Female Genital System and Reproductive Pathology Flashcards

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1
Q

Bartholin Cyst

A

Bartholin gland normally secretes lubrication into vestibule.

Usually unilateral enlarged painful cystic lesion secondary to inflammation and plugging of the gland.

Located at lower vestibule adjacent to the vaginal canal.

Generally women of reproductive age (infections/STD’s)

Not uncommon

Can be accompanied by abscess.

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2
Q

Condyloma

A

Warty neoplasm of vulvar skin, often large

MC due to HPV 6 and 11. (low risk based on DNA sequencing)

Characterized by koilocytic change

Rarely progresses to carcinoma

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3
Q

Lichen sclerosis

A

Thinning of epidermis and fibrosis of dermis

Leukoplakia w/ parchment-like vulvar skin

MC in postmenopausal women

Benign, associated w/ slightly increased risk of SCC

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4
Q

Lichen simplex chronicus

A

Hyperplasia of vulvar squamous epithelium

Leukoplakia w/ thick, leathery skin

Associated w/ chronic irritation and scratching

Benign; no increased SCC risk

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5
Q

Vulvar carcinoma

A

Arises from squamous epithelium of vulva

Rare

Presents as leukoplakia (biopsy may be required to distinguish from lichen sclerosis)

Etiology: May be HPV –> VIN (High risk - 16, 18, 31, 33) = 40-50 years old; or non-HPV related (long standing lichen sclerosis) = 70+ years old.

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6
Q

Extramammary Paget Disease

A

Malignant epithelial cell in the epidermis of the vulva

Presents as erythemetous, pruritic, ulcerated skin

*Key ddx is carcinoma (PAS +; Keratin +; and S100-) vs. melanoma (PAS-, Keratin -, and S100+)

Represents as carcinoma in situ (no underlying malignancy which is not the case w/ Paget’s disease of the breast)

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7
Q

Adenosis

A

Focal persistence of columnar epithelium in upper 2/3rds of vagina

Increased incidence in females exposed to DES (drug used to be given to mothers to prevent miscarriage) in utero

Can lead to clear cell adenocarcinoma

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8
Q

Clear cell adenocarcinoma

A

Malignant proliferation of glands with clear cytoplasm

Rare complication of DES-associated vaginal adenosis

Discovery of this and other complications lead to cessation of DES usage

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9
Q

DES complications in DES mom

A

Slightly increased risk of breast CA (estrogen like compound)

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10
Q

DES complications in DES daughter

A
  1. ) Adenosis –> clear cell adenocarcinoma

2. ) Smooth muscle problems in tubes/uterus. Increased ectopic risk.

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11
Q

Embryonal rhabdomyosarcoma

A

Malignant mesenchymal proliferation of immature skeletal muscle

Rare

Presentation: Bleeding and grape-like mass protruding from vagina or penis of child usually

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12
Q

Vaginal carcinoma

A

Carcinoma arising from squamous epithelium lining the vaginal mucosa

Usually related to high-risk HPV (16,18,31,33)

Precursor lesion is vaginal intraepithelial neoplasia (VAIN)

Regional lymph node spread: Lower 1/3 goes to inguinal nodes; Upper 2/3 goes to regional iliac nodes (due to embryological differences)

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13
Q

HPV infection

A

Sexually transmitted DNA virus

Infects lower genital tract, esp. cervix in transformation zone (strat squamous to simple columnar of exo/endo cervical border)

Persistent infection leads to risk for CIN

High risk: 16,18,31,33
Low risk: 6 and 11

High risk proteins:
E6: increases destruction of p53
E7: increases destruction of Rb

CIN: characterized by koilocytic change, nuclear atypia, and increased mitotic activity. Divided into grades based on cells involved.

CIN 1 - bottom 1/3 portion has dysplasia (reverses 66%)
CIN 2 - middle 2/3 has dysplasia (33% reverse)
CIN 3 - Almost all have dysplasia (rare reversal)
Carcinoma in situ (cannot reverse)

CIN progresses stepwise, but is not inevitable

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14
Q

Cervical carcinoma

A

Invasive carcinoma that arises from cervical epithelium

MC in middle-aged women (40-50)

Presents as vaginal bleeding or post-coital bleeding

Key risk factor is high risk HPV infection. Secondary factors include smoking (cervical and pancreas are two non-logical smoking related cancers) and immunodeficiency. (usually clears HPV infection)

Most common subtypes:
Squamous cell carcinoma (most common) and adenocarcinoma (rarer, but also due to HPV)

Often invade through anterior uterine wall into bladder –> hydronephrosis.

Local invasion over metastasis

Screen to catch dysplasia before it devleops into carcinoma.

Pap smear is gold standard for screening. Most successful screening tests ever developed. Look at nucleus/cytoplasm ratio etc.

Abnormal papsmear –> followed by confirmatory coposcopy and biopsy

Limitations of Pap smear: 1.) Inadequate sampling of transition zone (false negative).
2.) Limited efficacy in screeing for adenocarcinoma

Immunization: Effective in preventing HPV infections (HPV 6,11,16, and 18). Protection lasts for 5 years and must still undergo pap smears (31,33 and other high risks not covered)

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15
Q

Asherman Syndrome

A

Secondary amenorrhea due to loss of *basalis (regenerative layer of stem cells) and scarring

Result of overaggressive dilation and curretage (D&C)

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16
Q

Anovulatory cycle

A

Lack of ovulation

Results in estrogen-driven proliferative phase w/o progesterone-driven secretory phase

Common cause of dysfunction uterine bleeding, especially during menarche and menopause

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17
Q

Acute endometritis

A

Bacterial infection of endometrium

Usually due to retained products of conception

Presents as fever, abnormal uterine bleeding, and pelvic pain

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18
Q

Chronic endometritis

A

Chronic inflammation of endometrium

Characterized by
*plasma cells (lymphocytes are always present)

Common causes: retained products of conception, chronic PID, IUD, and TB

Presents with abnormal uterine bleeding, pelvic pain, and infertility.

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19
Q

Endometrial polyp

A

Hyperplastic protrusion of endometrium

Presents as abnormal uterine bleeding

Can arise as a side effect of tamoxifen

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20
Q

Enodmetriosis

A

Abnormal placement of endometrial glands and stroma outside uterine endometrial lining

Presents with dysmenorrhea (tissue cycles as well) and pelvic pain; may cause infertility.

3 theories:

  1. Retrograde theory
  2. Metaplastic theory
  3. Lymphatic dissemination theory

Common sites of involvement:

  • 1.) Ovary - chocolate cyst
    2. ) Uterine ligaments - pelvic pain
    3. ) Pouch of Douglas - pain with defecation
    4. ) Bladder wall- pain with urination
    5. ) Bowel serosa - abdominal pain and adhesions
  • 6.) Fallopian tube mucosa - scarring ( increased risk of infertility and ectopic)

“gunpowder” lesions in soft tissue.

Adenomyosis is endometriosis of myometrium

Increased risk of CA at site of endometriosis. Esp. at the ovary.

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21
Q

Adenomyosis

A

Endometriosis of the myometrium.

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22
Q

Endometrial hyperplasia

A

Increase in the amount of endometrium glands in comparison to the surrounding stroma.

*Consequence of unopposed estrogen.

Classically seen in postmenopausal obese women with uterine bleeding.

Classified histologically: Based on architectural growth and cellular atypia.

**Most important predictor for progression to CA is cellular atypia

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23
Q

Endometrial Carcinoma

A

Malignant proliferation of endometrial gland

Presents as postmenopausal bleeding

Arises via two distinct pathways:
1.) Hyperplasia pathway –> due to unopposed estrogen. Endometroid histology –> aged 50-60

2.) Sporadic pathway – cancer from an atrophic endometrium w/o precursor lesion. Serous/Papillary histology –> elderly. Driven by p53 mutations. Can get psammoma bodies. Very aggressive.

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24
Q

Leiomyoma

A

Benign proliferation of smooth muscle arising from myometrium

Related to estrogen exposure (premenopausal)

Multiple (vs. leiomyosarcoma) , well-defined white whorled masses (leiomyosarcoma will have necrosis/hemorrhage.

Rise during pregnancy and shrinks after menopause.

Usually asymptomatic

When present sx include abnormal uterine bleeding, infertility, and pelvic mass.

25
Q

Leiomyosarcoma

A

Malignant proliferation of smooth muscle arising from myometrium.

Arises denovo (not from leiomyoma)

Usually seen in postmenopausal women

Single lesion w/ necrosis and hemorrhage.

Necrosis, mitotic activity, and cellular atypia on histology.

26
Q

Hemorrhagic luteal cyst

A

Bleeding into corpus luteum.

Can cause “mass” within ovary.

27
Q

Follicular cysts

A

Due to degeneration of follicle.

Most women have some.

28
Q

Polycystic Ovarian Disease

A

Characterized by increased LH and low FSH.

LH:FSH >2

Many follicular cysts in the ovary.

High LH –> high androgen production –> hirusitism and estrone creation in androgen –> feedback inhibition of FSH –> no stimulation of follicle –> degeneration and formation of follicular cyst

Classical presentation:
Obese young woman with infertility, oligomenorrhea, and hirusitism

  • Some patients have insulin resistance
  • High circulating estrone levels increase risk for enodmeterial carcinoma
29
Q

Surface epithelial ovarian tumors

A

MC type of ovarian tumor

Derived from coelomic epithelium that lines ovary

Two MC subtypes are serous tumors and mucninous tumors. Both are usually cystic.

Can be endometrioid (usually carcinoma) and can have separate endometrioid carcinoma in endometrioid

Can be Brenner tumor (cells resemble urothelium)

Surface tumors present late.

Vague abdominal sx (pain, fullness). Signs of compression/urinary frequency.

Poor prognosis

*Epithelial carcinomas tend to spread locally especially to the perioneum (omental caking)

CA-125 is useful serum marker to monitor treatment response and screen for recurrence

30
Q

Cystadenoma

A

Benign tumor of ovary.

Composed of a single cyst w/ simple, flat lining

Most commonly in premenopausal women (30-40yrs. old)

Can be serous or mucinous based on fluid present and histology.

31
Q

Cystadenocarcinoma

A

Composed of complex cysts with thick, shaggy lining.

MC arises in post menopausal women (60-70 years old)

Cells invade into CT of cyst wall.

Can be serous or mucinous based on fluid present and histology.

BRCA1 mutation carriers have increased risk for serous carcinoma of the ovary and fallopian tube (can prophylactically remove)

32
Q

Borderline tumors

A

Features between benign and malignant tumors

Better prognosis, but still have metastasis capability.

33
Q

Germ cell tumors

A

2nd MC ovarian tumor (15%)

Usually occur in women of reproductive age (15-30)

Tumor subtypes mimic tissues normally produced in germ cells

34
Q

Cystic teratoma

A

Germ cell tumor that resembles fetus. 2-3 three layers present

MC germ cell tumor in females.

Bilateral in 10%

Benign

Presence of immature tissue (MC is neuroectoderm) or somatic malignancy (i.e. squamous cell carcionma of skin of teratoma) indicates malignant potential

Struma ovarii is a cystic teratoma composed primarily of thyroid tissue.

35
Q

Embryonal carcinoma

A

Composed of large primative cells.

Aggressive with early metastasis

36
Q

Endodermal Sinus Tumor

A

aka Yolk Sac Tumor

Malignant

MC germ cell tumor in children

Serum AFP is often elevated

Schiller-Duval (glomeruloid) bodies are seen on histology.

37
Q

Dysgerminoma

A

Composed of large cells with clear cytoplasm and central nuclei (oocyte)

MC malignant germ cell tumor

Testicular counterpart is seminoma

Good prognosis; responds to radiotherapy

Serum LDH is seen in serum.

38
Q

Choriocarcinoma

A

Germ cell tumor of placental orgin

Malignant proliferation of trophopblasts and synctiotrophoblasts w/o villi

Small, hemorrhagic tumor with early hematogenous spread ( cells are programmed to find blood vessels)

Can cause many metastasis with a small primary tumor.

High B-hcg

Poor response to chemotherapy

May also arise from complication of gestation (complete molar pregnancy; abortion; complete pregnancy) or as a spontaneous germ cell tumor. Gestation pathway responds well to chemotherapy.

39
Q

Struma Ovarii

A

cystic teratoma composed primarily of thyroid tissue.

40
Q

Sex cord stromal tumors

A

Tumors that resemble sex-cord stroma tissues of ovary

41
Q

Granulosa-theca cell tumor

A

Neoplasm of granulosa and theca cells

Often produce estrogen

Presents with signs of estrogen excess (Sx vary with age)

42
Q

Sertoli-Leydig Cell tumor

A

Sertoli cells form tubules

Leydig cells contain characteristic Reinke crystals

May produce androgen –> hirsutism or virilization

43
Q

Fibroma

A

Benign tumor of fibroblasts.

Associated with pleural effusion and ascites in osme patients (Meigs syndrome)

44
Q

Meigs syndrome

A

Fibroma of ovary that causes pleural effusion and ascites

45
Q

Kruckenberg tumor

A

Mucinous carcinoma that metastasizes to both ovaries.

MC is diffuse type gastric adenocarcinoma (signet-ring cell).

Can come from lobular carcinoma of breast or colon.

Mucinous tumor of ovary –> must ddx vs. surface mucous tumor –> key is unilateral (primary) vs. bilateral (metastasis)

46
Q

Pseudomyxoma peritonei

A

Abundant mucin in peritoneum –> Jelly Belly

Clasically seen in mucinous carcinoma of appendix.

Often metastsizes to the ovary.

47
Q

Ectopic Pregnancy

A

Implantation of fertilized ovum at site other than uterine wall

MC site is lumen of fallopian tube

Key risk factor is scarring

Classic presentation: Lower quadrant abdominal pain weeks after missed period. Surgical emergency

48
Q

Sponatneous abortion

A

Miscarriage of ferus (20 weeks before gestation)

Common; occurs in up to 1/4th of recognizable pregnancies

Presents as vaginal bleeding, cramp-like pain, and passage of fetal tissue.

Usually due to chromosomal anomolies.

Other causes include hypercoaguable state (lupus), congenital infection, and exposure to teratogens (esp. within 0-3 weeks)

49
Q

Placenta previa

A

Placenta implants in lower uterine segment and covers surgical os.

Needs C-section

50
Q

Placental abruption

A

Placental separates from decidua prior to delivery

Common cause of still birth

Presents with third trimester bleeding and fetal insufficiency.

Blood on the maternal suface on gross

51
Q

Placenta Accreta

A

Improper implantation of placenta into myometrium with little or no intervening decidua

Presents with difficult delivery of the placenta and post-partum bleeding

Often requires hysterectomy.

52
Q

Preeclampsia

A

Pregnancy induced HTN, proteinuria, and edema; arises in 3rd trimester

Due to abnormality of maternal-fetal vascular interface in placenta

Fibrinoid necrosis of vessels of placenta.

Can progress to ecclampsia or HELLP

53
Q

Ecclampsia

A

Preeclampsia with seizures

54
Q

HELLP

A

Preeclampsia with thrombotic microangiopathy inolving liver

Hemolysis, Elevated Liver enzymes, Low platelets.

Schistocytes

55
Q

Sudden Infant Death Syndrome

A

Death of a healthy infant (1 month to 1 year) without cause

Infants usually expire during sleep

Risk factors include sleeping on stomach, smoking in household, and prematurity.

56
Q

Hydatidiform mole

A

Abnormal conception characterized by swollen and edematous villi with prolifereation of trophoblasts

Uterus expands as if normal pregnancy is present. (bigger than normal and B-hcg is higher than expected)

Woman will begin to pass grape-like masses in early 2nd trimester.

With prenatal care dx by routine ultrasound in the early first trimester. Fetal heart tones are absent and “snow-storm” appearance on ultrasound.

Classified as complete or patial

Rx: is D&C

B-hcg monitored to ensure adequate mole removal and to screen for development of choriocarcinoma

57
Q

Partial mole

A

Genetics: Normal ovum fertilized by two sperm (or one sperm that dublicates its chromosomes) ; 69 chromosomes

Fetal tissue is present

Villous edema: some villi are hyropic and some are normal

Trophoblastic proliferation: Focal proliferation present around hydropic villi

Risk for choriocarcinoma: minimal

58
Q

Complete mole

A

Completely from dad

Genetic: Empty ovum fertilized by two sperm (or one sperm that duplicates chromosomes); 46 chromosomes

Fetal tissue: Absent

Villous edema: Most villi are hyropic

Trophoblastic proliferation: diffuse, circumferential proliferation around hydropic villi

Risk for choriocarcinoma: 2-3%

B-hcg is much higher (synctiotrophoblasts make B-hcg)