Case and Learning Objectives

Learning Objectives

1. Causes of vaginal discharge!

a. Infective (non-sexually transmitted)
 Bacterial vaginosis
 Candida
b. Infective (sexually transmitted)
 Chlamydia trachomatis
 Neisseria gonorrhoea
 Trichomonas vaginalis
 Herpes simplex virus
c. Non-infective
 Foreign bodies (e.g. retained tampons, condoms)
 Cervical polyps and ectopy
 Genital tract malignancy
 Fistulae
 Allergic reactions

Infection Organism Discharge Tests Treatment

Gonorrhoea Neisseria Watery / yellow. Endocervical Ciprofloxacin 500
gonorrhoea +/- dysuria, IMB, swab and mg stat.
pelvic pain. smear.
Rectal / throat
swabs.
Chlamydia Chlamydia Altered. Endocervical Doxycycline 100
trichomatis +/- dysuria, IMB, swab. mg bd PO 1/52.
ICB, PCB, lower First void urine Or: Azithromycin
abdominal pain. sample. 1g stat (if
pregnant).
Trichomona Trichomonas Offensive, High vaginal Metronidazole
s vaginalis vaginalis frothy, yellow / swab. 400mg bd PO 5-
green. Increased pH. 7/7.
+/- itchy and
sore
Bacterial Various Offensive, fishy, High vaginal Metronidazole
 vaginosis gram –ve white / yellow. swab. 400mg bd PO 5-
and +ve Increased pH. 7/7.
bacterium
Cervicitis Related to Purulent. Endocervical Doxycycline 100
NSU +/- PCB. swab. mg bd PO 1/52.
(Gon/Chl)
Candida Candida Curdy, white, Clinical Topical
albicans yeasty. diagnosis (but antifungal agent:
+/- itchy and can do a high Clotimazole.
sore vaginal swab). Or: Fluconazole
150mg PO stat.

2. Post-menopausal bleeding?
Causes of postmenopausal bleeding include: endometrial carcinoma; cervical
carcinoma; vaginal atrophy; endometrial hyperplasia +/- polyp; cervical polyps;
hormone-producing ovarian tumours; haematuria and rectal bleeding. The aim of
assessment and investigation of postmenopausal bleeding is to identify a cause
and exclude cancer. Assessment should start by taking a detailed history, with
identification of risk factors for endometrial cancer, as well as a medication
history covering use of HRT, tamoxifen and anticoagulants. Abdominal and
pelvic examinations should be carried out to look for masses. Speculum
examination should be performed to see if a source of bleeding can be identified,
assess atrophic changes in the vagina and look for evidence of cervical
malignancy or polyps. Ultrasound scan and endometrial biopsy are
complementary. Ultrasound scan can define endometrial thickness and identify
structural abnormalities of the uterus, endometrium and ovaries. Endometrial
biopsy provides a histological diagnosis. The measurement of endometrial
thickness aims to identify which women with postmenopausal bleeding are at
significant risk of endometrial cancer. If the examination is normal, the bleeding
has stopped and the endometrial thickness is < 5 mm on transvaginal ultrasound
scan, no further action need be taken.
a. Polyps—Polyps are usually noncancerous growths that develop from
tissue similar to the endometrium, the tissue that lines the inside of the
uterus. They either attach to the uterine wall or develop on the
endometrial surface. They may cause irregular or heavy bleeding.
 Polyps also can grow on the cervix or inside the cervical canal. These
polyps may cause bleeding after sex.
b. Endometrial atrophy—After menopause, the endometrium may
become too thin as a result of low estrogen levels. This condition is
called endometrial atrophy. As the lining thins, you may have abnormal
bleeding.
c. Endometrial hyperplasia—In this condition, the lining of the uterus
thickens. It can cause irregular or heavy bleeding. Endometrial
hyperplasia most often is caused by excess estrogen without enough
progesterone. In some cases, the cells of the lining become abnormal.
This condition, called atypical hyperplasia, can lead to cancer of the
uterus. When endometrial hyperplasia is diagnosed and treated early,
endometrial cancer often can be prevented. Bleeding is the most
common sign of endometrial cancer in women after menopause.

Although menstrual irregularity is normal during perimenopause, some unusual

bleeding can be a sign of a problem that needs medical attention:
 very heavy monthly bleeding, especially with clots
 bleeding after sexual intercourse
 spotting or bleeding between menstrual periods
 several menstrual cycles that are shorter than 21 days
 several periods that last three days longer than usual
 more than three months without a period

Cause Comment

Hormonal May cause an absence of periods (amenorrhea). Chronic failure to

imbalance* ovulate can result in an overgrowth of cells lining the uterus, which is a
risk factor for abnormal bleeding and for endometrial cancer.

Fibroids May cause heavy bleeding (menorrhagia). These benign tumors often
grow larger during perimenopause and tend to subside after
menopause.

Endometrial May cause heavy, prolonged, or irregular bleeding (often spotting).

polyps These benign growths of the uterine lining may or may not need to be
 removed.

Contraceptives Oral contraceptives may cause various irregular bleeding patterns

(skipped pills can cause bleeding between periods). Unmedicated IUDs
may increase menstrual flow; hormone-treated IUDs may reduce flow.

Thyroid problems Hypothyroidism can cause heavy bleeding. Both hypo- and
hyperthyroidism are associated with the absence of periods.

Clotting problems Irregular bleeding may be caused by inherited clotting disorders, such
as von Willebrand disease (a rare hereditary bleeding disorder that
impairs the blood's ability to clot).

Pregnancy Ectopic pregnancy, miscarriage, placenta previa, and other problem

pregnancies can cause irregular bleeding.

Polycystic ovary An endocrine disorder characterized by lack of ovulation and few or

syndrome absent periods. Periods that do occur may be heavy due to abnormal
buildup of the uterine lining.

*Possibly due to a change in weight, chronic stress, heavy exercise, illness,

perimenopause, or psychotropic medications.

3. Risk factor of cervical bleeding?

4. Cancer cervix! Risk factor, staging, definition, causes, pathophysiology!

Cervical cancer risk factors include:
a. Human Papilloma Virus Infection
HPV is the most important risk factor for cervical cancer, it is a group of more
than 150 related viruses, some of which causes papillomas, more commonly
known as warts. HPV infect cells on the surface of the skin, not the blood or
internal organs. Different type cause warts on different parts of the body. It
can be spread from one person to another during skin-to-skin contact. About
2/3 of all cervical cancer are caused by HPV 16 and 18.
b. Smoking
Tobacco by-products have been found in the cervical mucus of women who
smoke. These substances are believed to damage the DNA of cervix cells
and contribute to the development of cervical cancer. Smoking also makes
the immune system less effective in fighting HPV infections.
c. Immunosuppression
HIV puts women at higher risk for HPV infections. Another group of women
are those taking drugs to suppress immune response, such as those with
autoimmune disease or organ transplant.
d. Chlamydia Infection
It is spread by sexual contact and can cause pelvic inflammation, leading to
infertility. Women with chlamydia infection often asymptomatic and are at
higher risk of developing cervical cancer.
e. Diet low in fruits and vegetables
At increased risk.
f. Being overweight
more likely to develop adenocarcinoma of the cervix.
g. Long term use of oral contraceptives
Risk of cervical cancer goes up along the longer a woman takes OCs, and
goes back down again after the OCs are stopped. Cervical cancer risk was
doubled in women who took birth control pills longer than 5 years, but
returned to normal after 10 years stopped.
h. IUD use
Women who had ever used IUD had a lower risk, and also seen even in
women who had IUD for less than a year, and protective effect remained
after the IUDs were removed.
i. Having multiple full-term pregnancies
Women who had 3 or more full-term pregnancies have an increased risk of
developing cervical cancer.
j. Being younger than 17 at first full-term pregnancy
Almost 2 times more likely to get cervical cancer later in life.
k. Poverty
Low-income women do not have access to adequate health care services
 including Pap test, means they may not get screened or treated for cervical
pre-cancers.
l. Diethylstilbestrol (DES)
It is a hormonal drgs that was given to some women to prevent miscarriage
between 1940 and 1971. Women whose mother took DES develop clear-cell
adenocarcinoma of the vagina or cervix more often. Average age of women
when they are diagnosed with DES-related clear-cell adenocarcinoma is 19
years.
m. Having a family history of cervical cancer
Cervical cancer may run in some families, can increase the risk up to 3 times
than no one in the family had it.

Etiology  Major risk factors in HPV infections are:

 Sex at a young age

 Multiple sexual partners
 Promiscuous male partners
 History of sexually transmitted diseases

HIV infection is associated with a 5-fold increase in the risk of cervical cancer.

Pathophysiology

HPV infection must be present for cervical cancer to occur. On average, only 5%
of HPV infections will result in development of CIN grade 2 or 3 lesions within 3
years of infection and only 40% of CIN 3 lesions progress to invasive cervical
cancer with 30 years.

The following factors have been postulated to influence the development of CIN
3 lesions:

 Type and duration of viral infection.

 Host conditions that compromise immunity.
 Environmental factors.
 Lack of access to routine cytology screening.

Genetic susceptibility
 Genetic changes in several classes have been linked to cervical cancer. TNF is
involved in initiating the cell commitment to apoptosis, and the genes TNFa-8,
TNFa-572, TNFa-857, TNFa-863, and TNFG-308A have been associated with a
higher incidence of cervical cancer. Polymorphism in Tp53 (involved in apoptosis
and gene repair) associated with increased rate of HPV infection progressing to
cervical cancer.

HLA genes anomalies are associated with an increased risk. The chemokine
receptor-2 (CCR2) gene on chromosome 3p21 and the Fas gene in
chromosome 10q24.1 perhaps by disrupting the immune response to HPV. The
CASP8 gene (also known as FLICE or MCH5) has a polymorphism in the
promoter region that has been associated with a decreased risk of cervical
cancer.

Epigenetic modifications may also be involved in cervical cancer. Methylation is

the best understood and probably the most common mechanism of epigenetic
DNA modelling in cancer.

Human papillomavirus

Cancer study found that more than 90% of all cervical cancer worldwide are
caused by 8 HPV types: 16, 18, 31, 33, 35, 45, 52, and 58. Three types (16, 18,
and 45) cause 94% of cervical adenocarcinomas.

Table 1. Human Papillomavirus Types Associated with Cervical Cancer

Evidence for Cervical
HPV Alpha Group Types
Cancer Causation
Most carcinogenic HPV
1 16 type, known to cause
cancer at several sites
18,31,33,35,39,45,51,52,56,58,
Sufficient evidence
59
Limited evidence in
2A 68 humans and strong
mechanistic evidence
Limited evidence in
2B 26,53,66,67,70,73,82
humans
Classified by phylogenetic
analogy to HPV types with
30,34,69,85,97
sufficient or limited evidence in
humans
 Inadequate epidemiological
evidence and absence of
3 6,11
carcinogenic potential in
mechanistic studies
HPV = human papillomavirus.
HPV contain closed circular double-stranded DNA that encodes 6 early open
reading frame proteins (ie, E1, E2, E3, E4, E6 and E7), which function as
regulatory proteins, and 2 late open reading frame proteins (ie, L1 and L2),
which make up the viral capsid.

They are separated into 2 broad risk categories. Low risk types (eg, HPV 6 and
11) are associated with condylomata and a very small number of low-grade
squamous epithelial lesions (SILs) but are never found in invasive cancer. The
high-risk types (eg, HPV 16) vary in prevalence according to the cervical disease
state.

Upon integration into the human genome, the linearization of high-risk HPV DNA
places the E6 and E7 genes in a position of enhanced replication. E7 binds and
inactivates the Rb protein while E6 binds p53 and directs its degradation, and
the functional loss of the TP53 and RB genes leads to resistance to apoptosis,
causing uncensored cell growth after DNA damage. This ultimately results in
progression to malignancy.

Management

Immunization
Evidence suggests that HPV vaccines prevent HPV infection. The following 2
HPV vaccines are approved by the FDA:

 Gardasil (Merck, Whitehouse Station, NJ): This quadrivalent vaccine is

approved for girls and women 9-26 years of age to prevent cervical cancer
(and also genital warts and anal cancer) caused by HPV types 6, 11, 16, and
18; it is also approved for males 9-26 years of age

 Cervarix (GlaxoSmithKline, Research Triangle Park, NC): This bivalent

vaccine is approved for girls and women 9-25 years of age to prevent
cervical cancer caused by HPV types 16 and 18
 The Advisory Committee on Immunization Practices (ACIP) recommendations
for vaccination are as follows:

 Routine vaccination of females aged 11-12 years of age with 3 doses of either
HPV2 or HPV4

 Routine vaccination with HPV4 for boys aged 11-12 years of age, as well as
males aged 13-21 years of age who have not been vaccinated previously

 Vaccination with HPV4 in males aged 9-26 years of age for prevention of
genital warts; routine use not recommended

5. Staging and management! FIGO 1995!

Stage-based treatment
The treatment of cervical cancer varies with the stage of the disease, as follows:
a. Stage 0: Carcinoma in situ (stage 0) is treated with local ablative or
excisional measures such as cryosurgery, laser ablation, and loop excision;
surgical removal is preferred
b. Stage IA1: The treatment of choice for stage IA1 disease is surgery; total
hysterectomy, radical hysterectomy, and conization are accepted procedures
c. Stage IA2, IB, or IIA: Combined external beam radiation with brachytherapy
and radical hysterectomy with bilateral pelvic lymphadenectomy for patients
with stage IB or IIA disease; radical vaginal trachelectomy with pelvic lymph
node dissection is appropriate for fertility preservation in women with stage
IA2 disease and those with stage IB1 disease whose lesions are 2 cm or
smaller
d. Stage IIB, III, or IVA: Cisplatin-based chemotherapy with radiation is the
standard of care
e. Stage IVB and recurrent cancer: Individualized therapy is used on a
palliative basis; radiation therapy is used alone for control of bleeding and
pain; systemic chemotherapy is used for disseminated disease

6. IVA test!
VIA Procedure
Following are steps that are essential to performing VIA:
a. Assemble equipment and arrange equipment on the tray.
b. Ensure that the light source is working.
c. Assist woman onto the examination table after she has emptied her bladder.
d. Put on gloves and arrange equipment on the tray.
e. Inspect the external genitalia for the presence of lesions, papules, vesicles,
ulcerations, condylomata, discharge, redness, swelling, excoriation.
f. Tell the woman you will touch her. Check for inguinal lymph nodes.
g. Lubricate the speculum with clean, preferably warm, water.
h. Slowly and carefully insert the speculum without scraping the cervix with the
bills.
i. Adjust the speculum, so the entire cervix is in view and adjust the light as
needed.
j. Inspect the cervix for cervicitis, ectopy, nabothian cysts, ulcers, warts,
polyps, leukoplakia (thickened, white patches), or tumors. Look for vesicles,
small papules, or ulcers on the cervix. Is there any bleeding from the cervix,
especially after you touch it?
k. Observe the size and shape of the cervix and the external os.
l. Check for signs of infection such as vaginitis, cervicitis, or mucopurulent
discharge. Use a dry cotton swab to wipe away any discharge, blood, or
mucus from the cervix.
m. Identify the anterior and posterior lip of the cervix, red columnar epithelium,
pink squamous epithelium, the squamocolumnar junction, and the
transformation zone.
n. Observe all four vaginal fornices to make sure they are free from any growth.
o. Record any abnormal visual findings.
p. Soak a clean swab in 3% to 5% acetic acid and apply to the cervix liberally.
Wait at least 1 full minute for the acetic acid to be absorbed (use a watch).
Tell the woman that she might feel a slight burning sensation.
q. Check the transformation zone carefully, especially near the
squamocolumnar junction, for any dense, non-movable acetowhite areas in
the epithelium. Look around the entire transformation zone for any raised
and thickened white plaques or acetowhite lesions and note the following
characteristics described in Table 3. If acetowhite areas are identified, note
the location, extension, intensity of whiteness, borders and demarcations, as
well as size. Lesions vary in size, thickness, opacity, and border definition.
 Larger, thicker, more opaque lesions with clearly defined borders next to the
squamocolumnar junction suggest more severe cervical disease.

Characteristics of
Acetowhite
Lesions Comments

Location Is the acetowhite lesion near, abutting/touching, or

far away from the SCJ?
How much of the TZ does it occupy?

Extension Does the acetowhite area extend into the

endocervical canal?
Does it extend out toward the vaginal fornix?

Intensity of color Is the acetowhite area shiny white, pale white, or dull
white?
Are the lesions uniform in color?
Does the color intensity vary across the lesion?
Are there areas of erosion within the acetowhite
lesion?

Borders and Are the borders clear and sharp or indistinct diffuse
demarcation margins?
Are they raised or flat margins?
Are they regular or irregular margins?

Size Describe the extent or dimensions of the lesion and

the number of lesions

SCJ = squamocolumnar junction; TZ=transformation zone.

7. Why pale thin skin?

8. Cervical lesion? Cause?

9. Adnexa region of the uterus!
Adnexa refers to the area connecting to the uterus, such as the fallopian tubes
and ovaries. When a mass occurs in this region, it is referred to an adnexal
mass. Most adnexal masses develop in the ovary.

10. Atrophy of the lower genital tract

Vulvovaginal atrophy (VVA) is a
common and underreported condition
associated with decreased
estrogenization of the vaginal tissue.
Symptoms include dryness, irritation,
soreness, and dyspareunia with
urinary frequency, urgency, and urge
incontinence. It can occur at any time
in a woman's life cycle, although more
commonly in the postmenopausal
phase, during which the prevalence is
close to 50%. Clinical findings include
the presence of pale and dry
vulvovaginal mucosa with petechiae.
Vaginal rugae disappear, and the
cervix may become flush with the
vaginal wall. A vaginal pH of 4.6 or more supports the diagnosis of VVA. Even
while taking systemic estrogen, 10% to 20% of women may still have residual
VVA symptoms. Breast cancer treatment increases the prevalence of VVA
because the surgical, endocrine, and chemotherapeutic agents used in its
treatment can cause or exacerbate VVA. Local estrogen treatment for this group
of women remains controversial.

11. Pemeriksaan lab menopause! Pemeriksaan gynaecology!

12. Adnexal mass DD?

Differential Diagnosis of Adnexal Masses

Gynecologic

Benign ovarian

Corpus luteum cyst

Follicular cyst

Luteoma of pregnancy

Mature teratoma

Ovarian torsion

Polycystic ovaries

Serous and mucinous cystadenoma

Theca-lutein cyst

Malignant ovarian

Borderline tumors

Epithelial carcinoma

Ovarian germ cell tumor

Ovarian sarcoma

Sex-cord or stromal tumor

Benign nonovarian
 Ectopic pregnancy

Endometrioma

Hydrosalpinx

Leiomyoma

Tubo-ovarian abscess

Malignant nonovarian

Endometrial carcinoma

Fallopian tube carcinoma

Nongynecologic

Benign

Appendiceal abscess

Appendicitis

Bladder diverticulum

Diverticular abscess

Nerve sheath tumor

Pelvic kidney

Peritoneal cyst
 Ureteral diverticulum

Malignant

Gastrointestinal carcinoma

Krukenberg tumor (signet cell adenocarcinoma arising from the

gastrointestinal tract with metastasis to the ovary)

Metastasis from breast, colon, etc.

Retroperitoneal sarcomas

13. PAP Smear

The mainstay of cervical cancer screening for the last 60+ years has been the
Papanicolaou test. The Papanicolaou test, also known as the Pap test or the
Pap smear, was developed in the 1940s by Georgios Papanikolaou. It involves
exfoliating cells from the transformation zone of the cervix to enable examination
of these cells microscopically for detection of cancerous or precancerous
lesions.
Screening recommedations:
a. <21 years: no screening recommended.
b. 21 – 29 years: cytology (pap smear) alone every 3 years.
c. 30 – 65 years: HPV and cytology contesting every 5 years (preferred)
or cytology alone every 3 years (acceptable)
d. >65 years: no screening recommended if adequate prior screening has
been negative and high risk is not present

Preparation:

 The patient is not menstruating

 Avoid vaginal intercourse, douching, use of tampons, use of medicinal
vaginal cream or contraceptive cream for 24 – 48 hrs
 Pre-existing cervicitis should be treated prior to cervical screening
  Should proceed in the presence of bleeding or cervicitis, as these
symptoms may be related to cervical dyslasia or neoplasm, which may be
detected with cervical screening

Procedure:

1. Prepare the equipments: examination light, examination table with foot

supports, metal or plastic speculum, examination gloves, cervical spatula
and cytobrush, liquid-based cytology or glass slide and fixative.
2. Patient in lithotomy position.
3. Metal or plastic speculum is placed in the vagina, lukewarm water may be
used to lubricate and warm the speculum.
4. Transformation zone of the cervix is the region where squamous
epithelium replaces glandular epithelium and HPV has a predilection for
this region.
5. Discharge covering the cervix may be removed carefully using a large
swab, ensuring that the cervix is minimally traumatized.
6. Cervical broom or cervical spatula is applied to the surface of the cervix
and turned in a single direction to achieve an adequate sample for
cytology, making sure to rotate it at least 360o for the spatula and 5
rotations for the broom.
7. For thin prep the spatula and brush are to be swirled vigorously in the vial
10 times to release the specimen and then discarded.
8. When
conventional
cytology is to be
performed, the
specimens are
smeared on a
glass slide and
subsequently
sprayed with
fixative or placed
in 90% alcohol
solution.
Hasil menurut klasifikasi Papanicolaou

 Kelas I = negatif (tidak ditemukan sel-sel ganas)

 Kelas II = ada sel-sel atipik, tp tidak mencurigakan
 Kelas III = ada sel-sel atipik, curiga keganasan
 Kelas IV = ada kemungkinan tumor ganas
 Kelas V = jelas tumor ganas

Normalnya endocervix dibatasi glandular cells, sementara ectocervix dibatasi

squamous cells.
Jika ada abnormalitas pada squamous cells, namanya CIN (cervical intra-
epithelial neoplasia), jika ada abnormalitas pada glandular cells, namanya
CGIN (cervical glandular intra-epithelial neoplasia)

CIN

CIN 1:

 Perubahan ringan
 Mempengaruhi 1/3 atas lapisan serviks
 Bukan cancer dan pada kebanyakan kasus tidak berubah jadi cancer di
kemudian hari

CIN 2:

 Perubahan sedang
 Mempengaruhi 2/3 atas lapisan serviks

CIN 3:

 Perubahan berat (tapi bukan cancer)

 Mempengaruhi seluruh permukaan lapisan serviks

CGIN

Disebut juga dengan adenocarcinoma in situ (pre-invasive stage of

adenocarcinoma cervix)
Klasifikasi = low grade / mild and high grade /severe  equivalent dengan CIN 3
Bisa multifocal  >1 area karena dalam waktu bersamaan
 CGIN bukan cancer tapi jika tidak di treat, perubahan ini bisa berkembang
menjadi adenocarcinoma (cancer of the gland)

Results from cervical cytology specimens are reported according to the 2001
Bethesda System Classification, as listed below.[25]

Negative for intraepithelial lesion or malignancy

Epithelial cell abnormality

Squamous cell

 Atypical squamous cells (ASC) of undetermined significance (ASC-US) or

atypical squamous cells that cannot exclude HSIL (ASC-H)

 Low-grade squamous intraepithelial lesions (LSIL), includes human

papillomavirus (HPV), mild dysplasia, and CIN 1

 High-grade squamous intraepithelial lesions (HSIL), includes moderate to

severe dysplasia, carcinoma in situ, CIN 2, and CIN 3

 Squamous cell carcinoma

Glandular cell

 Atypical glandular cells (AGC), specify endocervical, endometrial, or not

otherwise specified (NOS)

 Atypical endocervical cells, favor neoplastic, specify endocervical or NOS

 Endocervical adenocarcinoma in situ (AIS)

 Adenocarcinoma

14. Myoma!

15. Tumour marker of ovarium cancer

Approximately 90% of ovarian cancers are celomic epithelial carcinomas and
contain a celomic epithelium–related glycoprotein, designated cancer (or
carcinoma) antigen 125. CA-125 can be localized in most serous, endometrioid,
and clear cell ovarian carcinomas; mucinous tumors express this antigen less
frequently.
 The American College of Obstetricians and Gynecologists and Society of
Gynecologic Oncologists guidelines for referring patients to a gynecologic
oncologist recommend referral for women with a pelvic mass suggestive of
ovarian cancer and a serum CA-125 value higher than 35 U/mL in
postmenopausal women or higher than 200 U/mL in premenopausal women.
16. Colposcopy

A cervical biopsy may be done to find cancer or precancer cells on the cervix.
Cells that appear to be abnormal, but are not yet cancerous, are called
precancerous. These abnormal cells may be the first sign of cancer that may
develop years later.
A cervical biopsy may also be used to diagnose and help treat these conditions:
a. Non-cancerous growth (polyps) on the cervix
b. Genital warts. These may mean that you have an infection with HPV.
HPV is a risk factor for cervical cancer.
c. Diethylstilbestrol (DES) exposure if your mother took DES during
pregnancy. DES raises the risk for cancer of the reproductive system.

Generally, a cervical biopsy follows this process:

 You will need to undress completely or from the waist down and put on a
hospital gown.

 You will be told to empty your bladder before the procedure.

 You will lie on an exam table, with your feet and legs supported as for a
pelvic exam.

 Your health care provider will put an instrument called a speculum into your
vagina. This will spread the walls of the vagina apart to reach the cervix.

 Often the health care provider will use a colposcope. This is an instrument
with a special lens like a microscope to help see the cervical tissues. The
provider will put colposcope at the opening of your vagina. It will not enter
your vagina.

 Your health care provider will look through the colposcope to find any
problem areas on the cervix or in the vagina.

 He or she may clean and soak the cervix with a vinegar solution (acetic
acid solution). This solution helps make the abnormal tissues turn white so
they are easier to see. You may feel a mild burning sensation. An iodine
solution may be used to coat the cervix. This is called the Schiller test.

 The type of biopsy done will depend on the size and shape of the abnormal
cells, as well as where they are.

 The health care provider may numb the area using a small needle to inject
medicine.

 He or she may use forceps (tenaculum) to hold the cervix steady for the
biopsy. You may feel some cramping when the tenaculum is put in place.

 The amount of tissue removed and where it is removed depend on the type
of biopsy. For a simple cervical biopsy, one or more small samples of tissue
will be removed using a special type of forceps. When this is done, you
may feel a slight pinch or cramp. Cells from the inside of the cervical canal
may be removed with a special tool called an endocervical curette or an
endocervical brush. This may also cause some cramping.

 For a cone biopsy, the provider may use a loop electrosurgical excision
procedure (LEEP) or the cold knife cone biopsy procedure. With the cold
knife cone biopsy, a laser or a surgical scalpel may be used to remove
tissue. This procedure needs regional or general anesthesia.
  Bleeding from the biopsy site may be treated with a paste-like topical
medicine. The provider may also use a probe (electrocauterization) or
stitches (sutures) to stop the bleeding.

 After a cone biopsy, the provider may pack the cervix with a pressure
dressing. Your provider will tell you how to remove this packing.

 The provider will send the tissue to a lab for testing.

17. Squamo-Columnar junction dysplasia

https://www.glowm.com/section_view/heading/Pathology%20of%20Cervical
%20Carcinoma/item/230

Definition of FIGO clinical staging for cervical cancer

Stage Definition

I     Carcinoma strictly confined to the cervix (extension to the corpus

should be disregarded)

  IA   Invasive cancer identified only microscopically; invasion limited to

stromal invasion with maximum depth of 5 mm and no wider than 7
mm (the depth of invasion should not be more than 5 mm taken from
the base of the epithelium, either surface or glandular, from which it
originates; vascular space involvement, either venous or lymphatic,
should not alter the staging)

    IA1 Measured invasion of stroma ≤3 mm in depth and ≤7 mm in width

    IA2 Measured invasion of stroma >3 mm and <5 mm in depth and ≤7 mm

in width

  IB   Clinical lesions confined to the cervix or preclinical lesions greater

than stage IA

    IB1 Clinical lesions no greater than 4 cm in size

    IB2 Clinical lesions greater than 4 cm in size

II     The carcinoma extends beyond the cervix but has not extended to
the pelvic wall or the lower third of the vagina

  IIA   Involvement of up to the upper two thirds of the vagina, with no

Stage Definition

obvious parametrial involvement

    IIA1 Clinically visible lesion ≤4 cm

    IIA2 Clinically visible lesion >4 cm

  IIB   Obvious parametrial involvement without involvement of pelvic

sidewall.

III     The carcinoma has extended to the pelvic wall; on rectal

examination, there is no cancer-free space between the tumor and
the pelvic wall; the tumor involves the lower third of the vagina; all
cases with a hydronephrosis or nonfunctioning kidney are included
unless they are known to be due to other causes

  IIIA   The carcinoma has spread to the lower third of the vagina but not to
the pelvic wall

  IIIB   The carcinoma has grown into the pelvic wall, or there is
hydronephrosis/non-functioning kidney

I     The carcinoma has extended beyond the true pelvis or has clinically
V involved the mucosa of the bladder or rectum

  IVA   Spread to adjacent pelvic organs

  IVB   Spread to distant organs

18. Endometrium di ovarium

19. Cara hitung kapan menopause dari hari pertama kali mens

20. Follow up for cervical cancer patients

Follow up of cervical cancer patients include:
a. Being examined by your doctor
b. Brushing a sample of cells from the cervix or colposcopy
c. Blood tests
d. X-rays
 e. CT scans or MRI scans
f. Liver ultrasound scans
The patients will be asked about how they are feeling and any side effects from
treatment. Also ask the patient if they had any new symptoms or are worried
about anything.
After the treatment take a sample of cells taken from the cervix using a small
brush or colposcopy repeated once a year. If the patient had their womb
removed, doctor may suggest taking a sample of cells from the top of the vagina
if you have unusual symptoms this is called vaginal vault test.
Cervical cells can be very difficult to interpret after radiotherapy, so the patient
will not continue to have regular tests as part of the cervical screening
programme. Using speculum at appointments to make sure there are no
problems.
Follow up is 3 to 4 month checkups to start with. Then if all is well at a year after
treatment they will change to 6 monthly for 2 years. And then yearly for another 3
years.
The most appropriate follow-up strategy has not been clearly stated. Clinical with
gynaecological examination including PAP smear are usually performed every 3
months for the first 2 years, every 6 months for the next 3 years and yearly
thereafter. SCC dosage in squamous cell carcinoma may be useful in patients’
follow-up if initially increased. PET/CT might have a role in early local recurrence
and metastasis detection.