Female gentila tract histology Flashcards

1
Q

What is cervical cytology and why use it

A

Study of clells from the cervix. Used to reduce incidence of cervical cancer by detecting pre-invasive lesions.

Early detecion ha sproved to decrease mortality from cervical cancer

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2
Q

Who gets cervical screening?

A

All woman aged 25-64 were invited from screening at 3 to 5 yearly intervals depending on their age.

Only for asymtpoamtic. If you have any symptoms you need gynae referral for investiagtions

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3
Q
A
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4
Q

What is the role of cytology

A
  • Cytology is the study of cells and is used to detect abnormalities in cells the cervix that are dyskaryotic or pre-cancerous
  • These changes are graded from borderline to severe dyskaryosis and depending on both persistent of abnormality or severity, women will be referred into colposcopy for further treatment
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5
Q

Role of Colposcopy

A
  • Colposcopy is used to obtain tissue samples of the cells that have been called abnormal on cytology
  • Flood cervix and where the samples need ot be taken from will turn white
  • These samples are graded as Cervical intraepithelial neoplasia and grades range from 1 to 3 depending on their severity
  • Any major discrepancies between the cytology and histology result are discussed as an MDT meeting where patient follow up and treatment are decided.
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6
Q

Liquid based cytology - what is this used for

A
  • Preferred method of sampel colelction, fixation, preparation and screenign in cervical cytology
  • Cells removed from cervix using the “cervex” brush and a 360degree rotation of the cervical os and ectocervix. This is repeated 5time. Previously this was done using aylesbury spatula.
  1. The cells colelcted on the brush ar eplaced immediately into pot of alcohol base dpreservative fluid. This is to prevent “drying out” of the sample which can cause diagnostic problems when screening.
  2. Sample processing - A hologic T5000 fully automated processing machine prepares the samples producing a circular preparation of the cells onto a slide. These are then stained with papaniolau staining technique on a fully automated platform.
  3. HMR 101 form or electornic ICE request to match sample pot and sent to lab. If discrepencies betwene pot and form then not accepted.
  4. Each slide takes 5-12mins to screen
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7
Q
A
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8
Q

WHat do staff look for in screenig of the cervical sample

A

Mostyl all normal but abnroamity indicators are:

  • Increased nuclear/cytoplasmic ratio
  • Irregular nuclea outline
  • Hyperchromasia (darkening) of nuclear chromatin and bi/multi nucleation of cells.
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9
Q

WHta is the only epithelium that repsonds to changes in oestrogen levels during menstrual cycle

A

Cervical epithelium

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10
Q

When does the cervical epithelium achieve full thickness

A
  • Day 14 as oestrogen levels peak and cervicla epitheliuma chieves full thickness. This offers protection against infectiona nd therefore this is “optimal” time ot take the sample.
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11
Q

Negative cells in cervical epithelium

A
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12
Q

What is ectropian in the cervix?

A
  • —When Oestrogen levels are high the cervix “bulks” up and causes the cells from the endocervical canal to evert out over the ectocervix and form a reddened area.
  • —This is known as an ECTROPIAN and is a normal condition.
  • —The cells causing the red area are endocervical cells from the canal.
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13
Q

The hsitolgoy and cytology appearance of endocervical cells

A

Picket fence.

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14
Q

Endocervicals - What happens when ectocervix eposed to acidity of vaginal canal

A
  • —The ectocervix is exposed to the acidity of the vaginal canal.
  • —Because of the fragile nature of endocervical cells, when they are exposed to this acid environment the cells undergo transformation into squamous cells to offer protection . This process is continuous, it is “normal” and is known as squamous metaplasia.
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15
Q

Squamous Metaplasia - how to recognise

A
  • Recognsided by dense opaqu blue cytoplasm and bizarre shapes/forms
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16
Q

Where do endometial cells shed from?

A
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17
Q

Endometrial cells - when are they seen normally

A
  • —Higher in the uterine body we find glandular cells called endometrials.
  • —These cells are seen “normally” at days 1- 14 and days 26-27 of the menstrual cycle it is therefore important for the patient to know the 1st day of her last menstrual period.
  • — If LMP is unknown, the patient is over 40 , and these cells are present they will be treated as suspicious and the patient will be referred for further treatment in gynaecology.
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18
Q

Infections in cervical samples

A
  • ¢All infections produce an excess of white blood cells (usually polymorphs) which can be troublesome when screening.
  • ¢They can obscure the cells and make the sample “inadequate” for interpretation and a repeat test will be requested by the laboratory.
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19
Q

Trichomonas Vaginalis

A

Can infect both men and women and patient spresent with yellow/green foul smelling discharge. It is a parasite and has no link to cervical cancer.

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20
Q

Candida albicans (thrush)

A
  • Yeats infection which occurd mainly in 16-35year old women
  • Hyphae and spores cna be observed whcih stain red
  • Inflammatory changes occur alongside infection
  • Treatable with drugs or cream (canesten)
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21
Q

What ar acitonomyces like organisms/ALO’s?

A
  • —These are related to true bacteria and are found in women using Intra Uterine Contraceptive Devices (IUCD).
  • —They usually appear as dark dense clusters with a central core and filaments protruding from the structure. The filaments aid in their identification.
  • — They are not linked to cervical cancer.
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22
Q

Herpes simplex virus (HSV)

A
  • 2 Types: Type 1 (lips + nose). T2 (genitalia)
  • Sexually transmtited and incurable ]Appears cyologically as large multinucleated cells with dense central cores.
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23
Q

Human Papiloma Virus (HPV)

A
  • —One of the most common infections
  • —It is a viral particle that has 100’s of variants some of which are causative of cervical cancer.
  • —Viral strains 6 ,and 11 are found in low grade lesions and don’t usually progress to cervical cancer, whereas strains 16 and 18, have been found to be present in almost all cervical cancers.
  • Found that repeated an/or prolonged infectionw ith hgih risk HPV can lead to cervical cancer
  • Under certain conditions the virus can invade and interrupt the nromal cell cycle leading to “turning on” of unihibited cells growth with the involvement of oncogenes E6 and E7.
24
Q

HPV screening

A
  • —In March 2012 HPV testing for women who presented with a first occurrence of a low grade abnormality on cytology commenced.
  • —In March 2013 any woman with a low grade abnormality or involved in annual follow up after treatment in Colposcopy were given an HPV test (Test of Cure)
  • —For both of these tests HPV was done as a triage test to routine screening.
  • —From March 2013, women who had previous treatment in Colposcopy and were being followed up with cytology at 12 monthly intervals (for 10 years) were given an HPV test.—If this was positive following an abnormal cytology patients were referred back to Colposcopy for further treatment but if negative they were given a 3 year recall then a normal recall of either 3/5 years depending on their age.
  • —From March 2020 the screening programme for the North East , and Yorkshire area will have fully converted to Primary HRHPV testing.

—The advantages are :

  • —A negative HRHPV result offers more protection for women than a negative cytology sample
  • —The call recall will be longer reducing stress and anxiety for women
  • —HRHPV testing with cytology triage has been found to be much more effective for disease detection in a vaccinated population.
25
Q

HPV Vaccine

A
  • Offers protection against viral strains 6,11,16 & 18. This wa sintroduced in 2006 to all 12-13year old children.
  • —The HPV vaccinated cohort are now starting to be screened in the UK and they will now be vaccinating boys as part of the programme.
  • —In Scotland the results from the vaccinated population have shown a decrease in the incidence of cervical cancer and this has been due to the high uptake of the vaccine by school children.
  • —It has also been found that the vaccinated population are also offering protection from cervical cancer in the non-vaccinated population.
  • ——In some third world countries use of the HPV vaccine has almost eradicated cervical cancer
26
Q

HPV ifnection - strains 6 and 11

A
27
Q

Grading abnormality in squamous cells of cervix

A
  • Mild dyskaryosis
  • Moderate dyskaryosis
  • Severe/?invasive dyskaryosis
  • High grade squamous dyskaryosis
    *
28
Q

Mild dyskaryosis in suqamous cells of cervix

A

¢ slight irregularity in the nuclear membrane

¢ slightly raised nuclear/ cytoplasmic ratio,

¢ chromatin is slightly clumped and hyperchromatic in the nucleus

¢ nucleus occupies 1/3 of the total cell area corresponds to the histological grade CIN 1.

29
Q

Moderate dyskaryosis squamosu cells of cervix

A

¢ more marked irregularity of the nuclear membrane

¢ nuclear /cytoplasmic ratio becomes higher

¢ chromatin clumping is much more pronounced.

¢chromatin very hyperchromatic (dark)

¢the nucleus occupies 2/3rds of the total cell area.

30
Q

Severe/ invasive dyskaryosis ins uqmaosu cells of cervix

A
  • —These cells are more likely to progress to cancer and treatment of such lesions should be carried out within 2 weeks of the cytology report being issued.
  • —Severely dyskaryotic cells which have not invaded through the epithelial basement membrane are still classed as pre-cancerous.
31
Q

High grade squamosu dyskaryosis

A
32
Q

Endocervical adenocarcinoma

A
33
Q

Endometrial and ovarian adenocarcinomas

A
34
Q

Other abnormalities in cervix - carcinomas

A

Extra-uterine carcinomas e,g bowel metastases, snall cell ca and lymphonas.

35
Q

Advantages of screening/vaccination

A
  • —Regular HRHPV testing with cervical cytology triage saves lives.
  • —The screening programme is constantly changing and HPV vaccination is now available for all girls and boys aged 13 years of age.
  • —A catch up vaccination programme is now available for girls aged 18.
  • —HRHPV primary screening will now determine patient treatment and follow up.
  • —HRHPV molecular testing has now been rolled out for use as a primary screening test with cytology triage.
  • —Women will need to be informed prior to their HRHPV test what the test involves and what the results mean
  • —In a fully vaccinated population cervical cancer could be eradicated !
36
Q

Future of HPV

A
  • — HRHPV is /has now been rolled out across England a primary screening tool (full conversion by 2020).
  • ——The service has become automated with fewer samples (approximately 10-15% requiring cytology screening).
  • — Fewer screening staff will be required and the merging of Laboratories has been started to reduce costs and realise savings from economies of scale.
  • — HPV is a molecular test which has changed cervical cytology from a screening to a diagnostic test.
37
Q

Key facts about endometrial cancer - symptoms

A
  • Most common invasive cancer of the female genital tract (7%)
  • Abnormal uterine bleeding
  • Childbearing age
  • Change in menstrual cycles
  • Postmenopausal
    • bleeding at least 12 months after cessation of menses OR unpredictable bleeding on HRT for 12months
38
Q

Aetiolgoy of endometrial cancer

A
  • omedian age at diagnosis - 60 years
  • 75% occur in post menopausal women
      • only 8% less than 45
    • -no screening test
    • diagnosis/once symptoms have started
    • Adenocarcinoma
39
Q
A
40
Q
A
41
Q

Two major pathogenic types of endometrial cancer

A

Type 1: Younger/peri menopausal women, obesity, associated with exces soestrogen, welld ifferentiated, superficial invasion, metastasis (infrequent), association with hyperplasia, genetic mutations (KRAS, PTEN, MLH1), better prognosis

Type 2: Older/ post menopusal women, poor differentiated carcinom (papillary serous, clear cell), deep myometrial invasion, often large bulky tumours, frequent LN metastasis, associated with atrophy, genetic mutation p53 *Erb-B2

42
Q

Type 1 endometrial cancer

A

o Younger/peri menopausal women

o Obesity

o Associated with excess oestrogen

o Well differentiated

o Superficial invasion

o Metastasis – infrequent

o Association with hyperplasia

o Genetic mutations KRAS, PTEN, MLH1

o Better prognosis

43
Q
A

Endometrial adenocarcinoma presenting as a fungating mass in the fundus of the uterus.

44
Q
A

Well-differentiated (grade 1) endometrioid adenocarcinoma with preserved glandular architecture but lack of intervening stromadistinguishing it from hyperplasia.

45
Q
A

Moderately differentiated (grade 2) endometrioidadenocarcinoma with glandular architecture admixed with solid areas.

46
Q
A

Poorly differentiated (grade 3) endometrioidadenocarcinoma with predominantly solid growth

47
Q

Type II Endometrial cell

A

o Older/post menopausal women

o Poorly differentiated carcinoma- papillary serous, Clear cell

o Deep myometrial invasion

o Often large bulky tumours

o Frequent lymph node metastasis

o Associated with atrophy

o Genetic mutations in p53 & Erb-B2

48
Q
A

Serous carcinoma of the endometrium with papillary growth pattern consisting of malignant cells with marked cytologic atypia including high nuclear-to-cytoplasmic ratio, atypical mitotic figures, and hyperchromasia.

49
Q
A

Accumulation of p53 protein in the nucleus

Immunocytochemistry.

50
Q

RFs for Endometrial cancer

A
  • Exposure to oestrogn** - risk increased with dose and time
  • Endogenous oestrogen - obesity, polycystic ovary syndrome, oligomenorrhea
  • Exogenous oestrogen - HRT, Tamoxifen
51
Q

Important hsitolgoy implciations of endometrialc ancer

A

oAggressive

oFrequent metastasis

oOften spread outside of the uterus at diagnosis

The tumor cells are irregular in size and have hyperchromatic nuclei with numerous mitotic figures (arrows).

52
Q

ENdometriosis

A
  • Present of endometrial like tissue outside the uteru,s which induces a chronic, inflamamtory reaction
53
Q

Endometrial sites

A
  1. Ovaries
  2. Uterine ligament
  3. Pelvic peritoneum
  4. Large and small bowel
  5. Appendix
  6. Cervical mucosa
54
Q

WHy is endometriosis an important condition

A
  • Infertility (20-50% of infertile women)
  • Dysmenorrhea (painful menstruation)
  • Pelvic pain
  • Features of invasion and metastasi - similae to malignant tumours
55
Q

2 theories of endometriosis

A

The metastatic theory - most widely accepted + plausable expalnation

Spread of endometrial tissue to distant sites through heamatogenous and lymphatic metastases

The metaplastic theory

Endometrium could arise directly from mesothelium of the pelvis or abdomen or embryonic development

56
Q
A

Endometirosis - in mucosa of colon

57
Q
A

Higher magnficiation reveals endometrial glands and stroma