NURS 301 The Mind Body Link.pdf

hfNURS 301 Test 1 Study Guide

Ch. 8 Stress

The Mind-Body Link

What goes on in the mind influences every part of the body

Because stress affects the mind, it can have a powerful effect on your body and your health

1/3 Americans are living with chronic (extreme) stress and so are 100% of nursing students!

Two kinds of stress:

oEustress- Good stress (ex. New job, planning wedding)

oDistress- Bad stress (ex. Terminal diagnosis, car wreck)

Hans Selye: Stress Theorist

Began early research on stress circa 1940 at McGill University

Applied physiological stressors to animals in the lab and studied responses.

 He found their responses to be a patterned, predictable chain of reaction, regardless of the type of

stress he put on them

Selye formulated the “stress as a response” theory and later named it the GAS Theory (General

Adaptation Syndrome)

Theories of Stress

Selye’s Theory of Stress

oDefinitions

 “Stress”- A non-specific response of the body to any demand made on it

“Stressors”- Any demand that induces stress: physical or emotional, pleasant or

unpleasant

Perception influences how a person responds to a stressor. For example, one

patient can be diagnosed with diabetes and think their life is over while

another patient can receive the same diagnosis and be relieved because she

thought she had terminal cancer!

oThree Stages of GAS Theory (For test, be able to identify a patient in each stage)

1. Alarm Reaction

Initial response to stressor

Activation of SNS- “Fight or Flight” (ex. Bear in the woods)

Ideally the alarm reaction phase is short! (1 min-24 hours)

Physical exam would show:

oVasodilation of skeletal muscles, vasoconstriction of reservoirs (skin,

kidneys, viscera) inc HR, inc RR, inc CO, inc SV, inc BP, dec GI, dec

Digestive enzymes (Know chart on page 102!)

oBlood shunted to core organs (brain, lungs, heart)

o increase in stress hormones (cortisol, Epi, NorEpi)

oHyperglycemia! It is important to check glucose every 6 hours to see

how patient is adapting to stress. The Liver mobilizes stored glucose

(glycogenolysis) to fuel the muscles. Hyperglycemia then leads to

increased infections such as hospital acquired pneumonia, slowed

wound healing, and immunocompromise (Always expect a hospital

patient to have increased blood glucose and poor wound healing!)

oTerms:

Stroke Volume- amt blood ejected per beat in mL

Cardiac Output- Amt blood pumped out per minute in L

Stress stimulates the Limbic Lobe which stimulates the Adrenal

Cortex (KNOW!)

oCerebral Cortex- processes stress stimuli

oLimbic System- relays information to hypothalamus

oHypothalamus- Releases CRH which activates SNS

oAnterior Pituitary- Releases beta-endorphins and ACTH

oAdrenal Cortex- Releases cortisol (STRESS HORMONE!)

oAdrenal Medulla- Releases catecholamines (Epi, Norepi)

2. Stage of Resistance

The amount of resistance is determined by the:

oPhysical state of the person

oNumber of stressors they have

oCoping abilities (strategies they have)

Goal=Adaptation! If no adaptation/coping, person moves to stage 3

(Exhaustion!)

3. Stage of Exhaustion

“Terminal Phase”

All energy for adaptation is exhausted

May see return of alarm phase

Can be terminal. Death can occur here if we don’t adapt

Later Theorists

oHolmes, Rahe and Masuda “stress as a stimulus”

oRichard Lazarus- “stress as a transaction”

Four Mediators of Stress-All four play huge roll in adaptation! (Know difference in hardiness, SOC, and

resilience)

1. Hardiness (how well someone deals with stress)

oA hardy patient has a clear sense of personal goals and values. They know what they’re in

for.

Ex. Patient going in for elective surgery has a plan

oHas a strong tendency toward interaction with the environment

oSense of meaningfulness is important

oAn internal rather than an external locus of control. (Internal is more powerful!)

Internal locus of control- Means the patient is in control and is the “captain of the

ship”

External locus of control- Patient lets environment control him; ex. Eeyore

2. Sense of Coherence (SOC)

oDeveloped by Antonovsky

oSeen as more powerful than hardiness- refers to how the person sees the world and their

place in it

oThree terms related to SOC:

1. Comprehensibility- The sense that internal and external stimuli are ordered and

make sense

2. Manageability- that there are resources available as needed

3. Meaningfulness- the sense that the demands that one faces are worthy of taking

3. Resilience (ability to “bounce back” and do better next time)

oMeans that one is resourceful, flexible, and a good problem solver

oEx. Student goes to remediation when she realizes she needs extra help

4. Attitude (Hassles vs. Uplifts)

oThe balance of the two within one’s life and how the stressor(s) is/are viewed

oSpeaks to ATTITUDE

Positive attitude can mean a quicker recovery

Pessimism can mean poorer health

Studies show link between stress and illness

Positive relationship between stress and infection (Increased cortisol can cause immunodeficiency)

Latent viruses (ex. The inactive Herpes virus becomes activated to cause cold sores when

stressed!)

AIDS (HIV)

Breast cancer incidence and recurrence (You can get cancer from stress!)

Heart disease (consistently elevated stress and cortisol levels wears on the heart! This is why a

“healthy” business manager may suddenly drop dead with an MI)

Accidents and suicide

What does stress do to the body? (Everything r/t immune system is decreased! Cortisol is only

increase)

Decreased # of natural killer cells (NKC’s)

Decreased # of cytokines (inflammatory mediators)

Decreased # of lymphocytes

Decreased # of phagocytes

Sustained elevations of cortisol result in increased blood sugar (Hyperglycemia!)

END result is Chronic Stress which leads to IMMUNOSUPPRESSION!

Theories

So, we have stress as a RESPONSE, stress as a STIMULUS, and stress as a TRANSACTION

Theories are not as important as how you will recognize stress in your patient at the bedside, and

how you will help your patient manage stress

Assisting Patients to Handle Stress (Know definitions! Know

which ones to do for which type of patient)

Biofeedback: Works best with patients who have or

desire control over their bodies (ex. Mind being

manipulated to control BP, HR, etc)

Relaxation: Opposite of fight or flight

Imagery: Seeing the fight (ex. Cancer patients

visualize chemo killing the cancer cells)

Hypnosis: relaxation plus imagery

Therapeutic Touch: Massage

Relaxation Breathing: 4x4 breathing technique. Have

patient inhale 4 sec, hold 4 sec, exhale 4 sec, rest 4

sec (KNOW for test! pg 105)



Music for Relaxation: Always take what the patient

wants into account. The patient may hate classical music, therefore this would not be stress

relieving for them!

Prayer: Spiritual encouragement

This is how we get

stressed induced illness!

Ch. 8 Test Review Questions

1. Determination of whether an event is a stressor is based on

a. Perception

2. Emotion focused coping

a. Join support group

3. Physiologic effect of stress on reticular formation

a. Inability to sleep night before administering self insulin injections

4. Encourage stressed patients to

a. Avoid exposure to upper respiratory infections

5. Person subject to chronic stress at high risk for

a. Colds and flu

6. During uncontrollable stressful circumstance, most effective

a. Emotion-focused coping

7. Before doing stress techniques, nurse should

a. Be personally familiar with them

8. Migraines occur during which stage of GAS

a. Exhaustion

9. Stress hormone released before oral exam

a. Cortisol

Ch. 30: Hematology

Definition

Hematology is the study of blood and blood forming tissues including the blood cells, the bone

marrow, the spleen and the lymph system

Bone Marrow

Soft center of bones- home of stem cells

Locations of bone marrow include sternum, ribs, scapulae, clavical, pelvis, flat cranial bones, end of

long bones

All blood cells (RBC’s, WBC’s, platelets) are produced in the RED bone marrow!

Aspirate stem cells from sternum or posterior iliac crest

#1 location for red bone marrow aspiration is the posterior iliac crest!

Three Types of Blood Cells

1. Erythrocytes (RBC’s)

2. Leukocytes (WBC’s)

3. Thrombocytes (platelets)

You can aspirate the red bone marrow to get some of these cells!

Pancytopenia= Anemia of all 3 cells! Worried about blood loss, infection, oxygenation

The Complete Blood Count (CBC) (Important in anemias!) Pg. 655

Normal Erythrocytes Levels

oMale= 4.7-6.1 million/mm3 (odd #’s)

oFemales= 4.2-5.4 million/mm3 (even #’s)

oBroad concept: Think “RBC’s 4-6”)

oLow RBC’s Oxygenation problem! Always think back to “ABC’s”

hbvHemolysis- destruction of damaged or abnormal RBC’s

Hemoglobin- Oxygen carrying capacity of RBC

o Combination of heme (iron) and globin (protein). It binds with oxygen and carbon dioxide

and represents the oxygen carrying capacity of RBC’s; it is low in cases of anemia and states

of hemodilution

oNormal Levels:

Male Hgb= 15-18 g/dL

Female Hgb= 12-16 g/dL

Hematocrit- Concentration of RBC’s in blood; “How low is the tank”

oIs measured as a percentage; it is the percentage of RBCs in relationship to total blood

volume; it is your best representative of blood volume loss

oNormal Levels:

Male Hct= 40-54%

Female Hct= 38-47%

Three other RBC indices that say a lot about anemia:

1. Mean Corpuscular Volume (MCV)= SIZE!

The measure of the average volume or size of a single RBC and is used in classifying

anemias

Normal MCV is 80-95 um (“Normocytic”)

Increased MCV= Macrocytic (more protein, iron, etc)

Decreased MCV- Microcytic (less protein, iron, etc)

2. Mean Corpuscular Hemoglobin (MCH)= WEIGHT!

The measure of the average amount (weight) of hemoglobin within an RBC

Iron weighs a lot!

Normal MCH is 27-31 pg

Increased MCH= Hyperchromia

Decreased MCH= Iron deficiency, hypochromia (likely low in iron)

3. Mean Corpuscular Hemoglobin Concentration (MCHC)- CONCENTRATION!

The measure of the average concentration or percentage of hemoglobin within a

single RBC

Normal MCHC is 32-36%

Increased MCHC= Hypochromia; in intravascular hemolysis

Decreased MCHC= Iron deficiency anemia, Thalessemia, spherocytosis

o**Read pg 667; Fig 31-6

Leukocytes

Normal level of WBC’s: 5,000-10,000 ul

Never Let Monkeys Eat Bananas!

Type Cell Normal

Range

Function

Granulocyte

Neutrophil 2,500-8,000 Phagocytosis, early phase of

inflammation

Eosinophil 50-500 Phagocytosis, parasitic

infections

Basophil 25-100 Inflammatory response, allergic

reaction

Agranulocytes

Lymphocyte 1,000-4,000 Cellular, humoral immune

response

Monocyte 100-700 Phagocytosis, cellular immune

response

oIncreased WBC’s means infection is hitting hard and fast! Neutrophils would be the first to

increase (First responders)

oDecreased WBC’s means Neutropenia and immunosuppression! This would be seen in

autoimmune diseases, chemo patient, longterm diseases, or aplastic anemias

oRationale: Patient is immunocompromised and will be dead in 72 hours! (WNL 2,500-8,000)

Leukopenia and Neutropenia (KNOW for test!)

WBC’s less than 4,000 and/or Neutrophil count below 1,000. Most likely both are occurring. But,

either one can deem the patient “neutropenic”

Patient is either fighting something and losing or they would be in trouble if they came in contact

with illness

Place the patient on Neutropenic Precautions:

oFrequent hand washing (for staff and family)

oPrivate room (Isolation precautions)

oLimit/Screen visitors

oRemove fresh flowers and plants from room

oNo fresh fruits, vegetables, and peppers from diet (nutritionists will steam the fruits and

veggies to kill germs)

oFrequent temperatures/monitor for signs of infections

*Best way to fight infection is hand washing!

Platelets

Normal Range: 150,000-450,000

Critical values at < 50,000 and > 1 million

oLess than 50,000 means patient will have imminent bleed

oOver 1 million means patient will have imminent thrombosis formation; ex. Pulmonary

embolism

Clotting:

oActivated by interstitial collagen

oAggregate and form a plug

oVascular response + plug + clotting factors= fibrin clot… stop the leak

Heparin Induced Thrombocytopenia (p.679)

oLife threatening, Allergic reaction forms clots d/t long term use of Heparin; more heparin is

required to maintain activated PTT

Spleen

Functions

a) Filters out old RBC’s and takes the hemoglobin from hemolysis and catabolizes the iron

b) Contains lots of lymphocytes and monocytes

Someone with spleen removed will be immunocompromised

c) **Sequesters/Stores 30% of platelets!

“Sequester” means the spleen calls in the platelets from the circulatory system into

the spleen

Splenectomy Patients

oSpleen stops “calling in” platelets causing blood levels of platelets to rise! (no storage unit)

oNot a huge problem generally

oPut on TED hose and pulsatiles (Thrombosis Precautions)

oIf their platelets are high, you may give heparin after surgery, which you wouldn’t do to a

normal surgical patient

oMain worry is INFECTION! The splenectomy patient will have a depleted ability to respond to

infection

Give patient prophylactic immunizations ( ex. Influenza, pneumococcal) before

splenectomy, or when patient is healthy. Don’t immunize when sick! Give the patient

time to recover

NeutropMeenic precautions when they come out of splenectomy surgery, then allow

more freedom 6 months- 1 year later once immune system is built back up to how it

was prior to surgery

Effects of Aging

Stem cells drop after age 30 and again after age 65

Hemoglobin drops after middle age

WBC increase less with infection (so you have to look for other signs of infection such as fever)

Ability to quickly respond to infection is what decreases!

Takes longer to reach homeostasis

Has to do with WBCs and RBCs (not really platelets)

What Should You Assess

Past history

Medications

Surgeries

Family history

Nutritional History

Signs of bleeding

Exercise level

Reproductive pattern/impotence

Lab values

LAB Studies

Erythrocyte Sedimentation Rate (ESR): The rate at which RBC settle in saline over a specified

period

oESR is basically the time it takes for RBC’s to float to bottom of solution

oNon-specific measure of inflammatory conditions (don’t know what type of infection or

where it is)

During inflammation, RBC’s are damaged and it takes longer for them to sink to the

bottom. Therefore, the larger the ESR, the more damaged the RBC’s, the more

inflammation.

Increased ESR= Increased Inflammation

oNormal Range of ESR:

Males- Up to 15 mm/hr

Female- Up to 20 mm/hr

Iron Metabolism Lab Tests: KNOW definitions! (pg. 657)

oSerum Iron: Iron + Proteins (50-150 mcg/dL)

oTIBC (Total Iron Binding Capacity): Proteins available to bind to Iron (250-410 mcg)

Iron binding capacity! How much iron could be bound if iron was sufficient

If there is not enough Iron to bind to the proteins, there will be extra proteins

available for binding! (INVERSELY related to serum iron)

Elevated TIBC: Iron deficiency

Decreased TIBC: Anemia, hemolysis, hemorrhage

oFerritin: Major Iron storage protein (10-300 mcg/dL)- Main protein! Acts in concert with iron

oTransferrin: Largest protein that binds with Iron (215-380 mcg/dL)

Better indicator of available iron for erythropoiesis. Iron bound to transferrin is readily

available for body to use

When transferrin is not bound to iron, it is just floating around, so it’s levels will be

high when iron is low. When transferrin is low there’s nothing for iron to bind to, so

serum iron will be high when transferrin is low! (INVERSELY related to serum iron).

oIron deficiency (low serum iron) would mean:

Increased TIBC

Decreased Ferritin

Increased Transferrin

oIron Overload (high serum iron) would mean:

Decreased TIBC

Increased Ferritin

Decreased Transferrin

Clotting Evaluation Lab Studies: (KNOW times!)

oProthrombin Time (PT)- assessment of clotting times for factors I, II, V, VII, and X (12-15

sec)

Coumadin: Factor VII (main) and X (PT)- A patient on Coumadin should have a longer

PT.

Coumadin is given long term

PT is an accurate measure of Coumadin efficacy (how well it’s working)

Increased PT: deficiency of clotting (blood too thin!)

Decreased PT: Vitamin K excess (too much clotting!)

oActivated Partial Thromboplastin Time (PTT)- assessment of clotting times for factors I,

II, V, VIII, IX, X, XI, XII (30-45 sec)

Heparin: Factor IX and X (PTT)- A patient on Heparin should have a longer PTT.

Heparin is given mainly in hospitals

If Heparin is working, PTT should be elevated.

oInternational Normalized Ratio (INR)- standardized method of reporting PT (2-3)

INR  PT Coumadin!

Measures PT across the world in the same language. PT may be reported as a 10 on

one machine in Virginia and a 15 on a machine in North Carolina. All lab machines

must be calibrated to spit out the same INR number!

Ex. If patient is on Coumadin, his INR should not be a 2 or a 3! It should have gone up

since his blood is thinner and taking LONGER to clot

Before giving Coumadin/Warfarin, check the PT and INR!

Before giving Heparin, check the PTT!

If PT, PTT, or INR is high, hold the drug and don’t do surgery! Their blood is too thin

already. If the numbers are low, it means they DEFINITELY need the drug (their blood

is too thick)!

Ch. 30 Test Review

1. Following aspiration from posterior iliac crest of patient with pancytopenia, nurse should-

a. A: Apply pressure over site for 5-10 minutes

b. Rationale: You’re worried about bleeding d/t low platelets! This will help most with clotting

1. Patient with elevated temperature and flank pain, which is most important to communicate to doctor

a. Neutrophils 950

2. Low MCV means

a. Small size of RBC’s

3. Patient is receiving heparin. Monitor:

a. PTT

4. Individual living at high altitude may normally have an increased RBC count because

a. Hypoxia caused by decreased atmospheric oxygen stimulates erythropoiesis

5. Malignant disorders that arise from granulocytic cells in the bone marrow will have the primary effect

of causing

a. Decreased phagocytosis of bacteria

6. Warfarin (Coumadin) that interferes with prothrombin production will alter the clotting mechanism

during:

a. Activation of thrombin

7. When reviewing the laboratory results of an 83 year old patient with an infection, nurse would find

a. Minimal leukocytosis (because one effect of aging is WBC increase less with infection)

8. Significant info obtained from hx r/t hematological system

a. Jaundice

9. While assessing lymph nodes

a. Lightly palpate superficial lymph nodes with pads of fingers

10. Normal lymph node

a. Firm, mobile node

11. Nursing care for pt immediately following bone marrow biopsy and aspiration includes;

a. Analgesics, lying still with pressure dressing intact, monitoring vital signs and assessing site for

excess drainage or bleeding

12. Splenectomy patient would have

a. Increased platelet levels (d/t loss of storage unit) and decreased immune function

13. Geriatric patient would have

a. Decreased hemoglobin

14. Nurse who suspects anemia should anticipate this test

a. Hgb

15. Patient with hemophilia will probably undergo this test

a. PTT (checks clotting factors in hemophilia patient)

16. Patient with bone marrow biopsy needs further teaching when he states

a. The type of antibiotic I need to take can be determined by this test

17. Anemic patient will need

a. Assistance with ambulation, monitored O2 sat, stool specimen for occult blood, daily rest period

18. Patient with prescription for ferrous sulfate should be taught

a. Foods high in Vit C will promote iron absorption

19. Patient with anemia may exhibit

a. Spoon-shaped nails

20. Patient prescribed erythropoietin

a. Should have his hgb checked twice a week

14.

Chatper 31: Hematological Disorders

Hemophilia

Hereditary bleeding disorder in MEN due to deficient clotting factors

There are 3 types of hemophilia depending on the different clotting factors absent:

1. A Type= Classic Hemophilia (80% of cases), Factor VIII is missing!

2. B Type= “Christmas Disease;” Factor IX is missing!

3. Von Willebrand Disease= Involves a congenitally acquired deficiency of the Von

Willebrand coagulation protein

Most common congenital bleeding disorder!

Medical Management of Hemophilia

oReplace clotting factor! (Replacement Therapy)

oGiven during crisis and before any procedures

oCryoprecipiate is retrieved from plasma containing the factor VIII and fibrinogen, frozen,

slowly thawed and administered

oFactor IX treated with Factor IX concentrate

oAssess for blood born infections, thrombosis, try to prevent hemarthroses in joints!

oMinor bleeds- Treat for 72 hours

oSurgeries- Treat for 10-14 days

oFactors are short lived so may even be continuous infusion

Nursing Management of Hemophilia

oGenetic counseling referral

oStop acute bleeds and administer factors

oJoint bleeds- rest joint, pack in ice, analgesics without aspirin, mobilize as soon as bleeding

is under control without weight bearing (ROM)- Blood will accumulate in joints!



Ex. If patient falls and is bleeding at the knee, rest the joint, pack it with ice, and give

analgesics (without Aspirin or other blood thinners) to prevent hemarthroses!

oAssess for intracranial bleeds and airway obstruction from hemorrhage into the neck and

pharynx

Monitor neurological status!

Anemia Overview

Anemia is defined as “deficiency in the number of erythrocytes, the quantity of hemoglobin, and/or

the volume of packed RBCs (Hematocrit)

There are diverse causes, but the three main categories of causes are:

oBlood loss/hemorrhage

oInadequate production from marrow

oToo much destruction

Compensation (Trying to reach homeostasis)

oShift oxygen from tissue to blood

oShunt blood from tissues that don’t need as much

oIncrease cardiac output, heart rate and stroke volume

oIncrease the number of RBCs produced (Erythropoiesis is stimulated!)

If hemoglobibn is increased, hematocrit will also be increased. If hgb is dec, hct dec. (except in crit

care)

Reticulocyte: Immature RBC

oIf there is an increased reticulocyte count, this means there has been a loss of mature RBCs

(ex. Hemorrhage). If there is a decreased reticulocyte count, this means there are not

enough RBC’s being produced

Iron Deficiency Anemia (See figure 31-6)

Most common type of anemia!

Heme synthesis is the problem. More gradual type of anemia.

Pregnant women need twice the amount of daily iron! This is why iron is found in prenatal vitamins

oNormal people need 1 mg of iron per day, pregnant people need 2 mg of iron per day

Causes: inadequate diet, poor absorption, GI bleed, menstruation, alcoholism

S&S:

oPallor (most common finding)

o Glossitis (Inflammation of the tongue; 2nd most common finding)

oCheilitis (Inflammation of the lips; 3rd most common finding)

oBurning of the tongue

oHeadache

oParesthesia

oPica may occur

Diagnosis: Full panel and diagnosis of cause

oLabs will show low hgb, low hct, high TIBC, low serum iron

oRBC’s will be microcytic and hypochromic (they’re “malnourished little cells!)

Tx: Treat the underlying cause and iron replacement

oOral iron is fine to give unless absorption is the issue! Never give enteric coated iron pills

because iron is absorbed in the duodenum

oIf poor diet is the issue, encourage patient to eat leafy greens!

Thalassemia Anemia

Thalassemia Minor- Person is heterozygous (one thalassemic gene, one normal); Mild form.

Patient may only get transfusions once a month

Thalassemia Major- Person is homozygous (two thalassemic genes); Severe condition. Patient

may need transfusions every week!

Etiology: GENETICS! CULTURE! Mediterranean and equatorial regions of Asian, Middle Eastern, and

African cultures

Predominant problem is inadequate production of hemoglobin! You have empty red blood cells

missing their hemoglobin! The goal of treatment is to keep Hgb >10

oRBC’s are microcytic and hypochromic

S&S:

oPale

oHyperplasia of the bone marrow- Erythropoiesis is stimulated d/t decreased oxygen

carrying capacity of the blood. This causes bone marrow hyperplasia and expansion of the

marrow space which leads to the thickening of the cranium and maxillary cavity

oThickening of cranium and maxillary cavity- Due to erythropoiesis stimulation

oGrowth retardation

oUltimately death

Tx: Palliative Transfusions and IV Desferal

oThe only treatment is palliative blood transfusions! (We can’t fix it, we just offer comfort)

oIt is important to monitor H&H as well as serum iron

oLots of transfusions leads to the accumulation of Iron. Therefore, you need to give Desferal

IV to bind to the iron to let it get excreted

Two Types of Megaloblastic (Macrocytic) Anemias:

1. Cobalamin/Vitamin B12 Deficiency/Pernicious Anemia

Cobalamin is Vitamin B12!

Etiology: Insufficient amount of intrinsic factor (IF). If there is no intrinsic factor protein in the

gut, you can’t absorb Vitamin B12, and you need Vitamin B12 to develop hemoglobin. No B12=

Anemia!

oPernicious Anemia is the most common cause

oChronic alcoholism- Alcohol destroys the mucosa of the stomach so they can’t absorb

iron

oGI surgery, Crohns, Ileitis, Diverticuli

Effects middle aged Scandinavians and African Americans

This is NOT a hemoglobin issue, it is a B12 issue! Therefore, RBC’s will be macrocytic and

normochromic. They are growing big to compensate for decreased B12

S&S: similar to iron deficiency, except you see neurological symptoms, all d/t hypoxia:

oParaesthesia

oAtaxia

oWeakness

oConfusion

oDementia

oBright red, smooth tongue d/t B12 deficiency

*Tx: 1000 ug Vitamin B12 IM every day for 2 weeks, then 4x a week until HCT is normal, then

monthly

oA patient could also be treated with nasal B12 inhalations after the initial treatment of

injections is completed

oYou can’t give B12 orally because the patient wouldn’t be able to absorb it d/t lack of IF!

Know that alcohol has NOTHING to do with intrinsic factor unless the patient is an alcoholic

2. Folic Acid Deficiency Anemia

Common Causes: (Think pregnancy and alcoholics!)

oPoor diets

oMalabsorption disorders (such as Crohn’s disease and ulcerative colitis)

oOral contraception

oPatients on anti-seizure drugs

oAlcohol abuse/anorexia

oHemodialysis patients (When blood is continuously filtered, folic acid is lost!)

Treatment:

oOral replacement therapy

Patient with poor diets or alcoholics have a folic acid deficiency! They need a “little yellow pill”



Folic Acid is used for DNA synthesis



This is not a hemoglobin issue either! It is a Folic Acid issue! Therefore, the RBC’s will be

macrocytic and normochromic

Anemia of Chronic Disease

Causes

oInflammatory diseases

oAutoimmune- Cells being attacked by the body (RBC destruction)

oInfectious disease

oMalignant disease

Treatment:

oTreat underlying disease! Until the underlying cause is discovered, give blood transfusions of

packed RBC’s

Aplastic Anemia (pg. 663)

What is it: Life threatening Stem Cell Disorder resulting in Pancytopenia! (The whole gang is

affected!)

oOther anemias have mainly to do with RBCs, but in Aplastic Anemia, every blood cell is

reduced!

o“Aplastic” means something is causing the stop of stem cell production. Give transfusions for

RBCs, give antibiotics for lack of WBCs, give platelets

oBone marrow is “on pause”

oThis is a “normocytic, normochromic” anemia (cells are fine, there is just not enough of

them!)

oThere is a low reticulocyte count, bleeding time is prolonged

Etiology:

oTwo Classifications of Aplastic Anemia:

Congenital

Acquired

Through cancer treatment

Treatment of infections

Pregnancy (can be a trigger)

Idiopathic (don’t know why)

Sequelae (Consequences of Aplastic Anemia):

oIncreased risk of infection- Even a low grade fever is a medical emergency! (d/t low WBC)

oFatigue and dyspnea (d/t low RBC)

oCardiovascular and Cerebral Vascular Response

o*Thrombocytopenia- Low platelets means predisposition to bleeding!

Sickle Cell Anemia (KNOW!)

Family of autosomal recessive genetic disorders caused by the abnormal properties conveyed to

RBC by mutated sickle cell hemoglobin

Affects African American, Mediterranean, Caribbean, South and Central America, Arabian, or East

Indian ancestry (basically all dark skinned people are genetically predisposed!)

RBC’s are crescent moon shaped SOME of the time! Involves hemolysis

The biggest priority in a SCA patient is pain! Main cause of pain is the lack of oxygen!

It isn’t the “sickling” that causes the problem. The patient has an increased oxygen demand on the

system and this increased oxygen demand causes the RBCs to sickle.

Increased oxygen demand can be due to infection, blood loss, stressors, or flu

Incidence of Sickle Cell

o1 in 375 births

oIncurable and often fatal by middle age

o*If both parents have the trait, there is a 25% chance that each pregnancy will result in a

child with sickle cell

Presentation of Sickle Cell Anemia:

oMuch like chronic anemia until a crisis

oVascular Occlusion! This leads to pain and tissue death.

Occlusion in capillary beds and other vascular systems causing symptoms similar to

MI or stroke causing INTENSE PAIN! The lower the oxygen, the worse the pain.

The primary symptom of SCA is pain!

To break up occlusion, give a vasodilator

It can last days to weeks. Often without known cause, may result in shock.

oRBC’s have a low concentration of hemoglobin, so their MCHC will be below 32%!

oHemolysis

Nursing Management of Sickle Cell Anemia

oTeam work is essential! A sickle cell patient will have SCA for life!

o**Lifestyle: Avoid high altitudes, hydrate well, don’t drink caffeine (vasoconstriction), treat

infections promptly, get Pneumovax and H flu vaccines

Ex. Sickle Cell Sam can’t climb Mt. Everest, get too hot/cold, go in crowds, exercise

vigorously, or get dehydrated! 

Infections are the most common precipitating factor

Always teach SCA patients to get vaccines!

oThe goal is to minimize the stressor. Ex. If the stressor is blood loss, give a transfusion

oTreat the areas of tissue necrosis- ex. Chronic leg ulcers result from hypoxia

o**Large doses of continuous narcotics to control pain during the crisis

Put oxygen on the patient and give them morphine to decrease the oxygen demand

and act as an analgesic. Morphine is the drug of choice for SCA patients!

Constantly change pain management drug so the patient will not build a tolerance

oTreatment: Stem cell transplant is the only possible cure! The problem is, stem cells must be

an identical match, so it practically has to come from an identical twin

Miscellaneous

Immune Thrombocytopenic Purpura (ITP) Priority is to give oral or IV corticosteroids

During blood transfusions, start the transfusion w/in 30 min of removing blood from blood bank,

then wait with the patient 15 minutes after starting the transfusion to check for reaction

Ch. 31 Test Review

1. Patient with pernicious anemia understands her treatment when she states:

a. I will need to take Cobalamin B12 either by shot or nasally for the rest of my life

b. Rationale: Know that alcohol has NOTHING to do with intrinsic factor unless the patient is an

alcoholic

2. Anemia with etiology of increased destruction of RBC’s and

a. African American with Sickle Cell Anemia

3. Discharge information for patient with sickle cell crisis:

a. Avoid exposure to crowds as much as possible during flu season!

b. Rationale: Iron has NOTHING to do with sickle cell anemia! Don’t let SCA pt have caffeine

4. Patient with hemophilia fell and has bleeding on knee joint. Nurse should immediately

a. Rest the knee to prevent hemarthroses

5. Severely anemic patient would exhibit

a. Dyspnea and tachycardia

6. Patient with microcytic, hypochromic anemia. Nurse would ask pt about

a. Daily intake of iron

7. Patient with severe anemia r/t peptic ulcer disease would include:

a. monitor stools for guaiac and instructions for high-iron diet

8. Nursing management for sickle cell patient

a. Monitor CBC, blood transfusion, iron chelation, optimal pain management, O2 therapy, rest,

DVT

prophylaxis

9. Complication of hyperviscosity of polycythemia

a. thrombosis

10. Patient with thrombocytopenia should

a. Dab her nose instead of blowing it

11. Patient with von Willebrand undergoing surgery would be treated with vWF and

a. Factor VIII

12. Neutropenic patient with a fever

a. Administer prescribed antibiotic STATE, blood cultures, monitor vital signs for septic shock

13. Most common type of leukemia in older adults

a. Chronic Lymphocytic Leukemia (CLL)

14. Multiple drugs used to treat leukemia and lymphoma b/c

a. the drugs work by different mechanisms to maximize killing of malingnant cells

15. Diff in Hodgkins and Non-Hodgkins Lymphoma

a. non-Hodgkins lymphoma can manifest in multiple organs

16. Patient with multiple myeloma becomes confused and lethargic

a. Hypercalcemia

17. After splenectomy, nurse expects to find

a. Increased platelet count

Ch. 16: Oncology- Cancer Formation, Development, and Treatment

Development

All tissue has stem cells

Stem cells activate and form new cells when:

oCells are damaged or die

oWhen the body needs more cells (like WBC’s)

Should go through normal cell division- cancer cells proliferate at same rate as other cells, but it is

indiscriminate and continuous!

Cancer cells are a mutation from the normal mother cell, but their morphology is different. They

become altered during the mitosis phase and pass down their mutations to their daughter cells.

Theory of Development

Initiation Phase

oThe “trigger” phase- something turns it on. Once initiation has occurred, it cannot “unoccur”

oInherited mutation (genetic predisposition)

Error occurs during DNA replication

oWhen host exposed to carcinogen

oMay be environmental, physical, or biological

oThis sets the cellular change into motion

oNot all altered cells establish a tumor, some commit cellular suicide (Apoptosis) which is

basically programmed cell death

Promotion Phase

oThis is the phase of reversible proliferation of altered cells

oPresence of a promoting agent creates the correct environment for development

oPromotion factors are reversible!

oLatent Phase: time frame from mutation until actual clinical evidence of disease (1-40

years) which includes the promotion phase

Length of latent phase is based on cellular division rate and environmental factors

If you are genetically predisposed, it’s not “if” you’ll get cancer, it’s “when!” That’s

why we want to limit carcinogens and promoting agents now so that it may have a 40

year long latent phase

Greater promotion means greater propensity to develop the tumor earlier

oInitiation has already occurred, now we’re adding:

Carcinogens- exacerbates/causes the cancer, can be a trigger or a promoter

Ex. Tobacco, alcohol

Promoting Agents- Makes environment more favorable for proliferation.

Ex. Obesity, fatty foods (time for the nurse to give some education!)

oThe degree the cell has mutated is important

oCritical Mass: when the cancer cells are detectable. Palpable when 1 cm in diameter (1

billion cancer cells). MRI can detect at about 0.5 cm

o**Immunological Escape: Most cancer cells are caught! Immunologic Escape is why we

get cancer.

How cancer cells evade the immune system:

a) Early cancer cells may have weak cell-surface antigens

oThis allows cancer cells to sneak through immunologic surveillance

b) Antigenic tolerance

oCancer coats itself so immune system recognizes cancer as a “normal

cell”

oThe immune system has developed tolerance to some tumor antigens

c) Overwhelming antigen exposure

d) Suppression of factors that stimulate T cells to react

o**Oncofetal Antigens: “reappearance of fetal antigens”

Markers to track tumor presence and development

Marker of how much cancer has proliferated

Indicator of how well treatment is working

oex. PSA will decrease if prostate cancer is getting better

Ex. CEA is an antigen produced in response to colon cancer. The higher the CEA

levels, the worse the cancer.

Progression Phase

oNow the tumor is actually present and is moving to tissue beyond the cancer site!

oMetastasis- spread of cancer to distant site

Two pathways of metastasis:

1. Vascular/Circulatory System

2. Lymphatic System

oSeeding of the tumor away from the primary tumor (tumor of origin; where it started)

Secondary tumor is where it metastasizes to

oUsually via blood or lymph

oCan be spread by physical manipulation

oProliferation of the primary tumor and mets (secondary tumor sites)

oEach cell type has its own typical pattern of mets and sites of colonization

oThe most common sites of metastasis (where we expect secondary tumors) are: (BBLLA)

a) Brain

b) Bone

c) Lung

d) Liver

e) Adrenals

* These are all very vascular sites! The tumors follow paths of least resistance

Histological Grading of Tumors

Based on morphology- how different cancer cells are from surrounding cells

There are two things we look at:

1. Appearance- how much the cancer cell looks like a normal host cell

2. Differentiation- how mature the cell is (ex. Well differentiated means very mature, slower

rate of growth)

oThe more rapidly the cell grows, the better it will respond to chemo

Grade I

oWell differentiated (mature)

oSlightly different from normal cells in appearance

Grade II

oModerately differentiated

oModerate dysplasia (moderate resemblance to mother cell)

Grade III

oPoorly differentiated

oSevere dysplasia (extremely different in appearance to mother cell)

oVery abnormal

Grade IV

oUndifferentiated (immature)

oAnaplasia (absence of any resemblance to mother cell)

makes it difficult to determine cells of origin!

oImmature, primitive cells

oMost difficult to treat and poorest response rate

Clinical Staging

Based on extent/SPREAD of disease

Stage O: Cancer in situ (self contained entity). It is not even invading local tissue!

Stage I: Tumor limited to tissue of origin, i.e. localized to the point of origin

oEx. Only the inner lying mucosa of the bowel is affected

Stage II: Limited local spread

oEx. Multiple layers of mucosa

Stage III: Extensive local and regional spread

oEx. Other tissue around the area is invaded

Stage IV: Metastasis (either in lymphatics or vascular system)

oMetastasis does not mean the primary tumor has “moved”, it means it has SPREAD to other

sites!

TNM Classification (Tumor Node Metastasis)

T= Primary tumor (size and invasiveness)

oT0= No evidence of primary tumor

oTis= Carcinoma in situ

oT1-4= Ascending degree of increase of tumor size and involvement

N= Regional lymph node involvement (presence or absence of regional spread to lymph nodes)

oN0= no involvement of nodes

oN1-4= ascending degree of node involvement (like clinical staging, but does not involve

metastasis. It is progressive lymphatic involvement)

oNx= cannot access nodes clinically

M= Distant metastasis

oM0= no evidence of distant mets (secondary tumor cells)

oM1-4= ascending degree of distant mets (How FAR away the tumor has traveled and how

MUCH has it spread (Distance AND Amount!)

Example of classification: This tumor is T1N1M1

Treatments

Goals of cancer treatment is to do one of the following:

a) Cure (Goal is not always to get rid of cancer)

b) Control

c) Palliation (Make patient feel better, control symptoms, better quality of life)

Four Treatment Modalities for Cancer: (Normally multiple treatments are used)

1. Surgical treatment

Prophylactic removal of non-vital organs can be used (ex. Remove breasts

before cancer occurs when oncofetal antigen markers are elevated and

immunological escape has not occurred yet)

Another option is to remove part of the tumor if it is attached to a vital organ

ex. The surgeon might remove part of a brain tumor to relieve pressure

2. Chemotherapy

3. Radiation

4. Biological and targeted therapy

Care of the Surgical Patient

Loss of self-image

Body alteration

Threat of reoccurrence- Once the trigger is turned on, it can’t be turned off!

“we got it all”- You may win the “battle,” but you are in the “war” for life! We need to get rid of

promoting agents so it doesn’t so it doesn’t come back soon

Chemotherapy

Use of chemicals as systemic therapy for cancer

Does not “target” a cancer cell, but certain types work better depending on where the cancer is.

Goal is to reduce the number of malignant cells in tumor site(s)

Mainstay for most solid tumors and hematologic cancers

Several factors determine response to chemotherapy:

1. Mitotic rate of tissue of origin- rapid rate means greater response to chemo

2. Size of tumor- small tumor means greater potential for response

3. Age tumor- young tumor responds better

4. Location of tumor- ex. only a few drugs are able to cross the BBB

5. Presence of resistant tumor cells- mutated cells resistant to chemo pass on resistance to

daughters

Chemotherapy Methods of Delivery

Oral

IM

IV (most common)- if given in a peripheral IV, check the site frequently! It has nothing to do with

the size of the IV, it has to do with the fact that it is in the vein. There is no chemo that kills ONLY

cancer cells

Intracavitary

Intrathecal (into spine to avoid the BBB; ex. Methotrexate)

Intra-arteria (into the artery supplying the cancerous tissue)

Perfusion

Continuous infusion

Subcutaneous

Topical (skin cancer)

Central Venous Access Devices

oMost of the time you need to give through a central line because chemo is a vesicant (does

tissue damage). We don’t want chemo to get in the tissue because it will cause cell death

oFor continuous or frequent chemo if the chemo is an extreme vesicant. Delivery through a

CVAD minimizes the risk of infiltration

oA way to avoid Extravasation- infiltration of drugs into tissues surrounding infusion site

causing local tissue damage

Care of the Chemotherapy Patient

Antiemetics for nausea and vomiting

Hair loss (alopecia)- tell patient to go get fitted for a wig early so they feel more in control

oNot all chemo will cause you to lose hair! If it does fall out, it will grow back, but will be

different

Watch blood counts for immunosuppression- put patient on Neutropenic Precautions

Monitor IV sites for Extravasations since chemo is a vesicant! Pain is the cardinal symptom of

extravasation

Encourage activities that require less energy

Nutritional concerns- eat lots of fruits and vegetables that are prepared by nutritionist!

Radiation Therapy

LOCAL treatment modality

Emission of energy through a space or material medium

Normal tissues are usually able to recover

Cancer cells are more likely to be permanently damaged

Low-Energy Beams

oExpend energy quickly, so they can only penetrate a short distance

oUseful for skin lesions

High-Energy Beams

oGreater depth of penetration

oSuitable for optimal dosing of internal targets while sparing skin

Care of the Radiation Patient

Nausea and vomiting

Skin Care! (Table 16-13, pg 285)

oUse non-scented lotions and mild soap such as Dove

oKeep open to air as much as possible

oDon’t wear tight clothing (a patient receiving radiation for breast cancer should not wear a

bra)

oAvoid temperature extremes! No ice pack or heating pads

o*Avoid chlorine, salt, or lake water! Don’t swim when skin is damaged; wait until 2-3 weeks

after radiation

oLimit sun exposure! Wear lots of sunscreen, long sleeves, hats, etc.

oFrequent cleansing of the perineal area for bowel cancer patients

Care of skin prior to treatment

Care of skin reactions

Observe for normal tissue damage

Maintain clarity of markings

Care of Patient Receiving Chemo and Radiation

A patient will rarely be on both chemo and radiation at the same time

Common side effects of chemotherapy and radiation include:

oBone marrow suppression (“myelosuppression”)- leads to pancytopenia! More profound with

chemo

oFatigue

oGI disturbance (especially r/t chemo and radiation of the gut; it stimulates the vomiting

center in the brain)

oIntegumentary and mucosal reactions (oral mucositis)

oPulmonary effects (congestive failure)

oReproductive effects

oCardiovascular- Pericardial effusion and pericarditis

Care of the Patient and Family

Emotional care- patients will need to feel in control!

Grief (anticipatory and final)

oDenial, Anger, Bargaining, Depression, Acceptance

Financial arrangements

Counseling group for the survivors

Managing survival guilt and anger

Reassigning of life roles

Leukemia Types (Pg 695 Table 31-25)

Leukemia is a cancer within the vascular system that is predominantly treated with chemo or a

stem cell transplant

The name of leukemia is based on 1) if it is acute or chronic, and 2) Type of cell involved

Four Main Types

1. AML- Acute Myelogenous Leukemia

2. ALL- Acute Lymphocytic Leukemia

3. CML- Chronic Myelogenous Leukemia

4. CLL- Chronic Lymphocytic Leukemia

Acute Myelogenous Leukemia (AML)

Acute (immature myeloblasts rapidly proliferating) and Myelogenous (r/t bone marrow)

Incidence: 60-70 years of age

oMakes up 25% of the Leukemias; 85% of all acute leukemias in adults

Clinical Manifestations:

oMouth sores, anemia, bleeding, headache, lymphadenopathy, fatigue, weakness

oHyperplasia of the bone marrow d/t increase in myeloblasts

oSudden and dramatic onset with infection and bleeding

Diagnosis:

oLabs: Low RBC, Hgb, Hct, and platelets (looks like pancytopenia!)

oLow to high WBC with lots of immature cells called myeloblasts, which are precursors to

granulocytes (there is an uncontrolled proliferation of myeloblasts!)

Treatment:

oStem cell and bone marrow transplant

Acute Lymphocytic Leukemia (ALL)

Acute (immature lymphoblasts rapidly proliferating) and Lymphocytic (r/t lymphatic system)

Incidence: before age 14 with the greatest number between age 2-9 (11%). Can occur in adults as

well, but much rarer (only 15% of adult leukemias)

oThink “little kids!”

Clinical Manifestations:

oFEVER is often present at time of diagnosis!

o Pallor, bruising, bleeding, weight loss, abdominal pain, CNS, hepato-splenomegaly, etc

oLeukemic meningitis occurs following arachnoid infiltrations (leukemia in the arachnoid

space of the spinal cord meninges)

Diagnoisis:

oLabs: Low RBC, Hgb, Hct, and platelets

oWBC can be low, normal, or high

oTransverse lines at ends of metaphysis of long bones

oProliferation of immature lymph cells called lymphoblasts

Treatment:

oCranial radiation and intrathecal Methotrexate

ALL crosses the BBB in young kids, so you need to give the medication intrathecally

directly into the spinal cord

oStem cell transplant

Chronic Myelogenous Leukemia (CML)

Chronic (slower progression, insidious, more mature cells) and Myelogenous (r/t bone marrow)

Incidence: between the ages of 25-60; peak around 45 years old (15%)

oThink “middle age!”

Clinical Manifestations:

oAsymptomatic early on

oDevelop fatigue, and then see sternal pain, joint tenderness, bone pain, massive

splenomegaly, and increase in sweating

Diagnosis:

oLabs:

 Low RBC, Hgb, and Hct.

High platelets early, then a drop.

Normal lymphocyte count (it is myelogenous!)

Treatment:

oTotal body radiation, bone marrow and stem cell transplant, alpha interferon,

oLeukapharesis- Try to lower WBC to reduce the risk of Leukemia-induced thrombosis

Chronic Lymphocytic Leukemia (CLL)

Chronic (slower progression, insidious, more mature cells) and Lymphocytic (r/t lymphatics)

Incidence: between ages of 50-70; more common in men. Rarely seen before age 30.

oThink “old people!”

oMost common adult leukemia

Clinical Manifestations:

oChronic fatigue, anorexia, splenomegaly

oIncreased incidence of infection, but clinically asymptomatic

oMay develop pain in lymph nodes that are swollen

Diagnosis

oMild anemia and thrombocytopenia with disease progression

oProliferation of lymphocytes in blood (more than normal)

oMore lymphocytes in the bone marrow

Treament:

oRadiation (total body, lymph node, spleen)

oSplenectomy, alpha interferon, colony stimulating factors to stimulate cell formation

oStem cell transplant

Chronic vs. Acute

Acute- Think rapid onset, immature cells!

oCharacterized by proliferation of immature cells.

oThey become defective past the myeloblast or lymphoblast stage, so that the blood does not

have the mature versions of these cells

Chronic- Think gradual onset, mature cells!

oInvolves more mature forms of WBC’s; Disease onset is more gradual (insidious)

Hairy Cell Leukemia

Chronic disease of lympho-proliferation involving B-lymphocytes that infiltrate the spleen and

bone marrow (B-lymphocytes proliferation)

Incidence:

oOnly 2% of all adult leukemias

oTypically males over 40 years old

Clinical Manifestations:

oSplenomegaly, pancytopenia, infection d/t impaired host defense

oCells have hairy phalanges!

Very treatable!

Unclassified Leukemia

Mixed presentation (more than one type of cancer cell is involved; some may be immature and

some may be mature)

Poor response/prognosis

Remission is the goal! We try to stop the cells from attacking, but the patient will never be cured for

life

Affects very small percentage of the population

Bone Marrow Biopsy

Used to diagnose leukemias, some lymphomas, and to stage solid tumors such as breast cancer

Posterior iliac crest is most common site

Sedate, cleanse site, local anesthesia (surface and deeper)

Bore into the periosteum, resulting pressure pain, then aspirate about ½ mL of fluid marrow

resulting in a suction pain

Apply pressure for 10-15 minutes, then bed rest for several hours post procedure

Lymph Node Biopsy

Open or closed (needle aspirate)

May be done under enhanced guidance

Pressure applied to avoid excessive bleeding

Observe for infection

Needle biopsy only indicates that the site aspirated does or does not have cancer cells

Start at primary site, and then move away. Aspirate many nodes!

Lymphoma: Hodgkins vs. Non-Hodgkins

Cancer of the lymphatic system

Hodgkins Lymphoma

o12% of all lymphomas

oMalignant condition characterized by the proliferation of giant, multi-nucleated cells called

Reed-Sternberg cells in the lymph nodes

Presence of Reed-Sternberg cells makes for easy diagnosis!

oNormally effects at age 15-35 or after 50… twice as many men as women

oSlow, insidious growth. Responds well to chemo (prognosis is 10 years and up)

oStays contained in lymphatic system

oThree associating factors have been identified:

Epstein Barr Virus

Genetic predisposition

Exposure to chemical toxins

Non-Hodgkins Lymphoma (NHL)

oHeterogenous group of malignant neoplasms

oNHL is the most common hematologic cancer and the 5th leading cause of cancer death

oMay see pancytopenia, but painless lymph node enlargement is the primary clinical

manifestation

oNo Reed-Sternberg cells!

oNHL’s tend to include extra-nodal sites (infects tissue outside the lymphatic system)

oMRI and lymph node biopsy can help determine patterns

oNot as controllable/contained

oPrognosis for NHL is generally not as good as Hodgkin’s

**Multiple-Myeloma

Plasma cell cancer that invades the marrow and destroys bone; think “Bone Cancer”

Twice as common in men than women. Appears after age 40 with peak around 65

Slow, very insidious. Developed over years.

Signs and Symptoms:

oGenerally only with advanced disease and presents as bone pain in ribs, spine, and pelvis

*Skeletal pain is major manifestation and is triggered by movement!

oOsteolytic lesions in skull, vertebrae, and ribs and bone destruction are common

oHypercalcemia can cause renal, GI, neurological changes such as anorexia and confusion

Demineralizing and decalcification of bone causes blood calcium levels to rise and

bones to become fragile

Loss of bone integrity leads to pathological fractures

oMay see granulocytopenia, thrombocytopenia, and anemia; Plasma cells are way too large!

Diagnosis:

oBlood and urine tests

oX-rays and bone marrow biopsy

Nursing Managemnt of Multiple-Myeloma

oHYDRATION! I&O to achieve urine output of 1.5-2 liters per day!

May require intake of 3-4 liters per day.

Adequate hydration will dilute the blood calcium. Extra Calcium must be excreted, so

the renal system is not happy! Give them 3-4 L of fluid/day to keep urine output

≥1.5-2 L/day

oFRACTURE PRECAUTIONS! Tell patient “When you get up, I will walk with you!”

You still want them to ambulate frequently (you strengthen the bone when you stress

it)

If they don’t ambulate, it will lead to contracture and deformity

 Give the patient analgesia before any ROM or ambulation exercise

oPain management- may use opiates and NSAIDS

Aredia- used for skeletal pain and instability; inhibits bone break down

oAdjust to impact of disease upon their life and also manage the chemo and/or radiation

therapy needed to treat the disease

Oncology Practice Questions

1. Cells in the bowel are poorly differentiated. This means:

a. Tumor cells look more like immature bowel cells

2. Patient vomiting after chemo. Nursing intervention:

a. Administer prescribed antiemetics 1 hour before tx

3. Patient with neutropenia. Nurse should take action when:

a. Visitors bring fresh peaches from home

4. Patient with multiple myeloma. Nursing intervention:

a. Maintain fluid intake of 3-4 L/day

5. Ovarian cancer report shows T2-N3-MX

a. Tumor is 4 cm in size involving the ovary and adjacent tissues

6. Chemo patient reports nausea

a. “Try eating several small meals throughout the day”

7. Platelet count of 25,000

a. Apply prolonged pressure to puncture site after blood sampling

8. Patient has mucositis d/t chemo

a. Obtain a culture of the lesions

9. Trends in incidence and death rates of cancer include:

a. African Americans have a higher death rate from cancer than whites

10. Features unique to cancer cells

a. Cells lack contact inhibition, cells return to a previous undifferentiated state, new proteins

characteristic of embryonic stage emerge on cell membrane

11. During stage of progression

a. Proliferation of cancer cells in spite of host control mechanisms

12. Primary protective role of immune system r/t malignant cells

a. Surveillance for cells with tumor-associated antigens

13. Primary difference between benign and malignant neoplasms

a. Characteristic of tissue invasiveness

14. Goals of cancer treatment are based on principle that

a. A combination of treatment modalities is effective for controlling many cancers

15. The most effective way of administering chemotherapeutic agent that is a vesicant is

a. Central venous access device

16. Patient undergoing brachytherapy

a. Requires use of radioactive precautions

17. Pancytopenia patient, report

a. Fever, fatigue, SOB

18. Nurse counseling chemo/radiation patient

a. Following successful treatment, a return to person’s previous functional level can be expected

19. Patient on chemo is losing weight and has no sense of taste

a. Discuss with physician the need for parenteral or enteral feedings

20. Patient with multiple myeloma is sleepy, confused, nauseous, and constipated

a. Hypercalcemia

21. Patient with anorexia, try to increase nutritional intake by

a. Adding items such as skim milk powder, cheese, honey, or peanut butter to food

22. Oral care for chemo patient at risk for oral tissue injury

a. 1 tsp salt in 1 L water mouth rinse

23. Biggest risk for myelosuppression patient

a. Risk for infection

24. Patient with diarrhea

a. Give bland, low fiber diet

25. Stage II cervical cancer

a. Has spread locally

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