Test Bank for Robbins Basic Pathology 10th Edition by Vinay Kumar, Abul K. Abba & Jon C. Aster 9780323353175 Chapter 1-24 | Complete Guide A+
TEST BANK FOR Robbins Basic Pathology (Robbins Pathology) 10th Edition by Vinay Kumar & Abul K. Abbas , ISBN: 9780323353175 |Chapters 1-24| Guide A+
Test Bank for Robbins Basic Pathology 10th Edition by Vinay Kumar, Abul K. Abba & Jon C. Aster 9780323353175 Chapter 1-24 | Complete Guide A+
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Chapter 19 – Female Genital System
Vulva
Vulvitis
Most common cause of Vulvitis is reactive inflammation in response to an exogenous
stimulus, which may be an irritant or an allergen. Vulvitis may also be caused by infections,
which often are sexually transmitted. An important complication of Vulvitis is obstruction of
the excretory ducts of Bartholin glands. This blockage may result in painful dilation of the
glands and abscess formation.
Nonneoplastic Epithelial Disorders
Lichen Sclerosis
Lichen Sclerosis is characterized by thinning of the epidermis, disappearance of rete pegs, a
zone of acellular, homogenized, dermal fibrosis, and a bandlike nonnuclear inflammatory cell
infiltrate. When the entire vulva is affected, the labia become atrophic and stiffened, and
the vaginal orifice is constricted. The pathogenesis is unclear, but presence of activate T
cells and increased frequency of autoimmune disorders in affected women suggest and
autoimmune etiology.
Lichen Simplex Chronicus
Lichen simplex chronicus is marked by epithelial thickening (particularly of the stratum
granulosum) and hyperkeratosis. These nonspecific changes are a consequence of chronic
irritation.
Tumors
Condylomas
Condyloma is the name given to any warty lesion of the vulva. On histological examination,
the characteristic cellular feature is koilocytosis, a hallmark of HPV infection.
Carcinoma of the Vulva
There appear to be two distinct forms of valvular squamous cell carcinomas that differ in
pathogenesis and course.
1. Carcinoma
a. Related to high-risk HPV strains
b. VIN = precancerous changes in epithelium
c. Smoking and immunodeficiency increase the risks
2. Squamous carcinoma
a. Reactive epithelial changes, lichen sclerosis
b. dVIN = subtle lesions
Extramammary Paget Disease
Paget disease is an intraepidermal proliferation of epithelial cells that can occur in the skin of
the vulva or nipple of the breast. Paget disease manifests as a red, scaly, crusted plaque that
may mimic the appearance of an inflammatory dermatitis. Usually there is no underlying
carcinoma.
, Vagina
Vaginitis
Vaginitis is a common condition that is usually transient and of no clinical consequence. It is
associated with the production of a vaginal discharge.
Candida albicans curdy white discharge
T. Vaginalis watery, copious gray-green discharge
o Sexually transmitted
Malignant Neoplasms
Squamous Cell Carcinoma
Extremely uncommon cancer that usually occurs in women older than 60 years in the setting
risk factors to those associated with carcinoma of the cervix. Often associated with HPV
infection lesions.
Clear Cell Adenocarcinoma
Clear cell adenocarcinoma, very rare tumor, was identified in a cluster of young women
whose mothers took diethylstilbestrol during pregnancy to prevent threatened abortion.
These lesions appear as red, granular foci lined by mucus-secreting or ciliated columnar cells
vaginal adenosis precursor of clear cell adenocarcinoma
Sarcoma Botryoides
Sarcoma botryoides is a rare form of primary vaginal cancer that manifests as a soft polypoid
masses. It usually is encountered in infants.
Cervix
Cervicitis
Inflammatory conditions of the cervix are extremely common and may be associated with
purulent vaginal discharge. Cervicitis can be classified as infectious, or noninfectious. Almost
all are sexually transmitted.
Chlamydia trachomatis
Neoplasia of the Cervix
HPV, the causative agent of cervical neoplasia, has a tropism for the immature squamous
cells of the transformation zone. HPV is detectable by molecular methods in nearly all cases
of cervical intraepithelial neoplasia (CIN) and cervical carcinoma. The E6 and E7 proteins of
‘high risk’ HPV variants inhibit p53 and RB, respectively, two potent tumor suppressors that
act to suppress the division of squamous cells as they mature.
High risk HPV progression to carcinoma
o Integrate into host cell genome
Low risk HPV condylomas
o Express E6 and E7 with different or weaker activities
o Do not integrate into host genome
Squamous Intraepithelial Lesion (SIL, Cervical Intraepithelial Lesion)
HPV-related carcinogenesis begins with the precancerous epithelial change termed SIL,
which usually precedes the development of an overt cancer by many years, sometimes
decades.
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