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GU / GYN & Renal > Pathoma: Female Genital System & Gestational Pathology > Flashcards

Pathoma: Female Genital System & Gestational Pathology Flashcards

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
Q

Vulva

Dysplastic precursor lesion characterized by koilocytic change, disordered cellular maturation, nuclear atypia, and increased mitotic activity

Histology

A

Vulvar intraepithelial neoplasia (VIN)

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26
Q

Vulva

Most common cause of non-HPV related vulvar carcinoma

Etiology

A

Long-standing lichen sclerosis

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27
Q

Vulva

Chronic inflammation & irritation eventually lead to carcinoma

Pathophysiology

A

Non-HPV related vulvar carcinoma

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28
Q

Vulva

Generally seen in elderly women (average age >70 years)

Epidemiology

A

Non-HPV related vulvar carcinoma

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29
Q

Vulva

  • Characterized by malignant epithelial cells in epidermis of vulva
  • Represents CIS; usually no underlying carcinoma

Histopathology

A

Extramammary Paget disease of the vulva

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30
Q

Vulva

Erythematous, pruritic, ulcerated vulvar skin

Clinical Presentation

A

Extramammary Paget disease of the vulva

Can also occur in nipple

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31
Q

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

A

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

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32
Q

Vulva

A

Extramammary Paget disease of the vulva

Microscopic Appearance

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33
Q

General

Vagina

A
  • Fibromuscular canal leading to cervix
  • Mucosa is lined by non-keratinizing squamous epithelium
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34
Q

Vagina

Focal persistence of columnar epithelium in upper vagina

Pathophysiology

A

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)

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35
Q

Vagina

Increased incidence in females exposed to diethylstilbestrol (DES) in utero

Etiology

A

Vaginal adenosis

DES: used to prevent pregnancy-related complications; can cross placenta

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36
Q

Vagina

A

Vaginal adenosis

Microscopic Appearance

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37
Q

Vagina

Malignant proliferation of glands with clear cytoplasm

Pathophysiology

A

Clear cell adenocarcinoma

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38
Q

Vagina

Rare, but severe complication of DES-associated vaginal adenosis

Etiology

A

Clear cell adenocarcinoma

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39
Q

Vagina

Malignant mesenchymal proliferation of immature skeletal muscle

Pathophysiology

A

Embryonal rhabdomyosarcoma

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40
Q

Vagina

Bleeding & a grape-like mass protruding from vagina / penis of a child (usually <5 yrs of age)

Clinical Presentation

A

Embryonal rhabdomyosarcoma

Also called sarcoma botryoides = “grape-like mass”

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41
Q

Vagina

Characteristic cell: rhabdomyoblast
* Cytoplasmic cross-striations
* Positive IHC staining for desmin & myogenin

Histology

A

Embryonal rhabdomyosarcoma

Cross-strations resemble skeletal muscle

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42
Q

Vagina

A

Embryonal rhabdomyosarcoma: grape-like masses

Gross Appearance

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43
Q

Vagina

Carcinoma of vaginal squamous epithelium

Histology

A

Vaginal carcinoma

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44
Q

Vagina

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

Etiology

A

Vaginal carcinoma

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45
Q

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

A

Vaginal carcinoma

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46
Q

General

Cervix

A
  • 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)
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47
Q

Cervix

A

Cervical transformation zone, normal

Clearly demarcated stratified squamous epithelium & columnar epithelium

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48
Q

Cervix

HPV infection

Pathophysiology

A
  • 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
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49
Q

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

A

Cervical intraepithelial neoplasia (CIN)

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50
Q

Cervix

Dysplasia involving < 1/3 of the thickness of epithelium

Histology

A

CIN 1

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51
Q

Cervix

Dysplasia involving < 2/3 of the thickness of epithelium

Histology

A

CIN 2

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52
Q

Cervix

Dysplasia involving almost entire thickness of epithelium

Histology

A

CIN 3

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53
Q

Cervix

Dysplasia involving entire thickess of epithelium

Histology

A

Cervical carcinoma in situ (CIS)

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54
Q

Cervix

A

CIN 3 / CIS

Dysplasia of almost entire thickness / Dysplasia of entire thickness

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55
Q

Cervix

Progression of CIN

Natural History & Complications

A

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

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56
Q

Cervix

Invasive carcinoma of cervical epithelium

Histology

A

Cervical carcinoma

Invasive = penetrates basement membrane; distinguishes from CIS

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57
Q

Cervix

Most commonly seen in middle-aged women (average age = 40-50 yrs)

Epidemiology

A

Cervical carcinoma

HPV infection occurs earlier (age 20-25 years)

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58
Q

Cervix

  • Vaginal bleeding, esp. postcoital
  • Cervical discharge

Clinical Presentation

A

Cervical carcinoma

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59
Q

Cervix

Key risk factor: high-risk HPV infection

Epidemiology

A

Cervical carcinoma

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60
Q

Cervix

Secondary risk factors: smoking, immunodeficiency (cervical carcinoma = AIDS-defining illness)

Epidemiology

A

Cervical carcinoma

Immunodeficiency –> impaired clearance of HPV infection

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61
Q

Cervix

Common subtypes of cervical carcinoma

Epidemiology

A
  1. SCC = 80% of cases
  2. Adenocarcinoma = 15% of cases

Both subtypes are related to HPV infection

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62
Q

Cervix

Consequences of cervical carcinoma

Natural History & Complications

A
  • 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
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63
Q

Cervix

Cervical carcinoma screening

Prevention

A
  • 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
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64
Q

Cervix

Pap smear

Prevention

A
  • 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

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65
Q

Cervix

A

High-grade dysplasia, Pap smear

Hyperchromatic nuclei & high N:C ratios

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66
Q

Cervix

HPV vaccine

Prevention

A

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

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67
Q

General

Endometrium & Myometrium

A
  • 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
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68
Q

Endometrium

Secondary amenorrhea (absence of menstruation) due to loss of basalis (regenerative layer of endometrium) & scarring

Pathophysiology

A

Asherman syndrome

Loss of basalis impairs regeneration & shedding of endometrium

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69
Q

Endometrium

Result of overaggressive dilation and curettage (D&C)

Etiology

A

Asherman syndrome

Curettage = scraping away of uterine wall; basalis can be scraped off

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70
Q

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

A

Anovulatory cycle

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71
Q

Endometrium

Bacterial infection of endometrium

Pathophysiology

A

Acute endometritis

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72
Q

Endometrium

Major cause of acute endometritis

Etiology

A

Retained products of conception (e.g., after delivery)
* Retained products act as nidus for infection

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73
Q

Endometrium

  • Fever
  • Abnormal uterine bleeding
  • Pelvic pain

Clinical Presentation

A

Acute endometritis

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74
Q

Endometrium

Chronic endometrial inflammation

Pathophysiology

A

Chronic endometritis

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75
Q

Endometrium

Characterized by presence of lymphocytes, plasma cells

Histology

A

Chronic endometritis

Lymphocytes normally in endometrium; plasma cells necessary for Dx

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76
Q

Endometrium

  • Retained products of conception
  • Chronic pelvic inflammatory disease (e.g., Chlamydia)
  • IUD
  • TB

Etiology

A

Chronic endometritis

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77
Q

Endometrium

  • Abnormal uterine bleeding
  • Pelvic pain
  • Infertility

Clinical Presentation

A

Chronic endometritis

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78
Q

Endometrium

Hyperplastic protrusion of endometrium

Histopathology

A

Endometrial polyp

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79
Q

Endometrium

Abnormal uterine bleeding

Clinical Presentation

A

Endometrial polyp

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80
Q

Endometrium

Can arise as side effect of tamoxifen
* Anti-estrogen effects on breast
* Weak pro-estrogen effects on endometrium

Etiology

A

Endometrial polyp

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81
Q

Endometrium

A

Endometrial polyp

Hyperplastic protrusion of endometrium w/ lymphocytes & plasma cells

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82
Q

Endometrium

Endometrial glands & stroma outside of uterine endometrial lining

Histology

A

Endometriosis

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83
Q

Endometrium

Most likely cause of endometriosis

Etiology

A

Retrograde menstruation with implanatation at an ectopic site

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84
Q

Endometrium

  • Dysmenorrhea (pain during menstruation)
  • Pelvic pain
  • Infertility (possibly)

Clinical Presentation

A

Endometriosis

Endometriosis cycles just like normal endometrium

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85
Q

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

A

Endometriosis

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86
Q

Endometrium

Implants classically appear as yellow-brown “gunpowder” nodules

Gross Appearance

A

Endometriosis

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87
Q

Endometrium

Complications of endometriosis

Natural History & Complications

A

Increased risk of carcinoma at site of endometriosis, especially in ovary

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88
Q

Endometrium

A

Endometriosis, “chocolate” cyst of ovary

Ovary with cystic lesion containing menstrual products

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89
Q

Endometrium

A

Endometriosis

Yellow-brown “gunpowder” nodules; involvement of soft tissues

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90
Q

Endometrium

Hyperplasia of endometrial glands relative to stroma

Pathophysiology

A

Endometrial hyperplasia

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91
Q

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

A

Endometrial hyperplasia

Unopposed proliferation results in hyperplasia

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92
Q

Endometrium

Post-menopausal uterine bleeding

Clinical Presentation

A

Endometrial hyperplasia

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93
Q

Endometrium

Classified based on architectural growth pattern (simple or complex) & presence / absence of cellular atypia

Histology

A

Endometrial hyperplasia

94
Q

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

A

Endometrial hyperplasia

95
Q

Endometrium

A

Endometrial hyperplasia

Crowded endometrial glands; high ratio of endometrial glands to stroma

96
Q

Endometrium

Malignant proliferation of endometrial glands

Histology

A

Endometrial carcinoma

97
Q

Endometrium

Most common invasive carcinoma of female genital tract

Epidemiology

A

Endometrial carcinoma

98
Q

Endometrium

Post-menopausal bleeding

Clinical Presentation

A

Endometrial carcinoma

99
Q

Endometrium

Arises via 2 distinct pathways:
1. Hyperplastic
2. Sporadic

Pathophysiology

A

Endometrial carcinoma

100
Q

Endometrium

Endometrial carcinoma, hyperplastic pathway

Pathophysiology

A
  • Most common: 75% of cases
  • Age at presentation: 60 years
  • Carcinoma arises from endometrial hyperplasia
101
Q

Endometrium

Endometrial carcinoma, sporadic pathway

Pathophysiology

A
  • Less common: 25% of cases
  • Age at presentation: 70 years
  • Carcinoma arises in atrophic endometrium with no evident precursor lesion
102
Q

Endometrium

Risk factors are related to estrogen exposure:
* Early menarche / late menopause
* Nulliparity
* Infertility with anovulatory cycles
* Obesity

Epidemiology

A

Endometrial carcinoma, hyperplastic

103
Q

Endometrium

Endometrioid type

Histology

A

Endometrial carcinoma, hyperplastic

104
Q

Endometrium

  • Serous type
  • Characterized by papillary structures with psammoma body (PB) formation
  • p53 mutation is common
  • Tumor exhibits aggressive behavior

Histology

A

Endometrial carcinoma, sporadic

Necrosis of papillae allows for calcification & PB formation

105
Q

Endometrium

A

Endometrial carcinoma

Growth = carcinoma; normal endometrium is smooth & shiny

106
Q

Endometrium

A

Endometrial carcinoma, endometrioid type

Normal endometrium-like but disorganized & overlapping, minimal stroma

107
Q

Endometrium

A

Endometrial carcinoma, serous type

Papillary architecture, FV cores; necrosis of papillae & PB formation

108
Q

Myometrium

Benign neoplastic proliferation of smooth muscle arising from myometrium

Histology

A

Leiomyoma (fibroids)

109
Q

Myometrium

Most common tumor in females

Epidemiology

A

Leiomyoma (fibrioids)

110
Q

Myometrium

Related to estrogen exposure
* Common in premenopausal women
* Often multiple tumors
* Enlarge during pregnancy & shrink after menopause

Etiology

A

Leiomyoma (fibroids)

111
Q

Myometrium

Multiple, well-defined, white, whorled masses that may distort uterus & impinge upon pelvic structures

Gross Appearance

A

Leiomyoma (fibroids)

112
Q

Myometrium

  • Usually asymptomatic
  • When present, symptoms include:
    • Abnormal uterine bleeding
    • Infertility
    • Pelvic mass

Clinical Presentation

A

Leiomyoma (fibroids)

113
Q

Myometrium

A

Uterine leiomyoma (fibroids)

Multiple, well-defined, white, whorled masses

114
Q

Myometrium

Malignant prolfieration of smooth muscle arising from the myometrium

Histology

A

Leiomyosarcoma

115
Q

Myometrium

Arise de novo

Pathophysiology

A

Leiomyosarcoma

Leiomyosarcomas do not arise from leiomyomas

116
Q

Myometrium

Usually seen in post-menopausal women

Epidemiology

A

Leiomyosarcoma

117
Q

Myometrium

Individual lesion with areas of necrosis & hemorrhage

Gross Apperance

A

Leiomyosarcoma

118
Q

Myometrium

  • Central necrosis
  • Mitotic activity
  • Cellular atypia

Histology

A

Leiomyosarcoma

119
Q

Leiomyoma vs. Leiomyosarcoma

A
  • 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
Q

General

Ovary

A
  • 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
Q

Ovary

A

Ovarian follicle, normal

Oocye = pink middle; Granulosa = purple cells inside; Theca = outside

122
Q

Ovary

A

Corpus luteum

Ovary = bottom right, white; Corpus luteum = top left, yellow

123
Q

Ovary

Multiple ovarian follicular cysts due to hormone imbalance

Histology

A

Polycystic ovarian disease (PCOD)

124
Q

Ovary

Affects 5% of reproductive-aged women

Epidemiology

A

Polycystic ovarian disease (PCOD)

125
Q

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

A

Polycystic ovarian disease (PCOD)

126
Q

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

A

Polycystic ovarian disease (PCOD)

127
Q

General

Ovarian tumors

A
  • 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
Q

Ovarian Tumors

Most common type of ovarian tumor

Epidemiology

A

Surface epithelial tumor

70% of cases

129
Q

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

A

Surface epithelial tumors

130
Q

Ovarian Tumors

Common subtypes of surface epithelial tumors

Epidemiology

A
  • 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
Q

Ovarian Tumors

Tumor composed of a single cyst w/ a simple, flat lining

Histopathology

A

Cystadenomas

Surface epithelial tumors, benign

132
Q

Ovarian Tumors

Most common in premenopausal women (ages 30-40)

Epidemiology

A

Cystadenomas

Surface epithelial tumors, benign

133
Q

Ovarian Tumors

  • Tumors composed of complex cysts with a thick, shaggy lining
  • Defining feature: invasion of cells into connective tissue of cyst wall

Histopathology

A

Cystadenocarcinomas

Surface epithelial tumors, malignant

134
Q

Ovarian Tumors

Most commonly arise in post-menopausal women (ages 60-70)

Epidemiology

A

Cystadenocarcinomas

Surface epithelial tumors, malignant

135
Q

Ovarian Tumors

Increased risk for serous ovarian & fallopian tube carcinoma

Etiology

A

BRCA1 mutation carriers
* BRCA1 carriers often undergo prophylactic salpingo-oopherectomy

136
Q

Ovarian Tumors

Less common subtypes of surface epithelial tumors

Epidemiology

A
  1. Endometrioid tumors
  2. Brenner tumors
137
Q

Ovarian Tumors

  • Composed of endometrial-like glands
  • Typically malignant
  • May arise from endometriosis
  • A/w endometrial carcinoma, endometrioid type (15% of cases)

Histopathology

A

Endometrioid carcinoma

138
Q

Ovarian Tumors

  • Composed of bladder-like epithelium
  • Usually benign

Histopathology

A

Brenner tumor

139
Q

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

A

Surface epithelial tumors

140
Q

Ovarian Tumors

A

Cystadenoma

Benign surface epithelial tumor; can be serous or mucinous

141
Q

Ovarian Tumors

Serum marker used to monitor treatment response & screen for recurrence of surface epithelial carcinoma

Approach to Therapy

A

CA-125

142
Q

Ovarian Tumors

  • 2nd most common type of ovarian tumor
  • Typically occur in women of reproductive age

Epidemiology

A

Germ cell tumors

15% of cases

143
Q

Ovarian Tumors

Subtypes of germ cell tumors

Histopathology

A

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
Q

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

A

Cystic teratoma

145
Q

Ovarian Tumors

  • Most common germ cell tumor in females
  • Bilateral in 10% of cases

Epidemiology

A

Cystic teratoma

146
Q

Ovarian Tumors

Cystic teratoma composed primarily of thryoid tissue
* Can result in hyperthyroidism

Histopathology

A

Struma ovarii

147
Q

Ovarian Tumors

Rule out malignant potential

Approach to Diagnosis

A
  • 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
Q

Ovarian Tumors

A

Cystic teratoma

Cystic tumor with hair, teeth / bone, skin

149
Q

Ovarian Tumors

Mass composed of large cells with clear cytoplasm & central nuclei
* Tumor cells resemble oocytes
* Testicular counterpart = seminoma

Histopathology

A

Dysgerminoma

“Dys-“ = bad (malignant); “-germ-“ = germ cells; “-oma” = mass

150
Q

Ovarian Tumors

Most common malignant germ cell tumor

Epidemiology

A

Dysgerminoma

151
Q

Ovarian Tumors

Serum LDH may be elevated

Approach to Diagnosis

A

Dysgerminoma

152
Q

Ovarian Tumors

  • Responds to radiotherapy
  • Good prognosis

Approach to Therapy

A

Dysgerminoma

153
Q

Ovarian Tumors

A

Dysgerminoma

Nests composed of round cells

154
Q

Ovarian Tumors

Malignant tumor that mimics yolk sac

Histopathology

A

Endodermal sinus tumor

155
Q

Ovarian Tumors

Most common germ cell tumor in children

Epidemiology

A

Endodermal sinus tumor

156
Q

Ovarian Tumors

  • Serum AFP is often elevated
  • Histology: Schiller-Duval bodies

Approach to Diagnosis

A

Endodermal sinus tumor

AFP = alpha fetoprotein; Schiller-Duval bodies = glomeruloid structures

157
Q

Ovarian Tumors

A

Endodermal sinus tumor

Schiller-Duval body = hallmark histological finding

158
Q

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

A

Choriocarcinoma

159
Q

Ovarian Tumors

High B-hCG
* Produced by syncytiotrophoblasts
* May lead to thecal cysts in ovary

Approach to Diagnosis

A

Choriocarcinoma

Characteristic lab finding

160
Q

Ovarian Tumors

Poor response to chemotherapy

Approach to Treatment

A

Choriocarcinoma, germ cell tumor variant

161
Q

Ovarian Tumors

  • Malignant tumor composed of large primitive cells
  • Aggressive with early metastasis
    • Primitive cells are designed to move & spread

Histopathology

A

Embryonal carcinoma

162
Q

Ovarian Tumors

Tumors resemble ovarian sex cord-stromal tissues

Histopathology

A

Sex cord-stromal tumors

163
Q

Ovarian Tumors

  • Neoplastic proliferation of granulosa & theca cells
  • Malignant, but minimal risk for metastasis

Histopathology

A

Granulosa-theca cell tumor

164
Q

Ovarian Tumors

Tumor is often estrogen-producing

Pathophysiology

A

Granulosa-theca cell tumor

165
Q

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

A

Granulosa-theca cell tumor

166
Q

Ovarian Tumors

Most common setting for granulosa-theca cell tumors

Epidemiology

A

Post-menopause

167
Q

Ovarian Tumors

Tumor composed of Sertoli cells & Leydig cells
* Sertoli cells –> form tubules
* Leydig cells –> between tubules

Histopathology

A

Sertoli-Leydig cell tumor

168
Q

Ovarian Tumors

Tumor may be androgen-producing

Pathophysiology

A

Sertoli-Leydig cell tumor

169
Q

Ovarian Tumors

  • Hirsutism
  • Virilization

Clinical Presentation

A

Sertoli-Leydig cell tumor

170
Q

Ovarian Tumors

Reinke crystals

Histology

A

Sertoli-Leydig cell tumor

Reinke crystals = hallmark histological finding

171
Q

Ovarian Tumors

Reinke crystals

Histology

A

Sertoli-Leydig cell tumor

Reinke crystals = hallmark histological finding

172
Q

Ovarian Tumors

Benign fibroblast tumor

Histopathology

A

Fibroma

173
Q

Ovarian Tumors

Meigs syndrome
* Pleural effusions
* Ascites

Clinical Presentation

A

Fibroma

174
Q

Ovarian Tumors

Syndrome resolves with removal of tumor

Approach to Therapy

A

Fibroma

175
Q

Ovarian Tumors

A

Ovarian fibroma

Solid tumor; white bands going through it represent fibrosis

176
Q

Ovarian Tumors

Metastatic mucinous tumor involving both ovaries

Histopathology

A

Krukenberg tumor

177
Q

Ovarian Tumors

Most common cause of Krukenberg tumor

Etiology

A

Metastatic gastric carcinoma, diffuse type

178
Q

Ovarian Tumors

Bilateral ovary involvement

Distinctive Clinical Manifestations

A

Bilaterality helps distinguish metastases from primary ovarian mucinous carcinoma (usually unilateral)

179
Q

Ovarian Tumor

Massive amount of mucus in peritoneum

Pathology

A

Pseudomyxoma peritonei

180
Q

Ovarian Tumors

Cause of pseudomyxoma peritonei

Etiology

A

Primary mucinous tumor of the appendix, usually with metastasis to ovary

181
Q

Gestational Pathology

Implantation of fertilized ovum at site other than uterine wall
* Most common site: lumen of fallopian tube

Pathophysiology

A

Ectopic pregnancy

182
Q

Gestational Pathology

Key risk factor for ectopic pregnancy

Epidemiology

A

Scarring
* Secondary to pelvic inflammatory disease
* Secondary to endometriosis

183
Q

Gestational Pathology

A

Ectopic tubal pregnany

Hemorrhage at rupture site of fallopian tube

184
Q

Gestational Pathology

Lower quadrant abdominal pain a few weeks after missed period

Clinical Presentation

A

Ectopic pregnancy

185
Q

Gestational Pathology

Treatment of ectopic pregnancy

Approach to Therapy

A

Surgical emergency

186
Q

Gestational Pathology

Major complications of ectopic pregnancy

Natural History & Complications

A
  • Hematosalpinx (bleeding into fallopian tube)
  • Rupture of fallopian tube
187
Q

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

A

Spontaneous abortion

188
Q

Gestational Pathology

  • Vaginal bleeding
  • Cramp-like pain
  • Passage of fetal tissues

Clinical Presentation

A

Spontaneous abortion

189
Q

Gestational Pathology

Most common cause of spontaneous abortion

Etiology

A

Chromosomal abnormalities
* Especially trisomy 21

190
Q

Gestational Pathology

Other causes of spontaneous abortion

Etiology

A
  • 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

191
Q

Gestational Pathology

Effects of teratogens on embryogenesis by weeks gestation at time of exposure

Pathophysiology

A
  • First 2 weeks: spontaneous abortion
  • Weeks 3-8: risk of organ malformation
  • Weeks 3-9: risk of organ hypoplasia
192
Q

Gestational Pathology

Effects of alcohol on embryogenesis

Pathophysiology

A
  • Most common cause of mental retardation
  • Facial abnormalities
  • Microcephaly
193
Q

Gestational Pathology

Effects of cocaine on embryogenesis

Pathophysiology

A
  • IUGR
  • Placental abruption
194
Q

Gestational Pathology

Effects of thalidomide on embryogenesis

Pathophysiology

A

Limb defects

195
Q

Gestational Pathology

Effects of cigarette smoke on embryogenesis

Pathophysiology

A

IUGR

196
Q

Gestational Pathology

Effects of tetracycline on embryogenesis

Pathophysiology

A

Discolored teeth

197
Q

Gestational Pathology

Effects of tetracycline on embryogenesis

Pathophysiology

A

Discolored teeth

198
Q

Gestational Pathology

Effects of warfarin on embryogenesis

Pathophysiology

A

Fetal bleeding

199
Q

Gestational Pathology

Effects of phenytoin on embryogenesis

Pathophysiology

A
  • Digit hypoplasia
  • Cleft lip / palate
200
Q

Gestational Pathology

Implantation of placenta in lower uterine segment, overlying cervical os (opening)

Pathophysiology

A

Placenta previa

201
Q

Gestational Pathology

Presents as third-trimester bleeding

Clinical Presentation

A

Placenta previa

202
Q

Gestational Pathology

Treatment of placenta previa

Approach to Therapy

A

Often requires delivery of fetus by caesarian section

203
Q

Gestational Pathology

Separation of placenta from decidua prior to delivery of fetus

Pathophysiology

A

Placental abruption

204
Q

Gestational Pathology

Common cause of stillbirth

Natural History & Complications

A

Placental abruption

205
Q

Gestational Pathology

Presents with third-trimester bleeding & fetal insufficiency

Clinical Presentation

A

Placental abruption

206
Q

Gestational Pathology

A

Placental abruption

Blood on surface that was in contact with decidua (maternal surface)

207
Q

Gestational Pathology

Improper implantation of placenta into myometrium with little or no decidua

Pathophysiology

A

Placenta accreta

Absence of decidua results in implantation of placenta into myometrium

208
Q

Gestational Pathology

Presents with difficult delivery of placenta & postpartum bleeding

Clinical Presentation

A

Placenta accreta

Placenta gets stuck as it is implanted in myometrium

209
Q

Gestational Pathology

Treatment of placenta accreta

Approach to Therapy

A

Often requires hysterectomy

210
Q

Gestational Pathology

Pregnancy-induced HTN, proteinuria, and edema
* Typically arises in 3rd trimester
* HTN can be severe –> headaches, visual changes

Pathophysiology

A

Preeclampsia

211
Q

Gestational Pathology

Cause of preeclampsia

Etiology

A

Abnormal maternal-fetal vascular interface in placenta

212
Q

Gestational Pathology

Eclampsia

Clinical Presentation

A

Preeclampsia + seizures

213
Q

Gestational Pathology

Treatment of preeclampsia

A
214
Q

Gestational Pathology

HELLP

Clinical Presentation

A

Preeclampsia + thrombotic microangiopathy involving the liver
* Hemolysis
* Elevated Liver enzymes
* Low Platelets

215
Q

Gestational Pathology

Treatment of preeclampsia

Approach to Therapy

A
  • Normal preeclampsia resolves with delivery
  • Eclampsia & HELLP warrant immediate delivery
216
Q

Gestational Pathology

Prevalence of preeclampsia

Epidemiology

A

Approx. 5% of pregnancies

217
Q

Gestational Pathology

Fibrinoid necrosis in vessels of placenta

Approach to Diagnosis

A

Preeclampsia

Classical finding resulting from very high blood pressure

218
Q

Gestational Pathology

  • Death of a healthy infant (1 month - 1 year old) without oviuous cause
  • Infants usually expire during sleep

Pathophysiology

A

Sudden infant death syndrome (SIDS)

219
Q

Gestational Pathology

SIDS risk factors

Epidemiology

A
  • Sleeping on stomach
  • Exposure to cigarette smoke
  • Premature birth
220
Q

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

A

Hydatidiform mole

221
Q

Gestational Pathology

Classically presents in 2nd trimester as passage of grape-like masses through vaginal canal

Clinical Presentation

A

Hydatidiform mole

Grape-like masses = large, edematous villi

222
Q

Gestational Pathology

Diagnosing hydatidiform mole

Approach to Diagnosis

A

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

223
Q

Gestational Pathology

Classes of hydatidiform mole

Histology

A
  1. Complete mole
  2. Partial mole
224
Q

Gestational Pathology

Partial mole

Histology

A
  • 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
225
Q

Gestational Pathology

Complete mole

Histology

A
  • 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%
226
Q

Gestational Pathology

Treatment of hydatidiform mole

Approach to Therapy

A

Suction curettage
* Subsequent B-hCG monitoring to ensure adequate mole removal & screen for choriocarcinoma

227
Q

Gestational Pathology

A

Complete hydatidiform mole

Swollen, grape-like villi

228
Q

Gestational Pathology

A

Complete hydatidiform mole

Hydropic villi = dilated; trophoblast proliferation = purple, middle

229
Q

Gestational Pathology

Causes of choriocarcinoma

Etiology

A
  • Gestational pathology:
    • Spontaneous abortion
    • Normal pregnancy
    • Hydatidiform mole
  • Ovarian tumor:
    • Spontaneous germ cell tumor
230
Q

Treatment of choriocarcinoma

Approach to Therapy

A
  • Gestational –> respond well to radiotherapy
  • Germ cell –> respond poorly to radiotherapy

GU / GYN & Renal (23 decks)

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