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imed3003 COPY > Pathology of the Cervix > Flashcards

Pathology of the Cervix Flashcards

1
Q

What is the cervix defined as?

A

Lower part of the uterus that is cylindrical, measuring 3cm in length and 2.5cm in diameter

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2
Q

What is the distal opening of the cervix called?

A

The os (opens into the vagina)

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3
Q

What happens to the cervix after several pregnancies?

A

A nulliparous (no deliveries ever) cervix the os is small and circular

A multiparous cervix os is transverse and slit-like

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4
Q

What epithelium lines the ectocervix (outside of the cervix)?

A

Stratified non-keratinising squamous epithelium

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5
Q

What epithelium lines the endocervix?

A

Columnar, mucous secreting epithelium

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6
Q

What is the squamo-columnar junction?

A

The point at which the squamous and columnar epithelium meet

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7
Q

What is clinically significant about the squamo-columnar junction?

A

Its position changes under hormonal influences during growth to young adult and then to adult.

Zone of transition is a location of lots of pathologies related to the cervix.

It is also called the transformation zone

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8
Q

What infective organisms cause chronic cervicitis?

A

Candidia

Trichomonas

Chlamydia and Gonorrhoea

Herpes simplex virus

Human papilloma virus

Others - Gardnerella, tubercolosis, syphilis, CMV, shistoma

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9
Q

What causes chronic cervicitis?

A

Affects almost all women to varying degrees

Squamous metaplasia at transformation zone obstructs cervical gland opening leading to cyst formation and stromal inflammation (acute and chronic)

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10
Q

What does chronic cervicitis look like when investigated?

A

Clinically the cervix appears red, inflamed and irregular with a wide transformation zone.

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11
Q

What causes candidiasis?

A

Overgrowth of commensal organsis.

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12
Q

What symptoms does candidiasis cause?

A

Generally causes vulvovaginitis with pruritis, burning and white discharge.

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13
Q

How is candidiasis treated?

A

Topical/oral antifungals

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14
Q

How is candidiasis diagnosed?

A

Cervical (pap) smear

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15
Q

How is trichomonas vaginalis spread?

A

Sexual contact.

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16
Q

What are the symptoms of trichomonas infection?

A

Patients may be asymptomatic or have yellow, frothy vaginal discharge

Vulvovaginal discomfort

Dysuria

Dyspareunia

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17
Q

How is trichomonas infection diagnosed?

A

Large flagellated ovoid protozoan that can be identified by pap smear.

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18
Q

What are the symptoms of chlamydia and gonorrhoea in females with cervicitis caused by these organisms?

A

Patients can be asymptomatic or can have pain, dysuria, discharge and bleeding.

Both infections, however, can ascend through uterus to cause pelvic inflammatory disease

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19
Q

What are potential complicaitons of pelvic inflammatory disease?

A

Acute complications include:

Peritonitis and bacteremia
Endocarditis, meningitis, and suppurative arthritis

Other sequelae include:

Infertility and tubal obstruction

Increased risk of ectopic pregnancy

Intestinal obstruction due to adhesions between bowel and pelvic organs.

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20
Q

What kind of infection does Herpes Simplex Virus - 2 cause?

A

HSV-2 usually involves genital mucosa.

Initial infection can cause systemic symptoms

Clinical symptoms seen in only 1/3 of people (red papules -> Vesicles -> Painful ulcers

Infection persists indefinitely and becomes reactivated at times of immunosuppression

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21
Q

How can HSV changes be visualized?

A

Pap smear shows swollen nuclei with multinucleation, ground glass chromatin with prominent nuclear membranes, and nuclear inclusions.

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22
Q

Who is HPV infection must common in?

A

Peak prevalence seen in 20-year-olds.

Most patients are asymptomatic

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23
Q

What kind of virus is HPV?

A

Double stranded DNA virus

Over 40 genotypes can infect the genital tract

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24
Q

Why is control of HPV important?

A

Divided into low and high oncogenic risk categories

Associated with condyloma, dysplasia and cancer in anogenital tract, oral cavity, and respiratory tract in both men and women

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25
Q

Do HPV viruses infect indefinitely?

A

No, infection usually is eliminated by host in 1 - 2 years. More oncogenic strains last longer than less oncogenic strains.

Persistent infections increase the risk of development of premalignant lesions and subsequent carcinoma.

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26
Q

What are the most common low risk HPVs? What are the most common high risk?

A

Lowest risk: HPV 11 and HPV6

High risk: 16 and 18.

newly discovered high risk: 31, 35, 52, 33

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27
Q

How does HPV affect people?

A

Integration of HPV into cell DNA allows for an overexpression of E6 and E7 viral genes which encode proteins.

Both E6 and E7 enhance degradation of p53 therefore interrupting cell death pathways.

E7 binds to p21 and prevents its function as a cell cycle inhibitor

E7 inactivates the retinoblastoma gene (Rb) blocking its proliferation-inhibitory function

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28
Q

What is condyloma acuminatum?

A

An exophytic lesion arising in transformation zone or ectocervix that has low oncogenic potential

29
Q

What causes condyloma acuminatum?

A

Usually associated with HPV6 and 11

30
Q

What does histology look like in condyloma acuminatum?

A

Exophytic lesion characterised by papillary fronds of thickened squamous epithelium with fibrovascular cores.

HPV cytopathic effect (large, irregular cytoplasm surrounding nucleus)

31
Q

What is koilocytosis?

A

Nuclear enlargement

Hyperchromasia

Binucleation

Cytoplasmic clearing

32
Q

What do premalignant lesions usually look like on cervix?

A

Flat lesions

33
Q

What is a cervical intraepithelial neoplasia?

A

Flat premalignant lesion of the cervix graded I - III depending on severity of dysplasia.

34
Q

How is cervical intraepithelial neoplasia diagnosed?

A

Based on identification of squamous cell nuclear atypia with variation in nuclear size and shape

Hyperchromasia

Coarse chromatin granules

Increased mitotic activity

35
Q

How is dysplasia graded in cervical intraepithelial neoplasia (CIN)?

A

CIN I has koilocytic atypia (Not as much maturation of cells to the surface)

CIN II has progressive atypia and expansion of dysplastic cells into middle third of the epithelium

CIN III Has diffuse atypia, loss of maturation, and expansion of dysplastic cells to epithelial surface.

**Dysplasia and koilocytic atypia are rising from base of epithelium all the way to the epithelial surface.

36
Q

What additional diagnostic tests allow diagnosis of CIN?

A

In situ hybridisation for high risk HPV DNA

Ki-67 showing proliferative activity throughout entire thickness of epithelium

37
Q

What protein is overexpressed in people with oncogenic HPV?

A

p16

38
Q

What terminology is used in cytology of cervical lesions (Pap smears)?

A

HPV infection shows Low grade squamous intraepithelial lesion (LSIL)

CIN I shows LSIL

CIN II shows High grade squamous intraepithelial lesion (HSIL)

CIN III shows high grade squamous intraepithelial lesion HSIL

*HPV infection and CIN I = low grade lesion

**CIN II and III = high grade lesion

39
Q

What is the prognosis of low grade squamous intraepithelial lesions like?

A

60% regress spontaneously

30% persist

10% progress to HSIL

LSIL do not often progress directly to invasive carcinomas.

These are managed by screening more often (less time between screenings)

40
Q

What is the prognosis of high grade squamous intraepithelial lesions like?

A

Significant malignant potential:

30% only regress

60% persist

10% progress to carcinoma

41
Q

How are HSILs treated?

A

By surgical removal of the transformation zone by LLETZ or cone biopsy

42
Q

How long do HSILs take to progress to invasive carcinomas?

A

Times vary from a few months to more than a decade. Very difficult to predict.

43
Q

What is the single most important factor for cervical cancer oncogenesis?

A

High oncogenic risk HPVs.

HPV16 alone accounts for ~60% of cervical cancer cases and HPV18 for another 10%

44
Q

What are the risk factors for cervical cancer?

A

Related to both host and viral characteristics:

HPV exposure (Age at first intercourse, multiple sexual partners, etc)

Viral oncogenicity (Persistent infection with high risk HPV subtypes)

Inefficiency of immune response (Immunosuppression/HIV infection)

Other risk factors (Smoking, coexisting infections, dietary deficiencies, OCP, hormonal changes)

45
Q

How common is cervical cancer?

A

500k new cases diagnosed each year.

250k deaths per year

46
Q

Where is cervical cancer most common and least common?

A

Most common: Underdeveloped countries (Sub-saharan Africa, Central and South America, Southeast Asia)

Least common: Western countries where screening has significantly reduced incidence of disease

47
Q

How does cervical cancer present?

A

Most are asymptomatic

Abnormal pap smear

Abnormal bleeding (post coital, intermenstrual)

Pain

Haematuria

Weight loss

48
Q

What does cervical cancer look like macroscopically?

A

Early lesions are only visible by colposcopy

Focal induration, ulceration, and elevated granular area that bleeds when touched

Advanced lesions can be endophytic or exophytic

49
Q

What do exophytic lesions look like?

A

Polypoid or papillary tumour mass

50
Q

What do endophytic lesions look like?

A

Ulcerated

51
Q

What is the most common types of cells to form cervical cancer?

A

Squamous cell carcinoma (accounts for 80% of cases)

This is because CIN III is the precursor lesion.

52
Q

What does cervical cancer consist of?

A

Nests and infiltrative tongues of malignant squamous cells invading the stroma.

53
Q

When is microinvasive squamous cell differentiated from CIN III?

A

When there is invasion of the basement membrane. (into the stroma)

SCC forms nests within the basement membrane eventually

54
Q

What percentage of cervical cancer are adenocarcinomas?

A

~15%

55
Q

What is the precursor lesion for adenocarcinomas?

A

Adenocarcinoma in situ

56
Q

What does histology of adenocarcinomas look like?

A

Proliferation of glandular epithelium composed of malignant endocervical cells with large, hyperchromatic nuclei and relatively mucin-depleted cytoplasm, resulting in dark appearance of the glands, as compared with normal endocervical epithelium

57
Q

What other tumours besides SCC and adenocarcinomas can cause cervical cancer?

A

Adenosquamous and neuroendocrine carcinomas (Account for remaining ~5%)

58
Q

What is the prognosis of adenosquamous and neuroendocrine carcinomas like?

A

Generally more aggressive and associated with less favourable prognosis

59
Q

Where do cervical carcinomas progress to usually?

A

Extends by direct spread to involve nearby tissues like bladder, ureters, rectum, and vagina

Local and distant lymph nodes can become involved

Distant metastases may be found in the liver, lungs, and bone marrow

60
Q

How is cervical cancer treated?

A

Depends on clinical stage:

Early carcinomas = cone biopsy only

Most = hysterectomy and lymph node dissection

Advanced = Surgery +/- adjunct radiotherapy and chemotherapy

61
Q

How effective is screening in preventing cervical cancer?

A

In Australia 80% of women diagnosed with cervical cancer did not participate in regular screening

Screening allows detection of precancerous lesions before they develop into invasive carcinoma.

62
Q

What test has replaced pap smear tests since 2017?

A

Cervical screening test

63
Q

How is a cervical screening test conducted?

A

Cells from transformation zone are obtained via spatula/brush

Liquid based medium

Molecular test for HPV DNA

Reflex cytology if HPV DNA is +ve

64
Q

What processes follow cervical screening tests?

A

If HPV is detected: reflex cytology is conducted.

If HPV infection is present ten referred to specialist for colposcopy

If low grade lesion is found repeat screening is done in 12 months and if still present referral to specialist again

65
Q

What does HPV vaccine (Gardasil) cover?

A

Reduces incidence of cervical cancer caused by HPV16 and 18 and condylomas caused by HPV 6 and 11.

Gardasil 9 also covers the next most common HPV types that are associated with cervical cancer (31, 33, 45, 52, and 58)

66
Q

When is HPV vaccine most effective?

A

When given to young people before they become sexually active.

Girls and boys aged 12 - 13 can receive HPV vaccine for free under national immunization program at their school.

67
Q

How effective has HPV vaccine been?

A

Program has already shown strong signs of success in reducing HPV infections, genital warts and precancerous lesions of the cervix

68
Q

Is routine screening still needed with the HPV vaccine?

A

Yes; vaccination does not protect against all types of cervical cancers or pre-existing HPV infections.

imed3003 COPY (48 decks)

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