SABA roll no 186 4th year MBBS Rawalpindi Medical university pathology presentation

1. SABA ROLL NO 186
4TH YEAR MBBS RMU
CERVICAL NEOPLASMS
•TRANSFORMATION ZONE
•HUMAN PAPILLOMA VIRUS
•SQUAMOUS INTRAEPITHELIAL LESIONS(SIL OR CIN)
•INVASIVE CARCINOMA
•ENDOCERVICAL POLYP
•ENDOMETRIOSIS

2. TRANSFORMATION ZONE
• The area between old squamo-columnar junction and new squamo columnar junction
is called transformation zone.
original squamo columnar junction (at the external os)
squamo columnar junction undergoes eversion (Ectropion or Ectopy)
Columnar cells exposed to acidic environment of vagina( created by Lactobacillus)
Squamous Metaplasia occurs
New Squamo-columnar junction formed
At puberty

4. Entropion_ Eversion
of Squamo-columnar
Junction
Formation of transformation Zone

5. HUMAN PAPILLOMA VIRUS
• Causative agent.
• Has tropism for immature squamous cells of the
transformation zone
• HPV 6 & 11 low risk genital warts
• HPV high risk cervical CA
• Integrate into host genome
Their inhibition leads to uncontrolled cellular replication (Dysplasia
And cancer)

6. RISK FACTORS
• Early age at first intercourse
• Multiple sexual partners
• Male partners with multiple previous sexual partners
• Persistent infection by high risk strains of papilloma
virus
• Immunodeficiency
• Smoking
• Family history is not a risk factor

7. CERVICAL INTRAEPITHELIAL LESION
(SIL) OR CIN
• Precancerous epithelial change
• Mean age ~30 years
• CAUSE:
HPV 6 & 11
• PATHOGENESIS:
HPV causes Dysplasia
HPV first infects basal epithelial cells
• TYPES:
Low grade SIL (or LCIN/LSIL) CIN I
Associated with productive HPV infection
Most regress
High grade SIL (or HCIN/HSIL) CIN II & CIN III
Increased proliferation
Arrested Epithelial maturation
Lower levels of viral Replication

8. MORPHOLOGY
• CIN I
Mild Dysplasia
Involves the lower 1/3rd of squamous eptelium
in the superficial layers
Resolves spontaneously
• CIN II
Moderate Dysplasia
Involves lower 2/3rd of squamous epithelium
Superficial layer still shows Differentiation
Progressive atypia
Occasional Koilocytosis

9. • CIN III
Severe Dysplasia
Involves all of the epithelium
Basement membrane spared (carcinoma in situ)
Koilocytosis absent

11. DIAGNOSIS
• PAP Smear
Screening Test
Cells are scraped from the Transformation Zone
• COLPOSCOPY
Visualizing the cervix by a scope
Ascetic acid used
Abnormal areas turn white
Biopsies of abnormal areas taken

12. TREATMENT
• LSIL
Managed conservatively
• HSIL
Surgical Excision(cone Biopsy)
Frequent follow ups smears required
• VACCINE
Quadrivalent vaccine (6, 11, 16, 18)
9-valent vaccine (6, 11, 18, 30, 31, 33, 45, 52, 58)

13. INVASIVE CARCINOMA OF CERVIX
• Include
Squamous cell carcinoma (75%)
Adenocarcinoma
Mixed Adeno squamous carcinomam (20%)
Small cell neuroendocrine carcinoma (<5%)
• CAUSE:
HPV 16 AND 18
• Risk Factors:
Smoking
HIV
• Mean age: 45yrs

14. MORPHOLOGY
• Microscopically:
Tongues and nests of squamous cells that produce
desmoplastic stromal response
• RANGE
May be well differentiated or poorly differentiated.
Well differentiated
Microscopic foci of stromal innvasion
Grossly conspicious exophytic tumors

15. • BARREL CERVIX:
Tumor encircles the cervix and penetrates into stroma
Identified by Direct palpation
• Can spread to pelvic lymph nodes
• Can extend to parametrial soft tissue

16. CLINICAL FEATURES
• Seen in women who:
Never had pap smear
Not screened for many years
• Unexpected Vaginal bleeding
• Leukorrhea
• Dyspareunia (painful coitus)
• Dysuria

17. TREATMENT
• Hysterectomy
• Lymph node dissection
• Radiation
• Chemotherapy

18. STAGING OF CERVICAL CANCER

19. ENDOCERVICAL POLYP
• Benign
• Polyploid masses
• Protrude out from endocervix (sometimes exocervix)
• SURFACE:
Smooth glistening surface
Underlying cystically dilated spaces
Mucinous secretions
Lining Epithelium: Simple columnar

20. • STROMA
Edematous
Contain scattered mononuclear cells
Superimposed Chronic Inflammation
Squamous Metaplasia
Ulceration
May Bleeding

21. ENDOMETRIOSIS
• Endometrial glands and stroma are located outside
thet uterus
• Abnormal endometrial tissue
• Multifocal
• Sites Of Implantation:
1. Ovaries
2. Rectal Pouch of Douglas
3. Uterine Ligaments
4. Fallopian Tubes
5. Rectovaginal Septum
6. Peritoneal Cavity/periumbilical tissues
7. Lymph nodes, lungs, heart, skeletal muscle, or bone

22. HYPOTHESIS
• REGURGITATION THEORY:
Menstrual backflow through the fallopian tubes
• BENIGN METASTASIS THEORY:
Vascular and lymphatic spread
• METAPLASTIC THEORY:
Coelomic metaplasia (Inappropraite differentiation of
pluripotent stem cells)
• EXTRAUTERINE STEM/PROGENITOR CELL THEORY:
Circulating stem cells from bone marrow differentiate into
endometrial tissue.

23. PATHOGENESIS
Endometrial Stromal cells
prostaglandin E2 Aromatase
Recruitment and activation Estrogen Production
of macrophages

24. MORPHOLOGY
• Functioning endometrium (undergoes cycling bleeding)
Blood collects Appear as red-brown nodules/implants
• Can coalesce
• Ovaries: large blood filled cysts (CHOCOLATE CYSTS)
•
• Widespread fibrosis
• Adhesions among pelvic structures
• Sealing of the tubal fimbriated ends
• Distortion of the fallopian tubes and ovaries

25. CLINICAL FEATURES
• Diagnosed in early adulthood (20s)
• 4 Ds
Dysmennorhea (painful mensus)
Dyspareunia (painful coitus)
Dyschezia (painful defecation)
Dysuria (painful urination)
• Lower abdominal discomfort
• Pelvic pain
• Intrapelvic bleeding
• Intraabdominal adhesions
• INFERTILITY

26. TREATMENT
• OCPs
• COX inhibitors
• Aromatase inhibitors
• Surgical removal of implants
• Infertility treatment