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203: Theme 3 > Pathology of the Female Reproductive Tract > Flashcards

Pathology of the Female Reproductive Tract Flashcards

1
Q

Give an overview of what happens to the microscopic structure of the vagina at puberty

A
  • oestrogen secreted by the ovary stimulates maturation of the squamous epithelial cells
  • Glycogen is formed within mature squamous epithelial cells
  • Glycogen in cells shed from the surface is a substrate for the vaginal anaerobic organism (lactobacilli)
  • Lactobacilli produce lactic acid keeping vaginal pH below 4.5
    • prevents infection
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2
Q

Describe the microstructure of the Ectocervix

A
  • made up of Stratified squamous epithelium
    • as the cells move up the cervix they mature and are eventually shed from the surface of the epithelium
    • multiple layers of cells on top of each other
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3
Q

Describe the microstructure of the Endocervix

A
  • made up of a single layer of tall mucin-producing columnar cells
  • has a tiny blind-ending channel known as clefts
    • these radiate out from the endocervical canal into the surrounding stroma
    • increases the surface area of the endocervix
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4
Q

Describe the formation of the transformation zone

A
  • During puberty, the cervix changes shape
  • The anterior and posterior lips of the cervix grow
  • The distal end of the endocervix opens
    • changes from a tubular shape to a funnel shape
  • makes the Distal Endocervical mucosa becomes exposed to the vaginal environment
  • The distal endocervical columnar epithelium is exposed to the acidic vaginal environment
  • It is not suited to this, so undergoes an adaptive change called metaplasia
  • Reserve cells in this area proliferate and mature to form squamous epithelium: This process is called squamous metaplasia
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5
Q

What is the definition of metaplasia?

A

a transformation of cell type from one kind of mature differentiated cell type to another kind of mature differentiated cell type

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6
Q

Review the cervical transformation zone

A
  • cells transform from columnar cells to squamous cells as it moves from the vagina to the cervix
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7
Q

What is this an image of

  • identify 3 key parts in this image
A
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8
Q

Describe the myometrium

A
  • Bundle of smooth muscle
  • very good vasculature and nerve supply
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9
Q

Describe the Endometrium in the Proliferative phase

A

formed of

  • Tubular glands
  • Specialised stroma
  • Blood vessels

Mitosis would be seen in the cells of the stroma and glands.

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10
Q

Describe the endometrium in the secretory phase

A

formed of

  • corkscrew glands
  • specialised stroma
  • blood vessel

secretion/ shedding would be seen in the glands

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11
Q

Define neoplasia

A

‘new growth’ – abnormal, uncoordinated and excessive cell growth.

persists following withdrawal of stimulus and associated with genetic alterations

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12
Q

Explain the behaviour of benign neoplasms

A
  • Remains localised and doesn’t invade surrounding tissues
  • Generally grow slowly
  • Good resemblance of parent tissue
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13
Q

What is the Leiomyoma of the myometrium?

A
  • aka Fibroid
  • a being neoplasm of the smooth muscle
  • it is slow0growing and is often localised
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14
Q

What are the consequences of benign neoplasms?

A
  • Pressure on adjacent tissue
    • bladder (frequency) Rectosigmoid (constipation)
  • Obstruction of lumen of a hollow organ
    • blocking endocervix
  • Hormone production
    • EPO producing polycythaemia
  • Transformation into a malignant neoplasm
  • Symptoms for the patient
    • abnormal uterine bleeding pain
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15
Q

Explain the behaviour of malignant neoplasms

A
  • Invade into surrounding tissues
  • Spread via lymphatics to lymph nodes and blood vessels to other sites (metastasis)
  • Generally grow relatively quickly
  • Variable resemblance to parent tissue
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16
Q

What are the key differences between malignant neoplastic tissue and normal tissue

A
  • loss of differentiation
  • loss of cellular cohesion
  • enlarged irregular dark nuclei
  • increased numbers of mitoses
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17
Q

What are the consequences of malignant neoplasms?

A
  • Destruction of adjacent tissue
  • Metastasis
  • Blood loss from ulcerated surfaces
  • Obstruction of a hollow viscera
  • Production of hormones
  • Weight loss and debility
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18
Q

Explain is the terminology used for neoplasms?

  • suffix?
  • malignant names based on origin?
A
  • Malignant epithelial tumours are carcinomas
  • Carcinomas are named for the epithelial cell type which they resemble
  • Carcinomas of glandular epithelium are called adenocarcinomas
  • Malignant stromal tumours are sarcomas
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19
Q

What is Dysplasia?

A
  • disordered growth and differentiation characterised by increased proliferation (more mitoses), atypia of cells and decreased differentiation
  • Dysplastic lesions may (but don’t always) progress to invasive malignancy
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20
Q

What is abnormal about this epithelium?

A
  • abnormal proliferation
    • the nuclear division saw throughout the epithelium rather than just in the basal area
  • abnormal differentiation
    • the nuclear in the cells do not mature- the nucleus is still large as it moves to the apical end of the endothelium
    • not very much accumulation of cytoplasm at the top where there should be
  • nuclear atypia - abnormal size and shape of the nucleus itself
    • the nucleus has angulated edges rather than smooth rounds
    • the chromatin has a gritty appearances
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21
Q

What are the different degrees of dysplasia that may be seen microscopically?

A
  • go from normal to CIN III
    • CIN 1 - 1 %
    • CIN 2 - 5%
    • CIN 3 - 40% likely to progress to SCC
  • allows you to predict the likelihood of developing invasive malignancy
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22
Q

Where is dysplasia more likely to occur?

A
  • Often occurs in sites where there is metaplasia
    • squamous metaplasia of the cervical transformation zone
    • squamous metaplasia of the bronchial epithelium
      • _​_increased in smoking to produce more resilient cells against the smoke
    • glandular metaplasia of the distal oesophagus
      • _​_gastric reflux leads to differentiation into cells that more resemble the gastric lining
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23
Q

What are the normal constituent cells found in a pap smear?

A
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24
Q

What is the difference between normal surface cells of the cervix and dysplastic surface cells?

A
  • Normal surface cells have a small nucleus and lots of cytoplasm
  • Dysplastic cells have a
    • a higher ratio of nuclear size to cytoplasmic volume,
    • the nuclei show the same features that we associate with malignancy
      • still have a large nucleus,
      • nuclear atypia,
      • irregular nuclear margin
      • gritty purple staining of the chromatin irregularly spread throughout the nucleus
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25
Q

What is the difference between dysplasia and carcinoma?

A
  • a carcinoma invades into the basement membrane
  • when an invasion is seen in the cell it moves from CIN to a carcinoma
26
Q

What is HPV?

A
  • Human Papillomaviruses (HPVs) infects the epithelium
    • has to infect basal cells
  • Confined to local site of infection without viraemia
  • Over 130 HPV types, some of which infect the anogenital mucosa
    • high-risk HPV: 16, 18
      • CIN and carcinoma
    • low-risk HPV: 6, 11
      • benign anogenital warts
  • Double-stranded DNA virus 7.9Kbp
27
Q

Review the way in which HPV can infect the cervical region

A
  • progress to a malignant stage when the HPV virus get’s incorporated in with the normal cervical cells
28
Q

What strategies are there to prevent cervical cancer?

A
  • HPV Vaccination
    • 16,18 then also 6, 11
  • Population-based screening
    • Cervical sample HPV test
    • Cervical sample cytology, only 15% get investigated at this level
  • Colposcopy
  • Treatment of high-grade dysplasia
    • Large Loop Excision of the Transformation Zone
29
Q

What are the conditions that HPV infection can cause?

A
  • genital warts (6,11)
  • pre-malignant and malignant cervical disease (16,18,31)
  • peri-anal cancers
  • cancers of the oral-pharnyx
30
Q

What is Endometrial cancer?

  • common endometrial cancer symptom?
A
  • Malignant neoplasm of glandular epithelium - adenocarcinoma
    • ​most endometrial cancers occur in the glands of the endometrium
  • 89% of women present with postmenopausal bleeding
    • necrosis of the tumour –> bleeding
31
Q

Give an overview of adenocarcinomas from a single site of the body and from different sites in the body

A
  • Adenocarcinomas arising at different sites in the body have different
    • risk factors,
    • pathogenesis,
    • appearances, behaviour
    • genetic abnormalities,
    • prognosis and treatment.
  • Among adenocarcinomas arising at a single site, there are
    • multiple subtypes, initially divided by different appearances and increasingly supplemented by understanding molecular genetic pathogenesis.
32
Q

What are the varying subtypes of endometrial adenocarcinoma by morphology?

A
  • Endometrioid - differentiation that resembles endometrial glands
  • Serous - resemble fallopian tube epithelium
  • Clear cell - clear cytoplasm
  • Mixed (components of the previous 3)
  • Undifferentiated / Dedifferentiated
    • not showing a normal pattern of glandular differentiation
  • Carcinosarcomas
    • can show some coexistent malignant mesenchymal differentiation
33
Q

What are the two groups/ demographics that present with different types of endometrial adenocarcinoma?

  • what distinguishes the two groups?
A
  • Age
    • Type 1: 50-60s
    • Type 2: 60s-70s
  • Cause
  • Morphologic types of tumour
    • T1: Endometroid
    • T2: Serous, mixed
  • Molecular genetic abnormalities
    • T1: MSI, PTEN, PAX2 loss
    • T2: P53mut, 1pdel., PAX2 loss
  • Precursor lesions
    • T1: EIN, atypical hyperplasia
    • T2: EIC
  • Prognosis and treatment
    • T1: good
    • T2: poor
34
Q

What is the precursor lesion to invasive squamous cell carcinoma in the cervix?

A
  • Cervical Intra-Epithelian Neoplasia (CIN)
    • the disease process is caused by dysplasia
35
Q

How can CIN be detected?

(Cervical Intra-Epithelial Neoplasia)

A
  • screening for HR HPV infection
  • looking for abnormal cells
  • examining the cervix by colposcopy
  • treating by LLETZ (loop)
36
Q

What is the precursor legion for endometrial carcinomas?

A
  • assumed to come from Atypical hyperplasia
    • ​closely packed glands that are enlarged
  • more difficult to diagnose when investigating
    • need better investigative methods?
37
Q

What are the risk factors for endometrial adenocarcinoma?

A
  • mostpenopausal women
    • peak between 55-65 y/o
  • the most common presenting feature is postmenopausal bleeding
  • Endogenous hormones and reproductive factors
  • Excess body weight
  • Diabetes mellitus and insulin
  • Exogenous hormones & modulators
  • Ethnicity
  • Familial (Cowden’s syndrome; HNPCC)
  • Smoking not a risk
38
Q

Give an overview of the link between endogenous hormones and endometrial cancer

  • what conditions may affect this?
A
  • Excess exposure to estrogen unopposed by progestogens
    • increased neoplastic growth in the endometrium
  • Being overweight increases estrogen levels in postmenopausal women
  • Overweight can disrupt ovulation and progestogen production in premenopausal women
  • Polycystic ovarian disease
    • prolonged exposure of the endometrium to unopposed estrogen that results from anovulation
  • Some rare ovarian neoplasms can produce estrogens
39
Q

Give an overview of the link between reproduction and endometrial cancer

A
  • Pregnancy and parity reduce the risk of endometrial cancer
  • Mechanism includes the break from unopposed oestrogen during pregnancy and the removal of abnormal cells at delivery
  • Early menarche and late menopause increase risk (reduced by 7% for each year fewer)
40
Q

Give an overview of the link between excess body weight and endometrial cancer

A
  • c 34 % endometrial cancers are linked to excess body weight
  • 2-3 times increased risk in overweight women
  • Increased risk begins with a moderately elevated BMI
  • Central adiposity (waist circumference and waist:hip ratios) may be more important than BMI

( links with DM and Insulin)

41
Q

Give an overview of the link between Diabetes mellitus and insulin, and endometrial cancer

A
  • Women with diabetes mellitus have a two-fold increased risk of endometrial cancer
  • Insulin and insulin-like growth factors may increase the effects of estrogen on the endometrium

Hard to separate the effect of insulin from excess body weight but a probably direct effect

42
Q

Give an overview of the link between exogenous hormones & modulators, and endometrial cancer

A
  • Hormone replacement therapy
    • unopposed estrogen (RR 6.0)
  • Tamoxifen (RR 2.0)

*relative risk*

43
Q

Give an overview of the link between ethnicity, and endometrial cancer

A
  • US studies show endometrial carcinoma is less common in African American women
    • 13 per 105 in African-American women
    • 23 per 105 in white
  • BUT this group has higher mortality (x4)
  • Many variables involved
    • Later stage at diagnosis ( less access to health)
    • Unfavourable tumour type
    • Sociodemographic factors and treatment
    • Comorbidities
44
Q

What are the tumour-specific parameters that inform behaviour and treatment?

A
  • Tumour Type
  • Tumour Grade
  • Tumour Stage
45
Q

What are the gradings for a neoplasm?

A
  • Well differentiated - Grade 1
  • Moderately differentiated - Grade 2
  • Poorly differentiated - Grade 3
  • grading reflected how much he tumour resembles its parent tissue
    • has to be done under the microscope
  • Normal endometrial epithelium matures to form glands
  • Adenocarcinomas also form glands
  • The fraction of the tumour forming glands is estimated as a percentage (then divided into three groups)
  • Tumour grade affects prognosis
46
Q

What is the staging for all neoplasms?

A

a T N M system exists

  • T for tumour: local spread
  • N for nodes: lymph node deposits
  • M for metastasis: metastatic deposits
47
Q

What is the grading system used in gynaecological tumours?

  • what is the system for Endometrial carcinoma
A

a FIGO system is used (Fédération Internationale de Gynécologie et d’Obstétrique)

  • Stage 1: Confined to corpus
  • Stage 2: Involving cervix
  • Stage 3: Serosa/Adnexa/Vagina/Lymph Nodes
  • Stage 4: Bladder, Bowel, Distant Metastasis
48
Q

What is the most common endometrial adenocarcinoma?

A
  • Endometroid
    • resembles the endometrial glands
49
Q

What congenital abnormalities are there of the cervix?

A
  • agenesis of the cervix
    • nor formation of the cervix
  • dysgenesis of the cervix
    • only part of the cervix has formed
  • no connection with the vagina
50
Q

Describe the anatomy of the cervix

A
  • the uterus is ~ 4 cm long
51
Q

Describe the appearance of the cervix in women

A
  • size and shape varies with age, hormonal state and parity
  • in nulliparous females it is barrel shaped with a small pinhole/ circular shaped external os
  • in parous women the cervix is bulky and the external os is slit-like
52
Q

Explain the histology of the normal cervix

A
  • Ectocervix: covered by non-keratinising, stratified squamous epithelium
  • Endocervix: lined by simple columnar epithelium that secrete mucus
  • Transformation zone: undergoes continuous metaplastic change as the squamous epithelium from the vagina changes to columnar epithelium
53
Q

What happens to the cervix after the Menopause?

A
  • the SCJ moves from outside the cervix into the canal due to a lack of oestrogen
  • so the transformation zone is now inside the endocervix rather than on the ectocervix
  • may require a profolactive loop during smear tests to check for any precancerous changes
54
Q

Describe the structure of the Cervix

  • stroma structure
  • blood supply
  • lymphatic drainage
  • nerve supply
A
  • the stroma of the cervix is made of collagenous connective tissue and is mad of approx 15% smooth muscle fibre
  • It’s blood supply is the descending branch of the uterine artery, and the venous drainage is the uterine veins
  • the lymphatic drainage is via
    • parametrium
    • obturator
    • int. ext, common illiacs towards the aorta
  • the nerve supply
    • pain with the parasympathetic nerves to S2-S4
55
Q

What is the function of the cervix?

A
  • produces mucus to facilitate sperm migration
  • acts as a barrier to ascending infection - mucus plug during pregnancy
  • holds a developing pregnancy in place
  • effaces and dilates to enable vaginal bith
56
Q

What physiological changes happen to the cervix during pregnancy?

A
  • hypertrophies
  • becomes softer due to increased vasculature
    • increased vascularity/ venous congestion (purple tinge)
  • glands are destined with mucus forming a mucus plug
  • prominent ectropion
    • migration of the columnar epithelium onto the ectocervix
  • remains elongated until the onset of labour when it begins to thin and dilate
57
Q

What normal physiological presentations of the cervix are there?

A
  • Cervical ectopy (ectropion) “erosion”
    • caused by oestrogen usually found in women on the COCP
  • Atrophic “cervicitis”
    • due to a lack of oestrogen usually found in postmenopausal women
58
Q

What is this an image of?

A
  • Gonorrhea infection of the cervix
59
Q

What is this an image of?

A
  • Trichomonas vaginalis infection
    • strawberry cervix
60
Q

What are risk factors that increase HPV related changes that lead to pre-cancer or cancer of the cervix?

A
  • smoking
  • multiple sexual partners
  • immune compromise
  • low socioeconomic status
61
Q

What is the treatment for cervical cancer?

A
  • for low-grade cancers 1a, there is a cone biopsy/excision
  • more severe cancers 1b: radical hysterectomy/ radical trachelectomy
    • if they are of child-bearing age and would like to have children, the radical trachelectomy surgery can be done where the uterus is attached to the vagina
  • if it’s grade >1b2 chemotherapy is advised

203: Theme 3 (6 decks)

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