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37 Cards in this Set
- Front
- Back
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Area most likely involved by HPV
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T zone
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Ectocervix
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Stratified non keratinixing squamous mucoa
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Endocervix
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Columnar epithelium that dips into the stroma to produce glands
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Pap smear
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Is not a diagnostic test, it is used for the presence of dx
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Cervicitis causes ?
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Herpes – ground glass nuclei
Syphillis – plasma cells Chlamydia – lymphoid germinal centers Gonorrhea – acute inflammation Trich – epithelial spongiosis Strep, ecoli, Staph |
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Do intranuclear inclusions indicate if the process is primary or secondary ?
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No
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What causes cervical metaplasia ?
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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.
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What is a nabothian cyst
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Entrapped endocervical cleft that continues to produce mucous. This is associated with inflammation and ulceration
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What does biopsy show for cervicitis ?
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Epithelial spongiosis
Submucosal edema erosions, necrosis or granulation tissue ALL THESE CHANGES MIMIC PRECANCEROUS LESIONS IN PAP SMEARS |
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Endocervical polyps
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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 |
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What percent of HPV is found in cancers and conylomas ?
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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 |
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Where is the HPV virus integrated into host DNA and where is it not ?
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Cancers – integrated, and condyloma not.
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How do E6 and E7 work ?
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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 |
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What are the risk factors for HPV ?
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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
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When patients are infected with 16 the first time and are infected with HPV again, is it 16 ?
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No it has ot be something else
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What is CIN ?
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1-mild,2-moderate,3-severe. Next step is SqCC. The pap smear helps prevent this
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Sq.CC
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When detected by pap smear these are called squamous intraepithelial lesion and are divided into low grade and high grade intrapepithelial layer
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Normal cervix
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Non-keratinizing squamous mucosa with gradual asceuding maturation with a single layer of basal cells – aka line at low resoution
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CIN-1
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Indistinguishable from condylomas. Usually low risk HPV. Koilocytes in the upper portion along with binucleation, dyskeratosis and basal layer proliferation
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LSIL
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Abnormal nuclei are 2.5-3 times the size of a normal intermediate cell
Koilocytes are elnarged and wrinkled nucleus |
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CIN-2
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Increased cytologic atypia with maturation only in upper third
Loss of polarity increasing pleomorphism abnormal mitosis hyperchromasia Associated with high risk HPV lesion |
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CIN-3
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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
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Cytology of HSIL
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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. |
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Sq. CC
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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 |
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What percent of SqCC are composed of large cells ?
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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
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What are the characteristics of Sq. CC ?
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Invasion into stroma
Loss of basement membrane Change in keratin production – makes them pinker Desmoplastic response |
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Staging 0,1,1a1,1a2,1b
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0 – CIN3
1-Confined to cervix 1a1-minimal microscopic invation 1a2-stromal invasion less than 5mm 1b-microscopic invasion greater than 5mm |
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Stage 1 survival ?
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80-90%
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Stage 2
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75% survival with carcinoma beyond cervic, the upper 2/3 of the vagina
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Stage 3
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Extends to pelvic side wall and extends to lower 1/3rd of vagina with 35% of survival
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Stage 4
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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
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Adenocarcinomas of the cervix
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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. |
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Mechanism of adenocarcinoma and cell structure
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Tumor invades the stroma, forms complex glands and nuclei become cigar shaped and stratified with apoptotic cells and mitosis
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Diagnosing cancer
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Pap smear to screen, however biopsy is required for definite confirmation
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How many patients with develop invasive carcinoma from CIN3?
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1 in 500
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Variable interval in precancer lesion to invasion. How would we deal with this ?
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Regular Pap Smears help detect abnormalities over time
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What is the pap reproduction now ?
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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
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