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Repro Phys 4 Flashcards

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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
TGF beta ________ cell growth
Inhibits
26
T or F: patients with breast cancer have a disrupted balance of TGF alpha and TGF beta
True
27
T or F: Excess estrogen results in immediate stimulation of mutant cell proliferation
FALSE -- takes several rounds of DNA replication and cell division for the mutant cells to be enough to cause cancerous growths
28
TGF alpha/TGF beta activates cell division
TGF alpha
29
How does the inflammation associated with cancer impact prostaglandin production?
Inflammation INCREASES PGE2 production
30
How does PGE2 interact with aromatase?
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)
31
How does obesity increase the risk of breast cancer
Adipose tissue creates more estrogen (estrone specifically)
32
Median age at diagnosis for cervical cancer
40-50 (middle aged women MC demographic)
33
What is the prognosis of localized cervical cancer? Metastatic?
Localized: 91.2% Metastatic: 18.9% (worse prognosis than breast cancer)
34
MC type of cervical cancer?
Squamous cell carcinoma
35
Which virus has a strong association with cervical cancer development?
HPV
36
Where does abnormal cell growth arise from in cervical cancer?
Squamocolumnar junction
37
Which strands of HPV is cervical cancer most associated with?
16 and 18
38
Which strands of HPV are considered more "harmless" (stronger association with genital warts)?
6 and 11
39
T or F: the new Gardasil vaccine only covers cancerous strands of HPV.
FALSE -- new vaccine covers cancerous strains (16, 18) as well as non-cancerous (6, 11) and five other strains of HPV
40
HIV/AIDS and history of transplant make patients who get HPV (more/less) likely to develop HPV associated cervical cancer
More
41
How does HPV lead to cervical cancer?
Persistent HPV infection causes CD4 and CD8 dysfunction --> impaired immune response --> cervical dysplasia (aka CIN)
42
T or F: Anyone who has had HPV will get cervical cancer
FALSE -- cervical cancer requires PERSISTENT HPV INFECTIONS to develop
43
What does E6 do?
Stops p53 from repairing mutated DNA
44
What does E7 do?
Inhibits production of Rb (Rb is a tumor suppressor) and promotes cell cycle progression THINK: 7 URB (sounds like 7 up)
45
What is the result of E6 and E7 being produced during HPV infection?
Unregulated cell cycle progression (no DNA repair or apoptosis without p53)
46
Normal functions of p53
DNA repair Cell cycle arrest Apoptosis
47
Cervical cancer results in a ____ of normal p53 functions
Loss
48
CIN classification
CIN 1 = mild (< 1/3 involved) CIN 2 = moderate CIN 3 = severe or carcinoma in situ (appearance: loss of cytoplasm)
49
Normally the endocervix has _____ cells and the ectocervix has ________ cells
Endo = glandular (columnar) cells Ecto = squamous cells
50
In cervical cancer, ______ cells migrate into the SCJ and are abnormally located in the ectocervix.
Glandular
51
Most likely location of lymphatic spread for cervical cancer
Parametrial and paracervical nodes
52
Most likely locations of hematogenous spread for cervical cancer
Lungs Liver Bone Ovaries
53
Median age at diagnosis for endometrial cancer
60s -- most cases are POSTMENOPAUSAL!
54
Prognosis for localized endometrial cancer? Metastatic?
Localized: 81% Metastatic: 18% 2nd worst prognosis of the gynecologic malignancies
55
Endometrial cancer risk factors
Obesity PCOS Increased estrogen exposure: estrogen treatments, i.e. tamoxifen, early menarche, late menopause, nulliparity) Older age
56
MC initial presentation of endometrial cancer
Abnormal vaginal bleeding --> get endometrial biopsy ASAP to r/o endometrial cancer
57
T or F: Pap smear is not an effective screening tool for endometrial cancer
True
58
Endometrial cancer findings on US
Thickened endometrial stripe (> 11 mm)
59
Genetic abnormalities associated with endometrial cancer
Ras, PTEN and p53 mutations
60
_____ mutation is associated with large, high grade tumors in endometrial cancer
p53
61
Endometrial cancer can be classified as _______ dependent or independent
Estrogen
62
Types of estrogen dependent endometrial cancer
Endometroid adenocarcinoma (MC) Endometroid with squamous differentiation Villoglandular Secretory Papillary serous
63
Endometroid is composed _____ differentiated, glandular elements
Well (as opposed to poorly)
64
Is estrogen dependent or independent endometrial cancer more common?
Estrogen dependent
65
Characteristics of estrogen independent endometrial cancer
Associated with p53 and HER2 mutations High grade More aggressive histology
66
Leiomyosarcoma
Malignant proliferation of a monoclonal tumor of myometrial smooth muscle Arises DE NOVO, not from a lesion or leimyomas
67
Ovarian cancer median age at diagnosis
63
68
Ovarian cancer prognosis if localized? Metastatic?
Localized: 50.8% Metastatic: 31.5% WORST PROGNOSIS OF ALL GYNECOLOGIC MALIGNANCIES!
69
Etiology of ovarian cancer?
Not fully understood, majority of cases considered sporadic
70
Ovarian cancer risk factors
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
Major variants of ovarian cancer
Epithelial Sex cord/germ cells
72
MC variant of ovarian cancer
Epithelial
73
Mutations associated with ovarian cancer
K-ras (oncogene) p53 BRCA HER2/neu overexpression (POOR prognosis)
74
MC type of epithelial ovarian cancer?
Serous adenocarcinoma
75
T or F: Direct invasion is possible in ovarian cancer
TRUE -- goes into uterus, sigmoid/rectum and uterine tubes
76
What is exfoliation in terms of tumor behavior?
Shedding tumor cells into adjacent body cavities --> tumor able to penetrate the peritoneum
77
What is omental caking?
Abdominal metastases implant on surfaces without deep implantation
78
Lymph nodes involved in spread of ovarian cancer?
Para-aortic Iliac and obturator RARELY the inguinal nodes
79
Which gynecologic malignancy is associated with local spread into the bladder leading to possible postrenal AKI?
Cervical cancer THINK: Cervix cant piss
80
In what age group are germ cord ovarian tumors more common?
Women of reproductive age (15-30)
81
MC type of breast cancer?
Invasive ductal carcinoma
82
MC type of ovarian cancer?
Serous adenocarcinoma

Physiology (4 decks)

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