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Physiology > Repro Phys 4 > Flashcards

Repro Phys 4 Flashcards

1
Q

What is the most common gynecologic malignancy worldwide?

A

Cervical cancer (due to lack of screening and HPV vaccine availability)

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2
Q

What is the general prognosis for localized breast cancer? Metastatic?

A

Localized: 99% 5 year survival rate
Metastatic: 31% survival rate

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3
Q

What are the different types of breast cancer in terms of receptors?

A

HR+/HER2+
HR+/HER2-
HR-/HER2+
HR-/HER2-

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4
Q

Out of all the types of breast cancer which has the worst prognosis and why?

A

HR-/HER- because it means the receptors will not be responsive to typical forms of treatment (hormones and antibodies) –> more aggressive

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5
Q

Which type of breast cancer is MC?

A

HR+/HER2+

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6
Q

What does it mean if a tumor is HR+?

A

It is likely to respond to hormonal treatment, i.e. tamoxifen or other SERMS, aromatase inhibitors

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7
Q

How does tamoxifen/SERMs work?

A

Block estrogen receptor to decrease estrogen exposure/effects

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8
Q

How do aromatase inhibitors work?

A

Block production of estrogen from sulfated DHEAS in granulosa cells

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9
Q

What does it mean if a tumor is HER2+?

A

It is responsive to antibody treatment

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10
Q

HR-/HER2- is more associated with BRCA1 or BRCA2?

A

BRCA1

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11
Q

What kind of hormones have HR receptors?

A

Progesterone and estrogen

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12
Q

Breast cancer risk factors

A

Increased estrogen exposure:
- early menarche
- late menopause
- obesity (adipose tissue increases estrogen production)
- nulliparity
- hormonal therapies for menopause
Increasing age
High alcohol consumption
1st degree relatives with BCA or prostate, pancreatic cancer

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13
Q

Breast cancer can be split into ______ and ______ in terms of histology

A

Invasive/infiltrating (MC)
Carcinoma in situ

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14
Q

What is the MC type of infiltrating breast cancer?

A

Ductal

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15
Q

Paget’s disease of the breast

A

Special kind of breast cancer that presents with nipple “eczema”

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16
Q

Phyllodes disease

A

Breast cancer with large tumor, little pain, and skin involvement

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17
Q

T or F: BRCA genes are tumor suppressors

A

T – BRCA MUTATION is what becomes a problem because patients cannot inhibit tumor growth

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18
Q

Which BRCA mutation results in higher likelihood of developing breast cancer?

A

BRCA1 (70% likelihood)

BRCA2 slightly lower lifetime risk for breast and ovarian cancer

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19
Q

Which BRCA mutation results in increased likelihood of developing non gynecologic cancers (pancreatic, prostate, uveal melanoma)?

A

BRCA2

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20
Q

Common mutations associated with breast cancer development

A

PTEN
p53
CHK2

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21
Q

PTEN, p53 and CHK2 are all (proto-oncogenes/tumor suppressor genes)

A

Tumor suppressor genes

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22
Q

MC location of breast cancer?

A

Upper outer quadrant (in/by axilla)

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23
Q

Pathophys of breast cancer

A

Estrogen hypothesis: mutation (inhibition of tumor suppressor or activation of proto oncogene) + excess estrogen exposure increases expression of genotoxic DNA elements –> estrogen releases TGF alpha –> breast tissue grows and transforms abnormally

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24
Q

TGF alpha _______ cell growth

A

Promotes

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25
Q

TGF beta ________ cell growth

A

Inhibits

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26
Q

T or F: patients with breast cancer have a disrupted balance of TGF alpha and TGF beta

A

True

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27
Q

T or F: Excess estrogen results in immediate stimulation of mutant cell proliferation

A

FALSE – takes several rounds of DNA replication and cell division for the mutant cells to be enough to cause cancerous growths

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28
Q

TGF alpha/TGF beta activates cell division

A

TGF alpha

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29
Q

How does the inflammation associated with cancer impact prostaglandin production?

A

Inflammation INCREASES PGE2 production

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30
Q

How does PGE2 interact with aromatase?

A

PGE2 INCREASES aromatase activity = more conversion of steroids to estrogen (worsens cancerous growth bc more estrogen can activate receptors and lead to TGF alpha release, angiogenesis, and cell proliferation)

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31
Q

How does obesity increase the risk of breast cancer

A

Adipose tissue creates more estrogen (estrone specifically)

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32
Q

Median age at diagnosis for cervical cancer

A

40-50 (middle aged women MC demographic)

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33
Q

What is the prognosis of localized cervical cancer? Metastatic?

A

Localized: 91.2%
Metastatic: 18.9%

(worse prognosis than breast cancer)

34
Q

MC type of cervical cancer?

A

Squamous cell carcinoma

35
Q

Which virus has a strong association with cervical cancer development?

A

HPV

36
Q

Where does abnormal cell growth arise from in cervical cancer?

A

Squamocolumnar junction

37
Q

Which strands of HPV is cervical cancer most associated with?

A

16 and 18

38
Q

Which strands of HPV are considered more “harmless” (stronger association with genital warts)?

A

6 and 11

39
Q

T or F: the new Gardasil vaccine only covers cancerous strands of HPV.

A

FALSE – new vaccine covers cancerous strains (16, 18) as well as non-cancerous (6, 11) and five other strains of HPV

40
Q

HIV/AIDS and history of transplant make patients who get HPV (more/less) likely to develop HPV associated cervical cancer

A

More

41
Q

How does HPV lead to cervical cancer?

A

Persistent HPV infection causes CD4 and CD8 dysfunction –> impaired immune response –> cervical dysplasia (aka CIN)

42
Q

T or F: Anyone who has had HPV will get cervical cancer

A

FALSE – cervical cancer requires PERSISTENT HPV INFECTIONS to develop

43
Q

What does E6 do?

A

Stops p53 from repairing mutated DNA

44
Q

What does E7 do?

A

Inhibits production of Rb (Rb is a tumor suppressor) and promotes cell cycle progression

THINK: 7 URB (sounds like 7 up)

45
Q

What is the result of E6 and E7 being produced during HPV infection?

A

Unregulated cell cycle progression (no DNA repair or apoptosis without p53)

46
Q

Normal functions of p53

A

DNA repair
Cell cycle arrest
Apoptosis

47
Q

Cervical cancer results in a ____ of normal p53 functions

A

Loss

48
Q

CIN classification

A

CIN 1 = mild (< 1/3 involved)
CIN 2 = moderate
CIN 3 = severe or carcinoma in situ (appearance: loss of cytoplasm)

49
Q

Normally the endocervix has _____ cells and the ectocervix has ________ cells

A

Endo = glandular (columnar) cells
Ecto = squamous cells

50
Q

In cervical cancer, ______ cells migrate into the SCJ and are abnormally located in the ectocervix.

A

Glandular

51
Q

Most likely location of lymphatic spread for cervical cancer

A

Parametrial and paracervical nodes

52
Q

Most likely locations of hematogenous spread for cervical cancer

A

Lungs
Liver
Bone
Ovaries

53
Q

Median age at diagnosis for endometrial cancer

A

60s – most cases are POSTMENOPAUSAL!

54
Q

Prognosis for localized endometrial cancer? Metastatic?

A

Localized: 81%
Metastatic: 18%

2nd worst prognosis of the gynecologic malignancies

55
Q

Endometrial cancer risk factors

A

Obesity
PCOS
Increased estrogen exposure: estrogen treatments, i.e. tamoxifen, early menarche, late menopause, nulliparity)
Older age

56
Q

MC initial presentation of endometrial cancer

A

Abnormal vaginal bleeding –> get endometrial biopsy ASAP to r/o endometrial cancer

57
Q

T or F: Pap smear is not an effective screening tool for endometrial cancer

A

True

58
Q

Endometrial cancer findings on US

A

Thickened endometrial stripe (> 11 mm)

59
Q

Genetic abnormalities associated with endometrial cancer

A

Ras, PTEN and p53 mutations

60
Q

_____ mutation is associated with large, high grade tumors in endometrial cancer

A

p53

61
Q

Endometrial cancer can be classified as _______ dependent or independent

A

Estrogen

62
Q

Types of estrogen dependent endometrial cancer

A

Endometroid adenocarcinoma (MC)
Endometroid with squamous differentiation
Villoglandular
Secretory
Papillary serous

63
Q

Endometroid is composed _____ differentiated, glandular elements

A

Well (as opposed to poorly)

64
Q

Is estrogen dependent or independent endometrial cancer more common?

A

Estrogen dependent

65
Q

Characteristics of estrogen independent endometrial cancer

A

Associated with p53 and HER2 mutations
High grade
More aggressive histology

66
Q

Leiomyosarcoma

A

Malignant proliferation of a monoclonal tumor of myometrial smooth muscle

Arises DE NOVO, not from a lesion or leimyomas

67
Q

Ovarian cancer median age at diagnosis

A

63

68
Q

Ovarian cancer prognosis if localized? Metastatic?

A

Localized: 50.8%
Metastatic: 31.5%

WORST PROGNOSIS OF ALL GYNECOLOGIC MALIGNANCIES!

69
Q

Etiology of ovarian cancer?

A

Not fully understood, majority of cases considered sporadic

70
Q

Ovarian cancer risk factors

A

Increased number of menstrual cycles (nulliparity, early menarche, late menopause)
Increasing age
Obesity
Family history of ovarian, breast, prostate or pancreatic cancer
Ethnicity: Eastern European, Ashkenazi Jewish

71
Q

Major variants of ovarian cancer

A

Epithelial
Sex cord/germ cells

72
Q

MC variant of ovarian cancer

A

Epithelial

73
Q

Mutations associated with ovarian cancer

A

K-ras (oncogene)
p53
BRCA
HER2/neu overexpression (POOR prognosis)

74
Q

MC type of epithelial ovarian cancer?

A

Serous adenocarcinoma

75
Q

T or F: Direct invasion is possible in ovarian cancer

A

TRUE – goes into uterus, sigmoid/rectum and uterine tubes

76
Q

What is exfoliation in terms of tumor behavior?

A

Shedding tumor cells into adjacent body cavities –> tumor able to penetrate the peritoneum

77
Q

What is omental caking?

A

Abdominal metastases implant on surfaces without deep implantation

78
Q

Lymph nodes involved in spread of ovarian cancer?

A

Para-aortic
Iliac and obturator
RARELY the inguinal nodes

79
Q

Which gynecologic malignancy is associated with local spread into the bladder leading to possible postrenal AKI?

A

Cervical cancer
THINK: Cervix cant piss

80
Q

In what age group are germ cord ovarian tumors more common?

A

Women of reproductive age (15-30)

81
Q

MC type of breast cancer?

A

Invasive ductal carcinoma

82
Q

MC type of ovarian cancer?

A

Serous adenocarcinoma

Physiology (4 decks)

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