Chapter 23: Concepts of Inflammation and the Immune Response

Purpose of Immunity
to neutralize, eliminate, or destroy organisms that invade the internal environm
ent.
without harming the body
Self- tolerance
Immune system cells distinguish self from non-self proteins and cells, which inc
lude infected body cells, cancer cells, and organisms.
This ability to recognize self versus non-self is necessary to prevent healthy b
ody cells from being destroyed along with invaders and is known as self-toleranc
e.
Failure to recognize ‘self’ = autoimmune disorder
Each person is unique; Antigens are unique for each person (if someone else anti
gen gets into your body then antigen antibody reaction takes place ) Antigens ar
e protein on the surface of our cells and when stimulated antibodies are made!
Question: At what point is our immune Fx the best?
A) Infancy
B) Teenager;
C) 20 to 30 years
D) 50 years and older (Nutrition and Age effect immune fx)
Answer C;
-This is why you don’t see many 30 yr olds in hospital. Infants are not good with
immune system b/c they don’t have one yet and an older adult has a lesser due to w
orn out system and older age;
Chronic diseases and conditions of immune system can wear a system out; Good nut
rition is needed for a good immune system;
So elders and malnutrition have decreased immune system fx;
Important lab values: serum albumin; protein; Prealbumin; ferritin (IRON); Hgb;
Clinical observation of good nutrition: BMI; muscle strength; skin color; skin i
ntactness; brittle dry nails; thin hair, etc; eyes (dry, sunken)
WBC needs protein to develop!!
- Corticosteroids depress immune system; chemotherapy;
Human Leukocyte Antigens Complex (HLA)
HLA = A unique universal product code for each person
Antigens are a normal part of the person; and act to stimulate an immune respons
e when they enter another person’s body
These antigens specify the tissue type of a person.

If an ‘encountered cell does not match the persons universal product code (HLA’s) th
en the immune system activates to neutralize, destroy, or eliminate the foreign
invader
Self-recognition
Human Leukocyte Antigens Complex (HLA)
Discovers of these complexes came from the trying to understand organ rejections
during transplantation.
Immune function effected by nutrition, drugs, disease, age; patients in the extr
emes of age have decreased function
Organization of the Immune System
Not confined to one organ or area of the body
Immune system cells come from the bone marrow.
Stem cells – undifferentiated cells (pluripotent)
Bone marrow starts with the stem cells; (stem cell can differentiate into any bl
ood cell needed for body)
Maturational pathway of any stem cell depends on body needs and presence of spec
ific-hormones (cytokines, factors)
Leukocytes (WBC) – protect body from invasion
Provide protection through defense actions
Erythrocytes
Thrombocytes
Three process needed for immunity
1. Inflammation
immediate, but short term; non-specific; may be localized or systemic;
helps to start the full immune response
2. Anti-body mediated immunity
B-lymphocytes
‘Humoral’ immunity
3. Cell-mediated immunity
T lymphocytes

Inflammation
* Provides immediate protection against the effects of tissue injury a
nd foreign proteins.
* The capability for inflammatory response is critical to health and w
ell-being.
* Causes visible symptoms and can rid the body of harmful organisms.
* Tissue damage may result from excessive inflammatory response.
* Does NOT mean that infection is present
Inflammatory process is NOT infectious but the infectious process is always infl
ammatory; (Tissue injury great example, twisted ankle, heart attack, blisters – in
flammatory process with no infection.. no foreign bacteria, etc that caused it)
(Infectious is invading) inflammation inhibits arterial blood supply and can cau
se tissue damage (localized); Some patients have a systemic inflammatory respons
e (injury localized) body responses to the injury, arteries dilate, BP drop, you’l
l see shock!!!; UO low, even when a dr does IV antibiotic they don’t get better (i
f its just inflammation it wont help) this is all called SIRS (Will put pt in IC
U) excessive inflammation;
Leukocytes
* Normal WBC count ~ 5,000 – 10, 000
* Differential normals
(must have ~ 3000 granulocytes to fight infections)
* Granulocytes (glandular in their cytoplasm) Infection fighting cells**
Segmented Neutrophils (Segs, aka PMNs) ~ 60% w/out these you’d always be sick! BI
G GUY!! Phagocytosis takes place by these guys; 1st responder EMS of white cells
;
* Bands < 5% (left-shift when ↑ )
Basophils < 1% secrete heparin and antihistamine and others; (heparin that keep
s capillary from making clots, temp, so the other cells can get to site of injur
y) Histamine to vasodilate (more cells can get there); Allergic response (hypers
ensitivity response) and increase with parasitic infestation;
Eosinophils < 2%
* Lymphocytes ~30%
* Monocytes ~ 3 %
Long Bones/Hip w/ Bone Marrow Bipsy (Hip bone is more activity); Typically on th
e site cleanse sites, topical pain med; (Bic pen size needle); when needle penet
rates down into bone marrow it hurts (esp as aspirating); Lidacain, fetal posit
ion (facilitate exposure to get down into muscle to bone) 10-15 min,
Risk for Hemorrhage (pressure, place on back, can use ice; visualize
and palpate site;
* Bone Marrow Biopsy
Jamshidi needle for Bone Marrow aspiration and biopsy
* Cell Types of Involved in Inflammation
Neutrophils
Monocyte/
Macrophage
(migrate and live in tissues as macrophages)
Basophils
Eosinophis
Infection
* Infection is usually accompanied by inflammation; however, inflammat
ion can occur without invasion by organisms.
* Inflammation does not always mean that an infection is present.
Sequence of Inflammatory Responses
* SIGNS of Inflammation: warmth, redness, swelling, pain, and decreas
ed function; (rush of blood to site, fluid in interstitial space)
* Stage I (vascular): change in blood vessels
* Phase I: constriction
* Phase II: hyperemia and edema
* Stage II (cellular exudate): neutrophilia, pus - If there is a infec
tion the white cells surround and engulf (clinically indication that that’s happen
is pus); if someone is neutropenic there is no destroying;
* Stage III (tissue repair and replacement)
Question Pt arriving at ER after injured in accident is experiencing swelling an
d pain at site. Nurse predicts the pt is experiencing which stage of inflammator
y response?
III
II;
Stage I
Answer C- Stage I phase II
Antibody-Mediated Immunity - B-Lymphocytes
- Released from BM and mature in lymphoid tissue (spleen, lymph nodes, t
onsils)
- Make specific antibodies against specific organisms or toxins
* An antigen enters the body; B cell recognizes antigen as non-self (n
ow sensitized) and divides forming a) plasma cells that produce antibodies & b)
memory cells; antibodies circulate within blood & body fluids (humoral, b/c the
y circulate in body fluids)
* Immunoglobulins = gamma globulins: IgG[KE1] , IgA, IgM, IgE, IgD
Disease multiple myloma
Immune Response: Two categories of Humoral Responses
1. Innate – natural within the person
* Can be a barrier to invasion or can be a destroyer
* Cannot be developed, or transferred from another, not adaptive
* Inflammatory response is innate
* No long term memory of the event
* Pathogen – PAMP – PRR--- Innate leukocyte --- Phagocytosis
* ----Target cell lysis
. Adaptive – in response to invasion
* Active- body makes the antibodies
Natural – without human interference, the body makes the antibody to the antigen a
fter an invasion; longest lasting & most effective (get exposed and healthy B c
ells make antibodies – and then if exposed again then they attack and destroy the
invading antigen)
Artificial – through immunization - invasion by an attenuated antigen; may requir
e ‘booster’ to retain protection; dead but enough properties to make antibodies to t
hat virus
* Passive – antibodies passed from one person to another (breast milk, or i
njection with antibodies made by another person/animal) short term
Humoral Immunity (B Lymphocyte) help against bacteria, etc. w/ antibody
* Acquired as a result of previous exposure
* Has the ability not only to distinguish self from nonself, but to re
cognize and destroy specific foreign agents based on the distinct antigenic prop
erties
* Mediated by the B lymphocytes (B cells)
* Every effective again extracellular microbes and their toxins
* B cells differentiate into antibody-secreting plasma cells
Cell-Mediated Immunity: T- Lymphocyte
* Help protect the body by differentiating self from non-self cells; non
-self cells most easily recognized by cell-mediated immunity are cancer cells an
d those self cells infected by organisms that live within host cells.
* Important in preventing the development of cancer and metastasis after
exposure to carcinogens.
* Have many subsets, each with specific functions
* Cancer (bad t lumph)

Helper/Inducer T-cells
* Most correct name is CD4+
* Helper/inducer T-cells easily recognize self cells versus non-self c
ells.
* Secrete lymphokines that enhance activity of other WBCs
* Help increase immune function
* Help maturation of WBCs
* Helper/inducer T-cells act as organizers in “calling in arms“ of various
squads of WBCs involved in inflammatory, antibody, and cellular defensive actio
ns to destroy or neutralize antigens.
* 600-1,200 CD4 cells per cubic millimeter of blood
* HIV to AIDs means they don’t have sufficient CD4 cells!!!! (T count wa
s _____)

Suppressor T-Cells
* Called theT8 + or the TS cells
* Help regulate cell-mediated immunity
* Prevent overreatction to non-self cells/proteins
* Secrete inhibitory lymphokines to inhibit growth and activity of imm
une system cells
* If balance of T8 > T4 then person at ↑ risk infection

Cytotoxic T Cells
* TC cells - a subset of suppressor cell
* Most effective against self cells infected by viruses or protozoa (p
arasites)

Cytokines
* Hormones produced by WBCs (monokines and lymphokines)
* Once the cytokine binds to a receptor site, the responder cells chan
ges its activity
* Control inflammatory and immune responses
* Examples: interleukins, interferons, colony stimulating factors, an
d tumor necrosis factors
(chart pg 375)
* CMI helps protect body by differentiating self from non-self & rids
body of abnormal malignant cells and cells invaded with harmful organisms. Cance
r is a failure of the CMI !
Transplant Rejection: Role of NK and cytotoxic T cells to destroy
* Hyperacute graft rejection: begins immediately and can’t be stopped (n
ot reversible) Occur if not matching up blood properly or if receipent has had m
any blood transfusion or freq transplanted organ;
* Acute graft rejection; within 1 -3 months; S/S organ dysfunction (sc
ar tissue developed so over time not good fx)
* Chronic rejection: chronic inflammation with scarring and replacemen
t of normal tissue with fibrous tissue
* Treatment of transplant rejection: immunosuppressive therapy: Cyclo
sporin (Sandimmune®), Imuran®, &
steroids (prednisolone); Monoclonal antibodies (nterleukin 2 antagonist) bi
nds to the IL-2 receptor sites & inhibits T cell growth
* Maintenance: Tacrolimus (Prograf®)
Pt receiving therapy w/ cyclosporine after transplant. Nurserec possible outcome
of long-term immunosupp. Therapy w/ this drug is? A low cost therapy for suppre
ssion of organ rejection; Possible serum sickness and anaphylaxis; risk for inf
ection; Increased risk for cancer development.
Chapter 27 Altered Cell Growth and Cancer Development
Pathophysiology
Hypertrophy is cell growth that causes tissue to increase in size by enlarging e
ach cell.
Hyperplasia is growth that causes tissue to increase in size by increasing the n
umber of cells.
Neoplasia is any new or continued cell growth not needed for normal development
or replacement of dead and damaged tissues.

Characteristics: Normal vs Malignant Cells

Normal
Slow cell division
Morphologically like the ‘parent’
Small nucleus
Perform specific functions
Adhere tightly together
Do not move away from site of origin; contact inhibition (touching, growth is
inhibited); stick together;
O Only divide & replace when needed and stop dividing
when cell touches cell
Have 23 pairs of chromosomes
Malignant
Rapid cell division
Are anaplastic (poorly differentiated = undifferentiated)
Need to look for terms like anaplasia (another name for differentiations) cancer
tx depends on how much it looks like parents cells;
Large nucleus
Have no useful purpose; only thing its good for is replicating (more growth of c
ells)
Don’t adhere to one another and will spread via blood, lymphatics, and body tissue
s;
Have no contact inhibition
Expand and invade other tissues
# chromosome pairs </ >/ = 23
- The faster the cells divide, the faster the growth of the tumor. As more cells
accumulate, the normal tissue b/c disrupted.
- Cancers spread by invasion and metastasis. Invasion = the direct migr
ation and penetration by cancer cells into neighboring tissues. Metastasis= the
ability of cancer cells to penetrate into lymphatic and blood vessels, circulat
e through the bloodstream, and then invade normal tissues elsewhere in the body.
Steps:
Cancer cells invade surrounding tissues and blood vessels
Cancer cells are transported by the circulatory system to distant sites
Cancer cells reinvade and grow at new locations
Blood from gut goes to liver and the liver takes out nutrients, and toxins etc.
if someone has gut cancer, the spread goes from gut to liver, then thru the hear
t to the lungs;
Naming – helps to determine site of origin
Carcinomas, the most common types of cancer, arise from the cells that cover ext
ernal and internal body surfaces. Lung, breast, and colon are the most frequent
cancers of this type in the United States.
Sarcomas are cancers arising from cells found in the supporting tissues of the b
ody such as bone, cartilage, fat, connective tissue, and muscle.
Lymphomas are cancers that arise in the lymph nodes and tissues of the body s im
mune system.
Leukemias are cancers of the immature blood cells that grow in the bone marrow a
nd tend to accumulate in large numbers in the bloodstream.
Learn these: Adeno = epithelial gland; hepato = liver; lipo= fat; lympho = lymp
hoid tissue; osteo = bone; rhabdo = muscle; squamous = skin; (others = chondro
= cartilage; erythro = red blood cells; hemangio = blood vessels; melano = pigme
nt cell; myelo= bone marrow)
If you hear sqaumous or basal skin cancers they are NOT life threatening (don’t sp
read to tissues); the American Cancer society does not report these, this kind w
ill be melanoma skin cancer!!
Cancer Development
Carcinogenesis/oncogenesis are names for cancer development
Malignant transformation occurs through the following steps:
Initiation (damage to DNA from carcinogens); T-lymphocytes is suppose to come in
and destroy
Promotion (enables CA cell to divide & grow)
Progression (continued growth, may change features)
Metastasis (spread to new locations via extension, local seeding, blood, lymphat
ics)
Carcinogenesis: transformation
Oncogene activation – cause normal Δ → CA (cancer)
Carcinogens: chemical (tobacco, hair dye), physical (radiation from sun, x-ray,
chronic irritation), viral, dietary (excesses & deficits) –
Excess nitrates and preservatives and “smoked” foods cause GI malignates)
Deficits - Low Vit A, low fibers causes slower movement (HIGH FIBER, wheat, barl
ey, beans, grains, crucierous veggies - Bro, cali, cabbage, brussel sprouts) oat
s, fruit, “raw” fruits, uncooked stuff and the peelings)
High Fiber foods: Wheat, barley, beans. Grains crucicerous veggies, oats, fruit
, “raw” foods & uncooked stuff
Crucicerous – broccoli, coliflower, cabbage, brussel sprouts
Personal factors, immune function, age, and genetic risk
Chemicals, radiation, viruses, and heredity all trigger changes;
DNA mutation genes can be mutated in several different ways;
Oncogenes stimulate dev of cancer by instructing cells to make protein that stim
ulate excessive cell growth and division (Normal cells regulate cell growth
Tumor Suppresor genes- If tumor suppressor genes absent cancers develop. Indivi
dual who inherit and increased risk of dev cancer often are born with defective
copy of a tumor suppressor gene. The person then may develop cancer b/c there n
o suppression to growth of abnormal cells
Immuntherapy tries to stimulate T-suppressor cells
Metastasis (blood or lymphatics)
Metastasis occurs through a progression of steps:
Extension into surrounding tissues
Blood vessel penetration
Release of tumor cells
Invasion
ü Local seeding (ovarian cancer)
ü Bloodborne metastasis
ü Lymphatic spread
Breast – bone/lung/brain; lung – bone/brain; GI – liver/lung; prostate – bone
If someone has lung cancer an it spreads to the brain it is really lung cancer i
n the brain and we must treat it as lung cancer;
Question: What is one of the common site of metastasis for breast cancer?
A. Brain
B. Lymph nodes
C. Pancreas
D. Pelvic
Rationale: Breast cancer commonly metastasizes to bone, lung, liver, and brain.
The lymph nodes are common for lung and melanoma. Pancreas is common for lung,
prostate to pelvic nodes, and colon cancer to liver.
Why cancer is dangerous?
Cancer cells can spread to distant parts of the body. For ex melanoma ( a canc
er of pigment cells) arising in skin can have cells that enter the bloodstream a
nd spread to distant organs like liver or brain. Cancer cell growing in the brai
n or liver can disrupt the fx of vital organs an are potentially life threatenin
g;
Question? Malignant tumor has metastasized from lung to brain? What type of canc
er is in brain?
Lung cancer in brain; use primary site when naming;
Cancer Classification
Cancer grading and staging help diagnosis, treatment, & prognosis.
Grading on the basis of appearance and activity: compares the CA cell with its n
ormal parent tissue. G1 – well differentiated, G4 – poorly differentiated, anaplasti
c
Staging classifies size of the CA, determines exact location and degree of metas
tasis at diagnosis. TNM (T – size of tumor; N – number of involved lymph nodes; M – me
tastatsize to another organ system);
Stage 1 limited disease, Stage 4 disease has spread; Stage refers to size of tu
mor! & extent of how much cancer does the person have
Question: Single most important risk factors is:
Bring a women
Family Hx
Cig Smoking
Advancing age
Rationale: Gender DOES NOT have a factor; AGE, according to the American Cancer
Society, advancing age is most important risk factor!!
External Factors & Carcinogenesis
Chemicals
Tobacco
ETOH (alcohol can be a contributor)
Physical
Chronic irritation
Radiation
UV (sun, tanning beds)
Ionizing (natural elements – radon, uranium, radium)
Bacterial
H-pylori (upper GI cancer) ulcers & GI malignances
Viral
Epstein-Barr –Burkitt’s lymphoma
Human papillomavirus (HPV) - genital
Dietary
High intake red meat & fats
High intake preservatives, additives including nitrites
Low intake of fiber, cruciferous vegetables, Vit A, Vit C (25 fiber/day)
Tobacco Use and Cancer: Among factors that cause cancer, tobacco smoking is grea
test public hazard. Cig smoke contains more than two dozen different chemicals
capable of causing cancer. 1 out of every 3 cancer death relating to cigarette s
moking
Lag Time – carcinogens initiate genetic alterations & Proliferations. Time is requ
ired. There can be a delay of several decades between exposure to a carcinogen a
nd the onset of cancer. For ex, exposure to carcinogens from smoking cigarettes
generally doesn’t develop into cancer for 20-30 years. ( Someone who was seriousl
y sun burned at 5 may not get skin cancer til they are 40)
When test is + for CA gene mutation, risk for CA development is HIGH, but test i
s NOT diagnostic for cancer!! Consider implications 1st; cancers with genetic im
plications: Breast, ovarian, some colon, esophageal/stomach
Cancer Risk & Aging: B/c a # of mutations usually must occur for cancer to arise
, chances of dev cancer increase as a person gets older b/c more time has been a
vailable for mutations to accumulate. Ex 75 old person is 100X more likely to d
ev colon cancer than a 25 yr old. B/c person are living longer than they did 50-
100 year ago they have longer exposure time to factor that may promote gene chan
ges linked to cancer. ACUTE LUEKEMIA in a 2 yr old is curable but in an adult is
not as promising; But Cancer is more likely to be seen in older adults;
Cancer Prevention: Primary
Avoidance of Carcinogens
Sun, tobacco, asbestos
Modification of risk factors
Dietary modification, sexual practices
Chemoprevention (to disrupt steps in CA development, reverse gen damage, halt pr
ogression of transformation)
Vit C/E, NSAIDS,
Removal of ‘at risk’ tissues (moles, colon polyps, mastectomy)
Healthy diet – increase fruit & veggies, and fibers – 5-9 servings of fruits and veg
gies daily;
Cancer Prevention: Secondary
Screenings
BSE (monthly) & Mammogram yearly p 40
Pap (yearly)
TSE (15 – 35 monthly)
PSA & DRE (yearly p 50)
Fecal Occult Blood Testing (FOBT) (yearly) & Colonscopy (@ 50 then q 5 -10 year
s)
Gene therapy – in the future
Question: Primary prevention would be
Yearly mammography for women older than 40 yr
Using skin protection during sun exposure at beach
Colonscopy at age 50
Yearly PSA and DRE for men older than 50
Answer is B, prevention!!
C A U T I O N
Change in bowel or bladder habits
A sore that doesn’t heal
Unusual bleeding
Thickening or lump
Indigestion or difficulty swallowing
Obvious change in a wart or mole
Nagging cough or hoarseness
Cancer may no have any warning: That is why screening for some cancers is import
ant.
Cancer doubling time (BSE) palpable mass; your fingers cant detect a mass in bre
ast til its around size of green pea (b4 big enough to be palpable in a breast i
t may have been there for years and divided around 30 some times)
Get Mammograpy after period; Cervical PAP – Early detection of cancer of uterine c
ervix; Prostate –DRE & PSA or TSE for testicaular cancer; Colon – FOBT & Colonscopy-
small amt of stool and test for blood
Question : In affluent countries, what percentage of people diagnosed with cance
r each year are cured of their disease? 50% (after 10 years without cancer, the
y are considered cured, some are after 5)
General Disease-Related Consequences of Cancer
Complications RT metastasis
If untreated, cancer
¡ Impairs immune and hematopoietic function, esp w BM invasion > ↓ WBCs, RBCs, plat
elets
¡ Alters gastrointestinal structure and function > obstruction, liver failure, ca
chexia (don’t want to eat and lose lots of wt)
¡ Motor and sensory deficits > nerve compression, bone involvement, SC compressio
n (Spinal Cord)
¡ Weakness and nerve involvement
¡ Decreases respiratory function, esp. when lungs involved
¡ Increased clotting (when long sitting, riding, job, etc is not present)
vComplementary Therapy – enhance affects if pt has positive outlook, mind and body
are def connected (psychoneuroimunology); Support pt more likely to do well; in
oncology we want to integrate therapeutic approaches; Power of prayer**
v Nutritional therapy
Well balanced diet
Nutritional support
Supplements
Tube Feedings
TPN
v Transfusion support
RBC
FFP
Platelets – can donate these (unless you take aspirin b/c it decreases stickin
ess)
Surgery as Cancer Treatment
Oldest form of cancer treatment used for:
¡ Prophylaxis
¡ Diagnosis ** Get tissue to determine if malignant
¡ Cure- if they can get all tissues they can cure it (all visible evidence of dis
ease)
¡ Control (cytoreductive = debulking) – remove bulk of disease not likely to cure (
You would do this for comfort measure like if it was blocking fecal matter etc)
¡ Palliation- diminish symptoms; debulking can be palliating too;
¡ Determining efficacy of therapy
¡ Reconstruction
Considered as local therapy
When it spreads by blood or lymph it may be in new location but amt is so limite
d that we don’t catch it (pt undergoes resection of colon, it hasn’t treated the pos
sible spread of somewhere else)
Nursing care of surgical client
Basic physical care same as for any other surgical client – remember your ABCs
Emotional impact of surgery – “what will they find?” “will they get it all?” “how can I liv
without my ……..?” Uncertainty
Grief – loss of body part, body function, loss if life
Radiation Therapy for Cancer
Purpose: to destroy cancer cells with minimal exposure of the normal cells to th
e damaging actions of radiation
Mechanism of action
¡ Cells are damaged by the radiation either outright or become unable to divide R
adiation therapy works by damaging cells. Normal cells are able to repair themse
lves, whereas cancer cells cannot.
Killing effects of radiation
Types of Radiation Therapy
Teletherapy – external beam therapy (Pt NOT radioactive; must be in same position
w/ every tx; usually 5X for 4-6 weeks)
Brachytherapy – Short, closeup therapy & Sourse is within client, Continuous (LD)
or intermittent (HD)
Client is radioactive, durin LD tx until isotope is eliminated – 48hr
Unsealed = given IV, PO, instillation; ex I^131 (radioactive iodine) Iodine is t
x for thyroids;
Sealed – implanted within tumor
Some stay in place forever b/c isotope life is so short
Preloaded – when placed in OR (placed in prostate) Pregnant ladies cant be in here
Afterloaded – special applicators placed, then radioactive implant loaded; excreta
are not radioactive; Preg lady can be in here
Considered as Local therapy
Radiation pysicsis (person who understands when too much radiation is bad for he
althy cells)
Side Effects of Radiation Therapy
Vary according to the site
Local skin changes and hair loss that will likely be permanent depending on the
total absorbed dose
Systemic effects:
¡ Altered taste sensations
¡ Fatigue related to increased energy demands
Inflammatory responses in healthy tissue cause tissue fibrosis and scarring
Bone marrow, hair and GI are fastest in dividing cells; if getting prostate “radia
tion” wont lose hair on but if radiation around lymph nodes they will have bone ma
rrow problems (have problems with esophageal and heart) Heart doesn’t respond to r
adiation; Lens of eye can tolerate radiation;

Nursing Care of Clients Undergoing Radiation Therapy

Teach accurate objective facts to help client cope.
¡ Alopecia, Bone Marrow suppression, proctitis, myocardititis, pneumonitis, fatigu
e
Administer skin care.
Do not remove markings.
Do not use lotions or ointments.
Avoid direct exposure of the skin to the sun.
Care for xerostomia (dry mouth). FOR LIFE!!! Good dental hygiene; hard candies,
liquids;
Destruction of sweat glands
Bone exposed to radiation is more vulnerable to fracture.
Loose fitting clothing, no exposure to heat or cold, Splash PAT; no LOTION, Per
fume, aftershave; no shaving
Question: A pt who is receiving radiation therapy for breast cancer would experi
ence which side ffect?
Sever fatigue : all pt with radiation can develop fatigue and can be debilitatin
g and may last for weeks to months.
Mucositis Mouth ulcers
Hair Loss
Nausea and vomiting
Tandum (device that fits in vaginal cannal and opens uterine cervix so when she
gets back to room the radiation seeds are placed in oval openings on side)
Someone with the implanted things (little smaller than speculum) will have a fol
ey and low residue diet (fiber) HOB lower
Brachytherapy – protect thyself!! Monitor amt of time you spend with pt, distance
b/t you and radiation source and protect with shielding; 30 min for the brady pt
(more than 1 pt assigned to this pt) PRIVATE ROOMS!!!!!
Skin care (dos and don’ts)

Types of RADIATION THERAPY

Teletherapy = external beam therapy
¡ Pt is NOT radioactive
¡ Pt must be in same position every treatment
¡ Usually 5 times a week for 4 – 6 weeks

Brachytherapy = short, close-up therapy & source is within the client, continuou
s (LD) or intermittent (HD)
¡ Client is ‘radioactive’ during the LD treatment until isotope is eliminated ~ 48 ho
urs
¡ Unsealed = given IV, PO, instillation; ex. I131
¡ Sealed – implanted within the tumor
¢ Some stay in place forever because the isotope life is so short
¢ Preloaded
¢ Afterloaded – special applicators then radioactive implant loaded; excreta are no
t radioactive

Protect ‘thyself’ (lead lying canaster and long tongs to pick up seeds)
Nursing Care when Clients Undergo Sealed Source Radiation Therapy
Private room
No children under 16
No staff that is pregnant/ no pregnant visitors
Visitors ½ hour a day
Stay 6 feet from source
Never touch radiation source with bare hands
Be careful to NOT dislodge source
All body secretions are radioactive – contact radiation safety officer if pt vomit
s
Floor where client walks, covered with protective covering
Foods on disposable plates
Flush toilet several times
Trash/linens kept in room until client is D/C
PPE – gloves & booties
Limited contact
Chemotherapy
Treating cancer with chemical agents
Considered as Systemic therapy, providing opportunity to kill metastatic cells
Major role in cancer therapy
Typically given IV, although some may be given orally; particularly lung cancer
that’s very fast growing but it is very very receptive to chemo;
Bone marrow (LETHAL), hair and GI can be hurt most by chemo;
Mechanism of Action
Chemotherapy – ability of the drugs to damage DNA and interfere with cell division
of the cancer cells
Tumors most sensitive to drugs are those with rapid growth
Will affect healthy cells as well as cancer cells
Normal cells affected more are those that have rapid growth such as skin, hair,
intestinal tissue, spermatocytes, and blood forming cells
Used to cure and increase survival time; prolong good quality of life
Some selectivity for killing cancer cells over normal cells
Cell cycle specific (means it only works on the cells in that specific cell cycl
e) Some cells will be in G0 – variable Quiescence; Prednisone gets them out of G0 –
it activates them and gets the off the “fat rockers” wont kill them but puts them in
active cycling phase; S Phase specific it will affect cells that are actively
making DNA but wont affect the ones in G1 G2, etc;
S (DNA synthesis 39%); G2 (Prep for mitosis 19%); M (Mitosis and cell division 2
%); G0 Quiescence (variable); G1 (Synthesis of components req for DNA synthesis
40%) we give combo drugs so we can hit multiple cell specifics

Chemotherapy Drugs
Antimetabolites --closely resemble normal metabolites and are “counterfeit” metaboli
tes that fool cancer cells into using the antimetabolics in cellular reactions w
hich impairs cell division.
5-FU (well tol. Drugs, wont lose hair or get sick)
Methotrexte (Mtx. SENSITIVITY NEED SUNSCREEN),
6-Mercaptopurine
Antitumor antibodies--damage the cells’ DNA and interrupt DNA or ribonucleic acid
(RNA synthesis); Not a micro; S phase very phase specific; VERY LIKELY TO CAUSE
THE SIDE EFFECTS!!
Bleomycin- unusal toxicity to lungs (lil to heart) after a certain dose that’s all
they can have for life.. watch COPD patients; Doxirubicin- (Adriamycin/Red devi
l) lose hair after 10 days, its cardiac toxic and they can only have a max dose/
life;
Mitomycin C- lose of Calcium;
Alkylating agents--cross link DNA, making the two DNA strands bind tightly toget
her inhibiting cell division
Busulfan (Cisplatin) – Easliy tolerated! Nephrotoxic so they need Creatinine (24hr
urine) clearance;
Chlorambucil, Cytoxan- Hemorrhatic cystisis, CCNU, Alkaran
Antimitotic agents--made of plant sources, interfere with the formation of micro
tubules, interfering with mitosis during cell division
Taxol – comes from tree bark,ethical issues with forest;
Vincristine (periwinkle plant), slow peripheral nerve production, neurotoxicity;
(sensation, muscle contraction,same issue as DM pt) slow gut;
Vinblastine – cause neurotoxicity same as vincristine;
Topoisomerase inhibitors--Enzyme need for DNA synthesis and cell division; Allow
s DNA to be copied, than it reattaches the DNA together ; Causes DNA breakage an
d cell death
VP16, VM 26
Miscellaneous chemotherapeutic agents--Inhibition of important enzyme systems; C
ompetition for important substances in metabolic pathways
Asparaganiase, Hydroxyurea
Combination chemotherapy--Increase effectiveness of several drugs; to produce cu
mulative effects; may prescribe one from each and prednisone to get max cell kil
l; each cancer
‘Rescue’ agent
¡ Leucorvan Folic acid used w/ Mext. Rescue healthy cells from excessive damage f
rom Mext (not a chemo really Folic acid) Timing of this drug is critical… know exa
ctly how soon after you admin Mxt when you should get this drug

Side Effects: alopecia, N/V, bone marrow suppression

Chemotherapy & the Cell Cycle
Noupegn- stimulates bone marrow to stimulate white cells
Nator max effect on bone marrow (Plasma, Leucocytes and platelets and erythrocyt
es in a tube separated) At low point they are at risk for infection;
Treatment Issues
Nadir- point after administration of drug that person bone marrow is most depres
sed;
NEEDS CBC prior to next tx cycle
We need to know that bone marrow has recovered and the WBC is normal range)
Need 3,000 granulocytes (neutrophils) to fight off; Most tx aren’t daily
Drug dosage – based on client’s body size (M2) Ht and Wt
Ø If they are 1.8M^2 and its 2mg we just multiply; Don’t have to know how to calcul
ate M2;
Drug schedule – timed to maximize cell kill; what tx plan for the pt
Drug administration –
¡ Extravasation of a Vesicants (causes severe tissue damage if
infiltrates) (Students don’t admin chemo)
¡ Put in new IV before doing chemo… lots of pt get picc line, central, etc to dimin
ish pain of stuck all the time and risk of extravasation is almost none;
¡ Mixing pharmacist and administering RN protect self
(absorbed through skin & mucous membranes; therefore wear spec
ial PPE)
¡ Special precaution with chemobio wastes kit

REMEMBER PROTECT THYSELF w/ chemo drugs

Verification of drug, route, dose, and schedule/ Cal check twice.
Extensive client education
Exposure from
Resp inhal
Skin absorption
Oral ingestion
OSHA guidelines
PPE (gowns, gloves) during prep and admin
Laminar-flow hoods during prep
Gowns and gloves handing body secretion of clients within 38 hr after chemothera
py
Hematopoietic Growth Factors
Epoetin (Epogen/Procrit)
Filgrastim (Neupogen) WBC stimulator, feel like ya got flu
Pegfilgrastim (Neulasta)
Oprelvekin (Neumega) – platelet release (At risk for bleeding)
Steriods
ü Prednisone stimulates bone marrow (activates G0 cells)
Antiemetics
Prochlorperazine (Compazine) Act CRAZY (Pyscho)
Promethazine (Phenergan) makes you sleepy; burn if rectal; slow if over IV and c
an cause psycho stuff;
Metoclopramide HCL (Reglan) – increases Gastric emptying, antiemetic properties as
well;
Ondansetron HCL (Zofran) – least side effects; common IV push
THC (meranaol) – generic of marijuana;
Routes of Admin (SYSTEMIC therpy)
Port-a-cath: occlusive dressing; aseptic tech;
IV
Oral (not many)
Intrathecal – (b/c most meds do not cross Blood-Brain barrier)
if pt has brain tumors then it must be directly placed in epidural so it is put
in CSF; If frequent use then they use ommaya reservoir (port-a-cath type techniq
ue, access by placing needle thru scalp into reservoir and med goes into ventric
les
Intravessicles (into bladder)
Intra hepatic (into kidney)
Femoral artery (osteogenic carcoma, save leg) heating/cooling;
Inhalation

Side effects of chemo- Side Effects of Chemotherapy

Alopecia or hair loss – wigs, caps,
Mucositis/stomatitis in the entire gastrointestinal tract
In mouth or whole GI tract (Candida every shift, ulcers in mouth) Listerine is t
oo strong (heavy alcohol), do cheap mouth washes and dilute with water b/c alcoh
ol is a drying agent;
lemon & glycerin swabs (lemon eats enamel away and glycerin is alcohol); Use sof
t bristle toothbrush.. gentle mouthcare;
Nystatin (magic mouthwash) will be administered if they have candida (an
tifungal); Bendryl, textrcycline, Lidacain (numbs mouth)
Stomatitis- not eating, pain, popsicle and ice works great before eating food; r
isk for infection and then into blood stream causing fungal septicemia; If mouth
looks red the other GI tracts looks same, swallow nystatin and magic mouth wash
;
Nausea and vomiting
If you know the drugs causes N/V give antiemetic; give another; serve cold food
instead of hot; Fluid and electrolyte; nutrition;
Skin Changes
Anxiety, sleep disturbance
Altered bowel elimination
Decreased Mobility
Bone marrow suppression
Leukopenia – granulocyte; neutropenic precautions
Wear glown gowns masks, Nec. Private room; No fruit baskets, no flowers, etc. (k
itchen orders, no salads, etc. MUST BE COOKED!!) pan cultures (cultures every or
ifice, urine, blood, sputum, stool, etc.) Broad spectrum get culture before you
admin med, (unless they cant produce sputum) Vitals q4
Thrombocytopenia – Risk for bleeding (lower platelet count higher risk 100,000 & <
ALL BIG RISKS)
no invasive procedures; maybe platelet transfusion; No hard dry crunchy foods; s
oft toothbrush or toothit; neumovax IM don’t do it for bleeding risks; (try to do
IM with small 23s, put lots of pressure, use deltoid, maybe use ice bag), check
vomit and stool and urine cause they can bleed anywhere b/c they don’t clot; NO AS
PIRIN or plyvax (no stickiness)
Anemia – Lack of oxygen delivery – confusion, headache, seizure, chest pain, angina,
 heart rate increases and irregular; constipation no bowel sounds, bloody diarrh
ea, abdominal cramps; fatigue & muscle cramps (claudiation – pain when walking, an
gina of legs)
May need transfusion, iron, PO iron dark teeth delivery w/ straw, black stool, V
it C inhances iron absorption, cast iron skillet b/c iron gets into food; IM iro
n (z-track) irritant and stain tissues; IV iron (Venofer) infusion, brown liquid
, must be protected from light and can cause anaphylaxis (swelling at IV sight,
respiratory stridor, bp drops, start drugs slow to see how pt tolerates it; FOOD
S in iron: Meat/fish/poultry, oranges, cantaloupe, strawberries, broc, tomato, p
otato, green peppers, grains ; DON’T GIVE spinach, chard, beet greens, rhubarb and
sweet potato
Question: What is the expected outcome rt hair loss for pt who is undergoing che
motherapy?
Hair loss may be permanent
Hair regrowth usually begin about 1 month after completion of chemotherapy;
New hair growth will likely be identical to previous hair growth in color and te
xture
Hormonal Manipulation
Some hormones make hormone-sensitive tumors grow more rapidly.
Some tumors actually require specific hormones to divide, therefore decreasing t
he amount of these hormones to hormone-sensitive tumors can slow the cancer grow
th rate and increase survival time.
Side Effects of Hormone Therapy
Androgens and antiestrogen receptor drugs cause masculinizing effects in women.
For men and women receiving androgens, acne may develop, hypercalcemia is common
, and liver dysfunction may occur with prolonged therapy.
Feminine manifestations often appear in men who take estrogens, and gynecomastia
can occur.

Tamoxifem- antiestrogen (hair growth, menopausal (hot flash, night sweat)

Immunotherapy: Biological Response Modifiers
Drugs that modify the client’s biologic responses to tumor cells
Cytokines: enhance the immune system
Interleukins, interferons
Side effects: generalized and sometimes severe inflammatory reactions, periphera
l neuropathy, skin rashes, increased depression

Gene Therapy
Experimental as a cancer treatment
Renders tumor cells more susceptible to damage or death by other treatments
Injection into tumor cells, enabling the immune system to better recognize cance
r cells as foreign and kill them
Monoclonal antibodies
Antisense drugs
Oncologic Emergencies
1. Sepsis – Can cause shock
2.Disseminated intravascular coagulation (DIC) – BLEEDING;
Collaborative management includes:
¡ Prevention (the best measure)
¡ Intravenous antibiotic therapy (for sepsis)
¡ Anticoagulants, cryoprecipitated clotting factors (for DIC)
3. Syndrome of Inappropriate Antidiuretic Hormone (SIADH) – reabsorb water, excret
e less water;
H20 is reabsorbed to excess by the kidney and put into system circulation.
SIADH is most commonly in CA of the lung
Showing hyponatremia (from dilution) showing in neuro;
Collaborative management includes:
¡ Fluid restriction
¡ Increased sodium intake
¡ Drug therapy with demeclocycline that works in opposition to
antidiuretic hormone
4. Spinal Cord Compression
Tumor directly enters the spinal cord or the vertebrae collapse from tumor degra
dation of the bone.
Tumors in the spine become a problem when they compress the spinal cord or nerve
s. This can lead to serious complications such as paralysis and loss of bladder
and bowel control. Others can destroy the vertebral bone that supports the spina
l cord making it unstable.
Incontinence; Cant walk; loss of motor and sensory fx;
Collaborative management includes:
¡ Early recognition and treatment
¡ Palliative
¡ High-dose corticosteroids
¡ High-dose radiation
¡ Surgery
¡ External back or neck braces to reduce pressure in the spinal cord
If there is a vertebral tumor with spinal cord compression this is a EMERGENCY!!
! IV steroid (decrease inflammation); Mid night, pt suddenly has bowel bladder
incontinent (breast and bone metastisis) 2-3 hr to get tumor OUT or undergone tx
to try to preserve spinal cord!!
5. Hypercalcemia
Occurs most often in clients with bone metastasis (bone is releasing Ca++)
From tumors that secrete PTH
From Bedrest
Generally develops slowly and body adapts but can be life threatening
Abnormal cardiac display (QT short)
Signs and symptoms of hypercalcemia may include:
Nausea / vomiting Fatigue/Lethargy
Stomach pain/constipation Anorexia
Extreme thirst Dry mouth
Moodiness/ Irritability Confusion
Frequent urination
Extreme muscle weakness
Irregular heart beat
Coma
Paralytic ileus
Abnormal behavior
Treatment for hypercalcemia
FLUIDS
Oral glucorticoids, calcitonin, mitramycin C, diuretics
Dialysis
6. Superior Vena Cava Syndrome (life threatening)
SVC is compressed or obstructed by tumor growth in upper chest (lymph nodes, lun
g cancer, etc blocks blood return in SVC into right Atrium). Block blood to ches
t and arms and head
Condition can lead to a painful, life-threatening emergency.
Signs include edema of face, edema of arms and hands, dyspnea, erythema, and epi
staxis. JVD, airway #1;
Late-stage signs include hemorrhage, cyanosis, change in mental status, decrease
d cardiac output, and hypotension.
Collaborative management includes high-dose radiation therapy, but surgery only
rarely.
7. Tumor Lysis Syndrome
Large numbers of tumor cells are destroyed rapidly; resulting in intracellular
contents being released into the bloodstream faster than the body can eliminate
them.
a.Hyperuricemia (Gout/uric acid kidney stones) When lots of cells die uric acid
is released an at risk for gout, stones, etc. give allopurinol
Collaborative management includes:
¡ Prevention
¡ Hydration
¡ Drug therapy (for hyperuricemia)
Allopurinol (Zyloprim); Probenecid (Benemid); Colchicine; NSAIDs
b. Hyperkalemia (Tall Tented T wave)
Drug therapy (for hyperkalemia)
Kayexylate
Loop or thiazide diuretics
Regular Insulin (IV) [and D50%]

The nurse is assessing for tumor lysis syndrome in a pt who has been receiving c
hemo? Hyperkalemia & hyper urcemia