Transcript Unit 8 - EarthLink

Unit 6
Blood Disorders
Gordons Functional Health Pattern
Activity - Exercise
Blood Conditions
• Unit objectives:
– Discuss the components, characteristics and functions of the
hematopoietic system.
– Compare the assessment data and the pathophysiologic
bases that occurs in blood disorders
– Discuss blood transfusion administration, reactions and
management
– Describe the various anemia’s in relationship to decreased,
increased and hemolysis of erythrocytes
– Discuss diagnostic tests, medical management and nursing
interventions for the anemia
Blood conditions
• Discuss the chronic conditions in which anemia can
occur.
• Describe sickle cell crisis and its management
• Differentiate between DIC and clotting problems
• Compare and contrast acute (ALL, ANLL) and
chronic (CML, CLL) leukemias, their clinical
manifestations and management.
• Compare and contrast lymphomas, multiple
myeloma, Hodgkin’s and non-Hodgkin’s lymphoma,
their diagnostic evaluations, clinical manifestations
and management.
• Discuss other FHP’s that might relate to
hematopoietic problems
Blood Conditions
REQUIRED READING:
•
Smeltzer: Chapter 33
Blood Conditions
• A & P review: blood
– Hematologic system  blood, bone marrow & reticuloendotheliaL
system [REM]
– Organs: Peripheral Lymphoid Tissue – sites for antigen processing
• Lymph nodes- small organs, < 5 mm in diameter, found throughout
body & interconnected w lymph vessels; provide RES & immune
functions; receive fluids taken up by lymphatic capillaries from
distal tissue sites. Macrophages w/I the node monitor the fluid for
foreign particulates & phagocitis them; found in large numbers in
abdominal & thoracic areas; called superficial nodes – lying close
to the body surface; when inflamed & swollen  palpated &
diagnostic
• Lymph nodules – modules found in mucosal epithelium lining in
resp, GI, and urogenital tracts.
Blood conditions
• Central Lymphoid Organs
– Spleen – largest lymphoid organ in body; functions  blood-clearing
process; assisting in recycling iron by capturing HgB released from
destroyed RBC’s, and removing particles from RBC’S w/o destroying the
cell itself; the pulp is divided into red zones & white zones (
accumulations of lymphocytes)
– Thymus – located in the mediastinum, reaches peak development
during childhood; endocrine organ secretes hormones that contributes to
maintenance of T-cells.
•
Blood
conditions
Bone marrow – one of largest organs in body, total weight in adult of about
3000 g (comparable to liver);
•
Visual appearance –red marrow – hematopoietic cells interspaced w
sinusoidal capillaries and yellow marrow – large number of adipose cells
–
–
–
–
–
Functions:
Stem cells – primitive; self-replicate, all blood cells are derived
An environment for the differentiation and maturation of blood cells
A storage site for large numbers of neutrophils & erythrocytes
Transformation of undifferentiated lymphocytes into mature
Hematopoiesis
Blood conditions
• Blood  mixture of cells- RBC’s, WBC’s, &
platelets, plasma
– Functions: supplies oxygen from the lungs &
absorbed nutrition from the GI tract to cells’
– Removing waste products from tissues to the
kidneys, skin & lungs for excretion
– Transporting hormones from their origin in the
endocrine glands to other areas of body
– Protecting the body from dangerous
microorganisms
– Promoting homeostasis ( the arrest of bleeding)
– Regulating body temperature by heat transfer
Composition of blood
• 8% of total body wt is blood; young female has
4-5 L, young male has 5-6 L
• Inverse relationship between blood volume & kg
of body wt  the less body fat, the more blood
per kg of body wt
• Arterial blood is bright red because of O2 bound
to Hgb & w/I RBC’s. venous blood is darker
• Blood is 3-4x more viscous [thick] than water.
• Blood is slightly alkaline, pH of 7.35 -745
[neutral pH is 7.0]
Plasma
• The liquid portion of the blood,
• 55% of blood
– 92% water, 7% protein, and < 1% nutrients, metabolic
wastes, resp gases, enzymes, hormones, clotting factors,
• 45% suspended particles [blood cells & platelets]
• Major function is to maintain blood volume
• Packed cell volume or hematocrit: the volume or % of
the RBC’s in sample –35% to 45%
– HcT can be  from loss of plasma (dehydration) or 
production of RBC’s (polycythemia)
– WBC’s & platelets -1 % of blood volume; form a buff coat or
white layer seen at interface of the RBC’s and plasma
RBC’s
• Erythrocytes
– carry O2 or hemoglobin to the cells & CO 2 back to lungs
– Assist with acid-base balance – carbonic anhydrase
– Structure: no nucleus, 7.5 um in diameter, depression on
flat side  very large surface area, to allow cell to change
shape passively as it goes thru capillaries.
– Production  erythropoises every minute, more than 100
million RBC’ s are formed to replace of destroyed cells.
• Precursor cells, proper microenvironment, & adequate supplies of
iron, vit B12, folic acid, protein, pyridoxine & traces of copper
• Arise from nucleated cells called hematopoietic stem cells
• Immature erythrocytes leave the bone marrow  circulation now
called reticulocytes  spleen  undergo conditioning  mature
erythrocytes  general circ. Life span 105-120 days
–  RBC production when O2 levels ↓ ; during pregnancy or
erythropoietin – healthy bone marrow can increase
production 6-7 x normal rate
RBC’s
• Erythrocytes
– Aged erythrocytes  fragile  rupture  release of
hemoglobin, “ghost cells”, taken up by macrophages 
hemoglobin broken down into heme (iron) goes to liver;
porphyrin  liver converts into bilirubin  excreted as bile
– Nutritional influences on RBC production
• Vit B12 – RBC maturation, nervous system function
– Not synthesized in body, must ingest from diet [meat, dairy products];
called extrinsic factor (outside the body), when digested from food, Vit B
12 binds w glycoprotein called intrinsic factor (inside body) in duodenum
for absorption in the blood
• Folic acid – a B-group vit,
– Synthesized by many plants & bacteria; food sources: vegetables & fruit
• Iron – essential to hemoglobin production.
– Adults 50 mg of Fe per 100 ml of blood; Hgb accounts for 2/3 of iron
(essential iron), 1/3 resides in bone marrow, spleen & liver. In Fe
deficiency develops these stores are reduced first, followed by a gradual
loss in Hgb
Platelets
• Platelets (thrombocytes)
• Are granular fragments from giant
multinucleated cells in red bone marrow
(megakaryocytes); takes 5 days to form & live
only 7 -10 days
• have two roles in homeostasis:
– Occlusion of small openings in blood vessels
– Provide chemical components leading to
coagulation
• Substances released from platelet aggregation activate
coag factors that provide for a stable clot or plug w fibrin
Role of liver & spleen
• Spleen – reservoir for erythrocytes – during
severe anemia
• Liver – fixed macrophages (Kupffer cells)
remove inanimate particulates & bacterial cells;
– Production of small quantities of erythropoietin
– Synthesis of plasma proteins & clotting factors
– Decomposition of Hgb into bilirubin
– Storage of iron in form of ferritin
Homeostasis
• Normal homeostasis – process that repairs vascular
breaks to reduce blood loss while maintaining the flow
of blood through vascular system; 3 components:
– Blood vessels, the platelets, & coagulation factors
– Work in 3 stages:
• Vascular phase  vasoconstriction of the vessel occurs
– Blood vessels supplying the site constrict (muscular tissue & reflex
nervous system reactions, serotonin is released.
• Formation of a platelet plug
– In circulation, recognize a disruption or alteration in the endothelial lining
of blood vessels  become sticky & adhere to one another
• Coagulation or formation of a fibrin clot
– If bleeding is severe, coagulation factors must join w platelets for form a
permanent clot
– once clot has served its purpose, it is balanced by fibrinolysis (clot
dissolution)
Homeostasis
• Clot formation: results in either one or two pathways:
table 1, pg 63 a
– Extrinsic pathway: initiated when tissue injury occurs outside
the vessel i.e.: burn
• Damaged tissue releases factor III (tissue thromboplastin) which
initiates the clotting cascade to form activated factor X  leads to clot
formation
– Intrinsic pathway: involves blood itself, i.e.: antigen –
antibody reactions & endotoxins;
• All factors for this reaction already in blood; pathway starts when
factor VII is exposed to a foreign surface  cascade of enzymatic
reactions to activate factor X
• Activated Factor X is responsible for conversion of prothrombin to
thrombin & soluble fibrinogen to insoluble fibrin clot (forms dense
interlacing threads to entrap cells)
Fibrinolysis
• Blood carries natural anticoagulants – heparin,
antithrombin
• Clot dissolves:
– Plasminogen is required to breakdown fibrin,
already in blood & in clot  turns into plasmin 
digests the fibrinogen & fibrin
Leukocytes (WBC’s)
• 5 types _classified according to presence or absence of
granules & staining characteristics of their cytoplasm
• Myeloid Stem cell  granulocytes 3 types:
– Neutrophils – primary cell to respond to an acute inflammatory
response, stored primarily in bone marrow
– Eosinophils – protect against parasitic infections & modulate IgE –
mediated allergic responses.
– Basophils – store heparin, histamine
• Agranulocytes (WBC w/o cytoplasmic granules) 2 types:
– Monocyte – released into circ as a immature phagocytic cell,  liver,
transform into macrophage with full phagocytic function
– Lymphocytes – some programmed to become T cells & others B cells in
bone marrow
• B cells function in antibody-mediated immune response to defend the body
against invasive types of bacteria,, bacterial toxins & some virus
• T cells are bases of cell-mediated immune functions that defend against
intracellular pathogens, fungi & virus
Anemia’s
•
•
•
•
Loss of RBCs
Decreased production of RBCs
Increased destruction of RBCs
Medical management is directed towards correcting
or controlling the cause and/or replacement of
RBCs
•
Nursing interventions are directed at managing
fatigue, maintaining adequate nutrition and
perfusion, complying with prescribed therapy, and
monitoring and managing potential complications
Types of Anemia
•
•
•
•
•
•
•
•
Anemias of Renal Disease and Chronic Disease
Aplastic
Iron Deficiency
Megaloblastic
Myelodysplastic Syndromes
Hereditary Hemochromatosis
Thalassemia
Sickle Cell
• Immune Hemolytic
Anemias
2. Anemia in renal dz – due to decreased production; deficiency of
erythropoietin and shortened RBC life span
3. Anemia in chronic disease – due to decreased production, deficiency
of erythropoietin and shorten RBC life span
4. Iron-deficiency anemia (chronic, microcytic, hypochromic)
a. Pathophysiology – inadequate absorption or excessive loss of
iron
b. clinical manifestations
Lab – low hbg, ↓total RBC, MCV, MCH & MCHC. Mild case may be
asymptomatic
c. Management/nursing
determine cause, iron preparations, diet, preventive education – diet
with foods high in iron – organ meats, beans, leafy vegetables,
raisins, molasses.
Pace/plan activities.
5. Magablastic anemia – caused by deficiencies of vitamin B12 and or
folic acid.
Anemias
1.
a.
b.
c.
Aplastic anemia (normochromic normocytic)
pancytopenia ↓ RBC,WBC,and Platelets
Pathophysiology – decrease in or damage to marrow
stem cells.
Clinical manifestation
Lab:↓RBC
gradual onset, weakness, dyspnea on exertion,
abnormal bleeding when thrombocytopenia present.
Management/nursing
bone marrow transplantation,
immunosuppressivetherapy, supportive therapy
(transfusions), preventive education.
Plan/pace activities and avoid trauma.
Anemias
6.
a.
b.
c.
7.
Vitamin B12 deficiency (pernicious anemia)
Pathophysiology – faulty absorption from the GI tract, lack of intrinsic factor
Clinical Manifestations
Lab - ↓ RBC, WBC, and MCH and  MCV and number of megaloblasts (by bone
marrow aspiration).
Schilling test
SXS – pale, fatigue, weakness, smooth sore red tongue, mild diarrhea, confusion,
paresthesia of extremities, difficulty maintaining balance.
Management/nursing
preventive education – vegetarians
vit B12 administration
support during tests
care of neuropathy problems
Folic acid deficiency – more commonly seen than Vit deficiency
a. Pathophysiology – folic acid deficiency
b. Clinical manifestations –
Lab – decreased serum folate – schilling test. Sxs – sore red tongue, no
neurological manifestations
c. Management/Nursing
diet – uncooked vegetables, green leafy vegetable, liver, citrus fruits, and yeast
folic acid supplementations.
Anemias
Hemolytic anemias:
1.
Major hallmarks – shortened RBC life span, abnormal increase in
the number of RBC destroyed and failure of the bone marrow to
replace destroyed RBCs
2.
Causes
trauma, chemical agents and medications, infectious agents,
systemic disease, antigen-antibody reactions
3.
Clinical manifestations
Lab:  retic count,  indirect bilirubin, ↓haptoglobuin and red cell
survival study.
SXS – pale, dyspnea, jaundice, cholelithiasis, splenomegaly,
hepatomegaly
•
Management/nursing
ID cause and correct
maintain fluid and electrolytes balance
02 administrations, preventive education, pace/plan activities
Anemias
Inherited hemolytic anemias
1.
2.
Herditary spherocytosis (congenital hemolytic jaundice, congenital
sphereocytic anemia). Inherited as a simple medelian dominant
trait
a. clinical manifestations – anemia, jaundice, splenomegaly
b. Management/nursing – splenectomy, O2 adm, blood
transfusion
Sickle Cell anemia
a. Pathophysiology – inheritance of the sickle hemoglobin gene
(Hbs)
b. Clinical manifestations – anemia, jaundice.
c. preventive education – avoid infections, cold temps.
supportive care – hydration, avoid high attitudes, folic acid
d. Sickle Cell Crisis – (occlusion of microcirculation)
clinical manifestations – severe pain, fever, and leukocytosis
management/nursing – control of pain, IV fluids, transfusions, O2
therapy.
Anemias
3. Thalassemia (Mediterranean anemia, cooley’s
anemia)
Characteristics – hypochromia, microcytosis,
hemolysis, variable degrees of anemia
a. Classified (according to affected globin chain)
- a-thalassemia – mild form
- b-thalassemia – more common form
- Thalassemia minor – asymptomatic
- Thalassemia major (cooley’s anemia) – severe
anemia, marked hemolysis of erythorytes,
jaundice. TX – splenomegaly, transfusions.
Anemias
4. Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD)
a.
Pathophysiology – a genetic defect of the RBC
b.
Clinical manifestations
Lab – G6PD
may be asymptomatic, jaundiced, pallor, increased reticulocyte,
Heins bodies
c.
Management/Nursing – preventive education, rest, fluids &
nutritious diet, transfusions
5. Acquired Hemolytic Anemias
Immune hemolytic anemia as a result from exposure of the RBC to
antibodies.
a. Clinical manifestation – fatigue, dyspnea, jaundice,
splenomegaly
b. Management/nursing – ID causative agent, corticosteroids,
blood transfusions, spleenectomy, immunosuppressive agents.
Polycythemia
•
•
•
•
•
Polycythemia Vera is a proliferative disorder in
which myeloid stem cells escape normal
control mechanisms
RBC, WBC, and platelet counts are elevated
Secondary Polycythemia is caused by
excessive production of erythropoietin
May occur as response to hypoxia or
neoplasms
Medical management is removal of cause or
therapeutic phlebotomy
Leukopenia and Neutropenia
• Leukopenia is condition of fewer WBCs
than normal, results from neutropenia or
lymphopenia
• Neutropenia results from decreased
production or increased destruction of
neutrophils
• Medical management varies depending on
cause
• Nursing management is towards
preventing and managing infections
Leukocytosis and Leukemias
• Leukocytosis is an increased level of
WBCs
• Leukemia is a neoplastic proliferation
of one particular cell
• Acute and Chronic Myeloid Leukemia
• Acute and Chronic Lymphocytic
Leukemia
• Agnogenic Myeloid Metaplasia
Leukemia
• Is a malignant ds of the blood-forming organs.
• 8% of all human cancers
– Most common in children & young adults – 80% are
lymphatic; 20% nonlymphatic; adults are opposite
• Cause unknown
• Risk factors: genetic factors; exposure to
ionizing radiation & chemicals (benzene);
medications ( alkylating agents); congenital
abnormalities (Down’s syndrome); presence &
infection w human T-cell leukemia virus type 1
[HTLV-1]
Leukemia
• Pathophysiology: uncontrolled proliferation of
leukocytes  lack of control  normal bone
marrow to be replaced by immature &
undifferentiated leukocytes (blast cells) 
circulate in blood & infiltrate blood forming
organs (liver spleen, lymph nodes)
• Classification: acute leukemia's are classified
according to their morphologic characteristics
& histo-chemical staining of blast cells 
indicates the % of immature cells in bone
marrow
Acute leukemia
• Acute = 50% of the marrow cells must be immature;
two major forms: lymphocytic & nonlymphocytic
leukemia
– Clonal disorders  a single lymphocyte stem cell undergoes
transformation  divide slowly & take longer to synthesize
DNA (blast phase leaving WBC’s undifferentiated or blasts
 block cell precursors & compete w normal cellular
proliferation “blocking out” the marrow & cause other cell
lines to stop production  causing pancytopenia ( a
reduction in all cellular components)
• Acute lymphoblastic leukemia (ALL)
– Most common in children (median age 11 yrs), acute
course—initial symptoms & w/o tx die 3-6 months, males >
females, more common in European – Americans
Acute Leukemia
• Acute adult nonlymphatic leukemia (AANLL) – more common in
adults, (median age 67 yrs), also called acute myeloid leukemia
(AML)
– involves the rapid accumulation of hematopoietic stem cells,
(differentiate into monocytes, granulocytes, RBC’s, and platelets)
• History: questions – exposure to radiation, chemicals, viruses,
& medications, occupation? Power plant or serving in military
• S&S: sudden onset of high fever, signs of abnormal bleeding
[bleeding gums, long menses, petechiae,  bruising, nose
bleeds],  fatigue & malaise, wt loss, night sweats & chills, c/o
abd or bone pain, appear acutely ill, dyspnic, & pale, enlarged
liver &lymph nodes; CNS involvement – HA, vomiting &
papilledema, blurred vision, meningeal irritation, intracranial
hemorrhage,  chemo does not pass the blood brain barrier
– psychosocial assessment  pts, families are shocked & fearful
Acute leukemia
• Neutropenic precautions- neutrophils < 2000 mm3,
necessary in prevention & limiting infections (chart
33-9, page 898)
• Bone marrow transplant – BMT is the administration
of 500-700 ml of marrow aspirated from the pelvic
bones of the patient during a remission (autologous
transplant) – most common; (allogeneic transplant)
– compatible donor – usually a parent or sibling.
• Transfusion of RBC’s & platelets – may be required
until the BM produces mature cells
• Radiation TX – adjunct to chemo when leukemic
cells infiltrate the CNS, skin, large mediastinal mass
Chronic Leukemia
• Chronic lymphatic leukemia (CLL) –involves
lymphocytes, (cells that circulate among the
blood, lymph nodes, lymphatic & lymphoid
organs); characterized by an uncontrollable
spread of abnormal, small lymphocytes (early
B lymphocytes)
• 33% of new leukemia cases annually in US are
dx as CLL.
• Least malignant form & progresses more
slowly than others, sometimes takes as long
as 15 yrs (WBC produced are more mature &
better to defend body against infection)
Chronic Leukemia
• Causes: unknown, several risk factors:  families,
suggesting heredity issues, possible genetic
predisposition, immunologic defects – ataxiatelangiectasia (vascular lesions formed by dilation of a
group of small vessels, birthmarks)
• Men > woman, and over the age of 50
• S&S: same as all types of leukemia;  anemia,
thrombocytopenia, & leucopenia; hx of malaise &
enlarged nodes, fever  susceptible to opportunistic
fungal, viral & bacterial infections, lost wt, any
bleeding, family hx of CLL, pale, enlarged liver or
spleen, skin has macular or nodular infiltrates
Chronic Leukemia
• Chronic myelogenous leukemia or chronic
granulocytic leukemia – characterized by abnormal
overgrowth of myeloblasts (all granulocytic
precursors)
– Gradual onset, WBC’s more mature
– Two phases: insidious chronic phase – originates in the
pluripotent stem cell w an initial finding of hyper cellular
marrow w a majority of normal cells; after approx 4 yrs. 
enters a blast crises or acute phase.
– Causes: 90% of pts have the abnormal Philadelphia
chromosome – thought to be induced by radiation or
carcinogenic chemicals; unidentified virus
– Occurs more commonly in young-to middle aged adults; 25
-60 yrs of age; slightly more men than women
The Lymphomas
• Neoplasms of cells of lymphoid
origin
• Hodgkin’s Disease
• Non-Hodgkin’s Disease
• Multiple Myeloma
Lymphoma’s
• Originating from the lymphatic system,
lymphoma is most common tumor of lymphoid
system; primary (thymus or BM) or secondary
tissue ( lymph nodes, spleen, tonsils)-most
arise from secondary
– Major subdivisions are: Hodgkin’s lymphoma /
Hodgkin's Disease (HD); Non – Hodgkin’s
lymphoma (NHL)
• 55,000 cases dx annually
Hodgkin’s Disease
• In 1832, Hodgkin described a ds w enlarged lymph
nodes starting in the neck & spreading throughout the
body & bx showed a distinctive large cell – called the
Reed-Sternberg cell – when the cell is absent the ds is
classified as NHL
• Incidence – 7500 new cases per yr, slightly more
males than females, strikes in young adult hood (ages
15 to 38) & a second peak later in life > 50, worse
prognosis
• Etiology – exact cause unknown, researchers suspect
an infectious component, ie: Epstein-Barr virus (organ
transplant recipients/ immunodeficiency ds, hx of
mononucleosis (2-3x), some studies show genetic
predisposition (Jews)
Hodgkin’s Disease
• Pathophysiology – painless progressive enlargement
of LN, caused by a proliferation of lymphocytes,
histiocytes, eosinophils & Reed – Sternberg giant
cells.
– Progressive & fatal if not treated, but one of the most curable
w tx (5yr survival rate > 90%)
• S &S- often are asymptomatic & present w painless
lymphadenopathy –
• . Nonproductive cough –X-ray shows a mediastinal
mass in 50% of pts;
• freq noc sweats & fever > 38 *C
• Dx: LN & bone marrow bx, Chest - X-ray; CT of
thoracic, abd & pelvis & staging laparotomy
Hodgkin’s Disease
• Staging: HD is divided into stages according to
the microscopic appearance of involved LN, the
extent & severity & prognosis
Hodgkin’s Disease
• Tx- begins w accurate classification & staging
– Radiation is used for early less extensive ds
– Stage 2 is combination of radiation & chemo used
for IIB, and III A & B,
– combo chemo for stage 4
Non-Hodgkin’s Lymphoma
• AKA – malignant lymphoma; comprises a group of
malignancies w a common origin in the lymphoid cells’
characterized by random proliferation of lymphocytes
• Ranges from aggressive, rapidly fatal to indolent
nodular varieties
– Less promising prognosis than HD
• ACS – estimates 55,000 new cases annually, &
25,000 related deaths; average age at dx is in 50’s
• 7 x more common than HD
• Between 1973 & 1992, a 75% increase in NHL
• 60 X more common in pts w AIDS
• 6th most common cause of cancer
• Men > woman;  in whites than other races
Non-Hodgkin’s Lymphoma
• Pathophysiology – an abnormal proliferation of neoplastic
lymphocytes –
• S&S – localized or generalized lymphadenopathy ( cervical,
axillary, inguinal & femoral), swelling is painless, nodes have
gradually enlarged over months or years; can be diffuse s&s
– B symptoms ( noc sweats, fever & wt loss, 1/3 have
hepatomegaly or splenomegaly
• Labs: CBC. ESR & peripheral smear,  LDH in advance
stages, uric acid, Ca,
• LN bx done for adenopathy > 3 weeks; B symptoms not
attributed to other causes, abnormal blood tests, Xray–
shows possible extranodular involvement, CT of abd & pelvis
• Disease staging
Non-Hodgkin’s Lymphoma
• Medical Management – tx is based on
classification of the cell & staging of ds. The ds
process may be slow enough that tx is saved
until ds takes a more aggressive path.
– Stage 1-11 radiation alone may be curative
• Intermediate-high grade lymphomas receive
combo chemo;
• combination chemo & radiation tx is done to
produce tumor shrinkage & remission
Nursing Management
• History & Physical– Any hx of HIV?, organ transplant, autoimmune ds, c/o
painless enlarged LN? fever, noc sweats, wt loss,
weakness & malaise, cough, dyspnea & chest pain (occur
20%  indicates lung involvement)
– LN  palpate chains infraclavicular, iliac, femoral sites
(involved nodes are painless, firm & rubbery in
consistency)& abdomen signs of hepatosplenomegaly?
& ascites? Skin lesions that look like nodules (20% of
cases),
– Psychosocial assessment – dx of cancer is devastating,
more common in older adult, effects retirement plans 
may lead to feelings of loss, grief, & anger.
Oncology
• Approx 1.2 – 1.3 million new cancers are dx each year
• Over 500,000 cancer deaths/ yr
• NCI = National Cancer Institute estimate 8.4 live today w a hx
of cancer
• Terminology:
– Tumor – lump, mass, or swelling (lay public use as a synonym for
cancer)
– Neoplasm – (Greek neos = new, plasis = molding); abnormal mass of
tissue serves no useful purpose & may harm the host organism
• Benign – usually a harmless growth that does not spread or invade other
tissues, does occupy space
• Malignant – harmful mass, capable of invasion of other tissues &
metastasis (spread) to distant organs
– Cancer – used to refer to malignant neoplasms; ds of the cell in which
normal mechanisms of control of growth & proliferation are altered, its
invasive, spreads directly to surrounding tissue and to new sites
– Oncology – refers to the medical specialty that deals w the dx, tx &
study of cancer
Oncology
• Mortality rate = the # of deaths caused by
cancer that occurs in a population in a given yr;
expressed as # of deaths due to cancer per
100,000 persons.
• Common misconceptions:
– Cancer is one disease --- cancer is many diseases
– The change from a normal cell to neoplastic cells is
a process not a single event or a single alteration in
cells; clinical manifestations are only the final
stages in the natural history of cancer
Bleeding Disorders
• Primary Thrombocythemia is a stem cell
disorder within the bone marrow
• Secondary Thrombocythemia is caused by
increased platelet production
• Thrombocytopenia can result from
decreased production of platelets within the
bone marrow, increased destruction of
platelets, or increased consumption of
platelets
• Idiopathic Thrombocytopenic Purpura may
be acute or chronic
Platelet Defects
• Qualitative defects can occur as
well as quantitative
• May be induced by aspirin or
NSAIDs
Hemophilia
• Hemophilia A caused by genetic defect that
results in deficient or defective factor VIII
• Hemophilia B caused by genetic defect that
results in deficient or defective factor IX
• X-linked traits affect males
• Von Willebrand’s Disease is a deficiency of
von Willebrand factor which is necessary for
VIII activity and platelet adhesion
Hemophilia
• Medical Tx goals –
– Stop topical bleeding ASAP
– Raise the level of antihemophilic factor (AHF) in
plasma – temporary supplies the missing factor
• Immediate transfusion of factor VIII & IX concentrate is
the primary tx  concentrates used, less risk of blood
volume overload (hepatitis & HIV remains a risk but now
better purification techniques are in place); the
procoagulant activity of AHF disappears rapidly, client
needs tx q 12 hrs until bleeding stops.
• Prognosis has  since AHF
Acquired Coagulation
Disorders
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•
•
•
•
•
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Liver Disease
Vitamin K Deficiency
Complications of Anticoagulant Therapy
Disseminated Intravascular Coagulation
Hyperhomocystinemia
Antithrombin III Deficiency
Protein C Deficiency
Activated Protein C Resistance and Factor V Leiden Mutation
Protein S Deficiency
Acquired Thrombophilia
Therapies for Blood Disorders
• Splenectomy may be necessary
after trauma or possible treatment
for some hematologic disorders
• Therapeutic Apheresis removes
certain cells from blood
• Therapeutic Phlebotomy is removal
of a certain amount of blood under
controlled conditions
Blood and Blood Component
Therapy
• Whole Blood
• White blood cells, red blood cells,
platelets and plasma
• Special preparations: Factor VIII,
Factor IX, albumin, immune
globulin
Transfusion
• Blood donation may be direct donation, standard or
autologous
• Transfusion complications
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–
Febrile, nonhemolytic reaction
Acute hemolytic reaction
Allergic reaction
Circulatory overload
Bacterial contamination
Transfusion-related acute lung injury
Delayed hemolytic reaction
Diseases transmitted by blood transfusion
Complications of long-term transfusion therapy
Iron overload
Peripheral Blood Stem Cell Transplantation and
Bone Marrow Transplantation
• May offer cure for some patients with
hematologic disorders
• Intensive chemotherapy with goal of
complete ablation of patient’s bone
marrow
• Stem cells from donor are infused into
patient
DIC
• Disseminated Intravascular Coagulation [DIC]
• Life threatening disorder in which bleeding & clotting
occur simultaneously; occurs acutely & in patients w
cancer or mothers carrying a dead fetus.
• Pathophysiology: involves an over activation of the
clotting mechanisms: tiny clots accumulate in the
microcirc (capillaries) throughout body, depleting the
body of its supply of clotting factors  microemboli
interfere w blood flow  ischemia & organ damage,
clots begin to lysis  fibrin degradation products
(FDP’s) – have an anticoagulation property of their
own) are released,  FDPs along w ↓ levels of
clotting factors  lead to massive internal bleeding:
brain, kidneys, lungs, heart, wounds & old puncture
sites
Nursing Management
• Nsg Dx: At risk for Sepsis, At risk for Bleeding (result
of thrombocytopenia secondary to tx), prone to Altered
Nutrition, at risk for Ineffective Management of
Therapeutic Regimen (Individuals & Family)
– Outcomes: the desired outcome for the client is that the ds
will become a chronic condition that the family can cope w in
a positive manner
– Interventions: hand washing (prevent infections), low
bacteria diet (excludes raw fruits, raw fish,) daily bathing,
good oral hygiene, administer abx, as ordered, analgesics
limit invasive procedures, monitor for fungal or viral
infections, bleeding precautions: soft toothbrushes, avoid
hard flossing, avoid blowing or picking nose, stool softeners
 avoid straining for BM’s, using tampons, use electric
razors, avoid rectal supp, limit injections, avoid aspirin, avoid
urinary catheters, use pressure reducing mattress, avoid
over inflation of B/P cuff & use rotation, use paper tape
DIC
• Causes: always occurs in response to another
type of disease or trauma; shock, cirrhosis,
glomerulonephrits, conditions causing release
of Factor III; fat emboli & snake bites, obstetric
conditions– abruptio placenta, retained dead
fetus
– Can occur anytime – women of childbearing age
who developed pregnancy- induced hypertension
– Not known how above disorders trigger DIC, but
intrinsic and/or extrinsic pathway of coag cascade is
activated
DIC
• Assessment:
– Hx: any chest, joint, back or muscle pain –severe
in DIC
– PE: assess skin for petechia, ecchymoses,
hematomas, epistaxis, bleeding from wounds,
vaginal bleeding in labor or pp, B/P ↓ , rapid
thready HR, restless, agitated, or confused,
oliguria present? Sense of impending doom, need
for multiple transfusions  fear, anxiety
– S &S occur acutely & develop w/I days or hours
– Mortality can reach 80%
DIC
• Expected Lab Values in DIC
Blood Component:
Role in Coagulation:
↓ platelets [< 100,000]
needed for clotting
↓ fibrinogen [<150 mg]
source of fibrin,
prolong thrombin time
↓the rate of fibrin
[> 15 sec]
production
prolong prothrombin PT reflects enzymes needed to
[> 15 sec]
convert fibrinogen
to fibrin are ↓
Prolong PTT
as above
positive D-dimers
antigen formed when the
[ > 500 ]
enzyme plasmin digests
clotted fibrin
DIC
• Management/nursing
– Correct precipitating factors – correct infections, delivery of
fetus, control bleeding
•
•
•
•
RBC’s –used to replace hypovolemia & to improve oxygenation
FFP- replaces clotting factors
Cryoprecipitate – best source for fibrinogen & factors V,VIII & XIII
Platelets – transfusion is used for platelet count falls below
100,000/mm3
– Use of heparin - reserved for clients w thrombosis seen in
acute renal failure and/or skin ischemia – low dose 300-500
u/hr
– Limit physical activity
– Bleeding precautions keep venipunctures to a minimum,
hold pressure for 10 min’s to puncture sites.