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
what are the gentics of type I endometrial carcinoma?
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%)
26
what are the gentics of type 2 endometrial carcinoma?
Endometrial serous carcinoma – P53 mutations in 90% – PI3KCA mutations in 15% Her-2 amplification • Clearcellcarcinoma – PTEN mutation – CTNNB1 mutation – Her-2 amplification
27
True or False: The hormone receptor expression of a tumour is a prognostic factor in endometrial cancer?
False it can indicate likely survival and response to therapy
28
True or False: Tumour ploidy affects prognosis in all endometrial tumours
True
29
True or False: Haploid tumours have better prognosis than diploid tumours
False diploid have better prognosis
30
True or False: The prognosis of endomeetrial caner is determined off 2 factors?
False determined by 4: grade - 3 grades stage - 4 stages ; measure of spread type ploidy
31
list examples of Gestational trophoblastic disease?
– Complete and partial mole – Invasive mole – Choriocarcinoma
32
what is thee malignant potential of complete and partial moles?
Partial mole - 0% malignant Complete mole - 2.5% malignant, 10% locally invasive
33
describe the chromosomal origin of a complete hydatidiform mole
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
describe the Chromosomal origin of partial hydatidiform mole
egg provides genetic material - 23X Then: A. 2 sperm fertilise this egg => 69XXY or 69XXX B. one 46XY sperm fertilise the egg => 69XXY
35
what is the origin and prognosis of choriocarcinoma?
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
what kind of condition is choriocarcinoma?
gestational trophoblastic disease germ cell tumour - can arise in ovary/testis
37
what is the origin of endometriosis?
– Metaplasia of pelvic peritoneum -> implantation of endometrium
38
retrograde menstraution is viisualised in which condition?
endometriosis
39
what is the difference between in situ and ectopic endometrial tissue?
Nothing Ectopic endometrial tissue is functional and bleeds at time of menstruation -> pain, scarring and infertility can develop hyperplasia and malignancy too
40
what is Adenomyosis?
Ectopic endometrial tissue deep within the myometrium
41
list some primary ovarian tumours
Surface epithelial Sex cord stromal Germ cell Non-specific: Sarcomas, Lymphomas
42
What is the most significant risk factor in ovarian caner?
genetic predisposition: • Family history of ovarian and breast cancers
43
which are the most common type of ovarian tumours? which are the most common MALIGNANT type of ovarian tumours
a - epithelial... more specifically SEROUS b - epithelial
44
what is the epidemiology of germ cell tumours?
bimodal distribution ; one peak 15-21 year olds one peak at 65-69
45
what are Sex cord-stromal tumors? epidemiology?
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
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.
Type 1 ovarian tumour
47
characterise type 2 ovarian carcinoma; eg causing mutations etc
High grade mostly of serous type • Aggressive • More than 75% have p53 mutations • No precursor lesions
48
Brenner tumour is an example of a ?
benign ovarian tumour
49
borderline tumours are precursors for?
Type 1 ovarian tumour
50
true/false: there are very reliable histological and molecular predictive markers for the behaviour of Bordeline ovarian tumours?
False! cant predict behaviour with anything!
51
true/false: borderline tumours invade
false
52
Benign tumours are lined by ______ ?
bland epithelium
53
ovarian Endometrioid Tumours are derived from ____?
1. surface epithelium of ovary (80%) | 2. endometriosis (10-20%)
54
which of the follwoing thas the best prognosis: serous, mucinous, endometroid ovarian tumour?
endometriod
55
which ovarian tumour has the strongest association with endometriosis?
clear cell carcinoma
56
most prevalent mutation in clear cell carcinoma?
PIK3Ca
57
most prevalent mutation in mucinous carcinoma?
K-Ras
58
P53 is most prevalent mutation in?
Endometrioid carcinoma High grade serous carcinoma
59
which tumour produces Teeth and hair? why?
Gerrm cell tumour: mature teratoma - Dermoid Benign differentiates into adult type tissues
60
characteristiics of Immature teratoma?
embryonic elements so: fast growing Mets to lymph nodes, lung, liver and other organs
61
Mature cystic teratoma with malignant transformation usually becomes what?
SCC - squamous cell carcinoma?
62
tumours with bilateral metastases composed of mucin producing signet ring cells - pathognomic of? origin?
Krukenberg tumours these metastises to ovaries gastric origin or beast
63
Papillary Hidradenoma presents where?
benign tumour of vulva
64
thee following are which type of malignancy in the vulva: * HPV or lichen sclerosus * VIN: vulval intraepithelial neoplasia
SCC - squamous cell carcinoma
65
HNPCC puts you at risk of which ovarian cancers?
1st - Endometroid carcinoma 2nd - mucinous tumours
66
ovarian cancer at age <30 years may be more likely to be due to ___?
HNPCC mutations rather than BRCA 1/2!
67
>90% BRCA1 carrier ovarian cancers are of what histology?
serous cystadenocarcinoma
68
thee following gamilial ovarian cancers have which inheritance pattern: familial breast-ovarian cancer syndrome site-specific ovarian cancer cancer family syndrome (Lynch type II)
autosomal dominant