Download Free Medical Pre-cancer and Malignant Disease of Vulva PowerPoint Presentation

Pre-cancer and Malignant Disease of Vulva PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Pre-cancer and malignant disease of vulva”.

This medical PowerPoint presentation is about pre-cancer and malignant disease of vulva. The vulva is the external genitalia of the female reproductive system, and like other parts of the body, it can develop pre-cancerous and cancerous conditions.

Pre-cancerous conditions of the vulva include Vulvar dysplasia and Vulvar intraepithelial neoplasia (VIN).

Malignant diseases of the vulva include Vulvar cancer and Pagets disease of the vulva.

Tags : Pre-cancer and malignant disease of vulva, external genitalia of the female reproductive system, Vulvar dysplasia, Vulvar intraepithelial neoplasia , Vulvar cancer, Pagets disease of the vulva, Gynaecology, Gynaecology PowerPoint presentation, Gynecologic Oncology, Gynecologic Oncology PowerPoint presentation

Published on : May 29, 2023 | Views : 763 | Downloads : 0

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Pre-cancer and malignant disease of vulva MA 張簡展照
Slide 2-

International Society for the study of Vulvar Disease
Slide 3-

Vulvar intraepithelial neoplasm
Slide 4-

Epidemiology & Risk factor Premenopausal (75%) No racial predisposition Similar to vulvar cancer HPV infection Cigarette smoking Immunodeficiency Immunosupression
Slide 5-

HIV positive womem Vulvovaginal / perianal intraepithelial neoplasia is more prevalent in HIV infected women (9 % & 1 %) 7% HIV positive with vulvovaginal or perianal condylomata acuminata  high-grade intraepithelial lesions
Slide 6-

Histopathology Table 2
Slide 7-

Human papillomavirusvaginal intraepithelial neoplasia grade 1. Note the surface spicules with partial uptake of Lugol's stain.
Slide 8-

(A) Vaginal intraepithelil neoplasia grade 2. (B) Vaginal intraepithelial neoplasia grade 3.
Slide 9-

Carcinoma in situ of the vulva(vulvar intraepithelial neoplasia grade 3)
Slide 10-

VIN III
Slide 11-

Subtypes of VIN III Basaloid– thickened epi. with flat, smooth surface, composed of atypical immature parabasal type cells with numerous mitotic figures and enlarged hyperchromatic nuclei Warty(condyloma) – undulating or spiking surface, condyloma appearance, cellular proliferation with numerous mitotic figures and abnormal maturation Differentiated (simplex) – thicked and parakeratotic epi. with elongated and anastomosing rete ridges, abnormal cells confined to parabasal and basal portion of the rete pegs with little or no atypia above the basal layers, basal cell positive to P53 which extend above the basal layers to epidermis, a precursor of HPV-negative vulvar cancer
Slide 12-

Vulvar hyperkeratosis
Slide 13-

Vulvar carcinoma in situ: carcinoma in situ extending into the hair follicle.
Slide 14-

Overview of pathogenesis Embryonic cloaca anogenital epithelium (cervix, vagina, anus, lower 3cm of rectal mucosa up to the dentate line) Susceptible to similar exogenous factors HPV !! CIN, VIN, VAIN, PAIN may multifocal !! The risk of neoplastic progression of VIN to invasive cancer :lower than CIN !! Genetic instability risk to invasive Dz.
Slide 15-

Distribution of VIN Unifocal Postmenopause No relationship to HPV Histology: differentiated type Multifocal Younger premenopausal Associated with HPV High grade & oncogenic HPV: 16,18,31 Interlabial grooves, post. fourchette, perineum 2/3 p’t of VIN
Slide 16-

Clinical manifestations Pruritus Altered appearance of the vulva Palpable abnormality Perineal pain or burning Dysuria 50% asymptomatic !!
Slide 17-

Diagnosis Physical examination --inspection & palpation (mass, color, ulcer) --most multifocal, non-hairy part --raised/verrucous white, red, brown, pink, gray, macular lesion
Slide 18-

Raised/verrucous white Changes that appear infectious (eg, condyloma acuminata) should be treated with a course appropriate therapy and Bx. if refractory or not resolve !!
Slide 19-

Red
Slide 20-

Brown
Slide 21-

Diagnosis-- Colposcopy Acetic acid -- 2-5% acetic acid, several minutes, dense acetowhite, punctation or vascular abnormality (may be a sign of invasive cancer) Toluidine blue -- 1% paint the vulva, wash with 1% acetic acid 2 mins later retained area -- False negative (infection, nonneoplastic ulceration) -- False positive ( thick hyperkeratotic lesions, ulcerated or abraded area absort only small amount of dye) Identify subclinical lesions, define the extent of disease
Slide 22-

Diagnosis Biopsy -- local anesthetic -- Punch Bx & Excisional Bx. Differential diagnosis -- Invasive squamous cell cancer, lichen sclerosis, planus -- difficult to distinguish esp. occur concurrent
Slide 23-

Treatment—Goal Prevent development of invasive vulvar cancer and relieve symptoms Preserve vulvar anatomy and function Based on biopsy results, extent of disease and symptom
Slide 24-

Treatment Wide local excision -- individual lesion with a 1 cm margin -- removal of epidermis -- satisfactory cosmetic result # remove small amount of dermis to insure invasive disease Skinning vulvectomy -- more extensive lesions -- removing the vascular skin along a avascular plane -- primary closure or use skin graft
Slide 25-

Treatment Laser ablation -- multi-focal or extensive -- cosmetic advantages -- effective in multiple small lesions (VIN I, II) -- evaluate the coexistent invasive cancer previously -- use colposcopy to control depth (1 mm) -- cure rate: 70% (1st), 1/3 need 2nd, 3rd Topical 5-FU -- conservative, preserve anatomy -- younger p’ts -- may result in buring pain, inflammation, edema and painful ulceration -- exclude invasive disease previously -- cure rate: 40-75%
Slide 26-

Treatment Imiquimod -- topical immune response modifier -- FDA-proved to treat anogenital warts -- treat multifocal VIN II or III… Topical immunotherapy, vaccines against HPV, photodynamic therapy, ultrasound surgical aspiration, chemopreventive agents…… Careful evaluation to exclude the presence of invasive squamous cell carcinoma is important prior to the therapy !!
Slide 27-

Prognosis Natural Hx. without Tx -- high grade: varies from persistence, progression to remission -- 9% untreated VIN III invasive cancer ( 8 yrs 內) Recurrence after Tx. -- at least 1/3 -- regardless to Tx. Modality -- Risk factors: high grade VIN, multiple focal or multicentric, positive margin on Bx. -- Long term F/U: 6 ms for 2 yrs 1 yr
Slide 28-

Vulvar Cancer
Slide 29-

Epidemiology & risk factor 4th common GYN cancer Postmenopause 65 y/o Cigarette smoking Vulvar dystrophy (eg, lichen sclerosis) VIN or CIN HPV infection Immunodeficiency Cx. cancer Hx. Northern European ancestry
Slide 30-

Clinical manifestations Unifocal vulvar plaque, ulcer or mass (most labia majora) 5% multifocal (evaluate vulvar and perianal skin, cervix, vagina) Synchromous second neoplasm (most cervical neoplasm): 22% Pruritus (vulvar bleeding, discharge, dysuria, enlarged groin LN…)
Slide 31-

Diagnosis Biopsy !! -- Determine the depth and nature of stromal invasion -- Taken from the center of the lesion -- If multiple abnormal areas: multiple biopsies to map -- Use acetic acid & colposcopy if not sure !
Slide 32-

Histopathology Squamous cell carcinoma -- Variant: verrucous carcinoma Melanoma Basal cell carcinoma Sarcoma Extramammary Paget’s disease Bartholin gland adenocarcinoma
Slide 33-

Squamous cell carcinoma Keratizing, differenrtiated or simplex type -- More common -- Older p’ts -- No related to HPV infection -- Associated with vulvar dystrophy Classic, warty or Bowenoid type -- HPV 16, 18, 33 -- Younger p’ts -- Most present with early stage >90% of vulvar malignancy, 2 subtypes
Slide 34-

Squamous cell carcinoma of the vulva, keratinizing type. The multiple pearl formations consist of laminated keratin.
Slide 35-

Early invasive carcinoma of vulva originating from vulvar intraepithelial neoplasia. An irregular nest of malignant cells extend from the base of rete pegs. Desmoplastic stromal reaction and chronic inflammation are useful diagnostic signs of stromal invasion. The depth of stromal invasion is measured from the base of the most superficial dermal papilla vertically to the deepest tumor cells.
Slide 36-

Cervical cancer: also strongly linked to persistent HPV infection…There is evidance that some high grade VIN and VAIN is a mono-clonal lesion derived from high grade or malignant cervical disease !!
Slide 37-

Verrucous carcinoma—a variant of SCC Verrous configuration Papillary fronds without central connective tissue core (typical of condyloma acuminata) Rarely metastasis to LN May local destructive Verrucous carcinoma of the vulva. Note the exophytic hyperkeratotic papillary fronds and endophytic bulky rete pegs with smooth borders.
Slide 38-

Melanoma 2nd common, 5% of primary, 3~7% of all melanomas Postmenopause, white, nonHispanic 68 y/o Pigmented lesion Most clitoris or labia minora Melanoma of the vulva involving the right labium minus.
Slide 39-

Vulvar melanoma. Spindle-shaped melanoma cells form interlacing bundles, and some contain melanin pigment (right upper corner). Epidermal invasion is evident in the form of Pagetoid migration (left upper corner).
Slide 40-

Vulvar cancer Basal cell carcinoma -- 2% / 2% -- postmenopausal Caucasian women -- locally invasive -- rodent ulcer with rolled edges and central ulceration -- high incidence of antecedent or concomitant malignancy Sarcoma -- 1-2% -- poor prognosis
Slide 41-

Extramammary Paget’s disease Intraepithelial adenocarcinoma < 1% 60~70 y/o Pruritus (70%), eczematoid appearance, well-demarcated, slightly raised edges with a red background, dotted with small pale islands Dx.: Bx. Histopathology ! Persistent pruritus with no response to antieczema therapy within 6 weeks Bx. !! Invasive adenocarcinoma may be beneath or within the surface lesion synchronous neoplasm !!
Slide 42-

Paget's disease of the labium major
Slide 43-

Paget's disease of vulva. The epidermis is permeated by abnormal cells with vacuolated cytoplasm and atypical nuclei. This heavy concentration of abnormal cells in the parabasal layers is typical of Paget's disease.
Slide 44-

Bartholin gland adenocarcinoma Rare, 57 y/o Duct lined by stratified squamous epi. which changes to transitional epi. as the terminal ducts are reached If squamous lesion related to HPV infection !! Bartholin gland tumor in a postmenopausal women or > 40 y/o Bx. to survey the malignancy !! Metastasis is common (due to rich vascular and lymphatic network)
Slide 45-

Mode of spread Direction extension to adjacent structure Lymphatic embolization: may occur early, begins at superficial inguinal LN drainage to deep inguinal and femoral LN pelvic lymphatics Inguinal-femoral lymph nodes
Slide 46-

Mode of spread Hematogenous dissemination -- typically late in the course -- rare in p’ts without inguinofemoral LN involvement
Slide 47-

Staging Clinical staging -- PE (palpate LN: inguinal, axillary, supraclavicular ) -- PV (Cx. Cytology, colposcopy of Cx, vagina & vulva due to multifocal lesions) -- Radiographic and endoscopic studied in large tumor or suspected metastasis
Slide 48-

Staging Surgical staging—FIGO -- Inguinofemoral LN status: the most important predictor of overall prognosis (clinical assessment of groin LN: false negative) -- Inguinofemoral lymphadenctomy (except stage IA) # Unilateral: unilateral lesion, distant from the midline # Bilateral: midline or bilateral lesions or unilateral lesion with positive ipsilateral LN
Slide 49-

ppt slide no 49 content not found
Slide 50-

Staging Less invasive means to assess LN status Sentinel node biopsy (unilateral) Reduce acute and long-term complications (1)Lymphoscintigraphy using radiolabeled human albumin and an intraoperative γ-detecting probe (2)Peritumor injection of isosulfan blue dye  Bilateral groin involvement is common in midline vulvar cancers  not suggest !!
Slide 51-

Treatment Goal -- Cure the cancer -- Minimize perioperative morbidity -- Maximize long-term psychosexual and physical well-being
Slide 52-

Treatment--SCC Stage IA Radical local excision without LN dissection Inguinofemoral LN metastases : <1 % Wide, deep excision of the lesion down to the inf. fascia of the urogenital diaphragm Clear margin: 2 cm (at least 1 cm)
Slide 53-

Treatment--SCC Stage IB Inguinofemoral LN metastases : >8 % Radical local excision + ipslateral inguinofemoral LN dissection ( lateralized lesion) or bilateral inguinofemoral LN dissection (central lesions)
Slide 54-

Treatment--SCC Stage II Modified radical vulvectomy + ipslateral / bilateral inguinofemoral lymphadenectomy Clear margin: at least 1 cm
Slide 55-

Small (T1) vulvar carcinoma at the posterior fourchette.
Slide 56-

Treatment--SCC Adjuvant R/T ? -- appears benefit those with two or more positive inguinal LN or positive/closes surgical margin -- The minimum number of nodes that should be examined is unclear !! -- GOG study: adjuvant R/T to high risk p’ts (> 4.1 cm tumor, positive margins, lymphovascular space invasion) with negative LN reasonable to consider !!
Slide 57-

Treatment--SCC Stage III and IV Radical vulvectomy combined with pelvic exenteration high morbidity !! Preoperative radiation therapy: downstage the tumor, allow a more conservative surgery Chemoradiotherapy: locally advanced vulvar cancer (cisplatin + 5-FU, Mitomycin + 5-FU
Slide 58-

Treatment--SCC Stage III and IV Neoadjuvant chemotherapy—for recurrent or locally advanced disease --Decreased tumor bulk and permit later resection --Result is inf. to chemoradiotherapy
Slide 59-

Treatment—Verrucous carcinoma Radical local excision Bx. suspicious LN, if positive inguinofemoral lymphadenectomy RT: contraindication !! (induce anaplastic transformation and increase the likehood of metastases) Recurrence: surgical excision
Slide 60-

Treatment Sarcomas -- Wide local excision -- Lymphatic metastases: uncommon # Exception: Rhabdomyosarcoma primary C/T + surgery Melanoma --10% vulvar cancer -- Wide local excision or radical vulvectomy -- depth /clear margin # < 1 mm 1 cm # 1~ 4 mm 2 cm # > 1 cm and extend to muscular fascia  local recurrent rate of local or radical vulvectomy is similar -- if central lesion groin LN dissection !!
Slide 61-

Treatment– Vulvar Paget’s disease Local excision or vulvectomy depend upon the extent of disease Poor prognostic markers: greater depth of invasion and lymphovascular involvement Moh’s micrographic surgery: lower recurrence rate RT or C/T ? Long-term F/U (high risk of recurrence) Annually inspection of vulva & survey tumors at other site (breast, lung, colorectum, gastric, pancreas, ovary)
Slide 62-

Treatment Bartholin gland cancer -- radical vulvectomy + bilateral groin & pelvic LN dissection --Extensive deep dissection Basal cell carcinoma -- locally aggressive but rarely metastasis -- Radical local excision without LN dissection
Slide 63-

Prognosis stage, tumor size, depth of invasion, capillary lymphatic space, older age, degree of nodal involvement
Slide 64-

Follow up Twice yearly Inspection, palpation of vulva, skin bridge and inguinal nodes Colposcopy & Bx. If suspicious
Slide 65-

Recurrent disease Local, inguinal or distant 5-yr survival rate: according to location -- Perineal : 60 % -- Inguinal and pelvic : 27 % -- Distant : 15 % RT add to surgery or C/T or a sole modality Salvage cytotoxic C/T: for distant metastases -- most active agents: those against squamous cell tumors at other sites ( Cisplatin, MTX, bleomycin, mitomycin C, cyclophosphamide) --duration of response usually low and short
Slide 66-

Treatment-- future Anti-EGFR tyrosine kinase inhibitors…
Slide 67-

Thank you for your attentions !!