HEMATOLOGY

OBJECTIVE 1 (Mandy)

This is pretty long and some of it is probably repeated in some of the objectives below it. 

Iggy pg 870-876

Review the anatomy and physiology of the hematologic system:

The hematologic system is the blood, blood cells, lymph, and organs involved with blood formation or blood storage. All
systems depend on circulation; thus any problem of the hematologic system affects total body health and well-being.

BONE MARROW:

Bone marrow is the blood-forming (hematopoietic) organ. It produces most of the cells of the blood, including red blood
cells (RBCs, erythrocytes), white blood cells (WBCs), and platelets. Bone marrow also is involved in the immune responses.

In the fetus, blood components are formed in the liver and spleen and, by the last trimester, the bone marrow. At birth, blood-
producing marrow is present in every bone. The flat bones (sternum, skull, pelvic and shoulder girdles) contain active blood-
producing marrow throughout life. As a person ages, the amount of blood-producing marrow decreases in the long bones and
in small, irregularly shaped bones. By the age of 18 years, blood production is limited to the ends of the long bones.

The bone marrow first produces stem cells. Stem cells are immature, undifferentiated cells that are capable of maturing into
any one of several types of blood cells: RBCs, WBCs, or platelets, depending on the body’s needs.

BLOOD COMPONENTS:

Blood is composed of plasma and cells. Plasma is part of the body’s extracellular fluid. It is similar to the interstitial fluid
found between tissue cells, but plasma contains several times more protein than interstitial fluid contains. The three major
types of plasma proteins are albumin, globulins, and fibrinogen.

Albumin increases the osmotic pressure of the blood, which prevents the plasma from leaking into the tissues. Globulins
have many functions, such as transporting other substances and protecting the body against infection. Globulins are also the
main component of antibodies. Fibrinogen is a protein molecule that can be activated to form fibrin. Fibrin molecules
assemble together to form structures important in the blood clotting process.

RED BLOOD CELLS:

Red blood cells (erythrocytes) are the largest proportion of blood cells. Mature RBCs have no nucleus and have a biconcave
disk shape. RBCs are able to change their shape without breaking as they pass through narrow, winding capillaries. The
number of RBCs a person has varies according to gender, age, and general health, but normal range is from 4,200,000 to
6,100,000/mm3.

RBCs start out as stem cells, enter myeloid pathway, and progress in stages to the mature RBC. Healthy mature RBCs have a
life span of about 120 days after being released into the blood. As RBCs age, their membranes become more fragile. These
old cells are trapped and destroyed in the tissues, spleen, and liver. Some parts of destroyed RBCs (e.g. iron), are recycled
and used to make new RBCs.

The RBCs produce hemoglobin (Hgb). Each normal mature RBC contains thousands of hemoglobin molecules. The heme
part of each hemoglobin molecule needs a molecule of iron. Only when the heme molecule is complete with iron can it
transport up to four molecules of oxygen (therefore, iron is a critical component of hemoglobin). The globin portion of
hemoglobin carries CO2. RBCs are also buffers and help maintain acid-base balance.

The most important feature of hemoglobin is its ability to combine loosely with O2. With only a small drop in O2 level in the
tissues, a greater increase in the transfer of O2 from hemoglobin to tissue occurs. Some problems change the speed and
amount of O2 released to the tissues.
The total number of RBCs a person has is carefully controlled through erythropoiesis (selevtive maturation of stem cells into
mature erythrocytes). This process ensures that enough RBCs are present for good oxygenation without having too many
cells that could “thicken” the blood and slow its flow. The trigger for control of erythropoiesis is tissue oxegenation. The
kidney produces the RBC growth factor erythropoietin at the same rate as RBC destruction occurs to maintain a constant
normal level of circulating RBCs. When tissue oxegenation is normal or high, the kidney reduces erythropoietin levels,
slowing the production of RBCs.

WHITE BLOOD CELLS (LEUKOCYTES):

White blood cells (WBCs), or leukocytes, perform actions critical to inflammation or immunity. The many types of WBCs all
have specialized functions. WBCs are formed in the bone marrow and are part of the hematopoietic system. See chapter 23
for WBC function.

PLATELETS:

Platelets are the third type of blood cells. They are the smallest of the blood cells, formed as fragments of a giant precursor
cell in the bone marrow.

Platelets stick to injured blood vessel walls and form platelet plugs that can stop the flow of blood from the injured site. They
also produce substances important to coagulation. They help keep blood vessels intact by beginning the repair of damage to
small blood vessels. They perform most of their functions by aggregation (clumping).

After platelets leave the bone marrow, they are stored in the spleen and then released slowly to meet the body’s needs.
Normally 80% of platelets circulate and 20% are stored in the spleen. Each platelet has a life span of 1 to 2 weeks.

ACCESSORY ORGANS:

The spleen and liver are important accessory organs of the hematopoietic system. They help regulate the maturation of blood
cells to help maintain hematologic homeostasis.

SPLEEN:

The spleen is located under the diaphragm to the left of the stomach. It contains three types of tissue: white pulp, red pulp,
and marginal pulp. These tissues all help balance blood cell production with blood cell destruction and assist the immunity.
White pulp is filled with WBCs, especially lymphocytes and macrophages. As whole blood filters through the white pulp,
unwanted cells (such as bacteria and old RBCs) are removed. Red pulp contains vascular enlargements (sinuses) that store
RBCs and platelets. Marginal pulp contains the ends of many arteries and other blood vessels.

The spleen destroys old or imperfect RBCs, breaks down the hemoglobin released from these destroyed cells, stores platelets,
and filters antigens. The client who has had a splenectomy has reduced immune functions. These clients are not as efficient at
ridding the body of disease-causing organisms and are at greater risk for infection and sepsis.

LIVER:

The liver is the main production site for prothrombin and most of the blood clotting factors. The proper liver function and
bile production are critical to the formation of vitamin K in the intestinal tract. (Vitamin K is essential for producing blood
clotting factors). Large quantities of whole blood and blood cells can be stored in the liver. The liver also converts bilirubin
to bile and stores extra iron within the protein ferritin. Small amounts of erythropoietin are produced in the liver.

PLATELET AGGREGATION:

Forming a platelet plug by causing platelets to clump together is essential for blood clotting. Platelets normally circulate as
individual cell-like structures. They are not attracted to each other and do not clump together until activated. Usually
activation causes platelet membranes to become sticky, allowing clumping to occur. When platelets become activated and
clump, they form large, semisolid plugs within the lumens and walls of the blood vessels and disrupt local blood flow. (These
platelet plugs are not clots and cannot provide complete hemostasis).
Some substances that cause platelets to clump include adenosine diphosphate (ADP), calcium, thromboxane A2, and
collagen. Platelet plugs start the cascade reaction that leads to fibrin clot formation and blood coagulation.

BLOOD CLOTTING CASCADE:

Blood clotting cascade is triggered by the formation of a platelet plug. The beginning of the cascade is rapidly amplified or
enhanced; that is, the final result is much larger than the triggering event. Cascades work like a landslide. A few small
pebbles rolling down a steep hillside can dislodge large rocks and pieces of soil, causing a final enormous movement of
earth. Just like landslides, cascade reactions are hard to stop once set into motion.

Intrinsic factors are problems or substances directly in the blood itself that first make platelets clump and then activate the
blood clotting cascade.

Extrinsic factors are when platelet plugs form as a result of changes in the blood vessels rather than in the blood. When
platelet plugs form in response to blood vessel changes, the response is said to be caused by extrinsic factors (outside the
blood). The most common extrinsic event is trauma that damages blood vessels and exposes the platelets to collagen.

Whether the platelet plugs were formed because of abnormal blood (intrinsic factors) or by exposure of substances from
damaged blood vessels (extrinsic factors), the end result of the cascade is the same: formation of a fibrin clot and
coagulation.

FIBRIN CLOT FORMATION:

Fibrinogen is a large, inactive protein made in the liver. The enzyme thrombin removes the end portions of the fibrinogen,
converting it to active fibrin. Individual fibrin molecules link together to form fibrin threads. The fibrin threads make a
netlike meshwork that forms the base of a blood clot.

FIBRINOLYSIS:

Because blood clotting occurs through a rapid cascade process, in theory it keeps forming fibrin clots whenever the cascade
is set into motion until all blood throughout the entire body has coagulated. Such widespread clotting would lead to death.
Whenever the blood clotting cascade is started, counterclotting or anticoagulant forces are also started. These forces limit clot
formation to damaged areas only so that normal blood flow is maintained everywhere else.

The fibrinolytic system dissolves the fibrin clot with special enzymes.

HEMATOLOGIC CHANGES ASSOCIATED WITH AGING:

Aging changes the cellular and plasma components of blood. Several factors cause a decreased blood volume in older adults.
Total body water is decreased among older adults. In addition, they tend ot have lower levels of plasma proteins and
decreased plasma osmotic pressure, which also causes some loss of blood volume into the interstitial space.

As bone marrow ages, it produces fewer blood cells. The total RBC and WBC counts are lower among older adults. Platelet
counts do not appear to change with age. Lymphocytes become less reactive to antigens and have loss of immune function.
Antibody levels and responses are lower in older adults. The WBC count does not rise as high in response to infection in
older people as in younger people.

THE REST IS COVERED BELOW ALONG WITH SOME OF WHAT I ALREADY INCLUDED

OBJECTIVE 2 (Amanda)

Iggy pg 882

Interpret a CBC and other hematologic tests, including clotting test to determine a client’s hematologic status.
OBJECTIVE 3 (Carol)

IDENTIY AND PRIORITIZE NURSING RESPONSIBILITIES DURING TRANSFUSION THERAPY.

Pg. 914 Med/Surg

BEFORE INFUSION:

1) Assess lab values

2) Verify the medical prescription
3) Assess the clients vital signs, urine output, skin color, and history of transfusion reactions.
4) Obtain venous access. Use a central catheter or 19 gauge needle if possible.
5) Obtain blood products from a blood bank. Transgfuse immediately.
6) With another registered nurse, verify the client by name and number, check blood compatability, and note expiration
times.

DURING INFUSION:

1) Administer the blood product using the appropriate filtered tubing.

2) If the blood product needs to be diluted, useonly normal saline solution.
3) Remain with the client during the first 14-30 minutes of the infusion.
4) Infuse the blood product at the prescribed rate.
5) Monitor vital signs.

OBJECTIVE 4 (Victoria)

Predict which type of blood product would be used for various hematologic problems.

Any blood component may be removed from a donor and transfused to a recipient. Components may be transfused
individually or collectively, with varying degrees of benefit to the recipient.

Transfusion therapy is the intravenous (IV) administration of whole blood or blood components for therapeutic purposes.
Most transfusions involve administration of allogenic units, units donated by an unknown compatible donor. Transfusions are
used to restore intravascular volume with whole blood or albumin, to restore the oxygen-carrying capacity of blood by
replacing red blood cells (RBCs), to replace clotting factors and/or platelets to reverse coagulopathy, or to replace white
blood cells in neutropenic clients. Transfusion of components separated from whole blood may be pooled, transferred into
one transfusion container, to facilitate infusion.

Transfused blood may be allogenic, donated by another person, or autologous, donated in advance by the client. Autologous
transfusion, or autotransfusion, is the collection and reinfusion of a client's own blood. This type of transfusion eliminates
compatability problems and reduces the risk for transmitting bloodborne diseases. The blood for an autologous transfusion is
commonly obtained by preoperative donation. Blood for an autologous transfusion can also be salvaged perioperatively
(during a surgical procedure), using a machine that washes and filters the blood to remove anticoagulants and activated
clotting factors before reinfusion into the client's circulation (American Association of Blood Banks [AABB], 2002).
(Clinical Nursing Skills & Techniques)

Red Blood Cell Transfusions RBSc are given to replace sells lost as a
result of trauma or surgery, anemic clients, or clients with problems that destroy RBCs or impair RBC maturation. Packed
RBCs are given to clients with a hemoglobin level less than 6g/dL (norm. 12-18g/dL).

Washed red blood cells (WBC-poor PRBCs)

Used for clients with a history of allergic transfusion reactions, and bone marrow transplant clients.

Platelet Transfusions
Platelets are given to clients with platelet counts below 20,000mm3 and to clients with thrombocytopenia who are actively
bleeding or are scheduled for an invasive procedure. Platelets are fragile and must be infused immediately after being
brought to the client’s room, usually over a 15- to 30-minute period.

Single Donor Platelets

Used for clients who are going to receive a bone marrow transplant or who need multiple platelet transfusions, or who have a
history of febrile or allergic reactions. They’re taken from just one donor and decrease the amount of antigen exposure to the
recipient, helping to prevent the formation of platelet antibodies.

Plasma Transfusions
Clients who are actively bleeding with a prothrombin time (PT) or partial thromboplastin time (PTT) greater than 1.5 times
normal are candidates for an FFP infusion.
May be given fresh to replace blood volume, or more commonly, plasma is frozen immediately after donation, forming fresh
frozen plasma (FFP). Freezing preserves the clotting factors, and the plasma can then be used for clients with clotting
disorders.

Cryoprecipitate Transfusions
Cryoprecipitate is a product derived from plasma; clients with a fibrinogen level of less than 100mg/dL are candidates for a
cryoprecipitate infusion. This highly concentrated blood product is also given to clients with clotting factor disorders such as
Hemophilia or von Willebrand’s disease.

White blood Cells

At some facilities, neutropenic clients with infections not responding to antibiotic therapy receive WBC replacement
transfusions. This practice is controversial because the potential benefit to the client must be weighed against the potential
severe reactions that often occur with WBC transfusions.

Table 43-6 Indications for Treatment with Blood Components

(Info from MED. Surg. pages 913-916)

OBJECTIVE 5 (Yvonne)

DISCUSS THE DEVELOPMENT, FORMS AND FUNCTIONS OF RBCs, WBCs, and PLATELETS. Iggy
pg 887. Martini’s Fundamentals of A&P chapter 19 (great chart on pg 658 for those who had Karen’s A&P)

RBCs, WBCs and platelets are the formed elements of blood.

RBC (erythrocytes) are the major cell in the blood (99.9%).Their function is to transport O2 from lungs to tissues
and carbon dioxide from tissues to lungs. Tissue oxygenation depends on keeping the circulating number of RBCs
within the normal range for the person’s age and gender. RBCs are developed in the red bone marrow.

WBC (leukocytes) and platelets make up 0.1% of formed elements in the blood. All WBCs except monocytes
complete their development in the bone marrow from stem cells. Unlike RBCs, WBC have nuclei and or
organelles but lack hemoglobin. Their primarily function is help defend body against invasion by pathogens and to
remove toxins, wastes and abnormal or damaged cells. They are divided into neutrophils (first to arrive at accident
scene), esosinophils, basophils, monocytes and lymphocytes. They circulated for only a short period traveling
through blood stream to enter damaged or problem areas into tissues.
Platelets’ function is for hemostasis: clump together and stick to vessel wall (platelet phase) activate intrinsic
pathway of coagulation phase. They remain in the bloodstream or in vascular organs and remain intact for 7-12
days; and are produced by megakaryocytes in bone marrow. They are cell fragments rather than individual cells.

OBJECTIVE 6 (Kulwinder)

Explain the process of homeostasis including the intrinsic and extrinsic factors.

Homeostasis/Blood Clotting

Homeostasis begins with the platelet formation and continues to the formation of a fibrin clot. (from Jake’s note) In
homeostasis, localized blood clotting occurs in damaged blood vessels while blood continues to circulate to all other areas.
Homeostasis is a complex process that balances the production of clotting and dissolving factors. It begins with the formation
of a platelet plug and continues with a series of events that eventually cause the formation of a fibrin clot. Intrinsic and
extrinsic factors are involved in blood clotting. Three sequential processes result in blood clotting: platelet aggregation with
formation of a platelet plug, the blood clotting cascade, and the formation of a complete fibrin clot.

PLATELET AGGREGATION

First step in blood clotting. Forming a platelet plug by causing platelets to clump together is essential for blood clotting.
Platelets normally circulate as individual cell-like structures. They are not attracted to each other and do not clump together
until activated. Usually activation causes platelet membranes to become sticky, allowing clumping to occur.

Intrinsic Factors

Intrinsic factors are problems or substances directly in the blood itself that first make platelets clump and then activate the
blood clotting cascade (Figure 42-4). These factors or conditions include antigen-antibody reactions, circulating debris,
prolonged venous stasis, and bacterial toxins. Continuing the cascade to the point of fibrin clot formation depends on the
presence of sufficient amounts of all the various clotting factors and cofactors (Table 42-2). (Antigen, antibody, circulating
debris, endotoxin are all intrinsic factors. Jakes note)

Extrinsic Factors

Platelet plugs also can form as a result of changes in the blood vessels rather than in the blood. When platelet plugs form in
response to blood vessel changes, the response is said to be caused by extrinsic factors (outside the blood). The most
common extrinsic event is trauma that damages blood vessels and exposes the platelets to collagen. Collagen then activates
platelets and causes clumping. The platelet plug is formed within seconds of the trauma. The blood clotting cascade is started
sooner by the extrinsic pathway because some of the steps of the intrinsic pathway are bypassed.(muscle damage exposure of
collagen jakes note) all info. Found in iggy 873 and some in Jake’s note

OBJECTIVE 7 (Maureen)

Predict which type of blood product would be used for various hematologic problems.

See page 913-916 in Iggy

Whole blood- trauma with massive blood loss.

RBCs- trauma or surgery, sickle cell anemia, other anemias

Platelets- patients with thrombocytopenia who are bleeding or about to undergo surgery, bone marrow recipients

Plasma- hypovolemia, clients with high PTT

Cryoprecipitate- Hemophiliacs
Granulocytes- clients with nuetropenia (caused by leukemia, chemo, radiation)

OBJECTIVE 8 (Okju)

Demonstrate an assessment of the hematologic system. (Iggy 879-883)

HISTORY
Demographic data- Bone marrow and immune activity diminish with age.
Family history and genetic risk- many bleeding disorders are inherited. Sickle cell disease is seen most often among African
Americans
Personal History- liver function, the presence of known immunologic or hematologic distorders and current drug use.
Because the liver makes clotting factors, ask about manifestations that may indicate liver problem, such as jaundice, anemia,
and gallstones. Ask the client use of warfarin, aspirin, NSAIDs.
Diet History- Dietary pattern can affect blood clotting. Diets high in fat and carbohydrates can cause many types of anemia
and decrease the functions of all blood cells. Chronic alcoholism can cause nutritional deficiencies and liver impairment,
both of which reduce blood clotting. Diets high in vitamin K may increase the rate of blood clotting.
Socioeconimic status- Assess the client's ability to understand and follow instructions related to diet, procedures and tests,
and therapeutic regimens. Ask about personal resources, such as finances and social support. A person with a poor income
may have a diet low in iron and protein.
Current health problems- Determine whether the client has had swelling of lymph nodes or excessive bruising or bleeding
and whether the bleeding was spontaneous or induced by trauma. Ask about the amount and duration o f bleeding after
routine dental work. Determine whether a woman has menorrhagia (excessive menstrual flow) and change of her pattern of
menstrual flow. If the client has had menstrual clots, ask her to estimate size. Assess dyspnea, palpitations, frequent
infections, fevers, recent weight loss, headaches, or paresthesias. Any or all of these symptoms may occur with hematologic
disease. The single most common symptom of anemia is fatigue. Ask client about feeling tired, needing most rest, or losing
endurance during normal activities. Determine whether they have other symptoms of anemia, such as vertigo, tinnitus, and a
sore tongue.

PHYSICAL ASSESSMENT
Skin- Inspect the color of the skin for pallor or jaundice and of the mucous membranes and nail beds for pallor or cyanosis.
Pallor of the gums, conjunctivae, and palmar creases indicates decreased hemoglobin levels. Assess the gums for active
bleeding in response to light pressure or brushing the teeth with a soft-bristled brush and any lesions or draining areas.
Inspect for petechiae (pinpoint hemorrhagic lesions in the skin) and large bruises (ecchymoses). Assess bleeding sites. Check
the skin turgor and ask about itching.

Check Oral mucosa. The tongue may be completely smooth in anemia or smooth and red in nutritional deficiencies. Inspect
and palpate all lymph nodes areas. Assess SOB. Observe for heaves, distended neck veins, edema, or signs of phlebitis.
Auscultate for murmurs, gallops, irregular rhythms, and abnormal BP. Systolic BP tends to be lower in clients with anemia. If
hypercellularity(abnormal increase in the number of cells present, as in bone marrow) is present, BP is higher than normal.
Severe anemias can cause enlargement of the right ventricle and heart disease.

RENAL AND URINARY ASSESSMENT

The kidneys have many blood vessels, and bleeding problems may manifest as overt or occult hematuria (blood in the urine).
Inspect a voided sample of urine for color. Hematuria may appear as grossly bloody red or dark brownish gold urine. Test the
urine for proteins with a urine test dipstick because hematologic problems may increase the protein content of the urine. Also
test the urine sample for occult blood (Hemoccult test).

MUSCULOSKELETAL ASSESSMENT
Rib or sternal tenderness is an important sign of hematologic malignancy. Examine the superficial surfaces of all bones,
including the ribs and sternum, by applying intermittent firm pressure with the fingertips. Assess the range of joint motion
and document any swelling or joint pain.

ABDOMINAL ASSESSMENT
The normal adult spleen is usually not palpable. An enlarged spleen, however, occurs with many hematologic problems. An
enlarged spleen may be detected by percussion, although palpation is more reliable. The spleen lies just beneath the
abdominal wall, under the ribs on the left side. When it is enlarged, the spleen can be identified by its movement during
respiration. During palpation have the client lie in a relaxed, supine position while you stand on the client's right and palpate
the left upper quadrant. Palpate gently and cautiously because an enlarged spleen may be tender and easily ruptured.
Palpating the edge of the liver in the right upper quadrant of the abdomen can detect hepatic enlargement, which is often
associated with hematologic problems. The normal liver may be palpable as much as 4 to 5 cm below the right costal margin
but is usually not palpable in the epigastrium.
A common cause of anemia among older adults is a chronically bleeding gastrointestinal lesion. If the lesion or open area is
located in the stomach or the small intestine, obvious blood may not be visible in the stool, or such a small amount is passed
each day that the client is not aware of it. Therefore obtain a stool specimen for occult blood testing.

CENTRAL NERVOUS SYSTEM ASSESSMENT

Examination of cranial nerves and neurologic function is important in hematologic assessment because some problems cause
specific nervous system manifestations. Vitamin B12 deficiency impairs cerebral, olfactory, spinal cord, and peripheral nerve
function, and severe chronic deficiency may cause permanent neurologic degeneration. Many neurologic problems can
develop in clients who have hematologic malignancies as a consequence of bleeding, infection, or tumor spread. When the
client with a known or suspected bleeding disorder has any head trauma, expand the assessment to include frequent
neurologic checks and mental status examinations (see Chapter 44). Assess fever, chills, and night sweats.

Diagnostic assessment- laboratory test. CBC.

OBJECTIVE 9 (Josh)

Discuss the significance of abnormal findings in a hematological system assessment. I included the tests with there
abnormal findings as well.

HEAD AND NECK ASSESSMENT

Check for pallor or ulceration of the oral mucosa. The tongue may be completely smooth in pernicious anemia and iron
deficiency anemia or smooth and red in nutritional deficiencies. These manifestations may occur with fissures at the corners
of the mouth. Assess for jaundice of the sclera.

Inspect and palpate all lymph node areas. Document any lymph node enlargement, including whether palpation of the
enlarged node causes pain. It is important to determine whether the enlarged node moves or remains fixed with palpation.

RESPIRATORY ASSESSMENT

Assess the rate and depth of respiration while the client is at rest as well as during and after mild physical activity (e.g.,
walking 20 steps in 10 seconds). Note whether the client can complete a 10-word sentence without stopping for a breath.
Assess whether the client is fatigued easily, has shortness of breath at rest or on exertion, or needs extra pillows to sleep
comfortably at night. Many anemias cause these symptoms.

CARDIOVASCULAR ASSESSMENT

Observe for heaves, distended neck veins, edema, or signs of phlebitis. Auscultate for murmurs, gallops, irregular rhythms,
and abnormal blood pressure (BP). Systolic BP tends to be lower than normal in clients with anemia. If hypercellularity is
present, BP is higher than normal. Severe anemias can cause enlargement of the right ventricle and heart disease.

RENAL AND URINARY ASSESSMENT

The kidneys have many blood vessels, and bleeding problems may manifest as overt or occult hematuria (blood in the
urine). Inspect a voided sample of urine for color. Hematuria may appear as grossly bloody red or dark brownish gold urine.
Test the urine for proteins with a urine test dipstick because hematologic problems may increase the protein content of the
urine. Also test the urine sample for occult blood (Hemoccult test).

MUSCULOSKELETAL ASSESSMENT
Rib or sternal tenderness is an important sign of hematologic malignancy. Examine the superficial surfaces of all bones,
including the ribs and sternum, by applying intermittent firm pressure with the fingertips. Assess the range of joint motion
and document any swelling or joint pain.

ABDOMINAL ASSESSMENT

The normal adult spleen is usually not palpable. An enlarged spleen, however, occurs with many hematologic problems. An
enlarged spleen may be detected by percussion, although palpation is more reliable. The spleen lies just beneath the
abdominal wall, under the ribs on the left side. When it is enlarged, the spleen can be identified by its movement during
respiration. During palpation have the client lie in a relaxed, supine position while you stand on the client's right and palpate
the left upper quadrant. Palpate gently and cautiously because an enlarged spleen may be tender and easily ruptured.

Palpating the edge of the liver in the right upper quadrant of the abdomen can detect hepatic enlargement, which is often
associated with hematologic problems. The normal liver may be palpable as much as 4 to 5 cm below the right costal margin
but is usually not palpable in the epigastrium.

A common cause of anemia among older adults is a chronically bleeding gastrointestinal lesion. If the lesion or open area is
located in the stomach or the small intestine, obvious blood may not be visible in the stool, or such a small amount is passed
each day that the client is not aware of it. Therefore obtain a stool specimen for occult blood testing.

CENTRAL NERVOUS SYSTEM ASSESSMENT

Examination of cranial nerves and neurologic function is important in hematologic assessment because some problems cause
specific nervous system manifestations. Vitamin B12 deficiency impairs cerebral, olfactory, spinal cord, and peripheral nerve
function, and severe chronic deficiency may cause permanent neurologic degeneration. Many neurologic problems can
develop in clients who have hematologic malignancies as a consequence of bleeding, infection, or tumor spread. When the
client with a known or suspected bleeding disorder has any head trauma, expand the assessment to include frequent
neurologic checks and mental status examinations (see Chapter 44).

Other clinical manifestations that occur with impaired hematologic function include fever, chills, and night sweats.

Psychosocial Assessment

The client with hematologic problems may have a chronic illness (e.g., hemophilia or cancer) or an acute episode of a
chronic disease (e.g., pernicious anemia). In either case, each person brings his or her own coping style to the illness.
Develop a rapport with the client and learn what coping mechanisms he or she has used successfully during past illness or
crises.

Ask the client and family members about social support networks, community resources, and financial health. A problem in
any of these areas can interfere with the client's adherence to therapy and, ultimately, recovery.

COMPLETE BLOOD COUNT

A complete blood count (CBC) includes a number of studies: red blood cell (RBC) count, white blood cell (WBC) count,
hematocrit, and hemoglobin level. The RBC count measures circulating RBCs in 1 mm3 of blood. The WBC count measures
all leukocytes present in 1 mm3 of blood. To determine the percentages of different types of leukocytes circulating in the
blood, a WBC count with differential leukocyte count is performed (Chapter 23). The hematocrit (Hct) is calculated as the
percentage of red blood cells in the total blood volume. The hemoglobin level is the total amount of hemoglobin in blood.

The CBC can measure other variables of the RBCs, including mean corpuscular volume (MCV), mean corpuscular
hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC). MCV measures the average volume or size
of a single RBC and is useful for classifying anemias. When the MCV is elevated, the cell is abnormally large (macrocytic),
as seen in megaloblastic anemias. When the MCV is decreased, the cell is abnormally small (microcytic), as seen in iron
deficiency anemia. The MCH is the average amount of hemoglobin by weight in a single RBC. The MCHC measures the
average amount of hemoglobin by percentage in a single RBC. When the MCHC is decreased, the cell has a hemoglobin
deficiency and is hypochromic, as in iron deficiency anemia.
RETICULOCYTE COUNT

Another hematologic test helpful in determining bone marrow function is the reticulocyte count. A reticulocyte is an
immature RBC that still has its nucleus. An elevated reticulocyte count indicates increased RBC production by the bone
marrow. Normally about 2% of circulating RBCs are reticulocytes. An elevated reticulocyte count is desirable in an anemic
client or after hemorrhage because this indicates that the bone marrow is responding appropriately to a decrease in the total
RBC mass. An elevated reticulocyte count without a precipitating cause usually indicates health problems, such as
polycythemia vera.

HEMOGLOBIN ELECTROPHORESIS

Hemoglobin electrophoresis detects abnormal forms of hemoglobin, such as hemoglobin S in sickle cell disease. Hemoglobin
A is the major type of hemoglobin in the normal RBC from an adult. Decreased hemoglobin A levels with increasing levels
of other types of hemoglobin indicate some hematologic problems, such as sickle cell disease.

LEUKOCYTE ALKALINE PHOSPHATASE

Leukocyte alkaline phosphatase (LAP) is an enzyme produced by normal mature neutrophils. Elevated LAP levels occur
during episodes of infection or stress. An elevated neutrophil count without an elevation in LAP level occurs with chronic
myelogenous leukemia

COOMBS' TEST

The two Coombs' tests (direct and indirect) are used for blood typing. The direct test detects the presence of antibodies (also
called antiglobulins) against RBCs that may be attached to a person's RBCs. Although healthy people can make these
antibodies, in certain diseases (e.g., systemic lupus erythematosus, mononucleosis, lymphomas) these antibodies are directed
against the client's own RBCs. The presence of these antibodies usually causes a hemolytic anemia.

The indirect Coombs' test detects the presence of circulating antiglobulins. The test is used to determine whether the client
has serum antibodies to the type of RBCs that he or she is about to receive by blood transfusion.

SERUM FERRITIN, TRANSFERRIN, AND TOTAL IRON-BINDING CAPACITY

Serum ferritin, transferrin, and the total iron-binding capacity (TIBC) tests measure iron levels. Abnormal levels of iron and
TIBC occur with hematologic problems, including iron deficiency anemia.

The serum ferritin test measures the amount of iron present as free iron in the plasma. The amount of serum ferritin is related
to the amount of intracellular iron and represents 1% of the total body iron stores. Therefore the serum ferritin level provides
a means to assess total iron stores. People with serum ferritin levels within 10 g of the normal range for their gender have
adequate iron stores; people with levels 10 g or more lower than the normal range have inadequate iron stores and have
difficulty recovering from any hemorrhagic event.

Transferrin is a protein that transports iron from the intestines to cell storage sites. Transferrin is not easily measured, but by
measuring the amount of iron that can be bound to serum transferrin indirectly one can determine whether an adequate
amount of transferrin is present. This test is the total iron binding capacity (TIBC) test. In healthy people only about 30% of
the transferrin is bound to iron in the blood. TIBC is measured by taking a sample of blood and adding measured amounts of
iron to it. TIBC is calculated when the blood no longer binds the iron but allows it to precipitate. TIBC increases when a
person is deficient in serum iron and stored iron levels. Such a value indicates that an adequate amount of transferrin is
present but less than 30% of it is bound to serum iron.

Tests Measuring Bleeding and Coagulation

CAPILLARY FRAGILITY TEST

The capillary fragility test, or Rumpel-Leede test, measures vascular hemostatic function. The intracapillary pressure in the
arm is increased by occluding venous outflow or by applying controlled negative pressure to a skin area. A blood pressure
cuff is usually inflated to a pressure halfway between the systolic and diastolic pressures. This pressure is maintained for 5
minutes and the petechiae that appear distal to the cuff are counted. Normally 5 to 10 petechiae appear. When the number of
petechiae that form increases, the cause of excessive bleeding or bruising is capillary fragility rather than poor platelet action.

BLEEDING TIME TEST

The bleeding time test evaluates vascular and platelet activity during hemostasis. A special spring-loaded lancet that makes a
uniform wound depth is applied to the forearm while a blood pressure cuff remains inflated at 40 mm Hg. Blood is blotted
from the site at 30-second intervals, and the time required for the bleeding to stop is recorded. Normal bleeding time ranges
from 1 to 9 minutes.

PROTHROMBIN TIME

The prothrombin time (PT) measures how long blood takes to clot. This test reflects how much of the clotting factors II, V,
VII, and X is present and how well they are functioning. When enough of these clotting factors are present and functioning,
the PT shows blood clotting between 11 and 13 seconds or within 85% to 100% of the time needed for a control sample of
blood to clot. PT is prolonged when one or more clotting factors is deficient, such as when liver disease is present. Sodium
warfarin (Coumadin, Warfilone ) therapy is also monitored using PT levels. Usually warfarin therapy is considered
appropriate when the PT is prolonged by one and a half to two times the client's normal PT value.

Facilities are using the PT test less often to assess blood clotting because control blood is taken from different people and
may not be the same even in one laboratory from one day to the next. To reduce PT errors as a result of control blood
variation or in some of the chemicals used in the test, the International Normalized Ratio (INR) is used to assess clotting
time.

INTERNATIONAL NORMALIZED RATIO

The INR measures the same process as the PT in a slightly different way: by establishing a normal mean or standard for PT.
The INR is calculated by dividing the client's PT by the established standard PT. A normal INR ranges between 0.7 and 1.8.
When using the INR to monitor warfarin therapy, the goal is usually to maintain the client's INR is between 2.0 and 3.0
regardless of the actual PT in seconds. It is important to remember, however, that the desired INR range for any client is
individualized for specific client factors.

PARTIAL THROMBOPLASTIN TIME

The partial thromboplastin time (PTT) assesses the intrinsic clotting cascade and evaluates the action of factors II, V, VIII,
IX, XI, and XII. PTT is prolonged whenever any of these factors is deficient, such as in hemophilia or disseminated
intravascular coagulation (DIC). Because factors II, IX, and X are vitamin K—dependent and are produced in the liver, liver
disease can decrease their levels and prolong the PTT. Heparin (Calciparin, Hepalean ) therapy is monitored by PTT.
Desired therapeutic ranges for anticoagulation are 1.5 to 2.0 times normal values.

Controversy exists as to whether this test is accurate when the blood sample is taken through a vascular access device (e.g.,
arterial line or a normal saline lock) instead of through a separate new venipuncture. With an appropriate discard, samples
obtained through vascular access devices accurately reflect the client's aPTT.

PLATELET AGGLUTINATION/AGGREGATION

Platelet aggregation, or the ability to clump, is tested by mixing the client's plasma with a substance called ristocetin. The
degree of clumping is noted. Aggregation can be impaired in von Willebrand's disease and during the use of drugs such as
aspirin, anti-inflammatory agents, psychotropic agents, and platelet inhibitors.

RADIOGRAPHIC EXAMINATIONS

Assessment of the client with a suspected hematologic abnormality can include radioisotopic imaging. Isotopes are used to
evaluate the bone marrow for sites of active blood cell formation and sites of iron storage. Radioactive colloids are used to
determine organ size and liver and spleen function.
The client is given a radioactive isotope intravenously about 3 hours before the procedure. The client is then taken to the
nuclear medicine department for the scan, where he or she must lie still for about an hour. No special client preparation or
follow-up care is needed for these tests.

Standard x-rays may be used to diagnose some hematologic disorders. For example, multiple myeloma causes characteristic
bone destruction, with a "Swiss cheese" appearance on x-ray.

OBJECTIVE 10 (Joe)

Compare the actions and uses of anticoagulants, fibrinolytics, and platelet inhibitors.
The folloing is found on 876-9 in iggy.

Anticoagulants

Anticoagulant drugs exert their effects by interfering with one or more steps involved in the blood clotting cascade.
Thus these agents prevent new clots from forming and limit of prevent extension of formed clots. Anticoagulants have no
categorized into heparin and vitamin k antagonist.

Fibrinolytics

Fibrinolytic drugs selectively degrade fibrin thread already present in the formed block clot. The mechanism to start
fibrin degradation is activation of the inactive tissue protein plasminogen to its active form, plasmin. Plasmin directly attacks
and degrades the fibrin molecule, having fewer effects on the fibrinogen molecule. Thus the action of fibrinolytic drugs is the
selective breakdown of formed fibrin clots with less effects on clot formation.
The use of fibrinolytic drugs result in the best clot breaking down with less disruption of blood clotting. These drugs
are the first line therapy for problems caused by small, localized formed clots such as myocardial infarctions, limited arterial
thrombosis, and thrombotic strokes.

Platelet Inhibitors

Platelet inhibitors are drugs that either prevent platelets from becoming active or prevent active platelets from
clumping together. The most widely used drug for this effect is aspirin, which inhibits the production of substances that can
trigger platelet activation, such as thromboxane. Other drugs change the platelet membrane, reducing its "stickiness", or
prevent activators from binding to platelet receptor sites.

OBJECTIVE 11 (Jodey)

Discuss the nursing implications for clients receiving any class of the class of drugs listed in objective 10.
Med/surg pg 877, table 42-3

Anticoagulants: Heparin: check client for bleeding, used for prevention of clot formations or extension, teach
client proper technique for home administration, keep prostamine sulfate on the unit while a client is receiving
heparin, client is most at risk for excessive bleeding in the first couple hours of receiving the drug, check client for
possible allergic reactions, monitor platelet count, H & H levels, coagulation level, check for blood in urine, stool,
emesis; check skin for increasing bruising or petechiae.
Low molecular weight heparins: Enoxaparin: Does not require monitoring of drug levels or aPTT and same as for
heparin. Dalteparin: Same as for heparin.

Vitamin K antagonists(warfarin): May be started while the client is still receiving heparin, instruct client that
bleeding precautions are still needed for at least a week after stopping the drug, warn clients not to take aspirin or
other platelet inhibitors unless prescribed by the health care provider who also prescribe the warfarin, instruct
clients to keep all appointments for drug level checks and not to self adjust drug dosages.
Fibrinolytics: Reteplase: Avoid venipuncture during and for one hour after administration, do not place clients in
a position in which the head is dependent to the body; assess neurologic status every 30 minutes for the first 3
hours after administration, assess any incisions, venipuncture sites, previous areas of trauma for bleeding.
Anistreplase: avoid venipunctures during and for four hours after drug administration and Alteplase: same as for
reteplase.
Streptokinase: Check client for mild and severe allergic reactions during and after treatment (rash, hypotension,
difficulty breathing, wheezing); keep emergency equipment and medications in client’s room, use bleeding
precautions when handling the client; assess for excessive bleeding at least every 15 minutes during and for 2
hours after drug administration. Assess for drug effectiveness during administration.
Urokinase: Use bleeding precautions for at least 24 hours after drug administration; assess for bleeding at least
every 2 hours for the first 24 hours. Assess client for manifestations of infection at least every shift during
hospitalization at least every shift during hospitalization; teach client to have regular monitoring for blood-borne
diseases for at least 1 year after therapy.

Platelet Inhibitors: Aspirin: Instruct clients to stop aspirin if wheezing occurs, instruct clients to discontinue
aspirin for at least a week before scheduled dental work, surgery and other invasive procedures. Teach clients to
take drug with food and to observe stools for evidence of bleeding (bright red blood, black tarry looking stools)
Abciximab: Teach client to observe for any skin rashes, swelling or difficulty breathing that may indicate an
allergy to the drug.
Clopidogrel(plavix): instruct clients to avoid dental work and invasive procedures while taking this drug or to
inform health care professionals that he or she is taking the drug, teach clients to take drug with food and to
observe stools for evidence of bleeding. Same as for aspirin.
Dipyridamole: Teach clients that their blood pressure could be lower than normal during position changes and that
they should move slowly when changing from a sitting or lying position to a standing position and also same as for
aspirin.

OBJECTIVE 12 (Jessica)

pg 884 IGGY

Prioritize the nursing care for a client after a bone marrow aspiration.

Bone Marrow aspiration or biopsy is often performed to evaluate the client’s hematologic status when other tests
show persistent abnormal findings. Post op care for this patient would consist of covering the site with a dressing
once bleeding is controlled and closely observe for 24 hours for bleeding and infection. Ice packs and mild
analgesic (non-aspirin) may be given for discomfort. Advise client to inspect site every 2 hours and to avoid
contact sports or trauma to the site for 48hrs. Info obtained from bone marrow aspiration reflects the degree and
quality of bone marrow activity, and cell counts.

OBJECTIVE 13 (Lori)

Chapter 42 in Iggy, too much to copy here, I hit the highlights.

Describe the indications, normal values, nursing implications, and patient teaching pre- and post-testing, for the
following tests:
Complete blood count with and without differential (CBC)
Serum Ferritin and Total Iron-Binding Capacity (TIBC)
Prothrombin Time (PT)/ International Normalized Ratio (INR)
Partial Thromboplastin Time (PTT)
Bleeding Time
Fibrin Split Products (FSP)
Bone Marrow Aspiration And Biopsy
d-dimer

A complete blood count (CBC) includes a number of studies: red blood cell (RBC) count, white blood cell (WBC) count,
hematocrit, and hemoglobin level. The RBC count measures circulating RBCs in 1 mm3 of blood. The WBC count measures
all leukocytes present in 1 mm3 of blood. To determine the percentage of different types of leukocytes circulating in the
blood, a WBC count with differential leukocyte count is performed (Chapter 23). The hematocrit (Hct) is calculated as the
percentage of red blood cells in the total blood volume. The hemoglobin level is the total amount of hemoglobin in blood.

Serum ferritin, transferrin, and the total iron-binding capacity (TIBC) tests measure iron levels. Abnormal levels of iron and
TIBC occur with hematologic problems, including iron deficiency anemia.

The serum ferritin test measures the amount of iron present as free iron in the plasma. The amount of serum ferritin is related
to the amount of intracellular iron and represents 1% of the total body iron stores. Therefore the serum ferritin level provides
a means to assess total iron stores. People with serum ferritin levels within 10 g of the normal range for their gender have
adequate iron stores; people with levels 10 g or more lower than the normal range have inadequate iron stores and have
difficulty recovering from any hemorrhagic event.

Transferrin is a protein that transports iron from the intestines to cell storage sites. Transferrin is not easily measured, but by
measuring the amount of iron that can be bound to serum transferrin indirectly one can determine whether an adequate
amount of transferrin is present. This test is the total iron binding capacity (TIBC) test. In healthy people only about 30% of
the transferrin is bound to iron in the blood. TIBC is measured by taking a sample of blood and adding measured amounts of
iron to it. TIBC is calculated when the blood no longer binds the iron but allows it to precipitate. TIBC increases when a
person is deficient in serum iron and stored iron levels. Such a value indicates that an adequate amount of transferrin is
present but less than 30% of it is bound to serum iron.

PROTHROMBIN TIME

The prothrombin time (PT) measures how long blood takes to clot. This test reflects how much of the clotting factors II, V,
VII, and X is present and how well they are functioning. When enough of these clotting factors are present and functioning,
the PT shows blood clotting between 11 and 13 seconds or within 85% to 100% of the time needed for a control sample of
blood to clot. PT is prolonged when one or more clotting factors is deficient, such as when liver disease is present. Sodium
warfarin (Coumadin, Warfilone ) therapy is also monitored using PT levels. Usually warfarin therapy is considered
appropriate when the PT is prolonged by one and a half to two times the client's normal PT value.

Facilities are using the PT test less often to assess blood clotting because control blood is taken from different people and
may not be the same even in one laboratory from one day to the next. To reduce PT errors as a result of control blood
variation or in some of the chemicals used in the test, the International Normalized Ratio (INR) is used to assess clotting
time.

INTERNATIONAL NORMALIZED RATIO

The INR measures the same process as the PT in a slightly different way: by establishing a normal mean or standard for PT.
The INR is calculated by dividing the client's PT by the established standard PT. A normal INR ranges between 0.7 and 1.8.
When using the INR to monitor warfarin therapy, the goal is usually to maintain the client's INR is between 2.0 and 3.0
regardless of the actual PT in seconds. It is important to remember, however, that the desired INR range for any client is
individualized for specific client factors.

PARTIAL THROMBOPLASTIN TIME

The partial thromboplastin time (PTT) assesses the intrinsic clotting cascade and evaluates the action of factors II, V, VIII,
IX, XI, and XII. PTT is prolonged whenever any of these factors is deficient, such as in hemophilia or disseminated
intravascular coagulation (DIC). Because factors II, IX, and X are vitamin K—dependent and are produced in the liver, liver
disease can decrease their levels and prolong the PTT. Heparin (Calciparin, Hepalean ) therapy is monitored by PTT.
Desired therapeutic ranges for anticoagulation are 1.5 to 2.0 times normal values.
Controversy exists as to whether this test is accurate when the blood sample is taken through a vascular access device (e.g.,
arterial line or a normal saline lock) instead of through a separate new venipuncture. With an appropriate discard, samples
obtained through vascular access devices accurately reflect the client's aPTT.

BLEEDING TIME TEST

The bleeding time test evaluates vascular and platelet activity during hemostasis. A special spring-loaded lancet that makes a
uniform wound depth is applied to the forearm while a blood pressure cuff remains inflated at 40 mm Hg. Blood is blotted
from the site at 30-second intervals, and the time required for the bleeding to stop is recorded. Normal bleeding time ranges
from 1 to 9 minutes.

BONE MARROW ASPIRATION AND BIOPSY

Bone marrow aspiration or biopsy is often performed to evaluate the client's hematologic status when other tests show
persistent abnormal findings. Results can provide important information about bone marrow function, including the
production of red blood cells (RBCs), white blood cells (WBCs), and platelets. Bone marrow aspiration and bone marrow
biopsy are similar invasive procedures. In a bone marrow aspiration, cells and fluids are suctioned from the bone marrow. In
a bone marrow biopsy, solid tissue and cells are obtained by coring out an area of bone marrow with a large-bore needle.

A physician's order and a signed informed consent are obtained from the client before a bone marrow aspiration or biopsy is
performed. Bone marrow aspiration may be performed by a physician, a sanctioned clinical nurse specialist, a nurse
practitioner, or a physician assistant, depending on the agency's policy and regional law. The procedure may be performed at
the client's bedside, in an examination room, or in a laboratory.

After learning what specific tests will be performed on the marrow, check the facility's procedure manual and the hematology
laboratory to determine how to handle the specimen. Some tests require that heparin or other solutions be added to the
specimen.
OBJECTIVE 14 (Brett)

Discuss the pathophysiology of the disorders listed below:

Sickle Cell Anemia: a genetic disorder that results in chronic anemia, pain, disability, organ damage, increased risk for
infection, and early death. The main problem is the formation of abnormal hemoglobin chains. In adults the normal
hemoglobin molecule has two alpha chains and two beta chains of amino acids. Normal adult hemoglobin called hemoglobin
A contains 98% to 99% HbA with a small percentage of a fetal form of hemoglobin. In sickle cell disease at least 40% of the
total hemoglobin contains an abnormality of the beta chains known as hemoglobin S. When RBCs having large amounts of
HbS are exposed to decreased oxygen states the abnormal beta chains contract and pile together within the cell distorting the
shape of the RBC. These cells assume a sickle shape, become rigid, clump together, and form masses of sickled RBCs that
block blood flow. The blocked blood flow leads to more blockage which can lead to more sickling and can result in tissue
damage from hypoxia. Conditions that cause sickling include hypoxia, venous stasis, low environmental or body
temperatures, acidosis, strenuous exercise, and anesthesia. When oxygenation returns to normal the cells shape returns to
normal, however, the hemoglobin remains twisted. These cells are more fragile and more easily broken. The average lifespan
of a RBC containing HbS is 12 to 15 days as opposed to 120 days of normal RBCs. Sickle cell disease causes periodic
episodes of extensive cellular sickling called crisis. These crises can occur as much as once a week or as little as once a year,
and occur due to conditions of hypoxemia, or low blood oxygen.

Fe Deficient Anemia: Adults usually have between 2 and 6g of iron, depending on the size of the person and the amount of
hemoglobin in the cells. About two thirds of this iron is contained in the hemoglobin; the other one third is stored in the bone
marrow, spleen, liver and muscle. With iron deficiency the iron stores are depleted first followed by the hemoglobin stores.
Iron deficiency anemia is common and can result from blood loss, poor intestinal absorption, and an inadequate diet. The
basic problem is a deficiency of iron for the developing RBC. Iron deficiency anemia can occur at any age but is more
common in women, older adults, and people with poor diets.

Vitamin B12 Deficient Anemia: Proper production of RBCs depends on adequate deoxyribonucleic acid (DNA) synthesis in
the precursor cells so that cell division and growth into functional RBCs can occur. All cell division requires adequate
amounts of folic acid to make DNA. One function of vitamin B12 is to activate the enzymes that move folic acid into the
cell, where DNA synthesis occurs. Vitamin B12 deficiency causes anemia by inhibiting folic acid transport and reducing
DNA synthesis in precursor cells. These precursor cells then undergo improper DNA synthesis and increase in size. This type
of anemia is called megaloblastic because of the large size of these abnormal cells. Vitamin B12 results from poor intake of
foods containing vitamin B12. Vegetarian diets, or diets lacking in dairy products can cause this deficiency, Conditions such
as small bowel resection, diverticula, tape worm, or overgrowth of intestinal bacteria can lead to poor absorption of vitamin
B12. Anemia caused by failure to absorb vitamin B12 (pernicious anemia) is caused by a deficiency of intrinsic factor which
is needed for intestinal absorption of vitamin B12. Vitamin B 12 deficiency anemia may be mild or severe, usually develops
s;owly, and produces few symptoms. Clients usually have jaundice and pallor as well as glossitis (a smooth beefy red
tongue), fatigue, weight loss, and may have paresthesias (abnormal sensations) in the feet and the hands, and poor balance.

Folic Acid Deficient Anemia: Manifestations are similar to those of vitamin B12 deficiency but nervous system functions
remain normal, and can cause megaloblastic anemia. The disease develops slowly and symptoms may be attributed to other
problems or diseases. The three common causes of folic acid deficiency are poor nutrition, malabsorption, and drugs.

Aplastic (Renal Failure) Anemia: is a deficiency of circulating red blood cells because of failure of the bone marrow to
produce these cells. It is caused by an injury to the hematopoietic precursor cell, the pluripotent stem cell. Aplastic anemia
usually occurs alone but usually occurs with leucopenia (a reduction in white blood cells) and thrombocytopenia (a reduction
in platelets). These three problems occur together because the damaged bono marrow loses the ability to produce any of these
cells. Pancytopenia (a deficiency of all three cell types) is common in aplastic anemia.

Polycythemia (primary and secondary): Polycythemia vera is a disease with sustained increase in blood hemoglobin levels
to 18 g/dL, an RBC count of 6 million/mm3, or a hematocrit of 55% or greater, PV is a cancer of the RBCs with three major
hallmarks: massive production of RBCs, excessive leukocyte production, and excessive production of platelets. Extreme
hypercellularity (cell excess) of the peripheral blood occurs in people with PV. At the time of diagnosis the client’s facial skin
and mucous membranes have a dark, flushed appearance. These areas appear purplish or cyanotic because the blood in these
tissues is poorly oxygenated. May have itching due to dilated blood vessels and varied tissue oxygenation. Blood viscosity is
increased causing an increase in peripheral resistance, superficial veins are distended, the thickened blood moves slowly
through the veins causing increased demands on the heart resulting in hypertension. In some areas stasis occurs causing
thrombosis (clot formation) which leads to hypoxia, anoxia, and later to infarction and necrosis. Tissues most at risk are the
heart, spleen, and kidneys. The number of cells in the blood is increased and the cells are not normal resulting in shorter cell
life which causes a rapid turnover in circulating blood cells which causes an increase in cell debris adding to sludging of the
blood. This debris includes uric acid and potassium which causes the symptoms of gout and hyperkalemia (elevated serum
potassium levels). Other manifestations of PV are poor oxygen carrying capacity and bleeding problems due to platelet
impairment.
Thrombocytopenia (IYP and TTP): is a decrease in the number of platelets below the number needed for coagulation.
Thrombocytopenia nay occur as a result of other conditions or treatments that suppress general bone marrow activity or
through processes that limit platelet formation or increase platelet destruction In idiopathic thrombocytopic Purpura (ITP) the
total number of circulating platelets is greatly reduced and even though plate production is normal. Clients with this disorder
make an antibody directed against the surface of their own platelets. The antibody wants the platelets making them more
likely to be destroyed by macrophages. These coated platelets are destroyed in the spleen due to a large number of
macrophages being produced in the spleen and the blood vessels of the spleen are long and twisted.ITP is most common in
women age 20 to 40 and among people with other auto immune disorders such as systemic lupus erythematosis.

Thrombotic thrombocytopenic Purpura (TTP) is a rare disorder in which platelets clump together abnormally on the
capillaries and few platelets remain in circulation. The client has inappropriate clotting, yet the blood fails to clot when
trauma occurs. The underlying cause of TTP appears to be an autoimmune reaction in blood vessel cells Manifestations
includes renal failure, myocardial infarction, and stroke. If untreated, this condition is often fatal in three months.

Disseminated intravascular coagulapathy occurs when the first stage of the coagulation process is abnormally stimulated.
Two distinct phases can be identified. First, when the clotting mechanism is triggered in the circulation, thrombin is
generated in greater amounts that can be neutralized by the body. Consequently there is rapid conversion of fibrinogen to
fibrin with the aggregation and destruction of platelets local and widespread fibrin deposition occurs in blood vessels.
Obstruction is caused by the thrombosis impendence of the blood flow with eventual necrosis of tissue concurrently the
fibromylitic mechanism is activated which causes extensive dystruction of clotting factors. With a deficiency in clotting
factors hemorrhage into vital organs is possible.

Hemophilia: is two different hereditary bleeding disorders resulting from deficiencies of specific clotting factors.
Hemophilia A is a deficiency of factor VIII and accounts for 80% of cases of hemophilia. Hemophilia B is a deficiency of
factor IX and accounts for 20% of cases. Hemophilia A mostly affects males non of whose sons will have the gene for
hemophilia and all of whose daughters will will be carriers. Before transfusions hemophilia A bleeding was so severe that
carriers rarely lived past the age of 3. Clinical signs are abnormal bleeding in response to trauma because of a deficiency of
the specific clotting factor. Clients with hemophilia do not bleed more often or more rapidly just for longer periods of time.
Hemophiliacs form platelets at the bleeding sight but the clotting factor deficiency impairs the clotting response and stable
fibrin clots do not form.

Neutropenia: is a reduction in the number of circulating neutrophils and is usually defined as a absolute neutrophil count
(ANC) of less than 1000/mm3. ANC is calculated by multiplying the total WBC count by the percentage of neutrophils and
bonds in the differential count.

Leukemia (ALL, CLL, AML, CML) Leukemia is a type of cancer with uncontrollable production of immature WBCs in
the bone marrow. As a result the bone marrow becomes over crowded with immature non functioning cells and production of
normal blood cells is greatly decreased. Leukemias are classified by cell type. Abnormal leukemic cells coming from
lymphoid pathways are lymphatic or lymphoblastic (ALL) or chronic lymphocytic (CLL). Leulemias in which the abnormal
cells come from the myeloid pathways are myeclotic or meylogenous(AML) or chronic myelogenous (CLL). Several
subtypes exist for each of these diseases which are classified according to the degree of maturity of the abnormal cell anf the
specific cell type involved.

Meyloma: is a white blood cell cancer that involves a more mature lymphocyte than either leukemia or lymphoma. There is
over growth of blymphocyte plasma cells in the bone marrow. These cwlla normally make antibodies. When they become
cancerous these plasma cells over produce both complete and incomplete antibodies or gama globlins. Fewer functional
RBCs, WBCs and platelets are produced. In addition to the excess antibodies myeloma cells produce excess cytokines that
increase the cancer cell growth rates and destroy bone. The excess antibodies are released into the blood increasing the serum
protein levels and clogging blood vessels in the kidneys and other organs. With out treatment the disease causes progressive
bone destruction, bleeding problems, kidney failure, immune suppression and death.

Malignant Lymphoma Hodgkins and Non Hodgkins: Hodgkins lymphoma is a cncer that can affect any age group it
occurs most often in people in their mid 20s and in people older than 50 years old. Possible causes include viral infections
and exposure to chemical agents. The cancer usually starts in a single lymph node or a line of lymph nodes and has the Reed-
Sternberg cell, a marker for hodgkins lymphoma. The disease progresses to other lymph tissue and other non lymph tissue.
Non Hodgkins includes all lymphoid cancers that do not have the Reed-Sternberg cell. There are more than 12 subtypes.
NHLs arise from altered B or T lymphocytes low grade lymphomas usually arise from B cell lymphocytes and progress
slower. They have longer survival times but are less responsive to treatment and cures are rare. High grade lymphomas are
aggressive tumors of mixed cell types with rapid growth. High grade lymphocytes are more responsive to chemotherapy and
chances for long term cure are greater.

OBJECTIVE 15 (Liz)

Describe the following

Anemia
Polycythemia
Thrombocytopenia
DIC
Hemophilia
Myeloma
Malignant lymphoma
thrombocytopenia

Sickle cell anemia

Disorder where the formation of abnormal hemoglobin chains. These cells form a sickle shape, become rigid, clump together,
and form masses of sickled RBCs that block blood flow. This leads to further tissue hypoxia. This is inherited and occurs in
all races but less often among white individuals, yet 10% of all African Americans are carriers of one sickle cell gene allele.
Pain is a common problem with sickle cell so administer pain medications, administer oxygen, hydrate, remove constrictive
clothing, promote venous return, elevate head of bed, and avoid taking BP. (chart 43-3)
Teach the client about risks for infection by thorough handwashing and anybody who comes in the room must where a mask.
If in hospital monitor CBC with differential WBC. For treatment other then medication is transfusion therapy.

Iron deficiency anemia

Can result from blood loss, poor intestinal absorption, and inadequate diet. Main problem is a decrease iron supply for RBC.
This is more frequent in women and older adults.
People who have this disorder should be evaluated for bleeding especially from GI tract. Treatment is to increase the oral
intake of iron thru diet. If iron losses are minimal, oral supplements can be given.

Vit B12 deficiency anemia

This is caused by vitamin B12 inhibiting folic acid transport and reducing DNA synthesis in precursor cells, these cells
undergo improper DNA synthesis. This is usually caused by poor intake of food. The S/S of this is severe pallor, severe
jaundice, smooth beefy red tongue, fatigue and wt loss. Treatment is increase B12 in diet or take a vitamin supplement.

Folic acid deficient

This can also form megoblastic anemia and the causes of this are poor nutrition, malabsorption, and drugs. High risk people
are older adults, debilitated clients with alcoholism, clients susceptible to malnutrition, and those with increased folic acid
requirements. Treatment includes eating plenty of foods that are high in folic acid and B12.

Aplastic anemia

Deficiency of circulating red blood cellsbecause of failure of the bone marrow to produce these cells. This may be caused by
long-term exposure to toxic agents, ionizing radiation, or infection. Blood transfusion are the mainstay of treatment for client
and immunosuppressant therapy helps clients who have aplastic anemia similar to autoimmune disorders. The last treatment
is splenectomy

Polycythemia

Is a disease with a sustained increase in blood hemoglobin levels to 18g/dL, and RBC of 6 and hematocreit of 55% or greater.
The blood of a client with this is hyperviscous or thicker blood. One type of polycythemia, polycythemia vera is fatal if left
untreated, they usually don’t live more then 2 years after diagnosed. S/S are in chart 43-6 and client education is in chart 43-
7. conservative treatment is repeated phlebotomies, removing RBC and reduce blood viscosity. Increasing hydration and
promoting venous return helps prevent clot formation. If this fails then need to start oral chemotherapy agents and radiation
therapy. Significant amount of ppl with pv end up developing acute leukemia.

Thrombocytopenia

Total number of circulating platelets is greatly reduced, even though platelet production in the bone marrow is normal. Body
makes an antibody directed against the surface of their own platelets and are then destroyed by macrophages. This client is at
great risk for bleeding. Treatment of medication involves immunosuppressants, and chemotherapy drugs. Blood replacement
therapy can occur if platelet count is less than 20,000. surgical procedure, splenectomy, would be the last result .

Thrombotic thrombocytopenic purpura

Is a rare disorder in which platelet clup together abnotmally in capillaries and too few platelets remain in circulation. This is
an underlying autoimmune disorders of the blood vessel cells. Treatment focuses on preventing platelet clumping and
stopping the underlying autoimmune process. This includes plasmaphoresis, inhibit platelet clumping like aspirin, and
immunosuppressive therapy.

Multiple myeloma

Is a wbc cancer that involves a more mature lymphocyte than either leukemia or lymphoma. There is overgrowth of the B-
lymphocyte plasma cells in the bone marrow. These overproduce both complete and incomplete antibodies and excess
cytokines that increase cancer growth. First signs are fatigue, easy bruising , and bone pain. Diagnosis is made by bone
marrow biopsy, xray findings of bone narrowing, and electrophoreses of plasma proteins. Standard treatment is
chemotherapy.

Hodgkin’s disease

Cancer that effects any age group and occurs usually in their mid-20’s and is more prevalent in men. Possible causes are
viral infections and exposure to chemical agents. First assessment finding is a large but painless lymph nodes usually in the
neck and then fever, malaise, and night sweats. The lymph node usually contains a cancer cell called reed-sternberg cell. Can
spread to non-lymphnoid tissue. Diagnosis is by a biopsy of a node and reveals reed-sternberg cells. Nursing management of
the client is focuses on the side effects of therapy following drug induced pancytopenia, N/V, skin problem at the site of
radiation, imparired hepatic function.

Non-hodgkins lymphoma

Includes all lymphoid cancers that do not have reed Sternberg cells. Enlarged lymph nodes mabe the only manifestation of
lymphoma because these nodes can arise from lymphoid cells in an tissue and can spread to any organ. Diagnosis is made
from features of cells obtained by biopsy of a node or mass. Treatment consists of radiation therapy and multiagent
chemotherapy. Nursing management includes helping the client deal with the psychosocial issues and side effects of the
cancer and treatments.

Hemophilia

Is two different hereditary bleeding disorders resulting from deficiencies of specific clotting factors. Women who are carriers
have a 50% chance of transmitting the gene to their daughters and to their sons. Hemophilia A usually affects males and all of
whose daughters will be carriers and not their sons. The bleeding disorder is so severe in type A that before blood transfusion
were available children rarely survived past 3 yrs old. Treatment consists of cryoprecipitate, which is so expensive that some
ppl cant afford it, but because it is made from human pooled serum there is a risk for viral contamination. Nursing
management involves education the client about the potential viruses and how to deal with these if they do occur.

DIC

Is a problem with blood clotting process which is triggered by many severe illnesses including cancer. Is usually caused by
(sepsis often a gram negative bacteria) the release of thrombin from cancer cells or by blood transfusions. Most often seen in
leukemia, adenocarcinoma of the lungs, pancreas, stomach and prostate. Teach clients and family member the early
manifestations of infection and sepsis and when to seek medical attention. Treatment focuses on reducing the infection and
halting the DIC process by IV initiated thereapy. During the early phase of DIC anticoagulant especially heparin are given to
limit clotting and prevent the rapid consumption of circulation clotting factors.

OBJECTIVE 16 (Kelly)

Describe the concept of self-tolerance. Iggy 360-361

Self tolerance is the ability to recognize self vs non-self (non self includes infected body cells, cancer cells and all invading
cells and organisms) this is necessary to prevent healthy body cells from being destroyed along with the invaders. The
immune cells are the only body cells capable of determining self from non-self. Self tolerance is possible because of the
different kinds of proteins present on cell membranes. Each person has unique proteins specific to only them, unless they
have identical twin, these are called a “universal product code” or a “cellular fingerprint” for that person. Because these
proteins are non-self to another persons immune system they are referred to as antigens, they are capable of stimulating an
immune response. Human Leukocyte Antigens (HLA) make up the code for each person. HLA’s are a normal part of each
person and act as antigens only if they enter another person’s body. These antigens specify the tissue type of each person.
The immune system cells come in contact with invader cells if they don’t match HLA they are attacked, neutralized or
destroyed.

OBJECTIVE 17 (Victoria)

Explain the difference between infection and inflammation

INFLAMMATION

Inflammation, sometimes called "natural" immunity, provides immediate protection against the effects of tissue injury and
invading foreign proteins. The ability to produce an inflammatory response is critical to health and well-being. Inflammation
differs from antibody-mediated immunity and cell-mediated immunity in two important ways:

1. Inflammatory protection is immediate but short term against the effects of injury or invading organisms. It does not
provide sustained, long-term immunity on repeated exposure to the same organisms.

2. Inflammation is a nonspecific body defense to invasion or injury and can be started quickly by almost any event.

Inflammation is nonspecific; the same tissue responses occur with any type of injury or invasion, regardless of the location
on the body or the specific initiating agent. Thus inflammation triggered by a scald burn to the hand is the same as
inflammation triggered by excess stomach acid or bacteria in the middle ear. How widespread the symptoms of inflammation
are in the body depends on the intensity, severity, duration, and extent of exposure to the initiating injury or invasion. For
example, a splinter in the finger triggers inflammation only at the splinter site, whereas a burn injuring 60% of the skin
surface results in an inflammatory response involving the entire body.

Inflammatory responses start tissue actions that cause visible and uncomfortable symptoms. Despite the discomfort, these
actions are important in ridding the body of harmful organisms. However, if the inflammatory response is excessive, tissue
damage may result. Inflammatory responses also help start both antibody-mediated and cell-mediated actions to activate a
full immune response.

Infection- A confusing issue about inflammation is that this process occurs in response to tissue injury, as well as to invasion
by organisms. Infection is usually accompanied by inflammation; however, inflammation can occur without invasion by
organisms. Examples of inflammation without infection include sprain injuries to joints, myocardial infarction, sterile
surgical incisions, thrombophlebitis, and blister formation. Examples of inflammation caused by noninfectious invasion by
foreign proteins include allergic rhinitis, contact dermatitis, and other allergic reactions. Inflammations caused by infection
include otitis media, appendicitis, bacterial peritonitis, viral hepatitis, and bacterial myocarditis, among many others. Thus
inflammation does not always mean that an infection is present. (Medical-Surgical Nursing pages 362-364)

OBJECTIVE 18 (Victoria)
Describe the basis for the 5 cardinal signs of inflammation

The purpose of inflammation and immunity is to neutralize, eliminate, or destroy organisms that invade the internal
environment. The leukocytes involved in inflammation are neutrophils, macrophages, eosinophils, and basophils.
Neutrophils and macrophages use phagocytosis to destroy and eliminate foreign invaders. Basophils and eosinophils act on
blood vessels to cause tissue-level responses.

The five cardinal manifestations of inflammation are: warmth, redness, swelling, pain, and decreased function. Inflammatory
responses occur in a predictable sequence. The sequence is the same regardless of the triggering event. Inflammatory
responses occur in three stages and the timing of the stages may overlap.

STAGE I (VASCULAR) In stage I of the inflammatory response, the early effects involve changes in blood vessels.
When inflammation results from tissue injury, this stage has two phases.

Phase I The first phase is rapid but short-term blood vessel constriction caused by trauma to blood vessel smooth muscle.
This phase lasts only seconds and may be so short that the person is unaware of it.

Phase II In the second phase, blood flow to the area increases (hyperemia) and swelling (edema) forms at the site of
injury or invasion. Injured tissues and the leukocytes in this area secrete histamine, serotonin, and kinins that constrict the
small veins and dilate the arterioles in the area of injury. These blood vessel changes cause redness and warmth of the tissues.
This increased blood flow increases delivery of nutrients to injured tissues.

Capillary leak also occurs, allowing blood plasma to leak into the tissues. This response causes swelling and pain. Edema at
the site of injury or invasion protects the area from further injury by creating a cushion of fluid. The extra fluid also can
dilute any toxins or organisms that have entered the area. The duration of these responses depends on the severity of the
initiating event.

The macrophage is the major cell involved in stage I of inflammation. The action is rapid because macrophages are already
in place at the site of injury or invasion. This action is limited because the number of macrophages is so small. To enhance
the inflammatory response, the tissue macrophages secrete several cytokines. One cytokine is colony-stimulating factor
(CSF), which triggers the bone marrow to increase the rate of white blood cell (WBC) production from 14 days to a matter of
hours. Some of the cytokines also increase the release of neutrophils from the bone marrow and attract them to the site of
injury or invasion, which leads to the next stage of inflammation.

STAGE II (CELLULAR EXUDATE)

In stage II, neutrophilia (increased number of circulating neutrophils) occurs, along with the formation of exudate, commonly
called pus.

The most active cell in this stage is the neutrophil. Under the influence of cytokines, the neutrophil count can increase up to
five times within 12 hours after the onset of inflammation. At the site of inflammation, neutrophils attack and destroy
organisms and remove dead tissue through phagocytosis.

In acute inflammation, the healthy person produces enough mature neutrophils to keep pace with invasion and prevent the
organisms from growing. At the same time, the WBCs and inflamed tissues secrete cytokines, which allow tissue
macrophages to increase and trigger bone marrow production of monocytes. This reaction begins slowly but its effects are
long lasting.

During this phase, the arachidonic acid cascade starts to increase the inflammatory response. This action begins by the
conversion of fatty acids in plasma membranes into arachidonic acid (AA). Then, enzymes (including cyclooxygenase)
convert AA into many chemicals that are further processed into the substances that continue the inflammatory response in the
tissues. These substances include histamine, leukotrienes, prostaglandins, serotonin, and kinins. Many anti-inflammatory
drugs stop this cascade by preventing cyclooxygenase from converting AA into inflammatory substances.

When an infection stimulating inflammation lasts longer than just a few days, the bone marrow cannot produce and release
enough mature neutrophils into the blood to keep pace with the growth of organisms. In this situation, the bone marrow
begins to release immature neutrophils, reducing the number of circulating mature neutrophils. This reduction of functional
neutrophils limits the helpful effects of inflammation and increases the risk for sepsis.

STAGE III (TISSUE REPAIR AND REPLACEMENT)

Although stage III is completed last, it begins at the time of injury and is critical to the final function of the inflamed area.

Some of the WBCs involved in inflammation start the replacement of lost tissues or repair of damaged tissues by inducing
the remaining healthy cells to divide. In tissues that are unable to divide, WBCs trigger new blood vessel growth and scar
tissue formation. Because scar tissue does not behave like normal tissue, loss of function occurs wherever damaged tissues
are replaced with scar tissue. The degree of function lost is determined by how much tissue is replaced by scar tissue.

Inflammation alone cannot provide immunity. Inflammatory cells must interact with lymphocytes to provide long-lasting
immunity. Long-lasting immune actions develop through antibody-mediated immunity (AMI) and cell-mediated immunity
(CMI).

TABLE 23-3 Stages of Inflammation

(Info from Medical-Surgical Nursing pages 367-368)

OBJECTIVE 19 (Amanda)

Compare and contrast the cells, purposes, and features of inflammation and immunity.

Inflammation:

“Inflammatory responses occur in a predictable sequence. The sequence is the same regardless of the triggering event.
Responses at the tissue level cause the five cardinal manifestations of inflammation: warmth, redness, swelling, pain, and
decreased function. Inflammatory responses occur in three stages and the timing of the stages may overlap (Table 23-3).”

The leukocytes involved in inflammation are neutrophils, macrophages, eosinophils, and basophils. Neutrophils and
macrophages use phagocytosis to destroy and eliminate foreign invaders. Basophils and eosinophils act on blood vessels to
cause tissue-level responses.

Although the neutrophils are the largest group of circulating leukocytes, each cell is small. This powerful army of small cells
is the first internal line of defense against invaders (especially bacteria) in blood and extracellular fluid. It is the granules
inside the neutrophils that destroy invaders by phagocytosis. The mature neutrophil has many granules containing different
enzymes that can degrade invaders.
The inflammatory function of macrophages is phagocytosis. Macrophages can easily distinguish between self and non-self
and are very effective at trapping invading cells. Unlike neutrophils, macrophages are able to renew their energy supplies and
enzymes needed to degrade foreign protein. Therefore each macrophage can take part in many phagocytic events.

Basophils have granules containing many chemicals (vasoactive amines) that act on blood vessels. These chemicals include
heparin, histamine, serotonin, kinins, and leukotrienes. When released into the blood, most of these chemicals act on smooth
muscle and blood vessel walls. Heparin inhibits blood and protein clotting. Histamine constricts small veins and respiratory
smooth muscles. Constriction of respiratory smooth muscle narrows airways and restricts breathing. Constriction of veins
inhibits blood flow and decreases venous return. This effect causes blood to collect in capillaries and small arterioles. Kinins
dilate arterioles and increase capillary permeability. These actions cause blood plasma to leak into the interstitial space
(vascular leak syndrome).

Eosinophils act against infestations of parasitic larvae. Eosinophil granules contain many different substances. Some
substances induce inflammation when released. In addition, enzymes from eosinophils degrade the vasoactive chemicals
released by other leukocytes and can limit inflammatory reactions. This is why the number of circulating eosinophils
increases during an allergic response.

Immunity:

Antibody-mediated immunity (AMI), also known as humoral immunity, involves antigen-antibody interactions to
neutralize, eliminate, or destroy foreign proteins. Antibodies are produced by B-lymphocytes (also known as B-cells).

The main functions of B-cells are to become sensitized to a specific foreign protein (antigen) and to produce antibodies
directed specifically against that protein. The antibody (rather than the actual B-cell) causes one of several actions to
neutralize, eliminate, or destroy that antigen.

The cells with the most direct role in AMI are the B-cells. Macrophages and T-lymphocytes (discussed later under Cell-
Mediated Immunity, p. 373) work with B-cells to start and complete antigen-antibody interactions. Therefore, for optimal
AMI, the entire immune system must function adequately.

The sustained immunity, or memory, function of antibody-mediated immunity (AMI) provides us with long-lasting immunity
to a specific antigen. Sustained immunity results from memory B-cells made during the lymphocyte sensitization stage.
These memory cells remain sensitized to the specific antigen to which they were originally exposed. On re-exposure to the
same antigen, the memory cells rapidly respond. First, the memory cells divide and form new sensitized blast cells and new
sensitized plasma cells. The blast cells continue to divide, producing many more sensitized plasma cells. The sensitized
plasma cells rapidly make large amounts of the antibody specific for the sensitizing antigen.

This ability of the memory cells to respond on re-exposure to the same antigen that originally sensitized the B-cell allows a
rapid and large immune (anamnestic) response to the antigen. So much antibody is made that usually the invading organisms
are removed completely, so that the person does not become ill. Because of this process, most people do not become ill with
chickenpox or other infectious diseases more than once, even though they are exposed many times to the causative organism.
Without the action of memory, people would remain susceptible to specific diseases on subsequent exposure to the
organisms, and no sustained immunity would be generated.

CELL-MEDIATED IMMUNITY

Cell-mediated immunity (CMI), or cellular immunity, involves many white blood cell (WBC) actions and interactions. This
type of immunity is provided by lymphocyte stem cells that mature in the secondary lymphoid tissues of the thymus and
pericortical areas of lymph nodes. Certain CMI responses influence and regulate the activities of antibody-mediated
immunity (AMI) and inflammation by producing and releasing cytokines. For total immunocompetence, then, CMI must
function optimally.

Cell Types Involved in Cell-Mediated Immunity

The WBCs with the most important roles in CMI include several specific T-lymphocytes (T-cells) along with a special
population of cells known as natural killer (NK) cells. T-cells have a variety of subsets, each of which has a specific function.
NK cells are most effective in destroying unhealthy or abnormal self cells. The non-self cells most often harmed by NK cells
are cancer cells and virally infected body cells.

The three T-lymphocyte subsets that are critically important for the development and continuation of CMI are helper/inducer
T-cells, suppressor T-cells, and cytotoxic/cytolytic T-cells.

Helper/inducer T-cells easily recognize self cells versus non-self cells. In response to the recognition of non-self (antigen),
helper/inducer T-cells secrete lymphokines that can enhance the activity of other WBCs.

Most lymphokines secreted by the helper/inducer T-cells increase immune function. These lymphokines increase bone
marrow production of stem cells and speed up their maturation. Thus helper/inducer T-cells act as organizers in "calling to
arms" various squads of WBCs involved in inflammatory, antibody, and cellular defensive actions to destroy or neutralize
antigens.

Suppressor T-cells prevent continuous overreactions (hypersensitivity) when a person is exposed to non-self cells or
proteins. This function is important in preventing the formation of autoantibodies directed against normal, healthy self cells,
which is the basis for many autoimmune diseases.

Cytotoxic/cytolytic T-cells destroy cells that contain a processed antigen's major histocompatibility complex (MHC). This
activity is most effective against self cells infected by parasites, such as viruses or protozoa.

Cell-mediated immunity (CMI) helps protect the body through the ability to differentiate self from non-self. The non-self
cells most easily recognized by CMI are cancer cells and those self cells infected by organisms that live within host cells.
CMI watches for and rids the body of self cells that might potentially harm the body. CMI is important in preventing the
development of cancer and metastasis after exposure to carcinogens.

OBJECTIVE 20 (Carol)

INTERPRET A WBC WITH DIFFERENTIAL TO INDICATE NO IMMUNE PROBLEM, AN ACUTE

BACTERIAL INFECTION, A CHRONIC BACTERIAL INFECTION, OR AN ALLERGIC REACTION.

Pg. 882, 365 Figure 23-6 in Med/Surg, Pg. 1513 in Wongs.

WBC count normal range is 5000-10,000/ul, international reference units are 5.0-10.0 x 10 (9) cells/L Increased levels are
associated with infection, inflammation, autoimmune disorders, and leukemia. Decreased levels may indicate prolonged
infection or bone marrow suppression.

Wongs says an allergic reaction s/s are: urticaria, pruritus, flushing, asthmatic wheezing, and laryngeal edema.

Figure 23-6 on page 365 shows the differential of a normal white blood cell count.

Differential: % /mm3
Total WBC 100 10,000
Segs 62 6200
Bands 5 500
Monos 3 300
Lymphs 28 2800
Eosin 1.5 150
Baso 0.5 50

OBJECTIVE 21 (Yvonne)

Explain how complement activation and fixation (one type of opsonization) assists in protection from infection. Pg
367 Iggy

In inflammation, opsonins coat a target cell –which is called opsonization—so its easier for a phagocytic cell to stick to it.
One type of opsonization is complement activation and fixation. Twenty different types of inactive complement proteins are
present in the blood. These proteins are made by the liver. With proper stimulation, each complement protein is activated,
joins other activated complement proteins, surrounds an antigen, and “fixes” or sticks to the antigen. Complement fixation
occurs quickly as a cascade or chain reaction.

OBJECTIVE 22 (Kulwinder)

Al l info found in iggy. 368-373

Compare the cells, function and protective actions of the AMI and CMI.

ANTIBODY-MEDIATED IMMUNITY

Antibody-mediated immunity (AMI), also known as humoral immunity, involves antigen-antibody interactions to neutralize,
eliminate, or destroy foreign proteins. Antibodies are produced by B-lymphocytes (also known as B-cells).

Purpose

The main functions of B-cells are to become sensitized to a specific foreign protein (antigen) and to produce antibodies
directed specifically against that protein. The antibody (rather than the actual B-cell) causes one of several actions to
neutralize, eliminate, or destroy that antigen.

Cell Types Involved in Antibody-Mediated Immunity

The cells with the most direct role in AMI are the B-cells. Macrophages and T-lymphocytes work with B-cells to start and
complete antigen-antibody interactions. Therefore, for optimal AMI, the entire immune system must function adequately.

B-cells start as stem cells in the bone marrow, the primary lymphoid tissue. Those stem cells destined to become B-cells
commit early to the lymphocyte pathway (see Figure 23-3). At the point of commitment, these stem cells are restricted to
lymphocyte development. The lymphocyte stem cells are released from the bone marrow into the blood. They then migrate
into many secondary lymphoid tissues, where maturation is completed.

Protective Actions:

Exposure: (invasion)

For a person to first make an antibody that can exert its effects on a specific antigen the antigen must first enter the person.
Not all exposures result in antibody production

Antigen Recognition

To begin making antibodies against an antigen the naïve unsensitized B cell must first recognize the antigen as non self. B
cells need the help of macrophages and helper inducer t cell to recognize an antigen.

Lymphocyte sensitization

Once the b cell recognizes the antigen as non self the b cell is sensitized to this antigen. A single naïve b cell can become
sensitized only once. B CELL CAN BE SESITIZED TO ONLY ONE TYPE OF ANTIGEN

Antibody release and production

Antibodies are produced by plasma cells. When fully stimulated each plasma cell can make as much as 300 molecules of
antibody per sec. each plasma cell produces antibodies specific only to the antigen that originally sensitized the parent B cell.

Antibody made by the plasma are released into the blood and other body fluids as free antibody. Each free antibody molecule
remains in the blood for 3 to 30 days.

Antibody antigen binding

Antibodies are Y shaped molecules.. the tips of the short arms fo the Y recognize the specific antigen and bind to it. Because
each antibody molecule has 2 tips each antibody can bind either to 2 separate antigens or to 2 areas of the same antigen

Antibody binging action:

The binging of antibody to antigen triggers reactions that neutralize, eliminate, or destroys the bound antigen. These actions
are:

Agglutination: is a clumping action that results from the antibody linking antigen together forming large
and small immune complexes.

Lysis: cell membrane destruction

Complement fixation: some classes of antibodies can remove or destroy antigen through complement
activation and complement fixation.

Precipitation: antibody molecules bind so much antigen that large insoluble antigen antibody complexes
are formed. Cannot stay in suspension in the blood.

Inactive neutralization: does not result in the immediate destruction of the antigen. Only small area of the antigen the
active site causes the harmful effects.

Sustained immunity

MEMORY: functions of antibody mediated immunity proviseds us with long lasting immunity to a specific antigen

CELL MEDIATED IMMUNITY: involves many WBC actions and interactions. This type of immunity is provided
lymphocyte stem cells that mature in the secondary lymphoid tissues of the thymus and periocortical areas of lymph nodes.

Cell Types Involved in Cell-Mediated Immunity

The WBCs with the most important roles in CMI include several specific T-lymphocytes (T-cells) along with a special
population of cells known as natural killer (NK) cells. T-cells have a variety of subsets, each of which has a specific function.

HELPER/INDUCER T-CELLS

The cell membranes of helper/inducer T-cells contain the T4 protein. Helper/inducer T-cells easily recognize self cells versus
non-self cells. In response to the recognition of non-self (antigen), helper/inducer T-cells secrete lymphokines that can
enhance the activity of other WBCs.

SUPPRESSOR T-CELLS

The membranes of suppressor T-cells contain the T8-lymphocyte antigen; Suppressor T-cells help regulate CMI.Suppressor
T-cells prevent continuous overreactions (hypersensitivity) when a person is exposed to non-self cells or proteins. This
function is important in preventing the formation of autoantibodies directed against normal, healthy self cells, which is the
basis for many autoimmune diseases.The suppressor T-cells secrete lymphokines that have an overall inhibitory action on
most cells of the immune system. These lymphokines inhibit both the growth and activation of immune system cells.

CYTOTOXIC/CYTOLYTIC T-CELLS

Cytotoxic/cytolytic T-cells are also called TC-cells. Because they have the T8 protein present on their surfaces, they are a
subset of suppressor cells. Cytotoxic/cytolytic T-cells destroy cells that contain a processed antigen's major
histocompatibility complex (MHC). This activity is most effective against self cells infected by parasites, such as viruses or
protozoa.Parasite-infected self cells have both self MHC proteins (universal product code) and the parasite's antigens on the
cell surface. This allows the person's immune system cells to recognize the infected self cell as abnormal, and the
cytotoxic/cytolytic T-cell can bind to it.When the cytotoxic/cytolytic T-cell binds to the infected cell's MHC complex, the
cytotoxic/cytolytic T-cell makes holes in the membrane of the infected cell and delivers a "lethal hit" of enzymes to the
infected cell, causing it to lyse and die. Once the lethal hit has been delivered to the infected cell, the cytotoxic/cytolytic T-
cell releases the dying infected cell and can then attack and destroy other infected cells that carry the same antigen MHC
complex.

NATURAL KILLER CELLS

Natural killer (NK) cells are also known as CD16+ cells and are very important in providing CMI. The actual site of NK cell
differentiation and maturation is unknown. Although this cell type has some T-cell features, it is not a true T-cell subset.NK
cells have direct cytotoxic effects on some non-self cells. Unlike cytotoxic/cytolytic T-cells, NK cells can exert these cell
killing effects without first being sensitized. Nor do they need to share any of the MHC proteins in common with the non-self
cell. The cell killing actions of NK cells are independent of the interactions of other white blood cells. NK cells conduct
"seek and destroy" missions in the body to eliminate non-self cells.NK cells are most effective in destroying unhealthy or
abnormal self cells. The non-self cells most often harmed by NK cells are cancer cells and virally infected body cells.

Cytokines

CMI regulates the immune system by the production and activity of cytokines. Cytokines are small protein hormones
produced by the many WBCs (and some other tissues). Cytokines made by the macrophages, neutrophils, eosinophils, and
monocytes are monokines; cytokines produced by T-cells are lymphokines.

Cytokines work like other types of hormone: one cell produces a cytokine, which in turn exerts its effects on other cells of
the immune system. The cells responding to the cytokine may be located close to or remote from the cytokinesecreting cell.
The cells that change their activity when a cytokine is present are "responder" cells. For a responder cell to respond to the
presence of a cytokine, the responder cell must have a specific receptor to which the cytokine can bind. Once the cytokine
binds to its receptor, the responder cell changes its activity.

Protection Provided by Cell-Mediated Immunity

Cell-mediated immunity (CMI) helps protect the body through the ability to differentiate self from non-self. The non-self
cells most easily recognized by CMI are cancer cells and those self cells infected by organisms that live within host cells.
CMI watches for and rids the body of self cells that might potentially harm the body. CMI is important in preventing the
development of cancer and metastasis after exposure to carcinogens.

OBJECTIVE 23 (Maureen)

Compare the different types of antibody-immunity (active and passive immunity) for their protection effectiveness
and duration of immunity. Iggy 372-3

Active Immunity

Active immunity occurs when antigens enter the body and the body responds by making specific antibodies against the
antigen. This type of immunity is active because the body takes an active part in making the antibodies. Active immunity can
occur under natural or artificial conditions.

NATURAL ACTIVE IMMUNITY

Natural active immunity occurs when an antigen enters the body without human assistance and the body responds by actively
making antibodies against that antigen (e.g., chickenpox virus). Most of the time, the invasion that triggers antibody
production usually also causes the disease. However, processes occurring in the body at the same time as infection create
immunity to that antigen. Thus the person will not become ill after a second exposure to the same antigen. This type of
immunity is the most effective and the longest lasting.

ARTIFICIAL ACTIVE IMMUNITY

Artificial active immunity is the protection developed by vaccination or immunization. This type of immunity is used to
prevent infections or illnesses (e.g., tetanus, diphtheria, polio) that have such serious consequences that avoiding the disease
altogether is most desirable. Small amounts of specific antigens are placed as a vaccination into a person. The person's
immune system responds by actively making antibodies against the antigen. Because antigens used for this procedure have
been specially processed (attenuated) to make them less likely to grow in the body, this exposure does not cause the disease.
Artificial active immunity lasts many years, although repeated but smaller doses of the original antigen are required as a
"booster" to retain the protection.

Passive Immunity

Passive immunity occurs when antibodies against an antigen are in a person's body but were not created there. Rather, these
antibodies are transferred to the person's body after being made in the body of another person or animal. Because these
antibodies are foreign to the receiving person, the antibodies are recognized as non-self and eliminated quickly. For this
reason, passive immunity only provides immediate, short-term protection against a specific antigen.

Natural passive immunity occurs when antibodies are passed from the mother to the fetus via the placenta or to the infant
through colostrum and breast milk.

Artificial passive immunity involves injecting a person with antibodies that were produced in another person or animal. This
type of immunity is used when a person is exposed to a serious disease for which he or she has little or no actively acquired
immunity. Instead, the injected antibodies are expected to inactivate the antigen. This type of immune protection is
temporary, lasting only days to a few weeks. Some of the problems in which artificial passive immunity may be used include
exposure to rabies, tetanus, and poisonous snake bites.

AMI works with inflammation to protect against infection. However, AMI can provide the most effective, long-lasting
immunity only when its actions are combined with those of cell-mediated immunity.

OBJECTIVE 24 (Okju)

Describe how the immune system responds to transplanted organs or tissues. (Iggy pg. 376)

Transplant rejection is a normal response of the immune system that can damage or destroy the transplanted organ.

Natural killer (NK) cells and cytotoxic/cytolytic T-cells also destroy cells from other people or animals. Although this action
is usually helpful, it is also responsible for rejection of grafts and transplanted organs. Because the solid organ transplanted
into the host is seldom a perfectly identical match of universal product codes (human leukocyte antigens [HLAs]) between
the donated organ and the recipient host, the client's immune system cells recognize a newly transplanted organ as non-self.
Without intervention, the host's immune system starts inflammatory and immunologic actions to destroy or eliminate these
non-self cells. This activity causes rejection of the transplanted organ. Graft rejection is a result of a complex series of
responses that change over time and involve different components of the immune system. Graft rejection can be hyperacute,
acute, or chronic.

HYPERACUTE REJECTION

Hyperacute graft rejection begins immediately on transplantation and is an antibody-mediated response. Antigen-antibody
complexes form in the blood vessels of the transplanted organ. The host's blood has pre-existing antibodies to one or more of
the antigens (including blood group antigens) present in the donated organ. The antigen-antibody complexes adhere to the
lining of blood vessels and activate complement. The activated complement in the blood vessel linings triggers the blood
clotting cascade, causing small clots to form throughout the new organ. Widespread clotting occludes blood vessels and leads
to ischemic necrosis, inflammation with phagocytosis of the necrotic blood vessels, and release of lytic enzymes into the new
organ. These enzymes cause massive cellular destruction and graft loss.

Hyperacute rejection occurs mostly in transplanted kidneys. The following clients are at greatest risk for hyperacute
rejection:

1. Those who have received donated organs of an ABO blood type different from their own
2. Those who have received multiple blood transfusions at any time in life before transplantation
3. Those who have a history of multiple pregnancies
4. Those who have received a previous transplant
The manifestations of hyperacute rejection are apparent within minutes of attachment of the donated organ to the host's blood
supply. The process cannot be stopped once it has started, and the rejected organ is removed as soon as hyperacute rejection
is diagnosed.

ACUTE REJECTION

Acute graft rejection occurs within 1 week to 3 months after transplantation. Two mechanisms are responsible. The first
mechanism is antibody mediated and results in vasculitis within the transplanted organ. This reaction differs from that of
hyperacute rejection in that blood vessel necrosis (rather than thrombotic occlusion) leads to the organ's destruction.
The second mechanism is cellular. Host cytotoxic/cytolytic T-cells and NK cells enter the transplanted organ through the
blood, penetrate the organ cells, start an inflammatory response, and cause lysis of the organ cells (Abbas & Lichtman,
2003).
Diagnosis of acute rejection is made by laboratory tests that show impaired function of the donated organ, along with biopsy
of the donated organ. Symptoms of acute rejection vary with each client and with the specific organ transplanted. For
example, when acute rejection occurs in a transplanted kidney, the client usually has some tenderness in the kidney area and
may have other general symptoms of inflammation.
An episode of acute rejection after solid organ transplantation does not automatically mean that the client will lose the new
organ. Drug management of host immune responses at this time may limit the damage to the organ and allow the graft to be
maintained.

CHRONIC REJECTION

The origin of chronic rejection is not clear, but it is similar to chronic inflammation and scarring. The smooth muscles of
blood vessels overgrow and occlude the vessels. Functional tissue of the donated organ is replaced with fibrotic, scarlike
tissue. Because this fibrotic tissue is not organ tissue, the transplanted organ's function is reduced in proportion to the amount
of normal tissue that is replaced by fibrotic tissue. This type of reaction is long-standing and occurs continuously as a
response to chronic ischemia caused by blood vessel injury. The results of chronic rejection are unique to different
transplanted organs. For example, in transplanted lungs, chronic rejection thickens small airways. In transplanted livers,
chronic rejection destroys bile ducts. In transplanted hearts, this process is called accelerated graft atherosclerosis (AGA) and
is the major cause of death in clients who have survived 1 or more years after heart transplantation (Augustine, 2000).
Although good control over host immune function can delay this type of rejection, the process probably occurs to some
degree with all transplanted solid organs. Because the fibrotic changes are permanent, there is no cure for chronic graft
rejection. When the fibrosis increases to the extent that the transplanted organ can no longer function, the only recourse is
retransplantation.

OBJECTIVE 25 (Josh)

Explain the actions and the short term and long terms effects of immunosuppressive drugs.(iggy page 377)

Immunosuppressive drugs such as cyclosporine, methotrexate, corticosteroids, and antithymocyte globulin (Kim, 2002). Care
is taken to avoid suppressing the new immune system to the extent that either the client is at risk for infection or the
transplanted cells stop engrafting.
Clients who take immunosuppressive drugs have an increased risk for infection and for cancer development.

Maintenance

The drugs used for routine immunosuppressive therapy after solid organ transplantation are combinations of specific
immunosuppressants (cyclosporine [Sandimmune, Neoral, Gengraf]), less specific immunosuppressants (azathioprine
[Imuran] or mycophenolate [CellCept, Myfortic]), and one of the corticosteroids, such as prednisone (Apo-Prednisone ,
Delta-sone ) or prednisolone (Delta-Cortef) (Table 23-6). Cyclosporine induces the specific and effective suppression of
rejection. This drug, however, induces major long-term adverse actions and is expensive (see the Resource Management box
on p. 378.) The dosage of all immunosuppressive agents is adjusted to the immune response of each client. Treatment with
these agents increases the risk for bacterial and fungal infections and for cancer development.

TABLE 23-6 Drugs Used to Prevent or Treat Transplant Rejection

OBJECTIVE 26 (Joe)

Describe the key nursing implications clients receiving immunosuppressive drugs.

• Place the client in a private room whenever possible.

• Use good hand washing technique before touching the client or any of his or her belongings.
• Ensure the client's room and bathroom are cleaned daily
• Do not use supplies from common areas for immunsuppressed clients. (ie keep a supply of drinking straws for the client
in their room)
• Limit the number of health care personnel entering the client's room.
• Monitor vital signs every four hours; not minor changes in temperature, which may suggest early sepsis.
• Inspect the client's mouth every 4 hours.
• Inspect open areas, such as IV sites, every four hours for manifestations of infection.
• Inspect the client's skin and mucous membranes at least every 8 hours.
• Change wound dressing daily.
• Obtain specimens of all suspicious areas for culture, and promptly notify physician.
• Assist the client in performing coughing and deep-breathing exercises
• encourage activity at appropriate level for the client's current health status
• change IV tubing daily
• limit visitors to healthy adults.
• Keep frequently used equipment in the room fore use by the client only (such as a stethoscope)
• Use strict aseptic technique for all invasive procedures
• Monitor the white blood cell count, especially the absolute neutrophil count daily.
• Avoid indwelling catheters
• Keep fresh flowers and potted plants out of the client's room.

OBJECTIVE 27 (Jodey)

Discuss the inflammation theory regarding the role of inflammation in disease processes.
Med/surg pg 363 (the chart in my objective I put in here cause it also has cell mediated and antibody mediated immunity
which Jake said today in lecture that we should refresh our memories on) Also the cells listed on the chart for the
inflammation response are listed on 364 and the following pages there after going into detail of their function and so on. It
would have been too long to add them to this objective.

Inflammation, sometimes called "natural" immunity, provides immediate protection against the
effects of tissue injury and invading foreign proteins. The ability to produce an inflammatory
response is critical to health and well-being. Inflammation differs from AMI and CMI in two
important ways:

1. Inflammatory protection is immediate but short term against the effects of injury or invading organisms. It does not
provide sustained, long-term immunity on repeated exposure to the same organisms.

2. Inflammation is a nonspecific body defense to invasion or injury and can be started quickly
by almost any event.

Inflammation is nonspecific; the same tissue responses occur with any type of injury or invasion,
regardless of the location on the body or the specific initiating agent. Thus inflammation triggered
by a scald burn to the hand is the same as inflammation triggered by excess stomach acid or
bacteria in the middle ear. How widespread the symptoms of inflammation are in the body depends
on the intensity, severity, duration, and extent of exposure to the initiating injury or invasion. For
example, a splinter in the finger triggers inflammation only at the splinter site, whereas a burn
injuring 60% of the skin surface results in an inflammatory response involving the entire body.

Inflammatory responses start tissue actions that cause visible and uncomfortable symptoms.
Despite the discomfort, these actions are important in ridding the body of harmful organisms.
However, if the inflammatory response is excessive, tissue damage may result. Inflammatory
responses also help start both antibody-mediated and cell-mediated actions to activate a full
immune response.

OBJECTIVE 28 (Jessica)

Discuss potential treatments for the inflammatory process.

Difficult to find precise info pg 74IGGY

Discusses the use of NSAIDS (non steroidal anti-inflammatory drugs) being very effective for inflammatory type
pain. Great for acute pain can be given orally or IV. Good for post-op pain. R.I.C.E (rest, ice, compression,
elevation) is used for inflammation from trauma. Ice works well for inflammation caused by injury. There are
specific anti-inflammatory drugs taken for systemic inflammation. Jake will hopefully cover this topic more
thoroughly; otherwise I will find out and post more soon.

OBJECTIVE 29 (Lori)

Define psychoneuroimmunology and discuss it’s implications on diseases of the immune system. P.199 Psych book

Psychoneuroimmunology: A Biopsychosocial Model

Cannon and Selye focused on the physical and mental responses of the nervous and endocrine systems to acute and chronic
stress. The psychoneuroimmunological model considers the immune system response, which is an integral part of the acute
or alarm phase (Mausch, 2000). Studies in psychoneuroimmunology (PNI) provided evidence that stress, through the
hypothalamic-pituitary-adrenal and sympathetic–adrenal medullary axes, can induce modulation of the immune system
(Yang & Glaser, 2002). The activation of the immune system sets up a bilateral process. Once activated by stress, the
immune system sends chemical messages (proinflammatory cytokines) to the brain. The brain then releases its own
cytokines, which signal the central nervous system to initiate a myriad of responses to help the body adapt to the stress. This
process changes neural activity in the brain, which in turn can alter everything that flows from neural activity—essentially
behavior, thought, and mood (Azar, 2001; DeAngelis, 2002). Thus, it seems that immune system responses are regulated by
the brain and behavior as well as by the presence of antigens (Lutz, Tarkowski, & Dudek, 2001). The PNI model helps
explain what clinicians and others have believed and witnessed for centuries: that there is a link between stress
(biopsychosocial), the immune system, and disease—a very clear mind-body connection that may alter health outcomes. The
immune response and the resulting cytokine activity in the brain also raise questions regarding the origins of psychological
and cognitive states such as depression and memory dysfunction.

PNI, as a purely biomedical framework, is still limited. There is a long way yet to go to show definite links between PNI
variables and disease; however, PNI research is becoming increasingly sophisticated. Investigators are examining how
psychosocial factors such as optimism and social support moderate the stress response; they are mapping the biological and
cellular mechanisms by which stress affects the immune system as well as testing new theories (DeAngelis, 2002).

TABLE 12-1 Some Reactions to Acute and Prolonged (Chronic) Stress

Acute Stress Can Cause

Prolonged Stress Can Cause

Uneasiness and concern

Anxiety and panic attacks

Sadness

Depression or melancholia

Loss of appetite

Anorexia or overeating

Suppression of the immune system

Lowered resistance to infections, leading to increase in opportunistic viral and bacterial infections

Increased metabolism and use of body fats

Insulin-resistant diabetes

Hypertension

Infertility

Amenorrhea or loss of sex drive

Impotence, anovulation

Increased energy mobilization and use

Increased fatigue and irritability

Decreased memory and learning

Increased cardiovascular tone

Increased risk for cardiac events (e.g., heart attack, angina, and sudden heartrelated death)

Increased risk of blood clots and stroke

Increased cardiopulmonary tone

Increased respiratory problems

OBJECTIVE 30 (Mandy)

Discuss the nursing implications for the following: Nutrition-related immunodeficiencies, Drug-induced
immunodeficiencies, and Radiation-induced immunodeficiencies:

This question is only asking for the nursing implications but I also summarized a little about each type of immunodeficiency.

Found in Iggy pg 448-450

Nutrition-related immunodeficiencies: Good nutrition is needed for proper immune function. WBCs are highly active cells
that constantly shed surface proteins and need nutrients to remake these components. Immunodeficiency related to nutrition
results from biologic, political, economic, and cultural factors. Immunodeficiency from poor nutrition can be prevented and
treated. Malnutrition can impair any aspect of immune function. The degree of impairment is related to the severity of
malnutrition. Nutrient excess, especially fats and carbohydrates, also have detrimental effects on immune function.

Protein-calorie malnutrition (PMC) affects all aspects of immune function. The greatest impairment occurs in cell-mediated
immunity, with decreased number of T-lymphocytes and thymic changes. The result is anergy (A state of immune
unresponsiveness) and increased risk for infection.

The incidence and severity of infectious disease increase among obese people. Impaired cell-mediated immunity and
decreased neutrophils activity occur with obesity, also making obese people at greater risk for infecting.

Here are some nursing implications:

• Nutritional counseling: Healthy eating and lifestyle, Food preparation, nutritional supplements.
• Measure height and weight when the client is admitted to the agency, reweighing at least weekly.
• Monitor the client’s ability to eat the prescribed diet and the amounts eaten.
• Obtain dietary consultation when needed.
• Assess and monitor laboratory values for serum albumin, prealbumin, and leukocyte counts.
• Use good hand washing before all contact with the client.
• Ensure that strict aseptic techniques are used for all invasive procedures.
• Assess the client every shift for manifestations of local or systemic infection and notify the physician of any
suspected infection.

Drug-induced immunodeficiencies: Several drug classes have major immunosuppressive effects. Some induce general
immunosuppression; others are more specific and target one part of the immune system more than another. Most cytotoxic
drugs interfere with all rapidly dividing cells. WBCs, including lymphocytes and phagocytes, rapidly divide and are
susceptible to this type of destruction. Corticosteroids are hormones used to treat many autoimmune diseases, neoplasms, and
endocrine disorders. Corticosteroids have both anti-inflammatory and immunosuppressive effects. They inhibit inflammation
by stabilizing blood vessel membranes and decreasing permeability, blocking the movement of neutrophils and monocytes.
Cyclosporine is a specific immunosuppressant that selectively suppresses the helper-induced T-lymphocytes by blocking
their growth and development. Cyclosporine is used to prevent organ transplant rejection and graft-versus-host disease.

Radiation-induced immunodeficiencies: Radiation is toxic to dividing and resting cells. Because most lymphocytes are
sensitive to radiation exposure can induce profound lymphopenia, causing general immunosuppression. Whether or not
immunodeficiency occurs after radiation therapy depends on the location and dose of radiation. Exposure to the iliac and
femur in adults can cause generalized immunosuppression because these bone areas are the primary blood cell-producing
sites.

Nursing implications for drug-induced immunodeficiencies and radiation-induced immunodeficiencies are similar and are
very similar to nutrition-related immunodeficiencies:

• Work closely with clients and other health care professionals to provide safe care to those at risk for infection.
• Good handwashing before contact with the client is essential for infection prevention.
• Health care professionals must use aseptic technique with any invasive procedure.
• Teach the client and family best practices to reduce the client’s risk for infection while at home. There is a long list of
client education of infection prevention on page 443 of iggy.

The main thing for anyone with immunodeficiencies is infection prevention and client education on how to avoid infection.

OBJECTIVE 30 (BRETT’s VERSION… we both did this one)

Discuss the nursing implications of the following:

Nutrition related immunodeficiencies: Good nutrition is needed for proper immune function. WBCS are highly active cells
that constantly shed surface proteins and need nutrients to remake these components. Protein calorie malnutrition can be
treated with supplements and should be started slowly. As clients consume calories and protein activity levels increase.

Drug induced immunodeficiencies; Several drug classes have major immunosuppressive effects. Most cytotoxic drugs
interfere with all rapid dividing cells. WBCs including lymphocytes and phagocytes rapidly divide and are susceptible to
these types of drugs. Corticosteroids keep T cells in the marrow reducing the number circulating resulting in lymphopenia
and suppressed cell mediated immunity. Corticosteroids interfere with immunoglobulin G production and reduce antibody
antigen binding. Cyclosporine is a specific immune suppressant that selectively suppresses the helper inducer T lymphocytes
by blocking their growth and development. Management of the client with treatment induced immunodeficiency aims to
improve immune function and protect him or her from infection. While the problem generally solves itself once
immunosuppressive therapy stops the potential for severe infections make this problem a major treatment concern.
Management revolves around preventing disease by hand washing and being careful with clients on immunosuppressive
drugs not to pass on infections.

Radiation Induced Immunodeficiencies: Radiation is toxic to dividing and resting cells. Lymphocytes are sensitive to
radiation therefore exposure can induce potential lymphopenia. The amount of immunosuppression depends on the amount
and location of the radiation.

OBJECTIVE 31 (Liz)

Describe best practices for reducing the risk for the nutrition related immunodeficiency, protein-calorie malnutrition?

• Measure height and weight when the client is admitted to the agency, reweighing at least weekly
• Monitor the client’s ability to eat the prescribed diet and the amounts eaten
• Obtain dietary consultation when needed
• Evaluate whether nutrients consumed are sufficient to meet basal and stress related energy needs
• Avoid prolonged use of standard IV fluids that provide less than 200 calories/L
• Assess and monitor laboratory values for serum albumin, prealbumin, and leukocyte counts
• Schedule tests and procedures so the that the client spends minimal time fasting

OBJECTIVE 32 (Kelly)

Explain how radiation-induced immunodeficiencies. Iggy 449

Radiation is toxic to dividing and resting cells. Because most lymphocytes are sensitive to radiation, exposure can induce
profound lymphopenia, causing general immunosuppresion. Whether or not immunodeficiency occurs after radiation
therapy depends on the location and dose of radiation. Exposure to the iliac and femur in adults can cause generalized
immunosuppresion because these bone areas are the primary blood cell producing sites.

OBJECTIVE 33 (Mandy)

Iggy pg 907

Describe best practices for the prevention of infection in an immunocompromised client:

• Avoid crowds and other large gatherings of people who might be ill

• Do not share personal toilet articles, such as toothbrushes, toothpaste, washcloths, or deodorant sticks, with others.

• If possible, bathe daily.

• Wash the armpits, groin, genitals, and anal area at least twice a day with an antimicrobial soap.

• Clean your toothbrush daily by either running it through the dishwasher or rinsing it in liquid laundry bleach and
water.

• Wash your hands thoroughly with an antimicrobial soap before you eat or drink, after touching a pet, after shaking
hands with anyone, as soon as you come home from any outing, and after using the toilet.

• Eat a low-bacteria diet, and avoid salads, raw fruits and vegetables, undercooked meat, pepper, and paprika.

• Wash dishes between uses with hot, sudsy water, or use a dishwasher.

• Do not drink water that has been standing for longer than 15 minutes.

• Do not reuse cups and glasses without washing.

• Avoid keeping turtles and reptiles as pets.

• Do not feet pets raw or undercooked meat.

• Take your temperature at least twice daily.

• Report any of the following manifestations of infection to your physician immediately: Temp. greater than 100 F;
Persistent cough (with or w/out sputum); pus or foul-smelling drainage from any open skin area or normal body
opening; presence of a boil or abscess; urine that is cloudy or foul smelling, or burning on urination.

• Take all meds. As prescribed.

• Avoid travel to areas of the world with poor sanitation or less-than-adequate health care facilities.

OBJECTIVE 34 (Christi)

"Identify drug categories that have the potential to reduce immune functions."

The following information explains in more detail but the gist is that for reducing immune function it's drugs known
as "immunosuppressants": cytotoxic drugs, corticosteroids, cyclosporine and "antibodies" aimed at certain
receptors. Med Surge pgs. 376-378 & 449

Drug-Induced Immunodeficiencies
Several drug classes have major immunosuppressive effects. Some induce general immunosuppression; others are more
specific and target one part of the immune system more than another.

CYTOTOXIC DRUGS

Most cytotoxic drugs interfere with all rapidly dividing cells. White blood cells (WBCs), including lymphocytes and
phagocytes, rapidly divide and are susceptible to this type of destruction. The result is a decrease in the number of
lymphocytes and phagocytic cells. Cytotoxic drugs interfere with the ability of lymphocytes to produce and release products
such as lymphokines and antibodies, causing general immunosuppression. Most cytotoxic drugs are used for cancer and
autoimmune disorders.

CORTICOSTEROIDS

Corticosteroids are hormones used to treat many autoimmune diseases, neoplasms, and endocrine disorders. Corticosteroids
have both anti-inflammatory and immunosuppressive effects. They inhibit inflammation by stabilizing blood vessel
membranes and decreasing permeability, blocking the movement of neutrophils and monocytes. These drugs disrupt the
synthesis of arachidonic acid, the main precursor for a variety of inflammatory chemicals.

Corticosteroids keep T-cells in the bone marrow, reducing the number of circulating T-cells and resulting in lymphopenia and
suppressed cell-mediated immunity.

Corticosteroids interfere with immunoglobulin G (IgG) production and reduce antibody-antigen binding. These drugs have
many effects that alter disease activity, and numerous side effects, including the following:

▪ Central nervous system changes, such as euphoria, insomnia, or psychosis

▪ Cardiovascular changes, such as hypertension or edema

▪ Gastrointestinal effects, such as gastric irritation, ulcers, and increased appetite (with weight gain)

▪ Other changes (e.g., hyperglycemia, muscle weakness, delayed wound healing, osteoporosis, and body fat
redistribution)

CYCLOSPORINE

Cyclosporine (Sandimmune, Neoral) is a specific immunosuppressant that selectively suppresses the helper-inducer T-
lymphocytes by blocking their growth and development. Cyclosporine is used to prevent organ transplant rejection and graft-
versus-host disease. This drug is occasionally used for disorders, such as uveitis, rheumatoid arthritis, and other autoimmune
diseases.

TREATMENT OF TRANSPLANT REJECTION

Rejection of transplanted solid organs involves all three components of immunity, although cell-mediated immune (CMI)
responses are most significant in the rejection process.

Maintenance

The drugs used for routine immunosuppressive therapy after solid organ transplantation are combinations of specific
immunosuppressants (cyclosporine [Sandimmune, Neoral, Gengraf]), less specific immunosuppressants (azathioprine
[Imuran] or mycophenolate [CellCept, Myfortic]), and one of the corticosteroids, such as prednisone (Apo-Prednisone ,
Delta-sone ) or prednisolone (Delta-Cortef) (Table 23-6). Cyclosporine induces the specific and effective suppression of
rejection. This drug, however, induces major long-term adverse actions and is expensive (see the Resource Management box
on p. 378.) The dosage of all immunosuppressive agents is adjusted to the immune response of each client. Treatment with
these agents increases the risk for bacterial and fungal infections and for cancer development.
Tacrolimus (Prograf) is used in maintenance therapy and rescue therapy. It is similar to erythromycin and specifically
suppresses T-cell actions, including production of interleukin-2 (IL-2). These effects occur through several mechanisms.
Without continuous stimulation by IL-2, helper/inducer T-cells and cytotoxic/cytolytic T-cells are slow to reproduce and do
not perform their usual functions. Suppression of these two cell populations allows the donated organ to remain free from
immunologic destruction. The general immunosuppression is not as profound and the host's risk for infection is not greatly
increased. Tacrolimus also prevents activation of unsensitized cytotoxic/cytolytic T-cells.

A newer approach to prevent transplant rejection for clients undergoing kidney transplantation is the use of monoclonal
antibodies directed against the IL-2 receptor site on activated T-cells (especially helper/inducer T-cells). These antibodies,
basiliximab (Simulect) or daclizumab (Zenapax), are given intravenously within 2 hours before the transplant surgery and
within the first few days after the surgery. By binding the antibodies to the IL-2 receptor site, T-cell growth and activation are
reduced for several months.
RESOURCE MANAGEMENT

TRANSPLANT REJECTION PROPHYLAXIS

Cost of Care

▪ The most useful agent in preventing rejection of transplanted solid organs is cyclosporin.

▪ Cost of maintaining therapeutic levels of this drug for an average-sized adult ranges between $1100 and $1500 per
month.

▪ Clients must take this drug daily for the life of the transplanted organ.

▪ The effectiveness of this drug is highly dependent on following manufacturer's directions for mixing and
administering.

▪ An antifungal agent, ketoconazole, when taken orally has been demonstrated to slow metabolism of cyclosporin and
maintain therapeutic blood levels at lower doses (about 40% to 50% of cyclosporin dose needed when taken without
ketoconazole).

▪ The cost of ketoconazole daily maintenance therapy is about $100 per month.

Implications for Nursing

Because of the high cost of medications to prevent transplant rejection, nurses need to incorporate proper medication
administration into their client teaching plans and reinforce this information frequently. Nurses can assist in cost reductions
by observing for sustained therapeutic blood levels of cyclosporin in clients and exploring what factors may be contributing
to this effect.

Data from Augustine, S. (2000). Heart transplantation: Long-term management related to immunosuppression,
complications, and psychosocial adjustments. Critical Care Clinics of North America, 12(1), 69–77; Drug Facts and
Comparisons. (2004). Drug facts and comparisons (58th ed.). St. Louis: Wolters Kluwer; and Personal communication, with
CVS Pharmacies, January 2004.

Rescue Therapy

Certain agents are used only to reduce the host's immunologic responses during rejection episodes, especially acute rejection.
These agents may be used in addition to or in place of the maintenance drugs in the host's normal treatment regimen.

ANTILYMPHOCYTE GLOBULIN

Antilymphocyte globulin (ALG) is an antibody (or group of antibodies) produced in an animal after the animal has been
exposed to human lymphocytes. The globulin can be made more specific by exposing the animal to human T-cells instead of
mixed lymphocytes. When these antihuman lymphocyte antibodies are given to humans, the antibodies selectively attack and
clear lymphocytes from body fluids, blood, and the transplanted organ. These agents are given only for a short time to
combat the acute rejection episode.
Most clients receiving ALG have some immunologic side effects, ranging from low-grade fever and malaise to serum
sickness and anaphylaxis. The side effects usually increase in intensity on repeated exposure to ALG.

MUROMONAB-CD3 (ORTHOCLONE OKT3)

Muromonab-CD3 is an antibody directed specifically against the human T-cell cell-surface antigen CD3. This antibody is
generated in mice rather than in horses. Because the agent is generated in mice, the clients receiving it rapidly develop
antimouse antibodies. These antimouse antibodies attack the CD3 and prevent its anti-T-cell activities. This antibody is most
effective against rejection during the first episode in which it is used. Its effect in combating graft rejection decreases with
each use.

Antibodies made in other animals, especially mice, cause side effects in humans because the animal proteins in the antibodies
are recognized as "foreign" by the human immune system. The incidence of side effects is decreasing because newer
antibodies have been "humanized." This process removes most of the mouse-specific proteins from the antibody and replaces
them with human specific proteins. The "humanized" antibodies made by mice now contain up to 95% human proteins rather
than mouse proteins.

TABLE 23-6 Drugs Used to Prevent or Treat Transplant Rejection

OBJECTIVE 35 (Amanda)

Mosby’s Diagnostic and Laboratory Test Reference 8th ed

 Define the following lab tests:
Rheumatoid Factor
Antinuclear Antibody Titer (ANA)
Erythrocyte Sedimentation Rate (ESR)
Serum Complement
Serum Protein electrophoresis
Serum immunoglobulins

p 825
Rheumatoid Factor: Blood test, negative result is <60 units/ml by nephelometric testing. Measures a type of IgM antibody
that acts as an antigen to the rest of the pt’s immune system (stimulates an immune response) known as rheumatoid factor
(RF). Approx. 80% of pt with rheumatoid arthritis have a positive RF titer. To be considered positive RF must be present in a
dilution greater than 1:80. Abnormal findings (increased levels) could indicate: rheumatoid arthritis, other autoimmune
diseases (eg., systemic lupus erythematosus), chronic viral infection, subacute bacterial endocarditis
Tuberculosis, chronic hepatitis, dermatomyositis, scleroderma, infectious mononucleosis, leukemis, cirrhosis, syphilis, renal
disease.

p. 90
Antinuclear Antibody Titer (ANA): blood test negative at dilution 1:40. This test is used to diagnose systemic lupus
erythematosus (SLE). “There are several different patterns of fluorocence seen through the UV microscome. When combined
with the specific subtype of ANA, the pattern can increase specificity of the ANA subtypes for the various autoimmune
diseases.” Since many patterns can be seen, increased levels (depending on pattern) may indicate: SLE, rheumatoid arthritis,
chronic hepatitis, periarteritis (polyarteritis) nodosa, dermatomyositis, scleroderma, infectious mononucleosis, raynaud’s
disease, sjogren’s syndrome, other immune diseases, leukemia, myasthenia gravis, cirrhosis.

P 404
Erythrocyte Sedimentation Rate (ESR): blood test with normal findings by Westergren method for:
• Male up to 15 mm/hr
• Female up to 20 mm/hr
• Child up to 10 mm/ hr
• Newborn 0-2mm/hr
Measures the rate that red blood cells (RBC) settle in saline or plasma over a specified time period. This test is not diagnostic
because it is not specific to any disease or disease process. It can be used to monitor disease therapy. Increased levels may
indicate: chronic renal failure, malignant diseases, bacterial infection, inflammatory diseases, necrotic tissue diseases,
hyperfibrinogenemia, macroglobulinemia, severe anemias such as iron deficiency or B12 deficiency. Decreased levels may
indicate: sickle cell anemia, spherocytosis, hypofibrinogenemia, polycythemia vera.

Last three are from Iggy, copied off page 397

Serum complement attaches to immune complexes in an attempt to destroy them. If a large amount of complement is used
in this lytic process, the concentration of free-floating complement in the blood diminishes. Normal values vary considerably,
depending on the laboratory technique used. An abnormal finding is indicated by a decrease in serum complement and is
seen primarily in clients with vasculitis.

In serum protein electrophoresis, the protein fractions of the plasma are measured, and an electrical current is used to
separate them. The level of alpha globulin is raised in acute inflammation; in chronic inflammatory conditions such as RA,
the level of gamma globulin is increased because of the increase in immunoglobulins.

The serum immunoglobulins can be separated into subtypes. In chronic inflammation, IgG is needed to combine with RF.
Thus in RA the IgG value is typically elevated.

OBJECTIVE 36 (Carol)

DESCRIBE THE FOLLOWING CONNECTIVE TISSUES DISORDERS/DISEASES, THE ROLE OF THE

IMMUNE SYSTEM WITH THE DISEASE AND THE MEDICAL AND NURSING MANAGEMENT.

Rheumatoid Arthritis: pg. 393,397,403 Med/Surg

Systemic lupus erythematosus pg. 409, 411, 412 Med/Surg

Rheumatoid arthritis is one of the most common connective tissue diseases and is the most destructive to the joints. It is a
chronic, progressive, systemic inflammatory autoimmune disease process that primarily affects the synovial joints, System
affects the body system, affecting many joints and other tissues.

In RA, autoantibodies (rheumatoid factors) are formed that attack healthy tissue, especially synovium, causing
inflammation. RF's consist mainly of immunoglobulin M and G, and they bind with antigens forming immune complexes.
Phagocytes attempt to engulf these complexes and as a result, release powerful enzymes such as cytokines. The B and T
lymphocytes of the immune systems are also stimulated and increase the inflammatory response.

Management of the disease. The health care provider, usually a rheumatologist, makes decisions about appropriate drug
therapy for clients with RA based on the severity of the disease. Mild disease is usually managed with NSAIDS or disease –
modifying agents. Other drugs are Immunosuppresive agents& steroids.

Systemic lupus erthymatosus is a chronic, progressive inflammatory connective tissue disorder that can cause major body
organs and systems to fail. It is characterized by spontaneous remissions and exacerbations and the onset may be acute or
insidious. The condition is potentially fatal, but the survival rate has improved dramatically most recently in countries where
SLE is diagnosed early and treated. Today more than 90% of clients with SLE are living 10 years afte diagnosis.
Improvements in determining the cause, diagnosis, and treatment of lupus account for the prolonged survival of these clients.

Lupus is thought to be an autoimmune process; that is, abnormal antibodies are produced and react with the clients tissues.
Antinuclear antibodies primarily affect the DNA withing th cell nuclei. As a result, immune complexes form in the serum
and organ tissues, which causes inflammation and damage. These complexes invade organs directly or cause vasculitis
which deprives the organs of arterial blood and oxygen.

Many clients with SLE have some degree of kidney involvement-the leading cause of death. Other causes of death from
SLE are cardiac and central nervous system involvement.

The aim of management of SLE is to treat the disease aggressively until remission. In addition to medications for skin
lesions, the health care provider often prescribes chronic steroid therapy to treat the systemic disease process. For renal or
CNS lupus, the health care provider may also prescribe immunosuppressive agents which are sometimes used for clients with
RA. Although clinical manifestations improve during remission, maintenance doses of these drugs are usually continued to
prevent further exacerbations of the disease. Observe for side effects and toxic effects of these medications and report their
occurrence to the physician.

OBJECTIVE 37 (Josh)

Discuss the bases and manifestations of allergy and autoimmunity.

Hypersensitivities/Allergies

Hypersensitivity or allergy is an increased or excessive response to the presence of an antigen (foreign protein or allergen) to
which the client has been previously exposed. These responses cause problems that range from uncomfortable (e.g., itchy,
watery eyes or sneezing) to life-threatening (e.g., allergic asthma, anaphylaxis, bronchoconstriction, or circulatory collapse).
The terms hypersensitivity and allergy are used interchangeably. Hypersensitivity reactions are classified into five basic
types, determined by differences in timing, pathophysiology, and clinical manifestations (Table 26-1). Each type may occur
alone or along with one or more other types.

Autoimmunity

Autoimmunity is a process whereby a person develops an inappropriate immune response. In this response, antibodies and/or
lymphocytes are directed against healthy normal cells and tissues. For unknown reasons, the immune system fails to
recognize certain body cells or tissues as self and thus triggers immune reactions. The responses, both antibody- and cell-
mediated, are similar to normal immune responses against invading organisms, but these reactions are now directed against
normal body cells. Causes of loss of recognition of self cells are not known.
Examples of diseases that have an autoimmune cause include systemic lupus erythematosus (SLE), polyarteritis nodosa,
scleroderma, rheumatoid arthritis, autoimmune hemolytic anemia, rheumatic fever, and Hashimoto's thyroiditis (Table 26-3).
Other diseases, such as type 1 diabetes mellitus, may have multiple causes, one of which is autoimmune.

Management of autoimmunities depends on the organ or organs affected. Anti-inflammatory drugs and immunosuppressive
drugs are commonly used along with symptomatic treatment.

OBJECTIVE 38 (Yvonne)

Explain the following hypersensitivity reactions. Include the medical and nursing management. Pg 454 Iggy

Type I IgE-mediated hypersensitivity

Type II cytotoxic hypersensitivity
Type III Immune complex hypersensitivity
Type IV Delayed hypersensitivity reactions
Type V Stimulatory reactions

Type I IgE-mediated hypersensitivity: Immediate- Most common type. Acute reaction- inflammation- occurs when IgE
responds to an antigen, such as pollen and causes the release of histamine and other vasoactive amines from basophils,
esosinophils and mast cells. Examples: hay fever, allergic asthma, anaphylaxis, allergic rhinitis. Allergens can be inhaled,
ingested, injected or by contact.

Monitor all types for signs of anaphylactic reaction which can be fatal.
N. I.: Identification through testing if unknown, obviously stopping the “culprit” and treatment with antihistamines,
corticosteroids, mast cell stabilizers, leukotriene antagonist (treats allergic rhinitis-“runny nose”), complementary and
alternative therapies, and/or desensitization

Type II cytotoxic hypersensitivity: Cytotoxic - Reaction of IgG with host cell membrane or antigen absorbed by host cell
membrane. Examples: autoimmune hemolytic anemia, Good pasture’s syndrome, myasthenia gravis.

Management: Assess patient’s knowledge, past history of uses and reactions. Discontinuation of the offending drug or blood
product. Plasmapheresis (Filtration of the plasma to remove specific substances) to remove auto antibodies maybe e
beneficial. Otherwise treatment is symptomatic. Monitor for signs of complications such as hemolytic crisis and renal failure
which may be life threatening.

Type III Immune complex hypersensitivity: Immune complex-mediated- Formation of immune complex of antigen and
antibody, which deposits in walls of blood vessels and results in complement release and inflammation. Examples: serum
sickness, vasculitis, systemic lupus erythematosus, rheumatoid arthritis.

Management: Treat fever, arthralgias, rash, lymphadenopathy, malaise, possibly polyarthritis and nephritis. Alert client to
possibility of serum sickness and what symptoms to look for whenever you give a foreign serum. Keep emergency
equipment and drugs close at hand in case the client has an anaphylactic reaction. Treatment is usually symptomatic;
antihistamines are given for itching and aspirin for arthralgias. Prednisone is given if symptoms are severe.

Type IV delayed hypersensitivity reactions: Delayed- Reaction of sensitized T-cells with antigen and release of
lymphokines, which activate macrophages and induce inflammation. Example: poison ivy, graft rejection, positive TB skin
test, sarcoidosis.

Management: removal of offending antigen is major focus. Treat symptomatically. Monitor reaction site and sites distal to
the reaction for circulation adequacy. Corticosteroids or other anti-inflammatory agents can reduce the discomfort and help
resolve the reaction more quickly.

Type V stimulatory reactions: Reaction of autoantibodies with normal cell-surface receptors, which stimulates a continual
overreaction of the target cell. Example: Graves’ disease, B-cell gammapathies.

Management: Involvement of only one organ, management focus on removing enough of the responding tissue to return the
function to normal. With Graves’ disease, thyroid tissue is either surgically removed or destroyed with radiation. If reaction
is more widespread, treatment focuses on reducing the production of auto antibodies through immunosuppression.
OBJECTIVE 39 (Kulwinder)

Discuss anaphylaxis prevention measures

All info found in iggy 459-460

HEALTH PROMOTION/ILLNESS PREVENTION

Because anaphylaxis has a rapid onset and a potentially fatal outcome (even with appropriate medical intervention),
prevention is critical. Teach the client with a history of allergic reactions to avoid allergens whenever possible, to wear a
medical alert bracelet, and to alert health care personnel about specific allergies. Some clients must carry an emergency
anaphylaxis kit (e.g., a bee sting kit with injectable epinephrine), or an epinephrine injector, such as the EpiPen automatic
injector (Dey, Napa, CA). The EpiPen device is an easy-to-use, spring-loaded injector that delivers 0.3 mg of epinephrine per
2-mL dose (Figure 26-3).

The medical records of clients with a history of anaphylaxis should prominently display the list of specific allergens. Ask the
client about drug allergies before giving any drug or therapeutic agent. Skin tests should be performed before giving any
substance that has a high incidence of causing anaphylactic reactions, such as iodine-containing dyes. Be aware of common
cross-reacting agents. For example, a client who is allergic to penicillin is also likely to react to cephalosporins because both
have a similar chemical structure. People who have an allergy to bananas are likely to have a latex allergy.

Take precautionary measures if an agent must be used despite a history of allergic reactions. Start an IV solution and place
intubation equipment and a tracheostomy set at the bedside. The client is often premedicated with diphenhydramine
(Benadryl, Allerdryl ). The substance is given first intradermally, then subcutaneously, and then intramuscularly in
increasing doses at 20- to 30-minute intervals so the initial dose by the next route does not exceed the final dose by the
previous route.

OBJECTIVE 40 (Maureen)

Discuss the nursing responsibilities for a client with anaphylaxis.

Interventions

Assess respiratory function first. Emergency respiratory management is critical during an anaphylactic reaction, because the
severity of the reaction increases with time. An airway must be established or stabilized immediately. Cardiopulmonary
resuscitation may be needed. Epinephrine (1:1000) 0.3 to 0.5 mL is given subcutaneously as soon as symptoms of systemic
anaphylaxis appear. This drug constricts blood vessels, improves cardiac contraction, and dilates the bronchioles. The same
dose may be repeated every 15 to 20 minutes if needed.

Antihistamines, such as diphenhydramine (Allerdryl , Benadryl) 25 to 100 mg are usually given IV, IM, or orally to treat
angioedema and urticaria. If needed, an endotracheal tube may be inserted or an emergency tracheostomy may be performed.

If the client can breathe independently, give oxygen to reduce hypoxemia. Start oxygen therapy via nasal cannula at 2 to 6
L/min or via face mask at 40% to 60% before arterial blood gas results are obtained. Monitor pulse oximetry to determine
oxygenation adequacy, with the goal of maintaining oxygen saturation greater than 90%. Arterial blood gases may be ordered
to determine therapy effectiveness. Use suction to remove excess mucous secretions, if indicated. Continually assess the
client's respiratory rate and depth. Assess breath sounds continually for bronchospasm and other abnormal breath sounds.
Elevate the bed to 45 degrees unless severe hypotension is also present.

For severe bronchospasm, the client is given theophylline 6 mg/kg IV over 20 to 30 minutes. If the client is taking
aminophylline regularly, no more than 3 mg/kg is given. Maintenance aminophylline (0.3 to 0.5 mg/kg/hr) is initiated. The
client may be given an inhaled beta-adrenergic agonist such as metaproterenol (Alupent) or albuterol (Proventil) via high-
flow nebulizer every 2 to 4 hours. Corticosteroids are added to emergency interventions, but they are not effective
immediately. Oral steroids are continued (at lower doses) after the anaphylaxis is under control to prevent the late recurrence
of symptoms.

Continually assess for changes in any body system or for adverse effects of drug therapy. For severe anaphylaxis, the client is
admitted to a critical care unit for cardiac, pulmonary arterial, and capillary wedge pressure monitoring. Observe the client
for fluid overload from the rapid drug and IV fluid infusions and report changes to the physician immediately. The client is
discharged from the hospital when respiratory and cardiovascular systems have returned to baseline.

OBJECTIVE 41 (Okju)

Identify the common drugs used as therapy for anaphylaxis. (Iggy pg. 460)

CHART 26-3 DRUG THERAPY for Anaphylaxis