This document discusses vulvar cancer, including its incidence, types, anatomy, etiology, clinical features, diagnosis, staging, treatment, prognosis, and complications. Some key points include:
- Vulvar cancer accounts for 0.6% of all malignancies and 4% of genital malignancies, with squamous cell carcinoma making up 90% of cases.
- Lymph node status is the single most important prognostic marker, with 5-year survival rates of 90% for node-negative patients and 50% for node-positive patients.
- Risk factors include HPV, VIN, smoking, immunosuppression, and history of other cancers.
- Diagnosis involves biopsy of any suspicious vulvar lesions.
Vaginal cancer is a rare type of cancer most common in women 60 and older.
Women are more likely to develop vaginal cancer if they have the human papillomavirus (HPV) or if your birth mother took diethylstilbestol (DES) when she was pregnant.
There are several types of vaginal cancer:
Squamous cell carcinoma
About 70 of every 100 cases of vaginal cancer are squamous cell carcinomas. These cancers begin in the squamous cells that make up the epithelial lining of the vagina. These cancers are more common in the upper area of the vagina near the cervix. Squamous cell cancers of the vagina often develop slowly. First, some of the normal cells of the vagina get pre-cancerous changes. Then some of the pre-cancer cells turn into cancer cells. This process can take many years.
The medical term most often used for this pre-cancerous condition is vaginal intraepithelial neoplasia (VAIN). "Intraepithelial" means that the abnormal cells are only found in the surface layer of the vaginal skin (epithelium). There are 3 types of VAIN: VAIN1, VAIN2, and VAIN3, with 3 indicating furthest progression toward a true cancer. VAIN is more common in women who have had their uterus removed (hysterectomy) and in those who were previously treated for cervical cancer or pre-cancer.
In the past, the term dysplasia was used instead of VAIN. This term is used much less now. When talking about dysplasia, there is also a range of increasing progress toward cancer - first, mild dysplasia; next, moderate dysplasia; and then severe dysplasia.
Adenocarcinoma
Cancer that begins in gland cells is called adenocarcinoma. About 15 of every 100 cases of vaginal cancer are adenocarcinomas. The usual type of vaginal adenocarcinoma typically develops in women older than 50. One certain type, called clear cell adenocarcinoma, occurs more often in young women who were exposed to diethylstilbestrol (DES) in utero (when they were in their mother’s womb). (See the section called "What are the risk factors for vaginal cancer?" for more information on DES and clear cell carcinoma.)
Melanoma
Melanomas develop from pigment-producing cells that give skin its color. These cancers usually are found on sun-exposed areas of the skin but can form on the vagina or other internal organs. About 9 of every 100 cases of vaginal cancer are melanomas. Melanoma tends to affect the lower or outer portion of the vagina. The tumors vary greatly in size, color, and growth pattern. More information about melanoma can be found in our document called Melanoma Skin Cancer.
Sarcoma
A sarcoma is a cancer that begins in the cells of bones, muscles, or connective tissue. Up to 4 of every 100 cases of vaginal cancer are sarcomas. These cancers form deep in the wall of the vagina, not on its surface. There are several types of vaginal sarcomas. Rhabdomyosarcoma is the most common type of vaginal sarcoma. It is most often found in children and is rare in adults. A sarcoma called leiomyosarcoma is seen more often in adults.
Vaginal cancer is a rare type of cancer most common in women 60 and older.
Women are more likely to develop vaginal cancer if they have the human papillomavirus (HPV) or if your birth mother took diethylstilbestol (DES) when she was pregnant.
There are several types of vaginal cancer:
Squamous cell carcinoma
About 70 of every 100 cases of vaginal cancer are squamous cell carcinomas. These cancers begin in the squamous cells that make up the epithelial lining of the vagina. These cancers are more common in the upper area of the vagina near the cervix. Squamous cell cancers of the vagina often develop slowly. First, some of the normal cells of the vagina get pre-cancerous changes. Then some of the pre-cancer cells turn into cancer cells. This process can take many years.
The medical term most often used for this pre-cancerous condition is vaginal intraepithelial neoplasia (VAIN). "Intraepithelial" means that the abnormal cells are only found in the surface layer of the vaginal skin (epithelium). There are 3 types of VAIN: VAIN1, VAIN2, and VAIN3, with 3 indicating furthest progression toward a true cancer. VAIN is more common in women who have had their uterus removed (hysterectomy) and in those who were previously treated for cervical cancer or pre-cancer.
In the past, the term dysplasia was used instead of VAIN. This term is used much less now. When talking about dysplasia, there is also a range of increasing progress toward cancer - first, mild dysplasia; next, moderate dysplasia; and then severe dysplasia.
Adenocarcinoma
Cancer that begins in gland cells is called adenocarcinoma. About 15 of every 100 cases of vaginal cancer are adenocarcinomas. The usual type of vaginal adenocarcinoma typically develops in women older than 50. One certain type, called clear cell adenocarcinoma, occurs more often in young women who were exposed to diethylstilbestrol (DES) in utero (when they were in their mother’s womb). (See the section called "What are the risk factors for vaginal cancer?" for more information on DES and clear cell carcinoma.)
Melanoma
Melanomas develop from pigment-producing cells that give skin its color. These cancers usually are found on sun-exposed areas of the skin but can form on the vagina or other internal organs. About 9 of every 100 cases of vaginal cancer are melanomas. Melanoma tends to affect the lower or outer portion of the vagina. The tumors vary greatly in size, color, and growth pattern. More information about melanoma can be found in our document called Melanoma Skin Cancer.
Sarcoma
A sarcoma is a cancer that begins in the cells of bones, muscles, or connective tissue. Up to 4 of every 100 cases of vaginal cancer are sarcomas. These cancers form deep in the wall of the vagina, not on its surface. There are several types of vaginal sarcomas. Rhabdomyosarcoma is the most common type of vaginal sarcoma. It is most often found in children and is rare in adults. A sarcoma called leiomyosarcoma is seen more often in adults.
Colorectal cancer is most common GI cancer
The rectum is the most frequent site involved
Adenoma-carcinoma sequence: Arises from adenoma in stepwise progression
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
7. Applied Anatomy
Single most prognostic marker – L N status
5 yr survival rate
No LN - 90%
LN - 50%
Superficial Inguinal Lymph node – Sentinal Lymph
Node
8.
9. Etiology
HPV
VIN
CIN
Lichen sclerosis
Squamous hyperplasia
Immunodeficiency
History of genital warts
Smoking
Alcohol
Immunosuppression
H/O Cervical or Vaginal cancer
Northern Europe ancestry
11. Clinical features
Postmenopausal female
(Mean Age – 65 yrs)
VIN
Vulval Pruritis
Lump or mass
Rare – bleeding/ulcerative lesions, discharge
Pain or dysuria
Large metastatic mass in groin
Other malignancies – HPV and smoking associated
14. Staging
IA Tumor confined to the vulva or perineum, ≤ 2cm in size
with stromal invasion ≤ 1mm, negative nodes
IB Tumor confined to the vulva or perineum, > 2cm in size or with
stromal invasion > 1mm, negative nodes
II Tumor of any size with adjacent spread (1/3 lower
urethra, 1/3 lower vagina, anus), negative nodes
15. Staging
IIIA Tumor of any size with positive inguino-femoral lymph
nodes
(i) 1 lymph node metastasis ≥ 5 mm
(ii) 1-2 lymph node metastasis(es) < 5 mm
IIIB (i) 2 or more lymph nodes metastases ≥ 5 mm
(ii) 3 or more lymph nodes metastases < 5 mm
IIIC Positive node(s) with extracapsular spread
16. Staging
IVA (i) Tumor invades other regional structures (2/3
upper urethra, 2/3 upper vagina), bladder mucosa, rectal
mucosa, or fixed to pelvic bone
(ii) Fixed or ulcerated inguino-femoral lymph nodes
IVB Any distant metastasis including pelvic lymph
nodes
17. Prognosis
Lymph nodes status
Lesion size
Histologic grade, tumor thickness, depth of stromal invasion, lymph-
vascular space involvement, tumor ploidy
Stage I – 79%
Stage II – 59%
Stage III – 43%
Stage IV – 13%
21. Stage Ia – Microinvasive T1a
Wide Local excision – deep upto dermis
Stage Ib & II – Early vulval cancer
Radical local excision plus Ipsilateral groin node
dissection
- 1 cm negative margin
- Extending up to inferior fascia of urogenital diaphragm
- Separate incision technique
Treatment
22. Treatment
Midline lesions
Anterior – clitoris sparing surgery – 8mm margin
Periclitoral lesion in young pt – small field RT with
concomitant chemosensitization
small lesion – 5000 cGy external radiation
f/b biopsy
23. Treatment
Stage II involving adjacent srtucture
Radical vulvectomy or radical local excision Plus
LN Dissection
Advanced disease
Surgery plus RT
plus
concomitant chemo
28. Closure of large defects
Small defects – primary closure without tension
Large – left open to granulate
Full thickness skin flap – rhomboid or mons pubis flap
Myocutaneous flap – gracialis
Tensior fascia lata myocutaneous graft
29. Management of LN
> 2 cm diameter
> 1 mm invasion
Surgery – trt of choice
Bilateral dissection - midline lesions, clitoris, post forchet
- unilateral bulky LN / multiple microscopic
LN
Bulky LN – debulking
Fixed unresectable LN - chemoradiation
30. Sentinal Lymph node biopsy
Criteria
1) unifocal primary tumour of 4 cm or less in diameter with >
1 mm invasion
2) no obvious metastatic disease on physical
examination/imaging
31. Postop management
Ambulation on day 1 or 2
DVT prevention
Subcutaneous heparin
pneumatic calf compression
Frequent dressing
Suction drainage of each side of the groin
Sitz bath
32. Early Postoperative Complications
Groin wound infection, necrosis, breakdown
En bloc operation – 53-85%
Separate-incision approach – 44%
UTI
Lymphocyst
DVT
Pulmonary embolism
MI
Hemorrhage
33. Late Complications
Chronic lymphedema
Recurrent lymphagitis or cellulitis
Usually responds to oral antibiotics
SUI
Introital stenosis
Femoral hernia (uncommon)
Depression, altered body image and sexual dysfunction
Pubic osteomylitis
Fistula
34. Recurrent Vulvar cancer
≥ 3 LN - 2/3 of vulvar cancer recur within first 2 years from initial
Tx.
Local recurrence
Margin status
Closer than 0.8cm -> 50% recur
Primary lesion larger than 4cm in diameter
Ipsilateral lymphovascular space invasion
Deep invasive tumour
Tx.
Additional surgery with myocutaneous graft
External beam therapy + interstitial needles
with chemotherapy
35. Regional and Distant Recurrence
Difficult
Poor prognosis
Radiation
Chemotherapy
Bleomycin and methotrexate & lomustine
Bleomycin and mitomycin C
Cisplatin, vincristine & paclitaxel
Response
Usually disappointing
Long-term survival is very uncommon
36. Role of Radiation Therapy
primary vulval ca.
Advanced disease
LN meta – microscopic, gross
Possible roles for RTx.
Involved or close surgical margin
Small primary tumor - primary Tx.,
Particularly clitoral or periclitoral lesion
37. Melanoma
Rare
Incidence : 0.1-0.19/100,000women
Second most common of vulvar malignancy
Postmenopausal white women
No symptoms (most)
Itching, bleeding, groin mass
Labia minora, clitoris
Vulvar nevi are junctional, precursor lesion to melanoma; thus,
should be removed
38. Histopathology
Mucosal lentiginous melanoma
Flat freckle, quite extensive, superficial
Superficial spreading melanoma
Most common, superficial
Nodular melanoma
Most aggressive, raised lesion
Penetrate deeply
Metastasize widely
¼ of cases of melanomas
Macroscopically amelanotic -> spread early
42. Bartholin Gland Carcinoma
Rare
Postmenopausal
Premenopausal
Honan’s criteria
The tumor is in the correct anatomic position
The tumor is located deep in the labium majus
The overlying skin is intact
There is some recognizable normal gland present
43. Bartholin Gland Carcinoma
Signs and Symptoms
Vulvar mass or perineal pain
10% of patients may be mistaken for benign cysts or
abscesses
Treatment
Radical vulvectomy with bilateral groin and pelvic LN
dissection
Fixed, involves adjacent structures-> postop radiation
and chemotherapy is preferable
The FIGO staging used for squamous lesions is not applicable to melanomas
Because the lesions are usually much smaller,
and the prognosis is related to the depth of tumor invasion rather than to the diameter of the lesion