DR N.C.

SWARTZ &
J.V. KHUTJWE 2023
CANCER OF THE CERVIX

Cervix – Lower portion of the uterus, contiguous

with the upper portion of the vagina

Comprises the exocervix and endocervix

Development of cancer begins with cells

changing from normal to pre-cancer (dysplasia)
and then to cancer

Mainly occurs in the transitional zone at the

squamo-columnar junction, an area in the cervix
where columnar cells change to squamous cells.

AKA Transformation zone

 EPIDEMIOLOGY

• Fourth most common cancer in women world wide

• Second most common cancer in Sub Saharan Africa
• The most common cancer among women in
Botswana and;
• The leading cause of cancer associated deaths in
Sub Saharan Africa, including Botswana.
• Globocan 2018
 TYPES OF CERVICAL CANCER
• A. Squamous cell Carcinomas
• Cancer of flat epithelial cell
• Account for 80% to 90% of the cervical cancers
• B. Adenocarcinomas
• Cancer arising from glandular epithelium
• 10% to 20%
Predisposing Factors of
Cervical Cancer
• Cervical Human Papilloma Virus (HPV) has been known to
be almost exclusively the cause of cervical cancer.
• HPV infection is a precursor to the development of
cervical dysplasia (Also known as Cervical Intraepithelial
Neoplasia [CIN] or Cervical Carcinoma in situ [CIS])
• (Latendresse, et al. 2010)
• Infection with Human Papillomavirus (HPV) accounts for
90% of all Cervical cancers
• Cervical cancer mainly caused by HPV 16 & 18 strains
 RISK FACTORS
• Human papilloma virus- Cause about 70% of cervical cancers
• Tobacco Smoking
• Multiple pregnancies
• Contraceptive use-long term
• Early age at onset of sexual activity
• Multiple sexual partners
• Immunosuppression
• -Persistent Infection with the high risk/ oncogenic types of HPV, predominantly type 16 and 18 can result in cervical
cancer
• -50% of adolescents and young women acquire HPV infection within 3 years of initiation of sexual intercourse some as
early as 3 months. Most of the infection is cleared spontaneously however by the immune system, and the majority of
these cases do not develop into cancer. Women with high grade CIN are more likely to progress to cervical cancer.
• -Other than HPV infection, the genetics of cervical cancer remain poorly understood.
• HPV causes the production of 2 proteins known as E6 and E7 which turn off some tumor suppressor genes.
• This may allow the cervical lining cells to grow too much and to develop changes in additional genes, which in some cases will lead to
cancer. (ACS, 2014)
• -IMPORTANCE OF VACCINATION; Available vaccinations that have been approved by the FDA.
EARLY SIGNS

• Thin watery vaginal discharge which can

be offensive
• Severe bleeding with clots
• Post coital bleeding
• Post menopausal bleeding
• Increase in menstrual flow
• Dyspareunia
LATE SIGNS
• Lower abdominal pains radiating to the flank & legs
• Oedema of the lower extremities
• Urinary symptoms: dysuria, urinary retention, frequency, haematuria
• Bowel symptoms: rectal bleeding, constipation, bowel obstruction
• Severe pv bleeding
DIAGNOSTIC PROCEDURES

• Pap Test- Ability to detect cancer early

• Colposcopy- Examination of the cervix under magnification after application of acetic
acid followed by a biopsy taken under a colposcope
• Endocervical curettage-removing some tissue lining from the endocervical canal.
Recommended when the upper limits of cervical abnormalities or the transformation
zone are not visualised
• Cone biopsy- recommended to obtain a larger wedge of tissue and to rule out invasive
cancer
CLINICAL STAGES
FIGO staging system [International Federation of Gynaecology & Obstetrics] is used
Based on the tumour size and whether it has spread
Stage I- Cancer is confined to the cervix
Stage II – Cancer invades the uterus but not the pelvic wall or the lower third of the vagina.
Stage III- Tumour extends to the pelvic wall and/or lower third of
the vagina and/or may cause hydronephrosis
Stage IV-Tumour invades the bladder/rectal mucosa and extends
beyond the true pelvis.
MEDICAL MANAGEMENT
Stage dependent

PRE INVASIVE CERVICAL CANCER

Cryotherapy : uses freezing gas (liquid nitrogen) to destroy precancerous cells on

the cervix
Laser Therapy: A carbon dioxide (CO2) laser beam is used to destroy abnormal
cervical tissue
Conization : Can be both for diagnostic and therapeutic purposes where the
cancerous lesion is removed
MEDICAL MANAGEMENT
INVASIVE CERVICAL CANCER
• Simple hysterectomy
• Radical hysterectomy & lymph
node dissection: Removal of entire
uterus, surrounding tissue, upper
part of vagina & lymph nodes
• Trachelectomy – Surgical removal
of the cervix; fertility conserving in
younger women.
• Radiotherapy
• ± chemotherapy; stage dependent.
Treatment Modalities and Nursing Management of the Woman With Cervical Pre-invasive or
Invasive Disease (Yarboro, Cancer nursing) for example

Treatment Modalities Nursing Management

Local therapies (eg, • Explain the disease. Assure patient that SIL (CIN) is not cancer.
laser cryosurgery, • Explain treatment and possible complications of treatment.
electrocautery) for • Discuss possibility of treatment failure.
preinvasive (CIN) • Instruct in self-care after treatment (no douching, tampons, sexual
disease intercourse for 2–4 weeks).
• Stress importance of follow-up care (next appointment, call physician if
fever, bleeding develops).
• Assess concerns related to sexual function (changes in libido, orgasm,
coital frequency, fertility).
• Assess for anxiety, depression, changes in body, self-image.
• Assess for psychological issues associated with sexually transmitted
disease (guilt, blame, mistrust).
Treatment Treatment
NursingModalities
Managementand Nursing Management of the Woman With
Modalities Cervical Pre-invasive or Invasive Disease (Yarboro, Cancer nursing)
Surgery Instruct patient preoperatively in use of incentive spirometer, importance of turning, coughing, deep
breathing, abdominal splinting, early ambulation, and use of antiemboletic stockings. Have patient do
return demonstration as indicated.
Review bowel preparation procedure.
Review need for IV, urinary catheter, colostomy, ileal conduit as indicated.
Begin ostomy teaching preoperatively as indicated.
Stress availability of pain medication.
Review use of patient-controlled analgesia as indicated.
Explore nonpharmacologic pain relief measures with patient.
Provide postoperative wound care.
Encourage patient to participate in wound care as indicated.
Assess concerns related to sexual function (changes in libido, orgasm, coital frequency, fertility).
Assess cultural beliefs as they relate to treatment (blood transfusions, avoidance of drugs, dietary
restrictions).
Assess spiritual needs/concerns.
Assess vital signs, body systems, lab values postoperatively.
Assess for deep-vein thrombosis.
Assess nutritional status, lymphedema, skin integrity hazards of immobility, alteration in sleep/rest
patterns.
Assess psychosocial functioning.
 Treatment Modalities and Nursing Management of the Woman With
Cervical Pre-invasive or Invasive Disease (Yarboro, Cancer nursing)

Treatment Modalities Nursing Management

Radiotherapy • Review treatment procedure (eg, external beam, intracavitary).

• Review side effects of therapy (eg, to skin, effect on blood values, vaginal
stenosis as indicated).
• Explain mobility restrictions with intracavity, interstitial radiotherapy as
indicated.
• Assess for deep-vein thrombosis.
• Encourage diversional activities to relieve boredom.
• Emphasize availability of pain relief measures.
• Explore nonpharmacologic pain relief measures with patient.
• Assess concerns related to sexual function (changes in libido, orgasm, coital
frequency, fertility).
• Assess cultural beliefs as they relate to treatment (blood transfusions,
avoidance of drugs, dietary
restrictions).
• Assess spiritual needs/concerns.
 Treatment Modalities and Nursing Management of the Woman With
Cervical Pre-invasive or Invasive Disease (Yarboro, Cancer nursing)

Treatment Modalities Nursing Management

Chemotherapy • Explain treatment (rationale for chemotherapy, name of chemotherapy
agents, nadir, method of
administration, side effects).
• Assess for symptom burden associated with treatment
• Assess psychological status of patient.
• Assess for anxiety, depression, changes in body, self-image.
• Assess effects of treatment on quality of life.
• Assess concerns related to sexual function.
• Assess cultural beliefs as they relate to treatment (blood transfusions,
avoidance of drugs, dietary
restrictions).
• Assess spiritual needs/concerns.
CANCER OF THE OVARY
• A collection of malignancies
• The complex and linked biologic functions of the ovary are
coordinated through various cells, each of which has neoplastic
potential
• Women have about 1.6% lifetime risk of developing ovarian cancer
• Most common after the age of sixty
TYPES OF
OVARIAN
CANCER
 • EPITHELIAL TUMOURS
• Most common type, accounts for >90% of
ovarian cancers
• Arises from the ovarian epithelium
• The ovarian epithelial tumours include:
TYPES OF • Serous tumours (50%)
OVARIAN • Mucinous tumours (25%)
CANCER • Endometroid tumours (15%)
• Clear cell tumours (5%)
• Transitional cell histology or Brenner
tumours(1%)
 GERM CELL CARCINOMAS

Arise from the ovary’s germinal elements

TYPES OF Account for 30% of all ovarian cancers

OVARIAN
CANCER Benign teratomas or Dermoid cysts are the most common
type, and affect mainly younger women

Malignant germ cell tumours comprise: yolk sac tumours,

immature teratoms, dysgerminomas, choriocarcinomas
and other less common types
 SEX CORD STROMAL TUMOURS

Most of them are confined to the ovary and rarely

spread
TYPES OF Account for 7% of the ovarian cancers

OVARIAN Common in women in their fifties to sixties

CANCER Treatment often involves surgery

Most of them are refractory to chemotherapy

 Nulliparity

Cigarette smoking

RISK Hormone Replacement Therapy

FACTORS Genetic factors

History of endometriosis
 Painless unless ovaries undergo torsion
Symptoms include:
Pelvic discomfort
Bloating

SYMPTOMS Urinary or bowel pattern changes

Heartburn
Early satiety
Abdominal pain
Abdominal distention- Ascites
STAGING
STAGING & PROGNOSIS
STAGE DESCRIPTION FIVE YEAR SURVIVAL RATE

1 Confined to the ovary 90-95%

2 Confined to the pelvis 70-80%

3 Intraabdominal spread 20-50%

4 Spread outside the abdomen 1-5%

 • Surgery
• salpingoopheroctomy
• ± hysterectomy
• omentectomy
TREATME • Pelvic lymphnodes sampling & excision
• If bulky disease; partial bowel
NT resection, splenectomy, and upper
abdominal surgery may be performed
• Chemotherapy
• Immunotherapy
• Accounts for 0.4% to 0.6% among
cancers among men in the USA &
Europe
• May represent up to 10% of cancers CANCER OF
in men in Africa, Asia and South
American countries THE PENIS
• More than 95% of penile cancers are
squamous cell carcinomas
 HPV infection
Smoking
RISK Phimosis
FACTORS
Age
HIV/ AIDS
 Growth or sore on the penis

Change in colour of the penis

A lump or thickening of the skin of the penis

Reddish or velvety rash

SYMPTOMS Foul smelling discharge or bleeding from the penis

Swelling

A lump in the groin

Unexplained pain on the glans

Itchiness or a burning sensation on any part of the penis

 Biopsy

DIAGNOSIS CT scan

Health History and Physical

examination
 Surgery

Penectomy (penile amputation- partial or total,

with possible removal or regional lymphnodes.

Chemotherapy
MANAGEMENT
Radiation therapy

Biotherapy
TESTICULAR CANCER
• Over 90% of testicular cancers start in the germ cells- responsible for sperm production
• Main types of germ cell tumours are Seminomas & Non-seminomas
• Some testicular cancers contain both seminoma and non-seminoma cells, and are called Mixed germ cell carcinomas
• SEMINOMAS
• Grow and spread relatively slow when compared to non seminomas
• Classified into two: i) Classical seminomas- most common- in ages 25-45
ii) Spermatocytic seminoma - found in older men & are
less likely to spread
TESTICULAR CANCER
• NON-SEMINOMAS
• Common in men in their late teens to the age of 30
• Four types have been identified; embryonal carcinoma, yolk sac carcinoma,
choriocarcinoma and teratoma.
• EMBRYONAL CARCINOMA
• Resemble tissues of early embryo when viewed under the microscope
• Rapid growth and can spread to distant organs
• Increased levels of alpha-fetoprotein (AFP) & human chorionic gonadotropin (HCG)
levels-Tumour markers
TESTICULAR CANCER
• YOLK SAC CARCINOMA
• Resemble a yolk sac of an early human embryo
• Most common form of testicular cancer in children, especially infants
• Successful response to treatment especially in children

• CHORIOCARCINOMA
• Rare and fast growing form of testicular cancer in adults
• Pure choriocarcinomas tend to spread to other organs including the lungs, brain etc.
• Mixed tumours have a relatively better disease trajectory
• Choriocarcinomas raise blood levels of HCG
TESTICULAR CANCER
• TERATOMA
• Rare tumours and do not increase neither AFP or HCG
• Areas resembling all the three layers of a developing embryo (ectoderm, mesoderm &
the endoderm)
RISK FACTORS FOR TESTICULAR CANCERS
An undescended testicle (cryptorchidism)
Family history of testicular cancer
HIV infection
Carcinoma in situ
Cancer in the other testicle
Age ( most common among men aged 20-34)
Race – More common in whites
Body size - higher risk in tall men
SIGNS & SYMPTOMS
• Lump or swelling in the testicle
• Breast growth or soreness- due to secretion of the human chorionic gonadotropin
hormone in high levels by some testicular cancers
• Early puberty in boys- Ledydig cell tumours produce androgens or male sex hormones,
leading to early puberty signs in boys
• Orchitis –inflammation of the testicle or epididymitis- inflammation of the epididymitis
• In advanced cancer; lower back pain, shortness of breath, chest pains, abdominal pains,
headaches and confusion in case of brain metastasis
DIAGNOSIS
Health history and physical examination
Blood tests for tumour markers
Ultra sound
Biopsy
X-rays
CT-scans
TREATMENT

Surgery: Orchiectomy- surgical removal of testicles

Radiation therapy- especially for seminomas
Chemotherapy
Stem cell transplant
Resource: American Oncology Society
PROSTATE
CANCER

• Common caner among men after skin cancer.

• The prostate is located below the bladder and
anterior to the rectum in men
• Together with the seminal vesicles, it produces
part of the fluid that makes semen
• The urethra is encircled by the prostate
• The size of the prostate increases as men age
PROSTATE CANCER
TYPES
• Almost all prostate cancers are adenocarcinomas
• These arise from glandular cells
• Other types are:
• Small cell carcinomas
• Neuroendocrine tumours
• Sarcomas

• Most prostate cancers grow slowly, but some can grow

and spread quickly
 • Age- rare in men below 40, but the risk increases rapidly
after the age of 50
• Race- more common in African American men and
Caribbean men of African descent
• Family history of prostate cancer
• Genetic factors- BRCA 2 mutations known to increase the

RISK
risk of breast and ovarian cancers, also increase the risk of
prostate cancer
• Men with Lynch syndrome; known to increase the risk of
FACTORS colon cancer, are also at risk of developing other cancers,
including prostate cancer
• High consumption of red meat and high fat foods
• Obesity
• Smoking
SIGNS & SYMPTOMS

Low and weak urine stream

Increased need to void especially at night
Blood in urine or semen
Erectile dysfunction
Painful hip, chest & back due to bone metastases
DIAGNOSIS
Screening of men aged 40 and above with a Prostate Specific
Antigen (PSA) blood test- early detection
PSA levels above 4ng/ml considered high, and may indicate
prostate cancer among other conditions
Health history and physical exam; including digital rectal
exam(DRE)
Prostate biopsy
PROSTATE CANCER GRADING
• GLEASON SCORE is used for grading prostate cancer
• Cancer cells are assigned a grade based on how abnormal they look when viewed under
a microscope
• The cells are graded on a scale of 1-5, grade 1 resembling normal prostate tissue, and
grade 5 barely resembling normal tissue because of gross mutation
• A Gleason score is the sum of most predominant tissue grade and the second most
predominant tissue grade
• For example, 3+4, to give a Gleason Score of 7 (intermediate grade)
• Higher grade cancers look more abnormal and are likely to grow and spread more rapidly
than low grade cancers
• A Glean Score of 8 to 10 indicates high grade or high risk prostate cancer
PROSTATE CANCER GRADING
PROSTATE CANCER GRADING
• The revised prostate cancer grading system called the grade group system was
introduced in 2014, by the International group of Urological pathologists.

Risk Group Grade Group Gleason Score

Low Grade Group 1 Gleason Score ≤ 6
Intermediate Favorable Grade Group 2 Gleason Score 7 (3 + 4)
Intermediate Unfavorable Grade Group 3 Gleason Score 7 (4 +3)
High Grade Group 4 Gleason Score 8
High Grade Group 5 Gleason Score 9-10
TREATMENT FOR PROSTATE CANCER
• Surgery
• Orchiectomy- Surgical removal of testicles
• Prostatectomy- Surgical removal of the prostate
• Hormonal Therapy- Androgen suppression therapy
• Chemotherapy
• Radiation Therapy
Common Tumour
Markers for Cancers
• A tumour marker test on its own is not
enough to screen for or diagnose cancer.
Tumour marker test results should be
combined with:
• a thorough medical history
• a physical exam
• other lab tests
• imaging tests
• https://cancer.ca/en/treatments/tests-
and-procedures/tumour-markers
 • If a tumour marker test is being used to monitor how
treatment is working, your test results may be
compared to results from before the start of treatment.
• If tumour marker levels decrease or return to normal, it
may mean that treatment is working, especially if levels
were increased before treatment.

Tumour • An increase in tumour marker levels may mean the

cancer is not responding to treatment, is growing or has

Markers
come back (recurred). A slight increase may not be
significant. The doctor looks at trends in the increase
over time.
• Chemotherapy treatment can cause a temporary
increase in tumour marker levels. This happens because
chemotherapy causes cancer cells to die quickly and
release large amounts of the tumour marker.
 Limitations of tumour markers
• There are limitations to tumour markers. Other tests are usually
needed to diagnose cancer or find out if cancer has come back after
treatment. Some limitations of tumour markers include:
• A non-cancerous disease or condition can increase tumour marker
levels. Some tumour markers can be high in people who do not have
cancer.
• Some tumour markers are specific to a particular type of cancer, while
others may be elevated in many types of cancer.
• Tumour marker levels may not rise until the cancer worsens. This is not
helpful for finding cancer early or finding out if cancer has come back
after treatment.
• Some cancers do not have known tumour markers.
• Some people do not have higher tumour marker levels even if the type
of cancer they have usually makes tumour markers.
E.g’s of Tumour Markers
https://cancer.ca/en/treatments/tests-
and-procedures/tumour-markers

• There are many different types of tumour markers, including:

• alpha-fetoprotein (AFP)- Germcell CAs (ovarian and testicular)
• cancer antigen 125 (CA125)- Ovarian CA
• cancer antigen 15-3 (CA15-3)- Breast CA
• carbohydrate antigen 19-9 (CA19-9)- Pancreatic CAs
• carcinoembryonic antigen (CEA)- Colorectal CAs
• human chorionic gonadotropin (hCG or beta-hCG)- gestational
trophoblastic disease (GTD) germ cell tumours of the ovary and testicle
etc.
• prostate-specific antigen (PSA)- Ovarian CA