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Pathology > Chapter 22 - Female Genital Tract > Flashcards

Chapter 22 - Female Genital Tract Flashcards

1
Q

cervix is divided into ______ and what is their epithelium

A

vaginal portio (visible to eye on exam - stratified nonkeratinizing squamous epithelium) and the endocervix (columnar, mucous-secreting epithelium)

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2
Q

point where the squamous and endocervical mucinous columnar epithelium meet

A

squamocolumnar junction

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3
Q

area in the cervix where the columnar epithelium is replaced by squamous epithelium

A

transformation zone

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4
Q

herpes simplex virus involves these female organs in decreasing order

A

cervix, vagina, vulva

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5
Q

HSV-1 gives rise to a _______ infection

A

oropharyngeal

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6
Q

HSV-2 gives rise to a ______ infection

A

genital mucosa and skin infection

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7
Q

clinically, what do the lesions of HSV look like initially and when they become more advanced in the female

A

red papules that progress to vesicles and then to painful ulcers with purulent discharge and pelvic pain

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8
Q

where does the herpes virus establish a latent infection

A

the lumbosacral nerve ganglia

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9
Q

reactivation of the herpes virus is more likely with which infection, and which group of people

A

HSV-2 and in immunocompromised women

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10
Q

in what stage of the virus can the virus transmit

A

active and latent phases

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11
Q

does HSV go into the fetus

A

yes during birth –> need cesarian section

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12
Q

anti-HSV Abs in serum indicates

A

recurrent/latent infection

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13
Q

conditions that may lead to symptomatic herpes infection

A

DM, antibiotics, pregnancy, compromised cell-mediated immunity

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14
Q

symptoms in herpes infection

A

vulvovaginal pruritus, erythema, swelling, curlike vaginal dishcarge

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15
Q

diagnosis of vaginal fungal infection, like Candida

A

pseudospores or filamentous funal hyphae in wet KOH

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16
Q

discharge in Trichomonas vaginalis

A

yellow, frothy vaginal discharge

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17
Q

vaginal/cervical mucosa in trichomonas vaginalis infection

A

fiery red appearance, dilation of cervical mucosal vessels –> STRAWBERRY CERVIX :)

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18
Q

main cause of baceterial vaginosis (vaginitis)

A

Gardnerella vaginalis

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19
Q

discharge from garderella vaginalis

A

thin, green-gray malodorous (fishy) vaginal discharge

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20
Q

pap smear of garnerella vaginalis

A

shaggy coat on coccobacilli

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21
Q

what effect does bacterial vaginosis have in pregnancy/labor

A

premature labor

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22
Q

common cause of PID

A

gonococcus (gram negative diplococcus) and chlamydia

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23
Q

site of initial involvement with gonococcus

A

endocervical mucosa

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24
Q

how do non-gonococcal infections following surgical procedures spread from the uterus

A

through lymphatic/venous channels instead of mucosal surfaces

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25
Q

acute complications of PID

A

peritonitis and bacteremia

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26
Q

late complications of PID

A

endocarditis, meningitis, and suppurative arthritis

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27
Q

bartholin cysts lined by

A

ductal squamous epithelium

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28
Q

presentation of bartholin cyst

A

painful unilateral cystic lesion that has been inflamed

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29
Q

lichen sclerosis involves thinning of what layer?

A

epidermis

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30
Q

surface appearance of lichen sclerosis

A

white smoothed out plaques that resemble parchment

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31
Q

lichen sclerosis is more common in pre/post menopausal women?

A

postmenopausal

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32
Q

lichen sclerosis is associated with an increased chance of developing

A

squamous cell carcinoma

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33
Q

squamous cell hyperplasia of the vulva is called

A

lichen simplex chronicus

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34
Q

clinically lichen simplex chronicus has an area of

A

leukoplakia (white plaque like mucosal thickening)

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35
Q

lichen simplex chronicus has an increased risk of..

A

NOTHING!! no predisposition to cancer.. but so sneaky its present at the margins of an established vulva cancer

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36
Q

sexually transmitted, benign warty lesions

A

condyloma acuminatum

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37
Q

what forms of HPV is condyloma acuminatum most associated with

A

6 and 11

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38
Q

what type of cytologic changes occur in condyloma acuminatum

A

koilocytotic atypia

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39
Q

koilocytotic atypia is characterized by

A

nuclear enlargement and atypia with a perinuclear halo

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40
Q

two groups of vulvar cancer, and they are associated with what

A

(1) basaloid and warty carcinomas - high risk HPVs 16 and 18,31 and (2) keritanizing squamous cell carcinomas not related to HPV infection

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41
Q

precancerous lesion of basaloid and warty carcinomas

A

classic vulvar intraepithelial neoplasia (classic VIN)

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42
Q

risk factors for vulvar carcinoma

A

reproductive-age women with young age at first intercourse, multiple sexual partners, or male partner with multiple sexual partners

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43
Q

keratinizing squamous cell carcinomas of the vulva typically arise in patients with

A

long-standing lichen sclerosus or squamous cell hyperplasia

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44
Q

mean age of keratinizing squamous cell carcinomas of the vulva

A

76 years

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45
Q

premalignant lesion for keratinizing squamous cell carcinomas of the vulva

A

differentiated vulvar intraepithelial neoplasia (differentiated VIN), VIN simplex

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46
Q

initial spread of vulvar cancer is to..

A

inguinal lymph nodes

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47
Q

vulva contains what kind of glands

A

modified apocrine sweat glands

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48
Q

you might confuse this with a carcinoma because of its tendency to ulcerate; a sharply circumscribed nodule on the labia majora/interlabial folds

A

papillary hidradenoma

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49
Q

pruritic red crusted sharply demarcated maplike area usually on the labia majora

A

extramammary paget disease

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50
Q

what layer can extramammary paget disease be found in

A

the epidermis of skin and adjacent hair follicles and sweat glands

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51
Q

what is seen on histology with extramammary paget disease

A

clear separation like a halo from the surrounding epithelial cells with mucopolysaccharide cytoplasm staining with PAS

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52
Q

how likely is it that invasion will develop in extramammary paget disease

A

rarely

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53
Q

how to differentiate extramammary paget disease from melanoma

A

a lack of mucopolysaccharides

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54
Q

exposure to DES to prevent abortions can lead to

A

congenital developmental anomalies like bifid vagina, vaginal adenosis, and clear cell carcinoma

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55
Q

normal vaginal epithelium –> vaginal adenosis when what?

A

Normally the vagina is lined by squamous epithelium (normally pale pink) – adenosis is when there is columnar persistence in the upper 1/3 (red granular areas)

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56
Q

where are gartner duct cysts located and what are they derived from

A

lateral walls of the vagina and derived from wolffian ducts

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57
Q

greatest risk factor for cancer of the vagina

A

previous carcinomma of the cervix or vulva

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58
Q

vaginal tumor occuring in kids less than 5 years old

A

embryonal rhabdomyosarcoma

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59
Q

what does an embryonal rhabdomyosarcoma look like

A

grapelike clusters –> polypoid rounded bulky masses that sometimes fill and project out of the vagina

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60
Q

second most common cancer in women

A

cervical carcinoma

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61
Q

normal vaginal and cervical flora is dominated by

A

lactobacilli

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62
Q

what is the lactobacilli’s role in the female

A

produce lactic acid maintaing vaginal pH at 4.5; produce bacteriotoxic H2O2

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63
Q

benign exophytic growth in the cervix producing irregular vaginal spotting

A

endocervcical polyps

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64
Q

most important factor in cerical oncogenesis

A

high oncogenic risk HPVs

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65
Q

high oncogenic risk HPVs

A

16&18

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66
Q

risk factors for cervical cancer

A

multiple sexual partners, male partner with multiple previous or current sexual partners, young age at first intercourse, high parity, persistent infection with high risk HPV, immunosuppression, HLA subtypes, oral contraceptive use, nicotine use

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67
Q

most of HPV infections will be cleared within

A

2 years, 50% cleared in 8 months

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68
Q

epithelium of cervix

A

large areas of immature squamous metaplastic epithelium

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69
Q

what is koilocytic atypia and what does it look like

A

changes that occur during replication of HPV; it has nuclear atypia and a cytoplasmic perinuclear halo

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70
Q

how does HPV activate the cell cycle, what specific parts of HPV activate the cycle

A

interfering with the function of Rb and p53; E7 and E6

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71
Q

what is the role of E7 and E6 in HPV

A

E6: degrades p53 and proteolyzes it inhibiting cell death, E7: cyclin E (E7) destroys hypophosphorylated Rb-E2F (active form) complex –> this complex usually inhibits S-phase entry of cell cycle

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72
Q

genetic abnormalities associated with HPV 16

A

deletions at 3p and amplifications of 3q

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73
Q

describe the dysplasia present in each classification of CIN and its grade of squamous intraepithelial lesion

A

CIN I - mild dysplasia/low-grade, CIN II - moderate dysplasia/high-grade, CIN III - severe dysplasia/high, CIN III - carcinoma in situ/high

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74
Q

what is the difference in the squamous cell distribution between high and low grade cervical lesions

A

low grade: squamous cells confined to lower one third of epithelium; high grade: expand to thwo thirds of epithelial thickness

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75
Q

there is an overexpression of what cell cycle regulatory protein in oncogenic HPVs

A

p16

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76
Q

what is p16 and what is its role in HPV infection

A

a cyclin kinase inhibitor that inhibits the cell cycle by preventing phosphorylation of RB; the E7 from the virus inactivates RB so cells proliferate and p16 can’t inhibit

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77
Q

most common HPV

A

HPV 16

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78
Q

most high grade cervical lesion develop from

A

low grade cervical lesions

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79
Q

immediate precursor of cervical squamous cell carcinoma

A

high grade squamous intraepithelial lesion

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80
Q

2nd most common tumor type of the cervix

A

cervical adenocarcinoma

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81
Q

low grade lesions of the cervix have what percent of a change to regress, persist and progress (progress to what)

A

60%, 30%, 10% to high grade

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82
Q

high grade lesions of the cervix have what percent of a change to regress, persist and progress (progress to what)

A

30%, 60%, 10% to carcinoma

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83
Q

peak incidence age of invasive cervical carcinoma

A

45 years

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84
Q

what do most patients with stage IV cervical cancer die from

A

consequence of local extension of tumor rather than distant metstases (like into bladder and ureters)

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85
Q

what part of the cervix is the pap test taken from

A

cervical transformation zone

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86
Q

available HPV vaccine types

A

6, 11, 16, 18

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87
Q

two major components of the endometrium

A

myometrium and endometrium

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88
Q

upper half to 2/3 of the endometrium

A

functionalis - shed during menses

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89
Q

lower 1/3 of the endometrium

A

basalis

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90
Q

what happens during the proliferative phase of the menstrual cycle

A

granulosa cells of developing follicle in ovary gives off estrogen causing the endometrium undergoes rapid growth

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91
Q

when does the endometrium slow its growth

A

ovulation

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92
Q

uterine bleeding not caused by any underlying organic/structureal abnormality

A

dysfunctional uterine bleeding

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93
Q

what is the cause of too much estrogen stimulation without the counteracting effect of the progestational phase

A

anovulatory cycle

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94
Q

when are anovulatory cycles the most common

A

menarche and perimenopausal period

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95
Q

what happens to the endometrium in an anovulatory cycle

A

mild architectural changesfrom prolonged endometrial stimulation

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96
Q

inadequate corpus luteum function resulting in low progesterone output and early menses

A

inadequate luteal phase

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97
Q

how does an inadequate luteal phase manifest clinically

A

infertility with increased bleeding or amenorrhea

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98
Q

what does biopsy of the endometrium show with an inadequate luteal phase

A

secretory endometrium that is late in its expected secretory characteristics by that date

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99
Q

under what conditions would acute endometritis arise

A

bacterial infections that arise after delivery or miscarriage

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100
Q

causative agents in acute endometritis

A

group a strep, staph

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101
Q

how would you treat an acute endometritis infection

A

removal by curettage with antibiotics

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102
Q

chronic endometritis occurs in these type of patients:

A

patients with chronic PID, postpartum/post abortion patients who have retained gestational tissue, IUDs, women with TB

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103
Q

what kind of cells are seen in chronic endometritis

A

plasma cells

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104
Q

what organism may be associated with chronic endometritis

A

Chlamydia

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105
Q

presence of endometrial tissue outside the uterus

A

endometriosis

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106
Q

sites of endometriosis in descending order

A

ovaries, rectovaginal septum, large/small bowel and appendix, fallopian tubes –> can have symptoms associated with where the tissue is

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107
Q

endometriosis presents clinically as…

A

infertility, dysmenorrhea, pelvic pain

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108
Q

what age group does endometriosis affect

A

women in active reproductive life, third/fourth decades

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109
Q

theories for endometriosis: (2)

A
  1. implanted at abnormal locations and retrograde menstruation through the fallopian tubes occur, possible reason for metastasis (2) endometrium could arise directly from coelomic epithelium
110
Q

what can happen to the ovaries in endometriosis

A

they can become filled with brown fluid from a previous hemorrhage –> CHOCOLATE CYST

111
Q

histologic diagnosis of endometriosis requires

A

endometrial glands and stroma

112
Q

symptoms of endometriosis

A

dysmenorrhea, dyspareunia, pelvic pain and possible pain on defection if the rectal wall is involved

113
Q

what is commonly a presenting complaint with endometriosis

A

infertility

114
Q

presence of endometrial tissue within the uterine wall

A

adenomyosis

115
Q

in adenomyosis, where does the endometrial tissue extend into

A

between the smooth muscle fascicles of the myometrium

116
Q

what does adenomyosis look like on histology

A

endometrial stroma with or without glands in the myometrium separated from the basalis

117
Q

symptoms of adenomyosis

A

menometrorrhagia, colickly dysmenorrhea, dyspareunia, and pelvic pain

118
Q

symptoms of endometrial polyps

A

asymptomatic or abnormal bleeding

119
Q

hyperplastic polyps are responsive to..

A

estrogen, not progestrone

120
Q

what cancer may arise within endometrial polyps

A

adenocarcinoma

121
Q

causes of endometrial hyperplasia

A

obesity, menopause, PCOD, granulosa cell tumors of the ovary, estrogen replacement therapy

122
Q

genetic alteration found in endometrial hyperplasia

A

inactivation of the PTEN tumor suppressor gene

123
Q

patients with what disease share a mutation with the one found in endometrial hyperplasia

A

Cowden syndrome

124
Q

types of endometrial hyperplasia

A

simple hyperplasia without atypia, simple hyperplasia iwth atypia, complex hyperplasia without atypia, complex hyperplasia with atypia

125
Q

which endometrial hyperplasia has glands with cystic dilation

A

simple hyperplasia without atypia

126
Q

which endometrial hyperplasia has increased # and size of glands with crowding and branching, intervening strom and abundant mitotic figures

A

complex hyperplasia without atypia

127
Q

how can you treat complex hyperplasia with atypia

A

hysterectomy

128
Q

most common invasive cancer of the female genital tract

A

endometrial carcinoma

129
Q

what age group does endometrial carcinoma arise in

A

postmenopausal women (55-65) because they present with postmenopausal bleeding

130
Q

most common type of endometrial carcinoma

A

type I carcinoma

131
Q

where does type I endometrial carcinoma invade into

A

myometrial invasion with extension into the periuterine structures by direct continuity

132
Q

metastases of type I endometrial carcinoma

A

lungs

133
Q

what are most typeI endometrial carcinomas called, and how do they look like on histology

A

endometrioid adenocarcinoma with gland patterns resembling normal endometrial epithelium

134
Q

type II endometrial carcinomas arise in what stage of the endometrium

A

endometrial atrophy

135
Q

what discharge can be found in type II endometrial carcinoma and what is another symptom

A

excessive leukorrhea (thick, whitish discharge from vagina), irregular or postmenopausal vaginal bleeding

136
Q

endometrial adenocarcinomas with malignant changes in the stroma

A

malignant mixed mullerian tumors

137
Q

in a malignant mixed mullerian tumor can differentiate into a variety of malignant components of what embryonic layer

A

mesodermal, like muscle, cartilage, osteoid

138
Q

what age group does malignant mixed mullerian tumors present in and what is a presenting symptom

A

postmenopausal womean with postmenopausal bleeding

139
Q

on gross appearance, malignant mixed mullerian tumors differ from adenocarcinomas because they are

A

fleshy, bulky, and protrude through the cervial os

140
Q

prognosis of malignant mixed mullerian tumors

A

highly malignant

141
Q

what kind of neoplasm is a leiomyoma (what is it composed of and malignant potential)

A

benign smooth muscle

142
Q

histology of leiomyomas

A

whorled pattern of smooth muscle bundles

143
Q

symptoms of leiomyomas

A

abnormal bleeding, compression of the bladder (urinary frequency), sudden pain on disruption of blood supply, imparied fertility

144
Q

how do you distinguish a leiomyosarcoma from a leiomyoma on histology

A

there is nuclear atypia, mitotic index, and zonal necrosis

145
Q

hydatids of morgagni are remnants of what and where is it found

A

mullerian duct, its a larger variety cyst near the fimbriated ennd of the fallopian tube

146
Q

paratubal cysts are filled with

A

clear serous fluid; 0.1-2 cm; fallopian tube cyst

147
Q

Where do cystic follicles of the ovary originate from?

A

Unruptuured graafian follicles or in follicles that have ruptured and immediately sealed

148
Q

Larger cystic follicles in the ovary may cause what symptom

A

Pelvic pain

149
Q

Uniform and usually b/l enlargement of the ovary with hypercellular stroma and luteinization of stromal cells (look like nests of cells with vacuolated cytoplasm)

A

Stromal hyperthecosis

150
Q

Most ovarian tumors are benign/malignant? And what age group do they occur in

A

Benign; 20-45 years

151
Q

Malignant ovarian tumors are more common in what age group?

A

45-65 years

152
Q

what 3 parts of the ovary do tumors derive from

A

(1) surface epithelium derived from the coelomic epithelium, (2) germ cells - migrate to ovary from yolk sac, (3) stroma of ovary (including sex cords)

153
Q

3 major histologic types of surface epithelium ovarian tumors

A

serious, mucinous, and endometrioid

154
Q

extent of peithelial proliferation in surface epithelium ovarian tumors (3 types, describe them)

A

benign (minimal proliferation), borderline (moderate proliferation), malignant (marked epithelial proliferation + stromal invasion)

155
Q

benign surface epithelium ovarian tumors can be broken down into 3 types

A

cystadenomas, cystadenofibromas, adenofibromas

156
Q

if borderline and malignant surface epithelium ovarian tumors have a cystic component and are malignant, what are they called

A

cystadenocarcinomas

157
Q

how are the surface layers of the ovary derived embryologically and what part gets transformed in ovarian tumors

A

mullerian ducts formed from the coelomic epithelium evolve into the 3 types of ovarian surface epithelium; this coelomic epithelium transforms into tumors

158
Q

serous surface epithelial ovarian tumors are lined by what type of cells and what are they filled with

A

cystic neoplasms lined by talll, columnar, ciliated and nonciliated epithelial cells and are filled with clear serous fluid

159
Q

most common malignant ovarian tumors, what age do they arise in

A

serous surface epithelial ovarian tumors; 20-45 years

160
Q

what percentage of serous surface epithelial ovarian tumors are benign/borderline/malignant

A

70% benign/borderline and 30% malignant

161
Q

risk factors for malignant serous surface epithelial ovarian tumors

A

nulliparity, family history, and heritable mutations

162
Q

what mutations increase susceptibility to ovarian cancer

A

BRCA1 and BRCA2

163
Q

borderline serous surface epithelium ovarian tumors have an increased number of ______ on histology

A

papillary projections

164
Q

serous surface epithelial ovarian tumors are mostly unilateral/bilateral

A

bilateral

165
Q

in benign serous surface epithilial ovarian tumors what is there an abundance of on histology

A

cilia

166
Q

which type of ovarian tumor has psammoma bodies

A

serous surface epithelium ovarian tumor

167
Q

most mucinous surface epithelium ovarian tumors are benign/malignant?

A

benign/borderline

168
Q

risk factor for mucinous surface epithelium ovarian tumor

A

smoking

169
Q

how does a mucinous tumor differ from a serous surface epithelium ovarian tumor (3)

A

rare surface involvement, mostly unilateral larger cystic masses, no cilia

170
Q

on histology, what kind of epithelial cells are present in mucinous surface epithelium ovarian tumors

A

columnar epithelial cells with apical mucin w/o cilia

171
Q

condition with extensive mucinous ascites, cystic epithelial implants on the peritoneal surfaces, adhesions, and frequently mucinous tumor involving the ovaries

A

pseudomyxoma peritonei

172
Q

how do endometriod tumors differ from serous or mucinous surface epithelial ovarian tumors

A

presence of tubular glands that look like benign/malignant endometrium

173
Q

in what disease state my endometriod surface epithelium ovarian cancers arise in

A

in the setting of endometriosis

174
Q

if you have a primary mucinous ovarian tumor and it presents bilaterally, what do you need to exclude

A

tumor of a non-ovarian origin

175
Q

which type of surface epithelium ovarian tumor has bilaterality that is typical

A

serous type

176
Q

if bilaterality is present in an endometriod surface epithelium ovarian tumor, what does this imply

A

extension of the neoplasm beyond the genital tract

177
Q

characterized by large epithelial cells with abundant clear cytoplasm similar to the hypersecretory gestational endometrium

A

clear cell adenocarcinoma

178
Q

what other disease may clear cell adenocarcinoma of the ovaries be associated with

A

endometriosis or endometriod carcinoma of the ovary

179
Q

what kind of epithelium does a brenner tumor have

A

nests of transitional type epthial cells like those from the urinary bladder

180
Q

brenner tumors are usually bilateral/unilaterl? what kind of tumors are they?

A

unilateral; adenofibroma

181
Q

if there is an ovarian tumor that has neoplastic epithium like the bladder, but without a brenner component, what is it

A

transitional cell carcinoma

182
Q

where will an ovarian tumor go if it extends past the capsule? and what symptom will it present with

A

it will seed the peritoneal cavity; presents with ascites

183
Q

marker for ovarian tumors

A

CA-125

184
Q

what can elevations in CA-125 also appear in other than ovarian tumors

A

peritoneal irritation

185
Q

what reduces the risk of ovarian cancer

A

fallopian tube ligation and oral contraceptive therapy

186
Q

at what stage of growth are ovarian tumors diagnosed

A

only diagnosed when they are large or originate on the ovarian surface where they easily spread to the pelvis

187
Q

most germ cell ovarian tumors are

A

benign cystic teratomas

188
Q

categories of ovarian teratomas

A

mature (benign), immature (malignant) and monodermal/highly specialized

189
Q

another name for benign ovarian teratomas and what age do they typically present in

A

dermoid cysts, young women of active reproductive years

190
Q

about 1% of dermoid teratomas most commonly undergo malignant transformation into what type of cancer

A

squamous cell carcinoma

191
Q

what kind of structures are found in an ovarian teratoma

A

collections of tissues and structures from all 3 germ layers

192
Q

most common specialized ovarian teratomas

A

struma ovarii and carcinoid

193
Q

specialized ovarian teratomas are unilateral/bilateral?

A

unilateral

194
Q

what kind of tissue is struma ovarii composed of

A

mature thyroid tissue

195
Q

what syptom might struma ovarii cause

A

hyperthyroidism

196
Q

where does the ovarian carcinoid tumor typically arise from

A

intestinal epithelium in a teratoma

197
Q

what does the ovarian carcinoid tumor produce and what syndrom may be associated with it

A

5-hydroxytryptamine and the carcinoid syndrome

198
Q

what age do malignant teratomas present in and what kind of tissue is found?

A

embryonal and immature fetal tissue and found mainly in prepubertal adolescents around 18 years

199
Q

risk factor for subsequent extra-ovarian spread in a malignant teratoma is based on the proportion of tissue containing:

A

immature neuroepithelium

200
Q

ovarian counterpart of the seminoma of the testis

A

dysgerminoma

201
Q

most dysgerminomas occur in what age group

A

2nd and third decades

202
Q

dysgerminomas are bilateral/unilateral

A

unilateral

203
Q

what is located in the fibrous stroma of a dysgerminoma

A

mature lympocytes and occasional granulomas

204
Q

dysgerminomas are benign/malignant

A

malignant

205
Q

what kind of prognosis do dysgerminomas have

A

good prognosis: responsive to chemo even if they extend beyond the ovary

206
Q

what is a yolk sac tumor rich in

A

alpha-fetoprotein and alpha1antitrypsin

207
Q

what kind of histology is seen in a yolk sac tumor

A

schiller-duval body

208
Q

what is a schiller-duval body

A

glomerulus-like structure composed of a central blood vessel enveloped by germ cells within a space lined by germ cells

209
Q

what is the clinical presentation of a yolk sac tumor

A

children or a young woman with abdominal pain and a rapidly developing pelvic mass

210
Q

extra-embryonic differentiation of malignant germ cells that have high levels of chorionic gonadotropins

A

choriocarcinoma

211
Q

how can you determin that a choriocarcinoma is of germ cell origin

A

you can only do this in a pre-pubertal girl because after this age you can’t exclude it from an ectopic pregnancy

212
Q

most ovarian choriocarcinomas exist with what other disease

A

other germ cell ttumors

213
Q

prognosis and chemo for ovarian choriocarcinomas

A

aggressive tumors that metastaze widely through bloodstream to lungs/liver and are unresponsive to chemo (unlike those that arise from placental tissue) - fatal :(

214
Q

tumor with granulosa and theca cell differentiation arising in postmenopausal women; what epithelial layer does it arise from

A

granulosa-theca cell tumor; sex-cord stromal

215
Q

what histology is seen with granulosa-theca cell tumors?

A

call-exner bodies

216
Q

what are call-exner bodies

A

small, distinctive, gland-like structures filled with acidophilic material

217
Q

what do granulosa-theca cell tumors give off

A

estrogen and inhibin (from granulosa cells)

218
Q

tumors arising in the ovarian stroma that are composed of fibroblasts; what epithelial layer is it from

A

fibromas; sex cord-stroma

219
Q

tumors arising in the ovarian stroma that are composed of plump spindle cells with lipid droplets; what epithelial layer is it from

A

thecomas; sex cord stroma

220
Q

what symptoms are associated with fibromas, thecomas, and fibrothecomas; what epithelial layer is it form

A

pelvic mass, ascites, hydrothorax only of the right side; sex-cord stroma

221
Q

Meigs syndrom is composed of…

A

ovarian tumor, hydrothorax, ascites

222
Q

tumors of the ovary that produce masculinization or least defeminzation

A

sertoli-leydig cell tumors/androblastomas

223
Q

sertoli-leydig cell tumors/androblastomas are usually bilateral/unilater? what epithelial layer are they derived from

A

unilateral; sex-cord stroma

224
Q

what is a consequence of sertoli-leydig cell tumors in women

A

virilization

225
Q

a ovarian tumor with lipid-laden cells and reinke crystalloids

A

hilus cell tumors, pure leydig cell tumors

226
Q

uncommon tumor composed of germ cell sand sex cord-stroma derivatives; individuals have abnormal sexual development and gonads of indeterminate nature

A

gonadoblastoma

227
Q

metastatic gastrointestinal neoplasia to the overies

A

krukenberg tumor

228
Q

what kind of cells are present in a krukenberg tumor

A

mucin-producing, signet-ring cancer cells of gastric origin

229
Q

pregnancy loss before 20 weeks gestation

A

spontaneous abortion or miscarriage

230
Q

causes of spontaneous abortion

A

chromosomal anomalies, luteal-phase defect, poorly controlled diabetes, other uncorrected endocrine disorders, vasculature disorders (antiphospholipid Ab syndrome, coagulopathies, HTN), infections (toxoplasma, mycoplasma, listeria, viral infections)

231
Q

implantation of the fetus in another site other than inside the uterus

A

ectopic pregnancy

232
Q

most common site of ectopic pregnancy

A

fallopian tubes!! other sites are ovary, abd cavity, intrauterine porition of fallopian tube

233
Q

predisposing condition to ectopic pregnancy

A

prior PID –> fallopian tube scarring, IUDs also increase risk

234
Q

fertilization and trapping of ovum within the follicle just at the time of its rupture results in

A

ovarian pregnancy

235
Q

what may develop of the fertilized ovum fails to enter or drops out of the fimbriated end of the tube

A

abdominal pregnancy

236
Q

tubal pregnancy is the most common cause of

A

hematosalpinx (blood-filled fallopian tube)

237
Q

consequence of fallopian tube rupture

A

massive intraperitoneal hemorrhage

238
Q

clinical presentation of an ectopic pregnancy

A

severe abdominal pain about 6 weeks after a previous normal menstrual period caused by a rupture of the tube –> pelvic hemorrhage

239
Q

what is a serious complication from ectopic pregnancy

A

hemorrhagic shock with signs of an acute abdomen

240
Q

identical twins are from what type of placenta

A

monochorionic

241
Q

in a monochorionic twin placenta, if there is a vascular anastomoses between the circulation of both twins

A

twin-twin transfusion syndrome

242
Q

placenta implants in the lower uterine segment or cervix with serious third-trimester bleeding

A

placenta previa

243
Q

if a patient had a complete placenta previa, how must the baby be delivered, and why does the baby have to be delivered this way

A

via cesarean section to avert placental rupture and fatal maternal hemorrhage during vaginal delivery

244
Q

partial or complete absence of the decidua with adherence of placental villous tissue directly to the myometrium and failure of placental separation

A

placenta accreta

245
Q

risk factors for poastpartum bleeding

A

placenta previa and history of previous cesarean section

246
Q

what are 2 ways infections in the placenta can develop, which is more common

A

ascending infection (most common) through the birth canal and hematogenous transplacental infection

247
Q

what does the amniotic fluid look like histologically with infection

A

polymorphonuclear leukocytic infiltrate with edema and congestion of the vessels

248
Q

what are the organisms that can cross through the placenta

A

TORCH (toxoplasmosis, others-syphilis, TB, listeriosis, rubella, CMV, herpes)

249
Q

how does preeclampsia present clinically

A

with HTN, edema, proteinuria in the last trimester

250
Q

what is it called when preeclampia patient becomes more seriously ill? and what additional symptom is seen with this state

A

ecclampsia with convulsions

251
Q

some women with sever preeclampsia can develop this syndrom composed of

A

HELLP syndrome - hemolysis, elevated liver enzymes, low platelets

252
Q

preeclampsia without proteinuria

A

gestational htn

253
Q

at what point of pregnancy does preeclampsia symtoms disapper

A

with delivery of the placenta

254
Q

what are the abnormalities associated with preeeclampsia

A

endothelial dysfunction, vasoconstriction, increased vascular permeability

255
Q

microscopic changes associated with preeclampsia

A

placental infarcts with increased syncytial knots and in the decidual vessels indicating abnormal implantation

256
Q

in what case will preeclampsia be found earlier than 34 weeks gestation

A

in patients wiht a hydatidiform mole

257
Q

what are indications for delivery no matter the age of the fetus with preeclampsia states

A

maternal end-organ dysfunction, fetal compromise, HELLP syndrome

258
Q

cystic swelling of the chorionic villi

A

hydatidiform mole

259
Q

hydatidiform moles are associated with an increased risk of..

A

persistant trophoblastic disease (invasive mole) or choriocarcinoma

260
Q

what ages are molar pregnancies more common in

A

far ends of reproductive life: teens and between ages of 40 and 50 years

261
Q

difference in ferilization in a complete and partial mole

A

complete: fertilization of an egg that has lost its chromosomes and genetic material is completely paternally derived - partial: fertilization of an egg with 2 sperm

262
Q

karyotype of complete and partial moles

A

complete: (46, XX or XY) and partial: (69,XXY or 92XXXY)

263
Q

complete mole histology

A

most villi enlarged and edematous with diffuse trophoblast hyperplasia arpimd tje emtore circumference of the villi

264
Q

which type of mole has an increased risk of choriocarcinoma

A

complete mole

265
Q

partial mole histology:

A

villous enlargement and architectural disturbance in only a proportion of villi

266
Q

what gene mutation in found in hydatidiform moles. are they in partial or complete moles

A

p57KIP2 in patial moles becuase it is maternally transcribed but paternally imprinted (complete moles have an emplty ovum)

267
Q

what lab value is elevated with a molar pregnancy

A

HCG

268
Q

how is choriocarcinoma dervied and what is its prognosis

A

malignant neoplasm of trophoblastic cells dervied from a previously normal or abnormal pregnancy ; its rapidly invasive and metastasizes widely but responds well to chemo (nearly 100% remission)

269
Q

most choriocarcinomas arise with what condition, what are some other common conditions

A

with hydatidiform moles, also in patients with previous abortions and 22% in normal pregnancies

270
Q

histology of choriocarcinomas

A

large pale areas of ischemic necrosis, foci of cystic softening and extensive hemorrhage

271
Q

how does choriocarcinoma manifest clinically

A

vaginal spotting of a bloddy, brown fluid

272
Q

what lab value is elevated in choriocarcinoma and where does metastases go

A

HCG, lungs

Pathology (9 decks)

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