Prostate Cancer: Presented To Dr. Fawad Rasool by

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PROSTATE CANCER

Presented to Dr. Fawad Rasool by:

UMER IBRAHEEM (41-M-14)


MUHAMMAD ZUBAIR (42-M-14)
MUHAMMAD JUNAID MALIK (84-M-14)
Introduction

Prostate cancer is a malignant neoplasm


that arises from the prostate gland.

Prostate cancer has an indolent course.


Epidemiology

Second leading cause of


cancer related deaths in males.

In US alone, nearly 220,000 men


were diagnosed in 2007.
Etiology(Probable risk factors)
• More than 70% of cases are diagnosed in men older than 65 years
Age

• African Americans have higher incidence and death rate because


testosterone is 15% higher in African American men as compared with white
Race males.

• Familial prostate cancer inherited in an autosomal dominant manner.


• Mutations in the CAG pattern in the androgen receptor gene, CYP17, SRDA2,
Genetic MSR1, can cause increased receptor activation.
Etiology (Possible risk factors)
•Clinical carcinoma incidence varies worldwide.
Environ •Latent carcinoma similar between regions.
mental

•Increased risk associated with high-meat and high-fat diet.


•Decreased intake of vit. D, vit. E, tomatos, and β -carotene increases risk.
Diet
•Does not occur in castrated men.
•Up to 80% are hormonally dependent. African Americans have 15% increased testosterone.
Hormon •Japanese have decreased 5 α -reductase activities .
al
Pathophysiology
◦ The prostate gland is a solid, rounded, heart-shaped
organ positioned between the neck of the bladder and
the urogenital diaphragm.
◦ The normal prostate is composed of acinar secretory
cells that are altered when invaded by cancer.
◦ The major pathologic cell type is adenocarcinoma
(>95% of cases).
The prostate
gland
Pathophysiology
◦ Normal growth and differentiation of the prostate
depends on the presence of androgens, specifically
DHT.
◦ The testes and the adrenal glands are the major
sources of circulating androgens.
◦ Hormonal regulation of androgen synthesis is mediated
through a series of biochemical interactions between
the hypothalamus, pituitary, adrenal glands, and testes.
Hormonal
regulation of
prostate
gland.
Pathophysiology

METASTATIC
SPREAD

Hematogenous Lymphatic
Local extension
dissemination drainage
Pathophysiology
Hematogenous
Lymphatic drainage visceral involvement
dissemination
• Lymph node metastases • Skeletal metastases from • lung, liver, brain, and
are more common in hematogenous spread adrenal glands are the
patients with large, are the most common most common sites of
undifferentiated tumors sites of distant spread. visceral involvement,
that invade the seminal • Sites of bone although these organs
vesicles. involvement include the are usually not involved
• The pelvic and lumbar spine, proximal initially.
abdominal lymph node femurs, pelvis, thoracic
groups are the most spine, ribs, sternum, skull,
common sites of lymph and humerus.
node involvement
TREATMENT
To decrease morbidity and mortality
caused by prostate cancer.

Desired Minimize toxicity associated with

Outcome prostate cancer treatment.

Advanced prostate cancer isn’t


currently curable so treatment should
focus on symptom relief and quality of
life.
Non Pharmacologic Therapy

There are four


non •Expectant Management
pharmacologic •Orchieotomy
approaches
used for •Radiation therapy
prostate cancer •Radical prostatectomy
management.
1.Expectant Management
Involves monitoring the
course of disease and
Also known as watchful initiation of therapy if the PSA & DRE every 6
waiting. cancer progresses or months.
patient become
symptomatic.

Advantages are avoiding


the adverse effects of
definitive therapies i.e
radiation and minimizing
the risk of unnecessary
therapies.
2.Orchiectomy

Bilateral orchieotomy or removal of testes.

Rapidly reduces circulating androgens to castrate levels ( <50ng/dL ).

Preferred initial treatment in patients with impending spinal cord


compression or ureteral obstruction.

Some patients find the procedure psychologically unacceptable and


many patients because of their advanced age are not surgical
candidates.
3. Radiation therapy

There • External Beam Radiotherapy:


• Doses of 70 to 75 Gy in patients with low-grade
are two prostate cancer and 75 to 80 Gy for those with
intermediate or high-grade cancer.

methods
• Brachytherapy:
• Permanent implantation of radioactive beads of
145 Gy Iodine or 124 Gy of Palladium. It is usually

used. reserved for low risk cancers.


Acute complications Chronic complications
from radiation therapy include proctitis,
include cystitis, proctitis, diarrhea, cystitis,
hematuria, urinary enteritis, impotence,
retention, penoscrotal urethral stricture &
edema & impotence. incontinence.
4.Radical Prostatectomy
Nerve sparing radical prostatectomy can be
performed in many patients; 50 to 80% regain sexual
potency within the first year.

Complications include blood loss, stricture formation,


incontinence, lymphocele, fistula formation,
anesthetic risk and impotence.

Because of significant and immediate mortality,


many patients may elect to postpone therapy until
symptoms develop.
Drugs of first choice

• Luteinizing Hormone-
Releasing Hormone
Agonists
Pharmacological • Gonadotropin-Releasing
Therapy Hormone Antagonists
• Anti-Androgens
• Combined Androgen
Blockade
• Chemotherapy
Drugs include leuprolide acetate,
leuprolide depot, leuprolide implant,
triptorelin depot, triptorelin implant,
goserlin acetate implant.

1.LH-RH Dosing interval ranges from once

Agonists monthly to every 16 weeks.

Common adverse effects include


disease flare up, hot flashes, erectile
impotence, decreased libido and
injection site reaction.
2.GnRH antagonists
It binds reversibly to GnRH
receptors in the pituitary
Major advantage over
There is only one drug in gland, reducing the
LHRH agonists is lack of
this class i.e. Degarelix production of
tumor flare.
testosterone to castrate
levels in 7 days or less.

Administered as a SC
injection every 28 days.
Drugs include Monotherapy is no
flutamide, longer
bicalutamide, recommended
nilutamide, due to decreased
enzalutamide. efficacy.

3.Anti-
Androgens Antiandrogens are
indicated for Adverse effects
advanced include
prostate cancer gynecomastia,
only when loss of libido, LFT
combined with abnormalities, GI
LHRH agonists or disturbances.
orchieotomy.
4.Combined Androgen Blockade
Also referred as maximal androgen deprivation or total
androgen blockade.

Combination of LHRH agonists or orchieotomy with


antiandrogens is most extensively studied CAB approach.

Major benefit is seen in patients with minimal disease.

It is appropriate to use either LHRH agonists as monotherapy


or CAB as initial therapy for metastatic prostate cancer.
Docetaxel 75mg/m² every 3 weeks,
combined with prednisone, 5mg
twice daily improves survival in
castrate-refractory prostate cancer.
Common adverse effects include
nausea, alopecia &
myelosuppression.
5.Chemotherapy
Cabazitaxel 25mg/m² every 3 weeks
with prednisone 10mg daily
significantly improves progression
free and overall survival.
Neutropenia, neuropathy and
diarrhea are most common
toxicities.
Monitor primary tumor size,
involved lymph nodes, and tumor
marker response such as PSA with
Evaluation definitive, curative therapy. PSA
level is checked every 6 months for
of the first 5 years, then annually.

therapeutic With metastatic disease, clinical


outcomes benefit can be documented by
evaluating performance status,
weight, quality of life, analgesic
requirements, and PSA or DRE at 3
month interval.

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