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GENITOURINARY

CANCERS
PROSTATE CANCER
 Most frequently diagnosed
malignancy and the second
leading cause of cancer death in
men.
 Global distribution of prostate
cancer reveals predominance in
the United States and Canada.
 Scandinavia and parts of
Carribean have higher rates while
Japan and China have extremely
lower rates.
 Among men diagnosed with prostate cancer,
98 % survive at least 5 years, 84 % survive at
least 10 years and 56 % survive 15 years.

COMMON RARE
• United states • Africa
• Northwestern • Central America
Europe • South America
• China
ETIOLOGY AND RISK FACTORS
 Appears as a result from interplay
between endogenous and
environmental influences.
 Risk factors: age, ethnicity and family
history
 Other risk factors: Increased fat
intake, consumption of red meat, and
increased dietary animal fat
 African men have greater melanin
deposition and have higher prostate
cancer rate.
 Men living in higher altitudes with less
exposure and Vit. D have higher rate
of prostate cancer
 Older than 65 years old
 Familial predisposition may occur in men who
have father or brother previously diagnosed with
prostate cancer
 HPC 1, BRCA 1, BRCA 2 mutations
 Endogenous hormones such as androgen and
estrogen
 Oldermen with vitamin D
deficiency
 Occupational exposure
 Farmingand pesticide
exposure
 Malignancies
in
chromosomes 1, 8, 10, 16,
17, and 20
PREVENTION, SCREENING, AND
DETECTION
 Advise patient to consume prudent low fat
and high fiber diet with consumption of
lycopene rich products.
 PSA (Prostate Specific Antigen) – a serine
protease produced by malignant cells in
the prostate.
Elevated levels in DRE (Digital Rectal
Exam, Benign Prostatic Hyperplasia and
prostatitis)
 American Cancer Society recommends to
start testing at age 40.
 Normal level: 2.6 to 4 ng/mL.
 An abnormal PSA is defined as a
value of 4.0 ng/ml or higher.
 National Comprehensive Cancer
Network includes in its guidelines
that PSA level of 2.6 ng/ml or
higher even in the presence of
normal DRE should be considered
for prostate biopsy.
CLASSIFICATION
 95 % are adenocarcinomas
 5 % are sarcomas and transitional cell tumors
 Neoplasm of prostate gland develop within the
peripheral zone
 Malignant growth spread locally into the seminal
vesicles, peritoneum, and bladder.
CLINICAL FEATURES
EARLY STAGE ADVANCED DISEASE
• Urinary hesistancy, • Bone pain and
frequency pathologic fractures
• Feeling of incomplete • Spinal cord
emptying of bladder
• Blood in the semen
compression
• Decreased ejaculatory • Hematuria
volume • Anemia
• Impotence
SYMPTOMS OF METASTASES
 Backache
 Hip pain
 Perineal and rectal discomfort
 Anemia
 Weight loss
 Weakness
 Nausea
 Oliguria
 Spontaneous pathologic fractures
DIAGNOSIS
 Elevated PSA
 Digital rectal exam provides
useful clinical information about
the rectum, anal sphincter, and
quality of stool.
 Biopsy
 Computed Tomography –
evaluation of nodes, tissue, and
organs and estimate prostatic
size
 MRI – evaluates extracapsular penetration beyond
the gland itself
 Fine needle aspiration – obtain prostate cells for
cytologic examination and determining the stage
of disease
 Radiolabeled monoclonal antibody capromal
pendetide with indium III (prostascint) an
antibody that can be used to detect either
recurrent prostate cancer at low PSA level/
metastatic disease.
STAGING AND GRADING
 T refers to tumor size, N refers to nodal status,
and M for metastasis.
 Prostate cancer is graded according to level of
cellular differentiation detected among biopsy
specimens.
 Gleason score is most commonly employed
grading system.
 Microscopic examination are rated on score of 1
to 5.
 Total scores ranges from 2 to 10.
 Higher
scores are more aggressive disease
and poor prognosis.
MANAGEMENT
 Radical Retropubic Prostatectomy –
complete removal of the prostate gland
with lymph node sampling.
-used with patient whose tumor is
confined to the prostate.
- complete surgical of the prostate,
seminal vesicles, tips of the vas deferens
and often the surrounding fat, nerves, and
blood vessels.
 Pelvic floor muscle strengthening exercises –
diminish incontinence.
 Anticholinergic or alpha adrenergic used for
prostatectomy induced incontinence.
 Radiation Therapy
1. Teletherapy (external)
Teletherapy (external beam radiation therpay)
EBRT may be given for 5 days per week for 7-8
weeks.
2. Brachytherapy (internal) involves the
implantation of the interstitial radioactive seeds
under anesthesia.
- Commonly used monotherapy treatment option
for the early clinically organ confined prostate
cancer.
 In this procedure the doctor uses 80 – 100 seeds
(depending on the prostate volume) and the
patient returns to home after the procedure.
 Patient should avoid close contact with pregnant
women and infants for up to 2 months.
 Advise to use condom during sexual intercourse
for 2 weeks after implantation to catch any seeds
that pass through the urethra.
Side effects : inflammations of the rectum, bowel
and bladder (proctitis, enteritis, and cystitis)
 Hormonal Therapy – 4 major types of hormonal
manipulation aimed for the disruption of androgen
stimulation: bilateral orchiectomy, lutenizing hormone
releasing hormone, antiandrogen, and estrogen therapy
 Androgen Deprivation Therapy- commonly used to
suppress androgenic stimuli to the prostate by decreasing
the level of circulating plasma testosterone or
interrupting the conversion to or binding of DHT.
 LHRH (lutenizing Releasing Hormone) agonists include
leuprolide (Lupron) and goserelin (Zoladex).
May be prescribed for patients who do not show adequate
serum testosterone suppression (less than 50 ng/mL) with
medical or surgical castration. LHRH agonists suppress
testicular androgen.
• Antiandrogen receptor antagonists
include flutamide (Eulexin), bicalutamide
(Casodex), and nilutamide (Nilandron).
Antiandrogen receptor antagonists cause
adrenal androgen suppression.
• When LHRH agonists are initiated, a
testosterone flare may occur, causing pain
in bony metastatic disease. Antiandrogens
given for the first 7 days may reduce this
uncomfortable symptom.
The most common uses of LHRH agonists
are the following:
• (1) in the adjuvant and neoadjuvant setting in
combination with radiation therapy;
• (2) after radical prostatectomy; and
• (3) in the treatment of recurrence indicated by an
elevation in the PSA but without clinical or x-ray
evidence.
Medical and surgical castration causes hot flushing
because these treatment modalities increase
hypothalamic activity, which stimulates the
thermoregulatory centers of the body.
Adrenal ablating drugs
 Ketoconazole (Nizoral) is used to inhibit cytochrome
P450 enzymes, which are required for the synthesis of
androgens and other steroids.
 High-dose ketoconazole lowers testosterone by
decreasing both testicular and endocrine production
of androgen.
 Administration of this medication requires steroid
supplementation to prevent adrenal insufficiency.
 Expectant management or watchful
waiting – involves no local therapy
or diagnosis with initiation of
treatment only when the patient
becomes symptomatic from either
locally advanced disease or
metastatic disease.
 Cryotherapy – direct application of
ice to the prostate gland via
percutaneously inserted cryogenic
probes.
 Chemotherapy
Some of the chemo drugs used to
treat prostate cancer include:
 Abiraterone Acetate
 Apalutamide
 Bicalutamide
 Docetaxel (Taxotere)
 Cabazitaxel (Jevtana)
 Mitoxantrone (Novantrone)
 Estramustine (Emcyt)
TESTICULAR CANCER
 Most common malignancy in men age 15-
35
 Account 1% for solid tumors among men.
 Highest incidence in Scandinivian
countries.
 Lowest incidence in Africa and Asia.
 Testicular cancer is classified as germinal
or nongerminal (stromal).
Secondary testicular cancers may also
occur.
Germinal Tumors
 Make up approximately 90% of all cancers of the testis;
 Germinal tumors are further classified as seminomas or nonseminomas.
 These cancers grow from the germ cells that produce sperm, thus the name
germinal tumors.
 Seminomas are slow-growing forms of testicular cancer that are usually found
in men in their 30s and 40s.
 Although seminomas can spread to the lymph nodes, the cancer is usually
localized in the testes.
 Nonseminomas are more common and tend to grow more quickly than
seminomas. It is often made up of different cell types and are identified
according to the cells in which they start to grow.
 Nonseminoma testicular cancers include choriocarcinomas (rare), embryonal
carcinomas, teratomas, and yolk sac tumors.
Nongerminal Tumors
 Nongerminal tumors account for less than 10% of
testicular cancers.
 These cancers may develop in the supportive and
hormone-producing tissues, or stroma, of the testicles.
 The two main types of stromal tumors are Leydig cell
tumors and Sertoli cell tumors.
 Although these tumors infrequently spread beyond the
testicle, a small number metastasize and tend to be
resistant to chemotherapy and radiation therapy.
Secondary Testicular Tumors
 Secondary testicular tumors are those that have
metastasized to the testicle from other organs.
 Lymphoma is the most common cause of secondary
testicular cancer.
 Cancers may also spread to the testicles from the prostate
gland, lung, skin (melanoma), kidney, and other organs.
 The prognosis with these cancers is usually poor because
they typically also spread to other organs. Treatment
depends on the specific type of cancer (ACS, 2009).
ETIOLOGY AND RISK FACTORS
 Occur in atrophic testis / cryptorchid
( undescended) testis
 Family history of testicular cancer
 History of prior germ cell testicular tumor
 History of trauma to the testis
 Men who are infected with HIV
 Alteration in chromosome Xq27
 Chromosome 1 alteration - found in cases of
testicular carcinoma
 Caucasian American men have a five times greater
risk than African American men and more than two to
three times greater risk than Asian, Native American,
and Hispanic American men.
 Occupational hazards, including exposure to
chemicals encountered in mining, oil and gas
production, and leather processing.
PREVENTION, SCREENING, AND
DETECTION

 Annualtesticular examination for


teenage male
 Monthly testicular self examination
 Teaching TSE, starting in
adolescence, alerts men to
the importance of seeking
medical attention if a
testicle becomes
indurated, enlarged,
atrophied, nodular, or
painful. TSE should be
performed monthly.
 Annual testicular
examination by a clinician
can reveal signs and lead
to early diagnosis and
treatment of testicular
cancer.
CLASSIFICATION
 GCT (seminoma, embryonal cancer, teratomas,
choriocarcinoma, and yolk sac tumor)
 Sex chord stromal / gonadal stromal tumor
 Mixed germ and stromal cell tumor
 Adrenal and Paratestical tumor
Diagnosis
 The tumor markers alpha-fetoprotein (AFP) and
betahuman chorionic gonadotropin (beta-hCG) may be
elevated in patients with testicular cancer. Tumor marker
levels in the blood are used for diagnosis, staging, and
monitoring the response to treatment.
 A chest x-ray to assess for metastasis in the lungs and a
transscrotal testicular ultrasound will be performed.
 Inguinal orchiectomy is the standard way to establish the
diagnosis of testicular cancer.
 Retroperitoneum, pelvis, and chest include an
abdominal/pelvic CT and chest CT (if the abdominal CT or
chest x-ray is abnormal).
Clinical Features
 Small painless mass
 Diffuse pain, swelling or
firmness of testis
 Normal testis is homogenous
in consistency and freely
movable
 Any nodular of fixed mass is
abnormal finding.
 Heaviness in the scrotum, inguinal area, or lower
abdomen.
 Backache (from retroperitoneal node extension),
abdominal pain, weight loss, and general weakness may
result from metastasis.
TREATMENT
 Seminoma therapy- removal of the affected
testiticle, radical inguinal orchiectomy, is initial
treatment for all stages of seminomas.
Stage I (IA,B,S ) – treated with 25- 30 Gy of
radiation to the infradiaphragmatic area including
the para-aortic lymph nodes.
Stage II A and II B- treated with postorchiectomy
RT, 35 – 40 Gy to the infradiaphragmatic and para-
aortic nodes and ipsilateral iliac nodes.
NONSEMINOMA THERAPY
 Stage I A Nonseminoma – nerve sparing
Retroperitoneal lymph node dissection (RPLND) or
observation
 Stage I B tumors – nerve sparing RPLND,
observation, or chemotherapy with RPLND being
the preferred option.
 Stage I S- treated with chemotherapy
 Stage II – chemotherapy and Radiation Therapy
 Radiation therapy is more effective with seminomas
than with nonseminomas. Postoperatively, radiation
may be used in early-stage seminomas.
 Chemotherapy may be used for seminomas,
nonseminomas, and advanced metastatic disease.
Cisplatin (PlatinolAQ) can be used in combination
with other chemotherapeutic agents, such as
etoposide (Toposar), bleomycin
(Blenoxane), paclitaxel (Taxol), ifosfamide (Ifex),
and vinblastine (Velban), and results in a high
percentage of complete remissions.
PENILE CANCER
 Rare disease in
industrialized countries.
 Account for 10 – 20 % of all
malignancies in parts of
Africa, Asia, and South
America, most notably in
Paraguay.
ETIOLOGY AND RISK FACTORS
 Associated with older age (6th or 7th decade
of life)
 Poor hygiene and accumulation of smegma
and irritants
 Phimosis and chronic inflammatory
conditions including balanoprosthitis and
lichen sclerosus et atrophicus, psoriasis
treatment with psoralen
 Sexual history and history of Condyloma
 Lack of circumcision
 Smoking
 Ultraviolet light treatment of psoriasis on Penis
TYPES OF PENILE CANCER
 Squamous cell carcinoma – 95% of cases
 Epidermoid penile cancer
 Verrucous carcinoma
 Adenocarcinoma carcinoma
 In situ carcinomas (Erythroplasia of Queyrat and
Bowen’s disease
 Basal cell penile cancer
 Melanoma
 Sarcomas
PREVENTION, SCREENING, AND
DETECTION

 Circumcision and prevention of


phimosis
 Treatment of chronic
inflammatory conditions
 Limiting PUVA treatment
 Smoking cessation and education
 Education regarding HPV infection
CLASSIFICATION

 High grade tumors and basaIoid and sarcomoid


subtypes are associated with nodal metastases
and poor survival
 Verrucous cancers rarely metastasizes
CLINICAL FEATURES
 Small papule or pustule to an
extensive fungating wound
 Burning or itching under the skin
 If neglected, lesions will
progress and foul smelling
discharges may be seen exuding
from beneath a phimotic,
nonretractive prepuce.
 Wartlike growth on the skin of penis
 Changes in skin color such as red rash
 Bluish growths
 Whitish patches
DIAGNOSIS
Penile cancer involves:
 Glans - most frequently (48%)
 Lesions of the foreskin (21|%)
corOnal sulcus (6%)
 Penile shaft (less than 2%)
 Urethra
 Regional or distant lymphnodes
 Physical examination is necessary – assessment
and palpation of penis and inguinal lymphnode.
- size,location, borderes,consistency, fixation,
and character and time of onset of penile lesion
should be noted.
 Incisionalbiopsy – assess the involvement of
surrounding tissue, determine the cell
types of the penile cancer
 Ultrasound examination and MRI – view
adjacent structures
TREATMENT
 Partial or total Penile
Amputation – gold standard of
therapy. Allow preservation of
enough penile stump to allow
for upright micturition and
sexual function.
 Partial penectomy is preferred to total penectomy
because patients can then participate in sexual
intercourse, stand for urination, and maintain
cosmesis.
 Topical chemotherapy with 5 fluorouracil cream
or biologic therapy.
 Wideexcisions or partial penectomies –
treatment of choice for small localized
tumor.
 Mohs micrographic surgery – systematic
excision of cancerous tissue under
complete microscopic control.
 Cryosurgery
 Electrodessication and curettage
 Ytrrium aluminium garnet (YAG) laser surgery
 Laser surgery – treatment of T1 and
T2 tumors and for local recurrence
following partial or total penectomy.
 Radiotherapy- for small T1N1 tumors
less than `4 cm in diameter. It treat
squamous cell carcinoma of the penis.
 Chemotherapy – used as an adjuvant
and neoadjuvant therapy. Indicated
for squamous cell penile tumors
Some of the drugs used to treat penile
cancer include:
 Cisplatin
 Fluorouracil (5-FU)
 Paclitaxel (Taxol®)
 Ifosfamide (Ifex®)
 Mitomycin C
 Capecitabine (Xeloda®)

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