Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Semester 4 > Repro Session 12 > Flashcards

Repro Session 12 Flashcards

1
Q

What are almost all cases of cervical cancer related to?

A

High risk HPV strains 16 and 18

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the pathogenesis of CIN and cervical carcinoma from HPV infection.

A

Infection of immature metaplastic squamous cells in transformational zone –> production of viral proteins in E6&7 –> inability to repair damaged DNA and inhibited apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the risk factors for cervical carcinoma associated with increased risk of HPV infection?

A

Sexual intercourse, early 1st marriage, early 1st pregnancy, multiple births, multiple partners, promiscuous partner, long-term use of OCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the risk factors for cervical carcinoma associated with the immune response to HPV infection?

A

Low SES class, smoking, immunosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why does having a partner with carcinoma of the penis increase the risk of developing cervical carcinoma?

A

Associated with HPV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is cervical intraepithelial neoplasia?

A

Dysplasia of squamous cells within the cervical epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the progression of CIN.

A

Starts as CINI, most of which spontaneously regress but some develop into CINII and CINIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the treatment options for the 3 stages of CIN?

A

I: follow-up +/- cryotherapy

II and III: superficial excision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How long does the progression of CIN typically take?

A

7 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the outcomes of CINIII?

A

30% regress, 10% progress to invasive carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does cervical carcinoma present?

A

~45% as screening abnormality or postcoital/intermenstrual/postmenopausal vaginal bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the distribution of types of cervical carcinoma?

A

80% SCC, 15% adenocarcinomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does cervical carcinoma of either type spread?

A

Locally by invasion to paracervical soft tissues, bladder, ureters, rectum, vagina; via lymph to paracervical, pelvic or para-aortic nodes; distally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the treatment for microinvasive cervical carcinoma?

A

Cervical cone excision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the 5-year survival rate for treated microinvasive cervical carcinoma?

A

100%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the treatment for invasive cervical carcinoma?

A

Hysterectomy +/- lymph node dissection, radiation, chemotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the 10-year survival rate for treated invasive cervical carcinoma?

A

62%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What frequently precedes endometrial adenocarcinoma?

A

Endometrial hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What changes are seen in endometrial hyperplasia?

A

Increase in gland:stroma ratio +/- abnormal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is endometrial hyperplasia associated with?

A

Prolonged oestrogen stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are risk factors for endometrial adenocarcinoma?

A

Anovulation, excess adipose tissue, OCP use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the treatment options for endometrial hyperplasia?

A

Simple: monitor

Complex/atypical/symptomatic: hysterectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the most common invasive cancer of the female genital tract?

A

Endometrial adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When does endometrial adenocarcinoma usually present?

A

55-75 y.o.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does endometrial adenocarcinoma typically present?

A

With irregular or postmenopausal vaginal bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Why does endometrial adenocarcinoma have a high 10-year survival rate?

A

Early symptoms are alarming so pts present early

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the two type of endometrial adenocarcinoma?

A

Endometrioid and serous carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the differences between the two type of endometrial adenocarcinoma?

A

Endometrioid: more common, mimics proliferative glands

Serous carcinoma: less common, poorly differentiated, aggressive with a worse prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How does endometrioid endometrial adenocarcinoma spread?

A

Myometrial invasion, direct extension to adjacent structures, local lymph nodes and distant sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How does serous carcinoma endometrial adenocarcinoma spread?

A

Tumour cells exfoliate and travel through Fallopian tubes where they can implant on peritoneal surfaces and cause death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Why is cervical carcinoma suitable for screening?

A

High incidence, simple and easy test, slow progression from identifiable precursor lesion and has a curative treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How is cervical carcinoma screening carried out?

A

Cells from transformational zone are scraped, stained with Papanicalou stain and examined by microscopy to look for dyskaryosis. Followed by colposcopy/biopsy if needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Why are molecular methods of cervical cancer screening not currently used?

A

Test for HPV in cervical cells is not available for all high risk types

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Why is cervical carcinoma screening required when there is an effective HPV vaccine in routine use?

A

Vaccine only protects for 10 years and is not effective against all high-risk types

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Who is invited for cervical carcinoma screening?

A

25-50 y.o. Females 3-yearly

50-65 y.o. Females 5-yearly (unless abnormal result)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is leiomyoma?

A

Benign tumour of smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the S/S of leiomyoma of the myometrium?

A

Asymptomatic or heavy/painful periods, urinary frequency, infertility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Do leiomyomas of the myometrium undergo malignant transformation?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How does leiomyoma of the myometrium appear macroscopically?

A

Well circumscribed, round, firm and whitish

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How does leiomyoma of the myometrium appear microscopically?

A

Well differentiated, appearing as normal smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is uterine leiomyosarcoma?

A

Uncommon tumour presenting at 40-60 y.o. and is highly malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Where does leiomyosarcoma metastasise to early in its disease process?

A

Lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Is uterine leiomyosarcoma associated with leiomyoma?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the treatment for leiomyosarcoma?

A

Total abdominal hysterectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Are the majority of ovarian tumours benign or malignant?

A

~80% benign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

At what age do benign ovarian tumours tend to present?

A

20-45 y.o.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

At what age do malignant ovarian tumours tend to present?

A

45-65 y.o.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Why is the prognosis of malignant ovarian tumours poor?

A

Often spread beyond ovary by the time of presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Where do malignant ovarian tumours spread before presentation?

A

50% to opposite ovary, liver, lungs, regional lymph nodes

50
Q

What are the S/S of non-functional ovarian tumours?

A

Abdominal pain, abdominal distension, urinary and GI S/S, ascites

51
Q

What are the S/S of non-functional ovarian tumours due to?

A

Invasion/metastases

52
Q

What are the S/S of functional ovarian tumours?

A

Mestrual disturbances, inappropriate sex hormones

53
Q

When is prophylactic salpingoophorectomy indicated in ovarian tumours?

A

Gene analysis positive for BRCA mutation

54
Q

What serum marker can be used for ovarian tumours?

A

CA-125

55
Q

What are the four cell origins of ovarian tumours?

A

Müllerian epithelium, germ cells, sex-cord stromal cells and metastases

56
Q

What are the 3 main histological types of Müllerian epithelial ovarian tumours?

A

Serous, mucinous, endometrioid

57
Q

How can all types of Müllerian epithelium ovarian tumour be classified?

A

Benign, borderline or malignant

58
Q

What are the risk factors for Müllerian epithelium ovarian tumours?

A

Nulliparity, low parity, BRCA1&2, smoking, endometriosis

59
Q

What is the consequence of serous Müllerian epithelium ovarian tumours being friable and fragile?

A

Often exfoliate and spread to peritoneal surfaces causing ascites

60
Q

How do mucinous Müllerian epithelium ovarian tumours appear macroscopically?

A

Large cystic masses filled with sticky fluid

61
Q

How are most mucinous Müllerian epithelium ovarian tumours classified?

A

Benign/borderline

62
Q

How can mucinous and endometrioid Müllerian epithelium ovarian tumours be differentiated microscopically?

A

Mucinous have glands with goblet cells, endometrioid have tubular glands resembling endometrial glands

63
Q

What is pseudomyxoma peritonei?

A

Exfoliation and invasion of tumour cells (commonly appendix) with epithelial implantation in the ovaries or peritoneal surfaces –> intestinal obstruction and mucinous ascites

64
Q

What are endometrioid ovarian tumours seen in 15-20% of cases of?

A

Endometriosis

65
Q

What associated condition do 15-30% of endometrioid ovarian tumours have simultaneously?

A

Endometrial endometrioid adenocarcinoma

66
Q

What are the 3 groups of ovarian germ cell tumours?

A

Mature (benign), immature (malignant), monodermal (highly specialised)

67
Q

What are the majority of germ cell ovarian tumours?

A

Benign cystic teratomas with many tissue types

68
Q

Who are germ cell ovarian tumours typically seen in?

A

Young women

69
Q

What is non-gestational choriocarcinoma?

A

Malignant ovarian germ cell tumour that is aggressive and fatal

70
Q

What do non-gestational choriocarcinoma secrete?

A

hCG

71
Q

What do yolk-sac tumours secrete?

A

Alpha-fetoprotein

72
Q

What type of tumours are yolk sac tumours?

A

Malignant ovarian germ cell

73
Q

What is stroma ovarii?

A

Monodermal ovarian germ cell tumour of benign functioning thyroid tissue

74
Q

What is the name of the malignant monodermal ovarian germ cell tumour that secretes 5HT?

A

Carcinoid

75
Q

How do carcinoid ovarian tumours lead to carcinoid syndrome?

A

Release 5HT that is not rapidly metabolised by the liver due to the venous drainage of the ovary

76
Q

Which cells can sex-cord stromal ovarian tumours resemble?

A

Sertoli, Leydig, granulosa, theca

77
Q

Who do granulosa cell ovarian tumours present in?

A

Post-menopausal women

78
Q

What are the effects of a granulosa cell tumour in a pre-pubertal girl?

A

Precocious puberty

79
Q

What are the effects of a granulosa cell tumour in an adult woman?

A

Endometrial hyperplasia and carcinoma, breast disease

80
Q

What is the peak incidence of of Sertoli-Leydig cell tumours?

A

Teens/20s

81
Q

What are the effects of Sertoli-Leydig cell tumours?

A

Delayed puberty, defeminisation, masculinisation inc breast atrophy, sterility, hair loss, hisutism, clitoral hypertrophy

82
Q

What are the most common origins of ovarian metastases?

A

Müllerian tumours from the uterus, Fallopian tubes, contralateral ovary, pelvis or peritoneum

83
Q

What non-Müllerian tumour metastases are seen in the ovaries?

A

GI tumours or lobular breast tumours

84
Q

What is a Krukenberg tumour?

A

Often bilateral metastatic GI tumour (usually stomach) within the ovaries

85
Q

How does a tumour in the stomach become a Krukenberg tumour?

A

Erodes through stomach wall, cells exfoliate and undergo trasceolomic spread

86
Q

Describe the epidemiology of vulval tumours.

A

Uncommon, ~3% of female genital tumours with 2/3 of pts >60 y.o.

87
Q

What are the types of vulval tumour?

A

Squamous cells carcinoma, basal cell carcinoma, extra mammary Paget’s disease, malignant melanoma

88
Q

What is the precursor to SCC of the vulva?

A

Vulvular intraepithelial neoplasia (VIN)

89
Q

What is VIN?

A

In situ precursor of SCC of the vulva with atypical squamous cells within the epidermis

90
Q

How is VIN identified macroscopically?

A

White patches on non-keratinised skin and brown patches on keratinised skin

91
Q

If SCC of the vulva presents in the 6th decade what is the likely association?

A

HPV

92
Q

Are the majority of vulval SCCs related to HPV?

A

No, ~70% unrelated

93
Q

Do vulval SSCs not related to HPV tend to present earlier or later than those that are related?

A

Later

94
Q

What risk factors are associated with non-HPV related vulval SSC?

A

Longstanding inflammatory and hyperplastic conditions of the vilva e.g. Lichen sclerosus

95
Q

What is lichen sclerosus?

A

Band of chronic inflammation above the BM leaves a sclerotic band of tissue. Autoimmune

96
Q

How do vulval SSCs spread initially?

A

Via lymph to inguinal, pelvic, iliac and para-aortic nodes

97
Q

Where can SCCs of the vulva spread outside of the lymphatic system?

A

Lungs and liver

98
Q

What treatment of vulval SCC gives 90% 5-year survival?

A

Vulvectomy and lymphadenectomy

99
Q

What is the most common site of extra-mammary Paget’s disease?

A

Vulva

100
Q

Describe extra mammary Paget’s disease of the vulva.

A

Itchy, red, scaly plaques in areas rich in apocrine glands

101
Q

What are tumours of gestation?

A

Tumours and tumour-like conditions that show proliferation of placental tissue

102
Q

What types of tissue may proliferate in gestational tumours?

A

Villous and /or trophoblastic

103
Q

Describe the pathogenesis of hyaditiform mole.

A

Cystic swelling of chorionic villi and trophoblastic proliferation creates a friable mass of thin-walled, translucent grape-like structures

104
Q

Who are the highest risk age groups for hyaditiform mole?

A

Teenagers and 40-50 y.o.

105
Q

How are hyaditiform moles usually diagnosed?

A

In early pregnancy by US or presenting as a miscarriage

106
Q

What other gestational tumours are hyaditiform moles associated with that are more aggressive and have a poorer prognosis?

A

Invasive mole and choriocarcinoma

107
Q

What is a complete hyaditiform mole?

A

Sperm fertilises an empty ovum that undergoes implantation to form a disorganised mass of trophoblast cells with no foetal tissue

108
Q

What is a partial hyaditiform mole?

A

2 spermatid fertilise 1 ovum so there is too much DNA and too much trophoblast resulting in trophoblast growth overtaking foetal tissue development resulting in a lack of foetal development

109
Q

How are hyaditiform moles managed?

A

Curettage and hCG monitoring

110
Q

What is an invasive mole?

A

Mole that penetrates/peforates the uterine wall

111
Q

Do invasive moles metastasise?

A

No

112
Q

When is a hysterectomy indicated in an invasive mole?

A

If local destruction causes uterine rupture

113
Q

What are the S/S of an invasive mole?

A

Vaginal bleeding, uterine enlargement, persistently high hCG

114
Q

What does persistently high hCG following curettage of hyaditiform mole indicate?

A

Invasive mole

115
Q

What treatment is used for invasive mole if the uterus is not perforated?

A

Chemotherapy

116
Q

How does gestational choriocarcinoma arise?

A

Normal/abnormal pregnancy with no villi present leads to a malignant neoplasm of trophoblastic cells

117
Q

How does gestational choriocarcinoma progress?

A

Rapidly invasive and metastasises widely

118
Q

What treatment does gestational choriocarcinoma respond well to?

A

Chemotherapy

119
Q

Describe the incidence of gestational choriocarcinoma presentations.

A

50% associated with complete moles, 25% after abortion, 22% after normal pregnancy, 3% in ectopic pregnancy

120
Q

What are the S/S of gestational choriocarcinoma?

A

Vaginal spotting, raised hCG

121
Q

What gives gestational choriocarcinoma a high cure rate unlike that seen in non-gestational choriocarcinoma?

A

Uterine evacuation and chemotherapy

Semester 4 (33 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions