Anemia

 Manifestation of a pathological process

 Identified through history & physical exam & classified by laboratory review

A deficiency in the... Erythrocyte Production

- Erythropoietin (EPO) is a glycoprotein
 Number of erythrocytes primarily produced in the kidneys
 Quantity or quality of hemoglobin o Increased number of stem cells
 Volume of packed RBC's (hematocrit) committed to RBC production
o Shortens the time to mature RBCs
Etiology - Lifespan of an RBC is 120 days
- 3 alterations in erythropoiesis may
 Blood loss decrease RBC production
 Impaired production of erythrocytes o  hemoglobin synthesis
 Increased destruction of erythrocytes o Defective DNA synthesis in RBC’s
o Diminished availability of
Classification erythrocyte precursors
 Morphological
o Cellular characteristics - descriptive,
objective laboratory information
 Etiological
o Underlying cause

Clinical Manifestations
 Hemoglobin levels used to determine the severity of anemia
 Mild anemia ⟶ no symptoms possible / palpitations, dyspnea, mild fatigue
 Moderate anemia ⟶ cardiopulmonary symptoms increased
 Severe anemia ⟶ affects many body systems

Pallor (decreased hemoglobin & blood flow to the skin)

Integumentary Jaundice (increased concentration of serum bilirubin)
Pruritus (increased serum & skin bile salt concentrations)
Heart & lungs attempt to provide adequate O2 to the tissues
Cardiac output maintained by increasing the HR & SV
Cardiopulmonary MI or angina pectoris may occur if O2 demands not met.
HF, cardiomegaly, pulmonary & systemic congestion, ascites, & peripheral edema can
develop if heart is overworked for long period of time

Nursing Implementation
 Blood or blood product transfusions
 Drug therapy (eg. erythropoietin & vitamins)
 Volume replacement
  Dietary and lifestyle changes
 Correcting the cause of the anemia is the ultimate goal
 Oxygen therapy

Age-Related Considerations
 Common in older adults due to chronic disease & nutritional deficiencies
 Signs & symptoms may go unrecognized or may be mistake for normal aging changes
o Pallor, confusion, ataxia, fatigue, worsening CVD & resp. problems

Types of Anemia
 Aplastic Anemia  a condition that occurs when your body stops producing enough new blood cells
o Types:
 Congenital – chromosomal alterations
 Acquired – results from exposure to ionizing radiation, chemical agents, drugs, viral &
bacterial infections
o Clinical manifestations
 Abrupt or gradual development
 Symptoms caused by suppression of any or all bone marrow elements
 Fatigue, dyspnea, cardiovascular & cerebral responses, neutropenia, thrombocytopenia
 Pancytopenia – decrease in RBC’s, WBC’s, & platelets
o Diagnostic studies
 Laboratory studies
o Nursing care
 Prevent complications from infection & hemorrhage
 Untreated = prognosis is poor
 Treatment = bone marrow transplantation OR immune-suppressive therapy
 Hemolytic Anemia  destruction or hemolysis of RBC’s at a rate that exceeds production
o Intrinsic hemolytic anemia = abnormal hemoglobin, enzyme deficiencies, & RBC membrane
abnormalities = usually hereditary
o Extrinsic hemolytic anemia = acqurited = damage caused by external factors
o Clinical manifestations
 Jaundice – destroyed RBC’s cause increased bilirubin
 Enlarged spleen & liver – hyperactive with macrophage phagocytosis of defective RBC’s
o Accumulation of hemoglobin molecules can obstruct renal tubules (tubular necrosis)
 Sickle Cell Disease  group of inherited, autosomal recessive disorders  genetic disorder & incurable
o Presence of an abnormal form of hemoglobin in the erythrocyte = hemoglobin S (HbS)
 HbS causes the RBC to stiffen & elongate
 Sickled cells cannot easily pass through capillaries or other small vessels & can
cause vascular occlusion, leading to acute or chronic tissue injury
 The resulting hemostasis promotes a self-perpetuating cycle of local hypoxia,
deoxygenation of more erythrocytes, & more sickling.
 Circulating sickled cells are hemolyzed by the spleen, leading to anemia
 Sickle shape in response to a decrease in O2 levels
 Substitution of valine for glutamic acid on the beta-globin chain of hemoglobin
o Types of SCD:
 Sickle cell anemia = most severe (HbSS)  Sickle cell trait (HbAS)
  Sickle cell-thalassemia  Sickle cell-HbC disease
o Clinical manifestations
 Sickling episodes – most commonly triggered by low oxygen tension in the blood
 Can be triggered by infection, dehydration, increased hydrogen ion concentration
(acidosis), increase plasma osmolality, decreased plasma volume, & low body
temperature
 Sickle cell crisis – severe painful acute exacerbation of sickling causes a vaso-occlusive
crisis
 This can cause shock which can cause severe oxygen depletion of the tissues & a
reduction in circulating fluid volume
 Typical client is asymptomatic, except during sickling episodes
 Symptoms = pain, swelling, pallor of mucous membranes, jaundice
o Complications
 Gradual involvement of all body systems
 Prone to infection (especially pneumonia)
 Organs most commonly affected = spleen, lungs, kidneys, & brain
 Acute chest syndrome = fever, chest pain, cough, pulmonary infiltrates, dyspnea
o Diagnostic studies
 Peripheral blood smear  Sickling test
 Electrophoresis of hemoglobin  Skeletal radiographs
 MRI
o Nursing care
 Alleviate symptoms of disease & complications
 Minimize end target-organ damage
 No specific treatment for SCD
 Client teaching  avoid high altitudes, maintain fluid intake, treat infections
 O2 for hypoxia & to control sickling
 Acute chest syndrome  antibiotics, O2 therapy, fluid therapy, transfusions
 Hydroxyurea = anti-sickling agent & erythropoietin in clients unresponsive to
hydroxyurea
 Hematopoietic stem cell transplant = can cure some clients
 Acquired Hemolytic Anemia 
o 3 extrinsic categories
 Physical factors = physical destruction of RBC’s results from the extreme force on the
cells
 Hemodialysis, extracorporeal circulation, prosthetic heart valves
 Immune reactions = antigen-antibody reactions destroy RBC’s
 Isoimmune reactions = antibodies develop against antigens; blood transfusions
 Autoimmune reactions = develop antibodies against their own RBC’s
 Infectious agents & toxins
 Foster hemolysis in 3 ways:
o Invading RBC’s & destroying contents
o Releasing hemolysis substances
o Generating an antigen-antibody reaction
 
Leukemia
A group of malignant disorders affecting blood & blood-forming tissues of bone marrow, lymph system,
& the spleen
o Accumulation of dysfunctional cells due to loss of regulation in cell division
o Fatal if untreated

Etiology & Pathophysiology

 No single causative agent – combination of genetic & environmental influences
 Associated with development
o Chemical agents ◦Chemotherapeutic agents
o Viruses ◦Radiation
o Immunological deficiencies
Classification
 Cell maturity & nature of disease onset = acute vs. chronic
o Acute – clonal proliferation of immature hematopoietic cells
o Chronic – mature forms of WBC, onset is more gradual
 Types = ALL, AML, CML, CLL

Clinical Manifestations
 Usually related to bone marrow failure
o Overcrowding by abnormal cells
o Inadequate production of normal marrow elements
 Inadequate marrow elements cause:
o Anemia
o Thrombocytopenia
o  number & function of WBC’s
 Leukemia cells cause…
o Splenomegaly, hepatomegaly, lymphadenopathy, bone pain, meningeal irritation, oral lesions, &
solid masses

Diagnostic Studies
 For diagnosing & classifying:
o Peripheral blood evaluation
o Bone marrow evaluation
 To identify cell subtype & stage
o Morphological, histochemical, immunological,
& cytogenetic methods Complete remission – no evidence of overt
disease is found on physical exam & bone
4 Therapy Stages marrow & peripheral blood normal.

 Induction therapy Partial remission – lack of symptoms & a

o Attempt to induce remission
o Seek to destroy leukemic cells in tissues,
peripheral blood, & bone marrow
normal peripheral blood smear – evidence
of disease in bone marrow.
Minimal residual disease – tumor cells that
cannot be detected by morphological exam
but can be detected by molecular testing.
 o Client may become critically ill
 Intensification therapy
o High-dose therapy
o May be given after induction therapy – same drugs at higher doses and/or other drugs
 Consolidation therapy
o After remission is achieved
o Eliminate remaining leukemic cells that may not be pathologically evident
 Maintenance therapy
o Lower doses of the same drug given every 3-4 weeks
o Goal is to keep the body free of leukemic cells

Chemotherapy Regimens
 Combination chemotherapy
o Mainstay treatment
o Three purposes:
  drug resistance
  drug toxicity using multiple drugs
 Interrupt cell growth at multiple points

Hematopoietic Stem Cell Transplant

 Goal is to totally eliminate leukemic cells using combinations of chemotherapy with or without total
body irradiation
 Eradicates client’s hematopoietic stem cells
 Replaced with those of an HLA -match (sibling, volunteer, identical twin) or replace with own stem
cells (autologous)

Acute Myelogenous Leukemia (AML)

 25% of all leukemias (80% of leukemias in adults)
 Abrupt, dramatic onset – serious infection or abnormal bleeding
 Uncontrolled proliferation of myeloblasts  hyperplasia of bone marrow & spleen

Acute Lymphocytic Leukemia (ALL)

 Most common type of leukemia in children
 Immature lymphocytes proliferate in the bone marrow – B-cell origin
 Symptoms may appear abruptly – fever & bleeding
 Insidious with progressive weakness, fatigue, pain, bleeding tendencies
o CNS manifestation common in ALL

Chronic Myelogenous Leukemia (CML)

 Excessive mature neoplastic granulocytes in bone marrow  move into peripheral blood in massive
numbers
o Ultimately infiltrate the liver & spleen
 Philadelphia chromosome  genetic marker
 Chronic stable phase  followed by acute, aggressive phase

Chronic Lymphocytic Leukemia (CLL)

 Production & accumulation of functionally inactive but long-lived, mature-appearing lymphocytes
 o B-cell involvement
 Lymph node enlargement is present through the body – increased incidence of infection
 Complications from early-stage CLL are rare
o May develop as the disease advances
o Pain, paralysis from pressure caused by enlarged lymph nodes