MEDSURG: HEMA

CHAPTER 28: ASSESSMENT OF HEMATOLOGIC

FUNCTION AND TX MODALITIES
Hema – BLOOD
Hematologic System – blood and blood forming sites,
bone marrow, and RES (reticuloendothelial system)
Blood
o Plasma: fluid portion
o 90% water
o 10% minerals, solutes, gases
o Blood Cells: erythrocytes, leukocytes,
thrombocytes
Hematopoiesis – formation of new blood cellular
components
BONE MARROW - site for blood product production
o Stem Cells: precursor cells; progenitor cells
involved in formation of blood components
o Myeloid: progenitor cells for the
production of
▪ Erythrocytes (RBC)
▪ Leukocytes (WBC)
▪ Platelets RBC: Erythrocytes (4.5 – 5.5 M /mm3)
o Lymphoid: – responsible for the Types:
production of o Hemoglobin – protein, giving the color RED;
▪ Lymphocytes carries oxygen
• T-lymphocytes = o Reticulocytes: immature RBCs (enters
responsible for bloodstream and matures there)
destroying pathogens Erythropoiesis – process of production of RBC by
via phagocytosis means of erythropoietin (hormone stimulates bone
• B-lymphocytes = marrow – kidneys)
releases antibodies Components needed for the production of new
o Stroma blood:
HEMATOPOEISIS – complex process of formation o Iron Stores and Metabolism
and maturation of blood cells. This occurs in bone o Vit. B12 and Folic Acid
marrow and begins with differentiation of stem cells Destruction - hemolysis
into either myeloid or lymphoid stem cells o RBC lifespan = 120 days

WBC: Leukocytes (4,500 - 11,000/mm3)

o Granulocytes – originates from bone marrow
o Eosinophils - allergy
o Basophils – blood clotting (releases heparin)
o Neutrophils – infection/existing
pathogen (via phagocytosis)
▪ Bands: left shift
o Agranulocytes – originates from lymph nodes
o Monocytes
o Lymphocytes
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▪ T-cells (destruction of HEMOSTASIS – response of blood after an injury
pathogens) o Prevent/stops bleeding
▪ B-cells (Ab) o Activates clotting factors
o Liquid-gel-clot-stop bleeding
PLATELETS: Thrombocytes (150,000 – 450,000)
o Thrombopoietin – hormone (produced by ASSESSMENT OF HEMATOLOGIC HEALTH
liver) to regulate production of platelets a. Health Hx
o Type of MGDF (Megakaryocyte Growth b. PE – usually pallor, tachycardia in response to
and Development Factor) blood loss
o Fibrin – major component of blood clotting c. Diagnostic Evaluation
o Aka Factor IA a. Hematologic studies - CBC
o 1st to activate after an injury to BV b. Bone marrow aspiration and biopsy –
Thrombocytopenia – platelet deficiency diagnose blood d/o (leukemia,
o Petechiae – pinpoint hemorrhagic lesions, myeloma)
prominent on trunk and anterior aspects of
lower extremities THERAPEUTIC APPROACHES
a. Splenectomy – removal of spleen
PLASMA and PLASMA PROTEINS a. Fue to splenomegaly – persistent infx
o Albumin – component responsible for b. Apharesis – sickle cell anemia, blood d/o
maintenance of oncotic pressure (pulls water a. Remove blood of pt. via centrifuge
into intravascular membrane/BV) and separate blood components
o Globulins – transport of lipids and fat-soluble; c. Hematopoietic stem cell transplantation
immune response (HSCT)
o Alpha – transports fat-soluble and d. Phlebotomy
lipids e. Blood component therapy
o Beta - transports fat-soluble and f. Special preparations
lipids
o Gamma – acts as antibodies BLOOD AND BLOOD PRODUCTS
(immunoglobulins – activated during Donor requirements
inflammatory response) Donation types: Table 28-4
o Impact on fluid Balance o Directed
o Standard
RETICULOENDOTHELIAL SYSTEM o Autologous
Histiocytes o Intraoperative blood salvage
o Kupffer cells – specialized type of cells o Hemodilution
produced in the liver Complications of donation
o Immune response; removes cellular Blood processing
debris/waste products Transfusion
o Limited to hepatic portal system - Common settings
(filters blood) - Pretransfusion assessment
o Peritoneal macrophages o 2 identifiers; ask pt
o Alveolar macrophages o ABO typing: should be a match
Spleen – lymphoid organ; filters lymph - Pt. Education
o collects old RBC - Transfusion process
o Reservoir for blood (temporary) o Correct administration techniques
o Activates when hemorrhage occurs per agency’s policies and procedures
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o chart 28-3, 28-4
Transfusion Complications
- Febrile nonhemolytic reaction – most
common reaction
o Fever, no destruction of RBC
(nonhemolytic)
o Chills, N&V, headaches, dizziness =
ex. May cytokines (causes immune
response)
o WBC – cytokines is present = causes
s/sx
- Acute hemolytic reaction - hemolysis
- Allergic reaction - mismatch
- Transfusion-associated circulatory
overload – rapid transfusion
- Bacterial contamination – improper
handling of blood
- Transfusion-related acute lung injury
- Delayed hemolytic reaction
- Disease acquisition chart 28-6
- Long term transfusion therapy
Nursing Management
- Stop
- Assess
- Notify primary provider and implement
prescribed treatments. Continue to monitor.
- Return blood
- Obtain any samples needed
- Document
Transfusion Alternatives chart 28-7
- Growth factors
- Erythropoietin
o For those who do not want to be
transfused with blood
o SubQ injection
- Granulocyte colony-stimulating factor
- Granulocyte-macrophage colony-stimulating
factor
- Thrombopoietin

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- Cardiac (less supply of O2), GI, neurologic,
respiratory sx
- Tongue changes – pernicious anemia
- Nail changes – clubbing
- Angular cheilitis – cracked or sores on
corners of mouth
- Pica – eats non-food items
Diagnostic Tests for Anemia
- Hgb & Hct
CHAPTER 29: MGMT OF PTS WITH NON- - Reticulocyte count
MALIGNAN HEMATOLOGIC D/O - RBC indices – identify N shape and size of
ANEMIA RBC, number of RBC
- Lower than N Hgb, fewer than N circulating - Iron Studies
erythrocytes - Vitamin B12
- Sign of underlying d/o - Folate
2 causes: - Haptoglobin and erythropoietin levels
- Hypoproliferative: defect in production of - Bone marrow aspiration – cannula insertion in
RBCs or underporduction hip bone/iliac crest
o Caused by Iron, Vit. B12, or Folate Medical Management of Anemias
Deficiency, decreased erythropoietin - Correct/control the cause
production (problems in kidney), - Transfusion of packed RBCs (golden
cancer, bone marrow damage standard)
- Hemolytic: excess destruction of RBCs - Treatment specific to type of anemia
o Caused by altered erythropoiesis, or - Dietary therapy
direct injury to erythrocyte. - Iron or Vit. Supplementation: iron,
o CHART 29-1 AND TABLE 29-1 folate, B12
o Results from RBC destruction - Transfusions
o Premature destruction of RBC results - Immunosuppressive therapy
in liberation of Hgb from erythrocytes - Other
in the plasma.
o Bilirubin concentration rises, and HEMOLYTIC ANEMIAS
increased erythrocyte destruction a. Sickle Cell Disease
leads to tissue hypoxia, which o Inherited blood d/o
stimulates erythropoietin production, o Abnormal mutation of beta hgb = HBB
reflected in an increased reticulocyte mutation
count. i. Changes in shape = “sickle-
Manifestations of Anemia shaped” “crescent-shaped”
Depends on the rapidity of the dev’t of ii. Accumulate = Obstructs BV =
anemia, duration of anemia, metabolic pain
requirements of pt. (deficiency), concurrent o Assessment: Health Hx and PE
problems (ex. Kidney problems), and i. Pain assessment
concomitant features. ii. Sickle cell crisis assessment
- Fatigue, weakness, malaise = less O2 iii. Blood loss: menses, potential
- Pallor (less circu RBC) or jaundice (hemolysis GI loss
= unconjugated bilirubin deposits)

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iv. Cardiovascular and oG6PD – enzyme that protects RBC
neurologic assessment from destruction
v. Lab: “S-shaped Hgb” d. Immune Hemolytic anemia
o Sx: swelling, fever, pain e. Hereditary hemochromatosis
i. Pain management is priority o Abnormally large amount of iron
o Chronic Skin ulcers of sickle cell deposits in the tissues/organs
(gangrene like) = due to vaso
occlusion caused by SC HYPOPROLIFERATIVE ANEMIAS
o Collaborative problems & potential a. Iron deficiency anemia – less iron intake
complications: b. Anemia in renal dx
i. Hypoxia, ischemia, infx a. Kidney = production of erythropoietin
ii. Dehydration (signals production of RBC)
iii. CVA – Ischemic stroke c. Anemia of inflammation
iv. Anemia d. Aplastic anemia – hypo/under production of
v. Acute and chronic kidney dx – blood components
low perfusion e. Megaloblastic anemia – larger than normal
vi. Heart failure RBC;abnormal function; caused by problem
vii. Impotence in DNA synthesis:
viii. Poor compliance a. Hypovitaminosis:
ix. Substance Abuse i. Folic acid deficiency
o Management: ii. Vit. B12 deficiency
i. Pain management b. Cell cycle stops at G1 phase – no
ii. Manage fatigue cellular division
iii. Infx prevention i. (N cycle is G1 (cell growth), S
iv. Promote coping (synthesis of DNA), G2 (cell
v. Educate on dx. Process growth), M (mitosis)
vi. Monitor complications
b. Thalassemia NEUTROPENIA
o Body abnormally generates abnormal o Decreased production or increased
Hgb destruction of neutrophils (<2000/mm)
o Hgb has 2 subtypes in a N person: o Monitor closely: Increased Risk for Infection
i. 2 Alpha chains o Absolute neutrophil count (ANC)
ii. 2 Beta chains o Medical Management: treatment depends
o In thalassemia, there is an imbalance on the cause
between the two o Nursing Management: Patient Education,
i. A-thalassemia – decrease a- prevent and manage complications
chains; increase b-chains
1. Causes RBC LYMPHOPENIA
hemolysis = jaundice o Lymphocyte count is less than 1500/mm3
ii. B-thalassemia - decrease b- o Causes:
chains; increase a-chains ▪ Exposure to radiation
1. Causes microcytic ▪ Long-term use of corticosteroids
anemia (immunosuppressants ex.
c. Glucose-6-phosphate dehydrogenase Betamethasone, dexamethasone)
(G6PD) deficiency • Suppresses bone marrow function
▪ Infections
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▪ Neoplasms IMMUNE THROMBOCYTOPENIA PRPURA (ICP) –
▪ Alcohol abuse relatively low amount of platelet without underlying
POLYCYTHEMIA cause
o Increased vol. of RBC PLATELET DEFECTS chart 29-9
o Secondary polycythemia HEMOPHILIA – lack of clotting factors
i. Excessive production of VON WILLEBRAND DISEASE chart 29-6, 29-8, table 29-3 - lack
erythropoietin from reduced of clotting factors
amounts of O2, cyanotic heart dx,
non-pathologic conditions or
neoplasms ASSESSMENT OF PATIENT W/ ANEMIA
ii. Results from neoplasms that a. Heath Hx and PE
stimulate erythropoietic b. Lab Data
production. a. CBC
o Medical Management: b. Peripheral blood smear – qty, size,
i. Treatment not needed if mild shape of blood products
ii. Treat underlying cause c. Presence of sx and impact of those in pt. life
iii. Therapeutic phlebotomy – most a. Fatigue – if can tolerate ADLs
common medical management b. Weakness
1. Remove excess blood thru c. Malaise
phlebotomy d. Pain
f. Not an anemia d. Nutritional assessment
g. Conditions causing polycythemia: e. Medications
o Smoking f. Cardiac and GI assessment
o OSA g. Blood loss: menses, potential GI loss
o COPD h. Neurologic Assessment
o Severe heart dx
o Living at high altitudes/exposure to Collaborative Problems and Potential
low levels of carbon monoxide Complications of the Patient w/ Anemia
o Heart failure (decreased O2 cannot sustain
heart)
BLEEDING DISORDERS o Angina
FAILURE OF HEMOSTATIC MECHANISMS o Paresthesias – numbness or tingling
hemostasis is the mechanism of our body to stop or sensation (peripheral neuropathy)
prevent bleeding o Confusion
Causes: o Injury r/t falls
o Trauma (esp. direct trauma to BV) o Depressed mood
o Platelet abnormality
o Coagulation factor abnormality Planning and goals for Pt. w/ Anemia
Med Mgt: specific blood products 1. Decreased fatigue
Nsg Mgt: limit injury (reduced risk of bleeding), 2. Attainment/maintenance of adequate
assess for bleeding, bleeding precautions nutrition
3. Maintenance of adequate tissue perfusion
SECONDARY THROMBOCYTOSIS 4. Compliance w/ prescribed therapy
THROMBOCYTOPENIA – decrease in platelet in the 5. Absence of complications
blood
Interventions for Pt. w/ Anemia
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1. Balance physical activity, exercise, and rest - Altered hemostasis mechanism causes
a. Provide sched massive clotting in microcirculation. As
2. Maintain adequate nutrition clotting factors are consumed, bleeding
3. Maintain adequate perfusion occurs.
4. Patient education to promote compliance w/ - Assessment:
medications and nutrition o Be aware: pt at risk for DIC
a. Causes, interventions, managements o Assess s/sx
pt could do o Assess for progression of thrombi and
5. Monitor VS, pulse oxi; provide supplemental bleeding
O2 PRN - Sx r/t tissue ischemia and bleeding
6. Monitor potential complications - Lab tests
- Treatment:
ACQUIRED COAGULATION DISORDERS o Treat underlying cause
Liver disease – defective clotting = hematoma (liver o Correct tissue ischemia
cirrhosis) o Replace F&E
Vit. K deficiency (needed for production of clotting o Maintain BP
factors) o Replace coagulation factors
Complications of anticoagulant therapy o Use heparin or LMWH = DOC
Disseminated Intravascular Coagulation / DIC o Goal: maintenance of hemodynamic
- Not a dx/ but a sign of underlying d/o status, intact skin and oral mucosa,
- Triggers: sepsis, trauma, shock, cancer, fluid balance, tissue perfusion,
abruptio placentae, toxins, allergic reactions enhanced coping, absence of
- Pathophysio: complications
o Formation of blood clots in o Interventions: target potential sites of
microcirculation (small BV) organ damage, monitor and avoid
o Activates clotting factors trauma and procedures/activities that
continuously increase the risk of bleeding and ICP
o Dissolves blood clot continuously - Collaborative problems & Potential
o Pt. bleed continuously Complications:
o Eventually, organ failures o Kidney injury
o Gangrene
o Pulmonary embolism or hemorrhage
o ARDS
o stroke
Thrombotic d/o
Hyperhomocycteinemia – elevated homocysteine
(needed for formation of blood clots) in the blood
Antithrombin deficiency
Protein C & S deficiency
Activated protein C resistance and factor V Leiden
mutation
Acquired thrombophilia
Malignancy
1.

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