CERVIX

NON- NEOPLASTIC
INFECTION
Infections constitute one of the most
common clinical complaints.


CERVICITIS
MENARCHE

INCREASED ESTROGEN

INCREASED GLYCOGEN UPTAKE BY SQUAMOUS CELLS

GLYCOGEN SUSTRATE FOR ENDOGENOUS MICROBES

RESULTS IN DROP IN pH

ENDOCERVIX UNDERGOES SQUAMOUS METAPLASIA

SQUAMOUS OVERGROWTH CLOSES CRYPT OPENINGS

NABOTHIAN CYSTS FORMS

INFLAMMATION OCCURS

ULCERATION

REPAIR



Chronic cervicitis
ENDOCERVICAL POLYPS
Inflammatory tumours
2-5% of adult women
Clincial: bleeding/ spotting
Macro:Soft mucoid endocervical mass
protuding from endocervical canal
Micro: loose fibromyxoid stroma, glands,
inflammation
CONDYLOMA ACUMINATUM
Common lesion of cervix
Caused by HPV (usually 6 &11)
Macro: Wart like / elevated flat area
Micro: Hyperplasia of squamous epithelium,
koilocytosis, nuclear atypia
SQUAMOUS NEOPLASIA
INTRAEPITHELIAL
-CIN / SIL/ CARCINOMA IN SITU

INVASIVE
-Large cell non keratinizing squamous cell
carcinoma
-Keratinizing squamous cell carcinoma
-Small cell carcinoma
INTRAEPITHELIAL AND INVASIVE
SQUAMOUS NEOPLASIA OF THE CERVIX
Epidemiological date imply a sexually
transmitted agent
HPV-most important agent
Risk factors:
Early age of first intercourse
Multiple sexual partners
Increased parity

Molecular evidence linking HPV to
cancer
HPV dna is detected in 95% of cervical cancers
High and low risk types
Viral (E6 &E7) genes of high risk HPV can disrupt the
cell cycle via upregulation of cyclin E, interrupt cell
death pathways by binding to p53, induce centrosome
duplication and genomic instability, prevent replicative
senescence by upregulation of telomerase
Virus integrated into host DNA in cancers and present
free (episomal) in condylomata and pre-cancers
Certain chromosome abnormalities are associated
with cancers with specific HPV strains
Vaccines against HPV can protect against pre-
cancers
HOWEVER HPV IS NOT THE
ONLY FACTOR
High % of young women infected with HPV
but only a few develop cancer
Co-carcinogens
Immune status
Nutrition
Smoking
OCP
High parity
Host gene alteration
Time
GLANDULAR NEOPLASIA
INTRAEPITHELIAL
-Adenocarcinoma- in-situ /CIGN

INVASIVE
-Adenocarcinoma
SQUAMOUS INTRAEPITHELIAL NEOPLASIA
CIN
PATHO: Early age at first intercourse
Multiple sexual partners
Male partner with multiple partners
HPV-16, 18
CIN usually starts at the squamo-columnar junction
Low grade CIN I may not progress
High grade CIN II&III are at higher risk of progression
Not all lesions begin as CIN I
CIN CARCINOMA ( months to 20 yrs)
CLINIC: 30 YRS for CIN II & III
MACRO: On colposcopy CIN characterized by white patches on the cervix after the
application of acetic acid. Distinct vascular mosaic or punctuation patterns
MICRO: I :koilocytic atypia
II :atypical cells in the lower layers of epithelium
III :atypical cells in involving all layers of the epithelium
INVES: Papanicolaou smear {superficial scraping of the cervix epithelium (squamous and
glandular) spread on a glass slide and stained with Papanicolaou stain to look for
atypical cells ( cells which do not look like normal cells)}
SQUAMOUS CELL CARCINOMA
CLINIC: 30-50 yrs
irregular vaginal bleeding (contact and spontaneous),
leukorrhea, dysuria
PATHO: Same as for CIN
MACRO: fungating / ulcerating / infiltrating
On colposcopy- highly abnormal vascular patterns
MICRO: 95%- Large cell ( non-keratinizing, keratinizing)
5% - Small cell
INVES: Biopsy for HPE
Natural Prog: Extends by continuity to involve every continuous
Structure ( peritoneum, bladder, ureter, rectum & vagina)
Local and distant lymph nodes
Distant mets: liver, lung , bone marrow
Cervical carcinoma
STAGING &
5 yr survival rate
0 : Carcinoma in situ (almost 100%)
I : Carcinoma confined to the cervix (80-90%)
II : Carcinoma beyond cervix-but not into
pelvic wall or lower third of vagina (75%)
III: Carcinoma extends into pelvic wall and
lower third of vagina (35%)
IV: Carcinoma has extended beyond the
true plevis or has involved the bladder
and the rectum (10-15%)
CAUSE OF DEATH: local extension of tumour with resultant uremia
Minimally invasive carcinoma
- Minimal microscopic invasion of stroma
Microinvasive carcinoma
- Microscopic invasion of carcinoma < 5mm
ENDOCERVICAL
ADENOCARCINOMA
10-15 % of cervical cancers
Macro: Mass in endocervical canal
Micro:Well differentiated adenocarcinoma
ADENOCARCINOMA IN SITU
Recognised as a precusor of invasive
adenocarcinoma
PAPANICOLAOU SMEAR
Should be periodically done- policy and recommendation varies
Suggested policy- ? Find out current policy of UH / Malaysia
Cytologic examination merely detects the possible presence of a
cervical cancer / precancer- it does not make an absolute diagnosis.
Definitive diagnosis- HPE of biopsy specimen

TREATMENT
SQUAMOUS
PRE-INVASIVE: PAP smear follow up ( for mild lesions)
Cone biopsy/ Loop excision etc
INVASIVE: Hysterectomy
Radiation- for extensive lesion


ADENOCARCINOMA
PRE-INVASIVE: Hysterectomy
INVASIVE: Hysterectomy + radiation+ chemotherapy

OTHER TUMOURS OF THE
CERVIX
Sarcoma
Lymphoma
Malignant melanoma