the normal structures of the cervix, including the ectocervix lined by squamous epithelium and the endocervix lined by columnar epithelium. It discusses pre-cancerous conditions like cervical intraepithelial neoplasia (CIN) and endometrial hyperplasia. It also covers other gynecological topics like hydatidiform mole, ectopic pregnancy, ovarian tumors, and breast fibroadenoma and invasive ductal carcinoma. Overall, the document provides an overview of the microscopic appearance of normal and pathological conditions of the female reproductive tract.
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0% found this document useful (0 votes)
7 views42 pages

Cervical and Endometrial Pathology Overview

This document summarizes the anatomy and histology of the female reproductive system. It describes the normal structures of the cervix, including the ectocervix lined by squamous epithelium and the endocervix lined by columnar epithelium. It discusses pre-cancerous conditions like cervical intraepithelial neoplasia (CIN) and endometrial hyperplasia. It also covers other gynecological topics like hydatidiform mole, ectopic pregnancy, ovarian tumors, and breast fibroadenoma and invasive ductal carcinoma. Overall, the document provides an overview of the microscopic appearance of normal and pathological conditions of the female reproductive tract.
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd

Dr Ismet M Nur Sp PA (K) MM

 The portio (ectocervix) :


covered by a stratified
nonkeratinizing squamous
epithelium
 Endocervix:
lined by columnar, mucus secreting
epithelium
 The point at which the squamous &
columnar epithelim meet is the
squamocolumnar junction
 The portion of the columnar ept.
that is replaced by squamous ept. is
termed “transformation zone”
Transformation zone
 Reserve cells in the transformation zone are
continuous with the basal cells of the ectocervix
 and may undergo having metaplasia become columnar
and squamous differentiated
 Transformation zone is the origin of precursor lessions
Colposcopic view of the cervix :
A. in the reproductive age woman
B. the postmenopausal cervix
Risk factor for cervical neoplasia:

 early stage at first intercourse


 multiple sexual partners
 increased parity
 A male with multiple previous sexual partners
 The presence of a cancer-associated HPV
 The persistent detection of high-riskHPV,
particularly in high concentration
 Exposure to oral contraceptives & nicotine
 Genital infections (chlamydia)
Normal Cervix
 normal ectocervix has a typical stratified Squamous
epithelium
 maturation cels,the eosinofilic cytoplasm expands
greatly and the cells are pushed upward into a stratum
 the cytoplasm becomes progressively flattened
 Cytoplasmic staining in superficial cell shows
exfoliating superficial squamous epithelial cells
Cervix normal
Cervical Precancer
Cervical precancers have been classified in :
 Displasia / Ca insitu system (mild and severe)
 Cervical intraepithelial neoplasia (CIN classification)
ex. CIN I,II,III
 Non Invasive Lession (Low grade / CIN I and High
grade / Ca Insitu/CIN III intraepithelial lession)
Cervical intra-epithelial neoplasia (CIN I)
 Mild dysplasia
 Low grade intraepithelial lesion
 Koilocytotic atipia :
Nuclear changes as enlargement and hiperkromasia
accompanied by cytoplasmic halos
 Koilocytotic atipia as the effect of active viral replication in the
maturing cells (Viral cytophatic effect)
 Few alteration in the lower third epithelial cells
(enlarged,crowded, hyperchromated, increased mitotic act)
 Often contain abundant papilloma Virus nucleic acid
Cervical intra-epithelial neoplasia (CIN I)
Cervical intra-epithelial neoplasia
(CIN II)
 Basal cells proliferation extend from one-third to two-
third of thickness of epithelium
 Atypical cells in the lower layers of squamous
epithelium
 Atypical cells shows changes in :
nucleo-cytoplasmic ratio
variation in nuclear size
increased mitotic figures ( abnormal mitosis and
hiperkromasi)
 they take on some of the characteristics of malignant
cells
Cervical intra-epithelial neoplasia
(CIN II)
Cervical intra-epithelial neoplasia
(CIN III)
 High grade intraepithelial lesion
 Carcinoma insitu
 The atypical cells extend into the upper third of
epitheliumuntil its totally replaced
 mitotic or abnormal mitotic figures are common and
are seen above the basal layer
 Progressive loss of differentiation
Cervical intra-epithelial neoplasia (CIN III)
Endometrial hiperplasia
1. Simple non-atypical hyperplasia
changes in glands of various size, producing
irregularity in gland shape, with cystic alteration
2. Complex atypical hyperplasia
increase in the number & size of endometrial
glands, with gland crowding, enlargement, and
irregular shape. Mitotic figures are commons
Endometrial hyperplasia
 Appears to be a response to excessive or uncoordinated
oestrogen production
 simplex or complex in form
 Associated with an increased risk of invasive
endometrial Ca
 risk complex >> simplex
 greatest in complex hyperplasia with atypia
 Heavy uterine bleeding is the most common symptom
Endometrial hyperplasia
Complex Hyperplasia
 Proliferation of the endometrial glands
 Many are irregular in shape and size, often with
papillary infolding
 Adjacent glands may be closely packed
 there is little intervening stroma
 nuclear and cytoplasmic pleomorf more often
 mitotic activity >>>
Complex Hyperplasia
Simplex Hyperplasia
 Endometrial lining becomes thickened by
proliferation of the endometrial glandular tissue
 Formation of numerous tiny cysts scattered among
normal endometrial glands
 Cysts result from dilated endometrial gland
 intervening stroma containing prominent thin-walled
blood vessels
Simplex Hyperplasia
Endometrial hyperplasia
Hydatidiform mole
 The condition known as hydatiform mole arises in
a small portion of pregnancies,after miscarriages
or terminations of pregnancy or even year after a
pregnancies
 Characterized by cystic swelling of the chorionic
villi, accompanied by variable trophoblastic
proliferation
 partial or complete
 complete mole: all or most chorionic villi are
edematous with central cystic spaces, diffuse
trophoblast hyperplasia, > 90% have a 46,XX
diploid pattern
Hydatidiform mole
Cisternae (Central cystic space ) are invested by a
layer hiperplastic cytotrofoblast and
syncytiotrophoblast
Some Tropholast cells lying free of the villi and
showing mild cellular pleomorfism
partial mole: some of the villi are edematous, the
trophoblasic proliferation is focal, the karyotype is
triploid (e.g 69,XXY)
wide spectrum of behaviour, some eradicated by
curretage, other persist, small number develop
malignancies as Chorio Ca
Feature Complete Partial mole
mole
Karyotype 46,XX (46,XY) Triploid
Villous All villi Some villi
edema
Trophoblast Diffuse, Focal, slight
proliferation cicumferential
Atypia Often present Absent
Serum hCG Elevated Less elevated
hCG in tissue ++++ +
Behavior 2% choriocarc. Rare chorioca.
Mola hydatidiform
Mola hydatidiform
Complete hydatidiform mole suspended in saline
showing numerous swollen
Ectopic pregnancy
 Implantation of the fetus in any site other than a
normal uterine location
 90% is within the tube, the other site are the ovary,
abdominal cavity, & intrauterine portion of fallopian
tube
 Ussually become dramatically apparent by severe
hemorrhage in the lumen often followed by tracking of
blood into peritoneal cavity
 only very rare of the pregnancies continue to near
normal term
Ectopic pregnancy
 Right: muscular wall of the tube
 Lumen:contains blood clot & chorionic villi, sheets
of trophoblast
 The epithelial lining of the tube has been replaced
by well-developed decidua
 Extensive haemorrhage into the lumen of the tube
 The trofoblast burrows into the wall of fallopian
tube leading to perforation
Ectopic pregnancy
Ovarian tumors
 Risk factor: nulliparity, family history & heritable
mutation. Higher freq. in unmarried woman and
in married woman with low parity
 Pathogenesis: mutations in both BRCA1 or BRCA2
(20%-60% by the age 70)
 Tumour may arise from epithelial, stromal,germ
cell, metastatic
 Classification: WHO Histological Classification
1993  surface epithelial-stromal tumors, sex
cord-stromal tumors, germ cell tumors, malignant
not otherwise specified, and metastatic
nonovarian cancer
Ovarian tumors
 Cystic cavity tends to be filled by complex branching
papillary structures
 These are covered by columnar cells that are crowded
and dysplastic
 The cells are stratified and form solid sheet
 Essential for diagnostic malignancy is evidence of
invasion tumour cells to stomal
Papillary cystadenocarcinoma serosum
ovarium
 This was a large tumor with
many cystic cavities filled with
watery fluid. One cystic cavity is
shown
 It is lined by deeply basophilic
epithelium which forms long
papilliferous processes.
 The epth. grown outwards,
penetrating the fibrous wall of
the cyst to reach the serosa
Fibroadenoma mammae
 Tend to be found in younger woman (20-35 years)
 Very rarely become malignant
 Forms a firm well-defined mass, up to about 3 cm in
diameter
 Are mixed tumours, in having both epithelial &
connective tissue components
Fibroadenoma mamae
Fibroadenoma mamae
 The tumor consist of both
stromal & glandular
hyperplasia
 The stromal underwent a
myxomatous degeneration
 The duct dilatated, & the
epithelial nuclei normal
 The nodules are
surrounded by bands of
denser fibrous tissue
Fibroadenoma mamae
 Pericanalicular pattern : Epithelial component of
rounded ducts that remain small and undistorted
stromal aroun them symetris and regular manner
 Intracanalicular pattern : The ducts appear elongated ,
flattened spaces compressed by nodular proliferation
of the stromal component
Invasive ductal carc. mamae
 Invading malignant epithelial cells form small ductal
stuctures
 Solid nest
 Stroma frequently fibrotic
Invasive ductal carc. mamae

 The tumor cell are polygonal hyperplastis, some give a ductuli


appearance with central necrosis
 The stromal is fully invaded by the tumor cells
Alhamdulillah..

Thank you

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