Download Thursday February 22, 2001

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts
no text concepts found
Transcript
Friday February 23, 2001, 11a, P022311
Pathology- Dr Mira
Scribe: Steve Hewitt
Proof: Tony Cauchi
Pathology of Female Genital Tract
Scribe note: Well, the good news is that we are done with the Translation part of the course. The bad, however, is that we’re not out of the
woods yet. After scribing this lecture I felt like unwinding by watching Sabado Gigante on Univision, or at least Robert Rodriguez’s Sundance
favorite El Mariachi, or maybe something by Pedro Almodovar. That said, Dr M started with Vulvar Cysts on page 365 of the notes.
The numbers that appear accompanying the slide headings refer to his power point presentation on the web.
http://www.macmed.ttuhsc.edu/Mira/gynecologic/index.htm
 Vulvar Cysts
o Most vulvar cysts are benign.
o Epidermal inclusion cysts are some of the most common cysts in the vulvar region. They are
usually secondary to trauma, i.e. child delivery or surgery done during delivery.
 Manifest as subq lesions that involve the labia majora or minora.
 Frequently seen in areas where an episiotomy has been performed, especially in
multiparous women. Also seen in posterior fornix secondary to lacerations during delivery.
 Slide- histo (photo 46-47): Cyst is lined by squamous epithelium and filled with
abundant keratinous debris, NOT sebum. This debris resembles sebum, however, and
these cysts are known clinically as sebaceous cysts.
 Slide (Photo 46-47): Dermal cyst with adnexal structures below the squamous
epithelium. In an epidermal cyst, however, there are no skin adnexa associated with the
lesion.
o Bartholin’s cysts are frequently secondary to inflammation of Bartholin’s glands- Bartholinitis,
abscesses.
 Can occur at any age, and reach a size of 3-5 cm.
 Inflammation causes glandular secretions to accumulate within the lumen of the duct.
Therefore, this is a cyst of the duct, NOT a cyst of the gland itself.
 Can be excised or marsupialized (incision the cyst and invagination of the flaps of the cyst
to allow drainage).
 Slide-gross (48): Bartholin’s cyst, as opposed to B’s abscess, involves no inflammation
of the surrounding skin. It is usually located in the vestibulum (posterolateral aspect of
introitus).
 Slide-histo (49): This is a cyst of the duct so it is lined by the transitional epithelium of the
duct. Frequently you see some transformation to squamous epithelium due to metaplasia.
Thus, you can see transitional or squamous epithelium, or both, depending on the
degree of squamous metaplasia present.
 Slide- histo (50): At high power, epithelium is similar to that of bladder or ureter. The
superficial cells are large, with large amount of cytoplasm, while those at bottom are
smaller with less cytoplasm.
o Mucous cysts arise from vestibular glands in the vulva and from the paraurethral (Skene’s)
glands.
 These are mucus glands, so the epithelium will stain for mucin using mucicarmin or
alcian blue.

Importantly, you will NOT see myoepithelial cells or smooth muscle underneath the
wall of the cyst. This is important to distinguish these cysts from others that may have
mucin content.
 Slide-gross (52): located in same area as Bartholin’s glands
 Slide- histo (53): lined with columnar mucinous epithelium without visible nuclei at the
base of the epithelium. Cytoplasm is filled with mucopolysaccharide, so PAS will stain
the cell pink. There are no myoepithelial cells or muscle present below the epithelium.
 Miscellaneous Benign Vulvar Lesions
o Ectopic breast tissue- can be seen in vulva. The glands in the vulva are essentially like those in
the breast, having the same embryologic origin. The vulvar glands can develop functional activity
similar to those in the breast.
 Slide-gross (55): soft, protruding mass of ectopic breast tissue on internal aspect of labia
majora. This mass can actually lactate during pregnancy. Keep in mind that any cyst that
occurs in the breast can also occur in ectopic breast tissue in the vulva- cancer,
fibroadenomas, and fibrocystic changes.
o Molluscum contagiosum- is caused by a poxvirus and is an STD; characterized by papules on
the skin with central umbilication where most of the viral inclusions are located.
 Can occur anywhere on the body; it’s an STD so contact with an infected part of the
body will produce the characteristic lesions.
 Slide-gross (57): lesions with central umbilicated area full of keratin debris and cells
containing molluscum bodies, which are viral inclusion bodies. The lesion will not
infiltrate the dermis so it is not a tumah
 Slide- histo (58): papillomatous proliferation with hyperkeratosis.
 Slide- histo (59): large pink inclusion bodies “in bottom layer of skin”= molluscum
bodies.
o Vestibular adenitis- unknown etiology, but “it’s a very annoying” inflammation of the vestibular
glands in the posterior introitus. It’s a very painful process that frequently ends up as ulcerations
of the introitus. Excision of the offending glands is the best treatment.
o Soft tissue tumors- there are many types that you see in other parts of the body that you also
can see in the vulva- lipomas, leiomyomas. The following tumors are found more commonly in the
vulva than elsewhere (although granular cell tumors are an exception).
 Granular cell tumors have been described in practically every organ and tissue in
the body.
 Cellular angiofibromas can be confused with sarcomas.
 Aggressive angiomyxoma and angiomyofibroblastoma are very characteristic of
the vulva, especially angiomyxoma because it can infiltrate into the vulvar and
perivulvar soft tissues.
 Slide- gross (60): This is how most soft tissue tumors will present- not exactly within
the vulva but outside in the labia majora or perineal/gluteal areas. Usually a subq
tumor that protrudes through the skin. This one is a lipoma.
 Angiomyofibroblastomas should be remembered in differential dx for soft tissue
tumors. These are usually well circumscribed, and histologically similar to aggressive
angiomyxomas. They differ in that angiomyxomas have infiltrative margins
 Slide- histo (62): Aggressive angiomyxoma has hypocellular stroma, large vessels
with thick walls, and proliferative myofibroblasts that infiltrate the surrounding tissue.
This is a very aggressive, locally invasive and destructive lesion, but it doesn’t
metastasize. Angiomyofibroblastomas have alternating areas of hypo- and
hypercellularity, and the vessels tend to be more capillary-like with thinner walls.
 Both of these lesions are important to know in vulvar soft tissue tumor
pathology.
 Skin tags and nevi are common.
 Papillary Hidradenoma
o The counterpart to the ductal papilloma of the breast because they are histologically similar.
o Well-circumscribed tumor margins. Characterized by papillary proliferation of epithelium within the
gland.
o Slide-gross (64-65): large nodules in the skin of the labia majora, or more commonly as
umbilicated lesions that can be confused with cancer or other inflammatory disease of the vulva
that produce ulcers or nodules with central umbilication.
o Slide-histo (66-67): again, similar to papilloma of the breast. Complex papillary proliferation that
“fills up the gland.” Usually the epithelium of these lesions is a double layer of epithelial cellscells on the surface are more columnar/cuboidal with round nuclei usually located at the base of
the cell, with myoepithelial cells at the bottom of the double layer.
o Staining with mucicarmin will yield a positive result because these tumors produce mucus.
 Vulvar Dystrophy
o This is an umbrella term for lichen sclerosus and squamous hyperplasia. These lesions can
coexist simultaneously. They are NOT premalignant lesions, but 10 % of squamous cell
carcinomas of the vulva actually develop in association with squamous hyperplasia or lichen
sclerosus. Additionally, both of these lesions can be accompanied by vulvar intraepithelial
neoplasias (VIN) (see below) or vulvar dysplasias.
o
Lichen sclerosus (previously known as lichen sclerosus atrophicus) can occur at any age
(newborn to postmenopausal women), but it is most common in postmenopausal women.
 Characterized by thinning of the epidermis and loss of rete pegs, with dermal fibrosis and
chronic “lichenoid” inflammation- the inflammatory cells infiltrate underneath the dermis.
 Patients tend to scratch these lesions, leading to hemorrhage and infection
 Slide- gross (69-70): (Robbins p 1041, 24-6) skin of vulva if white, shiny and smooth,
and its elasticity is lost. The skin is thin and “stretched out,” so introitus can be practically
obliterated. Lichen sclerosus can involve part or the entire vulva, including clitoris, labia
minora, and perineal/perianal skin. Disease can progress to destruction of entire labia
minora/majora
 Slide-histo (71): (p 1041, 24-7) similar findings in both male and female. Hyperkeratotic
skin with “big fat” layer of keratin on top of epidermis. Rete pegs and ridges are lost so no
papillae are evident underneath the skin- the skin is flat. Dermis is frequently edematous
and sclerotic
 Sometimes the capillaries of the skin dilate, allowing the “lichenoid infiltration” underneath
the lesion. Therefore, although the skin is thinning, it is still metabolically active (meaning
that there is no atrophy, which is why “atrophicus” was dropped from the disease name).
 There is usually no cellular atypia, but some can become dysplastic- thus don’t forget the
possibility of cancer in evaluation of lichen sclerosus.
o Squamous hyperplasia, previously known as hyperplastic dystrophy.
 Slide- gross (72): a much thicker, more leathery lesion (as opposed to lichen’s thin, white
lesion) that involves most of the vulvar skin.
 Slide-histo (73): (p 1042, 24-8) There is a very prominent hyperkeratinocytic hyperplasia
with long papillae/rete pegs. There is a “lichenoid” inflammatory infiltrate at the bottom. In
general, there will be a large thick layer of keratin under surface of skin.
 These lesions can be mixed with lichen sclerosus.
 Vulvar Intraepithelial Neoplasia (VIN)
o This is a precancerous lesion. The dysplasia seen is graded as mild, moderate or severe (VIN IIII), as well as carcinoma in situ.
o Associated with high-risk HPV types 16, 18 and some of the 30 group (last year’s scribe says
30 and 40 as well). These lesions can have many different types of clinical presentations.
o Slide-gross (B1): multiple hyperpigmented skin lesions of variable size with irregular borders.
This could be a melanocytic lesion OR carcinoma in situ.
o Slide-gross (B2): multiple white plaques/ leukoplakias covering labia majora.
o Leukoplakia is a clinical term that indicates a white plaque covering the vulvar skin. It does not
describe the underlying pathology of the lesion. All these lesions have hyperkeratosis, which is
why they look white, but underneath they can be inflammatory OR neoplastic. Therefore,
ALWAYS BIOPSY any leukoplakia in any woman at any age in order to dx any cancer present.
o Slide-gross (B3-B4-B5): Carcinoma in situ of the vulva can present as a hyperpigmented lesion
involving practically all the vulvar skin- labia majora/minora, clitoris. Lesions can be papular and
diffuse.
o Slide-histo (B6-B7): (p 1043, 24-10) dx of VIN depends on degree of proliferation of dysplastic
cells into the squamous epithelium. Mild dysplasia usually involves the inner third of the
epithelium, moderate extends into the “middle” of the epithelium, and “anything after that” (i.e.,
involving the full thickness of the epithelium) is severe dysplasia or carcinoma in situ. The cells
of carcinoma in situ are very large, with very little cytoplasm and hyperchromatic nuclei with
intense mitotic activity.
o Mitotic figures in the vulva are normally only seen in the basal cell layer; any mitosis outside of this
layer is abnormal and indicates dysplasia.
 Squamous Cell Carcinoma (SCC) of the Vulva
o May appear as leukoplakia so you must biopsy. ALL leukoplakias need to be biopsied.
o Prognosis of SCC depends mostly on depth of invasion, which is measured by biopsy. The
deeper the invasion, the greater the likelihood of metastatic disease to regional lymph nodes.
o Verrucous carcinoma is a type of SCC that has very good prognosis because it does not infiltrate
and therefore doesn’t involve lymphatics, making risk of metastasis very low.
o Slide-gross (B9, but not benign, B10): SCC usually presents as large, ulcerating lesions that
aren’t distinguishable from other inflammatory diseases. Usually has necrotic borders, and lesion
o
o
o
o
o
o
can become infected and covered with a purulent exudate. Thus, inflammatory conditions are
always in the differential dx of cancer, and cancer is always in the diff dx for inflammatory
conditions of the vulva. Can involve labia majora/minora, clitoris.
Slide-gross (B11): SCC has destroyed right side of labia majora and clitoris.
Slide-histo (B12): no different than SCC anywhere else. Tongues of squamous cells infiltrating
the stroma.
Slide-histo (B12): Sometimes the cells of SCC do not look extremely malignant. Cells in center
have abundant eosinophilic cytoplasm. Cells at periphery look more malignant, with more mitosis.
An infiltrative border indicates SCC, whereas a smooth border will indicate verrucous carcinoma.
So, no matter how well-differentiated the squamous epithelium, if you see an infiltrative margin,
then you’re looking at SCC.
Slide-histo (B13): Verrucous carcinoma has a very smooth border; it pushes against the dermis
rather than infiltrating. Can be difficult to differentiate from condyloma acuminatum
Slide-chart (B14): Illustrates how prognosis/depth of invasion relates to metastatic disease.
Lesions that are a cm or less have low chance of metastasis. Deeper lesions (2-3 cm) have about
a 12% chance of mets. 5 cm lesions have a 50% chance of mets. This is important because
survival rate for vulvar cancer drops tremendously when mets to regional lymph nodes occur.
Patients with SCC without mets have a 90-95% 5 year survival rate, but when mets occur survival
rates drop to 10-20%.
Depth of invasion (Slide B15) is measured from the tip of the rete pegs/papillae adjacent to the
tumor down to the deepest portion of the tumor. Can also be measured from skin surface, but this
will only allow measurement of the thickness of the tumor, not its maximal depth of invasion.