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Influenza vaccine: se: pain, red, swelling.

Myalgia, fever, NVD, HA

A febrile nonhemolytic reaction is caused by antibodies to donor leukocytes that remain in the unit of blood or blood
component; it is the most common type of transfusion reaction. It occurs more frequently in patients who have had
previous transfusions (exposure to multiple antigens from previous blood products) and in Rh-negative women who
have borne Rh-positive children (exposure to an Rh-positive fetus raises antibody levels in the untreated mother).
The diagnosis of a febrile nonhemolytic reaction is made by excluding other potential causes, such as a hemolytic
reaction or bacterial contamination of the blood product. The signs and symptoms of a febrile nonhemolytic
transfusion reaction are chills (minimal to severe) followed by fever (more than 1 C elevation). The fever typically
begins within 2 hours after the transfusion is begun. Although the reaction is not life threatening, the fever, and
particularly the chills and muscle stiffness, can be frightening to the patient.
This reaction can be diminished, even prevented, by further depleting the blood component of donor leukocytes;
this is accomplished by a leukocyte reduction filter. Antipyretic agents can be given to prevent fever; however,
routine premedication is not advised because it can mask the beginning of a more serious transfusion reaction.

Acute Hemolytic Reaction

The most dangerous, and potentially life-threatening, type of transfusion reaction occurs when the donor blood is
incompatible with that of the recipient (i.e., type II hypersensitivity reaction). Antibodies already present in the
recipients plasma rapidly combine with antigens on donor erythrocytes, and the erythrocytes are destroyed in the
circulation (i.e., intravascular hemolysis). The most rapid hemolysis occurs in ABO incompatibility. Rh
incompatibility often causes a less severe reaction. This reaction can occur after transfusion of as little as 10 mL of
PRBCs. Although the overall incidence of such reactions is not high (1:20,000 to 1:40,000 units transfused [Leo &
Pedal, 2010]), they are largely preventable. The most common causes of acute hemolytic reaction are errors in blood
component labeling and patient identification that result in the administration of an ABO-incompatible transfusion.
Symptoms consist of fever, chills, low back pain, nausea, chest tightness, dyspnea, and anxiety. As the
erythrocytes are destroyed, the hemoglobin is released from the cells and excreted by the kidneys; therefore,
hemoglobin appears in the urine (hemoglobinuria). Hypotension, bronchospasm, and vascular collapse may result.
Diminished renal perfusion results in acute renal failure, and disseminated intravascular coagulation may also
occur. The reaction must be recognized promptly and the transfusion discontinued immediately (see the Nursing
Management for Transfusion Reactions section).
Acute hemolytic transfusion reactions are preventable. Meticulous attention to detail in labeling blood samples
and blood components and accurately identifying the recipient cannot be overemphasized. Bar coding methods can
be useful safeguards in matching a patients wristband with the label on the blood component (Pagliaro, Turdo, &
Capuzzo, 2009); however, these methods are not fail proof and do not reduce the nurses responsibility to ensure the
correct blood component is transfused to the correct patient.

Allergic Reaction
Some patients develop urticaria (hives) or generalized itching during a transfusion; the cause is thought to be a
sensitivity reaction to a plasma protein within the blood component being transfused. Symptoms of an allergic

reaction are urticaria, itching, and flushing. The reactions are usually mild and respond to antihistamines. If the
symptoms resolve after administration of an antihistamine (e.g., diphenhydramine [Benadryl]), the transfusion may
be resumed. Rarely, the allergic reaction is severe, with bronchospasm, laryngeal edema, and shock. These reactions
are managed with epinephrine, corticosteroids, and vasopressor support, if necessary.
Giving the patient antihistamines or corticosteroids before the transfusion may prevent future reactions. For
severe reactions, future blood components are washed to remove any remaining plasma proteins. Leukocyte filters
are not useful to prevent such reactions, because the offending plasma proteins can pass through the filter.

Circulatory Overload
If too much blood is infused too quickly, hypervolemia can occur. This condition can be aggravated in patients who
already have increased circulatory volume (e.g., those with heart failure). PRBCs are safer to use than whole blood. If
the administration rate is sufficiently slow, circulatory overload may be prevented. For patients who are at risk for,
or already in, circulatory overload, diuretics are administered after the transfusion or between units of PRBCs.
Patients receiving fresh-frozen plasma or even platelets may also develop circulatory overload. The infusion rate of
these blood components must also be titrated to the patients tolerance.
Signs of circulatory overload include dyspnea, orthopnea, tachycardia, and sudden anxiety. Jugular vein
distention, crackles at the base of the lungs, and an increase in blood pressure can also occur. If the transfusion is
continued, pulmonary edema can develop, as manifested by severe dyspnea and coughing of pink, frothy sputum.
If fluid overload is mild, the transfusion can often be continued after slowing the rate of infusion and
administering diuretics. However, if the overload is severe, the patient is placed upright with the feet in a dependent
position, the transfusion is discontinued, and the primary provider is notified. The IV line is kept patent with a very
slow infusion of normal saline solution or a saline lock device to maintain access to the vein in case IV medications
are necessary. Oxygen and morphine may be needed to treat severe dyspnea (see Chapter 29).

Bacterial Contamination
The incidence of bacterial contamination of blood components is very low; however, administration of contaminated
products puts the patient at great risk. Contamination can occur at any point during procurement or processing but
often results from organisms on the donors skin. Many bacteria cannot survive in the cold temperatures used to
store PRBCs, but some organisms can do so. Platelets are at greater risk of contamination because they are stored at
room temperature. Recently, blood centers have developed rapid methods of culturing platelet units, thereby
diminishing the risk of using a contaminated platelet unit for transfusion.
Preventive measures include meticulous care in the procurement and processing of blood components. When
PRBCs or whole blood is transfused, it should be administered within a 4-hour period, because warm room
temperatures promote bacterial growth. A contaminated unit of blood product may appear normal, or it may have
an abnormal color.
The signs of bacterial contamination are fever, chills, and hypotension. These manifestations may not occur until
the transfusion is complete, occasionally not until several hours after the transfusion. As soon as the reaction is
recognized, any remaining transfusion is discontinued (see the Nursing Management for Transfusion Reactions
section). If the condition is not treated immediately with fluids and broadspectrum antibiotics, sepsis can occur.

Sepsis is treated with IV fluids and antibiotics; corticosteroids and vasopressors are often also necessary
(see Chapter 14).

Transfusion-Related Acute Lung Injury

Transfusion-related acute lung injury (TRALI) is a potentially fatal, idiosyncratic reaction that is defined as the
development of acute lung injury occurring within 6 hours after a blood transfusion. All blood components have
been implicated in TRALI, including IVIG, cryoprecipitate, and stem cells. TRALI is the most common cause of
transfusion-related death (Cherry, Steciuk, Reddy, et al., 2008).
The underlying pathophysiologic mechanism for TRALI is unknown but is thought to involve antibodies in the
donors plasma that react to the leukocytes in the recipients blood. Occasionally, the reverse occurs, and antibodies
present in the recipients plasma agglutinate the antigens on the few remaining leukocytes in the blood component
being transfused. Another theory suggests that an initial insult to the patients vascular endothelium causes
neutrophils to aggregate at the injured endothelium. Various substances within the transfused blood component
(lipids, cytokines) then activate these neutrophils. Each of these pathophysiologic mechanisms can contribute to the
process (Fung & Silliman, 2009). The end result of this process is interstitial and intraalveolar edema, as well as
extensive sequestration of WBCs within the pulmonary capillaries.
Onset is abrupt (usually within 6 hours of transfusion, often within 2 hours). Signs and symptoms include acute
shortness of breath, hypoxia (arterial oxygen saturation [SaO2] less than 90%; partial pressure of arterial oxygen
[PaO2] to fraction of inspired oxygen [FIO2] ratio of less than 300), hypotension, fever, and eventual pulmonary
edema. Diagnostic criteria include hypoxemia, bilateral pulmonary infiltrates (seen on chest x-ray), no evidence of
cardiac cause for the pulmonary edema, and no other plausible alternative cause within 6 hours of completing
transfusion. Aggressive supportive therapy (e.g., oxygen, intubation, fluid support) may prevent death.
Although TRALI can occur with the transfusion of any blood component, it is more likely to occur when plasma
and, to a lesser extent, platelets are transfused. One commonly used preventive strategy involves limiting the
frequency and amount of blood products transfused. Another entails obtaining plasma and possibly platelets only
from men or from women who have never been pregnant (and, consequently, are less likely to have developed
offending antibodies). The efficacy of this approach and its impact on the availability of these blood components
remain unclear (Mller, Porcelijn, & Vlaar, 2012).

Delayed Hemolytic Reaction

Delayed hemolytic reactions usually occur within 14 days after transfusion, when the level of antibody has been
increased to the extent that a reaction can occur. The hemolysis of the erythrocytes is extravascular via the RES and
occurs gradually.
Signs and symptoms of a delayed hemolytic reaction are fever, anemia, increased bilirubin level, decreased or
absent haptoglobin, and possibly jaundice. Rarely, there is hemoglobinuria. Generally, these reactions are not
dangerous, but it is important to recognize them because subsequent transfusions with blood products containing
these antibodies may cause a more severe hemolytic reaction. However, recognition is also difficult because the
patient may not be in a health care setting to be tested for this reaction, and even if the patient is hospitalized, the
reaction may be too mild to be recognized clinically. Because the amount of antibody present can be too low to

detect, it is difficult to prevent delayed hemolytic reactions. Fortunately, the reaction is usually mild and requires no
The complications that have been described represent a real risk to any patient any time a blood component is
administered. However, patients with long-term transfusion requirements (e.g., those with myelodysplastic
syndrome, thalassemia, aplastic anemia, sickle cell anemia) are at greater risk for infection transmission and for
becoming more sensitized to donor antigens, simply because they are exposed to more units of blood and,
consequently, more donors. A summary of complications associated with long-term transfusion therapy is given
inTable 32-5.
Iron overload is a complication unique to people who have had long-term PRBC transfusions. One unit of PRBCs
contains 250 mg of iron. Patients with chronic transfusion requirements can quickly acquire more iron than they can
use, leading to iron overload. Over time, the excess iron deposits in body tissues and can cause organ damage,
particularly in the liver, heart, testes, and pancreas. Promptly initiating a program of iron chelation therapy can
prevent end-organ damage from iron toxicity.

Hematopoietic stem cell transplantation (HSCT) is a therapeutic modality that offers the possibility of cure for some
patients with hematologic disorders such as severe aplastic anemia, some forms of leukemia, and thalassemia. It can
also provide longer remission from disease even when cure is not possible, such as in multiple myeloma.
Hematopoietic stem cells may be transplanted from either allogeneic or autologous donors. For most hematologic
diseases, allogeneic transplant is more effective; here, stem cells are obtained from a donor whose cells match those
of the patient. In contrast, the patients own stem cells are harvested and then used in autologous transplant.
(SeeChapter 15 for a detailed discussion of these procedures.)
In older patients, the bone marrows ability to respond to the bodys need for blood cells (erythrocytes, leukocytes,
and platelets) may be decreased. This decreased ability is a result of many factors, including diminished production
of the growth factors necessary for hematopoiesis by stromal cells within the marrow or a diminished response to
the growth factors (in the case of erythropoietin). In addition, in older patients, the bone marrow may be more
susceptible to the myelosuppressive effects of medications. As a result of these factors, when an older person needs
more blood cells, the bone marrow may not be able to increase production of these cells adequately. Leukopenia (a
decreased number of circulating leukocytes) or anemia can result.
Vitamin B12 and Folate Metabolism. Vitamin B12 and folate are required for the synthesis of deoxyribonucleic
acid (DNA) in RBCs. Both vitamin B12 and folate are derived from the diet. Folate is absorbed in the proximal small
intestine, but only small amounts are stored within the body. If the diet is deficient in folate, stores within the body
quickly become depleted. Because vitamin B12 is found only in foods of animal origin, strict vegetarians may ingest
little vitamin B12. Vitamin B12 combines with intrinsic factor produced in the stomach. The vitamin B12intrinsic
factor complex is absorbed in the distal ileum. People who have had a partial or total gastrectomy may have limited
amounts of intrinsic factor, and therefore the absorption of vitamin B12 may be diminished. The effects of either
decreased absorption or decreased intake of vitamin B12 are not apparent for 2 to 4 years.
Vitamin B12 and folate deficiencies are characterized by the production of abnormally large erythrocytes
calledmegaloblasts. Because these cells are abnormal, many are sequestered (trapped) while still in the bone
marrow, and their rate of release is decreased. Some of these cells actually die in the marrow before they can be
released into the circulation. This results in megaloblastic anemia.

Complete Blood Count

Without Differential
RBC (erythrocytes)

With Differential all +

Neutrophils (bands/stabs-immature)
(segmented- mature)

They carry hemoglobin to provide oxygen to tissues. The lifespan is 120 days. They are produced through
a process called erythropoiesis. It becomes a RBC when erythropoietin is released from the kidney or
liver which stimulates the bone marrow to produce the RBC. Mature erythrocytes have no nuclei.
Erythropoesis Myeloid stem cells produce erythroblasts (immature cells, aka reticulocytes). The cell then
matures which causes a loss of dark staining material and slight shrinkage. The mature RBC is then
released into circulation
Erythropoietin facilitates the transformation of myeloid stem cell to an erythroblast. If kidney detects low
levels of oxygen (when theres fewer red cells available to bind oxygen, or people that live in high
altitudes), erythropoietin levels increase. Increased erythropoietin stimulates the marrow to increase
production of RBCs. The whole process takes about 5 days.
Oxygen readily detaches from hemoglobin at sites where it is needed in the tissues where it is needed for
cellular metabolism.
Reticulocytes are slightly immature forms of RBCs. It occurs normally as a response to an increased
demand for erythrocytes as in bleeding or various disease states and when the liver or spleen take over as
the site of erythropoeisis.
Red blood cell destruction happens when they become trapped in small blood vessels and the spleen. They
are removed from the blood by the reticuloendothelial cells typically in the liver and spleen. Most of their
hemoglobin is recycled. Some hemoglobin breaks down to form bilirubin and gets secreted in the bile. Most
of the iron is recycled to form new hemoglobin molecules within the bone marrow. Small amounts are lost
daily in feces and urine, mentraual cycle.
It is regulated by:
1. O2 levels: A large molecule of Hemoglobin is on the surface of the RBC. HEME=iron and this is
where o2 attaches. Globin= protein and this is where co2 attaches.

2. Nutrition: Protein, iron, folate, B12, Niacin, and Vitamin C

RBC Polycythemia or Erythrocytosis

High altitude due to low o2 concentration

Physical training

Overproduction by bone marrow

Polycythemia vera is an increase in bone marrow production not due to hypoxia
Hypoxia due to increased secretion of erythropoietin
Dehydration due to increased RBC in the amount of fluid
Diarrhea, nausea, fever, diruetics, heat
Secondary polycythemia: caused by excessive production of erythropoietin. May occur in response
to dec o2 in heavy cig smoking, COPD, cyanotic heart disease, or high altitude. Can also occur from
neoplasms that stimulate erythopoetic production.

RBC Anemia

Where RBC and/or Hgb

Blood loss due to trauma
GI bleed
Nurtion deficiency of iron, folate, B6, Copper, B12
Hemolytic Anemai
Destruction of RBC
Bone marrow suppression
Leukemia where RBC are destroyed
Overhydration which dilutes the numbers of RBC
Lack of erythropoietin in kidney or liver disease

Iron Deficiency
Rate of iron absorption is regulated by the amount of iron already stored in body and by the rate
of erythrocyte production.
Iron is stored as ferritin. When it is needed, it is released into the plasma where it binds to
transferrin. Then it is transported into the membranes of the normoblasts in the marrow. There it
is incorporated into hemoglobin.
Iron is lost in feces, bile, blood, or mucosal cells from intestine
When there is iron deficiency, bone marrow iron stores are rapidly depleted. Hemoglobin
synthesis is depressed. Erythrocytes produced are small and low in hemoglobin.
Iron deficiency in an adult is usually indicative of blood loss from GI or heavy menstrual flow.
So low iron may be a sign of GI bleed or colon cancer.
1/3 of Hct. Men 13.2-17.3 women 11.7-16.0 preg 9.5-15 newborn 14-24, child 11-16. Heme= iron gives
piment. Glbin= protein. O2 carrying protin to distribute o2. Has 4 binding sites and that is saturated so o2
will be 100.


Abnormal type: hydradtion status

Cant use hgb to look at o2 sat
Iron def d/t low heme

It is a %. Proportion of RBC to plasma. Always consider hydration status. Should be x3 of hgb. Men 39-50%,
women 35-47%, newborn 55-68, child 36-40

Hct= plasma, RBC

Inverse relationship
Rbc are swimming in less fluid
Can result from burns, fluid loss, treat with hydration

Hct= plasma, same RBC or decreased RBC

True decreased rbc from massive blood loss
Values are normal at first then plasma volume returns to normal and RBC lost is still low. Treat with

Mean Corpuscular volume

MCV. measures size of RBC. Normocytic
Macrocytic: larger. Could indicate anemia d/t: VB12, folic acid, common in liver disease, recent alc intake,
can assess cirrhosis
Microcytic: could indicate iron def anemia, thalassemia or lead poisoning
RBC is 3, MCV is normal= lost RBC
RBC is 3, MCV is high= pernicious or folic acid
Mean Corpuscular Hemoglobin (MCH)
Amt of hgb on 1 RBC. It is a measurement of weight
Macrocytic: weigh more
Microcytic: wt less. Hypochromic is less color due to decreased hgb, iron def, thalassemis
Calculation of amt of 02 carrying hgb inside the RBCS
Mean corpuscular hemoglobin concentration
MCHC. % of hgb inside rbcs. Determines color.
Hyperchromic: none
Hypocromic: less color, less hgb concentration on cell= iron def, thalassemis
RBC distribution width
RDW. Indicates of varation in sixe. Only an increase is significant
Macrocytic: if RBC is larger the RDW is increased happens with folate or B anemia
Microcytic: if RBC is smaller it will increase RDW with iron def, thalassemia
Diet: protein, organs eggs, prune juice
Blood transufion
Drug therapy: erythropeitin, stims bone marrow (subq injection)

02 to stabalize
Bone Marrow
It is highly vascular. There are stem cells inside. When the stem cells are stimulated they complete
differentiation and grow into either:
1. Myeloid stem cells. They contain erythrocytes, leukocytes, and platelets.
2. Lyphoid Stem cells. They contain T or B lymphocytes.
WBC (Leukocytes) Normal value 4,000-11,000/ ul
Neutrophils: 50-70%, essential in preventing or limiting bacterical infection via phagocytosis, early
phase of inflammation to engulf pathogen. Arrive at injury one hour after the onset of an inflammatory
reaction and intitiate phagocytosis. Essential in preventing and limiting bacterial infection. They
differentiate in 10 days, stay in circulation from marrow for 6 hours, and die within 1-2 days. With an
infection, large numbers rapidly release into circulation!
Segs or segmented= more seniors
Bands or Stabs= more babies
Critical Value is less than 1000
Neutrophils Neutrophilia

Infection bacteria
Tissue injury

Neutrophils Neutropenia. You are at increased risk for infection. GI and skin are most
common areas of infection. Risk for infection also increases with the length of time that
neutropenia persists.

Viral diseases such as hepatitis, MMR, sepsis, mono- inc destruction

Bacterial infection- inc destruction
Chemo or radiation
Antiobiotics like Penicillin, Cephalosporin)
Psychotropic (Tricyclic Anti-depressants
Aplastic anemia due to medications or toxins- dec neutro
Metastatic cancer, lymphoma, leukemia-dec neutro
Myelodysplastic syndromes- dec neutron
Megaloblastic anemia- ineffective granulocytopoiesis
*dont always show sx

Eosinophils: 2-4%. Functions is phagocytosis, engulf antigen/antibody or parasites. Involved in allergic

reactions by neutralizing histamine; also digests foreign proteins. It has granules that contain histamine.

Allergic reaction because they neutralize histamine

Hodgkins Lymphoma
Rheumatoid Arthritis


Increased corticosteroids for therapy

Basophils: 0-2%. Functions: have chemical meidators released in response to tissue injury, allergic and
inflammatory response called hypersensivitiy reactions. They have cytoplasmic granules that contain
Heparin, Serotonin, Histamine. These levels increase during healing process

Rare Bone Marrow alterations


Nearly undetectable due to normal low levels

Allergic reaction
Acute infection

Lymphocytes: 20-40%. Function is cellular and humoral response. Responsible for immune system.
Primary function is to attack foreign material. They are produced from the lymphoid stem cells or the
thymus (T cells). They complete differentiation in lymph nodes and tissue of intestine and spleen. They are
the principal cell of the immune system, producing antibodies and identifying other cells and organisms as

3 types:
T lymphocytes: 60-90%. Function is the responsibility for cell-mediated immunity. It recognizes material
as foreign. It is like a surveillance system). Kills cells directly or releases lymphokines, substance that
enhances the activity of phagocytic cells. They are also responsible for delayed allergic reactions, rejection
of transplanted organs, and destruction of tumor cells. That is a process called cellular immunity
B lymphocytes: 4-25%. Function is the responsibility for humoral immunity. Many of them mature into
plasma cells to form antibodies which are a protein molecule that destroys foreign material by several
Plasma cell: Function is to secrete immunoglobulin, an antibody. This is also the mature form of B
Non T or B (natural killer): function is for immune defense system. They accumulate in the lypmphoid
tissue like the spleen, lymph nodes, and tonsils to mature there. They are potent killers of virus-infected
and cancer cells. They also secrete messenger proteins called cytokines to mobilize T and B cells into
Lymphocytes Lyphocytosis

Viral infection (mono, Hep)

Lymphocytes Lymphopenia

Autoimmune like lupus (SLE is systemic disease, no cure. Tx with immunosuppression. Black women
most. Runs in family)
When Neutrophils are increased

Monocytes: 4-8%. Function is phagocytosis of bacteria, dead cells, and tissue debris. Then migrate into
tissue and become macrophages. They are potent phagocytic cells and the 2nd to arrive at injury. They
transform into macrophages when they enter the tissues. Macrophages are active in spleen, liver,
peritoneum, and alveoli where they remove debris and phagocytize bacteria within the tissues.
Macrophages are particularly effective against fungi and viruses. They also digest old blood cells within the

Protozoan infection like malaria
Chronic condition like ulcerative colitis
Monocytic leukemia

Thrombocytes: Are also known as platelets. Their function is to provide a basis for coagulation to occur,
maintain homeostatis. They are a fragment of a megakaryocyte. They are formed from stem cells and are
stored in the spleen. They are produced in the marrow and are regulated in part by the hormone
thrombopoetin which stimulates the production and differentiation of magakaryocytes from the myeloid
stem cell.
Albumin is important for maintaining fluid balance because capillary walls are impermeable to albumin so
it creates an osmotic force to keep fluid in the vascular pace. It is produced by the liver and can bind to
medications and bilirubin. If you have impaired hepatic function, you may have low levels of albumin, and
therefore, a decrease in osmotic pressure which may develop into edema.

Malignant Tumors


Idiopathic purpua
Viral infections like AIDS
Chemotherapy and radiation


Condition of lower than normal hemoglobin. The amt of o2 to tissues is diminished.

With slow onset, levels of 9-11 may only have slight tachy on exertion and possibly fatigue.
If very active-more likely to have sx. Pt with hypothyroidism with decreased o2 needs may be
totally asymptomatic and a hemoglobin level at 10 g/dL. Pts with cardiac, vascular, pulm disease
may have very bad sx like dyspnea, chest pain, muscle pain, or cramping.
3 classifications. Whether the deficiency is caused by:
1. a defect in erythrocyte production: Hypoproliferative anemia. The marrow connot produce adequate
number of erythrocytes. It is reflected by a low or inappropriately normal reticulocyte count. It may result
from marrow damage due to medications like Chloamphenicol or chemicals like Benzene or lack of factors
like iron, B12, folic acid, erythropoeitn.
2. their destruction: Hemolytic anemia. Premature destruction of erythrocytes results in the liberation of
hemohlobin from the erythrocytes into the plasma. The resleased hemohlobin is converted in large part to
bilirubin so the bilirubin level rises. The erythrocyte destruction leads to tissue hypoxia, which in turn
stimulates erythropoietin production, the increased production is reflected in an increased reticulocyte
count as the bone marrow responds to the loss of erythrocytes. Hemolysis can result from an abnormality


within the erythrocyte itself as in sickle cell, glucose 6, immune hemolytic, or mechanical heart valve OR
direct injury.
Aged RBCs lose elasticity and become trapped in the liver and the spleen. During destruction, most of their
hemoglobin is recycled. Some breaks down and forms bilirubin to be secreted in bile.
How to differentiate between inadequate production or by destruction
A. the marrows ability to respond to decreased erythrocytes e/b an increased reticulocyte count in the
circulating blood
B. the degree to which young erythrocytes proliferate in the bone marrow nad the manner in which they
mature. This is shown on bone marrow aspirate.
C. the prescene or absence of end products of erythrocyte destruction within the circulation like increased
bilirubin level or decreased haptoglobin level.
3. by their loss: bleeding.
Assessment and diagnostic findings
Initially: Hgb, Hct, retic count, RBC indices, RDW, MCV. Also useful are iron and TIBC, % sat, ferritin, vit b12,
folate levels. May do bone marrow aspiration.
Complications of severe anemia
HF, paresthesia, delirium. Exacerbated angina in undxed HF.
Medical Management
Correct or control the cause of anemia. If severe, may need PRBC
Gerontologic Considerations
Most common hematologic contion. May cause decreased mobility, increased depression, increased risk for
falling and delirium when hospitalized. HR and CO dont increase as quickly so they have fatigue, dyspnea
and confusion.
Assessment: weakness, fatigue, malaise. Also pale skin and conjunctive, oral mucosa. Jaundice in
megaloblastic or hemolytic anemia. Smooth red tongue in iron deficiceny anemia. Beefy red and sore in
megaloblastic. Ulcerated mouth corners. Iron deficiency anemia presents cracing ice,s tartch or dirt aka
pica. Brittle nails, rigid and concave. Get med and alcohol hx. Extreme exercise can decrease erthropoisis
and erythrocyte survival. Vegetarians are RF megaloblastic anemia- they need b12 supp. Older needs b12
or folate. Cardiac status should be carefully assessed. When the hemoglobin level is low, the heart

attempts to compensate by pumping faster and harder in an effort to deliver more blood to hypoxic
tissue. This increased cardiac workload can result in such symptoms as tachycardia, palpitations,
dyspnea, dizziness, orthopnea, and exertional dyspnea. Heart failure may eventually develop, as
evidenced by an enlarged heart (cardiomegaly) and liver (hepatomegaly) and by peripheral edema.
Assessment of the GI system may disclose complaints of nausea, vomiting (with specific questions
about the appearance of any emesis [e.g., looks like coffee grounds]), melena [dark stools],
diarrhea, anorexia, and glossitis (inflammation of the tongue). Stools should be tested for occult
blood. Women should be questioned about their menstrual periods (e.g., excessive menstrual flow,
other vaginal bleeding) and the use of iron supplements during pregnancy. Neurologic examination is
also important because pernicious anemia affects the central and peripheral nervous systems.
Assessment should include the presence and extent of peripheral numbness and paresthesias, ataxia,
poor coordination, and confusion. Delirium can sometimes result from other types of anemia,
particularly in older adults. Finally, it is important to monitor relevant laboratory test results and to
note any changes over time


Iron Deficiency Anemia

From inadequate dietary intake, malabsorption, blood loss, hemolysis. Most common type is menstation
and preg. Need more iron. Most common cause in men and post meno women is bleeding from ulcers,
gastritis, inflammatory bowl disease, GI tumors. Chronic alc has blood loss from GI trat which causes iron
loas and eventually anemia. Other causes are iron malabsorption fter gastrectomy or celiac disease. Iron is
absorbed in the duodenum; we need apsorption ability. J tube for bypass of duodenum= no apsorption. It is
ahypoproliferative. The CBC will show NCV and reticulocyte. Other findings will be iron % sat and
ferritin. TIBC. Sx of anemia, and if prolonged they have: Pallor, Glottis: inflamed tongue, Chettis:
inflamed lips, HA, Paresthesia, Burning tongue. Brittle ridged nails, angular cheilosis. Can cause pallor,
dyspnea, tachy, malaise, fatigue, palp The signs go away after replacing iron. As risk if had mult preg GI
bleed or pica. Dx: definitive is bone marrow aspiration (will be low or absent) few people have this done.
HGB, hct, MCV, iron, Ferritin. total iron binding capacity d/t insufficient iron levels not enough there to
bind. After iron stores are depleted (as reflected by low serum ferritin levels), the hemoglobin level falls. The

diminished iron stores cause small erythrocytes to be produced by the marrow. Therefore, as the anemia progresses,
the MCV, which measures the size of the erythrocytes, also decreases. Hematocrit and RBC levels are also low in
relation to the hemoglobin level. Other laboratory tests that measure iron stores are useful but not as precise as
ferritin levels. Typically, patients with iron deficiency anemia have a low serum iron level and an elevated TIBC,
which measures the transport protein supplying the marrow with iron as needed (also referred to as transferrin)
Collaborative care Tx underlying cause. Diet iron: 150-200 take 1 hr before meal. Oral supp: just not
enteric coated. Parenteral supp: IM z track method watch for anaphylaxis. Blood transfusion. Hbg will
restore in a few weeks. Iron store will take 6-12 months. Can give IV iron if needed (a few administrations).
Teach: beef, calf liver, chicken liver, leafy gren, raisins, molasses, beans. Take orange juice too. Continue FE
supp even if feeling less fatigued. Ferrous sulfate SE: consip, cramp, NV- add stool softener or SR iron supp.
May cause stool to change color. Microcytic. Caused by chronic blood loss from minor gI bleed or colon fatigue, pallor, fissures of mouth, spooning fingernails, reduced exercise tolerance.
Is inherited.
Heterozygoud- minor: asymptomatic to mild sx. Microcytic and hypochromic. It is an inadequate production
of Hgb. Over prod of immature Absent or reduced globulin protein
Alpha thalessmia or beta thalassemia.
Hemolysis of RBCS
Homozygous is major: 2 genes called cooleys. Major disease process. Cooleys. Caused by defects in both
beta chains of hemoglobin molecule. It is severe microcytic anemia. Develop deformity of facial bones,
maxillary, hyperplasia, frontal bossing. Found in blacks, meds, se Asian. Manage with regular blood
transfusions to maintain hgb at 9-10. Chelating with Deferoxamine and monitor for toxicity.
Thalassemia Minor Sx:

Mild anemia

Thalassemia Major Sx:

Life threatening
Physical and mental delays
Splenomegaly, hepatomegaly, cardiomyopathy
Bone marrow hyperplasia



hbg, hct, tibc, transferrin, folate

reticulocytes, iron, bilirubin
No tx for minor. Major: low life expect. Blood transufion, chelating agents. Give deferasirox, deferiprone,
folic acid, zinc, splenectomy
Cobalamine B12 deficiency
Results from lack of intrinsic factor from pariatl cells of stomach. Is megaloblastic anemia. Macrocytic.
Defective maturation. Easily destroyed cells due to weak cell membranes. #1 cause is perricious= lack of
intrinsic factor as immune destroyed parietal cells. Can occur from GI surgery, chrons, celiac, divertic,
small bowel resect, alcoholism, PPIs, h2RB on reg basis bc they dec HCL acid that is needed for intrinsitc
factor, congenital pernicious anemia. It is a hypoproliferative. Pernicous anemia: macrocytic anemia
when B12 cant be absorbed in the distal small intesting d/t lack of intrinsic factor (produced by parietal
cells in stomach). May result after surg removal of stomach or from chronic gastritis causing dec intrinsic
factor. Autoimmune conitions may produce antibodies againstparietal cells. Sx may progress over 20 yrs.
Mild GI and mood swings to weak, fatigue, paresth hands/fingers, cog/mem, difficult walking. Later stages:
beefy red tongue, enlarged liver can lead to rt side HF. Hgb may be 7-8. B12 injection for life.
Beefy red tongue, anorexia, N V
Senses altered
Abdominal pain
Neuromuscular symptoms

cobalamin, hgb, hct

mcv, serum iron, transferring, ferritin
Shilling test: give b12, most will be excreted not absorbed
Collab care
Parental v b12, intranasal b12, oral b12.
Polycythemia Vera
An overproduction of all blood cells. Blood is viscous and can lead to HTN. Also known as primary
polycythemia. Proliferative disorder of myeloid stem cells. Bone marrow is hypercellular. RBC are highest
high. Hematocrit can exceed 60%. Can last for 10-20 years. The spleen resumes its embryonic function of
hematopoiesis and enlarges over time. The bone marrow may become fibrotic and not able to produce as
many cells its called burn out or spent phased. It my then involve myelofibrosis, MDS, or AML. Onset age is
65 yo more common in males than females. Survival rate exceeds 10 years. Death usually occurs from
thrombosis, hemorrhage, or rarely AML
Signs and symtoms:

Itchy skin* most distressing sx. Avoid temp change, alc, water.treat with interfereon alfa 2b not
antihist bc they dont work. Can also use serotonin uptake inhibitors. Do tepid or cool bath with
oatmal lotion or bakins soda


Red hands and feet- ruddy

Enlarged liver and spleen
Nose bleeds and easy bruising
Fullness and anorexia
Have sx of HF and stroke
Major concerns are stroke, MI, PE. So keep moving and monitor i/o
Angina, claudication, dyspnea, thrombophlebitis.
High BP

Diagnostic Findings

Dx is based on elevated erythrocyte mass, a normal o2, enlarged spleen

May see leukocytes and plateelts
Erythropoietin is not low


At risk for thromboses and may have stroke or MI.

Bleeding because platelets are large and somewhat dysfunctional. Can be significant bleeding.

Collaborative Care

Phlemobotomy every 2-3 months to pull off 500ml of fluid

Good hydration
Hydroxyurea to assist in halting proliferation
Objective is to reduce RBC count and rf thrombosis
Anagrelide to inhibit platelet aggregation. Side effects are HF, FVE, cardiac dysrhy, HF.
Can use low dose aspirin
Teach risk factors, DVT precautions, no alc, no iron supp or multivitamin

Folic Acid Deficiency

Megaloblastic (large RBC) from dematuration. It is Macrocytic. Is dangerous for unborn infants bc folic acid
prevents neural tube defects. Preg need 400/day. Is absorbed in small intestine stored in liver. Alcoholism
or not enough veggies can cause. May develop stomatitis and ulcerations on tongue. May have dysphagia,
flatulence, watery diarrhea
Can result from:

Poor nutrition
Drugs like Dilantin, Ohenobarbital, methotrexate
Hemodialysis: causes folic acid losses

Signs and symptoms

Usually slow onset, eventually will see:

Dyspepsia, beefy red tongue

Diagnostic Studies

Hgb, Hct, folate

MCV, serum Iron, Ferritin




Aplastic Anemia
Congenital or acquired (autoimmune, chemical, drugs, radiation, viral/bacteria. Decrease in all blood cells.
Called Pancytopenia. Normocytic resulting from decline in blood cell production r/t bone
marrow depression. Decline of all 3 blood cells. RBC decline gradual. WBC and PLTs faster, so it
appears as a chronic anemia. Can be heredity or acquired after bith. If sudden onset: hypoxia,
pallor, weak, fever, infections, low-grade fever, cellulitis in neck, nosebleed, waxy pale skin.
Hgb can be 7.
Signs and Symptoms

Related to anemia:
Fatigue, weak, infection, bleeding

Dianostic Studies

Hgb, Hct, WBC, RBC, Platelets

bleeding time, iron, TIBC


Remove causative agent

HSCT if younger than 55
Immunosuppresive therapy if older than 55
Regular blood transfusion will need chelating agent

Acute Blood Loss

Occurs from trauma, surgery, GI bleed
Signs and Symtoms

Thread pulse
Cool, clammy= shock


Replace volume loss

Packed RBCs

Sickle Cell Disease

This is a hemolytic anemia. You will see MCV and reticulocytes. It is an autosomal recessive disorder,
usually found at newborn screening. It is most common in Arifcan Americans. 1 in 500 live births. And
abnormal Hbg S which are stiff, elongated, sickle shaped cells.
Sickling episodes triggered by hypoxia
As a result of:

#1- Viral or bacterial infection like pneumonia due to hypoxia

Increased alititudes or stress
Surgery, blood loss
Blood becomes viscous and clump together

Signs and Symptoms

Excruciating pain, necrosis, full body response


Cronic anemia. Pain pallor, jaundice from hemolysis, fever, swelling of hands/feet which you may
see 1st in infant.
Tachypnea, fever, N,V
Hypertension, chest pain, cough, dyspnea
SOB, seizures, fever, vision changes, decreased peripheral pulses
Doecreased capillary refill
Pale to cyanotic
Lungs: pulmonary complications from occusion of vessels. PE, clot, pneumonia, dyspnea
Heart: MI, HF, cor pulmonale
Spleen: dysfunctional, atrophies, RF infection is high
Eyes: hemorrhage, retina detachment, blindness
Kidney: decreased perfusion, failure
Vascular: ulcer of skin

Diagnostic Studies

Hbg, Hct, Reticuloyctes, folate

iron, bilirubin
Blood smear
Sickling test
Genetic testing for recessive
Infection is common precipitating cause**

Nursing Diagnoses

Acute pain
Chronic pain
RC sepsis
RF skin integrity

Collaborative Care

Prevent: avoid high altitude. Crisis: bed rest to reduce energy expedinture.

* stop med that causes it
* treat neoplasm (which may cause neutropenia initally)
* coritocteroids if cause is immunologic disroder.
* granulocyte-colony stimulating factor or machrophage to increase neutrophil productioin when it's caused by
decreased production.
* withhold or reduce chemo treatment
* if fever--> means infection--> admit to hosp--> blood, urine, sputum, chest xray. Broad spectrum antibiotics
Nurse Management
* to assess the severity of neutropenia and risk of infection must assess ANC
lymphocyte count less than 1500. Can result from ionizing radiation, long-term use of cotricosteroids, uermia, infectionsparticularily vial, breast or lung cancer, adv hodgkins. If mild- without sequelae. If severe- can result in bacterial infection
d/t low B lymph or in opportunistic infection d/t low T lymph.


Bleeding Disorders
bone marrow may be stimulated to incraeses platelet production (thrombopoeisis). It may be a reactive response to sig
bleeding or general response to increased hematopoisis is in iron def anemia. the increase in platelets usually doesn't
result from increased production but from a loss in platelet pooling within the spleen.

Signs and Symptoms


vascular= localized
platelet issues= systemic
petechiae d/t small vessels
coagulation factor doesnt usually cause superficial bleeding, the bleeding occurs deeper in body. harder to stop

Medical Management
* transfusion
* if fibrinolysis is excessive, use aminocaproic acid to inhibit the process. use with caution- can result in thrombosis
* dental work may need transfusion before to minimize excessive bleeding
Secondary Thrombosis
increased platelet production. platelet function is normal. platelet survival time is normal or decreased. can be caused by
infection, chronic inflammatory, iron def, malig disease, actue hemmorhage, splenectomy

Signs and Symptoms

* sx related to hemorrhage or thrombosis
low platelet level. can result from decreased production of platelets in bone marrow, increased destruction, or increased
consuption as in using them to form clots

Signs and Symptoms

* bleeding at petichae don't start until less than 20,000. mostly along nasal and gingival, excessive menstration, dental
* less than 5000 potenial for fatal CNS or GI hemorrhage
* if platelets are dysfunction d/t MDS disease or meds like aspirin, the risk of bleeding is much greater when the platelet
count is not significantly reduced, becasue the function of the platelets is altered.
Diagnostic Findings
* deficient platelets from decreased procution like leukemia or MDS- bone marrow via aspiration and biopsy
* genetic would be autosomal dominant, autosomal recessive and x-linked mutation
* if destruction is the cause of thrombocytopenia, the marow shoes increased magakaryocytes and normal or maybe
increased platelet production as the body tries to compensate for decreased platelts in circulation


* Hep B or C can cause thrombocytopenia; so pt should be screened for it.

* need to exclude pseudothrombocytopenia. this is where the platelets aggregate and clump in the presence of EDTA,
which is the anticoagulant that is in the CBC tube for collection.dx with manual exam of spear
Medical Management
* try to treat the underlying cause
* if platelet production is impaired- platelet transuion may increase platelet count and stop bleeding or prevent
spontaneuous hemorrhage
* if excessive platelet destruction occurs- transfused platelets are destroyed, and platelet count doesn't increase.
* most common cause of excessive platelet destruction is immune thrombocytopenic purpura
* splenectomy may be useful. often is not an option though
* if pt has enlarged spleen d/t portal hypertension r/t cirrhosis, then it would cause more bleeding.
Nurse Management
* consider cause, duration, condition of pt
* prevent falls
Immune Thrombocytopenic Purpura
ITP more common in children and young women. Aka idiopathic thrombocytopenic purpura. Primary is
isolation. Secondary is autoimmune. It is characterized by desrtruction of normal platelets by unknown
stimulus. Antiplatelet antibodies deveop in the blood and bind to the platelets. The platelets are then
ingested and destroyed by the RES or tissue macrophages. Body compensates by increasing platelet
production in the marrow. Not as effective as thrombopoeitin and arent elevated. Viral illness may lead to
ITP. Meds like sulfa or lupus, pregnancy. Autoimmune condition, body attacks platelets and then pt is RF
bleeding. 1st line tx is corticosteroids to allow platelets to increase again. It will raise BGT so monitor CBG.
Give stool softener so no ICP rise because that would be RF intracranial bleeding. Dont transfuse platelets
bc they will be destroyed
Signs and symptoms

Many have no sypmtoms

Low platelet count is incidental as 30,000 or less than 5000
Common: easy bruising, heavy menses, petechaie on extremities or trunk
Wet purpura is GI, hempptysis. Have greater risk for intracranial bleeding
Platelets are functional, spontaneous bleeding doesnt usually occur
Tx only when bleeding is severe or less than 30000

Diagnostic findings

Hx, phys assess to exclude cause of thrombocytopenia and identify bleeding

Test for hep C and HIV (baby could be exposed, use barrier birth control, baby wont always get it.
If bone marrow aspirate may see megakaryocytes
Platelets usually at or less 20000
Some have H pylori, get rid of infection

Medical Management

safe platelet count rather than cure the disease

Stop med like sulfa or quinine
Use immunosuppressive agent, they block binding receptors on macrophages so platelets arent
Recommend to admin corticosteroid prednisone at 1mg/kg for 21 day and taper
Will rise within a few days
Can use azathioprine for maintenance therapy


IVIG to treat. Expensive

Splenectomy. At permanent risk for sepsis and should hav pneumovax haemophilus inful type b,
mengicoccal 2-3 weeks before splenectomy
Avoid platelet transufsions will be ineffective.

Nursing Management

Assess rf bleeding
Use of OTC herbs
Dont give sulfa, NSAID, aspirin
Recnent viral intracranial bleeding
Wet purpura and low platelet neuro assess
Avoid injection/rectal
They have fatigue
Avoid constipation and valsava, teeth flossing
Use elect razor, soft brush
Avoid vigorous sex
Monitor bone mineral density, give calcim and vit D

Platelet Defects
Quantitative: thrombocytopenia, thrombosis. Are relatively common.
Qualatative: # of platelets may be normal, but dont function normally
Now platelet function analyzer is used. Rapid and simple.
Peripheral smeal eval: assessing potential qualitative defects. Platelets are ofen hypogranular and pal and
may be larger than normal.
Aspirin may inuce platelet disorder. They reduce normal platelet aggregation and prolonged bleeding time
lasts several days after aspirin ingestion. If you have a coagulation disorder like hemophili or
thomboyctpoena it can be significant.
NSAIDS can inhibit platelet function, not as long of effect as aspirin.
ESRD, MDS, myltiple melyoma: from abonormal protein interfereing with flatelt function.
Cardiopulmonary bypass, herbal therapy
Labs/Clinical manifestations

PT and normal aPTT and platelet count could mean facter VII deficiency
PTT and normal PT and platelet could meal hemophilia or von Willebrand disease
Ecchymoses common, usually on extremities
RF bleeding after trauma or invasive procedure

Medical Management

If dysfunction d/t meds, stop them

Prevent by transfusing normal platelets before invasive procuedes
Use aminocaproic aicd to prevent bleeding after proceudres

Nursing management

Avoid OTC, herbal, nutription supplements, alcohol

Inform dentist before procedure

Clinically indistinguishable, can use lab tests. Both are X-linked traits, almost all are males. Females can
carry but are asymtpmatic. Dx at toddler age


Hemophilia A: genetic that result in deficient or defective factor VIII. 1 in 10,000 births
Hemophilia B: called Christma disease. Genetic defect that causes deficient or defective factor IX.
Clinical Manifestations

Manifested as hemorrhages
Depends of degree of deficiency and intensity
Mild factor VIII rarealy evelop hemorrhage spontaneous
Severe factor VIII freq henorrhages like hemarthrosos and hematoma. Require frequent VIII
replacement therapy
Most bleeding occurs into joints, knees, elbow, ankle, shoulder, wrist, hip
Pain in joint is first indication of bleeding. Then swelling and limited ROM
May have chronic pain like ankyloses (fixation)
Can be crippled before being an adult
Deep hematomas in muscle dec sensation, weakness, atrophy
Can have hematuria and GI bleed, mucous membrane
Most dangerous site of hemorrhage is head.
Clot formation is poor, wound healing is poor.
Bleeding is most common in dental extraction

Medical Management

Recombinant forms of factor VIII and X concentrates decreases the need for using factor
concentrates or fresh-frozen palsma. Give these when theres active bleeding
Prophylactic is good for severe factor VIII
If person develops antibodies to concentrates use plamaphereses or concurrent
ummunosuppressive during sig bleeding
Treatment is success when antibody titers remain low
Activated prothrombin complex concentrates use to control bleeding by improving fibrin clot
stability. Risks are thrombosis
Severe def screen b4 surgery
Aminocaproic acid inhibits fibrinolysis and therefore stabilizes the clot, very effective as adjunctive
measure afer oral surgery in tx mucosal bleeding
Desmopressin (DDAVP)- causes significant but transient rise in factor VIII levels
Mild forms of hemophilia A- desmopressin is extremely useful and reduces the need for blood
Desmopressin is NOT EFFECTIVE for severe factor VIII deficientcy

Nursing Management

Coping for children. Encourage self-sufficint, unneccesary trauma

Mild factor may not be dx until adult. Need education with activity restrictions
Home safety
Teach to amin factor concentrate at 1st sign of bleeding
Can do proph but need it 2-3 times per week
Avoid aspirin, NSAIDS, chamomile, nettle, alfalfa, alcohol, cold remedies
Apply pressure
Splints for joint or muscle hemorrhage
Avoid all injections, invasive procedures or give factor replacement b4
Wear med alert bracelet
Written emergency plan
During hemorrhagic observe close and assess for resp distress, LOC. VS until certain theres no
Analgesics for hematoma or hemorrhage to joint


Do genetic testing
Old people hep B an C common because they likely had a lot of blood transusions earlier in life.
Intracranial hemorrhage is 3rd most common cause of death. Mostly from joint disease not from
trauma. Likely to acurie inhibitors especially hemophilia A inhibiotrs increases with age. So they are
at risk for bleeding AND thrombosis
Coronary bypass graft surgery is super high risk bc stents are placed and cant use antiplatelet

Von Willebrand Disease

Usually inhereited as dominant trait. Affects males and females the same. It is caused by deficient of vWF,
which is necessary for factor VIII activity. It is also needed for platelet adhesion at site of vascular injury.
Factor VIII levels are mildly low like 15-50% low.
Type 1: most common. It is decreases in structurally normal vWF.
Type 2: variable qualitative defects based on subtype involved
Type 3: very rare. It is severe vWF deficiency and significant factor VIII deficieny.
Clinical Manifestations

Bleeding is usually mucosal.

Usually have recurrent nosebleeds, easy bruising, heavy menses, prolonged bleeding, post op
Usually dont have massive soft tissue or joint hemorrhage unless type 3

Diagnostic Findings

Normal platelet but prolonged bleeding and slight prolonged aPTT. Results can vary over time
Rely on values over time not just a single measure
Ristocetin cofactor or vWF collagen binding assay to measure vWF activity.
do vWF antigen, factor VIII
for type 2 suspiction do vWF multimers which measures specific subtype

Medical Management

goal is to replace defiecnt protein at time of bleeding or prior to procedure

desmopressin to prevent or manage mild bleeding after surgery for mild. Not use for type 3.
Provides transient increase in factor VIII coagulant active and may correct bleeding time. Can do IV
or intranassally. Contraindicated in unsable CAD. Side effects: HA, facial flushing, tachycardia,
hyponatremia, and rarely seizures
Humate-P and Alphante to replace. For 7-10 days after major surg and 3-4 days postpartum.
Aminocaproic acid to manage mild form of mucous bleeding
Platelet transfusion with significiat bleeding
No aspirin or herbs

Liver Disease
Most blood coagulation factors are synthesiszed in liver except for VIII. So if liver doesnt work good, there
will be diminished factors needed to maintain coagulation and hemostasis.
Prolonged PT unless caused by vit K defic may indicate severe hepatic dysfunction. Usually bleeding is just
echhymoses but the person is also at risk for sig bleeding with trauma or surgery. Transfusion of freshfrozen plasm be needed to replace clotting factor and prevent or stop bleeding. Person may have lifethreatening hemorrhage from peptic ulcer or esophageal varices. So then they will need fresh-frozen
plasma, PRBC and platlets.
Vitamin K Deficiency
Synthesis of many coagulation factors depend on vitamin K. a Vit K defic is common in malnutrition.
Prolonged use of some antibiodice decreases the intestinal flora that produce vitamin K so then it will


deplete vit K stores. Admin vitamin K such as phytonadoin via PO or subq, and will work quickly. So
adequate syntheses of coagulation factors is resfelcted by normalization of the PT.
Comlications of Anticoagulant Therapy
Anticoagulants are used to treat or prevent thrombosis. Warfarin or heparin can cause bleeding. The INR is
used to monitor the efficacy of anticoagulants that were measured by the PR. If the INR or aPTT is longer
than desired with no bleeding med can be stopped or dose decreased. Vitamin K is antidote for
warfarin. Protamine sulfate is antidote for heparin. Its not very effective though. If significant bleeding
use fresh-frozen plasma and it will replace vit k.
Disseminated Intravascular Coagulation
It is not a disease. It is a sign of an underlying condtion. It may be triggered by sepsis, trauma, cancer,
shoch, abrupto placentae, toxins, allergic reaction, and others. It is potentially life threatening.
What happens?

Underlying disease initaties the inflammation process and coagulation in the vasculatre.
The natural antigoaulant pathways in the body are simultaneously impaired
Fibrinolytic system is suppressed so that a massive amount of tiny clots form in the microcirculation
The coagulation time initially will be normal
As platelets and clotting factors form microthrombi coag fails
The paradoxical result of eccessive clotting is bleeding

Clinical manifestations

Usually as organ failure or dysfunction due to excessive clot formation.. ischemia!

Bleeding will be bad because the fibrinolytic system releases firbrin degradation products that are
super anticoagulants.
platelet and fibrinogen level PT, aPTT, thrombin time, fibrin degration products and d-dimers
Major mortality for ischemic thrombosis, frank hemorrhage, multi organ dysfunc syndrome
Mortality is based on ability to tx underlying
Bleeding from mucous, IV sites, GI and GU
Typically develop MODS, may exhibit these as result of microthromboses, macrothromboses,
May only see dec in platelet count first
Then will see sx of thrombus
Then bleeding

Diagnostic Findings

platlets fibrin degradation product, d-dimer, PT, aTT and fibrinogen level
D-dimer levels are more accurate to dx than fibin degradation products
PT and fibrinogen levels diagnose DIC!!

Medical management

Tx underlying cause
Correct ischemia, replace fluid, elect imbalance, admin vasopressor
Replace platelets if lots of bleeding
Cryopreciitate give to replace fibrinogen and V and VII
Fresh-frozen plasma give to replace other coagulation factors
Heparin is controversial. It may inhibit form of thrombi so thats good
Can use LMWH to prevent venous thromboembolism. It will be effective when plasma fibrinogen
concentation is normal and theres less bleeding.
Aminocaproic acid can be used with heparin
Dont use APC, its not approved anymore


Nursing management

Determine risk for DIC

Common cause are sepsis and acut prolyelocytic leukemia
Assess for sx of thrombi and bleeding
Watch lab values overtime. Not just one draw
Target potential sites of end-organ damage. Like kidneys, lung, brain, skin
May require dialysis if kidney is bad
If large bore dialysis catheter is needed, give paltelt and plasma transfusions
Liver: depleted albmin stores, not good synthesis of clotting factors
Monitor resp. do suctioning gently.
CNS: HA, visual change, altered LOC

Thronbotic Disorders
May cause excessive thrombosis that are arterial from platelet aggregation. May also be venous from
compromised platlets, red cells, thrombin.
May be from a decrease in clotting inhibitors, bad liver function, lck of fibronolytic enxymes, or tortouous
or atherosclerotic vessels
May first see as occult malignancy or complication from preexisting cancer.
Can be caused by hyperhomocysteinemia, antithrombin deficiency, protein C deficiency, protein S defic,
APC resistance and factor V Leiden deficiency.
Repeased episeods of thrombosis are called hypercoagulable states or thrombophilia
If it is due to inherited, need to do family genetic testing
May cause CVA, periph art occlusive disease
Need anticoagulation therapy. Time depends on extent and location.
Risk factors are contraceptives, cigs, obesity, tortous blood vessels, hx of thrombotic
If you take aspirin after completing anticoag therapy.. it reduces recurrent
May need lifelong anticoag therapy

Hyperhomocysteinemia: Homocysteine can promote platelet aggregation. A big risk factor for
venour thrombosis is the increased plasma levels of homocysteine. It can be hereditary, or result
from deficient folate, b12, b6. Giving supplements wont help
Antithrombin deficiency AT is a protein that inhibits thrombin and certain coag factors. Deficiency is
a hereditary contion that can cause venous thrombosis. Most common sites are DVT and mesentery. Often
reoccurs. Person tends to have heparin resistance so they may need a lot more of a dose. Encourage
family to be tested.

Protein C deficiency It is a vitamin K depenent enzyme synthesized in the liver. When it is activated, it
inhibits coagulation. If levels are low, the risk of thrombosis increases. Usually dont have sx until 20s. rare
complication is warfarin induced skin necrosis. Must then stop warfarin, give vitamin k and heparin and
fresh frozen plasma to reverse effects. may tx with purified protein C concentrate

Protein S deficieny Its a natual anticoagulant normally produced by liver. APC requires protiein S to
inactivate certain clotting factors. When levels are low, the inactivation process is diminished and risk for
thrombosis is increased. May see as early as 15 years old. Thromboses ususally occur in axillary,
mesenteric and cerebral veins. Warfarin induced skin necrosis is possible. Can acquire this. Can see in
pregnancy, DIC, liver dieseae, nepritic syndrome, HIV and use of L-asparaginase


Activated Protein C Resistance and Factor V Leiden Mutation APC resistance is common with
hypercoagulable states. It is an anticoagulant and if there is resisance to APC it increases risk for venous
thrombosis. 90% of time you will see molecular defect in the favotr V gene. This factor V Leined mutation
is more common cause of inherited hypercoagulability in whites.Factor V Leiden mutation synergistically
increases the risk of thrombosis with other rf like oral contracept, hyperhomocysteinemia, increased age.
Homozygous are bigger risk than heterozygous

Acquired Thrombophilia Do not have inherited or genetic causes. It is a result of inappropriate clot
formation usually caused by excess in antibodies or increase in clotting factors
Antiphospholipid syndrome: they reduce levels of annexin V which is a protein htat binds phospholipies
and has anticoagulant activity. Most common antiboides are either lups or anticardiolipin antibodies. It is
classified as primary or secondary. Malignancy: particularly stomach, pancreatic, lung, ovarian cancers.
The thrombosis occurs in unusual sites like portal, hepatic, renal vein or inferior vena cava. Anticoag can
be difficult to manage. LMWH is more effective than warfarin Medical management Primary method is to
use anticoagulation. Big risk of bleeding
Unfractionated Heparin Therapy Heparin is narurally occurring anticoagulant that enhances AT III and
inhibits platelet function. Usually given 2-3 times per day subq to prevent. To treat, it is given IV.
Therapeutic effect is monitored with serial aPTT, want a range to maintain 1.5 to 2.5 the control. A
complication is heparin-induced thrombocytopenia. It is a formation of antibodies. Risk factors are using
longer than 4 days, surgery, bovine. Women are at higher risk. A hallmark sign is decline in platelet count
4-14 days of heparin therapy. Stop therapy. Can give lepirudin and argatroban. Transisiton to warfarin if
possible.Heparin-associated thrombocytopenia is more common than HIT. Platelet declines and then
normalizes Low Molecular weight heparin therapy Include dalteparin, enoxaparin. Have longer halflife
and less variable than unfractionated. Dont need lab monitoring for dose adjustments. Contraindicated in
HIT. Stop warfarin 2-3 days before surgery and start heparin in its place. Then resume warfarin. Lmwh may
be resumed after surgery, and if so, d/c when warfarin level is achieved Warfarin (Coumadin) therapy
They are anticoagulants and antagonsits of vitamin K depenedt clotting factors. They bind to albumin and
are metabolized in liver. Have super long half-life. A pt with venous thromboembolus is first tx with heparin
and warfarin. When INR is reached, the heparin is stoped. Therapeutic range is 2-3 of the control. Need to
monitor closely. It is affected by lots of meds. Maintain consisitent amount of vitamin k in diet. Dabigatran
(Pradaxa) New oral direct throbin inhibitor. Reduces risk of CVA in a fib. Dont need INR or dose adjust.
Still has risk of bleeding. Expensive. Must stay in original packaging Nursing Management Avoid
immobility, crossing legs. Exercise and ambulate. Anti-embloism stocking. May have lowdose aspirin or
clopidogrel to alter platelet aggregation. May need lifelong anticoag with warfarin. Dont use bedrest.
Tobacco avoided

Acute Myeloid Leukemia

AML results from defect in hematopoitic stem cell that differentiates into all myeloid cells: monocytes,
neutrophils, basophils, eosinophils, erythrocytes, platelets. Older than 60 have more CNS and systemic
infection worse prognosis. Secondary AML is resistant to treatment
Sx: Without warning. Sx over a few weeks. Sx from insufficient production of normal blood cells. Fever
and infection from neutropenia. Weakness, fatigue, dyspnea on exertion, pallow from anemia, petichae,
echhymosis and bleeding from thrombocytopenia. Proliferation of leukemic cells shows pain from enlarged
liver or spleen, hyperplasia of gums, bone pain from expansion of marrow. Lymphadenopathy is rare.
Splenomegaly is rare Dx: Decreased erythrocytes, platelets. Total leukocyte can be low, normal, high,
percent of normal cells is decreased Bone marrow analysis shows excess of immature blast cells which is
HALLMARK DIAGNOSIS Care: Objective is for full remission where no leukemia is in bone marrow. Hard
to do. Induction therapy: chemo that needs hospitalization for several weeks. Uses cytarabine,
daunorubicin, or mixantrone, idarubicin. You will also eradicate normal myeloid cells and the pt will be
severly neutropenic. An ANC of 0 is not uncommon, anemia, thrombocytopenic. The pt will be very ill with
bacterial and fungal infection. Occas viral. Bleeding, mucosisits which causes diarrhea and bad nutrition.
Manage this by PRBC and platelets. Hematopoetic stem cell transplantation: HSCT. Need tissue match.


Goal is to destroy pts hematopoetic fxn of bone marrow. Then is resuced with donor stem cells. Big rf
infection and graft vs host

Chronic Myeloid Leukemia A mutuation in myeloid stem cell. Normal cells are produced but there is a
patho increased in blast cells. So bc there is no control of proliferation, the marrow expands into the
cavities of long bones and liver and spleen so they enlarge and are painful. Increases with age. In chronic
phase, have few sx and complications. Rare bleeding or infection. If it becomes acute phase which is a
blast crisis, the disease is more difficult to treat.
Sx: Most asymptomatic and leukos are 100,000 or more. May be sob or confused. Tender spleen Malaise,
anorexia, wt loss. Lymphadenopathy is rate. 3 stages are chronic, transformation, accelerated or blast
Medical management PO tyrosine kinase inhibitor iatinib mesylate: blocks signals wihin the
leukemia cells to prevent the cell from growing and dividing. Most useful in chronic phase. Can induse
remission. Dont use antacids or grapefruit. Watch acetaminophen. If doesnt work, add another or HSCT. In
transformation phase, may have bone pain and fever and wt loss. May become more anemic and
thrombocytopenic, with increased basophil level detected. Blast crisis: same meds as AML.. To reduce
leukocyte level use hydroxyurea

Acute Lymphocytic Leukemia ALL happens from uncontrolled proliferation of immature cells
(lymphoplasts) derived from lymphoid stem cell. Cell of origin is precursor to B lymph in 75%. Very
responsive to tx. HSCT can be successful even after second relapse
Sx: Immature proliferation impedes the development of normal myeloid cells so normal hematopoiesis is
inhbited and therefore will see decreaed granulocytes, erythro, platelets. Leukocyctes may by low or high.
Pain from enlarged liver or spleen and bone. CNS is freq a site for leukemic cells so may have HA, vomit.
Other areas are testes and breasts
Medical management Goal is remission w/out toxicity with rapid hematologic recovery. Tx is based on
genetic markers and risk factors. Preventative intrathecal chemo is key. Ingetral part are corticosteroids
and vinca alkaloids. Dexamethasone is preferred. Asparaginase is included. HSCT is controversial but can
be used

Chronic Lymphocytic Leukemia CLL common malignancy in older adults. Family hx. Malignant clone
of B lymphocytes. Cells are fully mature. Most survive more than 20 years. Complications like autoimmune
hemolytic anemia or idiopathic thrombocytopenia purpura can happen. This is because the immune
process with RES destroys the bodys own erythrocytes or platelets. Ppl have higher chance of having
other cancers in lung, bone, or skin. If they get Richters, its lyphadenophathy, splenomegaly, worse b sx
like fever night sweats and wt loss. Surivival is 6 months. T cell fxn is impaited Sx: Most asymptomatic.
Increased lymphocyte count is always present. Lymphadenopathy. Splenomegaly. B
sx: fever, drenching sweat, unintentional wt loss. T-cell fxn is impaired
Medical MAnagemtns Chemo agents like fludarabine and cyclophosphadmide in combo with rituxan.
Side effect of fludarabine is prolonged bone marrow suppression that looks like neutropenia, lymphopenia,
thrombocytopena so they are at risk for infection like peumo jirovect, listeria, myobact, herp. Bendustine
can be used with rituximab also

Myelodysplastic Syndromes MDS are group of clonal disorders of the myeloid stem cell that causes
dysplasia which is abnormal development in one or more types of cell lines. Most common feature is
dysplasia of erythrocytes which is manifested as a macrocytic anemia. Leukocytes like neutrophils and
platelets can be affected. Many cells die before being released from bone marrow. So number in circulation
is typically lower than normal. The cells do not function properly. The neutrophils have bad abilty to
destroy bacteria by phagocytosis. Platlets are less able to aggregate and are less adhesive. This results in
an increased risk for infection and bleeding, even though numbers arent super low. Primary MDS: ppl
older than 70. Initial findins are subtle. Secondary MDS: any age and results from prior toxic exposure to


chemicals including chemo. Poorer prognosis, resistant to treatment, more cytogenetic abnormalities and
evolves into AML.
Sx: Many are asymptomatic, dxd when CBC is drawn for other reasons. Fatigue is often there. Neutrophil
dysfunction puts pt at risk for recurrent pneumonias and other infections. Platelet function can be altered
so bleeding can happen. Overtime bone marrow can fail to produce enough so bone marrow failure. May
progress over time
Dx: CBC: macrocytic anemis; low leukos and platelets. Erythropoietin levels and reticulocyte count low. If it
involves AML: more immarture blast cells. DX IS bone marrow aspiration and biopsy
. Medical management HSCT is only cure, not viable for most d/t cormobidities or age. Low-risk are tx
with erythroid-stimulating agens like procit or aranesp. Chemo is traditionally used with disappointing
results. Most need freq RBC (for anemia), plateltet transufsions.. called transfusion dependence.High risk
disease the goal is to improve survival. Azacitidine and decitabine. Chelation therapy is a process that is used to
remove excess iron acquired from chronic transfusions. Iron is bound to the chelating agent and then excreted in the
urine. Because chelation therapy removes only a small amount of iron with each treatment, patients with chronic iron
overload from RBC transfusions need to continue chelation therapy as long as the iron overload exists, potentially for the
rest of their lives. Renal and liver dysfunction are possible, so serum creatinine and liver function tests should be
monitored and the medication held until the laboratory results return to baseline; the medication is typically resumed at a
reduced dose.
Essential Thrombocythemia
It is a stem cell isorder within the bone marrow. JAK2 promotes cell proliferation and resisitance to cell
death and hypersensisivity to erythropoietin and thrombopoietin. Marked increase in platelet production
consistently above 450,000. Size could be abnormal but life is normal. Cause unknown women more than
Sx: Many asymptomatic. Dxd during CBC for other reasons and seeing platelets. Sx are primarily from
vascular occlusion. HA, ischemia attack, diplopia. Spleen may be enlarged. Platelets substances cause
burining, warmth, redness. Bleeding from skin usually
Dx: Rule out other diseases. Dont use iron level. Analyze JAK2 protein. Bone marrow aspirate not usefull
Tx: Low aspirin. Hydroxyurea for lowering platelet count. May only cause dose related leukopenia.
Anagrelide but has worse side effects. Interferon alfa-2b has been shown to lower platelet counts by inhibiting
megakaryocyte differentiation. The medication is administered subcutaneously at varying frequency, most commonly
three times per week. Significant side effects, such as fatigue, weakness, memory deficits, dizziness, anemia, and liver
dysfunction, limit its usefulness. Moreover, it may not be effective in protecting from thrombotic complications.
Nursing management Patients with ET need to be educated about the risks of hemorrhage and thrombosis. The
patient is informed about signs and symptoms of thrombosis, particularly the neurologic manifestations, such as visual
changes, numbness, tingling, and weakness. Risk factors for thrombosis are assessed, such as obesity, hypertension,
hyperlipidemia, and smoking; measures to diminish these risk factors are encouraged. Patients taking aspirin should be
informed about the importance of taking this medication as well as the increased risk of bleeding. Patients who are at risk
for bleeding should be instructed about medications (e.g., aspirin, nonsteroidal anti-inflammatory agents [NSAIDs]) and
other substances (e.g., alcohol) that can alter platelet function. Patients taking interferon are taught to self-administer the
medication and manage side effects. Patients taking hydroxyurea should have CBCs monitored regularly; the dosage is
adjusted based on the platelet and WBC count.

Primary Myelofibrosis also known as agnogenic myeloid metaplasia or myelofibrosis with myeloid metaplasia, is
a chronic myeloproliferative disorder that arises from neoplastic transformation of an early hematopoietic stem cell. The
disease is characterized by marrow fibrosis or scarring, extramedullary hematopoiesis (typically involving the spleen and
the liver), leukocytosis, thrombocytosis, and anemia. Some patients have diminished leukocyte, platelet, and erythrocyte
counts (i.e., pancytopenia). Patients with myelofibrosis have increased angiogenesis (formation of new blood vessels)
within the marrow. Early forms of blood cells (including nucleated RBCs [immature RBCs] and megakaryocyte
fragments) are frequently found in the circulation. The cause is unknown but appears to evolve from a prior


myeloproliferative disorder (i.e., polycythemia vera, ET) in 25% of cases. As with ET and polycythemia vera, mutations of
the JAK2 protein are seen
Myelofibrosis is the rarest of the classic myeloproliferative diseases (ET, polycythemia vera, myelofibrosis). It is a
disease of the older adult, with a median age at diagnosis of 65 to 70 years, and is more common in males. Symptoms may
result from an often massively enlarged spleen, causing discomfort and early satiety; other signs and symptoms include
profoundfatigue, pruritus, bone pain, weight loss, infection and bleeding (from pancytopenia), and cachexia. Arterial or
venous thrombosis can occur but is less frequent than that found in polycythemia vera or ET. Average survival ranges
from 3 to 10 years based on the occurrence of such adverse prognostic indicators as anemia, leukocytosis, presence of blast
cells in the circulation, poor-risk cytogenetic results, and profound splenomegaly Common causes of death are heart or
liver failure, portal hypertension, complications of marrow failure, and transformation to AML. AML is especially difficult
to treat successfully in these situations.
Medical management HSCT is a useful treatment modality in younger, otherwise healthy people. For patients who
are not candidates for transplantation, medical management is directed toward palliation, reducing symptoms related to
cytopenias, splenomegaly, and hypermetabolic state. Although one third of anemic patients respond to the combination of
an androgen plus a corticosteroid, the primary treatment remains PRBC transfusion. Because of the prolonged
requirement for these transfusions, iron overload is a common problem. Iron chelation therapy should be initiated in
patients in whom survival is expected to exceed a few years. Hydroxyurea is often used to control high leukocyte and
platelet counts and to reduce the size of the spleen. Thalidomide or lenalidomide may be useful in improving anemia;
however, these drugs are not as effective in improving thrombocytopenia or in reducing an enlarged spleen. Newly
developed JAK2 inhibitors are being evaluated in patients with myelofibrosis; these agents appear to markedly reduce the
massive splenomegaly and improve pruritus and occasionally anemia, but they do not reduce fibrosis within the marrow
Enlarged spleen may be site of execessive destruction of blood cells. Pts may develop severe thrombocytopenia. A
splenectomy removes the trap and platelet counts may normalize over time. Post op complications: atelectasis,
pneumonia, abdominal distention, and abscess formation. Young children are at highest risk. Everyone is at risk for
infection, so they should receive pneumovax before surgery if possible. Pts should call MD if even minor s/s of infection
occur. Pts usually have even high number of platelets which can predispose to thromnotic or hemorrhagic problems. It
does not warrant any additional treatment.
may also be used to control the significant problems that result from a massively enlarged spleen. The mortality rate
associated with this procedure is 7% .Furthermore, a reactive thrombocytosis and leukocytosis can develop because the
cells are no longer sequestered out of the circulation. The decision to undergo splenectomy warrants careful consideration
of the advantages and disadvantages. Nursing management Splenomegaly can be profound in patients with
myelofibrosis, with enlargement of the spleen that may extend to the pelvic rim. This condition is extremely
uncomfortable and can severely limit nutritional intake. Analgesic agents are often ineffective. Methods to reduce the size
of the spleen are usually more effective in controlling pain. Splenomegaly, coupled with a hypermetabolic state, results in
weight loss (often severe) and muscle wasting. Patients benefit from very small, frequent meals of foods that are high in
calories and protein. Weakness, fatigue, and altered body image are other significant problems. Energy conservation
methods and active listening are important nursing interventions. The patient needs to be educated about signs and
symptoms of infection, bleeding, and thrombosis, as well as appropriate interventions if these occur. Ensuring that the
patient takes steps to decrease risks associated with developing thrombosis (e.g., smoking; obesity; or poorly controlled
hyperlipidemia, hypertension, or diabetes) can also be effective.

Hodgkin Lymphoma Rare. High cure rate. Men more then women. Starts in single node. Spreads by
contiguous extension along lymphatic system. Malignant cell is the Reed-Sternberg cell which is a gigantic
tumor cell that is unite and may be immature lymphoid. It is the pathologic hallmark and essential
diagnostic. The tumor is very heterogenous and may contain only a few reed-sternberg cells. Repeat
biopsy to establish dx. Cause is unknown, may be viral.
Sx: Enlargemtn of lymph node in neck. Painless, firm not hard. Cervical, supraclav, mediastinal. Can be
seen on chest xray. Puritiis is common, may have pain at site after alc consumption. Mild anemia. Leuko
or normal, platelet normal. ESR and copper level can assess disease activity. They have impaired cellular
immunity e/b absent or decreased reaction to skin sensitiveity tests. Infections are common. Assess for B
symtoms. PET good to identify residual disease. Staging Staging is numerical at 1 through 4 and then


either A or B Stage 1: single lymph node involvement Stage 2: 2 or more lymph node involvement on one
side of the diaphragm Stage 3: lymph node involvement above and below the diaphragm Stage 4:
involvement outside the diaphragm (liver, skin, spleen, bone marrow) A= absence of B symptoms B =
presence of B symptoms (fever, night sweats, wt. loss) Care: Chemotherapy Radiation Psychosocial
consideration Manage problems related to treatment (chemotherapy and radiation) doxorubicin
(Adriamycin), bleomycin (Blenoxane), vinblastine and dacarbazine

Non-Hodgkins Lymphoma All the lymphoid cancers that dont have the Reed-Sternberg cell. High
Grade Lymphomas: Aggressive with rapid growth More responsive to chemo Chances for long term cure
are greater Low grade Lymphomas: Longer survival rate, slower progression but cure is rare
Assess Large, painless lymph node, Fever, Malaise, Night sweats, Weight loss, Hepatomegaly,
Dx Biopsy (lymph and bone marrow) CXR. CT Scans. MRI spine
Collab care Chemotherapy Radiation Psychosocial consideration Manage problems related to treatment
(chemotherapy and radiation)

Multiple Myeloma
Malignancy of the Plasma cells. Plasma cells are activated B cells. B cells usually protect the body.
Abnormal protein produced instead. Cause is unknown. Exposure: radiation, chemicals, metals,
insecticides. Genetic factors. Viral infection
Assess: Bone pain Osteoporosis Signs and symptoms of: Hypercalcemia Anemia Thrombocytopenia
Dx Urine testing X-Rays, MRI, CT scan Serum Ca+ CBC
Collab care Seldom cured. Chemo, corticosteroids, biologic therapy, stem cell transplant. Adequate
hydration. Weight bearing exercise. Bisphosphonates (inhibit bone breakdown and hypercalcemia). Aredia
(pamidronate). Zometa (zoledronic acid) Didronel (etidronate).

MCV, MCH & MCHC all normal= normocytic, normochromic anemia. RBC low then acute blood
loss, or sickle cell anemia. MCV, MCH & MCHC all low= microcytic, hypochromic anemia. iron
deficiency, chronic blood loss, beta thalassemia. MCV, MCH & MCHC all high= Macrocytic
anemia. Vit. B12 deficiency, folic acid deficiency

CBC part 1

CBC part 2

Bone Marrow Aspiration/Biopsy

Assesses formation of blood cells, quantity, and quality
Used to document infection or tumor within marrow

Usually aspirated from iliac crest and occasionally sternum. Is ok for dxing anemia
Biopsy samples are taken from posterior iliac crest. It shows the architecture of bone marrow and
degree of cellularity. Pt is placed in lateral with one leg flexed or in prone position. CANNOT USE
Patient Preperation
Explain procedure
Give antianxiety if needed
Signed informed consent
Clean skin with aseptic technique
Anesthetize with local of the subq tissue
Pt will feel pressure, but aspiration will cause a sharp pain from suction. Teach them to take deep
breath or relaxation technique.
Do biopsy after aspiration, and in a different location.
Use surgical blade to make an incision first.
Pt feels pressure but not pain.
Assist in comfortable position and encourage deep breathing and relaxing.
Inform MD if pain occurs, can then give another anesthetic agent
Post procedure
Apply pressure for several minutes
Cover with a sterile dressing
May ace for 1-2 days, shouldnt have much discomfort
Warm tub bath and Tylenol can help
Avoid aspirin because of bleeding potential.
Hazards of aspiration or biopsy
Bleeding and infection.
RF bleeding is increased if platelet count is low or if they are taking aspirin or a med that alters
platelet function.
Blood transfusions Autologous: pts own blood. Used for elective surgeries. Start collecting 4-6
weeks before surgery. Give iron supplements. No draws 72 hrs before surgery. Primary advantage
is prevention of viral infections from another persons blood. Also, safer if theyve had reactions
in the past, prevents alloimunization, and avoiding complications of pt with alloantibodies. It can
only be transfused to the donor. If blood isnt needed, can freeze for up to 10 years. There is still
a risk for bacterial contamination. Contraindications: acute infection, severly debilitating
chronic disease, hgb <11, unstable angina, cardio or cerebrovasc disease, and possibly poor
control of epilepsy. Complications excessive bleeding at site (poor technique, bleeding disorder)

failure to apply enough pressure, excessive tourniquet pressure, laceration of vein. Fainting d/t
vasovagal reaction or too much fasting. Hypotension and syncope may occur in an erect position.
Pt should lie down or sit with head between knees. Watch them for 30 more mintes. Angina chest
pain may be precipated with undxed CAD. Seizure may happen if epileptic. Need further medical
eval for angina or seizure.
Transfusion of PRBC
1. Confirm that the transfusion has been prescribed.
2. Check that patients blood has been typed and crossmatched.
3. Verify that patient has signed a written consent form per institution or agency policy and agrees to
4. Explain procedure to patient. Instruct patient in signs and symptoms of transfusion reaction (itching,
hives, swelling, shortness of breath, fever, chills).
5. Take patients temperature, pulse, respiration, and blood pressure to establish a baseline and auscultate
lungs; assess for jugular venous distention to serve as a baseline for comparison during transfusion.
6. Use hand hygiene and wear gloves in accordance with standard precautions.
7. Use a 20-gauge or larger needle for insertion in a large vein. Use special tubing that contains a blood
filter to screen out fibrin clots and other particulate matter. Do not vent blood container.

1. Obtain packed red blood cells (PRBCs) from the blood bankafter the IV line is started. (Institution policy
may limit release to only 1 unit at a time.)
2. Double-check labels with another nurse or physician to ensure that the ABO group and Rh type agree
with the compatibility record. Check to see that number and type on donor blood label and on patients
medical record are correct. Confirm patients identification by asking the patients name and checking
the identification wristband.
3. Check blood for gas bubbles and any unusual color or cloudiness. (Gas bubbles may indicate bacterial
growth. Abnormal color or cloudiness may be a sign of hemolysis.)
4. Make sure that PRBC transfusion is initiated within 30 minutes after removal of the PRBCs from blood
bank refrigerator.
5. For first 15 minutes, run the transfusion slowlyno faster than 5 mL/min. Observe patient carefully for
adverse effects. If no adverse effects occur during the first 15 minutes, increase the flow rate unless
patient is at high risk for circulatory overload.
6. Monitor closely for 1530 minutes to detect signs of reaction. Monitor vital signs at regular intervals per
institution or agency policy; compare results with baseline measurements. Increase frequency of
measurements based on patients condition. Observe patient frequently throughout the transfusion for


any signs of adverse reaction, including restlessness, hives, nausea, vomiting, torso or back pain,
shortness of breath, flushing, hematuria, fever, or chills. Should any adverse reaction occur, stop
infusion immediately, notify primary provider, and follow the agencys transfusion reaction standard.
7. Note that administration time does not exceed 4 hours because of increased risk of bacterial
8. Be alert for signs of adverse reactions: circulatory overload, sepsis, febrile reaction, allergic reaction,
and acute hemolytic reaction.
9. Change blood tubing after every 2 units transfused to decrease chance of bacterial contamination.

1. Obtain vital signs and compare with baseline measurements.
2. Dispose of used materials properly.
3. Document procedure in patients medical record, including patient assessment findings and tolerance to
4. Monitor patient for response to and effectiveness of procedure.
Note: Never add medications to blood or blood products; if blood is too thick to run freely, normal saline
may be added to the unit. If blood must be warmed, use an in-line blood warmer with a monitoring

Transfusion of platelets or FFP

1. Confirm that the transfusion has been prescribed.
2. Verify that patient has signed a written consent form per institution policy and agrees to procedure.
3. Explain procedure to patient. Instruct patient in signs and symptoms of transfusion reaction (itching,
hives, swelling, shortness of breath, fever, chills).
4. Take patients temperature, pulse, respiration, and blood pressure to establish a baseline and auscultate
breath sounds to establish a baseline for comparison during transfusion.
5. Use hand hygiene and wear gloves in accordance with standard precautions.
6. Use a 22-gauge or larger needle for placement in a large vein, if possible. Use appropriate tubing per
institution policy (platelets often require different tubing from that used for other blood products).

1. Obtain platelets or fresh-frozen plasma (FFP) from the blood bank (only after the IV line is started.)


2. Double-check labels with another nurse or physician to ensure that the ABO group matches the
compatibility record (not usually necessary for platelets; here only if compatible platelets are ordered).
Check to see that number and type on donor blood label and on patients chart are correct. Confirm
patients identification by asking the patients name and checking the identification wristband.
3. Check blood product for any unusual color or clumps (excessive redness indicates contamination with
larger amounts of red blood cells).
4. Make sure that platelets or FFP units are administered immediately after they are obtained.
5. Infuse each unit of FFP over 3060 minutes per patient tolerance; infuse each unit of platelets as fast as
patient can tolerate to diminish platelet clumping during administration. Observe patient carefully for
adverse effects, including circulatory overload. Decrease rate of infusion if necessary.
6. Observe patient closely throughout transfusion for any signs of adverse reaction, including restlessness,
hives, nausea, vomiting, torso or back pain, shortness of breath, flushing, hematuria, fever, or chills.
Should any adverse reaction occur, stop infusion immediately, notify primary provider, and follow the
agencys transfusion reaction standard.
7. Monitor vital signs at end of transfusion per institution policy; compare results with baseline
8. Flush line with saline after transfusion to remove blood component from tubing.

1. Obtain vital signs and compare with baseline measurements.
2. Dispose of used materials properly.
3. Document procedure in patients medical record, including patient assessment findings and tolerance to
4. Monitor patient for response to and effectiveness of procedure. A platelet count may be ordered 1 hour
after platelet transfusion to facilitate this evaluation.
Note: FFP requires ABO but not Rh compatibility. Platelets are not typically cross-matched for ABO
compatibility. Never add medications to blood or blood products.