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Hematologic disorders
   The blood and the blood forming sites, including the
    bone marrow and the reticuloendothelial system

   Blood

    › Plasma

    › Blood cells

   Hematopoiesis
Blood


        Adult:
        •Female 4-5L
        •Males 5-6L
   Transport of:
    › Gases, nutrients, waste products
    › Processed molecules
    › Regulatory molecules

   Regulation of pH and osmosis

   Maintenance of body temperature

   Protection against foreign substances

   Clot formation
Antibodies & complements
–part of immune system




Clotting factor
Once activated, converted
to fibrin (threadlike protein
that forms blood clot
   Liquid part of blood
    › Pale yellow made up of 91% water, 9% other

   Colloid: Liquid containing suspended substances
    that don’t settle out
    › Albumin: Important in regulation of water movement
      between tissues and blood

    › Globulins: Immune system or transport molecules

    › Fibrinogen: Responsible for formation of blood clots
   Erythrocyte: RBC
   Leukocyte: WBC
    › Neutrophil
    › Monocyte
    › Eosinophil
    › Basophil
    › Lymphocyte: T lymphocyte and B lymphocyte
   Thrombocyte: platelet
Hematologic disorders
   Hematopoiesis or hemopoiesis:
    › Process of blood cell production
    › Fetus: liver, thymus, spleen, lymph nodes, red bone
      marrow
    › After birth: red bone marrow, for WBC in some
      lymphatic tissues

   Stem cells (hemocytoblast): All formed elements
    derived from single population
    › Proerythroblasts: Develop into red blood cells
    › Megakaryoblasts: Develop into platelets
19-
10
   Structure
    › Biconcave, anucleate

   Components
    › Hemoglobin (makes it red
      in color)
    › Lipids, ATP, carbonic
      anhydrase

   Function
    › Transport oxygen from
       lungs to tissues and
       carbon dioxide from
       tissues to lungs
Unable to divide, grow, or synthesize proteins


     Wear out in 100 to 120 days


     Removed by phagocytes in the spleen or liver


     New RBCs made by stem cells in bone marrow


     Production increases when oxygen level decrease or during
     pregnancy



Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
   Consists of:
    ›   4 globin molecules: Transport carbon dioxide (carbonic anhydrase
        involved), nitric oxide
         2 alpha and 2 beta globin chains
    ›   4 heme molecules: Transport oxygen
         Each heme contains 1 iron
         Iron is required for oxygen transport
    ›   Hemoglobin + oxygen = bright red
    ›   Hemoglobin with no oxygen = darker red
Erythrocytes: Levels in Blood


      Live only four (4) months or ~120 days


      Average RBC count:
            Males: 5.4 million/mm3
            Females: 4.8 million/mm3


      Outnumber white blood cells 1000:1



Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
   Happens in red bone marrow
   Components required:
    › Precursor cells: PROERYTHROBLAST
    › Proper microenvironment
    › Adequate supplies of iron, vitamin B12, folic acid, protein,
       pyridoxine and traces of copper
   Erythropoietin:
    › Hormone to stimulate RBC production
   During cell division, the process requires B
    vitamins folate and B12, necessary for synthesis
    of DNA.

   Iron is required for production of hemoglobin

   RBC production is triggered by low blood
    oxygen levels
Hematologic disorders
Hematologic disorders
Hematologic disorders
Hematologic disorders
Hematologic disorders
Hematologic disorders
Hematologic disorders
 Cytotoxic cells
 Helper cells
 Memory cells
 Suppressor cells
   IgG
    › chronic infxn, transplacental;

   IgA
    › external secretions; “mucosal paint”
    › through breastfeeding

   IgM
    › acute infxn; 1O response Ab, 1st produced by infants

   IgE
    › parasitic / allergic reactions

   IgD
    › no specific function; antigen-binding
Hematologic disorders
Hematologic disorders
   factor I (fibrinogen)
   factor II (prothrombin) – Vit K dependent
   factor III (tissue thromboplastin)
   factor IV (calcium)
   factor V (proaccelerin)
   factor VI (no longer considered active in hemostasis)
   factor VII (proconvertin) - Vit K dependent
   factor VIII (antihemophilic factor)
   factor IX (plasma thromboplastin component; Christmas factor) -
    Vit K dependent
   factor X (stuart factor) - Vit K dependent
   factor XI (plasma thromboplastin antecedent)
   factor XII (hageman factor)
   factor XIII (fibrin stabilizing factor).
Hematologic disorders
Spleen
    › Left upper quadrant of the abdomen behind abdomen
    › Produces RBC during fetal development
    › Filter function – remove old defective cells from circulation and
      breaks down RBC and recycles the iron to bone marrow

Liver
    › Receives blood from the spleen through portal circulation
    › Produce procoagulants necessary for hemostasis and blood
      coagulation
    › Storage of iron and B12
    › Detoxify drugs
    › Kupffer cells carry out phagocytosis
    › Bile production from erythrocyte destruction
Lymphatics
 Lymph capillaries
    › Carries lymph to the subclavian vein in the
     chest


   Lymph nodes
    › Small rounded structures that filter bacteria
     and foreign particles
Hematologic disorders
   Reduction below normal in the # of RBC,
    the quantity of hemoglobin and volume of
    RBC (hematocrit)

   Result from:
    › ↓RBC production
    › ↑RBC destruction
    › Acute or chronic blood loss
   Three broad categories

1. Loss of RBC- occurs with bleeding

2. Decreased RBC production
    › IDA
    › FADA
    › Thalassemia


3. Increased RBC destruction
   Normocytic
    ›   Normal RBC size
    ›   IDA

   Macrocytic
    ›   Large RBC due to impaired division of RBC precursor cells
    ›   Cobalamin and folate deficiency

   Microcytic
    ›   Small RBC

   Normochromic
    ›   Normal hemoglobin concentration

   Hypochromic
    ›   Decrease hemoglobin concentration

   Hyperchromic
    ›   Increased hemoglobin concentration
Hematologic disorders
   Iron Deficiency Anemia

    › dietary intake of iron is inadequate to produce
      hemoglobin

    › Most common type of anemia

    › May occur with removal of the duodenum

    › Associated with chronic blood loss.
  Iron Deficiency Anemia
Etiologic Factors

    1. Bleeding- the most common cause

    2. Mal-absorption

    3. Malnutrition

    4. Alcoholism
 Iron Deficiency Anemia
Pathophysiology

    › The body storage of iron decrease, leading
     to depletion of hemoglobin synthesis

    › The oxygen carrying capacity of
     hemoglobin is reduced tissue hypoxia
 Iron Deficiency Anemia
Assessment Findings

1. Pallor of the skin and mucous membrane

2. Weakness and fatigue

3. General malaise

4. Pica
Assessment Findings

5. Brittle nails

6. Smooth and sore tongue

7. Angular cheilosis
  Iron Deficiency Anemia
Laboratory findings

1.       CBC
     ›      Low levels of Hct, Hgb and RBC count

2.       Low serum iron, low ferritin

3.       Bone marrow aspiration- MOST definitive
   Iron Deficiency Anemia

Medical management
 1. Iron replacement
 2. Blood transfusion
Nursing Management
1. Provide iron rich-foods
     › Organ meats (liver)
     › Beans
     › Leafy green vegetables
     › Raisins and molasses

2. Administer iron
    › Oral preparations tablets- Fe fumarate, sulfate and
      gluconate
    › Advise to take iron ONE hour before meals
    › Take it with vitamin C
    › Monitor for adverse reaction like pyrosis (heartburn),
      constipation, diarrhea, dark stool
    › Continue taking it for several months even with normal iron
      level
Nursing Management
2. Administer iron
  › Oral preparations- liquid
     It stains teeth
     Drink it with a straw
  › Stool may turn blackish- dark in color
  › Advise to eat high-fiber diet and to ↑fluid
   intake to counteract constipation
Nursing Management
2. Administer iron
    › IM preparation
       Administer DEEP IM
       Include 0.5ml air in syringe to clear iron from the needle
       Use the Z-track method
    › Avoid vigorous rubbing
    › Can cause local pain and staining

   Note:
    › Iron should be taken for 2-3 mos after Hb level returns to
      normal
3. Administer packed red blood cell
   transfusion if patient is symptomatic
Hematologic disorders
   Normally hemoglobin contain 4 globin chains

   Decreased production of hemoglobin due to abnormal hemoglobin synthesis

   Reduced production or no production of 1 of the globin chains that make up
    hemoglobin


   Microcytic and hypochromic

   Autosomal recessive genetic disorder common among Mediterranean people.

   Chronic bone marrow hyperplasia

   Altered globin synthesis of hemoglobin

   Treatment causes chronic iron toxicity
   Thalassemia minor
    › Has 1 thalassemic and 1 normal gene with
      mild clinical manifestations
    › Requires no tx


   Thalassemia major
    › Has 2 thalassemic genes causing severe
     conditions
Hematologic disorders
Assessment:
1. Skin: pale/jaundiced


2.   Splenomegaly and hepatomegaly

3.   Thickened cranium and maxillary sinus space from
     bone marrow hyperplasia
Diagnostics:
1. CBC
     1. Anemia lower Mean corpuscular volume
2.   Hemoglobin electrophoresis
Nursing Management

1.   Administer BT and chelation therapy (remove heavy
     metals) to reduce iron overload
2.   Monitor for transfusion reactions or diseases
     acquired through transfusions
3.   Instruct about tx, medications and physical energy
     conservation techniques
4.   Strengthen client support and family systems.
Hematologic disorders
   Life-threatening stem cell disorder with many possible
    etiological mechanisms

   Decreased number of RBC as well as WBC and
    platelets

   Characterized as:
    › hypoplastic( incomplete development of a tissue or
      organ)
    › Fatty bone marrow
    › Pancytopenia (reduction in # of RBC, WBC and platelets)
CAUSATIVE FACTORS

1.       Environmental toxins- pesticides, benzene

2.       Certain drugs
     ›     Chemotherapeutic agents
     ›     Chloramphenicol
     ›     Phenothiazines
     ›     Sulfonamides

3.       Heavy metals

4.       Radiation
Pathophysiology

    Toxins cause a direct bone marrow
                 depression
                     ↓
          acellular bone marrow
                     ↓
 decreased production of blood elements
Hematologic disorders
   ASSESSMENT FINDINGS

1. fatigue
2. pallor
3. dyspnea
4. bruising
5. splenomegaly
6. retinal hemorrhages
    LABORATORY FINDINGS

1.   CBC
     ›   decreased blood cell numbers

2.   Bone marrow aspiration confirms the
     anemia- hypoplastic or acellular marrow
     replaced by fats
    Medical Management

1.   Bone marrow transplantation

2.   Immunosupressant drugs

3.   Rarely, steroids

4.   Blood transfusion
    Nursing management
1.        Assess for signs of bleeding and infection

2.        Pancytopenia plan of care to prevent
          complications like infection and bleeding.
     1.     Private room
     2.     Strict hand washing
     3.     Minimizing invasive procedures

3.        Provide client and family with support for
          lengthy hospitalization and tx
Hematologic disorders
   abnormally large RBC secondary to
    impaired DNA synthesis

   due to deficiency of Folic acid and/or
    vitamin B12
1. Folic Acid deficiency
     › Folate is required for DNA synthesis in erythrocyte formation

     › Without neurologic involvement

Causative factors

1.   Alcoholism

2.   Mal-absorption

3.   Diet deficient in uncooked vegetables

4.   Use of oral contraceptives
Pathophysiology of Folic acid deficiency

                       Decreased folic acid
                                 ↓
            impaired DNA synthesis in the bone marrow
                                 ↓
                   impaired RBC development
 impaired nuclear maturation but Cytoplasmic maturation continues
                                 ↓
                             large size
Assessment (Folate Deficiency)

1.    Poor nutrition
2.    Alcohol abuse
3.    Anorexia
4.    Impaired absorption in the small intestine
5.    Undergoing hemodialysis (folate is dialyzable)
6.    Certain drugs can block folate absorption
     1.   Oral contraceptives
     2.   Antiseizure drugs (phenytoin)
     3.   Antibiotics
Diagnosis (Folate deficiency)

1.    CBC
     1.   ↓ RBC, hgb & hct and ↑ MCV

2.    Serum folate levels are low

3.    Serum cobalamin is normal
Nursing Management

1.   Promote compliance with replacement therapy
     (1-5 mg oral folate/day)

2.   Administer prenatal vitamins in pregnancy

3.   Instruct on food high in folate such as leafy
     greens, liver, citrus fruits, nuts and grains
Hematologic disorders
Normal Condition:

Parietal cells of stomach secreted intrinsic
  factor to absorb ingested cobalamin
  (vit.b12)
Vitamin B12 deficiency
    (Pernicious Anemia)
     ›   Lack of intrinsic factor (needed for B12 absorption)
     ›   Common among Northern European ancestry over age of 40 and young African
         American

 Causative factors
1.  Strict vegetarian diet

2.   Gastrointestinal malabsorption

3.   Crohn's disease

4.   Yrs of Gastritis

5.   Gastrectomy
   Vitamin B12 deficiency

Pernicious Anemia
 Due to the absence of intrinsic factor secreted by
  the parietal cells

   Intrinsic factor binds with Vit. B12 to promote
    absorption
Assessment findings

1.    Weakness
2.    Fatigue
3.    Neurologic manifestations are present only in
      Vit. B12 deficiency
     1.   Weakness, paresthesia of feet and hands, impaired
          thought processes
4.    Coagulation deficiencies
 Assessment findings
Pernicious Anemia
    › Beefy, red, swollen tongue
    › Mild diarrhea
    › Extreme pallor
    › Paresthesias in the extremities
    Laboratory findings

1.   Peripheral blood smear- shows giant RBCs, WBCs with giant
     hypersegmented nuclei

2.   Very high MCV

3.   Schilling’s test
     ›   Radioactive vit B12 malabsorption is measured by small amount of
         secreted in urine
     ›   When vit B12 us administered with gastric IF parenterally, its absence in
         urine will diagnose pernicious anemia

4.   Intrinsic factor antibody test
   Medical Management

1. Vitamin supplementation
    Folic acid 1 mg daily

2. Diet supplementation
    Vegetarians should have vitamin intake


3. Lifetime monthly injection of IM Vit B12
    › w/o cobalamin replacement, patient can die in 1-3yrs.
   Since Pernicious anemia results from an
    inability to absorb cobalamin, dietary
    intake of the vitamin is not a treatment
    option, nor is bone marrow transplant
    Nursing Management

1.   Monitor patient

2.   Provide assistance in ambulation

3.   Oral care for tongue sore

4.   Explain the need for lifetime IM injection of vit B12
Hematologic disorders
   Decrease in erythrocyte precursor
    production that occurs in some chronic
    conditions

 End-stage renal failure
 Chronic liver disease
 Alcohol abuse
 hypothyroidism
Clinical Manifestations

   ALL ASSESSMENT FINDINGS FOR ANEMIA
                  APPLY
Diagnosis:
1. CBC
2. FERRITIN
  1. Iron stores may be high in contrast to IDA
    Nursing Management

1.   Facilitate diagnosis and tx if underlying, contributory
     condition

2.   Inform that this type of anemia does not respond to
     folic acid, iron or vitamin B12

3.   Erythropoietin therapy is administered to a client
     with anemia related to renal failure
Hematologic disorders
2 SITES OF HEMOLYSIS

1.       INTRAVASCULAR DESTRUCTION
     ›    Occurs within the circulation

2.       EXTRAVASCULAR DESTRUCTION
     ›    Occurs in liver, spleen, or bone marrow
CLASSIFICATION OF HEMOLYTIC ANEMIAS

1.       INTRINSIC HEMOLYTIC ANEMIAS
     ›        Usually hereditary
     ›        Defects in RBC themselves
         1.     Abnormal hgb = sickle cell anemia
         2.     Enzyme deficiencies = G6PD
         3.     Cell membrane abnormalities
CLASSIFICATION OF HEMOLYTIC ANEMIAS

2.       EXTRINSIC HEMOLYTIC ANEMIAS

     ›        Normal RBCs are damaged by external factors
     ›        Cause:
               antibodies, toxins,
               mechanical injury (prosthetic heart valves)
               dialysis,
               transfusion reaction
               trapping of cells within the liver and spleen
Hematologic disorders
Hematologic disorders
   A severe chronic incurable hemolytic anemia that results from
    heritance of the sickle hemoglobin gene.

   Produces specific mutant form of beta-globin

   Hypoxia-induced change in RBCs

   Associated with vascular occlusion and tissue infarction

   Anemia is caused by accelerated breakdown of abnormal RBC
 Causative   factor
 › Genetic inheritance of the sickle
   gene- Hbs gene
Pathophysiology

   Decreased O2, Cold, Vasoconstriction can
    precipitate sickling process
Pathophysiology
                             Factors
                                ↓
  cause defective hemoglobin to acquire a rigid, crystal-like C-
                       shaped configuration
                                ↓
           Sickled RBCs will adhere to endothelium
                                ↓
                  pile up and plug the vessels
                                ↓
                         ischemia results
                                ↓
                    pain, swelling and fever
Hematologic disorders
   Assessment Findings

1. jaundice

2. enlarged skull and facial bones

3. tachycardia, murmurs and cardiomegaly
Assessment Findings

   Primary sites of thrombotic occlusion: spleen,
    lungs and CNS

   Chest pain, dyspnea
   Assessment Findings

1. Sickle cell crises
    › Results from tissue hypoxia and necrosis

2. Acute chest syndrome
    › Manifested by a rapidly falling hemoglobin
     level, tachycardia, fever and chest infiltrates in
     the CXR
During the sickling crisis,

the sickling cells clog small capillaries and the resulting hemotasis
         promotes a self-prepetuating cycle of local hypoxia,
       deoxygenation of more erythrocytes and more sickling.

                          MEDICAL MGT:

       Administration of large doses of narcotic analgesics

                      Since pain last 4-6 days
Medical Management

1. Bone marrow transplant

2. Hydroxyurea

3. Long term RBC transfusion
Nursing Management

1. manage the pain
  › Support and elevate acutely inflamed joint
  › Relaxation techniques to reduce metabolic
    needs
  › analgesics
Nursing Management
2. Prevent and manage infection

  › Monitor status of patient


  › Initiate prompt antibiotic therapy
Nursing Management
3. Promote coping skills

  › Provide accurate information

  › Allow patient to verbalize her concerns about
    medication, prognosis and future pregnancy
Nursing Management
4. Monitor and prevent potential
   complications

  › Provide always adequate hydration

  › Avoid cold, temperature that may cause
    vasoconstriction
Nursing Management
4. Monitor and prevent potential
   complications

  › Leg ulcer
    Aseptic technique
Nursing Management
4. Monitor and prevent potential complications

  Priapism
     Sudden painful erection

     Instruct patient to empty bladder, then take a warm
      bath

5. Maintain F & E balance to reduce blood
   viscosity
Hematologic disorders
   Glucose-6-phosphate dehydrogenase

   Results from lack of an RBC enzyme that
    leads to RBC damage when metabolic
    needs of RBCs are increased.
   A group of X-linked familial hemolytic mutations of the
    gene

   Deficiency predisposes to oxidative denaturation of
    hemoglobin, with resultant red cell injury and lysis.

   Hemolysis occurs as the result of oxidative stress generated
    by either an infection or exposure to certain drugs.

   More common among males of Mediterranean or African
    descent
•Jaundice
             •Headache
Assessment
             •Dizziness
             •Easy fatigabilty
Diagnostic:

Use of G6PD assay or screening test

Quantification of G6PD levels during
 nonhemolytic phase
Nursing Management

1.   Provide periods of rest

2.   Provide adequate hydration

3.   Administer antibiotics and other tx as
     ordered to minimize complications.
Hematologic disorders
   Refers to an INCREASE volume of RBCs

   The hematocrit is ELEVATED to more than
    55%
   POLYCYTHEMIA VERA
    › Primary Polycythemia

      A proliferative disorder in which the
       myeloid stem cells become uncontrolled

      Neoplastic disorder where there is an
       increased in 3 types of blood cells
 POLYCYTHEMIA     VERA

Causative factor
  › unknown
   POLYCYTHEMIA VERA

   Pathophysiology
    › The stem cells grow uncontrollably


    › The bone marrow becomes HYPERcellular and all the
     blood cells are increased in number
   POLYCYTHEMIA VERA

Pathophysiology
    › The spleen resumes its function of hematopoiesis and
      enlarges

    › Blood becomes thick and viscous causing sluggish
      circulation

    › Overtime, the bone marrow becomes fibrotic
 POLYCYTHEMIA VERA
Assessment findings

    1.   Skin is ruddy, pruritic due to histamine release

    2. Splenomegaly in primary PV only

    3. headache, tinnitus

    4. dizziness, blurred vision

    5. Angina, intermittent claudication, dyspnea and
       thrombophlebitis
   POLYCYTHEMIA VERA

   Laboratory findings

    1. CBC- shows elevated RBC mass

    2. Normal oxygen saturation

    3. Elevated WBC and Platelets
 POLYCYTHEMIA VERA
Complications

    1.    Increased risk for:
         1.       Thrombophlebitis
                   Due to hypervolemia & hyperrviscosity,
                   Tx: active/passive leg exercise and ambulation
         2.       CVA
         3.       MI

    2. Bleeding due to dysfunctional blood cells
POLYCYTHEMIA VERA
Medical Management

    1. To reduce the high blood cell mass- PHLEBOTOMY

    2. Allopurinol

    3. Dipyridamole

    4. Chemotherapy to suppress bone marrow
   Nursing Management
    1. Primary role of the nurse is EDUCATOR

    2. Regularly asses for the development of complications

    3. Assist in weekly phlebotomy

    4. Advise to avoid alcohol and aspirin

    5. Advise tepid sponge bath or cool water to manage pruritus
Hematologic disorders
   Malignant disorders of blood forming cells

   characterized by UNCONTROLLED proliferation of
    WBC in the bone marrow- replacing marrow
    elements .

   The WBC can also proliferate in the liver, spleen
    and lymph nodes.
   named after the specific lines of blood
    cells afffected primarily
    › Myeloid
    › Lymphoid
    › Monocytic
   The leukemias are named also according
    to the maturation of cells

   ACUTE
    › The cells are primarily immature


   CHRONIC
    › The cells are primarily mature or diferentiated
   ACUTE myelocytic leukemia
   ACUTE lymphocytic leukemia

   CHRONIC myelocytic leukemia
   CHRONIC lymphocytic leukemia
   ETIOLOGIC FACTORS
    › UNKNOWM
    › Probably exposure to radiation
    › Chemical agents
    › Infectious agents
    › Genetic
PATHOPHYSIOLOGY of ACUTE Leukemia

   Uncontrolled proliferation of immature cells
                        ↓
       suppresses bone marrow function
                         ↓
    severe anemia, thrombocytopenia and
                granulocytopenia
PATHOPHYSIOLOGY of CHRONIC Leukemia

Uncontrolled proliferation of DIFFERENTIATED cells
                        ↓
  slow suppression of bone marrow function
                        ↓
               milder symptoms
   ASSESSMENT FINDINGS

   ACUTE LEUKEMIA
    › Pallor
    › Fatigue
    › Dyspnea
    › Hemorrhages
    › Organomegaly
    › Headache
    › vomiting
   ASSESSMENT FINDINGS

   CHRONIC LEUKEMIA
    › Less severe symptoms
    › organomegaly
LABORATORY FINDINGS

   Peripheral WBC count varies widely

   Bone marrow aspiration biopsy reveals a large
    percentage of immature cells- BLASTS

   Erythrocytes and platelets are decreased
Medical Management
1. Chemotherapy
2. Bone marrow transplantation
Nursing Management

    1. Manage AND prevent infection
    › Monitor temperature
    › Assess for signs of infection
    › Be alert if the neutrophil count drops
        below 1,000 cells/mm3
Nursing Management

2. Maintain skin integrity

3. Provide pain relief

4. Provide information as to therapy- chemo
    and bone marrow transplantation
Hematologic disorders
Read on the following remaining topics:

1.   Thrombocytopenia
2.   Disseminated Intravascular Coagulation
3.   Hemophilia
4.   Von Willebrand’s disease
5.   Neutropenia
On September 12, 2011, we will have
                  our
            UNIT EXAM
      on the following topics:

      Fluids and Electrolytes
               And
      Hematologic Disorders
NEXT TOPIC TO BE DISCUSSED WOULD BE:

    CARDIOVASCULAR DISORDERS
                AND
  PERIPHERAL DISORDERS BY S’ CLAY

  ENDOCRINE DISORDERS BY M’ LUDY
Hematologic disorders

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Hematologic disorders

  • 2. The blood and the blood forming sites, including the bone marrow and the reticuloendothelial system  Blood › Plasma › Blood cells  Hematopoiesis
  • 3. Blood Adult: •Female 4-5L •Males 5-6L
  • 4. Transport of: › Gases, nutrients, waste products › Processed molecules › Regulatory molecules  Regulation of pH and osmosis  Maintenance of body temperature  Protection against foreign substances  Clot formation
  • 5. Antibodies & complements –part of immune system Clotting factor Once activated, converted to fibrin (threadlike protein that forms blood clot
  • 6. Liquid part of blood › Pale yellow made up of 91% water, 9% other  Colloid: Liquid containing suspended substances that don’t settle out › Albumin: Important in regulation of water movement between tissues and blood › Globulins: Immune system or transport molecules › Fibrinogen: Responsible for formation of blood clots
  • 7. Erythrocyte: RBC  Leukocyte: WBC › Neutrophil › Monocyte › Eosinophil › Basophil › Lymphocyte: T lymphocyte and B lymphocyte  Thrombocyte: platelet
  • 9. Hematopoiesis or hemopoiesis: › Process of blood cell production › Fetus: liver, thymus, spleen, lymph nodes, red bone marrow › After birth: red bone marrow, for WBC in some lymphatic tissues  Stem cells (hemocytoblast): All formed elements derived from single population › Proerythroblasts: Develop into red blood cells › Megakaryoblasts: Develop into platelets
  • 11. Structure › Biconcave, anucleate  Components › Hemoglobin (makes it red in color) › Lipids, ATP, carbonic anhydrase  Function › Transport oxygen from lungs to tissues and carbon dioxide from tissues to lungs
  • 12. Unable to divide, grow, or synthesize proteins Wear out in 100 to 120 days Removed by phagocytes in the spleen or liver New RBCs made by stem cells in bone marrow Production increases when oxygen level decrease or during pregnancy Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
  • 13. Consists of: › 4 globin molecules: Transport carbon dioxide (carbonic anhydrase involved), nitric oxide  2 alpha and 2 beta globin chains › 4 heme molecules: Transport oxygen  Each heme contains 1 iron  Iron is required for oxygen transport › Hemoglobin + oxygen = bright red › Hemoglobin with no oxygen = darker red
  • 14. Erythrocytes: Levels in Blood Live only four (4) months or ~120 days Average RBC count: Males: 5.4 million/mm3 Females: 4.8 million/mm3 Outnumber white blood cells 1000:1 Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
  • 15. Happens in red bone marrow  Components required: › Precursor cells: PROERYTHROBLAST › Proper microenvironment › Adequate supplies of iron, vitamin B12, folic acid, protein, pyridoxine and traces of copper  Erythropoietin: › Hormone to stimulate RBC production
  • 16. During cell division, the process requires B vitamins folate and B12, necessary for synthesis of DNA.  Iron is required for production of hemoglobin  RBC production is triggered by low blood oxygen levels
  • 24.  Cytotoxic cells  Helper cells  Memory cells  Suppressor cells
  • 25. IgG › chronic infxn, transplacental;  IgA › external secretions; “mucosal paint” › through breastfeeding  IgM › acute infxn; 1O response Ab, 1st produced by infants  IgE › parasitic / allergic reactions  IgD › no specific function; antigen-binding
  • 28. factor I (fibrinogen)  factor II (prothrombin) – Vit K dependent  factor III (tissue thromboplastin)  factor IV (calcium)  factor V (proaccelerin)  factor VI (no longer considered active in hemostasis)  factor VII (proconvertin) - Vit K dependent  factor VIII (antihemophilic factor)  factor IX (plasma thromboplastin component; Christmas factor) - Vit K dependent  factor X (stuart factor) - Vit K dependent  factor XI (plasma thromboplastin antecedent)  factor XII (hageman factor)  factor XIII (fibrin stabilizing factor).
  • 30. Spleen › Left upper quadrant of the abdomen behind abdomen › Produces RBC during fetal development › Filter function – remove old defective cells from circulation and breaks down RBC and recycles the iron to bone marrow Liver › Receives blood from the spleen through portal circulation › Produce procoagulants necessary for hemostasis and blood coagulation › Storage of iron and B12 › Detoxify drugs › Kupffer cells carry out phagocytosis › Bile production from erythrocyte destruction
  • 31. Lymphatics  Lymph capillaries › Carries lymph to the subclavian vein in the chest  Lymph nodes › Small rounded structures that filter bacteria and foreign particles
  • 33. Reduction below normal in the # of RBC, the quantity of hemoglobin and volume of RBC (hematocrit)  Result from: › ↓RBC production › ↑RBC destruction › Acute or chronic blood loss
  • 34. Three broad categories 1. Loss of RBC- occurs with bleeding 2. Decreased RBC production › IDA › FADA › Thalassemia 3. Increased RBC destruction
  • 35. Normocytic › Normal RBC size › IDA  Macrocytic › Large RBC due to impaired division of RBC precursor cells › Cobalamin and folate deficiency  Microcytic › Small RBC  Normochromic › Normal hemoglobin concentration  Hypochromic › Decrease hemoglobin concentration  Hyperchromic › Increased hemoglobin concentration
  • 37. Iron Deficiency Anemia › dietary intake of iron is inadequate to produce hemoglobin › Most common type of anemia › May occur with removal of the duodenum › Associated with chronic blood loss.
  • 38.  Iron Deficiency Anemia Etiologic Factors 1. Bleeding- the most common cause 2. Mal-absorption 3. Malnutrition 4. Alcoholism
  • 39.  Iron Deficiency Anemia Pathophysiology › The body storage of iron decrease, leading to depletion of hemoglobin synthesis › The oxygen carrying capacity of hemoglobin is reduced tissue hypoxia
  • 40.  Iron Deficiency Anemia Assessment Findings 1. Pallor of the skin and mucous membrane 2. Weakness and fatigue 3. General malaise 4. Pica
  • 41. Assessment Findings 5. Brittle nails 6. Smooth and sore tongue 7. Angular cheilosis
  • 42.  Iron Deficiency Anemia Laboratory findings 1. CBC › Low levels of Hct, Hgb and RBC count 2. Low serum iron, low ferritin 3. Bone marrow aspiration- MOST definitive
  • 43. Iron Deficiency Anemia Medical management  1. Iron replacement  2. Blood transfusion
  • 44. Nursing Management 1. Provide iron rich-foods › Organ meats (liver) › Beans › Leafy green vegetables › Raisins and molasses 2. Administer iron › Oral preparations tablets- Fe fumarate, sulfate and gluconate › Advise to take iron ONE hour before meals › Take it with vitamin C › Monitor for adverse reaction like pyrosis (heartburn), constipation, diarrhea, dark stool › Continue taking it for several months even with normal iron level
  • 45. Nursing Management 2. Administer iron › Oral preparations- liquid  It stains teeth  Drink it with a straw › Stool may turn blackish- dark in color › Advise to eat high-fiber diet and to ↑fluid intake to counteract constipation
  • 46. Nursing Management 2. Administer iron › IM preparation  Administer DEEP IM  Include 0.5ml air in syringe to clear iron from the needle  Use the Z-track method › Avoid vigorous rubbing › Can cause local pain and staining  Note: › Iron should be taken for 2-3 mos after Hb level returns to normal
  • 47. 3. Administer packed red blood cell transfusion if patient is symptomatic
  • 49. Normally hemoglobin contain 4 globin chains  Decreased production of hemoglobin due to abnormal hemoglobin synthesis  Reduced production or no production of 1 of the globin chains that make up hemoglobin  Microcytic and hypochromic  Autosomal recessive genetic disorder common among Mediterranean people.  Chronic bone marrow hyperplasia  Altered globin synthesis of hemoglobin  Treatment causes chronic iron toxicity
  • 50. Thalassemia minor › Has 1 thalassemic and 1 normal gene with mild clinical manifestations › Requires no tx  Thalassemia major › Has 2 thalassemic genes causing severe conditions
  • 52. Assessment: 1. Skin: pale/jaundiced 2. Splenomegaly and hepatomegaly 3. Thickened cranium and maxillary sinus space from bone marrow hyperplasia
  • 53. Diagnostics: 1. CBC 1. Anemia lower Mean corpuscular volume 2. Hemoglobin electrophoresis
  • 54. Nursing Management 1. Administer BT and chelation therapy (remove heavy metals) to reduce iron overload 2. Monitor for transfusion reactions or diseases acquired through transfusions 3. Instruct about tx, medications and physical energy conservation techniques 4. Strengthen client support and family systems.
  • 56. Life-threatening stem cell disorder with many possible etiological mechanisms  Decreased number of RBC as well as WBC and platelets  Characterized as: › hypoplastic( incomplete development of a tissue or organ) › Fatty bone marrow › Pancytopenia (reduction in # of RBC, WBC and platelets)
  • 57. CAUSATIVE FACTORS 1. Environmental toxins- pesticides, benzene 2. Certain drugs › Chemotherapeutic agents › Chloramphenicol › Phenothiazines › Sulfonamides 3. Heavy metals 4. Radiation
  • 58. Pathophysiology Toxins cause a direct bone marrow depression ↓ acellular bone marrow ↓ decreased production of blood elements
  • 60. ASSESSMENT FINDINGS 1. fatigue 2. pallor 3. dyspnea 4. bruising 5. splenomegaly 6. retinal hemorrhages
  • 61. LABORATORY FINDINGS 1. CBC › decreased blood cell numbers 2. Bone marrow aspiration confirms the anemia- hypoplastic or acellular marrow replaced by fats
  • 62. Medical Management 1. Bone marrow transplantation 2. Immunosupressant drugs 3. Rarely, steroids 4. Blood transfusion
  • 63. Nursing management 1. Assess for signs of bleeding and infection 2. Pancytopenia plan of care to prevent complications like infection and bleeding. 1. Private room 2. Strict hand washing 3. Minimizing invasive procedures 3. Provide client and family with support for lengthy hospitalization and tx
  • 65. abnormally large RBC secondary to impaired DNA synthesis  due to deficiency of Folic acid and/or vitamin B12
  • 66. 1. Folic Acid deficiency › Folate is required for DNA synthesis in erythrocyte formation › Without neurologic involvement Causative factors 1. Alcoholism 2. Mal-absorption 3. Diet deficient in uncooked vegetables 4. Use of oral contraceptives
  • 67. Pathophysiology of Folic acid deficiency Decreased folic acid ↓ impaired DNA synthesis in the bone marrow ↓ impaired RBC development impaired nuclear maturation but Cytoplasmic maturation continues ↓ large size
  • 68. Assessment (Folate Deficiency) 1. Poor nutrition 2. Alcohol abuse 3. Anorexia 4. Impaired absorption in the small intestine 5. Undergoing hemodialysis (folate is dialyzable) 6. Certain drugs can block folate absorption 1. Oral contraceptives 2. Antiseizure drugs (phenytoin) 3. Antibiotics
  • 69. Diagnosis (Folate deficiency) 1. CBC 1. ↓ RBC, hgb & hct and ↑ MCV 2. Serum folate levels are low 3. Serum cobalamin is normal
  • 70. Nursing Management 1. Promote compliance with replacement therapy (1-5 mg oral folate/day) 2. Administer prenatal vitamins in pregnancy 3. Instruct on food high in folate such as leafy greens, liver, citrus fruits, nuts and grains
  • 72. Normal Condition: Parietal cells of stomach secreted intrinsic factor to absorb ingested cobalamin (vit.b12)
  • 73. Vitamin B12 deficiency (Pernicious Anemia) › Lack of intrinsic factor (needed for B12 absorption) › Common among Northern European ancestry over age of 40 and young African American Causative factors 1. Strict vegetarian diet 2. Gastrointestinal malabsorption 3. Crohn's disease 4. Yrs of Gastritis 5. Gastrectomy
  • 74. Vitamin B12 deficiency Pernicious Anemia  Due to the absence of intrinsic factor secreted by the parietal cells  Intrinsic factor binds with Vit. B12 to promote absorption
  • 75. Assessment findings 1. Weakness 2. Fatigue 3. Neurologic manifestations are present only in Vit. B12 deficiency 1. Weakness, paresthesia of feet and hands, impaired thought processes 4. Coagulation deficiencies
  • 76.  Assessment findings Pernicious Anemia › Beefy, red, swollen tongue › Mild diarrhea › Extreme pallor › Paresthesias in the extremities
  • 77. Laboratory findings 1. Peripheral blood smear- shows giant RBCs, WBCs with giant hypersegmented nuclei 2. Very high MCV 3. Schilling’s test › Radioactive vit B12 malabsorption is measured by small amount of secreted in urine › When vit B12 us administered with gastric IF parenterally, its absence in urine will diagnose pernicious anemia 4. Intrinsic factor antibody test
  • 78. Medical Management 1. Vitamin supplementation Folic acid 1 mg daily 2. Diet supplementation Vegetarians should have vitamin intake 3. Lifetime monthly injection of IM Vit B12 › w/o cobalamin replacement, patient can die in 1-3yrs.
  • 79. Since Pernicious anemia results from an inability to absorb cobalamin, dietary intake of the vitamin is not a treatment option, nor is bone marrow transplant
  • 80. Nursing Management 1. Monitor patient 2. Provide assistance in ambulation 3. Oral care for tongue sore 4. Explain the need for lifetime IM injection of vit B12
  • 82. Decrease in erythrocyte precursor production that occurs in some chronic conditions  End-stage renal failure  Chronic liver disease  Alcohol abuse  hypothyroidism
  • 83. Clinical Manifestations ALL ASSESSMENT FINDINGS FOR ANEMIA APPLY
  • 84. Diagnosis: 1. CBC 2. FERRITIN 1. Iron stores may be high in contrast to IDA
  • 85. Nursing Management 1. Facilitate diagnosis and tx if underlying, contributory condition 2. Inform that this type of anemia does not respond to folic acid, iron or vitamin B12 3. Erythropoietin therapy is administered to a client with anemia related to renal failure
  • 87. 2 SITES OF HEMOLYSIS 1. INTRAVASCULAR DESTRUCTION › Occurs within the circulation 2. EXTRAVASCULAR DESTRUCTION › Occurs in liver, spleen, or bone marrow
  • 88. CLASSIFICATION OF HEMOLYTIC ANEMIAS 1. INTRINSIC HEMOLYTIC ANEMIAS › Usually hereditary › Defects in RBC themselves 1. Abnormal hgb = sickle cell anemia 2. Enzyme deficiencies = G6PD 3. Cell membrane abnormalities
  • 89. CLASSIFICATION OF HEMOLYTIC ANEMIAS 2. EXTRINSIC HEMOLYTIC ANEMIAS › Normal RBCs are damaged by external factors › Cause:  antibodies, toxins,  mechanical injury (prosthetic heart valves)  dialysis,  transfusion reaction  trapping of cells within the liver and spleen
  • 92. A severe chronic incurable hemolytic anemia that results from heritance of the sickle hemoglobin gene.  Produces specific mutant form of beta-globin  Hypoxia-induced change in RBCs  Associated with vascular occlusion and tissue infarction  Anemia is caused by accelerated breakdown of abnormal RBC
  • 93.  Causative factor › Genetic inheritance of the sickle gene- Hbs gene
  • 94. Pathophysiology  Decreased O2, Cold, Vasoconstriction can precipitate sickling process
  • 95. Pathophysiology Factors ↓ cause defective hemoglobin to acquire a rigid, crystal-like C- shaped configuration ↓ Sickled RBCs will adhere to endothelium ↓ pile up and plug the vessels ↓ ischemia results ↓ pain, swelling and fever
  • 97. Assessment Findings 1. jaundice 2. enlarged skull and facial bones 3. tachycardia, murmurs and cardiomegaly
  • 98. Assessment Findings  Primary sites of thrombotic occlusion: spleen, lungs and CNS  Chest pain, dyspnea
  • 99. Assessment Findings 1. Sickle cell crises › Results from tissue hypoxia and necrosis 2. Acute chest syndrome › Manifested by a rapidly falling hemoglobin level, tachycardia, fever and chest infiltrates in the CXR
  • 100. During the sickling crisis, the sickling cells clog small capillaries and the resulting hemotasis promotes a self-prepetuating cycle of local hypoxia, deoxygenation of more erythrocytes and more sickling. MEDICAL MGT: Administration of large doses of narcotic analgesics Since pain last 4-6 days
  • 101. Medical Management 1. Bone marrow transplant 2. Hydroxyurea 3. Long term RBC transfusion
  • 102. Nursing Management 1. manage the pain › Support and elevate acutely inflamed joint › Relaxation techniques to reduce metabolic needs › analgesics
  • 103. Nursing Management 2. Prevent and manage infection › Monitor status of patient › Initiate prompt antibiotic therapy
  • 104. Nursing Management 3. Promote coping skills › Provide accurate information › Allow patient to verbalize her concerns about medication, prognosis and future pregnancy
  • 105. Nursing Management 4. Monitor and prevent potential complications › Provide always adequate hydration › Avoid cold, temperature that may cause vasoconstriction
  • 106. Nursing Management 4. Monitor and prevent potential complications › Leg ulcer Aseptic technique
  • 107. Nursing Management 4. Monitor and prevent potential complications Priapism  Sudden painful erection  Instruct patient to empty bladder, then take a warm bath 5. Maintain F & E balance to reduce blood viscosity
  • 109. Glucose-6-phosphate dehydrogenase  Results from lack of an RBC enzyme that leads to RBC damage when metabolic needs of RBCs are increased.
  • 110. A group of X-linked familial hemolytic mutations of the gene  Deficiency predisposes to oxidative denaturation of hemoglobin, with resultant red cell injury and lysis.  Hemolysis occurs as the result of oxidative stress generated by either an infection or exposure to certain drugs.  More common among males of Mediterranean or African descent
  • 111. •Jaundice •Headache Assessment •Dizziness •Easy fatigabilty
  • 112. Diagnostic: Use of G6PD assay or screening test Quantification of G6PD levels during nonhemolytic phase
  • 113. Nursing Management 1. Provide periods of rest 2. Provide adequate hydration 3. Administer antibiotics and other tx as ordered to minimize complications.
  • 115. Refers to an INCREASE volume of RBCs  The hematocrit is ELEVATED to more than 55%
  • 116. POLYCYTHEMIA VERA › Primary Polycythemia  A proliferative disorder in which the myeloid stem cells become uncontrolled  Neoplastic disorder where there is an increased in 3 types of blood cells
  • 117.  POLYCYTHEMIA VERA Causative factor › unknown
  • 118. POLYCYTHEMIA VERA  Pathophysiology › The stem cells grow uncontrollably › The bone marrow becomes HYPERcellular and all the blood cells are increased in number
  • 119. POLYCYTHEMIA VERA Pathophysiology › The spleen resumes its function of hematopoiesis and enlarges › Blood becomes thick and viscous causing sluggish circulation › Overtime, the bone marrow becomes fibrotic
  • 120.  POLYCYTHEMIA VERA Assessment findings 1. Skin is ruddy, pruritic due to histamine release 2. Splenomegaly in primary PV only 3. headache, tinnitus 4. dizziness, blurred vision 5. Angina, intermittent claudication, dyspnea and thrombophlebitis
  • 121. POLYCYTHEMIA VERA  Laboratory findings 1. CBC- shows elevated RBC mass 2. Normal oxygen saturation 3. Elevated WBC and Platelets
  • 122.  POLYCYTHEMIA VERA Complications 1. Increased risk for: 1. Thrombophlebitis  Due to hypervolemia & hyperrviscosity,  Tx: active/passive leg exercise and ambulation 2. CVA 3. MI 2. Bleeding due to dysfunctional blood cells
  • 123. POLYCYTHEMIA VERA Medical Management 1. To reduce the high blood cell mass- PHLEBOTOMY 2. Allopurinol 3. Dipyridamole 4. Chemotherapy to suppress bone marrow
  • 124. Nursing Management 1. Primary role of the nurse is EDUCATOR 2. Regularly asses for the development of complications 3. Assist in weekly phlebotomy 4. Advise to avoid alcohol and aspirin 5. Advise tepid sponge bath or cool water to manage pruritus
  • 126. Malignant disorders of blood forming cells  characterized by UNCONTROLLED proliferation of WBC in the bone marrow- replacing marrow elements .  The WBC can also proliferate in the liver, spleen and lymph nodes.
  • 127. named after the specific lines of blood cells afffected primarily › Myeloid › Lymphoid › Monocytic
  • 128. The leukemias are named also according to the maturation of cells  ACUTE › The cells are primarily immature  CHRONIC › The cells are primarily mature or diferentiated
  • 129. ACUTE myelocytic leukemia  ACUTE lymphocytic leukemia  CHRONIC myelocytic leukemia  CHRONIC lymphocytic leukemia
  • 130. ETIOLOGIC FACTORS › UNKNOWM › Probably exposure to radiation › Chemical agents › Infectious agents › Genetic
  • 131. PATHOPHYSIOLOGY of ACUTE Leukemia Uncontrolled proliferation of immature cells ↓ suppresses bone marrow function ↓ severe anemia, thrombocytopenia and granulocytopenia
  • 132. PATHOPHYSIOLOGY of CHRONIC Leukemia Uncontrolled proliferation of DIFFERENTIATED cells ↓ slow suppression of bone marrow function ↓ milder symptoms
  • 133. ASSESSMENT FINDINGS  ACUTE LEUKEMIA › Pallor › Fatigue › Dyspnea › Hemorrhages › Organomegaly › Headache › vomiting
  • 134. ASSESSMENT FINDINGS  CHRONIC LEUKEMIA › Less severe symptoms › organomegaly
  • 135. LABORATORY FINDINGS  Peripheral WBC count varies widely  Bone marrow aspiration biopsy reveals a large percentage of immature cells- BLASTS  Erythrocytes and platelets are decreased
  • 136. Medical Management 1. Chemotherapy 2. Bone marrow transplantation
  • 137. Nursing Management  1. Manage AND prevent infection › Monitor temperature › Assess for signs of infection › Be alert if the neutrophil count drops below 1,000 cells/mm3
  • 138. Nursing Management 2. Maintain skin integrity 3. Provide pain relief 4. Provide information as to therapy- chemo and bone marrow transplantation
  • 140. Read on the following remaining topics: 1. Thrombocytopenia 2. Disseminated Intravascular Coagulation 3. Hemophilia 4. Von Willebrand’s disease 5. Neutropenia
  • 141. On September 12, 2011, we will have our UNIT EXAM on the following topics: Fluids and Electrolytes And Hematologic Disorders
  • 142. NEXT TOPIC TO BE DISCUSSED WOULD BE: CARDIOVASCULAR DISORDERS AND PERIPHERAL DISORDERS BY S’ CLAY ENDOCRINE DISORDERS BY M’ LUDY