Pathology of the Vulva,Cervix and Endometrium Flashcards
Vulva Tumours
A vulva tumour can either be classified as benign and Malignant.
Benign: Condyloma Acuminatum
Premalignant lesions:
- Low grade CIN lesions
- High grade CIN lesions, including carcinoma in situ – HPV induced lesions
Malignant: Squamous Carcinoma
Benign: Condyloma Acuminatum
Young sexually active women, especially those with multiple partners, caused by HPV types 6 and 11.
The virus is sexually transmitted sexually
Macroscopic: Warty lesion, up to 5cm in diameter and are ususally multiple
Micro:scopic: Papillomatosis, acanthosis, hyperkeratosis and parakeratosis.
Koilocytes: Epithelial cells with an enlarged irregular nuclei cells and clear cytoplasm in the superficial epithelial layers – indication of HPV infection
Identical lesions may be found on penis
Malignant: Squamous Carcinoma
Previously rare and seen mainly elderly women(Cause is not clear)
Has become more common and is being seen in younger women,These tumours are caused by HPV (16&19) and are ass. with cervical carcinoma.
They start as small white areas of epithelial thickening but as they enlarge they ulcerate.
Spreads is mainly lymphatic to the inguinal nodes
Prognosis depends on the stage of the disease
Types of Infections
Herpes virus infection - STD, painful ulcer, intra-epidermal vesicle with virus inclusions
Syphilis – primary and secondary forms can affect the genitourinary tract
Granuloma inguinale – donovanosis, STD, chronic ulceration
Lymphogranuloma venereum – Chlamydia trachomatis, ulcer, granulation tissue, fibrosis, fistula, lymphadenopahty
Candida – common, chronic irritation and inflamation
Cervical Tumours: Carcinoma of the cervix
- Squamous carcinoma_ 90%
- Adenocarcinoma_ 5%\
- Adenosqaumous Carcinoma_ 3%
- Undifferentiated Carcinoma_ 2%
Classification of HPV-associated intraepithelial lesions of the cervix-Flat condyloma
CIN I-Mild dysplasia/Low Grade CIN
CIN II-Moderate dysplasia/High grade dysplasia
CIN III-Severe dysplasia or carcinoma in situ
Cytology Screening Programmes
Erroneously referred to as cervical cancer screening
Aim is to detect atypical cells in pre-invasive stage
Local measures as treatment – diathermy large loop excision of the transformation zone (LLETZ)
Cytology:
Simple, safe, non-invasive
Detect pre-cancerous changes in cervix
Majority from asymptomatic women
National screening program – lower mortality
Cytology detect abnormal (dyskaryotic) nuclei
Degree of abnormality may not always correlate with subsequent histological findings in a biopsy
Not reliable to detect invasion
Liquid-based cytology:
- Cells received suspended in fluid and prepared as a near monolayer on a slide and stained
- Replaced smearing of cells onto glass slide from a spatula
Clinical consequence of cervical cytology
The consequences of cervical cytology can be divided into Cytology finding and clinical conseqeuence
Cytology Finding
Unsatisfactory
Normal
‘Borderline’ changes or mild dyskaryosis
Persistent ‘borderline’ changes or mild dyskaryosis
Moderate / severe dyskaryosis
Clinical Consequence
Repeat immediately
3 or 5 yearly recall
Repeat in 6 months
Refer for colposcopy and biopsy
Refer for colposcopy and biopsy
Squamous Carcinoma
Description
Most common malignant tumour in black females in
South Africa, relatively common in white females.
Common throughout Africa, India and parts of South America. The incidence has fallen in most Western countries.
Age: 30 – 70 years.
Incidence is highest in communities with poor socio-economic conditions and where cytology screening is not done.
The risk factors and aetiology of Sqaumous Carcinoma
Sexual activity at an early age (16 or younger) Variety of sex partners Multiple pregnancies Numerous marriages Prostitution History of venereal disease Smoking
The risk facors indicate that the casusative agent is probably transmitted during sexual intercourse. The agent incriminated at present is HPV, ESP 16 AND 18, but it is possible that other agents may play a role.
The development of the carcinoma
The development of the carcinoma develops after a sequence of CIN I to II to III.
This usually takes place 10-20 yeras,but recently an alarming number of cases have been described where a CIN I lesion progresses to a carcinoma in 2 to 3 years.
The pathology of the Squamous Carcinoma
Macro: Initially a white or red area of thickening. Eventually an ulcer or exophytic lesion is formed. The lesion is friable and bleeds easily on contact. Common symptoms of carcinoma are intermenstrual bleeding and contact bleeding.
Micro: The usual features of the sqaumous carcinoma:
- Nests of pleomorphic squamous cells
- Keratinizing or non-keratinizing
- Infiltrate surrounding stroma
How does the spread of a squamous carcinoma occur:
Resasons death occurs:
Direct: Uterine corpus, vagina, parametrium, pelvic wall, bladder and rectum.
Lymphatic: iliac and para-aortic nodes
Haematogenous: rare
Death usually due to local disease:
- massive haemorrhage
- Bladder infiltration with urinary tract infections or
- Obstruction and renal failure
The prognosis of a squamous Carcinoma
Determined by the clinical stage of the disease at the time of diagnosis and the stage is related to a 5 year survival.
Stage 0: Carcinoma in situ 100%
Stage 1: Limited to cervix 90%
Stage 2: Spread to parametrium or upper vagina 60 %
Stage 3: Spread to pelvic wall or lower vagina 20
Stage 4: Metastases or bladder/rectum involvement5%
Adenocarcinoma
Less common than squamous carcinoma but more aggressive.
Increase in the incidence.
Aetiology uncertain, but HPV plays a role.
Smoking is a risk factor.
Precursor lesion: CGIN = cervical glandular intra-epithelial neoplasia, can also be picked up with routine Pap smear.
Endometritis
Most often seen after an intra-uterine pregnancy – especially with instrumentation or retained products.
Can be a complication of an IUD
Chlamydia: acute or chronic with lymphocyte infiltration and lymphoid follicles
Tuberculosis: secondary TB, granulomas are seen in the secretory phase of the menstrual cycle
Both conditions can be associated with infertility
Endometrial Polyps
Common perimenopausal and post menopausal
Presents with AUB – consists of dilated glands with prominent blood vessels in a fibrotic stroma
Tamoxifen – anti estrogen agent used in breast cancer. Paradoxically cause estrogen effects in the endometrium – can lead to hyperplasia or polyps
Endometrial Hyperplasia
Develops as a result of unopposed oestrogen stimulation and leads to thickening of the endometrium.
Some types of hyperplasia develop into endometrial carcinoma.
Symptoms of menorrhagia, post menopausal bleeding.
Sonar shows thickened endometrium. At D&C a larger volume of endometrium than normal is removed.
The source of oestrogen may be:
- Exogenous: oestrogen therapy
- Endogenous: produced by a granulosa cell tumour of the ovary, or the result of obesity( Fat cells convert androstenedione to estrogen)
The classification of Endometrial Hyperplasia
Simple hyperplasia: Increase in stroma and glands. Many glands are cystically dilated. No atypia. Little or no chance of malignant change.
Complex hyperplasia: Increase in glands which are branched and crowded. No cellular atypia. Small chance of malignant change.
Complex atypical hyperplasia: As above but with cellular atypia. Significant chance of malignant change.
Endometrial Tumours
Benign: Endometrial polyp
Malignant: Endometrial adenocarcinoma
Malignant mixed tumour ( MMMT)
Endometrial Carcinoma
Peak incidence 50 to 70 years, common in white patients(Rarely premenopausal)
Often associated with high oestrogen levels and often follows on hyperplasia – endometroid adenocarcinoma.
Sometimes no obvious underlying cause.
Risk factors ass. with Endometrial Carcinoma
- Anything that results in unopposed oestrogen stimulation.
- Obesity, especially in combination with diabetes and hypertension.
- Nulliparous women-Usually present with post menopausal bleeding.
