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Module 1
HEMATOLOGIC/IMMUNE/AUTOIMMUNE
W.PAWLIUK MPH MSNED RN CEN
COMPOSITION OF BLOOD
Blood
Composed of plasma and formed elements
Complex transport medium that performs vital pickup and
delivery services for the body
Keystone of body’s heat-regulating mechanism
Blood volume
Blood volume varies according to age, body type, sex, and
method of measurement
FORMED ELEMENTS OF BLOOD
Red blood cells (RBCs), also called erythrocytes
Description of mature RBCs
Have no nucleus and shaped like tiny biconcave disks
Do not contain ribosomes, mitochondria, or other organelles typical of
most body cells
Primary component is hemoglobin
Most numerous of the formed elements
Function of RBCs
Critical role in the transport of oxygen and carbon dioxide depends on
hemoglobin
FORMED ELEMENTS OF BLOOD (cont.)
Hemoglobin
Within each RBC are approximately 200 to 300 million molecules
of hemoglobin
Hemoglobin is composed of four globin chains, each attached to a
heme group
Hemoglobin is able to unite with four oxygen molecules to form
oxyhemoglobin to allow RBCs to transport oxygen where it is
needed
Anemia: a decrease in number or volume of functional RBCs in a
given unit of whole blood
FORMED ELEMENTS OF BLOOD (cont.)
Formation of RBCs
Erythropoiesis: entire process of RBC formation
Formation begins in the red bone marrow as hematopoietic stem
cells and goes through several stages of development to become
erythrocytes; entire maturation process requires approximately 4
days
RBCs are created and destroyed at approximately 100 million per
minute in an adult; homeostatic mechanisms operate to balance
the number of cells formed against the number of cells destroyed
FORMED ELEMENTS OF BLOOD (cont.)
Destruction of RBCs (Figure 17-8)
Life span of a circulating RBC averages 105 to 120 days
Macrophage cells phagocytose the aged, abnormal, or fragmented
RBCs
Hemoglobin is broken down and amino acids, iron, and bilirubin
are released
FORMED ELEMENTS OF BLOOD (cont.)
White blood cells (WBCs), also called leukocytes (Table 17-1)
Granulocytes
Neutrophils: approximately 65% of total WBC count in a normal blood
sample; highly mobile and active phagocytic cells
Eosinophils: 2% to 5% of circulating WBCs; numerous in lining of
respiratory and digestive tracts; capable of ingesting inflammatory
chemicals and proteins associated with antigen-antibody reaction
complexes; provide protection against infections caused by parasitic
worms and allergic reactions
Basophils: only 0.5% to 1% of circulating WBCs; motile and capable of
diapedesis; cytoplasmic granules contain histamine and heparin
FORMED ELEMENTS OF BLOOD (cont.)
Agranulocytes
Lymphocytes: smallest of the WBCs; second most numerous
WBC; account for approximately 25% of circulating WBCs; T
lymphocytes and B lymphocytes have an important role in
immunity: T lymphocytes directly attack an infected or
cancerous cell, and B lymphocytes produce antibodies
against specific antigens
Monocytes: largest leukocytes; mobile and highly phagocytic
cells
WBC numbers: normal blood usually contains 5000 to
9000 leukocytes, with different percentages for each type;
WBC numbers have clinical significance because they
change with certain abnormal conditions
FORMED ELEMENTS OF BLOOD (cont.)
Formation of WBCs
Granular and agranular leukocytes mature from the
undifferentiated hematopoietic stem cell
Neutrophils, eosinophils, basophils, and a few lymphocytes and
monocytes originate in red bone marrow; most lymphocytes and
monocytes develop from hematopoietic stem cells in lymphatic
tissue
BLOOD TYPES: BLOOD GROUPS
The ABO system
Every person’s blood belongs to one of four ABO blood groups
Named for antigens on RBC membranes
Type A: antigen A on RBCs
Type B: antigen B on RBCs
Type AB: both antigens A and B on RBCs; known as universal
recipient
Type O: neither antigen A nor B on RBCs; known as universal
donor
BLOOD TYPES: BLOOD GROUPS (cont.)
The Rh system
Rh-positive: Rh antigen is present on the RBCs
Rh-negative: RBCs have no Rh antigen present
Anti-Rh antibodies are not normally present in blood; anti-Rh
antibodies can appear in Rh-negative blood if it has come in
contact with Rh-positive RBCs
Anemia
Reduction in the total number of
erythrocytes in the circulating blood or in the
quality or quantity of hemoglobin
Impaired erythrocyte production
Acute or chronic blood loss
Increased erythrocyte destruction
Combination of the above
Anemia
Classifications
Morphology
Based on MCV, MCH, and MCHC values
Size
Identified by terms that end in “-cytic”
Macrocytic, microcytic, normocytic
Hemoglobin content
Identified by terms that end in “-chromic”
Normochromic and hypochromic
Anemia
Physiologic manifestation
Reduced oxygen-carrying capacity
Variable symptoms based on severity and the
ability for the body to compensate
Anemia
Risk factors
Advanced age, environmental exposure to chemicals, liver
disorders, autoimmune or other immunological disorders
Chronic anemia symptoms
Fatigue, weight loss, pallor, dyspnea on exertion,
hematochezia, sensitivity to cold, intermittent dizziness,
excessive menstration, paresthesias, uremia weakness, melena
Acute anemic symptoms
Fever, chest pain, acute heart failure, confusion, irritability
orthostatic hypotension, dyspnea, tachypnea, frank bleeding
Anemia
Pernicious anemia
Caused by a lack of intrinsic factor from the gastric
parietal cells
Required for vitamin B12 absorption
Results in vitamin B12 deficiency
Anemia
Pernicious anemia
Typical anemia symptoms
Neurologic manifestations
Absence of intrinsic factor on testing
Others
Loss of appetite, abdominal pain, beefy red tongue (atrophic
glossitis), icterus, and splenic enlargement
Anemia
Pernicious anemia
Treatment
Parenteral or high oral doses of vitamin B12
Anemia
Aplastic anemia
Pancytopenia
Pure red cell aplasia
Anemia’s compared
Pernicious
Aplastic
Lack of intrinsic factor
Rare, caused by bone
for absorption of B12
Could be congenital or
adult-onset gastric
mucosal atrophy
Develops slowly and as
hemoglobin decreases to
around 7-8 g/dl classic
symptoms start appearing
Treatment: Vitamin B12
marrow problems,
autoimmune disorders,
may also be congenital
Classic symptoms seen
Treatment is targeted at
the cause but can include
transfusions
Hemolytic Anemia
Destruction or hemolysis of RBCs at a rate that
exceeds production
Third major cause of anemia
Intrinsic hemolytic anemia
Abnormal hemoglobin
Enzyme deficiencies
RBC membrane abnormalities
Hemolytic Anemia (Cont’d)
Extrinsic hemolytic anemia
Acquired
Sites of hemolysis
Intravascular
Extravascular
Sequences of Events in Hemolysis
Hemolytic Anemia
Jaundice
Destroyed RBCs cause increased bilirubin
Enlarged spleen and liver
Hyperactive with macrophage phagocytosis of the defective
RBCs
Sickle Cell Disease (SCD)
Group of inherited, autosomal recessive disorders
Presence of an abnormal form of hemoglobin in the
erythrocyte
Hemoglobin S (HbS), abnormal
Sickle Cell Disease (Cont’d)
HbS causes the RBC to stiffen and elongate
Sickle shape in response to ↓ O2 levels
Substitution of valine for glutamic acid on the β-globin chain
of hemoglobin
Genetic disorder
Incurable disease, often fatal
Sickle Cell Disease
Etiology and Pathophysiology
Types of SCD
Sickle cell anemia
Most severe
Homozygous for hemoglobin S (HbSS)
Sickle cell thalassemia
Sickle cell HbC disease
Sickle cell trait (HbAS)
Sickle Cell Hemoglobin Aggregates and Alters
Shape of RBC
Sickle Cell Disease
Clinical Manifestations
Typical patient is asymptomatic except during
sickling episodes
Symptoms can be
Pain and swelling
Pallor of mucous membranes
Fatigue
Clinical Manifestations of Sickle Cell Disease
Sickle Cell Disease
Complications
Gradual involvement of all body systems
Usually fatal by middle age from renal and
pulmonary failure
Prone to infection
Pneumonia, most common infection
Sickle Cell Disease
Diagnostic Studies
Peripheral blood smear
Sickling test
Electrophoresis of hemoglobin
DNA testing
Skeletal x-rays
Magnetic resonance imaging (MRI)
Sickle Cell Disease
Nursing Management
Alleviate symptoms of disease complications
Minimize end-organ damage
No specific treatment for SCD
Patient teaching
Avoid high altitudes, maintain fluid intake, treat infections,
control pain
Sickle Cell Disease
Nursing Management (Cont’d)
O2 for hypoxia and to control sickling
Pain management
Acute chest syndrome
Antibiotics
O2 therapy
Fluid therapy
Sickle Cell Disease
Nursing Management (Cont’d)
Folic acid daily supplements
Blood transfusions in crisis
Hydroxyurea: Antisickling agent
Erythropoietin in patients unresponsive to hydroxyurea
Bone marrow transplant
Can cure some patients with SCD
Care plan for anemia
Example of Nursing Diagnosis
Fatigue r/t decreased oxygen supply to the body, increased cardiac
workload
Example of Outcome
Identify potential factors that aggravate and relieve fatigue by the
end of the shift as evidenced by patient self identifying activities that
cause increased fatigue
Intervention
Assess severity of fatigue level on scale of 0-10
Assess frequency, activities, and symptoms associated with increased
fatigue
Ackley
Care plan for anemia
ND: Impaired gas exchange r/t lack of RBC’s,
hemoglobin abnormalities
Outcome: within 3-24 hours patient has adequate
gas exchange as evidenced by HR and RR within 10%
of baseline
Intervention: Supplemental oxygen, monitor HR and
RR, Monitor oxygen saturation
Baird, Ch 10
Hemolytic Anemia
Destruction or hemolysis of RBCs at a rate that
exceeds production
Third major cause of anemia
Intrinsic hemolytic anemia
Abnormal hemoglobin
Enzyme deficiencies
RBC membrane abnormalities
Transfusion Responsibilities
Pretransfusion:
Verify prescription
Test donor’s/recipient’s blood for compatibility
Examine blood bag for identification
Check expiration date
Inspect blood for discoloration, gas bubbles, cloudiness
Transfusion Responsibilities (cont’d)
Provide patient education
Assess vital signs
Begin transfusion slowly, stay with patient first
15 to 30 minutes
Ask patient to report unusual sensations (e.g.,
chills, shortness of breath, hives, itching)
Administer blood product per protocol
Assess for hyperkalemia
Transfusion Reactions
Febrile
Anti WBC-antibodies
Multiple transfusions of PRBC, WBC, and/or platelet
transfusions
Develops chills tachycardia fever hypotension and tachypnea
Prevention WBC filters premedication's
Review local policies r/t fever definition
Transfusion Reactions
Hemolytic
Blood type or Rh incompatability
Antibody-antigen reaction
Mild to severe symptoms up to Disseminated intravascular
coagulation (DIC)
May be immediate or delayed
Manifested by apprehension, H/A, chest pain, low back pain,
tachycardia, hypotension, hemoglobinuria,
STOP THE TRANSFSION IMMEDIATELY !!!!!
Replace the entire IV infusion system from patient to bag, follow
local policy r/t post reaction testing
Transfusion Reactions
Allergic (anaphylactic)
May see urticaria, itching bronchospasm or anaphylaxis
Give leukocyte poor WBC, filtered, and/or irradiated blood to
patients with history
If anaphylaxis occurs this is an emergent situation, call a
code, stop the transfusion and follow code procedures
dependent on situation.
Transfusion Reactions
Bacterial
Contaminated blood products
Can lead to sepsis with symptoms of tachycardia, hypotension,
fever, chills and shock
Prevention by keeping blood products chilled
Multiple Myeloma
Pathophysiology
Overproduction of the B-lymphocyte that produce antibodies
and cytokines leading to bone destruction, clogging of blood
vessels in kidney and other organs and decreased amounts of
other cells produced in the marrow
May be asymptomatic but may progress to feelings of fatigue,
easy bruising and bone pain. May have unexplained fractures,
HTN, and infections
Testing will show elevated serum proteins and
immunoglobulin's, X-ray will show thinning bones
Multiple Myeloma
Interventions
Dependent on severity
Chemotherapy, steroids, bone marrow transplant
Supportive care is targeted to teaching about the
toxic effects of medications and for those
hospitalized, based on cell counts, isolation to
protect from infections
Purpose of Inflammation &
Immunity
Meet human need for protection by neutralizing,
eliminating, or destroying organisms invading the
internal environment
Organization of the Immune System
Immune system influenced by many systems
(e.g., nervous system, endocrine system, GI
system)
Stem cells – Immature, undifferentiated cells;
produced by bone marrow
Leukocytes (WBCs) – Protect body from effects
of invasion by organisms
Stem Cell Differentiation and
Maturation
Inflammation: “Innate Native
Immunity”
Any natural protective feature of a person
Provides immediate protection against effects of
tissue injury and foreign proteins—critical to
health and well-being
Causes visible symptoms and can rid body of
harmful organisms; tissue damage may
result from excessive response
Cell Types Involved in Inflammation
Neutrophils
Macrophages
Basophils
Eosinophils
Sequence of Inflammatory Responses
Five cardinal manifestations of inflammation:
Warmth
Redness
Swelling
Pain
Decreased function
Sequence of Inflammatory Responses
(cont’d)
Stage I (vascular) – Change in blood vessels:
Phase I—constriction
Phase II—hyperemia & edema
Stage II (cellular exudate) – Neutrophilia, pus
Stage III (tissue repair and replacement) –
WBCs trigger new blood vessel and growth
(angiogenesis) and scar tissue formation
Rheumatoid Arthritis (RA)
Common connective tissue disease, destructive
to joints
Chronic, progressive, systemic inflammatory
autoimmune disease; affects primarily synovial
joints
Transformed autoantibodies (rheumatoid
factors) form, attack healthy tissue causing
inflammation
RA Pathology
RA Collaborative Management
Assessment
Physical assessment/clinical manifestations:
Early—joint stiffness, swelling, pain, fatigue, generalized
weakness
Late—joints become progressively inflamed and quite
painful
RA Joint Involvement
RA Systemic Complications
Weight loss, fever, extreme fatigue
Exacerbations
Subcutaneous nodules
Respiratory, cardiac complications
Vasculitis
Periungual lesions
Paresthesias
RA Assessments
Psychosocial
Laboratory—rheumatoid factor, antinuclear
antibody titer, ESR, serum complement (C3 &
C4), serum protein electrophoresis, serum
immunoglobulins
Thrombocytosis can occur with late RA
Other diagnostic—x-ray, CT, arthrocentesis,
bone scan
RA Drug Therapy
Disease-modifying antirheumatic drugs
(DMARD)
Methotrexate (MTX)
NSAIDs
Biological response modifiers (BRM)
Neutralize alpha tumor necrosis factor (Humira,
Enbrrel)
Other:
Glucocorticoids
Immunosuppressive agents
(See pages 338-339 of Iggie)
RA Nonpharmacologic Interventions
Adequate rest
Proper positioning
Ice and heat application
Plasmapheresis (not common)
Complementary and alternative therapies
Promotion of self-management
Management of fatigue
Enhance body image
Care of RA
Promotion of self management
Manage fatigue
Enhance body image
Self-management
Home care
Lupus Erythematosus
Chronic, progressive, inflammatory connective
tissue disorder
Can cause major body organs/systems to fail
Spontaneous remissions and exacerbations
Autoimmune process
Autoimmune complexes tend to be attracted to
glomeruli of the kidneys
Often some degree of kidney involvement
Lupus Clinical Manifestations
Skin involvement
Butterfly rash
Polyarthritis
Osteonecrosis
Muscle atrophy
Fever and fatigue
Lupus Clinical Manifestations (cont’d)
Renal involvement
Pleural effusions
Pericarditis
Raynaud’s phenomenon
Neurologic manifestation
Serositis
Characteristic “Butterfly” Rash of
SLE
Assessments for Lupus
Psychosocial results can be devastating
Laboratory:
Skin biopsy (confirms diagnosis)
Immunologic-based laboratory tests
CBC (often shows pancytopenia)
Body system function
SLE Drug Therapy
Topical cortisone drugs
Plaquenil
Tylenol or NSAIDs
Chronic steroid therapy
Immunosuppressive agents
New drugs in clinical trials
Lupozor
Belimumab (Benlysta)
Monoclonal antibody medication
Care of SLE patients
Similar to RA
Also teach skin protection
monitoring of body temperature
increased temperature could be sign of exacerbation
Family education
Youtube videos of interest (cut-n-paste)
Anemia
Multiple myeloma
http://www.youtube.com/watch?v=pGTu
2aDbLpg
http://www.youtube.com/watch?v=2VJIg
RO7Yag
http://www.youtube.com/watch?v=SP7M
CBGyYfQ
http://www.youtube.com/watch?v=Jycz1
WBs-QQ
Lupus
http://www.youtube.com/watch?v=aGgV
CRg3OHI
http://www.youtube.com/watch?v=6_Uyf
3op8DI
Autoimmunity
http://www.youtube.com/watch?v=0z1qqf
4Ekb0
Rheumatoid arthritis
http://www.youtube.com/watch?v=0uwx
64YaxSk
http://www.youtube.com/watch?v=EPmF
4vWkuCk
http://www.youtube.com/watch?v=mIewj
ILmG5M
Transfusion reactions
http://www.youtube.com/watch?v=frYwX
cLv5yc