Female Genitalia Path Flashcards

1
Q

Herpes simplex clinical symptoms

A

Clinical symptoms will occur in ~1/3 of affected individuals

  • lesions 3-7 days after intercourse
  • painful red papules in vulva  vesicles  ulcers (contain virus particles)
  • leukorrhea (white discharge) when cervix or vagina is involved
  • systemic symptoms: fever, malaise, tender inguinal lymph nodes
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2
Q

Herpes simplex lesions & transmission

A

lesions heal spontaneously in 1-3 weeks, but infection remains latent in the regional nerve ganglia
-2/3 women suffer recurrence
transmission is possible whether active or latent phase
-greatest danger is to the neonate during birth
*may result in fatal systemic infection
-risk greatest during primary, active infections

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3
Q

Mycotic and yeast (Candida)

A

manifests as small white patches, leukorrhea, pruritus
10% of women are carriers
diabetes mellitus, oral contraceptives, and pregnancy promote development of infection
diagnosis: wet mount or culture

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4
Q

Trichomonas vaginalis

A
causes purulent discharge and discomfort
"strawberry cervix"
seen in 15% of women at STD clinics
frothy discharge due to
Trichomonas infection
“strawberry cervix”
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5
Q

Bacterial vaginosis

A

most common vaginal infection in women of childbearing age
imbalance of bacterial flora, favoring harmful types
risk factors: multiple partners, douching, pregnancy, smoking

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6
Q

Bacterial vaginosis symptoms

A

signs/symptoms: fish-like odor; gray discharge; burning/itching; frequently asymptomatic
especially important to treat during pregnancy: associated with PROM/premature birth
may ascend and cause pelvic inflammatory disease

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7
Q

Bacterial vaginosis Amsel’s criteria

A

diagnosis by Amsel’s criteria (3 of the following):
microscopic “clue cells“
fishy odor on adding 10% KOH to secretions
vaginal pH > 4.5
thin homogenous discharge

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8
Q

Pelvic Inflammatory Disease (PID)

A

pelvic pain, adnexal tenderness, fever, vaginal discharge
infection by: gonococci, chlamydiae, enteric bacteria
Postpartum and postabortion infections: staphylococci, streptococci, coliform bacteria, Clostridium perfringes

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9
Q

Gonococcal PID

A

inflammatory changes in affected glands (e.g., Bartholin gland) 2-7 days post inoculation
-acute suppurative reaction; inflammation mainly in the superficial mucosa, submucosa
-cervix involvement
common
organisms may disappear over time; proteolysis of inflammatory cells results in accumulation of serous fluid
treatment: easily controlled with antibiotics in early stages; more difficult if abscesses have formed

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10
Q

Gonococcal PID involves & spares

A

usually spares endometrium and involves tubes

  • acute suppurative salpingitis
  • tubal serosa hyperemic; layered with fibrin
  • tubal fimbriae leak exudate, the fimbriae seal to the ovary causing salpingo-oophoritis; tubo-ovarian abscess may develop
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11
Q

Postpartum and Postabortion PID

A

less exudation in tube lumens or mucosa, but greater deep involvement

  • infection spreads throughout the wall to involve the serosa, and spreads up the uterus via lymphatics or blood supply
  • bacteremia is a frequent complication
    treatment: much more difficult to control with antibiotics than gonococcal PID; surgical removal of organs may be necessary
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12
Q

Vulvar Non-Neoplastic Epithelial Disorders (VNED)

A

spectrum of inflammatory lesions of the vulva
characterized by white, scaly, plaquelike mucosal thickenings that produce vulvar discomfort and pruritus
-biopsy is indicated to distinguish from other diseases

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13
Q

Lichen sclerosus (chronic atrophic vulvitis)

A

leads to atrophy of labia, subepithelial fibrosis, narrowing of the introitus
most common after menopause

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14
Q

Lichen sclerosus histological features

A

atrophy of the epidermis (disappearance of rete pegs)
degeneration of basal cells of the epidermis
dermal fibrosis
bandlike lymphocytic infiltrate

unclear pathogenesis; believed to be autoimmune

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15
Q

Lichen simplex chronicus

A

non-specific condition that results from rubbing or scratching the skin to relieve pruritus
characterized by acanthosis and hyperkeratosis of vulvar squamous epithelium
-epithelium thickened; may show mitotic activity in basal and prickle layers

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16
Q

VNED-associated vulvar cancer

A
hyperplasia -> 
cellular atypia -> 
VIN (= carcinoma in situ)
treat with steroids
to prevent cancer development
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17
Q

Condyloma Acuminatum (Venereal Wart)

A

benign papillomavirus-induced squamous lesion with verrucous appearance
-typically caused by HPV types 6 and 11
frequently multiple and coalesce
involve perineal, vulvar, and perianal regions, vagina, sometimes cervix

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18
Q

Condyloma Acuminatum (Venereal Wart) histological

A

acanthosis, parakeratosis, hyperkeratosis, koilocytosis

-frequently regress spontaneously and not considered to be precancerous lesions (just STD marker)

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19
Q

Carcinoma and Vulvar Intraepithelial Neoplasia (VIN)

A

1/8th as frequent as cervical cancer
-3% of all genital cancers
most frequent in women 65-75 yoa
-15% in women VIN

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20
Q

Carcinoma and Vulvar Intraepithelial Neoplasia (VIN) most frequent symptom & sign

A

Most frequent symptom = long history of pruritus
-Less common = vulvar bleeding discharge, dysuria, pain
Most common sign = vulvar lump or mass
-May be fleshy, ulcerated, leukoplakic, or warty
-Most unifocal and on the labia majora
-Expert opinion recommends annual visual inspection of the external genitalia, even if the patient is no longer receiving annual Papanicolaou smears

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21
Q

Vulvar Carcinoma

A

No diagnostic features – diagnosis based on biopsy alone
Lymphohematogenous dissemination
-Inguinal and femoral nodes metastasis common; rarely pelvic nodes
-Lungs, liver, other internal organs
A rare variant of squamous cell carcinoma is the verrucous carcinoma, which presents as a fungating tumor that resembles condyloma acuminatum (isn’t associated with HPV, however)  biopsy any condyloma that doesn’t respond to therapy

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22
Q

Extramammary Paget Disease

A

Rare lesion of the vulva (sometimes perianal region) similar to Paget disease of the breast
-Manifests as pruritic, red, crusted lesion, usually on labia majora
*Sharply demarcated
*Sometimes with palpable submucosal thickening or tumor
~Prognosis is poor in uncommon cases associated with underlying carcinoma

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23
Q

Extramammary Paget Disease histology

A

Large tumor cells (Paget cells) distinguished by clear separation (“halo”) from surrounding epithelial cells
-Granular cytoplasm of Paget cells contains mucopolysaccharide that stains with periodic acid-Schiff (PAS)

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24
Q

Malignant Melanoma

A
Rare (5% of all vulvar cancers)
-2% of all melanomas in women
Peak incidence in 6th or 7th decade
Tumors rapidly enter a vertical growth phase following inception
-5-yr survival rate
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25
Q

Bartholin Cyst

A

obstruction of a Bartholin duct (usually due to preceding infection)
occur at all ages
symptoms: pain, local discomfort
cysts may become large (3-5 cm)
treatment: excision (recurrence likely) or marsupialization (opens the duct permanently)

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26
Q

Vaginal Intraepithelial Neoplasia and Squamous Cell Carcinoma

A

account for ~1% of malignant neoplasms of female genital tract
-(95% are squamous cell carcinomas)
most associated with HPV  greatest risk factor is previous cervical or vulvar cancer

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27
Q

Vaginal Intraepithelial Neoplasia and Squamous Cell Carcinoma

A

most often affects upper posterior vagina along junction with ectocervix

  • usually invades cervix and perivaginal structures by time of diagnosis
  • metastasize to iliac and inguinal nodes
    symptoms:
  • irregular spotting, leukorrhea
  • may be clinically silent until urinary or rectal fistulas develop
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28
Q

Adenocarcinoma(Clear Cell Carcinoma)

A

increased frequency in young women whose mothers had been treated with diethylstilbestrol (DES) during pregnancy (for a threatened abortion)
usually in upper anterior wall of vagina (may also occur in cervix)
most commonly discovered between 15-20 yoa
tumors contain vacuolated, glycogen-containing cells (= “clear cell”)

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29
Q

Diethylstilbestrol (DES) during pregnancy

A

FDA issued advisory in 1971

used by 4 million females between 1938-1971

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30
Q
Embryonal Rhabdomyosarcoma
(Sarcoma Botryoides)
A

uncommon; most frequent in children

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31
Q

Cervicitis

A

some degree of cervical inflammation may be found in virtually all adult women, and is usually of little clinical significance
inflammations common and associated with mucopurulent to purulent vaginal discharge
-discharge contains white cells, atypical epithelial cells (due to inflammation), and possible microorganisms
*presence of microorganisms IS NOT diagnostic of infectious cervicitis

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32
Q

Endocervical Polyps

A

innocuous, inflammatory tumors
2-5% of adult women; more common in multiparous
produce irregular spotting or bleeding
cured by curettage or surgical excision; malignant transformation rare (

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33
Q

Cervix: Intraepithelial and Invasive Squamous Neoplasia

A

Invasive carcinomas of the cervix arise from precursor lesions referred to as CIN (cervical intraepithelial neoplasia)
= SIL (squamous intraepithelial lesion)
Represents a continuum of dysplasia with indistinct boundaries for classification

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34
Q

CIN terminology

A

Represents the precancerous changes that can be detected by cytologic exam
Spectrum of morphologic changes, ranging from:
CIN I = mild dysplasia; koilocytotic atypia, nuclear enlargement, and hyperchromasia
CIN II = moderate dysplasia; loss of polarity, increased mitotic figures, pleomorphism
CIN III = severe dysplasia (carcinoma in situ)

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35
Q

Important things to remember…

A

not all lesions start as condylomata or as CIN I; may enter at any point
CIN may regress spontaneously (especially CIN I in young women)
-Among LSIL lesions (= CIN I)
*50-80% regress in adult women
*90% regress in women 13-21
Not all CIN will progress to cancer, but we treat as if it will (especially CIN II/III)
-When it does progress, may take upwards of 20 years

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36
Q

The role of HPV in cervical oncogenesis

A

HPV is the most important agent in cervical oncogenesis

  • “carcinogenic” types = 16 (primarily) and 18
  • all other HPV types are “probably” or “possibly” carcinogenic (as defined by WHO) except for types 6 and 11
  • A recent PCR test of a large international collection of cervical cancer specimens has shown that HPV DNA is present in 99.7% of cases!!!
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37
Q

risk factors of cervical cancer

A
cigarette smoking
 ↑ parity
 Oral contraceptives?
 Vit. A or C deficiency
 host factors
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38
Q

Invasive Carcinoma of the Cervix

A

Most (~75%) are squamous cell carcinomas

  • Occur at any age, but peak incidence is 40-45 years
  • Peak incidence of high-grade precancers (CIN II/III) is ~30 yoa
  • > 50 yoa in countries with screening programs is rare, as well as
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39
Q

CIN and Cervical Cancer: Cytologic Screening

A

ACS screening recommendations include:
Screening should begin approximately 3 years after the onset of vaginal intercourse and no later than 21 yoa.
Women who are >70 yoa with an intact cervix and who have had 3 or more consecutive, normal results, with no abnormal cytology in the past 10 years, can elect to cease screening
Cervical screening should be performed annually. At age 30, women who have had 3 consecutive normal cytology results may be screened every 2-3 years (unless immunocompromised or were exposed to DES in utero)
Screening following total hysterectomy for benign gynecologic disease is not indicated, but should be continued in those with subtotal hysterectomy or history of CIN II/III.
WHO is evaluating HPV testing as an adjunct to Pap smear screening

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40
Q

CIN and Cervical Cancer: Histologic Diagnosis

A

Colposcopic exam
Many Pap smear abnormalities do not signify a precancerous or cancerous lesion
Abnormalities confirmed by punch biopsy

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41
Q

CIN I

A

CIN lesions characterized by white patches on the cervix after application of acetic acid

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42
Q

CIN and Cervical Cancer: Treatment

A

CIN I = Pap smear follow-up
CIN II/III = cryotherapy, laser, LEEP (loop electrosurgical excision procedures), cone biopsy
Invasive cancer = hysterectomy and lymph node dissection; radiation if advanced
-Small cell undifferentiated (oat cell) tumors have worst prognosis

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43
Q

CIN and Cervical Cancer: Prevention

A

Modify risk factors (e.g., cigarette smoking, sexual behavior)
Vaccination with papillomavirus-like particles (VLPs) for a variety of oncogenic types

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44
Q

Body of Uterus and Endometrium

A

most common disorders result from endocrine imbalances, complications of pregnancy, and neoplastic proliferation
The most common problem is the occurrence of excessive bleeding during or between menstrual periods
-Causes are many, but the largest single group is the functional endometrial disorders

45
Q

Anovulatory Cycle

A

Most common cause of dysfunctional bleeding
Results in excessive and prolonged estrogenic stimulation without the development of the progestational phase that regularly follows ovulation
In most patients, the etiology is unknown
-probably a subtle hormonal imbalance
Most commonly occurs at menarche and the perimenopausal period
Failure of ovulation results in prolonged, excessive endometrial stimulation by estrogens
-The endometrial glands undergo mild architectural changes (persistent proliferation) and stromal breakdown may occur, resulting in bleeding in the middle of the menstrual cycle
-May also contribute to endometrial hyperplasia

46
Q

Inadequate Luteal Phase

A

Refers to the occurrence of inadequate corpus luteum function and a low progesterone output with an irregular ovulatory cycle
Manifests clinically as infertility with either increased bleeding or amenorrhea

47
Q

Endometrial changes induced by oral contraceptives

A

OCs containing synthetic or derivative ovarian steroids induce a wide variety of endometrial changes
-Changes most reminiscent of the decidua of pregnancy
Changes revert to normal on cessation of use

48
Q

Acute Endometritis

A

uncommon and limited to bacterial infections that arise post delivery or miscarriage
-Retained products of conception are the usual precipitating influence
MOs include Group A streptococci, staphylococci, et. al
Removal of the gestational fragments by curettage is followed by remission

49
Q

Chronic Endometritis

A

Occurs in the following settings (secondary disease):
patients suffering from chronic PID
in patients with postpartal or postabortal endometrial cavities (usually due to retained gestational material)
in patients with intrauterine contraceptive devices
in patients with TB (miliary spread or more commonly from drainage of tuberculous salpingitis)

In about 15% of cases, there is no obvious cause
Antibiotic therapy is indicated to prevent other sequelae (e.g., salpingitis)

50
Q

Adenomyosis

A

the presence of endometrial tissue in the uterine wall (myometrium)

  • Remains in continuity with the endometrium
  • Occurs in up to 20% of uteri
  • These tissues respond to the same hormonal stimulus as the endometrium and may bleed during menses
  • May cause menorrhagia, colicky dysmenorrhea, dyspareunia, and pelvic pain
51
Q

Endometriosis

A

the presence of endometrial glands or stroma in abnormal locations outside the uterus

  • Afflicts ~10% of women
  • Affects the following sites (in descending order of frequency): ovaries, uterine ligaments, rectovaginal septum, pelvic peritoneum, laparotomy scars, and rarely, in the umbilicus, vagina, vulva, or appendix
  • It often causes infertility, dysmenorrhea, pelvic pain and other problems
  • A disease of reproductive age (mostly in 20s and 30s)
52
Q

Risk Factors for Endometriosis

A

risk ↑ with exposure
to endometrial material
smoking, obesity ↓ risk

53
Q

Endometriosis:Clinical Course

A

Signs and symptoms include severe dysmenorrhea, dyspareunia, and pelvic pain due to intrapelvic bleeding and periuterine adhesions
-Pain on defecation indicates rectal wall involvement
-Dysuria reflects bladder involvement
-Intestinal disturbances indicate small intestine involvement
Menstrual irregularities are common and infertility in 30-40% of women
Malignancy may develop in this endometriotic tissue and may be considered an “at risk” epithelium

54
Q

Endometrial Polyps

A

sessile masses (usually 0.5-3cm in diameter) that project into the endometrial cavity
-May be single or multiple
-May be asymptomatic or cause abnormal bleeding
Of two histologic types: functional endometrium and, more commonly, hyperplastic endometrium (mostly cystic)
Seen in association with tamoxifen
Genetic alterations may play a role in their development
-Cells are clonal
-Contain chromosome rearrangements

55
Q

Endometrial Hyperplasia (Endometrial Intraepithelial Neoplasia)

A

Another cause of abnormal bleeding
Characterized by an increased gland to stroma ratio and abnormalities in epithelial growth relative to normal endometrium
Deserves attention because of its relation to endometrial carcinoma

56
Q

Endometrial Hyperplasia

A

linked to prolonged estrogen stimulation of the endometrium by anovulation or increased estrogen production
-Conditions promoting hyperplasia include: menopause, polycystic ovarian disease, functioning granulosa cell tumors of the ovary, excessive cortical function, and prolonged administration of estrogenic substances (e.g., HRT)

57
Q

Endometrial Hyperplasia subdivision

A

subdivided in to lower grade (simple) and higher-grade (atypical) subgroups:
Simple non-atypical hyperplasia
-Uncommonly progress to adenocarcinoma
-Reflect response to persistent estrogen stimulation
-Frequently evolve into cystic atrophy

58
Q

Complex atypical hyperplasias

A

aka, endometrial intraepithelial neoplasias (EIN)
dysplasia
increase in number and size of endometrial glands, with gland crowding, enlargement, and irregular shape
23% of patients eventually develop adenocarcinomas

59
Q

Endometrial Hyperplasia (Endometrial Intraepithelial Neoplasia) gene

A

shift in morphology from benign to precancerous often involves loss of PTEN gene expression

  • a tumor suppressor gene
  • In the absence of a normal gene, endometrial cells become more sensitive to stimulation by estrogens and, thus, prone to hyperplasia and carcinoma
60
Q

Carcinoma of the Endometrium

A

The most common invasive cancer of the female genital tract
-7% of all invasive cancers in women
Arise mostly in postmenopausal women (peak at 55-65 yoa)
-A higher incidence is seen in obesity, diabetes mellitus, hypertension, and infertility
-Tend to be seen in women who are single and nulliparous with a history of anovulation
-May be seen in patients with concomitant breast cancer
Causes postmenopausal (abnormal) bleeding (permits early detection and cure)

61
Q

Two general groups of endometrial cancer

A

1) Cancer that develops in relation to prolonged estrogen stimulation and endometrial hyperplasia
2) Cancer that does not exhibit hyperestrinism or pre-existing hyperplasia

62
Q

Carcinoma of the Endometrium:Hyperplasia-associated

A

Linked to obesity and anovulatory cycles
in postmenopausal women, there is greater synthesis of estrogens in body fat
Ovarian estrogen-secreting tumors confer higher risk
Rare in women with ovarian agenesis and early ovariectomy
Increased risk with estrogen replacement therapy
Inactivation of PTEN is common
Prolonged administration of DES may produce endometrial polyps, hyperplasia, and carcinoma
Most common type? adenocarcinoma
associated w estrogen excess

63
Q

Carcinoma of the Endometrium:Age-associated

A

Tend to acquire the cancer at a somewhat older age
more often papillary serous carcinomas, clear cell carcinomas, or squamous carcinomas
These tumors have a poorer prognosis due to their propensity to exfoliate and implant on peritoneal surfaces

64
Q

Carcinoma of the Endometrium: Clinical Course

A

May be asymptomatic for periods of time but usually produces irregular vaginal bleeding with excessive leukorrhea

65
Q

Leiomyomas

A
Perhaps the most common tumor in humans
-may be present in ~75% of reproductive age females 
*average 6.5 tumors/uterus! 
~but each is a unique clonal entity
~40% have chromosomal abnormalities
66
Q

Leiomyomas biopsy

A

benign tumors of smooth muscle
-demonstrate a whorled pattern of smooth muscle bundles on cut section
appear as sharply circumscribed, discrete, round, gray-white tumors varying in size from barely visible to massive tumors that can fill the pelvis

67
Q

Leiomyomas odd benign variants

A

benign metastasizing leiomyoma
-consists of a tumor that extends into vessels and migrates to other sites (most commonly lung)
disseminated peritoneal leiomyomatosis
-presents as multiple small nodules on the peritoneum

Leiomyomas may be asymptomatic or cause abnormal bleeding, bladder compression, sudden pain, and infertility
May be problematic in pregnancy

68
Q

Leiomyosarcomas

A

Uncommon malignant neoplasms
Arise de novo directly from the myometrium or the endometrial stroma undergoing smooth muscle differentiation
Equally common before and after menopause with a peak incidence at 40-60 years of age

69
Q

Leiomyosarcomas

Distinction from leiomyomas based on biopsy

A

Degree of nuclear atypia, mitotic index, and zonal necrosis

More than half metastasize to distant organs (lung, brain, bone)
5-yr survival rate = 40%

70
Q

Fallopian Tubes:Inflammations

A

Suppurative salpingitis may be caused by any pyogenic organisms (and often >1)
A tuberculous salpingitis is common in parts of the world where TB is prevalent
-It is rare in the U.S. (1-2%)

71
Q

Paratubal cysts

A

The most common primary lesions (excluding endometriosis) are minute 0.1-2 cm translucent cysts filled with clear serous fluid
Larger varieties found near the fimbriated end or in the broad ligaments are called hydatids of Morganii

72
Q

Fallopian Tubes Tumors

A

Tumors are uncommon
Benign tumors include adenomatoid tumors
Primary adenocarcinoma is rare
Occult carcinoma of the uterine tubes has been associated with BRCA mutations

73
Q

Ovaries

A
The most common types of lesions encountered in the ovary include functional or benign cysts
Intrinsic inflammations (öophoritis) are uncommon and usually accompany tubal inflammation
Rarely, a primary inflammatory disorder involving the ovarian follicles (autoimmune öophoritis) occurs and is associated with infertility
74
Q

Non-Neoplastic and Functional Cysts: Follicular and luteal cysts

A

Cystic follicles in the ovary are so common as to be virtually physiologic
-They originate in unruptured graafian follicles or in follicles that have ruptured and immediately sealed
Granulosa luteal cysts (corpora lutea) are normally present in the ovary
-They occasionally rupture and cause a peritoneal reaction

75
Q

Polycystic ovarian disease (PCOS)

A

formerly Stein-Leventhal syndrome
affects 3-6% of reproductive-age women
The central pathologic abnormality is numerous cystic follicles or follicle cysts
Patients with PCOS have persistent anovulation, obesity (40%), hirsutism (50%), and rarely, virilism
-Often associated with oligomenorrhea

76
Q

PCOS enzymes

A

It is now thought that a variety of enzymes involved in androgen synthesis are poorly regulated and are involved in the pathogenesis
Recent studies link PCOS to insulin resistance
-Administration of insulin mediators associated with resumption of ovulation

77
Q

Stromal hyperthecosis

A

disorder of ovarian stroma most commonly seen in postmenopausal women
characterized by uniform enlargement of the ovary (up to 7 cm)
-involvement is usually bilateral
Clinical presentation is similar to PCOS

78
Q

Ovarian Neoplasms

A

Among cancers of the female genital tract, the incidence of ovarian cancer ranks only below carcinoma of the cervix and endometrium
-Because many of these cancers cannot be detected early in their development, they account for a disproportionate number of fatal cancers
~ 80% of these tumors are benign and occur in between 20 and 45 yoa
-Malignant tumors are more common between 40 and 65 yoa

79
Q

Ovarian Neoplasms risk factors

A

Pathogenesis risk factors are less clear than for other genital cancers
Nulliparity, family history, and heritable mutations play a role
Gonadal dysgenesis in children is associated with a higher risk of ovarian cancer
Use of OCs and having a tubal ligation reduce risk in ♀s 40-59 yo
Genetic factors such as mutations in BRCA1 and BRCA2 increase susceptibility

80
Q

Ovarian neoplasms symptoms

A

Most are nonfunctional and tend to produce relatively mild symptoms until they have reached a large size
The most common symptoms are abdominal pain and distention, urinary and GI symptoms due to compression by tumor or cancer invasion, and abdominal and vaginal bleeding
-Benign forms may be entirely asymptomatic or incidental findings

81
Q

Ovarian Neoplasms:Tumors of Mullerian Epithelium

A

Most primary neoplasms fall into this category
There are three major types of such tumors: serous, endometrioid, and mucinous
May be small and grossly imperceptible or may fill the pelvic or abdominal cavities
They may be cystic (cystadenomas), cystic and fibrous (cystadenofibromas), and predominantly fibrous (adenofibroma)

The risk of malignancy is directly proportional to the amount of solid growth

82
Q

Tumors of Mullerian Epithelium Serous tumors

A

The benign and borderline types are most common between the ages of 20 and 50, and cystadenocarcinomas occur later in life on average
Bilaterality is common
-Should always exclude possibility of non-ovarian origin (metastatic spread)
Concentric calcifications (psammoma bodies) are characteristic
Biologic behavior depends on degree of differentiation, distribution, and characteristics of any peritoneal implants
-Unencapsulated surface tumors more likely to spread to peritoneum

83
Q

Tumors of Mullerian Epithelium Mucinous tumors

A

Occur principally in middle life (rare before puberty and after menopause)
80% are benign and 20% malignant
characterized by more cysts of variable size and less surface involvement
frequently bilateral
Associated with a condition called pseudomyxoma peritonei
-Ovarian tumor with extensive mucinous ascites, cystic epithelial implants on the peritoneal surfaces, and adhesions
-May result in intestinal obstruction and death

84
Q

Tumors of Mullerian Epithelium Endometrioid tumors

A

Account for ~ 20% of all ovarian cancers
-usually in older women (50-70 yoa)
Most are carcinomas
15-30% are accompanied by a carcinoma of the endometrium and 15% coexist with endometriosis

85
Q

Tumors of Mullerian Epithelium

Clear Cell Carciooma

A

An uncommon pattern of tumors of müllerian epithelium
Sometimes occur in association with endometriosis or endometrioid carcinoma of the ovary
5year survival rate of ~65% when tumors are confined to the ovary

86
Q

Tumors of Mullerian Epithelium

Cystadenofibroma

A

Tumors in which there is more pronounced proliferation of fibrous stroma that underlies the columnar epithelium

87
Q

Tumors of Mullerian Epithelium

Brenner tumor

A

Uncommon adenofibromas in which the epithelial component consists of nest of transitional cells resembling those lining the urinary bladder
Most are benign, but borderline and malignant types have been reported

88
Q

Ovarian Neoplasms:Clinical Course

A

All ovarian epithelial carcinomas produce similar clinical manifestations
Most commonly lower abdominal pain and abdominal enlargement
GI complaints, urinary frequency, dysuria, pelvic pressure
Malignant forms tend to cause progressive weakness, weight loss and cachexia
If the peritoneal cavity becomes seeded, massive ascites is common

89
Q

Ovarian Neoplasms: Clinical Course 2

A

Since ovarian carcinomas often remain undiagnosed until they are large or originate on the ovarian surface from which they readily spread to the pelvis, many patients already have lesions no longer confined to the ovary

  • Probably the reason for such poor 5 and 10 year survival rates
  • A potential screening tool is the use of a biological marker CA-125
  • Present in > 80% of serous and endometrioid carcinomas
90
Q

Ovarian Neoplasms:Prevention

A

Fallopian tubal ligation and OC therapy are associated with significant reductions in risk
Long term OC use or uterine tube ligation in patients with familial history (BRCA) have a reduction in risk by ~1/2

91
Q

Germ Cell Tumors: Mature (Benign) Teratomas

A

Most are cystic and known as dermoid cysts
-Derived from ectodermal totipotent cells
Usually found in young women during the reproductive years
-Are bilateral in 10-15% of cases
Characteristically are unilocular cysts containing hair and cheesy sebaceous material
-Within the wall, it is common to find tooth structures and calcification
About 1% undergo malignant transformation of any one of the components
-squamous cell carcinoma most common
The karyotype of all benign teratomas is 46,XX

92
Q

Germ Cell Tumors: Monodermal or Specialized Teratomas

A

almost always unilateral
Most common are struma ovarii
-composed entirely of mature thyroid tissue that can hyerfunction and cause hyperthyroidism
carcinoid tumors may arise from teratomal intestinal tissue

93
Q

Granulosa-Theca Cell Tumor

A

produce large amounts of estrogen

  • bleeding
  • linked to endometrial hyperplasia, endometrial carcinoma, breast carcinoma
94
Q

Metastatic tumors to ovary

A

uncommon
may appear as a large mass and resemble a primary tumor: a so-called “Krukenberg” tumor of ovary
-signet ring histologic pattern = adenocarcinoma
-usually metastatic from a GI primary

95
Q

Fibrothecoma

A

A right-sided hydrothorax in association with this tumor is known as Meig’s syndrome.

96
Q

Ectopic Pregnancy

A

most common site = fallopian tubes (~90%)
also ovary, abdominal cavity, and the intrauterine portion of the fallopian tube (cornual pregnancy)
According to your text, the most important predisposing condition (35-50% of cases) is PIDw/chronic salpingitis
sudden onset of severe abdominal pain and vaginal bleeding ~6-7 wks after normal menstrual period
-the invading placenta causes intratubal hematoma (hematosalpinx) and/or intraperitoneal hemorrhage
-tube rupture leads to pelvic hemorrhage → shock
Clinical examinations are not diagnostic, and no combination of physical exam findings exclude ectopic pregnancy
-~30% have no vaginal bleeding
-only 10% have palpable adnexal mass

97
Q

Ectopic Pregnancy diagnostic

A

ultrasound
-test of choice
-transabdominal ultrasound: EP suspected if no intrauterine gestational sac and β-hCG >6500mIU/ml
-transvaginal ultrasound: EP suspected if no intrauterine gestational sac and β-hCG >1500mIU/ml
urine pregnancy test
β-hCG measurement (should rise throughout normal pregnancy)
diagnostic curettage (could terminate desired pregnancy)

98
Q

Placental Abnormalities

A

Unlike first trimester bleeding, second and third trimester bleeding is usually secondary to abnormal placental implantation.
-occurs (on average) at 27-32 weeks gestation

99
Q

Abruptio placentae

A

premature separation, either partial or total, of a normally implanted placenta after 20 weeks of gestation
should be considered when there is a sudden onset of pain, with or without vaginal bleeding

100
Q

Placenta previa

A

implantation of the placenta over or near the internal os of the cervix
unknown etiology, but thought to be multifactorial
-multiple gestations, advanced maternal age, previous cesarean delivery, previous abortion, and possibly, smoking

101
Q

Placenta accreta

A

partial or complete absence of the decidua with adherence of the placenta directly to the myometrium

102
Q

Preeclampsia

A

formerly known as “toxemia of pregnancy”, but not associated w/bloodborne toxin
preeclampsia is the development of hypertension and proteinuria after 20 weeks of gestation
-your text includes edema, but this is no longer a diagnostic criterion
-severe preeclampsia may include oliguria, cerebral or visual disturbances, pulmonary edema, or cyanosis

103
Q

eclampsia

A

eclampsia is the new onset of seizures in a woman with preeclampsia
-occurs in 48 hours after delivery

104
Q

Gestational Trophoblastic Disease

A

constitutes a spectrum of tumors and tumor-like conditions characterized by proliferation of pregnancy-associated trophoblastic tissue of progressive malignant potential
traditionally divided into 3 overlapping morphologic categories: hydatidiform mole, invasive mole, and choriocarcinoma
-range from benign (hydatidiform mole) to highly malignant (choriocarcinoma)
-all elaborate hCG, and detected in higher amounts than in normal pregnancies (titers positively correlated with malignant potential)

105
Q

Hydatidiform Mole

A

characterized by cystic swelling of the chorionic villi (“bunch of grapes”) with variable trophoblastic proliferation
most patients present with spontaneous pregnancy loss or undergo curettage due to abnormalities in ultrasound
traditionally discovered at 12-14 wks (gestation “too large for dates”) but found earlier by hCG detection (hCG levels far exceed that of pregnancy’s age)
most common 40 yoa; higher incidence in Asian countries

106
Q

Invasive Mole

A

a complete mole that penetrates and/or perforates the uterine wall
-invades myometrium → may cause rupture and cause life-threatening hemorrhage
*hysterectomy may be required
-may spread locally to broad ligament and vagina
may embolize to different sites (lungs, brain) but do not grow as true metastases
less likely to be completely removed by curettage, so monitoring of hCG levels important

107
Q

Choriocarcinoma

A

rapidly invasive, widely metastasizing malignant neoplasm that arises from gestational chorionic epithelium or (less frequently) totipotential cells in the gonads or elsewhere
may derive from any form of previously normal or abnormal pregnancy
-much more common in some African countries (e.g., Nigeria)
-most arise from complete hydatidiform moles (~50%)
*previous abortions (~25%)
*normal pregnancies (~22%)

108
Q

in contrast to the moles, choriocarcinoma…

A

in contrast to the moles, choriocarcinoma does not classically produce a large, bulky mass
-are a hemorrhagic, necrotic mass
produces a bloody, brown, sometimes foul-smelling discharge
-usually appears after miscarriage, curettage, or normal pregnancy
-may not appear until months after pregnancy
by the time the tumor is discovered locally, has already metastasized
-favored sites (descending order) = lungs, vagina, bone, brain, liver, kidney
despite aggressiveness, current chemotherapy regimens have resulted in 100% cure rate