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CP > cervical and vulval pathology > Flashcards

cervical and vulval pathology Flashcards

1
Q

what is intraepithelial neoplasia?

A

it is a neoplastic change in the epithelium which is not yet invasive and almost all have the same aetiology which is HPV

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2
Q

what is the most common type of intraepithelial neoplasia?

A

cervical lintraepithelial neoplasia which is slightly lower down than cervical glandular intraepithelial neoplasm and it is a squamous epithelium type

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3
Q

what is dyplasia?

A

it is the earliest morpholigcal change of the multistage process of neoplasia and it a cytological feature of malignancy but is not invasive - it is in situ. Normal epithelium becomes neoplastic in dysplasia

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4
Q

what are the curatives for dysplasia?

A

removal - there is a high chance of progression and invasion if left

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5
Q

how do squamous cells reach the top?

A

they start as basal cells at the bottom and then mature, flatten on the surface

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6
Q

what are the stages of nuclei changes in dysplasia?

A

there is the first stage which is the enlargement of nuclei - to make nucleoli
the second stag is when the changes extend to the middle with mitosis and nuclear ratios becoming larger and then at the third stage there is hardly any maturation and the nucleoli are very large

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7
Q

what is the purpose of the cervical screening programme?

A

recognition of dysplastic changes giving us a chance to treat a potentially fatal disease before it arises as the abnormal cells have not yet acquired the ability for invasion so cannot spread - catch at CiN 1, 2 or 3

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8
Q

when does dysplasia become invasive?

A

when it breaches a membrane

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9
Q

what is HPV?

A

it is a double stranded DNA virus that has a 7,9kb circular genome and over 200 subtypes - not all are oncogenic but depends on the DNA sequence. Different types will affect different tissues and genital HPVs have low and high risk types. In most women the HPV is cleared by the immune system and poses no long term threat.

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10
Q

how are HPVs transmitted?

A

sexually - they can cross mucous membranes

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11
Q

what other cancers are high risk HPVs associated with?

A

penile intraepithelial neoplasia and squamous cell carcinoma - they are also involved in a subgroup of oral squamous cell carcinomas which have become common in more recent years

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12
Q

what does immunosupression lead to?

A

this can be due to disease or iatrogenic and can lead to extensive and multifocal intraepithlial neoplasia of the lower female genital tract due to poorly controlled HPV infection - smoking is also key in this

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13
Q

how is smoking thought to be a risk factor in cervical epithelium carcinoma?

A

smoking is known to decrease the numbers of APCs in cervical epithelium and therefore may cause local immunosupression

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14
Q

why are most types not seen?

A

they are not transmitted or are vaccinated against

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15
Q

what are low risk HPVs?

A

they are the ones that are associated with genital warts and other low grade cytological abnormalities - 6 and 11

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16
Q

what are high grade HPVs?

A

they are associated with high grade preinvasive and invasive disease and are 16 and 18 which are implicated in around 70% of cervical cancers

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17
Q

what is the prevalence of HPV DNA in cervical cancer?

A

around 99.7% of cervical cancers contain HPV DNA

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18
Q

how may types of HPV are associated with cervical cancer?

A

13 types

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19
Q

what is important to remember with HPV?

A

over 80% of people will get HPV in their lifetime as it lives on the skin, mucosa of the mouth, throat, cervix, vagina, vulva, anus and penis but most people will clear it themselves with natural immunity

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20
Q

what are types of HPV are high grade?

A

31 and 33

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21
Q

what do high and low grade cause?

A

low grade causes lower genital tract warts called condylomata which are benign squamous neoplasms and are very rare in malignant disease, high grade will cause high grade INs and invasive carcinomas

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22
Q

what are the two types of HPV vaccination?

A

cervarix which covers HPV 16 and 18 and gardasil which covers 6,11, 16, 18 and they are given for two doses as a baby or three after the age of 15

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23
Q

why are boys now also given the HPV vaccination?

A

to increase herd immunity and to reduce genital warts, anal and penile cancers, head and neck and oropharyngeal cancers

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24
Q

what are early and late genes?

A

early genes are the ones that are expressed at the onset of infection and control viral replication and on oncogenic viruses involved in cell transformation the late genes are the ones that code capside proteins

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25
Q

what are ORFs?

A

open reading frames - E6 and 7 are main ones targetted

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26
Q

how do HPVs work?

A

they integrate into the host genome and give the upregulation of E6, and 7 expression. The E 6 will then bind to and inactivate p53 which usually destroys mutated genes and the E7 beings the retinoblastoma proteins that are usually TSGs therefore there is an accumulation of cells that are neoplastic

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27
Q

what is the function of the p53 gene?

A

it mediated apoptosis in response to DNA damage - there is accumulations of genetic damage

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28
Q

what is the function of the RB1 gene?

A

it is a TSG that controls the G1/S cell cycle checkpoints - there is dysregulation of cell proliferation

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29
Q

where is cervical pathology higher?

A

in less developed countries

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30
Q

what is the anatomy of the cervix?

A

there is an endocervical canal which contains glandular crypts, external os is where the glandular epithelium changes to squamous and the ectocervix is lined with squamous.

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31
Q

what happens when menstruation starts?

A

the endocervical canal extends out and squamocolumnnar junction will no longer lie under the external os

32
Q

what area is susceptible to metaplastic change?

A

it changes to squamous epithelium and the endocervical canal is susceptible. It is an area of intraepithelial neoplasia and is where the smear test is. It is harder in post menopausal women as it pushes bacl into the canal

33
Q

what is the transformation zone?

A

it is the physiological area of squamous metaplasia - changes from glandular - these are taller cells

34
Q

what type of carcinoma is adenocarcinoma?

A

glandular

35
Q

where is cervical cancers the most common?

A

where the patients have not been to smear test and therefore do not have a CIN3 treated

36
Q

what is cervical intraepithelial neoplasm?

A

it is a low grade change that is unlikely to become invasive - only really occurs in those who smokse, use immunosupressants and other STIs and they are graded according to their abnormality - these are picked up in the cervical smear test

37
Q

what are the persistence, regression, progression and invasion features of CIN1,2 and 3?

A

CNI: regression: 60%, persistence - 30%, progression to CNIII - 10% and invasion - 1%
CIN2 - regression - 40%, persistence 40%, progression 10% and invasion 5%
CIN3 - regression - 33%, persistence 56% and invasion - 20-70%

38
Q

what is the issue with cervical screening?

A

the rate of cancer would be 50% higher if did not screen, there was a hope that 2/3 women less than 30 would be prevented if there was a 80% uptake however 1 in 4 women do not attend of the 5 million invited per year

39
Q

what is the frequency of screening?

A

the first invitation is at 25 years, and then from 25-39 is every three years. From 50-64 it is every 5 years and then not done past this unless not screened since 50 or there are recent abnormal signs

40
Q

why are the screens not done before 25?

A

there is no substantial evidence, can have obstetric consequences, there can be reactive changes which produce confusing cytology and there is a high HPV rate including high risk types but up to 80% will be cleared

41
Q

what is dyskaryosis?

A

it is abnormal nuclear changes and refers to the abnormal epithelial cells that are found in samples

42
Q

what will be found in cytology for screening?

A

if normal will have small nuclei and then will start with mild changes, there will be a viral halo around the nucleus if there is HPV present and then irregular changes and dyskaryosis with little cytoplasm

43
Q

what is the first line investigation of HPV?

A

high risk HPV testing and this replaced liquid based cytology

44
Q

what are the benefits of LBC?

A

it is automated screening, less false negatives and saves time

45
Q

how are smear tests dealt with?

A

HPV primary triage - high risk HPV are referred and the absence of this is ignored and goes for normal recall

46
Q

what are the outcomes of smear tests?

A

there will be:
no dyskaryosis - normal recall
borderline nuclear change and low grade dyskaryosis - HPV testing - if positive then refer for colposcopy and treatment
there may high grade dyskaryosis or malignancies which will go straight to referral and treatment stage

47
Q

what is the treatment following colposcopy?

A

large loop excision of the transformation zone or resection under local anasethetic and diathermy loop
pathohistological exam after to direct further treatment

48
Q

what is colposcopy?

A

examination of the cervix with a low powered stereoscopic microscope - cervix painted with acetic acid which will highlight potentially abnormal epithelium which can be resected

49
Q

what is the most important causative agent and risk factors for cervical squamous cell carcinoma?

A

high risk HPV is the most important causative factor but risk factors are smoking, immunosupression, male partner with lots of other partners, lots of sexual partners, high parity, low socioeconomic group and young age at first intercourse

50
Q

how will a cervical squamous cell carcinoma present?

A

commonly bleed, produce discharge and if late then signs and symptoms due to local spread such as urinary changes and hydronephrosis due to the effect on the ureter

51
Q

what is seen in cervical squamous cell carcinoma?

A

early invasion

52
Q

what are the similarities between cervical adenocarcinoma and SCC?

A

the presentation and spread, causative agent and treatment is the same

53
Q

what is the difficulty with CA?

A

it is agressive treatment due to radio resistance and poor prognosis

54
Q

what is the precursor for CA?

A

cervical glandular intraepithelial neoplasm

55
Q

how will glandular appear?

A

splattered - there will be stratification no basic orientation and less cytoplasm

56
Q

what is the treatment of cervical carcinoma?

A

LOOP excision at stage 1, at stage 2 there is chemo and radiotherapy and at stage 3 may just be palliative, specifically if has spread to neighbouring organs

57
Q

what is the FIGO staging for cervical carcinoma?

A

I - confined to the cervix
2 - invades beyond uterus but not to the pelvic wall
3 - extends to the pelvic wall and lower 1/3 vagina and uterus producing hydronephrosis
4 - invades to bladder, rectum or outside pelvis

58
Q

what are the metastasis for cervical carcinoma?

A

it is predictable through the pelvic and para-aortic lymph nodes and spreads through the blood to lungs and the bone

59
Q

what is the clinical presentation of cervical carcinoma?

A

warty white patches, or pigmented patches that are visualised by painting with toluidine blue

60
Q

what are the two classifications of vulvar intraepithelial neoplasms?

A

there is differentiated VIN or classical warty basaloid

61
Q

what are the features of classic?

A

it is graded VIN 1-3 and is related to HPV infection in younger women

62
Q

what are the features of differentiated VIN?

A

it is not graded and not HPV related - it occurs in older women and occurs in chronic dermatoses such as lichen sclerosus

63
Q

what is the behaviour of VIN?

A

35-50% will recur and the positive margins predict this. There is progression to invasive carcinoma in 4-7% that are treated and 87% of those that are not - the invasion is more likely to occur in post menopausal or immunocompromised women and there may be spontaneous regression particular in younger postpartum women

64
Q

what is vulvar squamous cell carcinoma?

A

it is the most common vulval cancer that accounts for around 90% and is associated with VIN or inflammatory dermatoses. It has a poor prognosis for the latter stages and is not as common in the latter stages

65
Q

for the type of VSCC that is associated with VIN, who does this affect?

A

it is in those who are HPV positive and less than 60y/o. It is also associated with lower genital tract neoplasia such as CIN

66
Q

for the type of VSCC that is associated with inflammatory dermatoses, who does this affect?

A

older people over the age of 70 that have lichen sclerosus or lichen planus - in symptomatic sclerosis there is a 15% risk of developing malignancy

67
Q

what is the risk of LN mets in invasion?

A

if the depth of invasion is less than 1mm then it is very rae, for 1-3mm then there is a 10% and for >4mm there is a 40% risk
for less than 1mm there is wide local excision, and for high risk mets there is lymph node sampling and groin node dissection with a sentinel node biopsy

68
Q

what is the result of pagets disease?

A

it accounts for 5% of vulval cancers at a mean age of 80. It results in pruritic, burning eczemtous patches and an in situ adenocarcinoma of the squamous mucosa. It can often recur following an excision

69
Q

what is the issue with pagets?

A

can develop into invasive adenocarcinoma and is 5% of regional malignant disease, it affects the bladder cervix an can be perianal and therefore want to exclude primary rectal carcinoma

70
Q

how does melanoma relate to cervical cancer?

A

it results in 5% of all vulval cancers at the mean age of 50-60. There is local recurrence in 1/3 and can spread to the urethra.

71
Q

what is the mode of spread of melanoma?

A

lymph or haematogenous - the depth of invasion correlates with LN involvement

72
Q

what is an important prognostic factor in melanoma?

A

the invasion

73
Q

how may melanoma present?

A

pigemented or not heavily. Rarely have no pigment at all which is known as amelanotic melanoma

74
Q

what is vulval squamous cell carcinoma associated with?

A

eroded plaques or ulcers, inflammatory dermatoses and VIN

75
Q

where does vulval SCC spread?

A

to the vagina and distal urehtra, ipsilaterally to inguinal LNs and contralateral LNs and deep iliofemoral LNs

CP (38 decks)

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