CERVICAL
CANCER
Presented by Batool Salah and Hala Marie
Supervised by Dr Hilda Salibi
OUTLINES
Epidemiology
Etiology
Clinical features
Diagnosis
Treatment
Complications
Epidemiology
Incidence: 7.4:100,000
Cervical cancer is the 3rd most common gynecological malignancy in
the US after endometrial and ovarian cancer.
Incidence is higher in countries without screening programs and HPV
vaccination.
Incidence has declined over the past 40 years due to screening and
HPVvaccination
Peak incidence: 35–44 years of age
Mortality: 2.2:100,000 women per year
1. Cervical cancer is the third most common cause of death due to a
gynecological malignancy after endometrial and ovarian cancer.
Mortality is highest in individuals aged 55–64 year
Cervix Anatomy
Cervical mass
Etiology
➢Human papillomavirus virus (HPV) infection
➢Infection with high-risk HPV genotypes is the main
cause of cervical cancer.
➢Nearly all squamous cell carcinoma of the cervix
and approximately 90% of adenocarcinoma of the
cervix are positive for HPV infection.
➢The major high-risk HPV types are HPV 16 and
HPV 18
Risk factor
For contracting HPV infection
✓Multiple sexual partners (strongest risk factor)
✓Early-onset of sexual activity
✓Multiparity
✓Immunosuppression (e.g., HIV infection, post-transplantation)
✓History of sexually transmitted infections (e.g., herpes simplex, chlamydia)]
Environmental risk factors
✓Cigarette smoking and/or exposure to second-hand smoke (for squamous
cell cancer types only)
✓In-utero exposure to diethylstilbestrol (DES)
✓Low socioeconomic status
Cervical intraepithelial neoplasia (CIN), a precursor of cervical cancer, typically
occurs in young adults (25–35 years).
Cervical intraepithelial neoplasia
HSIL LSIL CIN2
Pathology
•HSIL and invasive cervical carcinoma most commonly arise from metaplastic
squamous cell epithelium in the cervical transformation zone
Squamous cell carcinoma (∼ 80% of cases)
• Subtypes include large cell keratinizing, large cell nonkeratinizing, and papillary
squamous cell carcinoma.
•Irregular cell morphology
•Hyperchromatic cells with nonspherical nuclei, mitotic activity, and prominent
nucleoli
•Loss of basal membrane
•Precursor lesion: CIN or SIL
Pathology
Adenocarcinoma (∼ 20% of cases)
➢Subtypes include mucinous, endometrioid, clear-cell, and serous adenocarcinoma
➢The most common is the endocervical mucinous subtype
➢Precursor lesion: endocervical adenocarcinoma in situ
Clear-cell carcinoma of the cervix (CCC)
➢Rare form of cervical cancer (∼ 4% of all cervical adenocarcinomas)
➢Frequently associated with exposure to diethylstilbestrol (DES).
Atypical columnar epithelium with elongated nuclei
➢Small-cell carcinoma: ∼ 2% of cases
➢Neuroendocrine tumor
➢Infiltration of monotonous round atypical cells, arranged in a nesting pattern
➢Nuclei with salt-and-pepper chromatin
Grading
Grade1: less than 5% malignant undifferentiated cells
Grade2: 5% to 15%malignant undifferentiated cells
Grade3: more than 15%malignant undifferentiated cells
Spread of cervical carcinoma
Clinical features
Cervical cancer is usually asymptomatic in the early stages;
symptoms typically develop later in the course of the disease.
Early symptoms
✓Abnormal vaginal bleeding: irregular vaginal bleeding; heavy,
irregular menstrual bleeding; postcoital spotting
✓Abnormal vaginal discharge: blood-stained or purulent
malodorous discharge
✓Dyspareunia
✓Pelvic pain
Late symptoms: hydronephrosis, lymphedema, fistula formation
Cervical examination: ulceration, induration, or an exophytic
tumor
Staging
Staging
Diagnosis of Cervical Cancer
◻• Colposcopy:
Visual inspection of the cervix using magnification, with acetic
acid or Lugol’s iodine.
◻ • Cervical Biopsy:
Tissue sampling from abnormal areas for histopathology.
◻ • Endocervical Curettage (ECC):
Scraping cells from the endocervical canal.
◻ • Cone Biopsy (Conization):
Excision of a cone-shaped tissue sample (via Cold knife or
LEEP).
Prevention of Cervical Cancer
◻Primary Prevention:
• HPV Vaccination (Gardasil 9, ages 9–14; up to 26–45 years).
• Safe sexual practices (e.g., condom use).
• Health education about HPV and prevention.
◻Secondary Prevention:
• Regular cervical screening:
• Pap smear
• HPV testing
◻ Tertiary Prevention:
• Early treatment of precancerous or cancerous lesions to prevent
complications.
Complications
Direct complications of invasive cervical cancer
1. Local infiltration of organs:
➢Infiltration and compression of ureter → urinary obstruction → hydronephrosis → kidney
failure (bilateral obstruction is a potentially fatal complication)
➢Other organs often affected by the spread of cervical cancer include the rectum, bladder,
and vagina.
2. Fistula formation in locally advanced disease (e.g., rectovaginal, vesicovaginal,
urethrovaginal fistula)
➢Compression of veins or lymphatic vessels in the lesser pelvis → lymphedema of the lower
extremities
Metastasis
➢Bone metastasis: bone pain, pathologic fractures, spinal compression, hypercalcemia
➢Liver metastasis: abdominal pain, abdominal distention, nausea, jaundice
➢Lung metastasis: cough, hemoptysis, dyspnea, chest pain
➢Brain metastasis: headaches, seizures, cognitive deficits, focal neurological deficits
3. Cancer anorexia-cachexia syndrome (CACS)
Complications of radiation therapy
✓Vaginal stenosis
✓Postirradiation vaginitis (e.g., vaginal dryness,
dyspareunia)
✓Radiogenic cystitis/proctitis
✓Radiation may increase the risk of
complications like fistula formation.
Prognosis
Cervical cancer has the best prognosis out of the three main
gynecological cancers (ovarian, endometrial, and cervical
cancer).
➢The survival rates decrease with increasing FIGO stage [38]
➢Stage 0: > 93%
➢Stage I: 93%
➢Stage II: 63%
➢Stage III: 35%
➢Stage IV: 16%
Patients without lymph node involvement have a very good
prognosis, regardless of FIGO stage.
Main cause of death: uremia, often occurs secondary to bilateral
ureteral obstruction.
References
➢Amboss
➢kAPLAN STEP 2 Obstetrics and Gynecology