INTRODUCTION TO
CARE OF PATIENT WITH
CANCER
Objectives
• Define cancer and differentiate benign from malignant neoplasms.
• Discuss the theories of carcinogenesis, known carcinogens, and risk factors
for cancer.
• Compare the mechanisms and characteristics of normal cells with those of
malignant cells.
• Describe the effects of cancer on the body.
• Describe the laboratory and diagnostic tests used to diagnose cancer.
• Discuss the role of chemotherapy in cancer treatment.
• Discuss the use of surgery, radiation therapy, and biotherapy in the
treatment of cancer.
• Describe the nursing interventions required for selected oncologic
emergencies.
• Provide teaching to the client and family experiencing cancer.
• Use the nursing process as a framework for providing individualized care to
the client with cancer. *
•
OVERVIEW
• Progress in prevention, treatment, & survival
- Early detection
- Sophisticated diagnostic tests
- Aggressive chemotherapy, radiation,
surgery
- Effective management of side effects
- Bone marrow transplants
- Genetic research
- Biological response therapy*
Epidemiology
• Variables/Risk Factors
- Sex
– Women more prone to breast, uterus and cervix
– Men more prone to prostate, lungs
- Site
- Occupation
– Chemical factory workers. Farmer, radiology department personnel
- Age
– Older individuals
- Race
- Heredity/genetics
– With positive family history
- Obesity*
– Linked to breast and colorectal CA
- Socio-economic status
- Geographic's
– More common in urban dwellers
– Japan- stomach CA; US – breast CA*
- Environmental exposure
- Stress
Health Promotion
• Primary Prevention – control of risk factors
• Secondary Prevention – early detection
- CAUTION 7 WARNING SIGNS
- ACS Guidelines
• Tertiary Prevention – monitoring for
complications, symptom management,
support groups
•
WARNING SIGNS OF CANCER
C – Change in bowel & bladder habits
A – sore that does not heal
U – Unusual bleeding or discharge
U – unexplained sudden weight loss
U - Unexplained anemia
T – Thickening or lump in breast or elsewhere
I – Indigestion or difficulty in swallowing
O – Obvious change in wart or mole
N – Nagging cough or hoarseness of voice
Guidelines for early detection
of cancer
GENERAL BREAST
Cancer related Checkup: 20 - 40 Years:
18-40 years - every 3 years Breast exam by MD every 3
40 years & older - every year years
Breast self-exam every month
Baseline mammogram between
Health Counseling: ages of 35 and 39. Every yr. >40
Smoking cessation, avoiding sun
Exam for cancer of thyroid,
UTERINE/CERVIX
testes,
Sexually active people or 18 yr.
prostate, ovaries, skin, and lymph
> Papanicolaou (Pap) smear &
nodes.
yearly
• > pelvic examination
GUIDELINES FOR EARLY DETECTION OF
CANCER
PROSTATE COLON & RECTUM
50 yr. > Prostate Ages 40 years and older
Specific antigen Digital rectal exam every
<4mg/ml year
Combined with rectal
Ages 50 years and older
examination, nearly 90% Digital rectal exam every
of clinically significant
cancers can be detected. year
Stool for occult blood year
Protoscopic exam or flexible
TESTICULAR
15 - 45 yr.: Testicular self- sigmoidoscopy every 5 yrs
exam •
The Cell
• Cell cycle (Go, G1, S, G2,
mitosis)
• Normal Cell Characteristics
- Appearance
- Growth pattern
- Differentiated functions
- Non-migratory
Characteristics of Early
Embryonic Cells
• Rapid & continuous cell division
• Large nucleus
• Perform no differentiated functions
• Adhere loosely together
• Able to migrate
• Not contact inhibited
•
*Embroyonic Cell Testing
Commitment Phase of Early
Embryonic Cells
• Turn off proto-oncogenes
• Expression of specfic genes
•
Biology of Abnormal Cells
• Benign Neoplasm • Malignant Neoplasm
- Grow slowly - Grows rapidly
- Show specific - Anaplastic morphology
morphology - Large nucleus
- Small nucleus - Undifferentiated
- Differentiated functions - Adhere loosely
- Adhere tightly together together
- Grow orderly manner - Grow by invasion
- Non-migratory - Able to migrate
-
CHARACETERISTICS BENIGN MALIGNANT
SPEED OF GROWTH SLOWLY RAPIDLY
MODE OF GROWTH REMAINS LOCALIZED INFILTRATES
SURROUNDING TISSUES
CAPSULE ENCAPSULATED CAPSULATED
CELL CHARACTERISTIC WELL DIFFERENTIATED POORLY DIFFERENTIATED
MATURE CELL
RECURRENCE EXTREMELY UNUSUAL COMMON FOLLOWING
SURGERY
METASTASIS NEVER VERY COMMON
EFFECT OF NEOPLASM NOT HARMFUL TO HOST ALWAYS HARMFUL
PROGNOSIS VERY GOOD POOR
Carcinogenesis/Oncogenesis
• Steps of Malignant Formation
- Initiation (pure carcinogens)
- Latency Period
- Promotion
- Progression
Metastasis
• Malignant transformation
- Extension into surrounding tissue
• Tumor vascularization
- Penetration into blood vessels
• Blood vessel penetration
- Release of tumor cells into blood
• Arrest and invasion
- Invasion of tissue at site of arrest
•
The Development and Spread of Tumors
1. Lung cancer begins when epithelial cells lining the respiratory tract
start to reproduce an uncontrolled fashion.
2. These cells invade surrounding tissue, forming a mass in called a
tumor and, when hardened, a carcinoma.
3. Cancerous cells may penetrate blood and lymph vessels, to be
carried through the body until they reach a juncture through which
they cannot pass. At this point, they lodge and new tumors form.
Metastasis, the spreading of cancer from its original location to other
parts of the body, is the disease’s most destructive characteristic.
Routes of Metastasis
• Local Seeding
• Bloodborne
• Lymphatic
Secondary Tumors
Breast: Bone & lung
Prostate: Bone (spine & legs); Pelvic nodes
Lung Cancer: Brain, bone, liver, lymph nodes, pancreas
Melanoma: GI tract, lymph nodes, lung, brain
Colorectal: Liver, lymph nodes, adjacent structures
Cancer Classification
• Neoplasm
- Benign: suffix - oma
- Malignant: root sarco- or carcino-
• Tissue of origin
- Epithelial: glands, ducts, mucous membrane
- Connective tissue: bone, muscle, fat
- Hematopoietic: blood vessels, bone marrow,
lymph tissue
- Pigmented: pigmented producing skin
- Neural: Nerve Tissue
• Name of scientist describing tumor – Hodgkins, Wilms
Tumor Classification
• Grading – Histological make-up (cellular
aspects of tumor) Gx – G4
• Staging – exact location & extent of
spread @ diagnosis
– TNM Classification: Tx, To, T1,2,3,4 ; Nx, No,
N123
Mx, M0, M1
Phases of Cancer
• Pre-diagnosis
• Initial Diagnosis
• Treatment Phase
• Readmission Phase
• Reoccurrence
• Terminal
• Survival
Assessment
• History – depends on phase of cancer
- Focus on system of body
- Height, weight, vital signs
- Focus on effects of treatment
- Review medications
- Determine knowledge level
• Subjective Data
• Objective Data
Collaborative Assessment
• Laboratory blood tests
– CBC
– Platelet count
– WBC with differential
– Blood chemistry (ca ++; alkaline
phosphatase
– Coagulation studies (PT,Ptt)
– Tumor markers (specific for types of
cancer)
Collaborative Assessment
• Cytology Studies
• Biopsy
• Body Imaging – MRI, CT Scan
• Radiological Studies
• Ultrasound
• Endoscopies
• Immune Studies – antigen skin testing
•
Nursing Diagnoses
• Physiological
- Imbalanced nutrition
- Fatigue
- Altered comfort
- Altered oral mucosa
- Impaired skin integrity
- Disturbed sensory perceptions
Nursing Diagnoses
• Psycho-social
- Altered coping, individual/family
- Knowledge deficit
- Decisional conflict
- Grieving
- Powerlessness
- Hopelessness
- Altered body image
Surgical Interventions
• Purposes
- Diagnosis
- Cure
- Control
- Palliation
- Reconstruction
Surgical Interventions
• Biopsies – Needle, incisional,
excisional,staging
• Local Incision
• Wide Local Incision
• Wide Excision
• Extended Radical Excision
Radiation Therapy
• Treatment of disease with ionizing radiation - damage to
DNA leads to cell death
• Underlying Principles:
- Dose Determination
- Fractionalization
• Purposes
- Cure
- Control
- Palliation
• Radiation Treatment
• In this procedure the radioisotope cobalt 60 is used as the source of
gamma radiation. A high dose of gamma radiation is guided by
laser targeting to a localized area of treatment.
Radiation Therapy
• Tele “distant” therapy – beam radiation (Cobolt 60)
• Patient Preparation
Side Effects – Site Specific
• Skin Changes Local - skin changes - erythema, dryness, moist
desquamation, hyperpigmentation
• Head and Neck - mucous membrane
• Breast - erythema, swelling, discomfort
• Head/Brain - alopecia, CNS edema, motor & neuro deficits
• Pelvis & long bones - diarrhea, bone marrow suppression
• Lung & chest wall – pneumonitis, esophagitis
• Radiation Syndrome – effects not related to site
•
Brachytherapy
• Use of high energy radioactive materials within
body tissues
• Rationale: A very limited dose, directly absorbed
into malignant tissue for specific period of time
• Types
- Sealed isotopes (Molds, Plaques, Needles)
- Unsealed (orally or IV for dx. or Rx. Of
hyperthyroidism i.e.. iodine 131)
Brachytherapy – Safety Principles
• “Caution: Radioactive Material” sign
• Know type & place of implant
• Time, Distance, Shielding
• Body fluids precautions
• Wear dosimeter badge
• Never touch radiation source with bare
hands (Lead container & forceps in
room)
Chemotherapy
• Goals
- Cure
- Control
- Palliation
Pathophysiological Principles of
Chemotherapy
• Cell Kill Hypothesis – Any dose of Chemo.
Will destroy only a fraction of malignant
cells (Overhead)
• Cell Cycle Specific
• Cell Cycle Non-specific
• Combination Therapy (Tumor sensitivity,
side effects, variation in timing of drug
induced immunosuppression)
• Hormones and Steroids
Classification of Chemotherapeutic
Agents
• Alkylating Agents - Interferes with DNA
Replications
• Antimetabolites - Inhibits DNA Synthesis
• Nitrosoureas - Interfere with DNA replication and
repair.
• Antitumor antibiotics - Interfere with nucleic acid
synthesis and function, inhibits RNA synthesis
and DNA synthesis
• Plant Alkaloids) arrest or inhibits mitosis
• Hormonal Therapy
Dosage Calculation
• Remember the Five Rights:
– medication, time, route, dose, patient
• Calculate body surface area (BSA)
• Recalculate drug and dosage against order
• Check current labs
• Review drugs and potential side effects
• Verify informed consent
• Pre-medicate if ordered
•
Preparation
• OSHA Standards
- Reconstitute under Class II laminar
flow biological safety cabinet
- Wear protective clothing, latex gloves,
gown, mask, goggles
- Change protective clothing when
contaminated
- Careful disposal of drug contaminated
items
Routes of Chemo Therapy Administration
(overhead)
• Oral
• Intravenous
• Intra-arterial
• Isolated limb perfusion
• Intracavity
– Intra-peritoneal
– Intraventricular
– Intrathecal
– Intravesical
• Intraperitoneal
• Intraventricular
• intrapleural
Side Effects of Chemotherapy
• Gastrointestinal
- Nausea & Vomiting
- Mucositis/stomatitis
- Diarrhea & Constipation
• Fatigue
• Alopecia
• Infection
Side Effects of Chemotherapy
• Bone Marrow Suppression
- Anemia
- Neutropenia
- Granulocytopenia
- Leukopenia
- Thrombocytopenia
NIC – Nutrition/Nausea & Vomiting
• Explore food preferences
• Avoid spicy foods
• Monitor weight
• Assess for Sx. Of dehydration
• Small frequent meals
• Administer antiemetics
NIC – Mucositis/Stomatitis
• Assess oral mucosa
• Oral hygiene before & after meals
- Rinse mouth with ½ strength peroxide/saline
- Avoid alcohol or glycerine mouth washes
- Antimicrobal therapy
- Topical Anesthetics
- Soft diet, popsicles
- Artificial saliva
NIC - Alopecia
• Reassure that hair loss temporary
• Use mild shampoos, avoid dyes &
permanents
• Cut hair short & purchase hair piece
before loss
• Ice caps, pressure caps
•
NIC - Anemia
• Assess hemaglobin, hematocrit
• Encourage frequent rest periods
• Monitor packed red cell infusions
• Administer procrit if ordered
NIC – Risk for infection
• Monitor WBC – Handout on neutrapenia
(Absolute Neutraphil Count (ANC)
• Private room (CHIPS precautions) WBC > 1,000
mm3
• Avoid crowds
• Strict handwashing
• Low bacteria diet
• Monitor IV sites, arm pits, genitalia, anal areas
• Report temperature 100о F (38o C)
NIC - Thrombocytopenia
• Assess platelet counts <50,000 risk for
bleeding; < 20,000 very high risk for
hemorrhage
• Assess for bleeding any orifice,
petechiae, ecchymosis, hematomas
• Avoid intramuscular injections,
venopunctures
• Avoid trauma to anal area
•
Immunotherapy
Biological Response Modifiers
• Agents that restore, augment, or modulate
the host’s normal immune system
- Interleukins
- Interferons
• Agents that have direct antitumor effect
• Agents that block access to cancer cells
Breast Cancer
What is Breast Cancer?
•
• Abnormal cells develop from normal cells
in the breast to form tumors
•
• Tumor cells have genetic defects that
allow the cells to grow too rapidly and to
invade normal tissues
• 90% of women with breast cancer have
tumors due to spontaneous new
mutations arising in their breast tissue
as they age
What is Breast Cancer?
• The cause of these mutations is not
known
• 10% of women with breast cancer have
an inherited risk for cancer due to
genes passed on from their parents
•
Breast cancer: Steps in the
development of a tumor
•
• Cancers develop due to a series of
molecular changes in the the cells of the
breast
• These cellular changes lead to pre-
malignant tissues in the breast that can
be identified in a biopsy
• Cancers develop from a microscopic
group of cells that grow into larger
tumors over time
Stages of breast cancer?
• The rate at which a cancer will grow is
not predictable - some tumors grow
slowly, others rapidly
• The earlier a tumor is identified, the
better the chance for cure
• 95% of women with cancers less than
1/2 inch in size are cured
•
Breast Cancer: Statistics
• Breast cancer is the most common cancer
in American women
• 185,000 new cases this year
• 41,000 American women will die of breast
cancer - second only to lung cancer as a
cause of cancer death among women
• Lifetime risk for the average woman;
approximately one in nine will develop
breast cancer
What is my risk for
developing breast cancer?
• Age greater than 50 years
• History of breast cancer in a close
relative (mother/sister/daughter)
• 90% of women with breast cancer
have no relatives with the disease
Risks
• Finding of premalignant changes in
your breast tissue
• Never having children
• Having your first child after age 30
• Obesity - Alcohol - Estrogen therapy
•
What is my best defense against
breast cancer?
EARLY DETECTION
• Be aware of your personal risk for breast
cancer
• Have a screening mammogram every year
once you are 40 years old
• Have an annual breast exam every year after
age 40
Early Detection
• Practice monthly breast self exam
• See your doctor promptly if you note a
new breast lump or thickening
• Enjoy a healthy life: control your
weight, minimize alcohol, don’t
smoke, exercise
•
Why are mammograms important?
•
• Mammograms are sensitive xrays of
the breast
• Small, safe dose of radiation is used
• Minor discomfort due to pressure on
the breast is noted by some women
EARLY DETECTION LEADS TO CURE
Why are mammograms important?
• Mammograms can detect changes in
breast tissue that may be associated
with cancers and premalignant
changes
• Mammograms are the best means to
find early curable cancers - cancers
too small to be detected by touch
• 85% of cancers will show up on a
mammogram - 15% will not
What if I have an abnormal mammogram?
•
• See your doctor for a breast
examination
•
• Special mammogram will be done to
confirm if the finding is real
• Additional imaging tests - ultrasound -
for better definition
• Close follow-up imaging may be
recommended at 6 months or:
What if I have an abnormal
mammogram?
Biopsy may be recommended
Needle biopsy - Ultrasound directed
Needle biopsy - mammogram directed
Surgical biopsy
The tissue diagnosis is the most important
information in planning treatment
Most mammogram abnormalities are not
cancer; most are due to benign changes
What if I feel a lump in my breast?
•
•
• Go to you health care provider promptly for a
physical examination; don’t wait for your
annual examination
• She may refer you for breast imaging - even if
you had a mammogram less than one year
previously
• He may refer you to a Breast Center - or
specialist in breast care - a surgeon or medical
oncologist
EARLY DETECTION LEADS TO CURE
What if I feel a lump in my breast?
• A biopsy may be recommended,
depending on the features of the
lump
•
• Many lumps in the breast are NOT
cancer; benign fibrocystic disease
and benign tumors are common
•
How is the diagnosis of breast cancer made?
A suspicious sign on a mammogram or a
lump in the breast will indicate the need for
a tissue biopsy
A biopsy of the abnormal tissue is required
to make the diagnosis of breast cancer
A careful physical examination will give
signs about the stage of the cancer
size of tumor in breast
lymph node enlargement under arm
status of the opposite breast
How is the diagnosis of breast cancer
made?
Features of the tumor:
type of breast cancer - ductal,
lobular, etc
grade of the tumor
hormone receptor status
indicators of biologic growth rate
potential
c-erb
How is breast cancer treated?
1. SURGERY: to remove all the tumor
Breast preserving surgery - most
patients
Removal of the full breast - mastectomy -
may be required for some patients
2. DETERMINE THE STAGE OF THE
TUMOR: Remove some of the lymph
nodes under the arm to look for tumor
metastases
How is breast cancer treated?
3. ADJUVANT THERAPY: Medical therapy to
decrease the chance of tumor recurrence - to
improve the chances for cure
Chemotherapy - many different therapies
Hormonal therapy - tamoxifen, aromatase
inhibitors
4. RADIATION THERAPY - to prevent tumor
recurrence in the remaining breast tissue;
required for breast preserving therapy
•
Can breast cancer be prevented?
NSABP P1 Trial: showed that women with an
increased risk for breast cancer can have that risk
decreased by 40 - 50% by taking the anti-estrogen
medication tamoxifen
Tamoxifen benefited women with:
the breast cancer gene
age greater than 55 years
premalignant changes in previous biopsies
Side effects
very small increase in risk of cancer of the
uterus
blood clots
Can breast cancer be prevented?
• Who should be offered
chemoprevention?
•
• How long should we give this
medication?
• Are the long term effects satisfactory?
STAR Chemoprevention Trial
(Study of Tamoxifen against
Raloxifene)
• National clinical study that will enroll
22,000 women to test the
effectiveness of 2 different anti-
estrogens for the prevention of
breast cancer
STAR Chemoprevention Trial
(Study of Tamoxifen against Raloxifene)
Tamoxifen vs. Raloxifene
both are approved medications that selectively
block estrogen receptors
estrogen receptors are present on many tissues -
breast, bone, uterus, blood vessels, and many
others
Tamoxifen - breast cancer medication
Raloxifene - anti-osteoporosis medication
Compare the 2 groups of women for
development of breast cancer, possible side
effects or other benefits
STAR Chemoprevention Trial
(The Study of Tamoxifen against Raloxifene)
Eligibility for participation is based on a
5 year predicted risk for developing
breast cancer. The following factors
contribute to this calculated risk:
Age: post-menopausal women over the
age of 35
positive family history of breast cancer
history of benign breast biopsies
history of lobular carcinoma is situ on
previous breast biopsy
Cervical Cancer
Cervix
• Lower part of the uterus
• Connects the body of the
uterus to the vagina
(birth canal)
•
•
•
•
Source: American Cancer Society
Cervical Cancer
• Begins in the lining of the cervix
• Cells change from normal to pre-cancer
(dysplasia) and then to cancer
•
•
•
•
Source: American Cancer Society
Three Types
Squamous cell Carcinomas
Cancer of flat epithelial cell
80% to 90%
Adenocarcinomas
Cancer arising from glandular epithelium
10% - 20%
Mixed carcinoma
Features both types
Source: American Cancer Society
Statistics
• 10,520 new cases in the U.S. this year
• 3,900 will die
• 50% are diagnosed between ages 35 and 55.
• 20% at the age of 65 or over.
• Rarely occurs in women younger than 20
• Noninvasive is four times more common
• 74% decrease in deaths between 1955 and
1992 in the U.S.
• Death rate continuous to decline by 2% a year
Source: American Cancer Society
Lifetime Probability of Developing Cancer, by
Site, Women, US, 1998-2000
Site Risk
All sites 1 in 3
Breast 1 in 7
Lung & bronchus 1 in 17
Colon & rectum 1 in 18
Uterine corpus 1 in 38
Non-Hodgkin lymphoma 1 in 57
Ovary 1 in 59
Pancreas 1 in 83
Melanoma 1 in 82
Urinary bladder 1 in 91
Uterine cervix 1 in 128
Source:DevCan: Probability of Developing or Dying of Cancer Software, Version 5.1 Statistical Research and
Applications Branch, NCI, 2003. http://srab.cancer.gov/devcan
Signs and Symptoms
• Vaginal bleeding
•
• Menstrual bleeding is longer and heavier than usual
• Bleeding after menopause or increased vaginal
discharge
• Bleeding following intercourse or pelvic exam
•
• Pain during intercourse
•
•
•
Risk Factors
Human papillomavirus infection (HPV) – Primary factor
HPV 16, HPV 18, HPV 31, HPV 33, HPV 45
50% are caused by HPV 16 AND 18
Sexual behavior
Smoking
HIV infection
Chlamydia infection
Diet
Oral contraceptives
Multiple pregnancies
Low socioeconomic status
Diethylstilbestrol (DES)
Family history
Source: American Cancer Society
Prevention
Avoiding the risk factors
Especially HPV
Help for low-income women (NBCCEDP)
Having the Pap Test
3 years after first vaginal intercourse or by age 21.
Have test annually
Diagnosis
Cervical Cytology (Pap Test)
Cells are removed from the cervix and
examined under the microscope.
Can detect epithelial cell abnormalities
Atypical squamous cells
Squamous intraepithelial lesions
Squamous cell carcinoma (likely to be invasive)
Source: American Cancer Society
Diagnosis
Additional testing
Colposcopy
Cervix is viewed through a colposcope and the
surface of the cervix can be seen close and
clear.
Cervical Biopsies
Colposcopic biopsy – removal of small section
of the abnormal area of the surface.
Endocervical curettage – removing some tissue
lining from the endocervical canal.
Cone biopsy – cone-shaped piece of tissue is
removed from the cervix
Staging
FIGO System (International Federation Of Gynecology and Obstetrics)
Has five stages – 0 to 4
Stage 0 Carcinoma in situ
Stage 1 Invaded cervix, but has not spread.
Stage 2 Has spread to nearby areas, not leaving pelvic area.
Stage 3 Cancer has spread to the lower part of the vagina.
Stage 4Cancer has spread to nearby organs; metastasis.
Source: American Cancer Society
Survival Rate
• 5-year survival rate is 92% for earliest stage
•
• 71% for all stages combined
•
•
•
•
•
•
Source: American Cancer Society
Treatment
Surgery
Preinvasive cervical cancer
Cryosurgery
Laser surgery
Conization
Invasive cervical cancer
Simple hysterectomy
Removal of the body of the uterus and cervix.
Radical hysterectomy and pelvic lymph node dissection
Removal of entire uterus, surrounding tissue, upper
part of the vagina, and lymph nodes from the
cervix.
Radiation
Chemotherapy
What’s new in cervical cancer
research and treatment?
• HPV test
• HPV vaccine
•
• Radical trachelectomy procedure
• Other clinical trials
•
•
Source: American Cancer Society
Prostate
Cancer
"You and Your Prostate,"
produced by the
Australian Department of Veterans' Affairs
.
Urethra
Central
zone
Transitional zone
Fibromuscular
zone
Urethra
Ductus
deferens Capsule
Peripheral zone
nld.by/e/current/stat13.htm#15
Lobes of the Prostate
Anterior lobe
Median lobe
Lateral lobe
Posterior lobe
Image Source: SEER Training Website
Zones of the Prostate
• Peripheral
• Central
• Transitional
Image Source: SEER Training Website
Prostate Cancer Facts
#1 cancer in men (non-skin)
1/6 men diagnosed
Estimate 230,000 new cases in 2006
1/34 men die of prostate cancer
Estimate 27,000 deaths in 2006
70% over 65 y.o. at diagnosis
90% diagnosed at early stage
Over past 20 years, survival 67% to
97%
Risk Factors
Male
Age
Race
Higher rate in African-American, lower in
Asian
Family history (1st degree relatives)
Diet?
Symptoms
• a difficulty in starting to pass urine
• a weak, sometimes intermittent flow of urine
• dribbling of urine before and after urinating
• a frequent or urgent need to pass urine
• a need to get up several times in the night to
urinate
• a feeling that the bladder is not completely
empty
• rarely, blood in the urine
Prostatic Specific Antigen
Protein produced by cells of prostate gland
Test introduced in 1986
Age influenced
40 - 49 / 2.5
50 - 59 / 3.5
60 - 69 / 4.5
70 - 79 / 6.5
Elevated indicates possible CA dx
PSA 4 – 10 indicates 25-35% risk of cancer
diagnosis
PSA 10 – 20 indicates 65% risk of cancer diagnosis
PSA > 20 indicates possible metastatic disease
Free PSA
PSA that
circulates in
blood w/o
carrier protein
The lower the %
of free PSA, the
greater the risk
of CaP
Free PSA >
www.marinurology.com 24%
probably
benign
DRE
• PSA can be falsely
elevated
• DRE does not
palpate entire
prostate gland
• Abnormal:
nodules, hard
spots, soft spots,
enlarged
Screening
AUA recommendation:
American College of
Annual PSA, DRE Preventive Medicine:
Caucasion > 50 Recommends against
y.o. routine screening
Annual PSA Af-Am tests (PSA/DRE)
males > 40 OR Men over 50 w/10
men w/+ FH years life should be
told about benefits
& harms of
ACS: Annual tests men
screening
> 50 y.o. IF 10 years
of life expected
(earlier AA men, +
FH)
Biopsy (TRUSP)
• Hypoechoi
c shows
abnorma
l area
needing
biopsy
Transrectal
sonogram of the
prostate. Looking up
from the feet of a
patient toward his
head.
Other Workup
• Bone scan
• CT abdomen/pelvis
• PET scan
• Chest x-ray
Histology
99% Adenocarcinoma
1% Other
Sarcoma, small cell, other
PIN – do NOT abstract
30% men will go on to
develop CaP
Close follow-up
recommended for 2
years
visualsonline.cancer.gov
www.prostate-cancer.org
Grade Priority (FORDS)
1. Gleason’s grade
2. Terminology
Differentiation (well differentiated,
moderately differentiated, etc)
3. Histologic grade
Grade I, grade II, grade III, grade IV
4. Nuclear grade only
Grade Conversion
Gleason’ Gleason’ Histo Terminology SEER
s Score s Pattern Grade Code
2, 3, 4 1, 2 I Well 1
differentiated
5, 6 3 II Moderately 2
differentiated
7, 8, 9, 10 4, 5 III Poorly 3
differentiated
Partin nonogram
Doctors need PSA, Gleason score, and
clinical staging items (PE)
Can determine probability of:
Organ-confined disease
Extraprostatic extension
Seminal vesical invasion
Lymph node involvement
urology.jhu.edu/prostate/partintables.php
TABLE I. Clinical Stage T1c (nonpalpable, PSA elevated)
PSA Pathologic Stage Gleason Score
Range
(ng/ 2-4 5-6 3+4=7 4+3=7 8-10
mL)
4.1–6.0 Organ confined 90 (78–98) 80 (78–83) 63 (58–68) 52 (43–60) 46 (36–56)
Extraprostatic 10 (2–22) 19 (16–21) 32 (27–36) 42 (35–50) 45 (36–54)
extension
Seminal vesicle (+) — 1 (0–1) 3 (2–5) 3 (1–6) 5 (3–9)
Lymph node (+) — 0 (0–1) 2 (1–3) 3 (1–5) 3 (1–6)
6.1– Organ confined 87 (73–97) 75 (72–77) 54 (49–59) 43 (35–51) 37 (28–46)
10.0
Extraprostatic 13 (3–27) 23 (21–25) 36 (32–40) 47 (40–54) 48 (39–57)
extension
Seminal vesicle (+) — 2 (2–3) 8 (6–11) 8 (4–12) 13 (8–19)
Lymph node (+) — 0 (0–1) 2 (1–3) 2 (1–4) 3 (1–5)
Collaborative
Staging:
Prostate
CS Extension – Clinical/Notes
1: Do not include prostatectomy info
2: Explains codes
10 – 15: clinically INapparent
20 – 24: clinically apparent (palpable,
radiology)
30: Not know if clinically apparent
31, 33, 34 OBSOLETE about apex
41 – 49 extension beyond prostate
CS Extension – Clinical/Notes
3: Talks about apex, but that is in SSF now
4: 13 – 14 when TURP done
5: Prostatic urethra involvement no effect
6: “Frozen pelvis” definition
7: AUA stages included
8: Pathologic tissue of other organs
9: Explains how mapping works
CS Extension - Clinical
Clinically Inapparent
00 in situ §Not palpable
10 – T1 NOS §Not visible on
≤ 5%
13 – T1a ≤ 5%
imaging
§Not visible on sono
14 – T1b > 5%
§Incidental finding
15 – T1c because
§Latent
of needle biopsy §Occult
> 5%
www.upmccancercenters.com
CS Extension - Clinical
Clinically Apparent
20 – T2 NOS 1 §Palpable
lobe §Nodule
21 – T2a ≤ ½ §Induration
lobe §Firm, Irregular
22 – T2b > ½
§Visible on imaging
§Extracapsular
lobe extension
23 – T2c both
§Visible on sono
lobes §Hypoechoic
24 – Stage B
§Streaky
densities
NOS
30 – Localized
CS Extension - Clinical
• 41 - T3 NOS thru
capsule NOS T3a
• 42 – T3a unilateral
• 43 – T3a bilateral T3a
• 45 – T3b seminal
vesicle
• 49 – T3 NOS T3b
Periprostatic
extension NOS
www.upmccancercenters.com
CS Extension - Clinical
• 50 – T4 extension to/
fixation to adjacent
• 52 – T4 muscles,
ureter
• 60 – T4 pelvic wall or
bone, “frozen”
pelvis
• 70 – T4 further
contiguous
extension
•
www.upmccancercenters.com
• 95 No evidence
CS Evaluation Fields (CS/TS)
0 PE, Imaging, clinical; no path, no c
1 autopsy
Scope, biopsy, no surg resection, no c
2 aut
Bx of extraprostatic tissue p
3 Autopsy (dx before death) p
4 Surg resect w/o neoadjuvant p
5 Surg resect WITH neoadjuv, clinical c
6 Surg resect WITH neoadjuv, path y
8 Autopsy (dx unknown pre death) a
9 Unk if surg resect, not documented c
CS Lymph Nodes
• Prostate is
inaccessible organ
(pg 14)
• 00 None
• 10 Regional LNs
• 80 LNs NOS
• 99 Unknown
•
• CS Reg Nodes Eval,
# Pos, # Eval
Use Standard Table www.upmccancercenters.com
CS Mets at Dx
• Prostate is inaccessible
organ
• 00 None
• 11 Common iliac LN
• 12 Other distant LN
• 30 Bone mets (not direct*)
• 35 – 30 + 11 or 12
• 40 Other distant mets
• 45 Mets NOS
• 50 40 - + 11 or 12
• 55 40 - + 30 or 35
• 99 Unknown
Site Specific Factors
SSF 1 PSA Value SSF 2 PSA
000 Test not done 000 Test not done
001 - < 0.1 010 Positive
002 – 989 actual # 020 Negative
990 - ≥ 99.0 ng/ml 030 Borderline
999 Unknown 080 Order, results ??
999 Unknown
oHighest PSA prior to bx or tx
oUse same value for SSF1 and SSF2
Why PSA Twice?
PSA varies by age & race patient
< 40 y.o. < 2.0 ng/ml
40-50 y.o. < 2.5 ng/ml
51-60 y.o. < 3.5 ng/ml
61-60 y.o. < 4.5 ng/ml
> 70 y.o. < 6.5 ng/ml
PSA varies norms by lab method
Generally, 4-10 ng/ml borderline
SSF 3 Pathologic Extension
Notes
1. Prostatectomy info only
2. Prostatectomy done as first course
3. Involvement prostatic urethra not matter
4. Apical or distal urethral margin, bladder base
or neck margin + w/o extension = 040
5. 031, 033, 034 OBSOLETE about apex
6. If incidental dx, code appropriately per path
7. “Frozen pelvis” definition
8. AUA stages included
9. Explains how mapping works
SSF3 similar to CS Extension
• 095 No evidence
3-digit code primary
No T1 codes
• 096 Unknown if
024 absent prostatectomy done
040 Margins involved • 097 No prostatectomy
045 = T3b w/in first course
048 = T3a • 098 Prostatectomy
048 extracapsular
performed but not
extension first course
•
SSF 4 Prostatic Apex
1 No involvement
2 Into/arising in
3 Arising in
4 Extension into
5 Apex extension
unk
1st number =
www.upmccancercenters.com clinical
SSF4 Apex
• 1 No involve – statement of normal apex
or neg on path
• 2 Into/arising NOS – can’t be determined
where cancer started (avoid this code)
• 3 Arising in – If apex is ONLY site of
cancer
• 4 Extension to – cancer present in other
parts + apex
• 5 Unknown – no description; no
prostatectomy
SSF 5 & 6
SSF 5 Gleason’s pattern SSF 6 Gleason’s
Note 1 explains what to do score
if only 1 number • Note 1 same
If more than one • Add the 2 patterns
Gleason’s pattern, use • If more than one,
the one from the use largest
largest specimen specimen
Different from other rules
where we code to the
worst
This is not instructions
for grade of tumor
If multiple Gleason’s in
Treatment
Observation
Beam RT
Hormone
Experimental
Seed RT
Surgery
Watchful Waiting
• aka Active Surveillance
• PSA q 6 mos
• Slow growing cancer
• Delay for other diseases to improve
• Comorbidities prevent other tx
•
Surgery
TURP
CRYOSURGERY
kidney.niddk.nih.gov www.nemc.org
Prostatectomy
Perineal,
Retropubic,
Suprapubic –
depends on patient
anatomy and
surgical history
Nerve-sparing
Robotic
www.prostate-cancer.org
Brachytherapy
www.prostate-cancer.org
Beam Radiation
IMRT
3-D
Prostate sitting on rectum
www.prostate-cancer-radiotherapy.org.uk
Hormone Therapy
LHRH analogs
Lupron, Zoladex
Androgen blockades
Casodex, Eulexin,
Nilandrone
Estrogen therapy
(DES)
NOT orchiectomy
www.upmccancercenters.com
Other
Chemotherapy
Hem Tsplt & Endocrine
Not first course
Procedures Stage IV
Endocrine surgery or
Hormone refractory
radiation
Bilateral
Could have
subcapsular orchi
Could have testicular
prosthesis
Experimental
Hyperthermia
Laser ablation
Alternative medicine
Pomegranate juice
Ginseng
Fasting
Mini-trampoline
Vitamin D
Vaccines
www.cdc.gov/cancer/prostate/screening
Treatment for Recurrence/Mets
Hormones
Orchiectomy
Radiation to mets
Radioisotopes
strontium-89 (Metastron)
samarium-153 (Quadramet)
Chemotherapy
Follow-Up (NCCN Guidelines)
OBSERVATIO
CURATIVE STAGE IV
N §PSA q 6 mos x 5 §PSA q 3-6 mos
yr §H&P w/sx
§ < 10 years?
§DRE q year x 5 discussion
§ H&P q 6 yr
mos
§ 10 years?
§ PSA &
DRE q
6 mos
§ Repeat
bx at 1
year
LUNG CANCER
Lung Cancer: Defined
• Uncontrolled growth of malignant cells in
one or both lungs and tracheo-bronchial
tree
• A result of repeated carcinogenic irritation
causing increased rates of cell
replication
• Proliferation of abnormal cells leads to
hyperplasia, dysplasia or carcinoma in
situ
Picture of the Lungs
Lung Cancer in the US
• According to 2004 statistics,
there were 1,800,000
173,770 new cases and 1,600,000
1,400,000
160,440 deaths yearly 1,200,000
1,000,000
800,000
• More deaths from lung 600,000
cancer than prostate, 400,000
200,000
breast and colorectal 0
1 3 5 10
cancers combined
New Cases
• Decreasing incidence and Deaths
deaths in men; continued
increase in women
Women & Lung Cancer
• 80,660 new cases were reported in 2004
- Account for 12 % of all new cases
• 68,510 deaths were reported in 2004
- An increase of 150% between 1974
and 1994
• Women are more prone to tobacco effects -
1.5 times more likely to develop lung
cancer than men with same smoking habits
•
Where Does it Come From?
Radiation Exposure
Smoking
Environmental/ Occupational Exposure
Asbestos
Radon
Passive smoke
Smoking Facts
Tobacco use is the
leading cause of lung
cancer
87% of lung cancers are
related to smoking
Risk related to:
age of smoking onset
amount smoked
gender
product smoked
depth of inhalation
Where does it travel?
•
• Lymph Nodes, Brain, Liver, Adrenal,
Gland, Bones
• 40% of metastasis occurs in the
Adrenal Gland
Diagnosis
History and Physical exam
Diagnostic tests
Chest x-ray
Biopsy (bronchoscopy, needle biopsy,
surgery)
Staging tests
CT chest/abdomen
Bone scan
Bone marrow aspiration
PET scan
Symptoms
cough
dyspnea
hemoptysis
recurrent infections
chest pain
Syndromes/Symptoms secondary
to regional metastases:
Esophageal compression dysphagia
Laryngeal nerve paralysis hoarseness
Symptomatic nerve paralysis Horner’s
syndrome
Cervical/thoracic nerve invasion Pancoast
syndrome
Lymphatic obstruction pleural effusion
Vascular obstruction SVC syndrome
Pericardial/cardiac extension effusion,
tamponade
Two Lung Cancer Cells,
Classified
Non Small Cell Small Cell Lung
Lung Cancer Cancer (SCLC)
(NSCLC)
Oat Cell
Adenocarcinoma
Intermediate
Squamous Cell Carcinoma
Combined
Large Cell Carcinoma
Treatment and Staging
NSCLC
Stage Description Treatment Options
Stage I a/b Tumor of any size is found only in the Surgery
lung
Stage II a/b Tumor has spread to lymph nodes Surgery
associated with the lung
Stage III a Tumor has spread to the lymph nodes Chemotherapy followed by
in the tracheal area, including chest wall radiation or surgery
and diaphragm
Stage III b Tumor has spread to the lymph nodes Combination of
on the opposite lung or in the neck chemotherapy and
radiation
Stage IV Tumor has spread beyond the chest Chemotherapy and/or
palliative (maintenance)
care
SCLC
• Limited Stage
Defined as tumor involvement of one lung,
the mediastinum and ipsilateral and/or
contralateral supraclavicular lymph nodes or
disease that can be encompassed in a single
radiotherapy port.
•
• Extensive Stage
Defined as tumor that has spread beyond one
lung, mediastinum, and supraclavicular lymph
nodes. Common distant sites of metastases are
the adrenals, bone, liver, bone marrow, and
brain.
• Cancerous Human
Lung
• This dissection of human
lung tissue shows light-
colored cancerous
tissue in the center of
the photograph. the
tissue surrounding the
cancer is black and
airless, the result of a
tarlike residue left by
cigarette smoke.
Conclusion
• Smoking cessation is essential for
prevention of lung cancer.
• New screening tools under way.
• Clinical trials under way.
• New treatments under way.
• Treatment can palliate symptoms and
improve quality of life.
• Read first bullet again!!
•
Gastric Cancer
Gastric Cancer :Biology
• There are several Hystological
types of Gastric Cancer of
which adenocarcinoma is by far
the most frequent.
•
• Sarcomas and Lymphomas can
also occur.
•
• This presentation refers basically
to adenocarcinoma.
Gastric Cancer Prevention
Biology: Hystopathology
Two types of adenocarcinoma
are recognized:
1. Intestinal: resembles colon
cancer, can be polypoid or
ulcerated, occurs usually in the
distal stomach and has a
prolonged pre-cancerous
phase.
Gastric Cancer Prevention
Biology: Histopathology
2. Difuse: Extends widely with no
distinct margins and the glandular
structure is rarely present.
Patients tend to be younger and
have a worst prognosis.
Gastric Cancer Prevention
Biology: Histopathology
•
• Adenocarcinoma is considered
early when it´s confined to the
mucosa and sub-mucosa,
irrespective of lymph node
affection.
• Otherwise it’s called advanced.
Gastric Cancer Prevention:
Epidemiology
•
• Infrequent before 40 years of age.
• Twice as frequent in men than in
women.
• Leading cause of death from
cancer worldwide.
Gastric Cancer Prevention:
Epidemiology
•
• Highest incidence in Japan, South
America and Eastern Europe.
• Adjusted rate worldwide is 15.62
per 100 000
• Adjusted rate for Latin America is
variable.
Gastric Cancer Prevention:
Epidemiology
• In the United States the incidence
has been decreasing and
unexplainedly the cancer has
migrated proximally.
Gastro-esophageal lesions are
more frequent than antral lesions.
Gastric Cancer: Risk Factors
and Primary Prevention
• Gastric Cancer is a very
common disease that carries
a high mortality.
• The diagnosis in early phases,
when better results should be
expected, is difficult due to the
unspecifity of early symptoms.
Gastric Cancer: Risk Factors and
Primary Prevention
• Recognition of risk factors and
application of strategies directed
towards their elimination are of
paramount importance.
• We will discuss the most probable
and convincing risk factors
related to this disease.
Gastric Cancer Prevention:
Chronic Atrophic Gastritis
•
•Chronic Atrophic Gastritis is
thought to be the initial
step in the development
of most Gastric Cancers.
Gastric Cancer Prevention:
Chronic Atrophic Gastritis
Chronic Atrophic Gastritis
has been shown to appear
in patients with:
1. Tobacco use.
2. H. pylori infection.
(cont.)
Gastric Cancer Prevention:
Chronic Atrophic Gastritis
3. Diets with high levels of
nitrites, nitrates, salt and
smoked foods.
4. Previous Gastric Surgery.
5. Pernicious Anemia.
•
Gastric Cancer Prevention:
Tobacco
•Smoking increases the risk of
Gastric Cancer by 50% to 60%
•It is estimated that smoking
tobacco is responsible for
11% of all Stomach Cancers
worldwide.
Gastric Cancer Prevention:
Tobacco
•Tobacco use decreases the
levels of Carotenoids and
Vitamin C which act as
protective agents against
this disease.
Gastric Cancer Prevention:
Tobacco
•
•Tobacco use is associated
with Helycobacter pylori
infection which in turn
leads to Atrophic Gastritis.
•
Gastric Cancer Prevention:
Tobacco
•
•Smoking cessation returns
the risk to that of the
general population after 20
years.
Gastric Cancer Prevention:
Helycobacter pylori
• H. pylori is associated with a two
to sixfold increase in the risk of
developing Gastric Cancer.
• Many believe that genetic and
environmental factors also
need to be present for H. pylori
to cause cancer.
Gastric Cancer Prevention:
Helycobacter pylori
•
•In 1994 the World Health
Organization designated
H. pylori a Group 1 carcinogen
Gastric Cancer Prevention:
Dietary Factors
• Consumption of fruit, vegetables
and fiber has shown, in the
majority of controled studies
published, a protective effect
against Gastric Cancer.
• This effect is probably due to
Vitamin C or carotenes.
Gastric Cancer Prevention:
Dietary Factors
•Nitrates and nitrites found in
salted, smoked and dried
foods lead to atrophic
Gastritis which in turn leads
to Gastric Cancer.
Gastric Cancer Prevention:
Genetic Factors
All of the following genetic
factors have been shown to
increase the risk of Gastric
Cancer.
•
Gastric Cancer Prevention:
Genetic Factors
•Blood type A.
•Hereditary non-polyposis
colorectal cancer.
•e-cadherin gene mutations.
•A first degree relative with
Gastric Cancer.
Gastric Cancer Prevention:
Genetic Factors
•
•Presently they are not subject
to preventive measures
except for prophylactic
gastrectomy in e-cadherin
mutations.
Gastric Cancer Prevention:
Secondry Prevention
• Secondary prevention is the
“early” detection of cancer
through screening.
• This is done in populations where
the disease is a major health
problem.
• Examples of this approach can be
found in Japan and Costa Rica.
Gastric Cancer Prevention:
Secondary Prevention
•
•In Japan gas-contrast Stomach
Fluorography is done in the
mass population.
(cont.)
Gastric Cancer Prevention:
Secondary Prevention
•
• Those considered abnormal
(about 13%) will undergo
further studies, including
endoscopy and biopsy.
•
Gastric Cancer Prevention:
Conclusions
The best primary
prevention strategies are:
Gastric Cancer Prevention:
Conclusions
•Smoking avoidance or
cessation.
•Diets rich in fruit, vegetables
and fiber.
•Avoidance of salted, smoked
and poorly preserved foods.
•Erradication of H. pylori.
Gastric Cancer Prevention:
Conclusions
•
•Mass screening is a
viable strategy in high
risk populations.
• Double-Contrast
Barium X Ray of the
Large Intestine
• used to detect colorectal
cancer. Barium, an X-
ray opaque material or
contrast medium is
used. The American
Cancer Society
recommends people
over age 50 have a
double-contrast barium
enema every 5 to 10
years.
Leukemia
Leukemia
any of several types of cancers that affect
RBC, WBC and platelets.
• Blood cells (bone marrow)
• leukemia begins when an immature blood
cell in the marrow, (progenitor cell),
becomes cancerous,
• the marrow becomes crowded with
cancerous cells
• suppresses the production of healthy
blood cells
• Pale skin,
• fatigue, and
• shortness of breath are signs of anemia
• Nose bleeds, gum bleeding, a tendency to
bruise easily, and pinhead-sized red
spots on the skin
• prone to infection.
• two principal characteristics: the lineage of blood cell that becomes
cancerous, and how rapidly the disease progresses. A leukemia is
classified as myelocytic or myelogenous if the malignant cells have
descended from the progenitors of red cells, granulocytes,
macrophages, or platelets. If the leukemic cells have descended from a
lymphocyte precursor cell, the leukemia is referred to as lymphocytic.
• Myelocytic or lymphocytic leukemia can be acute or chronic, terms that refer
to the patient’s life expectancy if the disease remains untreated. Acute
leukemias develop rapidly, and without prompt treatment, the
suppression of normal blood cell production is so severe that death
occurs in a matter of weeks. In the chronic leukemias, patients may
survive for several years or more without treatment because the effects
of leukemic cells on the structure and function of the marrow develop
more slowly and are less severe. In chronic myelocytic leukemia, for
example, the leukemic cells can often complete their development and
become functional blood cells. In chronic lymphocytic leukemia, the
leukemic lymphocytes do not function normally, but in many cases the
abnormal cells do not severely inhibit normal blood cell development.
• The four major forms of leukemia—
• acute myelocytic,
• chronic myelocytic,
• acute lymphocytic,
• chronic lymphocytic
• Myelocytic leukemia—both acute and chronic forms—can occur at any age,
but more than 90 percent of cases occur in adults, and the risk of
developing the disease increases dramatically after the age of 50.
• Acute myelocytic leukemia is the most common form of leukemia in the
United States, with 12,000 new cases diagnosed each year. About 4,600
new cases of chronic myelocytic leukemia are diagnosed each year.
• Chronic lymphocytic leukemia occurs rarely before the age of 45 and
increases in incidence with each succeeding decade.
• Acute lymphocytic leukemia, by contrast, can occur at any age, but about
half the cases occur in children under the age of 19, with the peak
incidence occurring at about 4 years of age. In the United States, chronic
lymphocytic leukemia accounts for about 9,700 new cases of leukemia
each year, and acute lymphocytic leukemia, for about 4,000 new cases.
• Intensive radiation exposure or moderately intense exposure for
long periods
• Exposure to certain chemicals
• Tobacco smoking appears to increase the incidence of this form of
leukemia.
• Chemotherapy drugs
• Two viruses, human T-cell leukemia viruses (HTLV) I and II, are
known to cause T-cell leukemia,
• Genetic factors
• Bone marrow biopsy and blood cell tests are the primary techniques
used to diagnose leukemia.
• Blood tests that monitor blood cell counts
• staining of cells with various chemical dyes
• chest X rays and examination of the spinal fluid for leukemic cells
• Chemotherapy - mainstay of treatment for
both acute and chronic leukemias. In
acute leukemias
• Antibiotics and transfusions of red cells
and platelets help sustain patients
whose blood counts are dangerously
low because they are receiving intensive
chemotherapy.
• radiation
• stem cell transplantation (bone marrow transplantation).
• Immunotherapy
• The goal in treating acute leukemias is to kill enough leukemic cells
to produce a remission