Female Genital System Flashcards
1
Q
……is a specific vulvar infection that is not an STD
A
Candidal vulvitis
2
Q
HPV is a associated with……..(vulvar diseases)
A
Condyloma accuminatum, VIN, one type of vulvar squamous cell carcinoma
3
Q
Compare lichen scelrosus & lichen simplex chronicus
Both present clinically as…..
A
- Scelrosus: chct by atrophic thinning epithelium, usually with dermal fibrosis. It carries inc risk of developing squamous cell carcinoma
- Simplex chronicus: chct by thickening of epithelium usually with an inflammatory infiltrate
Leukoplakia
4
Q
VIN I & condyloma accuminatum are associated with….
A
Low risk starins of HPV 6 & 11
5
Q
Describe morphology of vulvar condyloma accuminatum
A
G: multiple may be papillary elevated (acuminata) or flat & red, pink in colour
M: consists of tree like proliferation of startified squamous epithelium with pecularr perinuckear cytoplasmic vacuolations & nuckear atypia called koilocytosis attributed to viral effect.
6
Q
Mention grades of VIN
A
Mild dysplasia (I)
Moderate dysplasia (II)
Severe dysplasia (III)
Carcinoma in situ
7
Q
HPV 16 is present in 80-90% of……
A
Cases of high grade VIN (II & III)
8
Q
Most common microscopic variety of vulvar carcinoma is …..
A
Squamous cell carcinoma
9
Q
Compare HPV-related cases & unrelated cases of squamous cell carcinoma of vulva
A
Related: in middle-aged women, usually proceeded by VIN. Cigarette smoking & immunodeficinecy increase risk of prgression into carcinoma. Poorly differentiated
Non-related: older women, . Associated with lichen sclerosus & lichen simplex chronicus. Usually well-differentiated
10
Q
Describe morphology of Paget disease of vulva
A
G: red crusted sharply demarcated areas mostly on labia majora that may mimic appearance of inflammatory dermatitis
M: chct by large epithelioid vacuolated cells infiltrate singly or in clusters within epidermis
11
Q
Sarcoma botryoides occurs in……., the microscopic picture is…….
A
Young girls
It is a rhabomyosarcoma with myxomatous areas
12
Q
Clear cell adenocarcinoma occurs in women whose mothers took…..during pregnancy
A
Diethylstilbestrol (DES)
13
Q
List causes of PID
A
- Gonococcal infection is most common cause
- Postpartum or postabortal: staph, strept, coliform bacteria
- Chlamydial infection
14
Q
List complications of PID
A
- Salpingitis: salpingo-oophritis, pyosalpinx & tubo-ovarian abscess. Untreated cases lead to infertility if bilateral
- Acute suppurative peritonitis, localized or generalized. Fibrous adhesions & blockage of oviducts
- Blood spread leading to bacteremia, septicemia & systemic pyaemia
- Intestinal obstruction: due to adhesions between small bowel & pelvic organs
15
Q
Describe microscopic features of chronic cervicitis
A
There is infiltrtion by many inflammatory cells & nabothian cysts
The mucosa may show squamous metaplasia with/out reactive atypia
16
Q
Describe pathogenesis, morphology & C/P of endocervical polyp
A
Path: inflammation trauma pregnancy have been implicated
Morphology: G: may be small & sessile to large & soft, M: made up of CT stroma containing dilated mucus secreting glands & covered by columnar epithelium may show squamous metaplasia
Clinically resents with post coital bleeding or vaginal discharge & backache
17
Q
Describe pathogenesis of cervical neoplasia
A
-HPV shows tropism to immature epitheliumin the transformation zone, detected in nearly all cases of CIN & cervical carcinoma
-The main risk factors for developing CIN include:
1. Early age of onset of sex intercourse
2. Multiple high risk sex partners
3. Persistent HPV infection: HPV 16 & 18 strains integrate into host genome & produce E6 & E7 proteins that inactivate p53 & RB genes. Affected cells become transformed capable of autonomous growth
4. Cofactirs as immunodeficiency, gene mutations & smoking
18
Q
Describe classification of CIN
A
- CIN I: mild dysplasia where dysplastic changes take place in lower 1/3 & shows koilocytotic changes
- CIN II: moderate dysplasia, dysplastic changes extend into middle third of epithelium. Itvtakes form of delayed maturation of keratinocytes & superficial layer shows more differentiation & may show koilocytotic changes
- CIN III: severe dysplasia, complete loss of maturation, greater atypia * mitoses, koilocytotic changes are usually absent
For simplification, CIN I is termed low-grade squamous intraepithelial lesion & CIN II & III are termed high-grade squamous intraepithelial lesion
19
Q
Mention diagnostic methods for CIN
A
- Exfoliative cytology & Pap smear, most successful cancer screening test
- HPV detection by molecular methods
- Colposcopy:
A. Schiller’s test, involves painting teh cervix with a solution of lugol’s iodinenormal cervix is rich in glycogen & stains, neoplastic foci fail to stain
B. Painting cervix with 5% acetic acid, areas of white epithelium (aceto-white areas) with abnormal vascular patterns (mosaic or ounctutation) - Biopsy: punch or scraping
20
Q
List most common invasive carcinomas in order of prevalenr
A
- Squamous cell carcinoma (75%)
- Adenocarcinoma & adenosquamous carcinomas (20%)
- Small-cell neuroendocrine carcinomas (<5%)
21
Q
Cervical squamous cell carcinoma peak age is …..
A
45, 10 to 15 yrs after CIN detection
22
Q
Describe morphology of squamous cell carcinoma of cervix
A
G: develops in transformation zone usually friable bleeds to touch may be fungating mass projecting into vagina, ulcerative type, infiltrative type
M: coventional squamous cell crcinoma grades 1-4
23
Q
Describe spread of cervical carcinoma
A
Local to vgina urinary bladder rectum uterus broad ligaments
Lymphatic to iliac sacral and hypogastric nodes
Blood borne in lte and advanced cases
24
Q
Describe clinical features of cervical carcinoma
A
- Patients usually present with vaginal bleeding, postcoital leukorrhea, dyspareunia dysurua.
- Malignant fistula vesicovaginal or rectovaginal
- Pyometria
- Uraemia is acommon cause of death
25
Acute suppurative endometritis shows infiltration by………
Neutrophils & pus cells
26
Diagnosis of chronic non-specific endometritis depends on…..
Plasma cells
27
…..is common with IUD
Actinomyces israeli
28
Describe etiology of endometriosis
1. Regurgitation theory: from menstrual flow with subsequent implantation
2. Metaplastic theory: due to endometrial differentiation from coelomic epithelium
3. Vascular & lymphatic dissemination theory for extrapelvic lesion
4. Extrauterine stem/progenitor cell: bone marrow cells differentiate into endometrial tissue
29
Describe pathogenesis of endometriosis
Studies suggest it is not only misplaced by also abnormal as:
1. Produces large amounts of inflammatory mediators esp PGE2
2. The unflammation results from recruitment of & activation of macrophages by factors made by endometrial stromal cells
3. Stromal cells also make aromatas leading to local estrogen production
-These factors enhance survival & persistance of the endometriotic tissue within a foreign location, which helps explain benefifical effect of COX-2 inhibitors
30
Ovarian endometriosis shows……due to….
Chocolate cyst
periodic bleeding with each menstrual cycle at site
31
Describe microscopic pic & effects of adenomyosis
M: nests of stroma &/or glands seen deep in myometrium
Effects: uterine enlargement as this endometrial tissue shows reactive hypertrophy of myometrium resulting in thickened uterine wall. Dysmenorrhea & pelvic pain before menses
32
Describe etiology of endometrial hyperplasia
Exposure to high levels of estrogen compred to progestin due to:
1. Failure of ovulation with abnormal persistance of Graafian follicle
2. Administration of estrogenic steroid
3. Estrogen producing diseases as PCO & granulosa-theca cell tumors
4. Obesity as adipose tissue converts steroid precursors to estrogen
33
Describe microscopic classification of endometrial hyperplasia & its prognosis
Classified according to presence of cytologic atypia into:
1. Hyperplasia without atypia (cells lining glands are columnar epithelium with inc number of mitosis) carries a low risk (1-3%) for progression to endometrial carcinoma
2. Hyperplasia with atypia (cells lining glands are atypical) also called EIN RISK OF PROGRESSION TO CANCER IS 20-50%
34
When hyperplasia with atypia is discovered in patient no longer desiring fertility……is done
In younger patient ttt is…..
Hystrectomy
High dose progestin in attempt to presesrve uterus
35
Regardless cytologic atypia microscopic exam of endometrial hyperplasia may show….or….form
Simple/complex
36
The most common tumor of uterus is……
Leiomyoma
37
Describe gross features of leiomyoma
1. The uterus is enlarged may be uniform or more common irregular & firm in consistency
2. Leiomyomas are sharply circumscribed rounded nodules with whorly cut surface
3. May be single more common multiple
4. Apparent encapsulation due to compression of surrounding tissue
5. Occur within myometrium (interstitial) or submucous protruding into cavity or subserosal
38
Describe the microscopic features of leiomyoma
Consist of interlacing bundles of smooth muscle fibers with dense collagenous bundles, stroma is vascular
39
List pathological changes & effects of leimyoma
1. Hyaline/cystic degeneration
2. Necrosis in the center, pedunculated mass may undergo tosrsion
3. Infection & suppuration rarely occur in submucus leiomyoma
4. Pathological calcification
5. Red degeneration
6. Malignant change into sarcoma is extremely rare
40
Explain the occurrence of red degeneration in leiomyoma
Associated with pregnancy & OCP. Leiomyoma becomes soft & hemorrhagic & infarcted due to thrombosis of vessels or twisting of pedicle. Clinically patients may complain of abdominal pain, vomiting & fever
41
Describe CP of leiomyoma
May be asymptomatic or associated with:
Uterine bleeding, urinary bladder disorders, impaired fertility, spontaneous abortion; fetal malpresentations & postpartum Hges
42
Mention genetic risk factors for each of the following
1. Leiomyoma
2. Endometrioid adenocarcinoma
3. Serous carcinoma
1. Rearrangements of ch6 & 12
2. Mutations in Mismatch repair genes (Lynch syndrome) & tumor suppressor gene PTEN (Cowden syndrome)
3. TP53 mutations
43
Mention risk factors of endometrioid carcinoma
1. Prolonged estrogen stimulation as in endometrial hyperplasia
2. Infertility
3. DM
4. HTN
5. Obesity
44
Describe microscopic features of subtypes of endometrial cancer
1. Endometrioid carcinoma: resembles normal endometrial glands graded I-III, may show squamous differentiation, if squamous element is malignant it is called acanothosquamiys carcinoma. May show secretory or mucinous diff
2. Serous: shows small tufts or papillae with high nuclear atypia. They are highly aggressive
45
Mention CP of endometrial cancer
Age is…..
Leucorrhea & irregular uterine bleeding in postmenopausal female, symptoms of spread
55-65 yrs
46
Describe microscopic pic of leiomyosarcoma
It varies from tumors resembling leiomyoma to widely anaplastic neoplasms, can be differentiated into leiomyoma by presence of necrosis, cytologic atypia, mitotic activity
47
Mention causes of abnormal endometrial bleeding in:
1. Prepuberty
2. Adolescnce
1. Precocious puberty
2. Anovulatory cycle
48
Mention causes of abnormal endometrial bleeding in:
1.Perimenopausal bleeding
2. Postmenopuasal bleeding
1. Anovulatory cycle, irregular shedding, organic lesions (carcinoma, hyperplasia, polyps)
2. Organic lesions & endometrial atrophy
49
Mention causes of abnormal endometrial bleeding in reproductive age
1. Complications of pregnancy (abortion, trophoblastic disease, ectopic pregnancy)
2. Anovulatory cycle
3. Organic lesions
4. Ovulatory dysfunctional bleeding (inaqdeuate luteal phase)
50
List complications of salpingitis
1. Extension of infection through the fimbrial end of the tube to the peritoneum leading to pelvic peritonitis which may be generalized
2. Extension of infection to near-by ovary leading to tubo-ovarian abscess
3. Chronicity, hydrosalpinx, pyosalpinx
4. Sterility if bilateral
5. Ectopic pregnancy
51
Describe hydrosalpinx
Chct by obliteration of fimbriated end with dilatation of tube, the wall is whitish thin & translucent contains serous clear fluid
52
Describe pathogenesis of tubal pregnancy
1. Factors that retard passage of conceptusalong tube as ch salpingitis & congenital tubal diverticulae
2. Factors that inc tubal receptibility as in endometriosis with attraction of fertilized ovum to this site
53
What is the gross pic & fate of tubal pregnancy
G, the tube is distended by haemorrhagic clot enmeshing chorionic villi
F: most end in tubal abortion or perforation with release of blood into peritneal cavity & subsequent intraperitoneal Hge
54
STIC have mutations of…..
TP53
55
Follicular cyst originates from…..
Describe its gross & micro pic
Unruptured Graafian follicle or in follicles that ruptured & immediately sealed
G: unilocular cyst varying in size 1 to 5 cm single/multiple, unilateral/bilateral. The outer surface is smooth, wall is thin & cyst contains clear watery fluid
M: lined by granulosa cells surrounded by theca interna cells
56
Describe CP of follicular cyst
1. Occasionally, become palpabe masses & produce pelvic pain
2. They may be estrogen secreting causing menstrual irregularities
57
Describe theca luein cells
They are associated with high level of circulating gonadotrophin as in pregnancy, hydatidiform mole, choriocarcinoma & in patients recieving gonadotrophin therapy. Leads to hyperplastic & luteinized theca interna cells
Hge & rupture may need surgical intervention
58
Describe gross & mic pic of PCO
G: both ovaries are uniformly enlarged 2-5 times n size, the ovaries show thickened capsule & studded by multiple small cysts 0.5 to 1.5 cm in diameter
M: they show thickened tunica albuginea with cystic follicles lined with granulosa cells with hyperplastic luteinized theca interna, no corpora lutea, no/rare corpora albicantia
59
Describe CP of PCOS
1. Hyperoestrinism: resulting in endometrial hyperplasia & abnormal uterine bleeding
2. Stein-Leventhal syndrome: chct by 2ry amenorrhea, sterility & PCO
3. Virilism: manifested by hirsutism of a progressive nature, voice changes & breast atrophy
60
Dsecribe morphology of chocolate cyst
1. Cyst wall is thick & fibrotic with a smooth or shaggy red brown inner lining & covered by dense fibrous adhesions
2. Cyst contents are red brown chocolate material
61
List risk factors for ovarian neoplasms
Nulliparity, familty history, germline mutation in tumor suppressor genes as BRACA 1&2
62
Compare type I & II neoplasms
Type I: progress from benign tumors & may give rise to low-grade carcinoma
Type II: These are ovarian tumors that arise from inclusion cysts in ovarian cortex or fallopian tube epithelium via intraepithelial precursors. They demonstrate high grade features & are commonly of serous histology
63
The most common ovarian epithelial tumor is……
Classify it
Serous tumors
1. Benign (60%)
2. Borderline (15%)
3. Malignant (25%)
64
Mention 2 variants of benign serous cyst
Serous cystadenofibroma
Papillary serous cystadenoma
65
What differentiates borderline & malignant tumors of ovary?
Borderline show cytologic atypia but no stromal invasion
Malignant show both
66
Classify mucinous tumors
Mucinous cystadenoma (80%)
Borderline mucinous tumors (10%)
Mucinous cystadenocarcinoma (10%)
67
Endometrioid tumors of ovary are usually……
Malignant
68
Describe morphology & prognosis Brenner tumors
G: most are unilateral, ranging from few cm uoto 20 cm. Most are circumscribed, solid, firm & rubbery. Less commonly, they may have a cystic component
M: nests of transitional epithelial nests in fibrous stroma
P: most are benign but malignant & borderline tumors have been described
69
Describe gross features of malignant epithelial tumors
They may be cystic, solid, or partly cystic & partly solid
Papillary outgrowths could be seen either internally (endophytic) or externally (exophytic)
The contents are serous, mucoid and or hemorrhagic. Areas of hge & nec are common.
70
Granulosa cell tumors are most common in……
Postmenopausal females
71
Describe microscopic pic if granulosa cell tumors
Composed of cuboidal cells with nuclear longitudinal groove (coffee-bean nucleus) & are arranged in diff patterns:
1. Trabecular
2. Insular (i.e. in compact groups)
3. Microfollicular
4. Diffuse sarcomatoid
72
Describe clinical features of granulosa cell tumors
In pre-menarchal period: it leads to precocious puberty
In reproductive period: abnormal bleeding, endometrial hyperplasia, uterine leiomyoma, fibrocystic disease & breast carcinoma
In post-menopausal period: abnormal bleeding ensues with the possibility of endometrial hyperplasia & carcinoma
Biological behaviour of such tumor is unpredictable
73
Describe mic pic of thecoma
Composed of spindle-shaped theca cells arranged in a fibroma-like pattern, foci of luteinization are seen, hence the yellow tinge
74
Describe CP of Sertoli-Leydig cell tumor of ovary
Secrete testosterone leading to defeminization i.e. amenorrhea, atrophy of breast, followed by musculinization i.e. hirsutism, enlarged clitoris & male voice
They are rarely malignant
75
Describe mic pic of dysgerminoma
Composed of immature cells with central nuclei, prominent nucleoli arranged in cords or groups, supported by fibrous tissue stroma infiltrated by lymphocytes.
76
Endodermal sinus tumors occurs in females in age……
between 10-20 yrs
77
Describe mic pic of yolk sac tumor
Microcystic pattern formed by a loose network of flat or cuboidal cells, Schiller-Duval body is pathognomonic; central blood vessel enveloped by germ cells within a space similarly lined by germ cells, resembles glomerulus.
Alpha fetoprotein tumor marker is markedly raised
78
What is Meig’s syndrome?
Ovary fibroma that reaches a large size compressing the lymphatics leading to ascites & hydrothorax.
79
Krukenberg tumor origin is from……
GIT or breast
80
Mention CP & complications of ovarian tumors
1. Asymptomatic (30%)
2. Abdominal mass
3. Pressure symptoms (on venous drainage, bladder, ureter)
4. Hormonal effects
5. Symptoms due to complications:
a. Torsion
b. Pseudomyxoma pertonii (implantation of mucinous tumor cells in peritoneum)
c. Infection
d. Sterility
e. Malignant transformation
f. Meig’s syndrome
81
Mention the tumor marker for the following:
1. Epithelial ovarian cancer
2. Mucinous ovarian cancer
3. Choriocarcinoma, embryonal carcinoma
4. Granulosa cell tumor
5. Endodermal sinus tumor, embryonal carcinoma
1. CA-125
. CEA
4. HCG
4. Inhibin
5. AFP
82
Complete mole is caused by……
Fertilization of emoty egg by 2 sperms yielding diploid karyotype.
83
Describe morphology of complete mole
G: uterus is enlarged, cavity is filled with mass of grapelike structures of thin-walled translucent greyish white cysts, weighs more than 200 g, no fetl parts identified
M: the cysts are.composed of hydropic swelling of chorionic villi, the interior being filled with an avascular loose myxoid stroma, trophoblastic proliferation produces hyperplastic sheets of cyto & syncytiotrophoblasts. Cytologic atypia may be present.
84
Describe CP & Complications of complete mole
CP: +ve pregnancy test, uterine enlargement greater than normal pregnancy, vaginal bleeding (3rd to 4th month), greatly elevated HCG
Complications: choriocarcinoma (2.5%), invasive mole (10%), HCG level is most percise for follow-up
85
Partial mole occurs due to…..
Fertilization of normal egg by 2 sperms
86
Describe morphology & CP of partial mole
G: uterus is enlarged, few vesicles & fetal parts are seen
M: villous edema involving a portion of villi & trophoblastic proliferation is focal & slight
CP: similar to complete mole but HCG is not as high. They have minimal risk for complications.
87
Invasive mole differs from choriocarcinoma as it….
Does not metastasize
88
Describe effects of invasive mole
1. Uterine bleeding, st rupture uterus
2. Abortion
3. High HCG in urine
89
Half of Choriocarcinoma is preceded by…..
Hydatidiform mole
90
Describe mic pic of choriocarcinoma
The tumor is formed of cytotrophoblastic & syncitial cells invading uterine wall, blood vessels & lymphatics
There NO stroma or blood vessels but areas of necrosis & extravasated blood are usually present
Chorionic villi are not formed
91
Choriocarcinoma is sensitive to….
Chemotherapy
