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Endo/Repro > Cervix > Flashcards

Cervix Flashcards

1
Q

What does the cervix consist of?

A
  • External vaginal portion (ectocervix) and the endocervical canal
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2
Q

What is visible on vaginal examination?

A
  • Ectocervix
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3
Q

What covers the ectocervix?

A
  • Mature squamous epithelium that is continuous with the vaginal wall
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4
Q

What covers the endocervix?

A
  • Columnar, mucus secreting epithelium
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5
Q

What is the squamocolumnar junction?

A
  • The point where the squamous and columnar epithelium meet
  • Position is variable and changes with age and hormonal influence (in general, the junction moves up the canal with age)
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6
Q

What is squamous metaplasia?

A
  • The replacement of the glandular epithelium
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7
Q

What is the transformation zone?

A
  • The area of the cervix where the columnar epithelium coexists with the squamous epithelium
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8
Q

What happens to the SCJ during reproductive years?

A
  • SCJ moves out onto the ectocervix (calle ectropion)
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9
Q

What happens to the SCJ as a women ages beyond reproductive years?

A
  • Retreats up into the endocervical canal
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10
Q

What happens during menarche in response to estrogen production?

A
  • Maturation of the cervical and vaginal squamous mucosa
  • Formation of intracellular glycogen vacuoles in the squamous cells
  • As the squamous cells shed, they glycogen provides a substrate for various bacteria,like lactobacilli, which is the dominant bacteria in a normal vagina
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11
Q

What does lactobacillus do in the vagina?

A
  • Produces lactic acid to keep the vaginal pH under 4.5 in order to suppress growth of other organisms like Candida
  • At low pH, lactobacilli produces H2O2 which is bacterial toxic
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12
Q

What happens if the vagina becomes alkaline?

A
  • Hydrogen peroxide production decreases
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13
Q

What can cause the vagina to become alkaline?

A
  • Bleeding
  • Sexual intercourse
  • Vaginal douching
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14
Q

What is an exogenous source that causes the pH to rise in the vagina?

A
  • Antibiotics that suppress lactobacilli
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15
Q

What are endocervical polyps?

A
  • ## Common benign exophytic growths that arise within the endocervical canal
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16
Q

What do endocervical polyps look like?

A
  • Vary from small, sessile bumps to large polypoid masses that may protrude through the cervical os
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17
Q

What is the main significance of endocervical polyps?

A
  • May be the source of irregular vaginal spotting or bleeding that arouses suspicion of some more ominous lesion
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18
Q

What is the treatment for endocervical polyps?

A
  • Simple curette or surgical excision
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19
Q

What viruses are considered oncogenic viruses?

A
  • HTLV-1
  • Epstein Barr virus
  • Hep B and C
  • Merkel cell carcinoma
  • Kaposi sarcoma associated herpesvirus
  • HPV
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20
Q

What does HPV affect?

A
  • Any squamous cell component (Vulva, Vagina, and Cervix)
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21
Q

What are the highest risk types of HPV?

A
  • 16, 18, 31, and 45
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22
Q

What are the primary low risk types of HPV?

A
  • 11 and 6
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23
Q

What is HPV?

A
  • Non-enveloped, double stranded, circular DNA virus with an icosahedral capsid
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24
Q

What proteins compose HPV?

A
  • E1-E7

- L1 and L2

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25
Q

What does the E5 protein do in HPV?

A
  • Stimulates cell proliferation and prevents differentiation

- Downregulates surface MHC class I expression

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26
Q

What does the E6 protein do in HPV?

A
  • Downregulates cell cycle control through p53 inactivation/degradation
  • Induces malignant transformation together with E7
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27
Q

What does the E7 protein do in HPV?

A
  • Keeps cells active in the cell cycle through Rb inactivation
  • Induces malignant transformation together with E6
28
Q

What cells does HPV infect?

A
  • Immature basal cells of the squamous epithelium in areas of epithelium breaks or immature metaplastic squamous cells
29
Q

What cells are most susceptible to HPV infection?

A
  • Immature squamous cells in the transformation zone

- As a result, this is where the majority of cervical precursor lesions and cervical cancers develop

30
Q

What cell type is safe from HPV infection?

A
  • Mature superficial squamous cells that cover the cervix, vagina, or vulva
31
Q

How is HPV integrated into the host genome in the low risk types of HPV?

A
  • In types 6 and 11, the HPV genome is maintained in a nonintegrated episomal form
32
Q

How is HPV integrated into the host genome in the high risk types of HPV?

A
  • In types 16 and 18, the HPV genome is integrated into the host genome
33
Q

What happens to the cells once HPV in integrated into the genome?

A
  • Viral genome starts expressing the early proteins that maintain the keratinocytes in a rapidly dividing state
  • Productive replication is established such that the viral genome is amplified to more than 1000 copies and expression of capsid proteins is induced
  • Once the expression of capsid proteins is induced, infectious virions are synthesized and released
34
Q

Why is it theorized that there is a delayed immune response in HPV?

A
  • Could be due to the fact that the complete cycle takes place above the basal layer and does so without directly triggering cell lysis
35
Q

What does HPV protein E6 do to cause cell immortalization?

A
  • Block p53 which is the guardian of the genome

- Increase telomerase expression

36
Q

What does HPV protein E7 do to cause cell immortalization?

A
  • Inhibit p21 which causes increased CDK4/cyclin D which blocks RB-E2F
  • Inhibits RB-E2F causing cell cycle to continue
37
Q

What are some qualities of HPV infections?

A
  • Extremely common and mostly asymptomatic
38
Q

What is the peak age of onset for HPV positivity?

A
  • Age 20-24
39
Q

Does the immune system clear most HPV infections?

A
  • Yes, 50% are cleared in 8 months and 90% are cleared in 24 months
40
Q

What about HPV causes an increased risk for cervical cancer?

A
  • Persistent infection

- Infection with HPV alone is not sufficient for carcinogenesis

41
Q

What else is needed with HPV for carcinogenesis?

A
  • Cotransfection with a mutated RAS gene results in full malignant transformation
42
Q

What are some environmental factors that act in concert with HPV to increase the risk of cervical cancer?

A
  • Cigarette smoking
  • Coexisting microbial infections
  • Dietary deficiencies
  • Hormonal changes
43
Q

Why has cervical cancer decreased in mortality?

A
  • We did not have a screening test for it
44
Q

What is the screening test for cervical cancer?

A
  • Pap smear
  • It detects cervical precursor lesions, some of which would have progressed to cancer if not treated
  • Can also detect low-stage, highly curable cancers
45
Q

What is the best system when regarding patient management?

A
  • The two tiered system
46
Q

What is the two tiered system?

A
  • A system that classifies growth as either low grade or high grade
  • This is done to determine treatment options (observation vs surgical treatment)
47
Q

What does the low grade squamous intraepithelial lesion designation cover?

A
  • HPV (HPV)

- CIN I (mild dysplasia)

48
Q

What does the high grade squamous intraepithelial lesion designation cover?

A
  • CIN II (moderate dysplasia)

- CIN III (severe dysplasia and carcinoma in situ)

49
Q

What is LSIL associated with?

A
  • High level of viral replication but only mild alteration in growth of infected cells
  • 80% of cases are associated with high-risk HPV serotypes
50
Q

How are most cases of LSIL treated?

A
  • No like premalignant lesion

- Observation/HPV testing/biopsy

51
Q

Which SIL is more common?

A
  • LSIL (10x more)
52
Q

Does LSIL progress directly to invasive carcinoma?

A
  • No
53
Q

What is seen in HSIL?

A
  • Dysregulation of the cell cycle by HPV leads to increased cellular proliferation, decreased or arrested epithelial maturation, and lower rate of viral replication
  • Derangements may be irreversible
54
Q

What does HSIL develop from?

A
  • Most develop from LSIL
55
Q

What is HSIL associated with?

A
  • 100% are associated with high risk serotypes (HPV 16)

- Considered high risk for progression to squamous cell carcinoma (takes place over several decades)

56
Q

What is a punitive marker for HPV infections?

A
  • Overexpression of p16
57
Q

What is the average age of a patient with cervical carcinoma?

A
  • 45-50
58
Q

What are the histological types of cervical carcinoma?

A
  • Squamous cell carcinoma (80%)
  • Adenocarcinoma (15%)
  • Mixed adenosquamous or neuroendocrine (5%)
59
Q

Who are most cervical cancers seen in?

A
  • Women who were not in regular screening program
60
Q

What is done when a pap smear is abnormal?

A
  • Colposcopic examination of the cervix and vagina is performed to identify the lesion
  • Mucosa is examined with a magnifying glass following application of acetic acid which will highlight abnormal epithelium as white spots
  • Cone biopsy
61
Q

What are the different stages of cervical cancer?

A
  • Stage 0: carcinoma in situ
  • Stage 1: confined to cervix
  • Stage 2: carcinoma extend beyond cervix but not to the pelvic wall (involves vagina)
  • Stage 3: carcinoma has extended to the pelvic wall
  • Stage 4: carcinoma has extended beyond true pelvis or has involved the mucosa of bladder or rectum
62
Q

Where does cervical cancer metastasize to?

A
  • Primary pelvic nodes first then para-aortic nodes

- Distant mets to lung, other nodes, liver, and bone (can be the initial presentation)

63
Q

What is death mainly due to in cervical cancer?

A
  • Complications related to local tumor invasion rather than distant mets
64
Q

What are some of the vaccines for HPV?

A
  • Gardasil (gardasil 9)

- Cervarix

65
Q

Who is vaccinated for HPV?

A
  • All girls and boys who are 11 or 12
  • Could be started at 9
  • Recommended for young women through age 26 and young men through age 21
66
Q

What are some special cases of people who are recommended to get the HPV vaccine?

A
  • Young men who have sex with men
  • Young men who identify as bisexual or gay or who intend to have sex with men through age 26
  • Young adults who are transgender through age 26
  • Young adults with certain immunocompromised conditions through age 26

Endo/Repro (31 decks)

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