L2 - Pathology of female repro tract 2 Flashcards
DYSPLASIA
i) what is it?
ii) how may dysplastic cells look? what do they not do?
iii) what does recognising dysplastic lesions allow?
iv) what are the three features of dysplasia?
v) how may proliferation be affected in dysplastic cells? how can this been seen
vi) how may cells look at the top compared to the bottom of a healthy and a dysplastic epithelium? how many chromatin look in dysplastic cells?
i) a pre malignant state of cells
ii) look like malignant cells but dont cross the basement membrane
iii) recognition allows early treatment before invasion occurs
iv) abnormal growth and differentiation
- abnormal maturation
- nuclear atypia
v) more proliferation = more mitoses
vi) healthy = shrinkage of nuclei and increased cyto as the cell moves up/reduced mitoses at top
dysplastic = no difference between cells in top and bottom of epithelia
- see gritty chromatin in dysplastic cells
SITES OF DYSPLASIA
i) where does dysplasia often occur?
ii) give examples of this occuring in the a) cervix, b) bronchus
c) oesophagus? what do cells change to and from?
iii) does malignancy arise from the new or old cell type?
iv) are cells at the surface of a dysplastic epithelium the same or different to those at the surface of a normal epithelium?
i) at sites of metaplasia
ii) a) cervix - columnar > strat sq in the transformation zone
b) bronchus - columnar > squamous (due to smoking)
c) oesophagus - strat squamous > columnar/glandular (due to reflux - becomes like stomach)
iii) malignancy arises from the new cell type
iv) cells at surface of dysplastic ep are different to those at the top of a normal epithelium
SMEAR TEST
i) what three cell types are acquired in a smear test?
ii) how do normal surface cells of the cervix look (nuclei and cytoplasm)
iii) how do dysplastic cells look? (nucleus and cyto)
iv) how does the chromatin look in dysplastic cells?
v) what differentiates between dysplasia and carcinoma in the cervix?
i) endocervical cells (columnar), squamous cells, metaplastic squamous cells
ii) normal cells have a small nucleus and lots of cytoplasm
iii) dysplastic cells have a bigger nuclei size/irreg margins and lower cytoplasmic volume
iv) gritty chromatin
v) invasion through the basement membrane
HUMAN PAPILLOMAVIRUS
i) what area does it infect? does it stay confined or spread?
ii) what type of virus is it?
iii) name two high risk and two low risk strains? what may low risk HPV cause?
iv) which cells does it infect first?
v) what pattern of infection is seen in low grade lesions? what happens differently in high grade lesions?
i) infects the epithelium and stays confined
ii) double stranded DNA virus
iii) high risk - 16 and 18
low risk - 6 and 11 = anogenital warts
iv) infects basal cells of the epithelium first
v) low grade - cycle of virus limited to cycle of cell (virus replicates in cell as it moves up but then shed off)
- high grade - integration of virus into host genome and manufactures cell proliferating proteins
EPIDEMIOLOGY OF GYNAE CANCERS
i) what area of the world is cervical cancer most prevalent?
ii) what area of the world is endometrial cancer most prevalent?
iii) how is the incidence of cervical cancer changing in europe?
i) cervical cancer is most prevalent in the developing world eg east and west africa
ii) endometrial cancer is most prevalent in north america and europe
iii) incidence of cervical cancer is declining in europe
INCIDENCE OF CERVICAL CANCER
i) when the main peak age of cervical cancer? around what age is a second peak seen?
ii) what is the birth cohort effect? when has this occured in relation to cervical cancer?
iii) what is creating a new birth cohort?
i) main peak age is 25-45
- also a second peak in older women 80-84
ii) birth cohort effect is when a group of people experience different circumstances to those born immediately before or after them
- reflects seperate peaks in cervical cancer and women reaching sexual debut during WW1&WW2
iii) HPV vaccination is creating a new birth cohort
