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Module 203 Theme 3 > Pathology of the female reproductive tract > Flashcards

Pathology of the female reproductive tract Flashcards

1
Q

What are some changes to the vagina during puberty

A

Oestrogen secreted by the ovary stimulates the maturation of squamous epithelial cells

glycogen is formed within mature squamous epithelial cells

glycogen in cells shed from the surface and anaerobically metabolised by lactobacilli to make lactic acid which keeps pH below 4.5

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2
Q

What are the 3 parts of the cervix from inside to outside

A

Endocervix, transformation zone and ectocervix

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3
Q

What cells line the ectocervix

A

covered by stratified squamous epithelium

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4
Q

What cells line the endocervix

A

Single-layer of tall, mucin making columnar cells.

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5
Q

How does the cervix change in puberty

A

The cervix changes shape, the lips grow, the distal end of the endocervix opens and the endocervical mucosa becomes exposed to the vaginal environment (transformation zone)

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6
Q

What happens to the transformation zone once exposed to the acidic vaginal environment

A

The distal endocervical columnar epithelium is exposed to the acidic vaginal environment which it is not suited for so they undergo metaplasia.

reserve cells proliferate and form squamous epithelium (squamous metaplasia)

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7
Q

What is metaplasia

A

The transformation of a mature differentiated cell type to another kind of mature differentiated cell type.

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8
Q

Outline the metaplastic squamous epithelium and its stages

A

At first, the metaplastic squamous epithelium is thin and delicate but with time (proliferation n maturation increase) it comes to be as strong and well-formed as that on the ectocervix

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9
Q

The endometrium changes appearance, what is the structure in the proliferative phase (before ovulation)

and then in the secretory phase

A

1) tubular glands
2) specialised stroma
3) blood vessels

secretory

1) cork screw glands
2) specialised stroma
3) blood vessels

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10
Q

What is neoplasia

A

‘new growth’- abnormal, uncoordinated and excessive cell growth.
persists following withdrawal of stimulus and associated with genetic alterations

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11
Q

What are the consequences of benign neoplasms

A

Pressure on adjacent tissue

obstruction of the lumen of a hollow organ

hormone production

transformation into a malignant neoplasm

symptoms for the patient

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12
Q

What are clinical problems of benign neoplasms

A

Pressure on adjacent tissues
-bladder (frequency),
rectosigmoid (constipation)

obstruction to the lumen of a hollow organ
-adjacent (ureters) blocking
endocervix

hormone production
-erythropoietin producing polycythaemia

transformation into a malignant neoplasm
- probably malignancy arises de novo

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13
Q

How do neoplasms behave

A

Malignant
- invade into surrounding tissues

  • spread via lymphatics to lymph nodes and blood vessels to other sites (metastasis)
  • generally grow relatively quickly
  • variable resemblance to the parent tissue.
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14
Q

What are the consequences of malignant neoplasms

A

Destruction of adjacent tissue

metastasis

blood loss from ulcerated surfaces

obs of a hollow viscera

production of hormones

weight loss and debility

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15
Q

What is dysplasia or CIN (cervical intra-epithelial neoplasia)

A

Disordered growth & differentiation characterized by increased proliferation, atypia of cells & decreased differentiation

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16
Q

Where does dysplasia often occur

A

Often occurs in sites where there is metaplasia

  • squamous metaplasia of the cervical transformation zone
  • squamous of the bronchial epithelium
  • glandular metaplasia of the distal oesophagus
17
Q

How do we analyse cervical cells

A

Via a pap test, cervical ‘smear test’, cells are grabbed and studied.

normal surface cells have a small nucleus and lots of cytoplasms

dysplastic cells have a higher ratio to nuclear size and cytoplasmic volume.

18
Q

What is the difference between dysplasia and carcinoma

A

The difference is the invasion through the basement membrane

19
Q

What effect does HPV have on the cervix

A

HPV infection causes CIN and cervical cancer.

HPV infect epithelium and are confined to the local site of infection

20
Q

Which high-risk HPV is associated with CIN

A

HPV 16, 18

21
Q

Which low-risk HPV types are associated with anogenital warts

A

HPV 6, 11

22
Q

What are some strats to prevent cervical cancer

A

HPV vax, HPV test and sample cytology, colposcopy, treatment of high-grade dysplasia and large loop excision of the transformation zone.

23
Q

What is the endometrium

A

The inner layer, composed of glands in a specialised stroma with a specialised blood supply.

growth, maturation and regression of all 3 components is coordinated during each menstrual cycle.

24
Q

Where is endometrial cancer predominantly located and what type of carcinoma is it

A

Endometrial cancer is predominantly in the glands therefore it is an adenocarcinoma.

25
Q

briefly, where are adenocarcinomas found and what are the diff risk factors

A

adenocarcinomas arise at diff sites in the body, there are multiple subtypes and have different risk factors, pathogenesis, genetic abnormalities, behaviour, prognosis and treatment

26
Q

name the subtypes of endometrial adenocarcinoma by morphology (microscopic appearance)

A

Endometroid, show differentiation that resembles endometrial glands

serous, thought to resemble fallopian tube epithelium

clear cell, have clear cytoplasm

mixed (components of all 3)
undifferentiated
carcinosarcomas.

27
Q

What is the precursor lesion to Invasive squamous cell carcinoma, what is the disease process and how do we detect HPV infection?

A

the precursor lesion to invasive squamous cell carcinoma is CIN
the disease process is called dysplasia

  • we detect CIN by screening for HPV Infection
  • looking for abnormal cells
  • examining the cervix by colposcopy
28
Q

What is the precursor lesion to endometrial carcinoma

A

Assumed to be atypical hyperplasia.

29
Q

What are risk factors for endometrial cancer

A
  • endogenous hormones and reproductive factors
  • excessive body weight
  • diabetes mellitus and insulin
  • exogenous hormones and modulators
  • ethnicity
  • familial
  • smoking, not a risk
30
Q

why is endogenous hormones a risk for endometrial cancer

A

Excess exposure to estrogen unopposed by progestogens

overweight increase estrogen levels in postmenopausal women and disrupt ovulation in pre mp women.

31
Q

How are neoplasms graded

A

grading reflects how much a tumour resembles its parent tissue
well-differentiated grade-1
moderately differentiated grade-2
poorly differentiated grade-3

32
Q

How are tumours staged

A 
How far in the body the tumour has spread
TNM system
T-  tumour: local spread
N- nodes: lymph node deposits
M- metastasis: metastatic spread

Module 203 Theme 3 (5 decks)

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