CANCER CONCEPT_SIR MANLOD [30 hours] 3.

Definition of Terms
REFERENCES: a. Aberrant Cellular Growth
 MedSurg Books for Cancer - Alteration in normal cellular
 Anatomy books (check my gdrive; growth
AnaPhy folder) - Occurs when the cells escape
the normal control in growth and
THE CELL differentiation
1. What is Cancer? b. Apoptosis
a. A disease process - Programmed cellular death
- Cells proliferate abnormally c. Carcinoma
- Ignore regulating signals in the - Specific form of CA or malignant
env’t surrounding cells. tumor arising from epithelial
b. Medical Term: Malignant cells
Neoplasm o Squamous, cuboidal,
- synonymous w cancer mucosa, etc.
o however, not all - If non-epithelial: Sarcoma (e.g.
neoplasm is malignant! muscles, gleal cells)
o Not all tumors are d. Carcinoma in Situ

cancers - “in situ” – on site

o No metastasis yet(?)
- Neoplasm which remains
confined on the site of the origin
- Usually stage 1 or 2 in CA
- Enclosed cyst
e. Cyst
- Closed sac having a district
membrane and developing
abnormally in a body cavity or

2. Role of CA Nurse structure

a. Provide support - Filled w air, fluid, and other

- to the patient and family substances

- via a wide range of physical, - Tumor: abnormal growth of

emotional, social, cultural and tissue

spiritual crises f. Differentiation

- holistic care - Aka specialization

- Extent to which tissue cells
resemble normal cells
- CA cells can be differentiated
as:
o Well-differentiated: CA
cells can be identified
o Undifferentiated: CA
cells resemble stem
cells; hard to originate
(mostly composed of
hematoblast: stem cell
for blood products)
g. Metastasis
- Spread of cancer cells from
primary tumor to distant sites
- Usually stage 4 in CA
h. Neoplasm
- Abnormal mass of tissue that
serves no useful purpose and
may harm host organism
- Synonymous to tumor
i. Neoplastic progression
- Worsening of the cell’s
biological potential, w the
passage of time neoplasm
becomes more malignant
- E.g. from tumor → carcinoma in
situ → regional invasion →
metastasis
j. Oncogenes
- Inducing genes
- Promote cell proliferation and
are capable of triggering
cancerous characteristics
- “sira na genes”; DNA damage
- Mutate from proto-oncogenes
k. Oncology
- Field or study of cancer
- Medical specialty that deals w
the dx, txt and study of CA
(case to case basis)
l. Progression
- Phenomenon by which
malignancies attain their fxn
slowly
m. Proto-oncogenes
- Benign forms of oncogenes
necessary for some normal
cellular fxns especially G&D
- Carcinogens trigger the
conversion of proto-oncogenes
to oncogenes
n. Sarcoma
- Malignant tumor arising from
non-epithelial tissue
o. Tumor
- Lump, mass, swelling or
enlargement
- Solid neoplasm
p. Tumor suppressor gene
- Genes which inhibit cell division
and survival
4. Parts of The Cell e. Ribosome
- Important role in protein
synthesis
- Contain concentrations of RNA
f. Smooth Endoplastic Reticulum
- Synthesizes fatty lipids
- Plays role in detoxification
g. Rough Endoplastic Reticulum
- Transportation of proteins
h. Cell Membrane
- Controls exchange of materials
inside and outside of cell
a. Nucleus
i. Cytosol
- Contains DNA
- Intracellular gel-like fluid where
- Controls cellular activity
many chemical reactions occur
- Plays central role in heredity
j. Flagellum
o Each chromosome
- Used for locomotion
contains thousands of
k. Mitochondrion
hereditary units called
- Cell’s power plant
genes
l. Lysosome
b. Nucleolus
- Breaks down molecules that
- Ribosome (ribosomal proteins)
enter the cell
production
m. Centrioles
o Sites of synthesis of
- Important role in cell division
rRNA n. Cytoskeleton
o Assembly of rRNA and - Provides structural organization
proteins into ribosomal
units
- Made up of clusters of protein,
DNA and RNA
o Not enclosed w a
membrane
c. Nuclear Membrane
- Has pores
d. Golgi Apparatus
- Modifies and distributes
secretory production
5. The Cell Cycle
6. Interphase Periods
a. Interphase
- Longest phase
- G1: “first growth” – growth and
normal metabolic processes
occur
o Longest period
o May take a week to
complete
o Neurons stop at G1 (no
DNA replication)
- S phase: “synthesis phase”
where DNA replication happens
o To prep cell for mitosis
- G2: “gap/secondary growth
phase” - growth and proliferation
of cells happen
o Organelles are
duplicated
b. Prophase
c. Metaphase
d. Anaphase
e. Telophase
f. Cytokines
7. Checkpoints in Cell Cycle
<before it can proceed to another phase>
a. Checkpoint 1: before synthesis
phase
- aka G1 checkpoint
- Cells will check for cell size,
abundant nutrients, growth
factor, absence of DNA
damage/unusualities
- If met, proceed to synthesis
phase
o If not, may stop
b. Checkpoint 2: before start of M
phase or prophase
- Check for DNA damage and
completeness of DNA
replication
o If unmet, may stop
c. Checkpoint 3: before anaphase
- Aka spindle checkpoint
- Are all chromosomes attached
to the spindles?
- Halts until the chromosomes are
completely attached to spindles
8. Regulators in Cell Cycle 9. Tumor Suppressor Gene
a. Cyclins
- Different types per stage in the
interphase
b. Cyclin-Dependent Kinases
(CDK)
- Activate cyclins by attaching to
the latter via phosphorylation
- Inc. can lead to activation in a. Physiology
different target cells - DNA damage [start]
- Activate diff. fxns in cell cycle - Activation of P53 and TSG cells
o E.g. inc. CDK in G1 → o Checks if DNA is

promote cell growth reparable

c. Anaphase-Promoting Complex /
Cyclosomes (APC/C)
- Cohesin
- Add ubiquitin protein to securin
o Leads to the breakdown
of securing and
separase (securin-
separase complex)
- Separase acts on cohesion via
hydrolyzation which leads to
breakdown of chromosomes
o Anaphase occurs
- Proteasome function is
o If reparable, cell cycle
recur
o If irreparable, P53
activate apoptosis
- Activate P21 (CDK inhibitor)
- CDK inhibitor attach to CDK –
Cyclin complex
- Cell cycle stops
b. 3 functions
- Activation of CDK inhibitor →
Stops cellular division
- DNA repair
- Cellular apoptosis

necessary for normal maturation <Cancer occurs if these 3 are inhibited>

of P-glyco-protein
o Part of the ubiquitin-
proteasome pathway
- Proteasome inhibition could
decrease the accumulation of P-
glyco-protein in the membranes
of cancer cells → inc. apoptosis
 - E.g. BPH
10. Cell Differentiation d. Metaplasia
- Change to another cellular type
- Nagiba ang constitution ng cells
- E.g. cardio-esophageal
sphincter (GERD);
o “reddish” area is
indicative of metaplasia
o Aka Barret’s espohagus
e. Dysplasia
- Deranged cellular growth
a. Stem Cell - Iba-iba/assorted (big cells, small
- develops into more specific cells,etc.)
types of cells - Cancer
- e.g. stem cell → muscle cell, f. Hypertrophy and hyperplasia
sex cell, etc. - Inc. in both size and number
12. Contact Inhibition
11. Cellular adaptive process a. Definition
- Enables noncancerous cells to
cease proliferation and growth
when they contact each other
b. Growth Properties of normal
cells
- Has contact inhibition
- Covers a surface as a
monolayer
c. Growth Properties of
<occurs in response to stress>
Cancerous cells
a. Hypertrophy
- No contact inhibition
- Inc. in cellular size
- Multi-layer
- Physical activity/mobility may
o Clump/pile up one
induce hypertrophy
above the other
b. Atrophy
- Dx test for cancer: biopsy
- Dec. in cellular size
13. Cell’s Regenerative Ability
- Immobility can trigger atrophy of
a. Labile
cells
c. Hyperplasia
- Inc. in numbers
 - Cells that routinely divide and hydrocarbons
replace cells that have a limited (e.g. vehicle
lifespan emissions, oil
- Fast regeneration refineries,
- E.g. hair, skin, mucous smoke)
membranes, GI tract o Foods and
b. Stable preservatives
- Cells that have a long lifespan w  Nitrates
normally a low rate of division  Talc
but can rapidly divide if needed  Food
- Local regeneration sweeteners
- E.g. bone, liver (largest gland) - Radiation
c. Permanent or Fixed o Ionizing radiation
- Cells that never divide (cancer induction)
- E.g. neurons, cardiac, RBC o Frequent X-ray
o Radioactive isotopes
ALL ABOUT CANCER o Sunlight/ UV rays
1. Factors contributing to dev’t of cancer
o Radon
a. Oncogenic viruses + Oncogene
o Electromagnetic
- Proto-oncogene when exposed
radiation
to oncogenic virus can develop
c. Immunologic defects
into an oncogene
- Autoimmune
o Oncogene theory by
d. Age
Francis Rous (1911)
- Depending on the type of
- E.g. HPV (a type of oncogenic
cancer
virus) → cervical cancer
e. Gender
- Needs a host
- Colorectal cancer is common in
b. Carcinogens
males > females
<Most famous factor associated w
o + middle-aged to elderly
cancer cell mutation>
clients
<Chronic exposure>
- Breast, cervical or ovarian
- Chemical
cancer in females are often
o Industrial compounds
linked with hormonal changes
 Vinyl chloride
f. Heredity
(e.g. asbestos)
- Inc. risk in acquiring cancer due
 Polycyclic
to genetics
aromatic
 - But depends on observation of The more frequent the mitosis,
lifestyle practices The more rapid the rate of
- E.g. Hodgkin’s disease is not growth
familial
g. Poverty b. Cell surface and membrane
- Vices, lack of financial alteration
resources can contribute to - Proteins in the plasma
development of cancer membrane help identify if cells
h. Stress are damaged or not (via T cells)
i. Lifestyle practices - Cell surface loses its contact
- Obesity, vices, etc. inhibition → tumor growth
2. Oncogene c. Metabolic changes
< induce cell proliferation > - MYC genes activate cell
a. MYC and RAS genes are often metabolism
affected (and etc.) o Inc. in glycolysis →
b. Pathophysiology inc. metabolic rate in
- Proto-oncogenes appear to be cells =
normal genes inc. demand of glucose
- Behavior may be altered d/t o Grabe kain ng cells →
o Incorporation of inc. cell proliferation
retrovirus OR - Hence, PET scan is done as a
o Mutation (physical or dx test for cancer (makes use of
chemical carcinogen) a glucose contrast dye)
- Transformation o Cancer cells show up
- Oncogene as “bright spots” or
- Cell proliferation “darker areas” on PET
o Uncontrolled cellular scans
growth o These spots/areas
- Anaplasia represent cells that are
3. Characteristics of Cancer cells using more sugar →
a. Anaplasia more of the radioactive
- Describe lack of normal cell substance are absorbed
proliferation and differentiation (hypermetabolic state)
in cancerous tissue d. Antigenic changes
- General Rule: - TSG activates
The more undifferentiated the
tumor,
 via superior vena cava and
travel to the diff parts of the
body via circulation →
metastasis
STAGES IN CANCER DEV’T d. Regional Invasion
- Cellular proliferation
- Loss of contact inhibition
- Secretion of cystic substance
e. Hyalurodinase: destroys
intracellular cementic
substances
- Destroys encapsulation of in situ
cancer

1. Initiation 4. Mechanism of Metastasis

a. Initial exposure of carcinogenic <Metastasis – cancer has spread>

agents to normal cells →

genetic mutation
b. Decreased TSG activity**
2. Latency/Promotion
a. “silent area”
b. Adaptive processes occur (e.g.
hyperplasia)
3. Progression
a. Hyperplasia develops to
dysplasia
b. From dysplasia, cells can
progress to an in situ cancer a. Invasion of neoplastic cells to
(encapsulated cancer cells) adjacent cells (regional
4. Invasion invasion) caused by:
a. If the capsules in in situ cancer - Inc. tumor size
breaks, it becomes an invasive - Loss of tumor cohesiveness
cancer - Destruction of the supporting
b. Starts locally (regional invasion) tissues of an organ
c. Affects lymphatic system, - Factors in the host response to
primarily the blood vessels tumor cell invasion
- Once in the subclavian artery, b. Spread of tumor cells via:
cancer cells can go to the heart - Lymphatic system
 o Brain does not contain c. Lysosomal hydrolyses
lymphatic capillaries - Induce metastasis
d. All 3 causes loss of tumor
cohesiveness
- Blood vessels
- Direct expansion of tumors in
body cavities
o Occurs as cells travel
throughout the cavity to
develop new growth or
other serosal surfaces
o E.g. ovarian cancer
(pelvic cavity is proximal
to intestines; expands
directly and affects
intestines)
o E.g. brain cancer (gleal
cells can spread via
gravity; closely proximal
to spinal cord)
 Pons
responsible for
survival reflex
c. Establishment and growth of
tumor cells at the secondary site
- Tumor develops its own
vascularization in the new site
and has the ability to infiltrate
adjacent tissue bc its not
encapsulated
5. Destructive enzymes produced by
malignant cells
a. Collagenases
- Induce metastasis
b. Plasminogen activators
- Protect tumor cells from
apoptosis
CHARACTERISTICS NORMAL MALIGNANT
1. Mitotic Division  Leads to 2 daughter cells  Leads to multiple
daughter cells
2. Appearance  Homogenous in size, shape  Larger & grows more
& growth rapidly than normal,
heterogeneous
o Rapid growth d/t
constant need
for glucose
consumption
o V fast cellular
metabolism

 Not cohesive, irregular

pattern of expansion
 Cohesive, forms regular
patterns of expansion
 Larger, more prominent
nucleus
 Uniform in size to nucleus

 Lack of pattern in
 Well differentiated
organization
o Growth pattern
o Growth pattern
3. Growth Pattern  Do not invade adjacent  Invade adjacent tissue
tissue

 Proliferation in response to  Proliferation in response

specific stimuli to abnormal stimuli
o E.g. bones o Kahit walang
proliferate in stimulus, still
response to injury proliferates
such as fractures,
running, etc.

 Grows in ideal condition

 Grows in adverse
 condition

 Cell birth = cell death

 Cell birth > cell death

 Stable cell membranes

 Loss of control as a
result of cell membrane
change

 Constant predictable growth

 Erratic growth rate
rate

 Cannot grow out of specific

environment  Able to break of cells
that migrate through
blood stream/ lymphatic
channels
4. Functions  Have specific designated  No useful purpose
purpose

 Contribute to overall well-  Parasitic

being of host

 Functions in specific
 No normal function,
predetermined manner
causes damage instead
5. Others  Chromosomes remain  Chromosome aberration
constant throughout cell occur as cells mature
division

 Cannot invade, erode or  Invades, erode and

spread spreads

 Have own bld supply

BENIGN TUMORS
1. Definition
a. “-oma”
- Means tumor
- Usually attached to a term for a
parent tissue of the tumor
o (e.g. Adenomyoma)
o Adenoma – gland
Myo – muscle
Oma – tumor
b. When one or more parent tissue
enters into the formation of
neoplasm
2. Three (3) Most Common Benign Tumors
a. Fibroma
- Grows anywhere in the body
- Encapsulated, harmless tumor
and may cause symptoms
unless they press in a bone or
nerves (cause obstruction)
- Usual manifestation: bulging
- Can be removed or not
(optional)
b. Lipoma
- Very common benign tumor
(adipose tissue)
- Poorly encapsulated
- Very large in size
- May put pressure on
surrounding tissue as they
expand
- Pain d/t compression of nerve
endings
- Growths in the skin.
o subcutaneous layer; fat
- Occurs in large surface areas of
skin like the back, trunk, arms,
shoulders and neck
c. Leiomyoma
- Smooth muscle in origin
o GI tract: uterus,
stomach, etc.
- Rarely become malignant
COMMON MALIGNANT TUMORS
1. Carcinoma
a. Carcinoma in situ
- Localized and can be removed
surgically but can become
invasive and eroding into
surrounding tissue.
- Must be removed completely to
prevent mitosis of cancer cells
2. Sarcoma
a. Malignant Fibrosarcomas
- May originate from benign
fibromas
- bulky, well differentiated tumor
b. Bronchogenic Carcinoma
- 90% of all cases of lung CA
- Usually develops in lower
trachea and lower bronchi
- Excision of tumor (choice) but
readily gives rise to metastasis
- Metastasis: surgery
contraindicated
o Difficult
o Small-cell carcinoma:
very small in size (not
visible to naked eye)
PARENT TISSUES
1. Adeno – Glandular tissue
2. Angio – Blood vessel (smooth)
3. Basal cells – epithelium, mainly sun
exposed area (last layer of epidermis)
4. Embryonal – gonads
5. Lympho – lymphoid tissue
6. Melano – pigmented cells of epithelium
(also part of the last layer of epidermis)
7. Myo – muscles
8. Osteo – bone
CLASSIFICATION OF NEOPLASM
TISSUE OF ORIGIN BENIGN MALIGNANT
1. Connective Tissue

2. Fibrous Tissue  Fibroma  Fibrosarcoma

3. Adipose Tissue
 Lipoma  Liposarcoma

4. Bone
 Osteoma  Osteogenic sarcoma
5. Epithelium

6. Skin  Papilloma  Squamous cell

o Tabi ng basal cells carcinoma
7. Bone marrow  Leukemia

8. Muscle tissue  Multiple myeloma

o Myelin cells are
also affected

9. Smooth muscle  Leiomyosarcoma

 Leiomyoma
10. Nerve tissue

11. Nerve fibers  Neuroma  Neurogenic sarcoma

12. Meninges
 Meningioma  Malignant meningioma
13. Gonads  Dermoid cyst  Embryonal carcinoma

COMPARISON: BENIGN AND MALIGNANT CELLS

CHARACTERISTIC BENIGN NEOPLASM MALIGNANT NEOPLASM
1. Spread of growth  Grows slowly  Usually grows rapidly,

 Usually continues to grow  Tends to grow

throughout life unless relentlessly throughout
 surgically removed life

 May have periods of  Rarely, neoplasm may

remission regress spontaneously
2. Mode of growth  Grows by enlarging and  Grows by infiltrating
expanding surrounding tissues

 Always remains localized  May remain localized (in

situ) but usually

 Never infiltrates surrounding infiltrates other tissues

tissues
3. Capsule  Almost always contained  Never contained within
within a fibrous capsule a capsule

 Capsule does not prevent  Absence of capsule

expansion of neoplasm but allows neoplastic cells
does prevent growth by to invade surrounding
infiltration tissues

 Capsule advantageous  Surgically removal of

because encapsulated tumor tumor is difficult
can be removed surgically
4. Cell characteristics  Usually well-differentiated  Usually poorly
differentiated

 Mitotic figures absent or  Large numbers of

scanty normal and abnormal

mitotic figures present

 Mature cell

 Anaplastic cells absent  Cells tend to be

anaplastic
5. Recurrence  Recurrence extremely  Recurrence common
unusual when surgically following surgery
removed because tumor cells

6. Metastasis  Metastasis never occurs
7. Effect of neoplasm  Not harmful to host unless
located in area where it
causes compression of
tissue or obstruction of vital
organs
 Does not produce cachexia
8. Prognosis  Very good
 Tumor generally removed
surgically
spread into surrounding
tissues
 Metastasis is very
common
 Always harmful to host,
results in death unless
removed surgically or
destroyed by radiation
or chemotherapy
 Causes disfigurement,
disrupted organ
function, and nutritional
imbalances
 Depends on cell type
and speed of diagnosis
 Poor prognosis
indicated if cells are
poorly differentiated and
evidence exists of
metastatic spread
 Good prognosis
indicated if cells still
resemble normal and
there is no evidence of
metastasis
GRADING AND STAGING - M0/Mo: no distant metastasis
1. Grading - M1, M2, M3: ascending degree of
a. Acc to histologic or cellular distant metastasis
characteristics of tumor f. Wilm’s tumor has stage 5 cancer
b. Histopathology - Affects both kidneys but individual
- Gx: grade cannot be assessed ang pag rate per kidney
- G1: well-differentiated grade o e.g. stage 3 ang left kidney
- G2: moderately well-differentiated tas stage 2 yung right
grade
- G3: poorly differentiated GENERAL CLINICAL MANIFESTATIONS
- G4: undifferentiated 1. Pain
2. Staging a. Types of Cancer Pain
a. Quantifies the ddx/ identify the - Acute pain: starts suddenly
spread of ddx - Chronic pain: lasts more then 6
b. Legend months
- T: tumor b. Nsg Respos for Pain
o extent of primary tumor; size - Help patients and families to
- N: nodes take an active role in managing
o involvement of regional lymph pain.
nodes - Provide education and support
- M: metastatic involvement to correct fears and
o extent of metastasis misconceptions about opioid
c. T Staging use.

- Tx: tumor cannot be adequately o E.g. codaine,

assessed demepherol, morphine,
- T0: no evidence of primary tumor Vicodin
- TIS: Carcinoma in situ - Bone CA is the most painful
- T1, T2, T3, T4: progressive increase type of CA
in tumor size and/ or involvement 2. Bleeding
d. N Staging a. Thrombocytopenia
- Nx: regional lymph nodes cannot be - Most common cause of bleeding
assessed clinically in CA pts
- N0/No: no evidence of regional node - May be d/t angiogenesis,
- N1, N2, N3: increasing involvement physical injury
of regional lymph nodes b. Nsg Respos for Bleeding
e. M Staging - Encourage to use a soft, not
- Mx: not assessed stiff, toothbrush and an electric
 not straight edged, razor to
prevent bleeding
- Provide soft foods, increase
fluid intake and stool softeners,
as ordered
- Handle and move joints and
extremities gently to minimize
risk for spontaneous bleeding
- Serum hemoglobin and
hematocrit are monitored
carefully for changes indicating
blood loss
- The nurse test all urine, stool,
and emesis for occult blood
o occult blood: may not
be as obvious as active
bleeding
o melena: upper GI tract
bleeding (small
intestine)
o hematochezia: fresh
blood (large intestine)
c. Neurologic Assessment for
Bleeding
- Administer fluid and blood
products as ordered
o BT common for
leukemia pts
- Vasopressor agents are
administered as prescribed to
main blood pressure and ensure
tissue oxygenation
3. Infection
a. immunocompromised d/t txt
administered like radiation and
chemotherapy
(immunosuppressant)
b. Inc. risk for bacterial infection
- Streptococcus &
Staphylococcus species
c. Nsg Respos for Infection
- Administer antibiotics promptly
- Strict asepsis
- Encourage appropriate hygiene
- Encourage patient to cough and
perform deep breathing
exercises
4. Anorexia-Cachexia Syndrome
a. Inc. Protein metabolism &
Carbohydrate metabolism
b. Nsg Respos for Anorexia-
Cachexia Syndrome
- Food should be prepared in
ways that make it appealing
- Unpleasant smells and
unappetizing looking foods are
avoided
- Provide small, frequent meals
- Encourage oral hygiene before
mealtime to make meal more
pleasant
- If adequate nutrition cannot be
maintained by oral intake,
nutritional support via the
enteral route
o TPN
DETECTION AND PREVENTION FOR
CANCER
1. Primary Prevention Measures
a. Optimal dietary pattern and
lifestyle changes
- Avoid obesity
- Decrease consumption of salt-
cured, smoked and nitrate-cured
foods
- Increase intake of fresh
vegetables
- Increase fiber intake, vit. A, vit.
E, and foods rich in vit. C
- Reduce alcohol intake
b. Minimize exposure to
carcinogens
- Stop smoking
- Avoid exposure to chemicals,
asbestos fiber and constant
environmental dust
- Avoid radiation exposure
- Avoid overexposure to the sun
c. Obtain adequate rest and
exercise to reduce stress
2. Secondary Prevention
< Early Detection >
a. Health Hx & PE
b. Screening Methods
- Mammography, Pap smear,
Prostate exam, digital rectal
exam
- Self – care practices
o Breast self-exam
o Testicular exam
- Sigmoidoscopy and fecal occult
blood test
c. Teaching Early Warning Signs
of Cancer
- Change in bowel or bladder
movement
- A sore / wound that does not
heal
- Unusual bleeding or discharge
- Thickening of breast/ lump
- Indigestion / dyspepsia
- Obvious change in wart or mole
- Nagging/ hoarseness
- Unexplained weight loss
- Prolonged anemia
3. Diagnosis of Cancer
a. Extensive Testing to:
- Determine the presence of
tumor and its extent.
- Identify possible spread of
disease or invasion of other
body tissues.
- Evaluate the function of involved
and uninvolved body system
and organs.
- Obtain tissue and cell of
analysis, including evaluation of
tumor stage and grade.
b. Nsg Respos for Dx Tests
- Help relieve fear and anxiety by:
o Explaining the tests to
be performed
 Be specific in
your
explanations;
don’t be vague
(e.g. “para
mayo ka
ma’am”)
 o The sensations likely to
be experienced
o Patient's role in the test
procedures
4. Diagnostic Tools
a. Lab Tests
- CBC & Differential count
o Inc. WBC may be
indicative of ALL
o Inc. of RBC may be
indicative of aplastic 5. Cytologic Examination
anemia
 immature RBCs
 does not carry
O2
 low Hgb count
o Inc. in Ca can indicate
bone metastasis
o Dec. in Ca can indicate
liver cancer
- Serum Electrolytes
- Examination of body fluids
o Bence Jones CHON -
urine study
 increase 6. Oncologic Imaging
multiple
myeloma
o Guaiac Test - Occult
blood
 GI bleeding
- Tumor Markers or Protein
associated with specific cancer
o Serum prostate-specific
antigen (PSA)
o Alpha-fetoprotein (AFP)
o Carcinoembronic
Antigen (CEA)
o Homovanillic Acid
(HAV)
o Vanillylmandilic Acid
(VMA)
o B-Human Chorionic
Gonadotropin (B-HCG)
o Adrenocorticotropic
Hormone (ACTH)
- Radioimmunoassay
- Flow Cytometry
a. Papanicolaou Test (Pap smear)
- screening test that examines
cervical scrapings for
abnormality.
o cervicovaginal
discharge (CVD)
o Lithotomy position
o 2 specimens kunin:
specimen and
discharge
- It is used to detect inflammation,
infection, premalignant changes,
and malignancy of the cervix
a. Radiographs / X-ray
- Chest X-ray
- Mammograms
- CT scan / MRI
o MRI is bigger than CT
scan
- Positron Emission Tomography
(PET)
- Biopsy
 o For brain CA
3. Prophylactic Surgery
7. Invasive Diagnostic Techniques a. Removes nonvital tissues likely
a. Biopsy to develop cancer
b. Cyst Aspiration 4. Palliative Surgery
c. Cystoscopy a. Goal:
- Bronchoscopy - to make the patient as
- Sigmoidoscopy comfortable as possible AND
- Colonoscopy - to promote a satisfying and
8. Management of Pts w Neoplastic Ddx productive life for as long as
a. Goals: possible.
- Cure 5. Reconstructive Surgery
- Control a. Nsg Respos for Nsg Mgt
- Palliation - Complete a thorough pre-
SURGERY operative assessment.
1. Dx Surgery - Provide education and
a. 3 Methods: emotional support.
- Excisional Biopsy - Communicate frequently with
- Incisional Biopsy the health team members.
- Needle Biopsy - Assess the patient’s responses
2. Surgery as Primary Txt to the surgery and monitor
a. Goal possible complications.
- To remove entire tumor or as - Provide comfort.
much as possible AND - Initiate as early as possible
- Any involved surrounding tissue, plans for discharge, follow-up
including regional lymph nodes and home care and treatment to
b. 2 common procedures: ensure continuity of care.
- Local incision - Patients and family are
- Wide or Radical Excision encouraged to use community
c. New Approaches resources such as the Philippine
- Video: lap Cancer Society.
- Salvage surgery
- Electrosurgery
- Cryosurgery: liquid nitrogen
- Chemosurgery
- Laser surgery: Inc. precision
o usually for brain cancer
- Stereotactic Radiosurgery
 - Kinds of Teletherapy:
RADIOTHERAPY o Kilo voltage therapy
1. Definition device
a. Use of ionizing radiation to o Linear Accelerators and
interrupt cellular growth betatron machines
2. Indications o Gamma Rays
a. Cure CA o Particle Beam radiation
b. Control malignant ddx o Intraoperative Radiation
- when a tumor cannot be
therapy (IORT)
removed surgically OR
b. Internal Radiation Implantation
- when local nodal metastasis is
aka Brachytherapy
present
- Kinds of Implants:
c. Prophylactic use
o Sealed
d. Palliative use
o Unsealed
3. 2 Types of Ionizing Radiation
- 2 Types of Sealed Radioisotope
a. Electronic Rays
(SR)
- E.g. X-rays and gamma rays
o Intracavity Radioisotope
b. Particles
o Interstitial Radioisotope
- electrons, beta particles,
- SR: Intracavity Radioisotope
protons, neutrons and alpha
o For gynecologic CA
particles.
o Inserted into specially
4. Effects of Radiation Therapy
a. Alters the DNA molecule within positioned applicators

the cells of the tissue after the position is

- breaks the strands of the DNA verified by X-ray

helix causing cell death. o Used Cesium137 or

b. Ionizes constituents of body Radium226

fluids especially water - Nsg Respos for Intracavity

- results in the formation of free Radioisotope

radicals and irreversibly o Remain in place for

damaging the DNA. prescribed period and

- Cells may die immediately OR it then are removed,
may initiate cellular suicide generally 24-72 hours.
(Apoptosis). o Patients are maintained
5. 2 Types of Radiation Therapy on bed rest and log
a. External Radiation aka rolled.
Teletherapy
 o An indwelling catheter is - Place a sign on the patient’s
inserted. door and on the patient’s chart
o Low residue diets and indicating that the patient is
anti-diarrheal agents, receiving internal radiation
such as diphenoxylate therapy.
(Lomotil) - Observe principles of time and
- SR: Interstitial Radioisotope distance.
o For txting prostate, - Check all linens, bedpans and
pancreatic or breast CA emesis basin routinely to see if

o May be temporary or the sealed source has been

permanent depending accidentally lost from the tissue.

on the radioisotope - If sealed source is dislodged,

used but has not fallen out of the

o usually consists of patient’s body, notify the x-ray

seeds, needles, radiation department at once.

ribbons, beads, wires or o If fallen out, do not pick

small catheters it up with bare hands.

positioned to provide a Use forceps and place it

local radiation source in a lead container.

and less frequently - Most patients are placed on bed

dislodged. rest and instructed to remain in

o Iridium192, iodine125, certain positions so that the

Cesium137, Gold198 emanations from the element

and Radon222 will reach the correct area.

c. Principle of Radiation Protection - Visitors will spend limited time in

- 3 factors: the room to 30 minutes daily,

o The distance between seeing that visitors maintain a 6-

foot distance from the radiation
the nurse and the
source.
patient.
- Prohibit visits by children or
o The amount of time
pregnant visitors.
spent in actual proximity
e. Common Side Effects for
to the patient
External Radiation
o The degree of shielding
- Head and Neck
provided
o irritation of oral mucous
d. Precautionary Measures for
membranes with oral
Internal Radiation
- Place pt in a private room
 pain and risk of
infection.
o Loss of taste.
o Irritation of the pharynx - Head and Neck
and esophagus with o mucositis, oral pain and
nausea and indigestion. risk for infxn and
o Increase ICP anorexia

- Chest g. Skin Care Txt

o Inflammation of lung - Apply the special skin care

tissue with increase lotion 4x a day starting

susceptibility to immediately.

infection. - Do not wash off treatment

- Abdomen markings.

o nausea, vomiting, o Tattoos, if done, are

diarrhea, anorexia permanent.

- Pelvis - Keep skin clean and dry.

o diarrhea, cystitis, sexual o Expose the skin to air

dysfunction, Urethral as much as possible.

and rectal stenosis - Protect the skin in the treatment

- General SE area from the sun and cold by

o Skin: change in texture using scarves, hats or other

and/or color, moist clothing.

desquamation(rare); - Cornstarch may be used for dry,

alopecia itchy skin.

o Blood: bone marrow - Irritated skin, a different lotion

may be needed.
depression with
- Bathing – clear water and pat
leukopenia, anemia and
dry.
thrombocytopenia.
o Use mild soap.
o Depressed Immune Fxn
- Clothing: wear soft, loose cotton
o Fatigue
clothing over the treatment area.
f. General SE for Internal
- Shampooing – use baby
Radiation
shampoo.
- Elevated temp.
- Shaving – use electric razors.
- Cervical Implant
- Do not rub or scratch the skin in
o Urinary frequency,
the treatment area.
diarrhea, N/V and
anorexia
 - Do not use lotions or creams not with subsequent local
approved by the doctor. therapy.
- Do not use deodorants,
perfumes or make-up in the
treatment area. 3. Classes of Antineoplastic Drugs
- Do not use ice packs or heating a. Alkylating Agents
pads - Non-phase specific
- Do not use tape in the treatment - Act on performed nucleic acids
area. by creating defects in tumor
h. Post Removal of Source DNA
- Betadine douche - Cause cross-linking of DNA
- Enema strands
- Out of bed o can permanently
- Avoid direct sunlight interfere with replication
- Cream and transcription.
- Common AE:
CHEMOTHERAPY o Acute myelogenous
1. Definition leukemia
a. Systemic intervention o Irreversible infertility
b. Indications o Nephrotoxicity
- Ddx is widespread o Hemorrhagic cystitis
- Risk of undetectable ddx is high
- 5 Subclasses:
- Tumor cannot be resected and
o Nitrogen mustards
is resistant to radiation therapy
(Mechlorethamine)
2. 2 Types of Chemotherapy
o Nitrosoureas
a. Adjuvant chemotherapy
(Carmustine)
- Started after initial txt w either
o Alkyl sulfonates
surgery or radiation therapy
(Bisulfan)
b. Neoadjuvant chemotherapy
o Triazines (Decarbazine)
- Preoperative use of
o Ethylenimines
chemotherapy
(Thiotepa)
o To reduce the bulk AND
- E.g.
lower the stage of a
o Cisplatin,
tumor making it
o Chlorambucil,
amenable to surgery
even to possible cure o Cyclophosphamide,
o Bisulfan
b. Antimetabolites
- Phase-specific
o Work best during S
phase
- Have little effect in G0
- Subclasses:
o Folic Acid Analogues
(Methotrexate)
 also used in
ectopic
pregnancy
o Pyrimidine analogues
(5-Flourouracil)
o Cystocine arabinoside
(ARA-C)
o Purine analogues (6-
Mercaptopurine)
- S/S of AE:
o N/V
o Stomatitis
o Diarrhea
o Alopecia
o Leukopenia
c. Cytotoxic Antibiotics
- Derived from various
Streptomyces species
- Generally too toxic to be used
as antibacterial agents
- MOA:
o Disrupt DNA replication
and RNA transcription.
(cell cycle non-specific)
o Create free radicals
which generate breaks
in DNA and other forms
of damage.
o Bind to almost
everything they come in
contact with and kill
cells, probably by
damaging cell
membrane.
- E.g.
o Actinomycin D,
o Doxorubucin
o Bleomysin
o Mithramycin
o Mitomycin-C
d. Plant Alkaloids (PA)
- 2 Main Groups from plant
sources
o Vinca Alkaloids
o Etoposide
 pancytopenia
e. PA: Vinca Alkaloids
- E.g. Vincristine & Vinblastin
- MOA:
o Phase-specific acting
during mitosis.
o Bind to a specific
protein that promotes
chromosome migration
during mitosis and
serves as a conduit for
neurotransmitter
transport along axons.
- Toxicity: affect the nervous
system
o Depression of deep
tendon reflexes
o Paresthesias
o Motor weakness
 o Cranial nerve
disruptions
o Paralytic ileus
f. PA: Etoposide
- E.g. Eposin, Etopophos,
Vepesid, VP-16
- MOA:
o Inhibits enzyme
topoisomerase II, which
aids in DNA unwinding,
and by doing so causes
DNA strands to break.
o Acts in all phases of the
cell cycle, causing
breaks in DNA and
metaphase arrest.
- Toxicity:
o Bone marrow
suppression
o N/V
o Hypotension
g. Hormone and Hormone
Antagonists (HHA)
- 2 main groups:
o Corticosteroids
o Hormone Antagonists
h. HHA: Corticosteroids
- E.g. Predisone
o main hormone used
- MOA:
o Phase-specific (G1);
o Binds to specific
intracellular receptors,
repressing transcription
of memory RNA and
thereby altering cellular
function and growth.
- SE
o Impaired healing
o Hyperglycemia
o Hypertension
o Osteoporosis
o Hirsutism
i. HHA: Hormone Antagonists
- Work w hormone-binding
tumors
o For breast, prostate and
endometrium CA
- E.g.
o Tamoxifen – competes
w estradiol receptors in
breast tumors
o Diethystilbestrol –
competes with hormone
receptors in endometrial
and prostate tumors
o Anti-androgen
(Flutamide) AND
Luteinizing hormone –
releasing hormone
block testosterone
synthesis in prostate
cancer.
j. Miscellaneous Agents
- Cisplatin (Alkylating agent)
- An organic drug containing
platinum and chlorine atoms
o Platinum complexes
react by binding to and
causing crosslinking of
DNA
 o Ultimately triggers
apoptosis
- Most active in the G1 subphase
- Toxic effect: Reversible renal
tubular necrosis
4. Chemotherapeutic Administration
a. Oral route
b. IM or SC
c. IV – most common, provides
better absorption
- Risk: infxn & phlebitis
- Mgt for IV
o Smallest needle gauge
o Aseptic technique
o Monitor IV site frequently
o Change IV fluids q4
5. Types of IV Chemotherapy
a. Central Venous Catheter
Infusion
- Continuous or intermittent
infusion
- Risk:
o Infxn
o Catheter clot
o Sepsis
o Needle malposition
- Mgt:
o Aseptic technique
o infxn
o infiltration from
malposition
c. Intra-arterial Route
- Delivers agents directly to tumor
in high concentration while
decrease drug systemic toxic
effect
- Risk:
o Infxn
o Bleeding at catheter site
o Clotting at site
- Mgt for Intra-arterial Route
o dressing change daily
and assess infection
o Irrigate/flush catheter
o Avoid kinks in tubing
d. Intraperitoneal
- For ovarian and colon CA
- High concentration of agents
delivered to peritoneal cavity via
catheter, then, drain
6. Chemotherapy Safety Guidelines
a. Obtain special training
b. Wear: gloves, disposable,
closed, long-sleeved gown
c. Label prepared drugs
appropriately
d. Double bag drugs prepared –

o Monitor site daily transport

o Flush catheter daily/ e. Clean any accidental spill

f. Dispose all used materials
between use
appropriately
o Assess for signs of infxn
g. Dispose all syringes and
b. Venous Access Device
needles intact
- Prolonged infusion
7. SE & Nsg Mgt
- Risk:
a. GI System
- N/V
o Antiemetics 4-6 hrs
before initiated
o Withhold fluids/foods 4-
6 hours before
o Support food
preferences
o Small frequent feeding/
meals – Calories and
CHON
- Diarrhea d/t toxicity
o Antidiarrheal
o Everyday perineal care
o Monitor K, Na, & CL
level
- Constipation d/t drug affecting
nerve endings of GIT
o Inc. fiber and fluids
o Have stool softeners
- Stomatitis
o Good oral hygiene
o Rinse w Lidocaine
before meals
o Cleansing rinse w plain
H2O OR dilute a water-
soluble lubricant after
meal
o KY jelly to cracked lips
o Avoid spicy and acidic
foods
b. Hematologic System
- Thrombocytopenia
o Platelet (below 150T –
300T)
o Shorter lifespan
- Leukopenia
o WBC (below 5T – 10T)
- Leukopenia Mgt
o Careful handwashing
technique/aseptic
technique
o Reverse isolation
o Assess for respiratory
infection
o Avoid crowds or people
with infection
- Anemia Mgt
o Adequate Rest
o Monitor Hgb and Hct
count
o O2 PRN
c. Integumentary System
- Alopecia (2 – 3 wks)
o Temporary
o Support and
encouragement
o Wear wig
d. Renal System
- Direct damage to kidney
(excretion)
o Frequent voiding
o Inc. OFI
o Allopurinol (Zyloprim) to
prevent uric acid
formation
e. Reproductive System
- Infertility/mutagenic damage to
chromosomes
- Banking sperm
f. Neurologic System
- d/t repeated use of Vincristine
- S/S
o Hearing loss
o Paralytic ileus
o Loss of tendon reflex