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37 Cards in this Set

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Area most likely involved by HPV
T zone
Ectocervix
Stratified non keratinixing squamous mucoa
Endocervix
Columnar epithelium that dips into the stroma to produce glands
Pap smear
Is not a diagnostic test, it is used for the presence of dx
Cervicitis causes ?
Herpes – ground glass nuclei
Syphillis – plasma cells
Chlamydia – lymphoid germinal centers
Gonorrhea – acute inflammation
Trich – epithelial spongiosis
Strep, ecoli, Staph
Do intranuclear inclusions indicate if the process is primary or secondary ?
No
What causes cervical metaplasia ?
This usually occurs due to inflammation. Glycogenated cells are shedded by the cervical cells at menarche, allowing the bacteria to grow. Thisleads to a drop in vaginal pH. Then there is metaplasia from columnar to squamous.
What is a nabothian cyst
Entrapped endocervical cleft that continues to produce mucous. This is associated with inflammation and ulceration
What does biopsy show for cervicitis ?
Epithelial spongiosis
Submucosal edema
erosions, necrosis or granulation tissue
ALL THESE CHANGES MIMIC PRECANCEROUS LESIONS IN PAP SMEARS
Endocervical polyps
2-5% of women
Cause bleeding
Arise in endocervical cana
Composed of thick walled, fibromyxoid stroma, dilated mucous glands and inflammation
This could be a reason for spotting, and therefore once removed the bleeding stops
What percent of HPV is found in cancers and conylomas ?
85% in cervical cancers and 90% of cervical condylomas(low risk HPV)
High risk HPV 16, 18 contained viral oncogenes E6 and E7 which caused the virus to cause dx
Where is the HPV virus integrated into host DNA and where is it not ?
Cancers – integrated, and condyloma not.
How do E6 and E7 work ?
E6 binds to P53 accelerating its degradation
E7 binds to RB gene affecting cell cycle regulation
Other chromosomal abnormalities have been associated with high risk HPV cancers
What are the risk factors for HPV ?
Having multiple sexual partners over a long period of time will ensure that one develops HPV. Multiple risk factors are minor risk factors, smoking, parity, fam hx, other genital infections
When patients are infected with 16 the first time and are infected with HPV again, is it 16 ?
No it has ot be something else
What is CIN ?
1-mild,2-moderate,3-severe. Next step is SqCC. The pap smear helps prevent this
Sq.CC
When detected by pap smear these are called squamous intraepithelial lesion and are divided into low grade and high grade intrapepithelial layer
Normal cervix
Non-keratinizing squamous mucosa with gradual asceuding maturation with a single layer of basal cells – aka line at low resoution
CIN-1
Indistinguishable from condylomas. Usually low risk HPV. Koilocytes in the upper portion along with binucleation, dyskeratosis and basal layer proliferation
LSIL
Abnormal nuclei are 2.5-3 times the size of a normal intermediate cell
Koilocytes are elnarged and wrinkled nucleus
CIN-2
Increased cytologic atypia with maturation only in upper third
Loss of polarity
increasing pleomorphism
abnormal mitosis
hyperchromasia
Associated with high risk HPV lesion
CIN-3
If you cannot tel top from bottom then CIN3. This has completel loss of maturaltion with abnormal cells in all layers. There is increased mitoses and abnormal mitosis and is associated with high risk HPV
Cytology of HSIL
Increased nuclear to cytoplasmic ration
Hyperchromatic nuclei with notches and irregularities
Single cells. The worse the lesion gets the less the koilocytes. Hence no koilocytes here.
Sq. CC
Peak incidence 40-45
It can be exophytic ulcerating or infiltrative- with direct extension to other pelvic organs, LN, or distant metastasis to the liver lungs or bone marrow
What percent of SqCC are composed of large cells ?
95% of keratizining (well diff ) or non keratinizing (mod diff). Small subset are poorly diff and have poor prognosis with early lymphatic spread and metastatic disease
What are the characteristics of Sq. CC ?
Invasion into stroma
Loss of basement membrane
Change in keratin production – makes them pinker
Desmoplastic response
Staging 0,1,1a1,1a2,1b
0 – CIN3
1-Confined to cervix
1a1-minimal microscopic invation
1a2-stromal invasion less than 5mm
1b-microscopic invasion greater than 5mm
Stage 1 survival ?
80-90%
Stage 2
75% survival with carcinoma beyond cervic, the upper 2/3 of the vagina
Stage 3
Extends to pelvic side wall and extends to lower 1/3rd of vagina with 35% of survival
Stage 4
Beyond pelvis and now involved the bladder, rectum or distant metastasis with 10-15% survival. This can lead to local extension and obstruction of the ureters causing pyelonephritis and uremia rather than distant metastasis
Adenocarcinomas of the cervix
Arise from endocervical glands
Associated with HPV18 (more common than 16)
Older age group
Can be mixed adenosquamous cell carcinoma – worse prognosis
Clear cell ardenocarcinoma – most frequent cancer in DES exposed women. The daughters in utero came up wth these carcinomas.
Mechanism of adenocarcinoma and cell structure
Tumor invades the stroma, forms complex glands and nuclei become cigar shaped and stratified with apoptotic cells and mitosis
Diagnosing cancer
Pap smear to screen, however biopsy is required for definite confirmation
How many patients with develop invasive carcinoma from CIN3?
1 in 500
Variable interval in precancer lesion to invasion. How would we deal with this ?
Regular Pap Smears help detect abnormalities over time
What is the pap reproduction now ?
Negative pap, negative HPV for three consective times, then they can space it out for three years. They should still be saem at that point