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Pathoma: Female Genital System & Gestational Pathology Flashcards

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1
Q

General

Vulva

A
  • Anatomically includes skin & mucosa of female genitalia external to the hymen
    • Labia majora & minora
    • Mons pubis
    • Vestibule
  • Lined by squamous epithelium
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2
Q

Vulva

Cystic dilation of Bartholin gland

Pathophysiology

A

Bartholin cyst

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3
Q

Vulva

Bartholin glands

Anatomy

A
  • One present on each side of the vaginal canal
  • Produce mucus-like fluid that drain via ducts into lower vesibule
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4
Q

Vulva

Unilateral, painful cystic lesion at lower vestibule adjacent to vaginal canal

Clinical Presentation

A

Bartholin cyst

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5
Q

Vulva

Results from inflammation & obstruction of Bartholin gland

Etiology

A

Bartholin cyst

Inflammation associated w/ infections, STDs

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6
Q

Vulva

Usually seen in reproductive-aged women

Epidemiology

A

Bartholin cyst

Infections, STDs more common in this age group

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7
Q

Vulva

  • Warty neoplasm of vulvar skin
  • Often large
  • Rarely progress to carcinoma

Morphology

A

Condyloma

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8
Q

Vulva

Most common cause of condyloma

Etiology

A

Low-risk HPV types 6, 11

Condyloma acuminatum

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9
Q

Vulva

2nd most common cause of condyloma

Etiology

A

Syphilis

Condyloma latum

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10
Q

Vulva

Koilocytes

Histology

A

Condyloma acuminatum (HPV-associated condyloma)

Koilocyte = HPV hallmark; raisin-like nucleus w/ perinuclear halo

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11
Q

Vulva

A

Condyloma acuminatum

Microscopic appearance

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12
Q

Vulva

A

Condyloma acuminatum

Koilocytic change: raisin-like nucleus w/ perinuclear halo

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13
Q

Vulva

  • Thinning of epidermis & fibrosis of dermis
  • Benign; slightly increased risk of SCC

Pathophysiology

A

Lichen sclerosis

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14
Q

Vulva

Leukoplakia (white patch) w/ parchment-like vulvar skin

Clinical Presentation

A

Lichen sclerosis

Parchment-like = paper-thin

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15
Q

Vulva

Most commonly seen in post-menopausal women

Epidemiology

A

Lichen sclerosis

Post-menopause: atrophy of epithelium & fibrosis of dermis

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16
Q

Vulva

  • Hyperplasia of vulvar squamous epithelium
  • Benign; no increased risk of SCC

Pathophysiology

A

Lichen simplex chronicus

Hyperplasia due to chronic irritation & scratching of skin

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17
Q

Vulva

Leukoplakia with thick, leathery vulvar skin

Clinical Presentation

A

Lichen simplex chronicus

Thick & leathery due to hyperplasia

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18
Q

Vulva

Associated with chronic irritation & scratching

Etiology

A

Lichen simplex chronicus

Chronic irritation & scratching results in hyperplasia

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19
Q

Vulva

Carcinoma of vulvar squamous epithelium

Histology

A

Vulvar carcinoma

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20
Q

Vulva

  • Presents as leukoplakia
  • Biopsy may be required to distinguish from other causes of leukoplakia

Diagnosis

A

Vulvar carcinoma

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21
Q

Vulva

  • Rare; makes up small % of female genital cancers
  • May be HPV or non-HPV related

Etiology

A

Vulvar carcinoma

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22
Q

Vulva

Cause of HPV-related vulvar carcinoma

Etiology

A

High-risk HPV types 16, 18

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23
Q

Vulva

  • Risk factors are related to HPV exposure
    • Multiple sexual partner
    • Early first age of intercourse
  • Exposure generally occurs at reproductive age
    • Carcinoma typically seen at age 40-50 yrs

Epidemiology

A

HPV-related vulvar carcinoma

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24
Q

Vulva

Arises from VIN precursor lesion

Pathophysiology

A

HPV-related vulvar carcinoma

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25
# Vulva Dysplastic precursor lesion characterized by koilocytic change, disordered cellular maturation, nuclear atypia, and increased mitotic activity | Histology
Vulvar intraepithelial neoplasia (VIN)
26
# Vulva Most common cause of non-HPV related vulvar carcinoma | Etiology
Long-standing lichen sclerosis
27
# Vulva Chronic inflammation & irritation eventually lead to carcinoma | Pathophysiology
Non-HPV related vulvar carcinoma
28
# Vulva Generally seen in elderly women (average age >70 years) | Epidemiology
Non-HPV related vulvar carcinoma
29
# Vulva * Characterized by malignant epithelial cells in epidermis of vulva * Represents CIS; usually no underlying carcinoma | Histopathology
Extramammary Paget disease of the vulva
30
# Vulva Erythematous, pruritic, ulcerated vulvar skin | Clinical Presentation
Extramammary Paget disease of the vulva | Can also occur in nipple
31
# Vulva Must be distinguished from melanoma, which can occasionally occur in the vulva * Paget cells: PAS-pos, keratin-pos, S100-neg * Melanoma: PAS-neg, keratin-neg, S100-pos | Diagnosis
Extramammary Paget disease of the vulva * Keratin-pos = epithelial cell --> carcinoma * PAS-pos = epithelial cell --> carcinoma * S100- = not melanoma | Keratin: intermediate filament in epithelial cells; PAS stains for mucus
32
# Vulva
Extramammary Paget disease of the vulva | Microscopic Appearance
33
# General Vagina
* Fibromuscular canal leading to cervix * Mucosa is lined by non-keratinizing squamous epithelium
34
# Vagina Focal persistence of columnar epithelium in upper vagina | Pathophysiology
Vaginal adenosis * During development, stratified squamous epithelium from lower 1/3 of vagina (derived from urogenital sinus) should grow upward to replace the columar epithelium lining the upper 2/3 of the vagina (derived from Mullerian duct)
35
# Vagina Increased incidence in females exposed to diethylstilbestrol (DES) in utero | Etiology
Vaginal adenosis | DES: used to prevent pregnancy-related complications; can cross placenta
36
# Vagina
Vaginal adenosis | Microscopic Appearance
37
# Vagina Malignant proliferation of glands with clear cytoplasm | Pathophysiology
Clear cell adenocarcinoma
38
# Vagina Rare, but severe complication of DES-associated vaginal adenosis | Etiology
Clear cell adenocarcinoma
39
# Vagina Malignant mesenchymal proliferation of immature skeletal muscle | Pathophysiology
Embryonal rhabdomyosarcoma
40
# Vagina Bleeding & a grape-like mass protruding from vagina / penis of a child (usually <5 yrs of age) | Clinical Presentation
Embryonal rhabdomyosarcoma | Also called sarcoma botryoides = "grape-like mass"
41
# Vagina Characteristic cell: rhabdomyoblast * Cytoplasmic cross-striations * Positive IHC staining for desmin & myogenin | Histology
Embryonal rhabdomyosarcoma | Cross-strations resemble skeletal muscle
42
# Vagina
Embryonal rhabdomyosarcoma: grape-like masses | Gross Appearance
43
# Vagina Carcinoma of vaginal squamous epithelium | Histology
Vaginal carcinoma
44
# Vagina Usually related to high-risk HPV (16, 18) | Etiology
Vaginal carcinoma
45
# Vagina * Arises from VAIN precursor lesion * Spread to regional lymph nodes: * Cancer from lower 1/3 --> inguinal lymph nodes * Cancer from upper 2/3 --> iliac lymph nodes | Pathophysiology
Vaginal carcinoma
46
# General Cervix
* Anatomically comprises "neck" of uterus * Divided into ectocervix & endocervix * Ectocervix: visible on vaginal exam; stratified squamous epithelium, non-keratinizing * Endocervix: lined by single layer of columnar epithelial cells * Transformation zone = junction between ectocervix & endocervix; lined by immature squamous epithelial cells * Susceptible to infections (i.e., HPV)
47
# Cervix
Cervical transformation zone, normal | Clearly demarcated stratified squamous epithelium & columnar epithelium
48
# Cervix HPV infection | Pathophysiology
* Sexually transmitted DNA virus that infects lower genital tract (especially transformation zone) * Infection is usually cleared by acute inflammation * Approx. 90% of HPV infections are cleared * Persistent infection increases risk of CIN * Risk of CIN depends on HPV genotype: * Low-risk HPV: types 6, 11 * High-risk HPV: types 16, 18 * High-risk HPV types produce E6 & E7 proteins * E6 --> increases destruction of p53 * E7 --> increases destruction of Rb * Loss of TSGs increases risk for CIN
49
# Cervix * Characterized by koilocytic change, disordered cellular maturation, nuclear atypia, and increased mitotic activity within the cervical epithelium * Grading is based on the extent of epithelial involvement by immature dysplastic cells | Histology
Cervical intraepithelial neoplasia (CIN)
50
# Cervix Dysplasia involving < 1/3 of the thickness of epithelium | Histology
CIN 1
51
# Cervix Dysplasia involving < 2/3 of the thickness of epithelium | Histology
CIN 2
52
# Cervix Dysplasia involving almost entire thickness of epithelium | Histology
CIN 3
53
# Cervix Dysplasia involving entire thickess of epithelium | Histology
Cervical carcinoma in situ (CIS)
54
# Cervix
CIN 3 / CIS | Dysplasia of almost entire thickness / Dysplasia of entire thickness
55
# Cervix Progression of CIN | Natural History & Complications
Classic stepwise progression through CIN 1, CIN 2, CIN 3 and CIS to become invasive SCC * CIN progression to carcinoma takes 10-20 yrs * Progression not inevitable --> CIN 1 often regresses * Higher grade of dysplasia: * More likely to progress to carcinoma * Less likely to regress to normal
56
# Cervix Invasive carcinoma of cervical epithelium | Histology
Cervical carcinoma | Invasive = penetrates basement membrane; distinguishes from CIS
57
# Cervix Most commonly seen in middle-aged women (average age = 40-50 yrs) | Epidemiology
Cervical carcinoma | HPV infection occurs earlier (age 20-25 years)
58
# Cervix * Vaginal bleeding, esp. postcoital * Cervical discharge | Clinical Presentation
Cervical carcinoma
59
# Cervix Key risk factor: high-risk HPV infection | Epidemiology
Cervical carcinoma
60
# Cervix Secondary risk factors: smoking, immunodeficiency (cervical carcinoma = AIDS-defining illness) | Epidemiology
Cervical carcinoma | Immunodeficiency --> impaired clearance of HPV infection
61
# Cervix Common subtypes of cervical carcinoma | Epidemiology
1. SCC = 80% of cases 2. Adenocarcinoma = 15% of cases | Both subtypes are related to HPV infection
62
# Cervix Consequences of cervical carcinoma | Natural History & Complications
* Tumors tend to grow locally & do not metastasize until very late in diease course * Cervical cancers tend to produce local symptoms * Advanced tumors often invade through anterior uterine wall into bladder, resulting in obstruction of ureters * Hydronephrosis with postrenal failure is a common cause of death in advanced cervical carcinoma
63
# Cervix Cervical carcinoma screening | Prevention
* Goal is to identify CIN before progression to carcinoma * Begins at age 21; performed every 3 yrs * Gold standard = Pap smear * Most successful cancer screening test ever
64
# Cervix Pap smear | Prevention
* Cells are scraped from transformation zone & analyzed under microscope * Dysplastic cells are classified as low grade (CIN 1) or high grade (CIN 2/3) * High grade dysplasia is characterized by: * Hyperchromatic (dark) nuclei * High N:C ratios * Abnormal Pap smear is followed by confirmatory colposcopy & biopsy * Limitations: * Inadequate sampling of transformation zone (false negative screening) * Limited efficacy in screening for adenocarcinoma | Colposcopy = visualization of cervix w/ magnifying glass
65
# Cervix
High-grade dysplasia, Pap smear | Hyperchromatic nuclei & high N:C ratios
66
# Cervix HPV vaccine | Prevention
Immunization is effective in preventing HPV infection * Quadrivalent vaccine covers HPV 6, 11, 16, 18 * Abs against HPV 6, 11 prevent condylomas * Abs against HPV 16, 18 prevent CIN & carcinoma * Pap smears still necessary due to limited number of HPV types covered by vaccine
67
# General Endometrium & Myometrium
* Endometrium = mucosal lining of uterine cavity * Myometrium = smooth muscle wall underlying endometrium * Endometrium is hormonally sensitive * Proliferative phase: endometrial growth driven by estrogen * Secretory phase: endometrial preparation for implantation driven by progesterone * Menstrual phase: shedding occurs with loss of progesterone support
68
# Endometrium Secondary amenorrhea (absence of menstruation) due to loss of basalis (regenerative layer of endometrium) & scarring | Pathophysiology
Asherman syndrome | Loss of basalis impairs regeneration & shedding of endometrium
69
# Endometrium Result of overaggressive dilation and curettage (D&C) | Etiology
Asherman syndrome | Curettage = scraping away of uterine wall; basalis can be scraped off
70
# Endometrium * Lack of ovulation * Results in estrogen-driven proliferative phase without a subsequent progesterone-driven secretory phase * Proliferative glands break down & shed resulting in uterine bleeding * Common cause of dysfunctional uterine bleeding * Especially during menarche & menopause | Pathophysiology
Anovulatory cycle
71
# Endometrium Bacterial infection of endometrium | Pathophysiology
Acute endometritis
72
# Endometrium Major cause of acute endometritis | Etiology
Retained products of conception (e.g., after delivery) * Retained products act as nidus for infection
73
# Endometrium * Fever * Abnormal uterine bleeding * Pelvic pain | Clinical Presentation
Acute endometritis
74
# Endometrium Chronic endometrial inflammation | Pathophysiology
Chronic endometritis
75
# Endometrium Characterized by presence of lymphocytes, plasma cells | Histology
Chronic endometritis | Lymphocytes normally in endometrium; plasma cells necessary for Dx
76
# Endometrium * Retained products of conception * Chronic pelvic inflammatory disease (e.g., Chlamydia) * IUD * TB | Etiology
Chronic endometritis
77
# Endometrium * Abnormal uterine bleeding * Pelvic pain * Infertility | Clinical Presentation
Chronic endometritis
78
# Endometrium Hyperplastic protrusion of endometrium | Histopathology
Endometrial polyp
79
# Endometrium Abnormal uterine bleeding | Clinical Presentation
Endometrial polyp
80
# Endometrium Can arise as side effect of tamoxifen * Anti-estrogen effects on breast * Weak pro-estrogen effects on endometrium | Etiology
Endometrial polyp
81
# Endometrium
Endometrial polyp | Hyperplastic protrusion of endometrium w/ lymphocytes & plasma cells
82
# Endometrium Endometrial glands & stroma outside of uterine endometrial lining | Histology
Endometriosis
83
# Endometrium Most likely cause of endometriosis | Etiology
Retrograde menstruation with implanatation at an ectopic site
84
# Endometrium * Dysmenorrhea (pain during menstruation) * Pelvic pain * Infertility (possibly) | Clinical Presentation
Endometriosis | Endometriosis cycles just like normal endometrium
85
# Endometrium * Most common involved site: ovary * Results in classic chocolate cyst * Other sites of involvement: * Uterine ligaments (pelvic pain) * Pouch of Douglas (pain with defecation) * Bladder wall (pain with urination) * Bowel serosa (abdominal pain & adhesions) * Fallopian tube mucosa (scarring increases risk for ectopic tubal pregnancy) * Uterine myometrium involvement = adenomyosis | Pathophysiology
Endometriosis
86
# Endometrium Implants classically appear as yellow-brown "gunpowder" nodules | Gross Appearance
Endometriosis
87
# Endometrium Complications of endometriosis | Natural History & Complications
Increased risk of carcinoma at site of endometriosis, especially in ovary
88
# Endometrium
Endometriosis, "chocolate" cyst of ovary | Ovary with cystic lesion containing menstrual products
89
# Endometrium
Endometriosis | Yellow-brown "gunpowder" nodules; involvement of soft tissues
90
# Endometrium Hyperplasia of endometrial glands relative to stroma | Pathophysiology
Endometrial hyperplasia
91
# Endometrium * Consequence of unopposed estrogen * Obesity * Polycystic ovarian syndrome (PCOS) * Estrogen replacement therapy (ERT) * Results in continuous proliferative phase with no subsequent secretory or menstrual phase | Etiology
Endometrial hyperplasia | Unopposed proliferation results in hyperplasia
92
# Endometrium Post-menopausal uterine bleeding | Clinical Presentation
Endometrial hyperplasia
93
# Endometrium Classified based on architectural growth pattern (simple or complex) & presence / absence of cellular atypia | Histology
Endometrial hyperplasia
94
# Endometrium Most important predictor for progression to carcinoma is cellular atypia * Simple hyperplasia w/ atypia often progresses to cancer * Complex hyperplasia w/o atypiaa rarely progresses | Natural History & Complications
Endometrial hyperplasia
95
# Endometrium
Endometrial hyperplasia | Crowded endometrial glands; high ratio of endometrial glands to stroma
96
# Endometrium Malignant proliferation of endometrial glands | Histology
Endometrial carcinoma
97
# Endometrium Most common invasive carcinoma of female genital tract | Epidemiology
Endometrial carcinoma
98
# Endometrium Post-menopausal bleeding | Clinical Presentation
Endometrial carcinoma
99
# Endometrium Arises via 2 distinct pathways: 1. Hyperplastic 2. Sporadic | Pathophysiology
Endometrial carcinoma
100
# Endometrium Endometrial carcinoma, hyperplastic pathway | Pathophysiology
* Most common: 75% of cases * Age at presentation: 60 years * Carcinoma arises from endometrial hyperplasia
101
# Endometrium Endometrial carcinoma, sporadic pathway | Pathophysiology
* Less common: 25% of cases * Age at presentation: 70 years * Carcinoma arises in atrophic endometrium with no evident precursor lesion
102
# Endometrium Risk factors are related to estrogen exposure: * Early menarche / late menopause * Nulliparity * Infertility with anovulatory cycles * Obesity | Epidemiology
Endometrial carcinoma, hyperplastic
103
# Endometrium Endometrioid type | Histology
Endometrial carcinoma, hyperplastic
104
# Endometrium * Serous type * Characterized by papillary structures with psammoma body (PB) formation * p53 mutation is common * Tumor exhibits aggressive behavior | Histology
Endometrial carcinoma, sporadic | Necrosis of papillae allows for calcification & PB formation
105
# Endometrium
Endometrial carcinoma | Growth = carcinoma; normal endometrium is smooth & shiny
106
# Endometrium
Endometrial carcinoma, endometrioid type | Normal endometrium-like but disorganized & overlapping, minimal stroma
107
# Endometrium
Endometrial carcinoma, serous type | Papillary architecture, FV cores; necrosis of papillae & PB formation
108
# Myometrium Benign neoplastic proliferation of smooth muscle arising from myometrium | Histology
Leiomyoma (fibroids)
109
# Myometrium Most common tumor in females | Epidemiology
Leiomyoma (fibrioids)
110
# Myometrium Related to estrogen exposure * Common in premenopausal women * Often multiple tumors * Enlarge during pregnancy & shrink after menopause | Etiology
Leiomyoma (fibroids)
111
# Myometrium Multiple, well-defined, white, whorled masses that may distort uterus & impinge upon pelvic structures | Gross Appearance
Leiomyoma (fibroids)
112
# Myometrium * Usually asymptomatic * When present, symptoms include: * Abnormal uterine bleeding * Infertility * Pelvic mass | Clinical Presentation
Leiomyoma (fibroids)
113
# Myometrium
Uterine leiomyoma (fibroids) | Multiple, well-defined, white, whorled masses
114
# Myometrium Malignant prolfieration of smooth muscle arising from the myometrium | Histology
Leiomyosarcoma
115
# Myometrium Arise de novo | Pathophysiology
Leiomyosarcoma | Leiomyosarcomas do not arise from leiomyomas
116
# Myometrium Usually seen in post-menopausal women | Epidemiology
Leiomyosarcoma
117
# Myometrium Individual lesion with areas of necrosis & hemorrhage | Gross Apperance
Leiomyosarcoma
118
# Myometrium * Central necrosis * Mitotic activity * Cellular atypia | Histology
Leiomyosarcoma
119
Leiomyoma vs. Leiomyosarcoma
* Leiomyoma (benign) * Multiple masses * Well-defined, white, whorled masses * Premenopausal women --> driven by estrogen * Leiomyosarcoma (malignant) * Single masses * Necrosis & hemorrhage at center of mass * Post-menopausal women
120
# General Ovary
* Functional unit of ovary is the follicle * A follicle consists of an oocyte surrounded by granulosa & theca cells * LH stimulates theca cells --> induces androgen production * FSH stimulates granulosa cells --> conversion of androgen to estradiol * Drives proliferative phase of endometrial cycle * Estradiol surge induces LH surge --> leads to ovulation * Marks beginning of secretory phase * After ovulation the residual follicle becomes a corpus luteum, which primarily secretes progesterone * Drives secretory phase which prepares endometrium for possible pregnancy * Hemorrhage into corpus luteum can result in hemorrhagic corpus luteal cyst, esp. in early pregancy * Degeneration of follicles results in follicular cysts * Small numbers of follicular cysts are common in women and have no clinical significance
121
# Ovary
Ovarian follicle, normal | Oocye = pink middle; Granulosa = purple cells inside; Theca = outside
122
# Ovary
Corpus luteum | Ovary = bottom right, white; Corpus luteum = top left, yellow
123
# Ovary Multiple ovarian follicular cysts due to hormone imbalance | Histology
Polycystic ovarian disease (PCOD)
124
# Ovary Affects 5% of reproductive-aged women | Epidemiology
Polycystic ovarian disease (PCOD)
125
# Ovary Characterized by increased LH & low FSF (LH:FSH > 2) * Increased LH induces excess androgen production from theca cells --> hirsutism * Androgen is converted back to estrone in adipocytes * Estrone feedback decreases FSH --> cystic degeneration of follicles * High levels of circulating estrone increase risk for endometrial cancer | Pathophysiology
Polycystic ovarian disease (PCOD)
126
# Ovary Classic presentation: obese young woman with infertility, oligomenorrhea, and hirsutism * Some patients have insulin resistance & may develop type 2 diabetes mellitus 10-15 years later | Clinical presentation
Polycystic ovarian disease (PCOD)
127
# General Ovarian tumors
* Ovary is composed of three cell types: * Surface epithelium * Germ cells * Sex cord stroma * Tumor can arise from any of these cell types or from metastases
128
# Ovarian Tumors Most common type of ovarian tumor | Epidemiology
Surface epithelial tumor | 70% of cases
129
# Ovarian Tumors * Derived from coelomic epithelium that lines ovary * Coelomic epithelium embryologically produces epithelial lining of: * Fallopian tubes (serous cells) * Endometrium * Endocervix (mucinous cells) | Histology
Surface epithelial tumors
130
# Ovarian Tumors Common subtypes of surface epithelial tumors | Epidemiology
* 2 most common subtypes of surface epithelial tumors: * Serous tumors: full of watery fluid * Mucinous tumors: full of mucus-like fluid * Both subtypes are usually cystic * Both types can be benign, borderline, or malignant * Borderline tumors have features in between benign & malignant tumors
131
# Ovarian Tumors Tumor composed of a single cyst w/ a simple, flat lining | Histopathology
Cystadenomas | Surface epithelial tumors, benign
132
# Ovarian Tumors Most common in premenopausal women (ages 30-40) | Epidemiology
Cystadenomas | Surface epithelial tumors, benign
133
# Ovarian Tumors * Tumors composed of complex cysts with a thick, shaggy lining * Defining feature: invasion of cells into connective tissue of cyst wall | Histopathology
Cystadenocarcinomas | Surface epithelial tumors, malignant
134
# Ovarian Tumors Most commonly arise in post-menopausal women (ages 60-70) | Epidemiology
Cystadenocarcinomas | Surface epithelial tumors, malignant
135
# Ovarian Tumors Increased risk for serous ovarian & fallopian tube carcinoma | Etiology
*BRCA1* mutation carriers * *BRCA1* carriers often undergo prophylactic salpingo-oopherectomy
136
# Ovarian Tumors Less common subtypes of surface epithelial tumors | Epidemiology
1. Endometrioid tumors 2. Brenner tumors
137
# Ovarian Tumors * Composed of endometrial-like glands * Typically malignant * May arise from endometriosis * A/w endometrial carcinoma, endometrioid type (15% of cases) | Histopathology
Endometrioid carcinoma
138
# Ovarian Tumors * Composed of bladder-like epithelium * Usually benign | Histopathology
Brenner tumor
139
# Ovarian Tumors * Clinically present late --> poor prognosis * Vague abdominal symptoms: pain, fullness * Signs of compression: urinary frequency * Epithelial carcinomas tend to spread locally, especially to peritoneum | Clinical Features
Surface epithelial tumors
140
# Ovarian Tumors
Cystadenoma | Benign surface epithelial tumor; can be serous or mucinous
141
# Ovarian Tumors Serum marker used to monitor treatment response & screen for recurrence of surface epithelial carcinoma | Approach to Therapy
CA-125
142
# Ovarian Tumors * 2nd most common type of ovarian tumor * Typically occur in women of reproductive age | Epidemiology
Germ cell tumors | 15% of cases
143
# Ovarian Tumors Subtypes of germ cell tumors | Histopathology
Germ cell tumor subtypes mimic tissues normally produced by germ cells 1. Fetal tissue --> cystic teratoma; embryonal carcinoma 2. Oocytes --> dysgerminoma 3. Yolk sac --> endodermal sinus tumor 4. Placental tissue --> choriocarcinoma
144
# Ovarian Tumors * Cystic tumor composed of fetal tissue derived from 2-3 embryologic layers * Embryologic layers: skin, hair, bone, cartilage, gut, thyroid, etc. * Benign tumor composed of mature tissue * Presence of immature tissue (usually neural) or somatic malignancy (usually SCC of skin) indicates malignant potential | Histopathology
Cystic teratoma
145
# Ovarian Tumors * Most common germ cell tumor in females * Bilateral in 10% of cases | Epidemiology
Cystic teratoma
146
# Ovarian Tumors Cystic teratoma composed primarily of thryoid tissue * Can result in hyperthyroidism | Histopathology
Struma ovarii
147
# Ovarian Tumors Rule out malignant potential | Approach to Diagnosis
* Teratomas are benign * Need to confirm that the tumor is benign * Presence of immature tissue = immature teratoma * Can spread outside region --> malignant potential * Most common: neural ectoderm * Presence of cancerous tissue within teratoma * Somatic malignancy --> malignant potential * Most common: SCC of skin
148
# Ovarian Tumors
Cystic teratoma | Cystic tumor with hair, teeth / bone, skin
149
# Ovarian Tumors Mass composed of large cells with clear cytoplasm & central nuclei * Tumor cells resemble oocytes * Testicular counterpart = seminoma | Histopathology
Dysgerminoma | "Dys-" = bad (malignant); "-germ-" = germ cells; "-oma" = mass
150
# Ovarian Tumors Most common malignant germ cell tumor | Epidemiology
Dysgerminoma
151
# Ovarian Tumors Serum LDH may be elevated | Approach to Diagnosis
Dysgerminoma
152
# Ovarian Tumors * Responds to radiotherapy * Good prognosis | Approach to Therapy
Dysgerminoma
153
# Ovarian Tumors
Dysgerminoma | Nests composed of round cells
154
# Ovarian Tumors Malignant tumor that mimics yolk sac | Histopathology
Endodermal sinus tumor
155
# Ovarian Tumors Most common germ cell tumor in children | Epidemiology
Endodermal sinus tumor
156
# Ovarian Tumors * Serum AFP is often elevated * Histology: Schiller-Duval bodies | Approach to Diagnosis
Endodermal sinus tumor | AFP = alpha fetoprotein; Schiller-Duval bodies = glomeruloid structures
157
# Ovarian Tumors
Endodermal sinus tumor | Schiller-Duval body = hallmark histological finding
158
# Ovarian Tumors * Malignant tumor composed of cytotrophoblasts & syncytiotrophoblasts * Mimics placental tissue, but villi are absent * Small, hemorrhagic tumor with early hematogenous spread * Tumor is derived from trophoblasts * Trophoblasts are genetically programmed to find & invade blood vessels | Histopathology
Choriocarcinoma
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# Ovarian Tumors High B-hCG * Produced by syncytiotrophoblasts * May lead to thecal cysts in ovary | Approach to Diagnosis
Choriocarcinoma | Characteristic lab finding
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# Ovarian Tumors Poor response to chemotherapy | Approach to Treatment
Choriocarcinoma, germ cell tumor variant
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# Ovarian Tumors * Malignant tumor composed of large primitive cells * Aggressive with early metastasis * Primitive cells are designed to move & spread | Histopathology
Embryonal carcinoma
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# Ovarian Tumors Tumors resemble ovarian sex cord-stromal tissues | Histopathology
Sex cord-stromal tumors
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# Ovarian Tumors * Neoplastic proliferation of granulosa & theca cells * Malignant, but minimal risk for metastasis | Histopathology
Granulosa-theca cell tumor
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# Ovarian Tumors Tumor is often estrogen-producing | Pathophysiology
Granulosa-theca cell tumor
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# Ovarian Tumors Presents with signs of estrogen excess; varies with age * Prior to puberty: precocious puberty * Reproductive age: menorrhagia or metorrhagia * Menorrhagia = abnormally heavy flow * Metorrhagia = uterine bleeding independent of menstruation * Post-menopause: endometrial hyperplasia with post-menopausal bleeding
Granulosa-theca cell tumor
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# Ovarian Tumors Most common setting for granulosa-theca cell tumors | Epidemiology
Post-menopause
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# Ovarian Tumors Tumor composed of Sertoli cells & Leydig cells * Sertoli cells --> form tubules * Leydig cells --> between tubules | Histopathology
Sertoli-Leydig cell tumor
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# Ovarian Tumors Tumor may be androgen-producing | Pathophysiology
Sertoli-Leydig cell tumor
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# Ovarian Tumors * Hirsutism * Virilization | Clinical Presentation
Sertoli-Leydig cell tumor
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# Ovarian Tumors Reinke crystals | Histology
Sertoli-Leydig cell tumor | Reinke crystals = hallmark histological finding
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# Ovarian Tumors Reinke crystals | Histology
Sertoli-Leydig cell tumor | Reinke crystals = hallmark histological finding
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# Ovarian Tumors Benign fibroblast tumor | Histopathology
Fibroma
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# Ovarian Tumors Meigs syndrome * Pleural effusions * Ascites | Clinical Presentation
Fibroma
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# Ovarian Tumors Syndrome resolves with removal of tumor | Approach to Therapy
Fibroma
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# Ovarian Tumors
Ovarian fibroma | Solid tumor; white bands going through it represent fibrosis
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# Ovarian Tumors Metastatic mucinous tumor involving both ovaries | Histopathology
Krukenberg tumor
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# Ovarian Tumors Most common cause of Krukenberg tumor | Etiology
Metastatic gastric carcinoma, diffuse type
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# Ovarian Tumors Bilateral ovary involvement | Distinctive Clinical Manifestations
Bilaterality helps distinguish metastases from primary ovarian mucinous carcinoma (usually unilateral)
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# Ovarian Tumor Massive amount of mucus in peritoneum | Pathology
Pseudomyxoma peritonei
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# Ovarian Tumors Cause of pseudomyxoma peritonei | Etiology
Primary mucinous tumor of the appendix, usually with metastasis to ovary
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# Gestational Pathology Implantation of fertilized ovum at site other than uterine wall * Most common site: lumen of fallopian tube | Pathophysiology
Ectopic pregnancy
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# Gestational Pathology Key risk factor for ectopic pregnancy | Epidemiology
Scarring * Secondary to pelvic inflammatory disease * Secondary to endometriosis
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# Gestational Pathology
Ectopic tubal pregnany | Hemorrhage at rupture site of fallopian tube
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# Gestational Pathology Lower quadrant abdominal pain a few weeks after missed period | Clinical Presentation
Ectopic pregnancy
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# Gestational Pathology Treatment of ectopic pregnancy | Approach to Therapy
Surgical emergency
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# Gestational Pathology Major complications of ectopic pregnancy | Natural History & Complications
* Hematosalpinx (bleeding into fallopian tube) * Rupture of fallopian tube
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# Gestational Pathology Miscarriage of fetus occurring before 20 wks gestation * Usually occurs during 1st trimester * Common; occurs in up to 1/4 of recognizable pregnancies | Pathophysiology
Spontaneous abortion
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# Gestational Pathology * Vaginal bleeding * Cramp-like pain * Passage of fetal tissues | Clinical Presentation
Spontaneous abortion
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# Gestational Pathology Most common cause of spontaneous abortion | Etiology
Chromosomal abnormalities * Especially trisomy 21
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# Gestational Pathology Other causes of spontaneous abortion | Etiology
* Hypercoagulable states (e.g., antiphospholipid syndrome) * Congenital infection * Exposure to teratogens * Esp. in first 2 weeks of embryogenesis * Effect depends on dose, agent, and time of exposure | Etiology
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# Gestational Pathology Effects of teratogens on embryogenesis by weeks gestation at time of exposure | Pathophysiology
* First 2 weeks: spontaneous abortion * Weeks 3-8: risk of organ malformation * Weeks 3-9: risk of organ hypoplasia
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# Gestational Pathology Effects of alcohol on embryogenesis | Pathophysiology
* Most common cause of mental retardation * Facial abnormalities * Microcephaly
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# Gestational Pathology Effects of cocaine on embryogenesis | Pathophysiology
* IUGR * Placental abruption
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# Gestational Pathology Effects of thalidomide on embryogenesis | Pathophysiology
Limb defects
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# Gestational Pathology Effects of cigarette smoke on embryogenesis | Pathophysiology
IUGR
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# Gestational Pathology Effects of tetracycline on embryogenesis | Pathophysiology
Discolored teeth
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# Gestational Pathology Effects of tetracycline on embryogenesis | Pathophysiology
Discolored teeth
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# Gestational Pathology Effects of warfarin on embryogenesis | Pathophysiology
Fetal bleeding
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# Gestational Pathology Effects of phenytoin on embryogenesis | Pathophysiology
* Digit hypoplasia * Cleft lip / palate
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# Gestational Pathology Implantation of placenta in lower uterine segment, overlying cervical os (opening) | Pathophysiology
Placenta previa
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# Gestational Pathology Presents as third-trimester bleeding | Clinical Presentation
Placenta previa
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# Gestational Pathology Treatment of placenta previa | Approach to Therapy
Often requires delivery of fetus by caesarian section
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# Gestational Pathology Separation of placenta from decidua prior to delivery of fetus | Pathophysiology
Placental abruption
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# Gestational Pathology Common cause of stillbirth | Natural History & Complications
Placental abruption
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# Gestational Pathology Presents with third-trimester bleeding & fetal insufficiency | Clinical Presentation
Placental abruption
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# Gestational Pathology
Placental abruption | Blood on surface that was in contact with decidua (maternal surface)
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# Gestational Pathology Improper implantation of placenta into myometrium with little or no decidua | Pathophysiology
Placenta accreta | Absence of decidua results in implantation of placenta into myometrium
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# Gestational Pathology Presents with difficult delivery of placenta & postpartum bleeding | Clinical Presentation
Placenta accreta | Placenta gets stuck as it is implanted in myometrium
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# Gestational Pathology Treatment of placenta accreta | Approach to Therapy
Often requires hysterectomy
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# Gestational Pathology Pregnancy-induced HTN, proteinuria, and edema * Typically arises in 3rd trimester * HTN can be severe --> headaches, visual changes | Pathophysiology
Preeclampsia
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# Gestational Pathology Cause of preeclampsia | Etiology
Abnormal maternal-fetal vascular interface in placenta
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# Gestational Pathology Eclampsia | Clinical Presentation
Preeclampsia + seizures
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# Gestational Pathology Treatment of preeclampsia
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# Gestational Pathology **HELLP** | Clinical Presentation
Preeclampsia + thrombotic microangiopathy involving the liver * **H**emolysis * **E**levated **L**iver enzymes * **L**ow **P**latelets
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# Gestational Pathology Treatment of preeclampsia | Approach to Therapy
* Normal preeclampsia resolves with delivery * Eclampsia & HELLP warrant immediate delivery
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# Gestational Pathology Prevalence of preeclampsia | Epidemiology
Approx. 5% of pregnancies
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# Gestational Pathology Fibrinoid necrosis in vessels of placenta | Approach to Diagnosis
Preeclampsia | Classical finding resulting from very high blood pressure
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# Gestational Pathology * Death of a healthy infant (1 month - 1 year old) without oviuous cause * Infants usually expire during sleep | Pathophysiology
Sudden infant death syndrome (SIDS)
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# Gestational Pathology SIDS risk factors | Epidemiology
* Sleeping on stomach * Exposure to cigarette smoke * Premature birth
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# Gestational Pathology * Abnormal conception characterized by swollen & edematous villi with proliferation of trophoblasts * Uterus expands as if a normal pregnancy is present, but uterus is much larger and B-hCG much larger than expected for date of gestation | Pathophysiology
Hydatidiform mole
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# Gestational Pathology Classically presents in 2nd trimester as passage of grape-like masses through vaginal canal | Clinical Presentation
Hydatidiform mole | Grape-like masses = large, edematous villi
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# Gestational Pathology Diagnosing hydatidiform mole | Approach to Diagnosis
With prenatal care, moles are diagnosed by routine ultrasound in early 1st trimester * Fetal heart sounds are absent * "Snowstorm" appearance | "Snowstorm" appearance = classic radiologic finding
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# Gestational Pathology Classes of hydatidiform mole | Histology
1. Complete mole 2. Partial mole
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# Gestational Pathology Partial mole | Histology
* Genetics: normal ovum fertilized by 2 sperm / 1 sperm w/ 2x chromosomes; 69 chromosomes * Fetal tissue: present * Villous edema: some hydropic villi, some normal * Trophoblastic proliferation: focal proliferation around hydropic villi * Risk for choriocarcinoma: minimal
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# Gestational Pathology Complete mole | Histology
* Genetics: empty ovum fertilized by 2 sperm / 1 sperm w/ 2x chromosomes; 46 chromosomes * Fetal tissue: absent * Villous edema: most villi are hydropic * Trophoblastic proliferation: diffuse, circumferential proliferation around hydropic villi * Risk for choriocarcinoma: 2-3%
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# Gestational Pathology Treatment of hydatidiform mole | Approach to Therapy
Suction curettage * Subsequent B-hCG monitoring to ensure adequate mole removal & screen for choriocarcinoma
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# Gestational Pathology
Complete hydatidiform mole | Swollen, grape-like villi
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# Gestational Pathology
Complete hydatidiform mole | Hydropic villi = dilated; trophoblast proliferation = purple, middle
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# Gestational Pathology Causes of choriocarcinoma | Etiology
* Gestational pathology: * Spontaneous abortion * Normal pregnancy * Hydatidiform mole * Ovarian tumor: * Spontaneous germ cell tumor
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Treatment of choriocarcinoma | Approach to Therapy
* Gestational --> respond well to radiotherapy * Germ cell --> respond poorly to radiotherapy

GU / GYN & Renal (23 decks)

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