Flashcards in Pathology - Nichols Deck (62):
lining (membrane) of body passages and cavities that communicate directly or indirectly with the exterior (commonly containing mucin-secreting glands)
outermost layer (covering) of an organ in a serosal cavity (peritoneal, pleura or pericardial) consisting of fibroelastic tissue covering by mesothelium continuous with the lining of the cavity
acellular fibrous (collagenous) membrane separating the organized cellular elements of a tissue from the interstitium (space b/w organized cellular element of a tissue)
purely cellular avascular layer covering and lining all the external and internal surfaces of the body and associated glands
supportive connective tissue around the parenchyma
-functional tissue of an organ, which performs the function of the organ
-fragmented glands and stroma, and degenerating blood
Why does menstruation occur?
to slough infection
What role does estrogen play in menstruation?
lack of it allows it to occure
What role does progesterone play in menstruation?
What role do the arteries play?
vasoconstrict, vasospasm, cut off blood supply causing ischemic necrosis
Proliferative Endometrium (early)
-straight glands lined with pseudostratified epithelium and stroma with spindle-shaped cells
Early Secretory Endometrium
-prominent basal cytoplasmic vaculoes (begin 36-48 hrs post-ovulation and are evidence that it has occurred)
-tortuous dilated glands containing secretions
Granulasa cells produce?
-themselves to convert androgens from thecal cells to estradiol by aromatase during the proliferative phase
What happens to granulosa cells after ovulation?
-the turn into granulosa lutein cells that produce progesterone
How would a granulosa cell tumor manifest clinically in a child?
How would a granulosa cell tumor manifest clinically in an adult?
abnormal uterine bleeding
Would a granulosa cell tumor manifest differently after menopause?
What happens to the corpus luteum if fertilization of the ovum occurs?
-keeps producing hormones, progesterone is key
What happens to corpus luteum if NO fertilization of the egg occurs?
-single cell layer of modified peritoneal mesothelial cells, overlying stroma of spindle-shaped cells
# of ovarian tumors from serosal surface?
-90% of malignant ones
Histology of Fallopian Tube
-papillary epithelium and muscular wall
-lined by ciliated epithelium
Histology of Uterus
-myometrium composed of smooth muscle
-transition from stratified squamous epithelium (exocervix) to columnar epithelium of cells with abundant cytoplasmic mucin (endocervix)
Metaplastic squamous cells
-in cervical transformation zone
-prone to infection with HPV, which can progress to squamous cell carcinoma
-prevented by Pap smear to detect dysplasia before it becomes carcinoma
Breast Duct lining?
-two-cell layer of inner epithelial and outer myoepithelial cells, surrounded by basement membrane
90% or breast cancers are?
-in situ before they are invasive, and in situ carcinoma can look very much like hyperplasia, but hyperplasia will leave the layer of myoepithelia cells in place
What do prolonged high levels of progesterone do?
-produced by corpus luteum
-transform spindle-shaped stromal cells of proliferative endometrial stroma into enlarged rounded cells with abundant smooth pink cytoplasm in a process called decidualization
-large, rounded stromal cells
-abundant smooth eosinophilic cytoplasm
Diseases of Vulva?
-inflammation, non-noeplastic epithelial disorders, dysplasia, tumors
Diseases of Vagina?
-inflammation, dysplasia, tumors
Diseases of Cervix?
-inflammation, dysplasia, tumors
Diseases fo Corpus?
-menstrual cycle, inflammation, adenomyosis, abnormal bleeding, endometrial hyperplasia, tumors
Diseases of Tubes?
-inflammation & ectopic pregnancy
Diseases of Ovary
STD, commonly affects vulva
-sexually transmitted (HSV I or II)
-common in young age
-painful papules progressing to vesicles & ulcers on vulva, vagina, cervix
-nuclear inclusions, multi-nucleation
-transmitted during neonate delivery
STD, gential wart, intraepithelial dysplasia, invasive carcinoma
STD, cervicitis, endometritis, salpingo-oophoritis
STD, Skene gland adenitis, cervicitis, endometritis, salpingitis
-about 10% of women
-predisposition: DM, pregnancy, oral contraceptives
-white mucosal surface w/curdy white vaginal discharge, discomfort, itching
-caused by flagellated protozoa
-sexually transmitted (must treat partner)
-15% of women
-heavy, foamy, gray-green vaginal discharge, mucosal irritation & itching
-feed on squamous cells
Pelvic Inflammatory Disease (PID)
-caused by Gonococcus, Chlamydia, Mycoplasm, enteric bacteria (in postpartum)-streptococci, staphlococci
-presents with vaginal discharge, pelvic pain, fever, adnexal tenderness
-vulva, vagina, cervix, endometrium, & adnexa re involved
Pathology of Gonorrheal PID
-spread: ascending from vestibular glands to vagina-cervix-corpus & adnexa
-acute suppurative salpingitis
-pyosalpinx (resolved: hydrosalpinx)
Complications of Gonorrheal PID
-infertility (from tube closure)
-sepsis (endocarditis, bacteria in blood)
-abnormal implantation site of the fetus
-most common: fallopian tubes
-sudden abdominal pain, acute abdomen, shock-like presentation about six to twelve weeks following a previous menstrual period
-early diagnosis is critical
Endometrial Histology: Proliferative Phase
-straight glands with pseudo-stratified epithelium
-negative for mucin production
-stroma is composed of spindle cells with scant cytoplasm, high mitotic rate
Endometrial Histology: Secretory Phase
-postovulation: basal secretory vacuoles decreasing mitotic activity, simple epithelial layer
-late phase: tortuous, dilated glands, prominent secretory activity, prominent stromal spiral arteries, decidulization
Endometrial Histology: Menstrual Phase
-progressively decreasing estrogen and progesterone levels
-extravasation of red blood cells into the stroma
-leukocytic infiltration of stroma
-disintegrating glands & stroma
Postmenopausal (atrophic) Endometrium
-inactive, simple or cystic glands
-no evidence of proliferation or secretion
-dense, inactive stroma
-can be reversed by exogenous hormones/or tumor producing hormones
Endometrial Hyperplasia Etiology
-prolonged, abnormally high estrogenic stimulation without progesterone effect
Endometrial Hyperplasia Conditions
-Estrogen producing tumors
Endometrial Hyperplasia Foms
-simple with/without atypia
-complex with/without atypia
Molecular Pathology of Hyperplasia & Carcinoma
-inactivation of PTEN tumor suppressor gene through deletion and/or inactivation
-normally unopposed estrogen increases PTEN production
-PTEN inactivation increases the gland sensitivity to estrogen
Simple Endometrial Hyperplasia
-glandular crowing, irregularly shaped glands with stroma
Complex Endometrial Hyperplasia
-complex glandular architecture with stroma
Complex Endometrial Atypical Hyperplasia
-glands are crowded with almost total exclusions of stroma b/w them
-cytological atypia is present