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Pathoma > 13_Female Repro > Flashcards

13_Female Repro Flashcards

1
Q

Vulva = skin & mucosa external to the _____

A

hymen

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2
Q

The vulva is lined by ______ epithelium

A

squamous

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3
Q

Bartholin Cyst- basic pathology & typical patient it is seen in?

A

Cystic dilatation of the Bartholin Gland

  • It arises due to inflammation & obstruction of the gland or duct
  • Usually occurs in women of reproductive age b/c often related to infection / STI
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4
Q

Are Bartholin Cysts usually unilateral or bilateral?

A

Unilateral

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5
Q

Classic Clinical Presentation of Bartholin Cyst?

A
  • Woman of reproductive age
  • Unilateral painful, cystic lesion
  • Lower vestibule adjacent to vaginal canal
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6
Q

Condyloma

A

Warty neoplasm of vulvar skin, often large

  • Most commonly due to HPV 6 or 11 (low-risk)
  • Characterized by koilocytic change
  • Rarely progresses to carcinoma
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7
Q

General/classic histologic manifestation of HPV?

A

Koilocytic change (cell looks crinkled, raisin-like)

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8
Q

How is the determination made as to whether HPV is High-risk or Low-risk?

(refers to “risk” of developing subsequent carcinoma)

A

DNA sequencing

Low-risk types: 6 & 11 (cause Condylomas)
High-risk types: 16, 18, 31, & 33 (cause Dysplasia)

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9
Q

Lichen Sclerosis - basic pathology & presentation?

A
  • Thinning of the epidermis & Fibrosis of the dermis
  • Leukoplakia w/ “parchment-like” vulvar skin
  • Most commonly presents in post-menopausal women
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10
Q

Lichen Simplex Chronicus- basic pathology & presentation?

A
  • Hyperplasia of vulvar squamous epithelium
  • Leukoplakia w/ thick, leathery vulvar skin
  • Associated w/ chronic irritation & scratching
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11
Q

Vulvar Carcinoma - how common is it?

A

Relatively rare- accounts for only a small percentage of female genital cancers

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12
Q

Vulvar Carcinoma- presentation?

A

Presents as Leukoplakia
- Biopsy may be required to distinguish carcinoma from other causes of leukoplakia (Lichen Sclerosis, Lichen Simplex Chronicus)

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13
Q

Vulvar Carcinoma- Etiology(ies)?

A

2 Etiologies:

  1. HPV-related pathway (16, 18)
    - – Arises from VIN
  2. Non-HPV-related pathway (6, 8)
    - – Arises from longstanding Lichen Sclerosis
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14
Q

HPV-related Vulvar Carcinoma:

  • Etiology?
  • Typical age?
A
  • Due to high-risk HPVs (16 & 18)
  • Arises from Vulvar Intraepithelial Neoplasia (VIN)
  • 40-50 yrs. age
    (get HPV @ 20-25, then takes 10-15 to develop neoplasia)
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15
Q

Non-HPV-related Vulvar Carcinoma:

  • Etiology?
  • Typical age?
A
  • Arises from Longstanding Lichen Sclerosis
  • Chronic inflammation & irritation that eventually leads to carcinoma
  • Generally seen in elderly, postmenopausal women (>70 yrs.)
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16
Q

Extramammary Paget Disease - basic pathology & presentation?

A
  • Malignant epithelial cell in the epidermis of the vulva
  • Represents carcinoma in-situ, usually no underlying carcinoma
  • Presents as erythematous, pruritic, ulcerated skin
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17
Q

Paget cells (carcinoma) vs. Melanoma:

  • PAS?
  • Keratin?
  • S100?
A

Paget cells: PAS +, Keratin +, S100 -

Melanoma: PAS -, Keratin -, S100 +

(PAS not as important as other 2 in distinguishing)

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18
Q

Etiology of Paget Disease of the nipple vs. the vulva?

A

Paget Disease of Nipple = means there is a cancer somewhere in the breast

Paget Disease of Vulva = usually NO underlying cancer

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19
Q

Lichen Sclerosis- risk of cancer?

A

Benign, however is associated w/ slightly increased risk of Squamous Cell Carcinoma

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20
Q

Lichen Simplex Chronicus- risk of cancer?

A

Benign, no increased risk of Squamous Cell Carcinoma

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21
Q

The mucosa of the vagina is lined by what type of epithelium?

A

Non-keratinizing Squamous Epithelium

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22
Q

Adenosis

A
  • Focal persistence of columnar epithelium in upper ⅓ of vagina (from Malarian duct –> normally replaced by squamous epithelium)
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23
Q

Adenosis- risk of cancer?

A

Increases risk of developing Clear Cell Adenocarcinoma

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24
Q

Clear Cell Adenocarcinoma

A
  • Malignant proliferation of glands w/ clear cell cytoplasm
  • Rare complication of DES-associated vaginal adenosis

(discovery of this & other complications led to cessation of DES usage)

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25
Q

a) Where is the upper ⅓ of the vagina derived from?
b) What about the lower ⅔ of the vagina?
c) What type of epithelium lines each part?

A

a) Upper ⅓ = Mullerian Duct
b) Lower ⅔ = Urogenital Sinus (UGS)
c) Both are lined by non-keratinizing Squamous Epithelium. The upper ⅓ is originally Columnar, however during development is replaced by squamous epithelium (EXCEPT in the case of Adenosis, where there is focal persistence of columnar epithelium in the upper ⅓)

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26
Q

There is an increased incidence of Adenosis in females exposed to _____ in-utero

A

DES

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27
Q

Embryonal Rhabdomyosarcoma - basic pathology?

A

Malignant mesenchymal proliferation of immature skeletal muscle

(very rare)

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28
Q

Embryonal Rhabdomyosarcoma- presentation?

A
  • Bleeding, grape-like mass protruding from the vagina or penis of a child
  • Usually <5 yrs. old
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29
Q

2 important characteristics of Rhabdomyoblast (malignant cell of Embryonal Rhabdomyosarcoma)

A
  • Cytoplasmic cross-striations

- Positive IHC staining for Desmin (muscle cell IF) & Myoglobin

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30
Q

Vaginal Carcinoma - basic pathology?

A
  • Carcinoma arising from squamous epithelium lining the vaginal mucosa
  • Usually related to high-risk HPV (16, 18, 31, 33)
  • Precursor lesion is vaginal intraepithelial neoplasia (VAIN)
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31
Q

What is the precursor lesion for Vaginal Carcinoma?

A

Vaginal Intraepithelial Neoplasia (VAIN)

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32
Q

Where are the typical locations for regional lymph node spread of vaginal tumors?

A

Cancer from upper ⅓ of vagina –> Regional Iliac Nodes

Cancer from lower ⅔ of vagina –> Inguinal Nodes

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33
Q

The Exocervix is lined by __a__ epithelium.

The Endocervix is lined by __b__ epithelium

A

a) squamous

b) columnar

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34
Q

What is the “Transformation Zone” in the Lower Genital Tract (LGT)?

Why is this important pathologically?

A

It is where the squamous epithelium of the exocervix meets the columnar epithelium of the endocervix.

This is one of the most common sites of HPV infection in the LGT (persistent infection leads to risk for CIN)

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35
Q

What 2 proteins do “high-risk HPVs” make that make them high-risk?

A

High-risk HPVs make 2 proteins:

  1. E6: increases destruction of p53 (HPV16)
  2. E7: increases destruction of Rb (HPV18)
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36
Q

General difference between dysplasia (CIN 1-3) & carcinoma in-situ?

A

CIN 1-3 (cervical intraepithelial neoplasia) involves increasing amounts of the epithelium from the basal layer.
Once the entire epithelial layer is included, it is considered carcinoma in-situ.

  • Carcinoma in-situ is IRReversible
  • CIN 1-3 are all reversible (1>2>3)
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37
Q

How do you distinguish invasive carcinoma vs. carcinoma in-situ (CIS)?

A

Invasive carcinoma goes through the basement membrane

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38
Q

Classic presentation of invasive cervical carcinoma?

A

Presents as vaginal bleeding, typically in a 40-50 yr old woman
(also post-coital bleeding or bleeding after intercourse is classic)

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39
Q

Primary & secondary risk factors for invasive cervical carcinoma?

A

Primary – high risk HPV infection (16, 18)

Secondary – Smoking, immunodeficiency

40
Q

What types of cancers does smoking tend to cause?

A
  1. Organs it has direct contact w/ upon smoking – Oropharynx, Esophagus, Lungs
  2. Anything urine touches b/c kidney filters carcinogens from blood → Kidneys, ureters, bladder
  3. 2 randoms to remember – Cervix & Pancreas
41
Q

T or F?

Cervical carcinoma is an AIDS-defining illness in a HIV+ patient.

A

True

42
Q

Most common subtypes of cervical carcinoma?

Which are ass’d w/ HPV?

A

Squamous CC - Exocervix - much more common

Adeocarcinoma - Endocervix

BOTH subtypes are ass’d w/ HPV

43
Q

Classic finding in an advanced cervical tumor?

A

Hydronephrosis w/ post-renal failure

Tumor invades bladder & blocks ureters
(cervical cancers tend not to metastasize outside of local area until very, very late )

44
Q

What is the confirmatory test for an abnormal pap smear?

A

Colposcopy w/ biopsy

(introduce a magnifying glass into vaginal canal to view cervix, can apply acid to visualize abnormal areas & collect BIOPSY)

45
Q

2 major limitations of pap smear?

A
  • Inadequate sampling of transition zone may not pick up area w/ cancer – false negative
  • Does not detect Adenocarcinoma as well (incidence of adenocarcinoma has not dec’d significantly since use of pap smear)
46
Q

Which strains of HPV are prevented by the Quadrivalent vaccine & for how long is this effective?
Are pap smears still necessary if you’ve had the vaccine?

A

HPV 6, 11, 16, & 18

Protection lasts about 5 years

Pap smears are still necessary to cover the other HPV subtypes
(or to pick up non-HPV ass’d neoplasias)

47
Q

Asherman Syndrome - Cause & Pathology?

A

Secondary amenorrhea due to loss of basalis (stem cell layer of endometrium) & scarring

This is a result of overaggressive dilation & curettage (D & C)

48
Q

Dx?

Secondary amenorrhea due to loss of basalis & scarring w/ a Hx of overaggressive dilation & curettage.

A

Asherman Syndrome

49
Q

Acute Endometritis - Cause & pathology?

A

Bacterial infection of endometrium

Usually due to retained products of conception

50
Q

Acute Endometritis - Classic presentation?

A
  • Fever
  • Abnormal uterine bleeding
  • Pelvic pain
51
Q

Chronic Endometritis - characterized by what type of cells?

A 
Plasma cells
(these must be seen in endometrium in order for it to be called chronic endometritis)
52
Q

Chronic Endometritis - Common causes?

A
  • Retained products of conception
  • Chronic PID (chlamydia)
  • IUD
  • TB (granulomas present)
53
Q

Chronic Endometritis - Classic presentation?

A
  • Abnormal uterine bleeding
  • Pelvic pain
  • Infertility
54
Q

Endometrial Polyp - Classic presentation?

A

Abnormal uterine bleeding

55
Q

Endometrial polyps may arise as an adverse effect what drug?

A

Tamoxifen

b/c of its pro-estrogenic effects on endometrium

56
Q

Endometriosis - pathology?

A

Abnormal placement of both endometrial glands & stroma outside of the uterus/endometrial lining

  • Non-neoplastic
  • Characterized by cyclic bleeding (menstrual type) from ectopic endometrial tissue, resulting in blood-filled “chocolate cysts)
  • In ovary or on peritoneum
57
Q

Endometriosis - Classic presentation?

A
  • Severe menstrual-related pain (dysmenorrhea)
  • Painful intercourse (dyspareunia)
  • Infertility
  • Menorrhagia (cyclic, menstrual-type bleeding from ectopic endometrial tissue)

Uterus is normal sized (as opposed to Adenomyosis)

58
Q

Endometriosis - Causes?

A

Retrograde menstrual flow

59
Q

Endometritis - Tx?

A

Gentamycin + Clindamycin

— w/ or w/out Ampicillin

60
Q

What specific cell type are you always looking for on a pap smear?

A

Koilocytes, to indicate dysplasia

wrinkled, “raisinoid” nuclei, some of which have clearing or a perinuclear halo

61
Q

Endometriosis - Tx?

A

Oral contraceptives, NSAIDs, Leuprolide, Danazol

62
Q

Name the anatomical site of involvement of the following symptom seen in a patient w/ Endometriosis:
- Chocolate cyst

A

Ovaries

63
Q

Name the anatomical site of involvement of the following symptom seen in a patient w/ Endometriosis:
- Pelvic pain

A

Uterine Ligaments

64
Q

Name the anatomical site of involvement of the following symptom seen in a patient w/ Endometriosis:
- Pain w/ urination

A

Bladder wall

65
Q

Name the anatomical site of involvement of the following symptom seen in a patient w/ Endometriosis:
- Pain w/ defecation

A

Pouch of Douglas

66
Q

Name the anatomical site of involvement of the following symptom seen in a patient w/ Endometriosis:
- Abdominal pain & adhesions

A

Bowel serosa

67
Q

Name the anatomical site of involvement of the following symptom seen in a patient w/ Endometriosis:
- Scarring

A

Fallopian tube mucosa

68
Q

Pathogenesis of Chocolate Cyst?

A

Endometriosis implants inside an ovary & goes through cycles of growing & shedding, building up more & more blood inside the cyst

69
Q

Adenomyosis - Pathology?

A

Endometriosis that involves the myometrium

  • increased risk of carcinoma
70
Q

Adenomyosis - Classic presentation?

A
  • Menorrhagia
  • Dysmenorrhea
  • Pelvic pain

Uterus is enlarged (as opposed to endometriosis that doesn’t involve the myometrium)

71
Q

Adenomyosis - Tx?

A

Hysterectomy

72
Q

Endometrial Hyperplasia - pathology?

A

Hyperlasia of endometrial glands relative to the stroma

consequence of unopposed estrogen

73
Q

Endometrial Hyperplasia - Causes?

A

Unopposed estrogen

postmenopausal - estrogen lowers but progesterone is absent, so the limited estrogen that’s left is unopposed

74
Q

Endometrial Hyperplasia - Clinical presentation?

A

Postmenopausal uterine bleeding

75
Q

What is the most important predictor for progression to carcinoma?

A

Cellular Atypia

76
Q

Endometrial Carcinoma is a malignant proliferation of _________

A

endometrial glands

77
Q

Endometrial Carcinoma - Clinical presentation?

A

Postmenopausal bleeding

78
Q

2 distinct pathways leading to Endometrial Carcinoma?

A
  1. Hyperplastic pathway
    - Carcinoma arises from Hyperplasia
    - Risk factors: Estrogen exposure
    - Avg. age = 50-60 yrs
    - Histology = Endometrioid
  2. Sporadic pathway
    - Carcinoma arises in atrophic endometrium
    - No evident precursor lesion
    - Avg. age = 70 yrs.
    - Histology is usually serous (papillary)
    - p53-driven (aggressive)
79
Q

Which of the 2 endometrial carcinoma pathways is driven by p53 mutations?

A

Sporadic

80
Q

Which pathway of endometrial carcinoma is more likely to have psammoma bodies on histology?

A

Sporadic

papillary, finger-like growths become calcified, leading to psammoma bodies – concentrically arranged calcifications

81
Q

Leiomyoma - pathology?

A

Benign proliferation of smooth muscle arising from myometrium

82
Q

Leiomyoma - Causes?

A

Related to estrogen exposure

83
Q

Leiomyoma - gross appearance?

A

Multiple, well-defined white whorled masses

important for differentiation w/ leiomyosarcoma

84
Q

Dx?

Tumor of myometrium that has multiple, well-define white whorled masses.

A

Leiomyoma

85
Q

Leiomyoma - Clinical presentation?

A
  • Premenopausal women
  • Usually asymptomatic
  • – IF they have symptoms, they would be abnormal uterine bleeding, infertility, &/or pelvic mass
  • Enlarge during pregnancy
  • Shrink after menopause
86
Q

Leiomyosarcoma - Clinical presentation

A
  • Postmenopausal women (>70-80 yrs.)
  • Single mass/lesion w/ necrosis or hemorrhage in center
  • Necrosis, mitotic activity, & cellular atypia
87
Q

T or F?

Leiomyomas run the risk of turning into a Leiomyosarcoma.

A

FALSE

Leiomyosarcomas develop de novo & do NOT arise from leiomyomas!

88
Q

What is the residual follicle called just after ovulation?

What is its primary secretion?

A

Corpus Luteum

Primarily secretes Progesterone

89
Q

2 key distinctions in gross appearance of Leiomyoma vs. Leiomyosarcoma?

A
  1. Leiomyoma = usually multiple.
    Leiomyosarcoma = usually singular.
  2. Leiomyoma = White, whorly regular masses
    Leiomyosarcoma = Necrosis or hemorrhage in center of mass
90
Q

Leiomyosrcoma - pathology?

A
  • Malignant proliferation of smooth muscle arising from the myometrium
  • Arises de novo (NOT from leiomyoma)
  • Single lesion w/ necrosis & hemorrhage
91
Q

BRCA1 gene mutation carriers have an increased risk of both breast cancer & what else?

A

Serous Carcinoma of the Ovary & Fallopian Tube

92
Q

Dx?

Ovarian tumor that contains cells that resemble Urothelium.

A 
Brenner tumor 
(surface epithelial carcinoma of the ovaries)
93
Q

Dx?

Ovarian tumor ass’d w/ Endometriosis.

A 
Endometrioid tumor
(surface epithelial carcinoma of the ovaries)
94
Q

15% of patients w/ Endometrioid Carcinoma of the ovaries will also have a separate Endometrioid Carcinoma in the ______.

A

Endometrium

95
Q

General types of Ovarian Tumors most common in each age group:

  • 15-30 yrs.
  • 35-40 yrs.
  • 60-70 yrs.
A

15-30 yrs. = Germ cell tumor (reproductive age)

35-40 = Benign Surface Epithelial tumor

60-70 = Malignant Surface Epithelial tumor

Pathoma (3 decks)

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