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ABBEY MSII Unit 1 > Pathoma Female Reproductive > Flashcards

Pathoma Female Reproductive Flashcards

1
Q

What type of epithelium does the vulva have?

A

squamous

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2
Q

What does the vulva include?

A

skin and mucosa of the female genitalia external to the hymen (labia major, minora, mons pubis, vestibule)

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3
Q

What presents as a unilateral, painful cystic lesion at the lower vestibule adjacent to the vaginal canal?

A

bartholin cyst

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4
Q

What is the Bartholin gland?

A

present on each side of vaginal canal - produces mucus-like fluid that drains via ducts into the lower vestibule

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5
Q

What presents as a warty neoplasm of vulvar skin?

A

condyloma

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6
Q

What causes condylomas?

A

HPV types 6 or 11 and secondary syphilis

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7
Q

What is characterized by thinning of the epidermis and fibrosis of the dermis of the vulva and presents as a white patch?

A

lichen sclerosis

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8
Q

Who most commonly gets lichen sclerosis?

A

postmenopausal women

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9
Q

Is lichen sclerosis benign or malignant?

A

benign, but associated with slight increased risk for squamous cell carcinoma

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10
Q

What is characterized by hyperplasia of the vulvar squamous epithelium and presents as leukoplakia with thick, leather vulvar skin?

A

lichen simplex chronicus

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11
Q

What is associated with lichen simplex chronicus?

A

chronic irritation and scratching

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12
Q

Is lichen simplex chronicus benign or malignant?

A

bening with NO increased risk of squamous cell carcinoma

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13
Q

What presents as leukoplakia (white patch)

A

lichen sclerosis and vulvar carcinoma

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14
Q

What is a way to distinguish between HPV related vulvar carcinoma and non-HPV related vulvar carcinoma?

A

HPV related: high risk - get around age 40-50 non HPV: long standing lichen sclerosis in post menopausal women

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15
Q

What type of carcinoma is vulvar carcinoma?

A

squamous

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16
Q

What presents as erythematous, pruritic, ulcerated vulvar skin?

A

extramammary paget disease

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17
Q

What is extramammary paget disease characterized by?

A

malignant epithelial cells in the epidermis of the vulva

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18
Q

What is the difference between paget disease of the nipple as opposed to the vulva?

A

nipple: almost always associated with underlying carcinoma vulva: represents carcinoma in situ - no underlying carcinoma

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19
Q

How is extramammary paget disease distinguished from melanoma?

A

melanoma = PAS-, keratin-, S100+ paget cells PAS+, keratin +, S100-

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20
Q

What is PAS?

A

marks mucous (present in paget cells but not melanoma cells)

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21
Q

What is S100?

A

defining stain of melanomas

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22
Q

What is the mucosa of the vagina lined with?

A

non-keratinizing stratified squamous epithelium

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23
Q

What has focal persistence of columnar epithelium in the upper vagina?

A

adenosis

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24
Q

What do women who were exposed to diethylstilbestrol (DES) in utero have increased incidence of?

A

adenosis

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25
Q

What is a complication of DES-associated vaginal adenosis?

A

clear cell adenocarcinoma

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26
Q

What presents as bleeding and a grape-like mass protruding from vagina or penis of a child?

A

embryonal rhabdomyosarcoma

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27
Q

What is embryonal rhabdomyosarcoma?

A

malignant mesenchymal proliferation of immature skeletal muscle

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28
Q

What is the characteristic cell of embryonal rhabdomyosarcoma?

A

rhabdomyoblast which exhibits cytoplasmic cross-striations

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29
Q

What do rhabdomyoblast stain for?

A

desmin (intermediate filament in muscle cells) and myogenin (nuclear transcription factor present in immature skeletal muscle)

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30
Q

What is the precursor lesion for vaginal carcinoma?

A

vaginal intraepithelial neoplasia (VAIN)

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31
Q

What causes vaginal carcinoma?

A

high-risk HPV (16,18,31,33)

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32
Q

What type of cells are on the exocervix? endocervix?

A

exo: nonkeratinizing squamous epithelium endo: single layer of columnar transformation zone between the two

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33
Q

What typically infects the transformation zone?

A

HPV DNA virus

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34
Q

HPV infection

A

typically eradicated by acute inflammation - persistent infection is what leads to increased risk for cervical dysplasia (CIN)

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35
Q

What does high risk HPV produce?

A

E6 and E7 proteins E6 = increased destruction of p52 and E7 = increased destruction of Rb (both tumor suppressor proteins)

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36
Q

What is characterized by koilocytic change, disordered cellular maturation, nuclear atypia, and increased mitotic activity within the cervical epithelium?

A

CIN cervical intraepithelial neoplasia

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37
Q

What is the difference between dysplasia and carcinoma?

A

dysplasia is reversible

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38
Q

Who is cervical carcinoma most commonly seen in?

A

middle aged women (40-50 years)

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39
Q

How does cervical carcinoma typically present?

A

vaginal bleeding (esp post coital) and/or cervical discharge

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40
Q

What are the key risk factors for cervical carcinoma?

A

high-risk HPV, smoking, immunodeficiency (because immune system usually gets rid of viruses)

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41
Q

What are the two common subtypes of cervical carcinoma?

A

squamous cell and and adenocarcinoma

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42
Q

What happens with advanced tumors of cervical carcinoma?

A

invade anterior uterine wall into bladder, block ureters, cause hydronephrosis with postrenal failure (most common cause of death)

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43
Q

How are high-grade dysplastic cells characterized?

A

hyperchromatic (dark) nuclei and high nuclear to cytoplasmic ratios

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44
Q

What are abnormal Pap smears followed by?

A

colposcopy (visualization of cervix) and biopsy

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45
Q

What are the two limitations of the Pap smear?

A

inadequate sampling (false negatives) and limited efficacy in screening ADENOCARCINOMA

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46
Q

What does the HPV vaccine cover?

A

types 6, 11, 16, 18

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47
Q

What drives growth of the endometrium?

A

estrogen

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48
Q

What drives preparation of the endometrium for implantation?

A

progesterone

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49
Q

What drives shedding of the endometrium?

A

lack of progesterone

50
Q

Secondary amenorrhea due to loss of the baseless (regenerative layer of the endometrium) and scarring is known as…….

A

asherman syndrome

51
Q

What is an anovulatory cycle?

A

lack of ovulation resulting in an estrogen-driven proliferative phase without a subsequent progesterone-drive secretory phase

52
Q

When do anovulatory cycles typically happen?

A

menarche and menopause

53
Q

What are the most common cause of acute endometritis?

A

retained products of conception (after delivery/miscarriage) - retained products act as a nidus for the bacterial infection of the endometrium

54
Q

How does acute endometritis typically present?

A

fever, abnormal uterine bleeding, pelvic pain

55
Q

What is chronic endometritis characterized by?

A

lymphocytes and plasma cells (plasma cells most important!!!! bc lymphocytes are normally found in endometrium)

56
Q

What are causes of chronic endometritis?

A

retained produced of conception, chronic pelvic inflammatory disease (eg chlamydia), IUD, TB (see granulomas)

57
Q

How does chronic endometritis present?

A

abnormal uterine bleeding, pain, infertility

58
Q

What is a side effect of tamoxifen? What are the effects on breast/endometrium?

A

endometrial polyp on breast: anti-estrogenic effects; on endometrium: pro-estrogenic effects

59
Q

What is endometriosis?

A

endometrial glands and stroma outside of the uterine endometrial lining

60
Q

How does endometriosis present?

A

dysmenorrhea (pain during menstruation), pelvic pain

61
Q

What is the most common site of involvement in endometriosis?

A

ovary = chocolate cyst

62
Q

What does involvement of the pouch of Douglas in endometriosis cause?

A

pain with defecation

63
Q

What is adenomyosis?

A

involvement of the uterine myometrium with endometriosis

64
Q

What is endometrial hyperplasia, and what causes it?

A

hyperplasia of endometrial glands relative to stroma caused by unopposed estrogen

65
Q

What is the most common invasive carcinoma of the female genital tract?

A

endometrial carcinoma

66
Q

How does endometrial carcinoma present?

A

postmenopausal bleeding

67
Q

What are the two pathways that endometrial carcinoma can arise? Which is more common?

A

hyperplasia and sporadic - hyperplasia more common

68
Q

What are the risk factors for the hyperplasia pathway of endometrial carcinoma?

A

estrogen exposure - early menarche/late menopause, nulliparity, infertility with anovulatory cycles, obesity (anything with unopposed estrogen)

69
Q

What happens in the sporadic pathway of endometrial carcinoma?

A

carcinoma arises in an atrophic endometrium with no evident precursor - usually in women over 70

70
Q

What are common characteristics of endometrial carcinoma?

A

histology: serous with papillary structures - psammoma (fluid) body formation also p53 mutation common aggressive tumor

71
Q

What is a leiomyoma?

A

benign neoplastic proliferation of smooth muscle arising from myometrium most common tumor in females

72
Q

What are characteristics of leiomyomas?

A

common in premenopausal women, often multiple masses, enlarge during pregnancy, shrink after menopause due to estrogen levels/exposure*

73
Q

What is present in the gross exam of a leiomyoma?

A

multiple, well-defined, white, whorled masses that may distort the uterus (usually asymptomatic)

74
Q

What are the differences between a leiomyoma and leiomyosarcoma?

A

leiomyosarcoma is malignant - always de novo NEVER from leiomyomas - usually seen in POSTmenopausal women - usually only a SINGAL lesion on exam with necrosis and hemorrhage (as opposed to multiple white, whirled masses)

75
Q

What is the functional unit of the ovary?

A

follicle

76
Q

What is the function of LH?

A

acts on theca cells to induce androgen production

77
Q

What is the function of FSH?

A

stimulates granulosa cells to convert androgen to estradiol (drives the proliferative phase of the endometrial cycle)

78
Q

What does estradiol do?

A

induces LH surge leading to ovulation (marks the beginning of the secretory phase)

79
Q

What happens to the follicle after ovulation?

A

becomes the corpus lute which secretes progesterone (drive the secretory phase)

80
Q

What is polycystic ovarian disease? (PCOD)

A

multiple ovarian follicular cysts due to hormone imbalance

81
Q

What is PCOD characterized by?

A

increased LH and low FSH (LH:FSH >2) increased LH = increased androgen production causing hirsutism and the extra androgen is converted to estrone in adipose tissue - extra estrone = decreased FSH = cystic degeneration

82
Q

What are the two types of surface epithelial tumors?

A

serous and mucinous

83
Q

What is a cystadenoma?

A

benign surface epithelial tumor that is composed of a single cyst with a simple, flat lining (premenopausal women)

84
Q

What is a cystadenocarcinoma?

A

malignant surface epithelial tumor - complex cysts with thick, shagge, lining (postmenopausal women)

85
Q

What do BRCA1 mutation carrier have an increased risk for?

A

serous carcinoma of the ovary and fallopian tube

86
Q

endometrioid tumor

A

surface epithelial tumor - composed of endometrial-like glands and usually malignant - may arise from endometriosis

87
Q

brenner tumor

A

surface epithelial tumor composed of bladder-like epithelium - usually benign

88
Q

How do surface tumors present clinically?

A

late with vague abdominal symptoms (pain and fullness) or signs of compression (urinary frequency)

89
Q

Which cancer has the worst prognosis of the female genital tract cancers?

A

surface epithelial carcinoma = tend to spread locally esp to peritoneum

90
Q

What sit eh serum marker used to monitor treatment response and screen for recurrence of a surface epithelial tumor?

A

CA-125

91
Q

What are the four subtypes of germ cell tumors? When do they typically occur?

A

fetal tissue, oocytes, yolk sac, placental tissue occur during reproductive age typically

92
Q

Cystic teratoma

A

germ cell tumor - cystic tumor composed of fetal tissue - most common, benign

93
Q

Under what circumstances can cystic teratoma become malignant?

A

presence fo immature tissue (esp neural) or somatic malignancy (cancer within the teratoma)

94
Q

Struma ovarii

A

teratoma composed primarily of thyroid tissue (causes hyperthyroid)

95
Q

Dysgerminoma

A

germ cell tumor - composed of large cells with clear cytoplasma and central nuclei resembling OOCYTES - malignant - good prognosis responding to radiotherapy - high LDH

96
Q

Endodermal sinus tumor

A

malignant tumor that mimics the YOLK SAC - most common germ cell tumor in children; serum AFP elevated

97
Q

What tumor presents with schiller-ducal bodies in histology?

A

endodermal sinus tumor (schiller duval = glomerulus-like structures)

98
Q

Choriocarcinoma

A

malignant tumor - composed of cytotrophoblasts and syncytiotrophoblasats mimicking PLACENTAL TISSUE - high b-hCG characteristic - poor response to chemotherapy

99
Q

Embryonal carcinoma

A

malignant - composed of large primitive cells

100
Q

Why is embryonal carcinoma so aggressive?

A

have the ability to move and spread easily since the cells are primitive

101
Q

granulosa-theca cell tumor

A

sex cord-stromal tumor - neoplastic proliferation of granulosa and theca cell - often produces estrogen presenting with signs of estrogen excess - malignant but minimal risk for metastasis

102
Q

What happens in a sertoli-leydig cell tumor?

A

mimics testicle because it is composed of sertoli cells that form tubules and leydig cells

103
Q

What is characteristic of sertoli-leydig tumors?

A

reinke crystals

104
Q

Fibroma

A

benign tumor of fibroblasts - associated with pleural effusions and ascites (meigs syndrome) - resolves with removal of tumor

105
Q

Krukenberg tumor

A

metastatic mucinous tumor that involves both ovaries - most commonly due to metastatic gastric carcinoma

106
Q

Pseudomyxoma peritonei

A

massive amounts of mucus in peritoneum - due to mutinous tumor of the appendix - usually has metastasis to the ovary

107
Q

ectopic pregnancy

A

implantation of fertilized ovum at a site other than uterine wall - most common is fallopian tube

108
Q

What is the key risk factor for ectopic pregnancy?

A

scarring (secondary to pelvic inflammatory disease or endometriosis)

109
Q

What is the most common cause of spontaneous abortions?

A

chromosomal anomalies, hypercoagulable states, congenital infection, exposure to teratogens (esp first 2 weeks)

110
Q

What most likely happens when a teratogen is introduced in weeks 3-8 of pregnancy?

A

risk of organ malformation

111
Q

What most likely happens when a teratogen is introduced in months 3-9 of pregnancy?

A

risk of organ hypoplasia

112
Q

What is placenta previa?

A

implantation of the placenta in the lower uterine segment; placenta overlies cervical os - presents as third-trimester bleeding

113
Q

What is placental abruption?

A

separation of placenta from decidua prior to delivery of fetus - common cause of still birth

114
Q

What is placenta accreta?

A

improper implantation of placenta into the myometrium with little or no intervening decide - presents with difficult delivery of placenta and postpartum bleeding

115
Q

What is eclampsia?

A

preeclampsia with seizures (need to remove placenta)

116
Q

What is HELLP?

A

preeclampsia with thrombotic microangiopathy involving the liver -characterized by Hemolysis, Elevated Liver enzymes, and Low Platelets

117
Q

What is hydatidiform mole?

A

abnormal conception characterized by swollen and edematous villi with proliferation of trophoblasts

118
Q

What are signs of a hydatidiform mole?

A

uterus is much larger and b-HCG is much higher than expected

119
Q

How does hydatidiform mole classically present?

A

in the second trimester as passage of grape-like masses through vaginal canal - “snowstorm” appearance on ultrasound

120
Q

What are the differences between a complete mole and a partial mole?

A

complete mole is “completely from dad” - empty ovum, two sperms - 46 chromosomes, no fetal tissue, hydraulic villi, risk for choriocarcinoma

121
Q

Choriocarcinoma from which pathway respond well to chemotherapy?

A

gestational pathway (as composed to the germ cell pathway)

ABBEY MSII Unit 1 (4 decks)

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