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Path - Histopath > Gynae pathology > Flashcards

Gynae pathology Flashcards

1
Q

what is the causative organism in BV? type of organism?

A

Gardnerella vaginalis

gram negative bacillus, non-spore-forming, nonmotile coccobacilli

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2
Q

list the adverse effects of mycoplasma genitalium?

A

causes miscarriage and chorioamnionitis

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3
Q

what are the routes of PID infection and which organisms are implciated in each?

A

From STI -
Chlamydia, gonorrhoea:
starts from the lower genital tract LGT and spreads upward via mucosal surface

From Abortion -
Staph, stept, coliform bacteria and clostridium perfringe:
– usually start from the uterus and spread by lymphatics and blood vessels upwards
– deep tissue layer involvement

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4
Q

list some complications of PID?

A
  • Peritonitis - with spread to peritoneum
  • Intestinal obstruction due to adhesions
  • Bacteremia
  • Infertility
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5
Q

how does salpingitis usually occur?

prognosis & complications?

A

Usually direct ascent from the vagina

can resolve
Complications:

  • Adhesions to ovary
  • Tubo-ovarian abscess • Peritonitis
  • Hydrosalpinx
  • Infertility
  • Ectopic pregnancy
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6
Q

which is the 2nd most common cancer affecting women worldwide

A

cervical cancer

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7
Q

what is the pre-malignant phase of cervical cancer?

A

cervical intraepithelial neoplasia

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8
Q

apart from HPV, what are the other causes of cervical cancer?

A

5%:

  • Many sexual partners
  • Sexually active early
  • Smoking
  • Immunosuppressive disorders
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9
Q

what are the presentations of low and high risk HPVs?

A

Low: oral and genital warts
- low grade lesions only

High: cancers - cervical mainly but anal, vaginal, vulval and penile cancers too
- low and high grade lesions

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10
Q

what are the most common High Risk HPVs?

A

HPV 16 & 18 -> cervical cancer

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11
Q

what are the most common Low Risk HPVs?

A

HPV 6 & 11

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12
Q

describe the Disease progression from HPV infection to CIN? what comes after this?

A

after infecton with HPV, abnormal cells develop.

this can develop to CIN 1 -> 2 -> 3 (mild, mod, severe)

after decades from first HPV infection, carcinoma (dyskaryosis) can occur after CIN 3

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13
Q

which are the High and Low-grade squamous intraepithelial lesions (LSILs)

A

Low:
Abnormal cells
CIN 1

High:
CIN 2,3

carcinoma is NOT an SIL

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14
Q

what is CGIN?

A

Cervical Glandular Intra-epithelial Neoplasia

squamous epithelial involvement is more common than this subtype

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15
Q

what defines the change from CIN -> invasive carcinoma?

A

Invasion through the basement membrane

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16
Q

What is hpv infection like in the general population of women? why?

A

one study showed that most women are exposed to HPV at some point in life

immune system fight off in most cases - no signs withinn 2 years

repeat infection with high risk subtypes can lead to pre-malignant changes

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17
Q

How does HPV transform cells ??

A

Virus Two proteins E6 and E7

These inactivate two tumour suppressor genes:

E7 - Retinoblastoma gene (Rb)
E6 - P53

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18
Q

What are the 2 distinct biological states of HPV infection?

A
  1. Non productive or latent infection
    - cellular effects of HPV infection are not seen
    - can only detect infection via molecular methods
  2. Productive viral infection
    -Viral DNA replication occurs independently of host
    chromosomal DNA synthesis
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19
Q

how does Hybrid Capture II (HC2) HPV DNA Test work?

A

kind of like FISH:

contains long Synthetic nucleic acids/ RNA with fluorescent markers

theese bind to hpv dna

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20
Q

which are the current HPV vaccines?

what do they protect against?

A
  1. Cervarix
    - Bivalent. HPV 16, 18
    - Vaccine intervals: 0, 1, 6 months
  2. Gardasil
    - Quadrivalent. HPV 6, 11, 16, 18
    - 0, 2, 6 months
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21
Q

what advice to give to a woman about gettin the vaccine?

A

not therapeutic - > won’t change incidence if have already been infected b4

you can still contract HPV infection - just the less dangerous subtypes. 75% protection

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22
Q

the endometrium has which cell types?

A

glands and stroma

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23
Q

list some causes for endometrial hyperplasia?

A

persistent estrogen exposure state:

Perimenopausal
Persistent anovulation
Polycystic ovary (PCO)

Granulosa cell tumours ovary
unopposed Estrogen therapy (alone)

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24
Q

what are the types of ewndometrial cancer? origins?

A

Type I: 80-85%
 Endometrioid, mucinous and secretory adenocarcinomas
 Younger age
 oestrogen dependent
 Often associated with atypical endometrial hyperplasia
 Low grade tumours, superficially invasive

Type II: 10-15%
 Serous and clear cell carcinomas
 Older, postmenopausal
 Less oestrogen dependent
 Arise in atrophic endometrium
 High grade ,deeper invasion,higher stage
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25
Q

what are the gentics of type I endometrial carcinoma?

A

Require 4 mutations from the following:

  • PTEN (10q23; 37-61%)
  • PI3KCA (39%) (mainly codons 9 and 20)
  • K-ras (10-30%)
  • CTNNB1 (14%-44%)
  • FGFR2 (16%)
  • P53 (10%)
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26
Q

what are the gentics of type 2 endometrial carcinoma?

A

Endometrial serous carcinoma
– P53 mutations in 90%
– PI3KCA mutations in 15% Her-2 amplification

• Clearcellcarcinoma
– PTEN mutation
– CTNNB1 mutation
– Her-2 amplification

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27
Q

True or False:

The hormone receptor expression of a tumour is a prognostic factor in endometrial cancer?

A

False

it can indicate likely survival and response to therapy

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28
Q

True or False:

Tumour ploidy affects prognosis in all endometrial tumours

A

True

29
Q

True or False:

Haploid tumours have better prognosis than diploid tumours

A

False

diploid have better prognosis

30
Q

True or False:

The prognosis of endomeetrial caner is determined off 2 factors?

A

False

determined by 4:

grade - 3 grades
stage - 4 stages ; measure of spread
type
ploidy

31
Q

list examples of Gestational trophoblastic disease?

A

– Complete and partial mole
– Invasive mole
– Choriocarcinoma

32
Q

what is thee malignant potential of complete and partial moles?

A

Partial mole - 0% malignant

Complete mole - 2.5% malignant, 10% locally invasive

33
Q

describe the chromosomal origin of a complete hydatidiform mole

A

ALL genetic material from father/sperm - via duplication of genetic material OR dual fertilisation (2 sperm, 1 egg)

egg provides no genetic material

ends up 46XX, 46XY

34
Q

describe the Chromosomal origin of partial hydatidiform mole

A

egg provides genetic material - 23X

Then:
A. 2 sperm fertilise this egg => 69XXY or 69XXX

B. one 46XY sperm fertilise the egg => 69XXY

35
Q

what is the origin and prognosis of choriocarcinoma?

A

cancer of the trophoblast - placenta

It is preceded by:
50% molar pregnancies
then miscarriage
then normal pregnancies

rapiid distant metastises - early haematogenous spread to lungs

responds well to chemo

36
Q

what kind of condition is choriocarcinoma?

A

gestational trophoblastic disease

germ cell tumour - can arise in ovary/testis

37
Q

what is the origin of endometriosis?

A

– Metaplasia of pelvic peritoneum

-> implantation of endometrium

38
Q

retrograde menstraution is viisualised in which condition?

A

endometriosis

39
Q

what is the difference between in situ and ectopic endometrial tissue?

A

Nothing

Ectopic endometrial tissue is functional and bleeds at time of menstruation -> pain, scarring and infertility

can develop hyperplasia and malignancy too

40
Q

what is Adenomyosis?

A

Ectopic endometrial tissue deep within the myometrium

41
Q

list some primary ovarian tumours

A

Surface epithelial
Sex cord stromal
Germ cell

Non-specific:
Sarcomas, Lymphomas

42
Q

What is the most significant risk factor in ovarian caner?

A

genetic predisposition:

• Family history of ovarian and breast cancers

43
Q

which are the most common type of ovarian tumours?

which are the most common MALIGNANT type of ovarian tumours

A

a - epithelial… more specifically SEROUS

b - epithelial

44
Q

what is the epidemiology of germ cell tumours?

A

bimodal distribution ;
one peak 15-21 year olds
one peak at 65-69

45
Q

what are Sex cord-stromal tumors?

epidemiology?

A

a group of tumours derived from the stromal component of the ovary and testis.

In females:

  1. Granulosa cell tumours
  2. Sertoli–Leydig cell tumours - testosterone producing ovarian tumour
  3. Thecal cell tumours - thecomas
  4. Fibromas
    epidemiology: post menopause
46
Q

Which tumour presents as following:

  • Usually present as large stage I tumours
  • Mutations in K-ras, BRAF, PI3KCA and HER2, PTEN and beta– catenin
  • Arise from have precursors; eg endometriosis
  • Include low grade serous, low grade endometrioid, mucinous and tentatively Clear cell carcinoma.
A

Type 1 ovarian tumour

47
Q

characterise type 2 ovarian carcinoma; eg causing mutations etc

A

High grade mostly of serous type
• Aggressive
• More than 75% have p53 mutations
• No precursor lesions

48
Q

Brenner tumour is an example of a ?

A

benign ovarian tumour

49
Q

borderline tumours are precursors for?

A

Type 1 ovarian tumour

50
Q

true/false:

there are very reliable histological and molecular predictive markers for the behaviour of Bordeline ovarian tumours?

A

False!

cant predict behaviour with anything!

51
Q

true/false:

borderline tumours invade

A

false

52
Q

Benign tumours are lined by ______ ?

A

bland epithelium

53
Q

ovarian Endometrioid Tumours are derived from ____?

A
  1. surface epithelium of ovary (80%)

2. endometriosis (10-20%)

54
Q

which of the follwoing thas the best prognosis:

serous, mucinous, endometroid ovarian tumour?

A

endometriod

55
Q

which ovarian tumour has the strongest association with endometriosis?

A

clear cell carcinoma

56
Q

most prevalent mutation in clear cell carcinoma?

A

PIK3Ca

57
Q

most prevalent mutation in mucinous carcinoma?

A

K-Ras

58
Q

P53 is most prevalent mutation in?

A

Endometrioid carcinoma

High grade serous carcinoma

59
Q

which tumour produces Teeth and hair?

why?

A

Gerrm cell tumour: mature teratoma - Dermoid

Benign

differentiates into adult type tissues

60
Q

characteristiics of Immature teratoma?

A

embryonic elements so:

fast growing
Mets to lymph nodes, lung, liver and other organs

61
Q

Mature cystic teratoma with malignant transformation usually becomes what?

A

SCC - squamous cell carcinoma?

62
Q

tumours with bilateral metastases composed of mucin producing signet ring cells - pathognomic of?

origin?

A

Krukenberg tumours

these metastises to ovaries

gastric origin or beast

63
Q

Papillary Hidradenoma presents where?

A

benign tumour of vulva

64
Q

thee following are which type of malignancy in the vulva:

  • HPV or lichen sclerosus
  • VIN: vulval intraepithelial neoplasia
A

SCC - squamous cell carcinoma

65
Q

HNPCC puts you at risk of which ovarian cancers?

A

1st - Endometroid carcinoma

2nd - mucinous tumours

66
Q

ovarian cancer at age <30 years may be more likely to be due to ___?

A

HNPCC mutations rather than BRCA 1/2!

67
Q

> 90% BRCA1 carrier ovarian cancers are of what histology?

A

serous cystadenocarcinoma

68
Q

thee following gamilial ovarian cancers have which inheritance pattern:

familial breast-ovarian cancer syndrome
site-specific ovarian cancer
cancer family syndrome (Lynch type II)

A

autosomal dominant

Path - Histopath (21 decks)

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