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Pathology III > Cervical Pathology & Gynecologic Cytology > Flashcards

Cervical Pathology & Gynecologic Cytology Flashcards

1
Q

what is the “transitional zone”

what is its clinical significance

A

aka squamocolumnar junction

the junction between the endocervix (lined with squamous epithelium) and ectocervix (lined with mucus secreting columnar epithelium)

immature squamous cells in the transition zone are highly susceptible to infection by HPV, which is why the cervix is a more common location for SCC than is the vulva/vagina

ectocervix = blue arrow, endocervix = black arrow

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2
Q

what is squamous metaplasia?

where is the cervix can it occur?

A

transition from columnar cells → squamous cells

occurs in endocervix: columnar cells become squamous, loss of mucous production

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3
Q

follicular cervicitis

cause

morphology

A
  • cause = various; often chlamydia trachomatis
  • morphology - germinal center formation
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4
Q

HSV cervicitis- morphology

A
  • multinucleated epithelial cells with
    • intranuclear inclusions
    • nuclear changes - molding, chromatin margination
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5
Q

endocervical polyp

  • cause
  • clinical
  • morphology - gross, microscopic
A
  • cause - n/a
  • clinical
    • common, benign
    • can cause bleeding (typically how its found)
  • morphology
    • gross - small or large well-circumscribed mass
      • may protrude thru external os
    • micro - loose, fibromyxoid stroma with larger, thicker walled central vessels
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6
Q

what are the low and high risk HPVs?

what do each lead to?

A
  • high risk = HPV 16, 18
    • associated with dysplasia, carcinoma of
      • vulva, vagina, cervix
        • vuvla: U-VIN, HPV-dependent SCC
          • tho HPV-independent SCC m/c than HPV dependent
        • vagina: VaIN, SCC
        • cervical: LSIL, HSIL, SCC
      • tonsils, oropharynx
  • low risk = HPV 6, 11
    • → condyloma accuminatum
    • usually not associated with dysplasia/carcinoma
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7
Q

HPV - general

  • prevalence
  • presentation
  • sequelae
A
  • most common STI
  • most often asymptomatic (and not detected on pap smear)
  • sequelae
    • 90% of HPV infection clear within 2 years
    • persistent infections are more increase risk of dysplasia /carcinoma
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8
Q

HPV - pathogenesis

A
  • HPV infects immature squamous cells (NOT mature squamous cells on the cervical surface) that are either
    • in the basal layer and accessible due to damage to the mucosal surface, or
    • at the cervical transitional zone
  • HPV’s genome codes for several oncoproteins
    • 6 early (E) proteins
      • E6, E7 are key: inactivate key cell-cycle checkpoints that inhibit cell proliferation & allow for cell damage repair, resulting in uncontrolled proliferation & immortalization in genetically unstable cells
        • E6
          • binds & degrades p53
          • has an anti-apoptotic effect
          • up regulates telomerase expression
        • E7
          • degrades retinoblastoma (Rb)
          • inhibits p21, p27
    • 2 late (L) proteins
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9
Q

E6 has what roles in the pathogenesis of HVP?

A

E6 = oncoprotein

  • degrades p53 (controls from G1 → S transition) resulting in
    • uncontrolled proliferation
    • replication of damaged DNA
  • has an anti-apoptotic effect, which
    • allows chromosomal mutations to accumulate
  • up regulates telomerase expression
    • immortalizes infected, mutated cells
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10
Q

E7 has what roles in the pathogenesis of HPV?

A
  • E7
    • has selective apoptotic affect
      • apoptosis of cells with wild type p53
      • anti-aptoptic effects in cells with mutated p53
    • degrades retinoblastoma (Rb) (inhibits E2F transcription factor), resulting in
      • uncontrolled proliferation
      • accumulation of p16 (- feedback)
    • inhibits p21, p27 (CKIs at G1 → S checkpoint)
      • uncontrolled proliferation
      • replication of damaged DNA
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11
Q

discuss the classification of cervical intraepithelial neoplasia (CIN)

A

CIN I-III: 3 tiered based on degree of dysplasia

  • CIN I - mild dysplasia
  • CIN II - moderate dysplasia
  • CIN III - severe dysplasia

associated with squamous intraepithelial lesion (SIL) classification: two tiered, based on 1. level of viral replication, 2. alteration to host cells, 2. pre-malignancy status

  • low grade SIL (LSIL)
    • high rate viral replication / mild alterations to host cells
    • not pre-malignant
    • CN-I
  • high grade SIL (HSIL)
    • low rate viral replication/ inc host cell proliferation
    • pre-malignant (treated as high risk)
    • CN-II, CN-III
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12
Q

LSIL (low grade squamous epithelial lesions)

  • cause
  • clinical
  • morphology
  • dx
  • sequelae
A

class of (CIN): represents a productive HPV infection

  • cause - almost always high risk HPV (HPV-16)
  • clinical - NOT pre-malignant
  • morphology microscopic
    • high rate viral replication / mild alterations to host cells
    • CIN-I:
      • mild expansion of basal layer ( < ⅓ total epithelium )
      • mitosic figures seen only in lower ⅓
      • individual cells are:
        • LARGER than CIN-II, III
        • LOWER N:C ratio than CIN-II, III
  • dx - p16 negative
  • sequelae
    • 60% regress
    • 30% persist
    • 10% progress to HSIL
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13
Q

high grade squamous intraepithelial neoplasia (HSIL)

  • cause
  • clinical
  • morphology
  • diagnosis
  • sequelae
A

class of CIN: represents progressive dysregulation of cell cycle

  • cause - always d/t high risk HPV (HPV-16)
  • clinical - pre-malignant (treated as high risk)
  • morphology
    • low rate viral replication / inc host cell proliferation
    • CN-II, CN-III
      • basal layer
        • CN-II: basal layer > ⅓ epithelium
        • CN-III: immature basal cells have reached epithelial surface
      • mitotic figures:
        • in all layers of epithelium (both)
      • individual cells:
        • CIN-II: smaller than CIN-I, higher N:C than CIN-I
        • CIN-III: smaller than CIN-II, higher N:C ratio than CIN-II
  • dx - P16 +
  • sequelae
    • 30% progress
    • 60% persists
    • 10% progresses to SCC
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14
Q

how does LSIL vs HSIL progress?

A
  • LSIL - 10% progresses to HSIL (mostly regresses)
    • does NOT ever directly progress to SCC
  • HSIL - 10% progresses to SCC
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15
Q

identify

A

positive p16 immunohistochemical stain

  • brown stain of cytoplasm & nuclei
  • stains HSIL and other high risk HPV infections (SCC) positive
  • p16 is a tumor suppressor gene that activates Rb (which then lowers cell proliferation)
    • in a persistent HPV infection, E7 degrades RB, leading to accumulation of p16 trying to activate it
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16
Q

what female reproductive tract cancers would stain positive for p16? negative?

A
  • positive
    • any HPV-dependent SCC
    • VaIN
    • HSIL
  • negative
    • HPV-independent SCC (vulvular)
    • LSIL
17
Q

cervical cancer - general

  • cause
  • clinical
    • prevalence/incidence
    • presentation
    • screening
  • includes what neoplasms?
A
  • cause
    • high risk HPV (HPV-16 > HPV-18) almost always associated
    • higher incidence also seen in
      • persons sexual active young/ with more partners
      • lower socio-economic class
      • smokers
  • clinical
    • prevalence - 3rd most common cause of cancer in women worldwide
    • presentation - takes years to develop (from persistent HPV)
    • gold standard for screening - pap smear
      • a leading cause of death in women w/out pap smears
  • m/c types of:
    • SCC (80%)
    • adenocarcinoma (15%)
18
Q

outline the procedure for giving a pap smear

A
  • using a spatula/brush, the cervical transformation zone is circumferentially scraped
  • then, the specimen is processed one of two ways
    • immediately smeared on glass & sprayed with fixative (traditional)
    • placed in a vial of liquid fixative that is spun down to remove mucus, pus & blood, then placed on a slide (liquid based)
19
Q

what is the specificiy of the pap smear?

why is this the case?

A

70% sensitive

this is b/c a lot of other reactive conditions can mimick dysplasia

20
Q

what is the sensitivity of the paper smear?

why is this the case?

A

80% sensitive

  • this is b/c dysplastic cells may be missed or not present
    • cells might get missed because of
      • poor sampling on dr’s part
      • presence of obscuring
        • blood (ex-pt on period), or
        • inflammatory cells
      • if a traditional method
        • air drying can produce an artifact over sample
        • smear can be too thick
21
Q

what are the advantages/disadvantages of a liquid-based pap smear

A

advantages

  • more sensitive
    • reduces risk of sampling error: no air-dying artifact, no risk of too thick/poorly prepared smear
  • can also test for:
    • HPV DNA testing
    • gonorrhea
    • chlamydia

disadvantages

  • more expensive
22
Q

what are pap screening recommendations?

A
  • initial screening
    • first screen
      • at 21 yrs, or
      • within 3 yrs of onset sexual activity
    • then every 3 years thereafter until the age of 30
  • after 30:
    • if neg thus far for high risk HPV (16,18): screen every 3-5 years
    • is pos thus far for high risk HPV (16,18): screen every 6-12 mos

if abnormal cytology at ANY AGE: perform colposcopic examination of cervix/vagina for biopsy

23
Q

what vaccines protect against HPV?

which HPVs do they cover?

vaccines are recommended for what populations/at what age?

for how long are HPV vaccines protective?

A
  • 3 vaccines protect against HPV - Cervarix, Gardasil, Gardasil 9
    • cover 16, 18 (high risk): all 3
    • cover 6, 11, 16, 18: Gardasil & Gardasil 9
    • covers against 9 HPVs: Gardasil 9
  • vaccination recommendations:
    • population dependent
      • any HPV vaccine is always recommended for:
        • boy/girls age 11-12 (can start at age 9), or
        • females age 13-26 that did not previously get a vaccine
      • Gardasil or Gardasil 9 recommended for
        • men age 13-21 not previously vaccinated
        • men 22-26
          • with certain immunocompromising conditions
          • who are gay, bisexual
          • transgender & not previously vaccinated
    • always given in 2 doses
  • vaccine provides coverage for up to 10 years
24
Q
A

normal vaginal squamous cells

25
Q
A

LSIL (CN-I)

26
Q
A

HSIL (CN-II)

27
Q
A

HSIL (CN-III)

28
Q
A

keratinizing SCC

29
Q
A

non-keratinizing SCC

30
Q
A

adenocarcinoma

31
Q
A

adenocarcinoma

Pathology III (5 decks)

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