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1 Hematology Review Questions 1. What is the unique nature of a stem cell and what does it mean to be “committed”? a.

The bone marrow first produces stem cells. These blood stem cells are immature, unspecialized (undifferentiated) cells that are capable of becoming any one of several types of blood cells: RBCs, WBCs, or platelets, depending on the body’s needs. b. The next stage in blood cell production is the committed stem cell (precursor cell). A committed stem cell enters one growth pathway and can at that point specialize (differentiate) into only one cell type. i. Committed stem cells actively divide but require a specific growth factor for specialization. 2. What is the difference between intrinsic and extrinsic clotting factors? a. Intrinsic clotting factors—problems or substances directly in the blood itself that first make platelets clump and then trigger the blood clotting cascade. i. Circulating debris, prolonged venous stasis b. Extrinsic clotting factors—outside of the cell than can induce platelet plugs to form. i. Trauma, inflammation, bacterial toxins, or foreign proteins ii. The blood-clotting cascade is started sooner by this pathway because some of the steps of the intrinsic pathway are bypassed.

3. What is the difference between anticoagulants and thrombolytics? a. Anticoagulants- work by interfering with one or more steps involved in the bloodclotting cascade. So they prevent new clots from forming and limit or prevent extension of formed clots. Anticoagulants cannot break down existing clots. b. Thrombolytics- break up existing clots. i. First line therapy for problems caused by small, localized, formed clots such as myocardial infarction (MI), limited arterial thrombosis, and thrombotic strokes. 4. What lab values are evaluated to determine coagulation status? What are their “normal” ranges? a. CBC w/ or w/o differential i. RBCs: males 4.7-6.1 million/mm3 females 4.2-5.4 million/mm3 ii. WBCs: 5,000-10,000/mm3 iii. Platelets: 150,000-400,000/mm3 iv. Hemoglobin: male (14-18 g/dL), female (12-16 g/dL) v. Hematocrit: males (42-52%), females (37-47%) vi. Reticulocyte Count: <2% of circulating RBCs (immature RBCs) vii. Prothrombin Time (PT: 11-12.5 seconds (time it takes for blood to clot) viii. International Normalized Ratio (INR): goal of 2-3 secs for patients on coumadin therapy ix. Partial Thromboplastin Time (PTT): 20-40 seconds depending on lab x. Coombs Test: should be negative 1. Positive findings indicate antibodies to RBCs

Bone marrow biopsy. Low environment or body temperature. How does iron deficiency anemia develop and who is at an increased risk for its development? Development: In 3 stages: Iron stores in body decreased. Dehydration. early death. Anesthesia 8. brittle nails. has a low dietary intake of iron or an increased need for iron or excessive blood loss. disability. increase risk for infection. Absence of neurological problems in folic acid deficiency anemia marks the only difference between these two anemias. pain. What is the significance of folic acid in RBC production? a. Triggers: Hypoxia. orthostatic hypotension.describe important post-procedure assessment and nursing care a. 11. 9. How does one develop SSA and what are some “triggers” contributing to a flare-up? Discuss methods of prevention and treatment of “flare-ups” SSA is an Autosomal recessive genetic disorder. Invasive procedure requiring informed consent c. What are the classic assessment findings in the client with anemia? Pallor. High altitudes. Ativan) ii. tachycardia. and thrombocytopenia. Anyone who is malnourished. avoid contact to area iii. headaches 7. . i. Nervous system functions remain normal because folic acid deficiency does not affect nerve function. Bone marrow aspiration. Strenuous exercise. cool skin.solid tissue and cells obtained by coring out an area of bone marrow with a large bore needle. How is folic acid deficiency and vitamin B12 deficiency anemia differentiated? a. b. Don’t give aspirin or Motrin 6. Local anesthetic as well as sedative (Versed. Venous stasis. leukopenia. Discuss the procedure behind bone marrow biopsies. mild analgesic. Infection. What is pancytopenia and in what disease states is it common? a. Cover site with dressing. Pancytopenia is a deficiency of all three cell types causing aplastic anemia. SOB.2 5. Monitor closely for 24 hours for bleeding/infection. dyspnea.cells and fluids suctioned from marrow d. Alcohol use. organ damage. Performed to evaluate the patient’s hematologic status when other tests show persistent abnormal findings. 10. Decreased oxygen saturation. All cell division requires adequate amounts of folic acid to make DNA. Vitamin B12 moves folic acid into cells so DNA synthesis can occur. Aplastic anemia is a deficiency of circulating RBCs because of failure of the bone marrow to produce these cells. Production of RBCs depends on adequate DNA synthesis in the precursor cell so that cell division and growth into functional RBCs can occur. Acidosis. e. Ice packs. fatigue. Iron stores in hemoglobin depleted. Nursing interventions: i.results in chronic anemia. Insufficient iron for developing RBCs (Hgb deficient RBCs). Pregnancy.

Prolonged hospitalizations are common while the patient is immunosuppressed. 12. From the myeloid pathway: myelocytic or myelogenous b. Induction therapy— intense and consists of combination chemotherapy (cytosine arbinoside and daunorubicin). alopecia (hair loss). PV is a cancer of the RBCs with an increase in number of circulating RBCs leading to hyperviscous blood. or infection. intense itching. which can be caused by long-term exposure to toxic agents and drugs. which causes symptoms of gout and hyperkalemia. What is the standard treatment for leukemia and what are the associated complications? Why may a client who has received previous treatment for cancer develop a different type of cancer later in life? a. and later to infarction and necrosis. d. In some highly vascular areas. Clinical manifestations of leukemia are most related to bone marrow depression and effects of decreased tissue perfusion r/t anemia. SE: N/V. Cancer with uncontrolled production of immature WBCs in bone marrow. Excessive production of platelets b. blood flow may become so slow that stasis occurs. Manifestations of PV: facial skin and mucous membranes dark and flushed with purple/cyanotic appearance. This debris includes uric acid and potassium. complete remission of all manifestations of disease. Shorter life spans and increased cell production cause a rapid turnover of circulating blood cells which leads to increasing amounts of cell debris (released when cells die) in the blood. Drug therapy for Acute Leukemia: i. occluding blood vessels. d. and cardiac toxicity. bleeding 13. Goal is to achieve a rapid. Why is someone with polycythemia vera at risk for tissue hypoxia? a.3 1. HTN. c. liver toxicity. kidney toxicity. . Leukemias are classified by cell type i. ionizing radiation. diarrhea. Caused by an injury to the pluripotent stem cell (immature precursor cell for RBCs). risk for gout and hyperkalemia. adding to the general “sludging” of the blood. Primary ND: increased risk of infection and bleeding 14. The blood vessel occlusion leads to tissue hypoxia. anoxia. risk for thrombosis. stomatitis (mouth sores). Excessive leukocyte production iii. What is the difference between lymphocytic and myelogenous leukemia? a. The presence of the Philadelphia chromosome is the hallmark of chronic myelogenous leukemia (CML) c. From the lymphoid pathway: lymphocytic or lymphoblastic ii. Vascular stasis causes thrombosis (clot formation) within the smaller vessels. Massive production of RBCs ii. Many times reason is unknown. 3 hallmarks: i.

The graft is actually trying to attack the host tissue and cells. Presence of “B symptoms” less common . anemia v. Standard treatment for patients with Leukemia is a bone marrow transplant (hematopoietic stem cell transplant). iii. i. Treatment includes radiation in earlier stages and combination chemotherapy for later stages. Spreads in an orderly fashion.right upper quadrant abdominal pain. HIV or chemical agents iv. The immunocompetent cells of the donated marrow recognize the patient’s (recipients) cells. B symptoms—intermittent fever. Diagnosis through node biopsy and presence of Reed-Sternberg (RS) cells. vi. weight loss. Failure to engraft—donated stem cells fail to grow in the bone marrow and function properly. Hodgkin’s lymphoma is a malignancy of the lymph nodes that originates in a single lymph node or chain of nodes. and liver enlargement. Maintenance therapy—prescribed for months to years after successful induction and consolidation therapies. lymphadenopathy. Clinical manifestations: lymphadenopathy and extranodal involvement (lesions of bone. Purpose is to maintain the remission achieved. drenching night sweats. May be caused by viral infections: EBV. Complications: 1. Discuss the process of bone marrow transplantation. “B symptoms” 1. Consolidation therapy—treatment occurs early in remission and its intent is to cure. mediastinal mass found on X-ray. GI tract. Symptoms of liver failure. and CNS) 1. ascites. This is done by ridding client of leukemic cells via high dose chemotherapy and sometimes total body irradiation and then performing the transplant.4 ii. skin. painless mass in neck often first sign. ii. c. Clinical manifestations: enlarged. Veno-occlusive disease—the blockage of liver blood vessels by clotting and inflammation. i. i. 15. 4. and organs as foreign and start an immunologic attack against them. Bleeding and infection 2. b. Non-Hodgkin’s lymphoma includes all lymphoid cancers that do not have the ReedSternberg cell. weight gain. 3. b. Hodgkin’s and non-Hodgkin’s lymphoma are characterized by abnormal proliferation of lymphocytes. What does it mean to “engraft”? discuss potential complications associated with BMTs and possible treatments for each 16. Does not spread through lymphatic system in orderly fashion 2. Distinguishing feature—Reed-Sternberg (RS) cells iii. host disease—mostly in allogenic (from sibling or matched unrelated donor) transplants. tissues. jaundice. Graft vs. What are the main differences in diagnosing Hodgkin’s and non-Hodgkin’s Lymphoma? a.

Spinal cord compression and paraplegia c. i. and pelvis ii. Thalidomide causes severe birth defects patient at increased risk for infection . Treatment includes radiation. which can lead to renal failure. Multiple myeloma cells also produce excess cytokines that increase cancer cell growth rates and destroy bone. Renal failure ix. Diagnosis i. Weakness and fatigue iii. Steroids. Plasmapheresis (to selectively take out bad cells) and bone marrow transplant iii. Thus the disorder is called a “gammopathy”. When they become cancerous these plasma cells overproduce antibodies (gamma globulins).azathioprine (Imuran) used to inhibit immune system production of antiplatelet autoantibodies 3. 17. Causes decreased production of immunoglobulin and antibodies and increased levels of uric acid and calcium. i. IV Immunoglobulin. Treatment i. ii. spine. Describe the pathophysiology behind multiple myeloma. Autoimmune thrombocytopenia—number of circulating platelets reduced with normal bone marrow production. chemotherapy. Bone (skeletal) pain especially in the ribs. These cells normally make antibodies. There is an overgrowth of B-lymphocyte plasma cells in the bone marrow. Patients make an antibody directed against the surface of their own platelets (an antiplatelet antibody).000/mm3 2.used when platelet count <20. Splenectomy. Biopsy of lesions d. iii. Osteoporosis & fractures vi. Platelet transfusion. Treatment: prevent bleeding episodes!!! 1. Chemotherapy (dexamethasone w/ or w/out thalidomide or bortezomib) 1. The abnormal plasma cells produce an abnormal antibody (myeloma protein or the Bence Jones protein) found in the blood and urine. How is multiple myeloma typically diagnosed and treated? a. Assessment: i. What are the main differences between autoimmune and thrombotic thrombocytopenia purpura? How are each treated? a.5 ii. and even bone marrow transplant because there is nodal involvement. Anemia v. The antibody coats the surface of the platelets. Bone X-ray—Swiss cheese ii.prevent destruction of antibody coated platelets 4. Thrombocytopenia and leukopenia vii. Cancer of mature WBC. ii. Elevated immunoglobulin levels iv. Recurrent infections iv. b. Elevated calcium and uric acid levels viii. Urinalysis shows Bence Jones proteinuria and elevated total serum protein level iii. Bisphosphanates to slow bone damage and reduce pain and risk of fractures 18. making them more likely to be destroyed by macrophages.

0. Vital signs after 15 minutes and then every hour . pain from chronic bleeding into joints. Thrombotic thrombocytopenia—platelets clump together in capillaries with too few remaining in circulation. ABO compatibility required 2. Clumping results in vessel occlusion and ischemia. abnormal bleeding for longer period of time c. PT or PTT >1. i. Treatment: prevent platelet clumping and stop the underlying autoimmune process 1.w/in 15 minutes of starting transfusion c.6 b. Labs: prolonged partial thromboplastin time (PTT) and a normal prothrombin time (PT/INR) d. deficiency in clotting factor VIII (hemophilia A).9NS flush (others may cause clotting) v. Treatment: a regularly scheduled and/or intermittent infusions of factor VIII cryoprecipitate and blood transfusions 20. What is the pathophysiology behind hemophilia? What are the main differences between Hemophilia A & B and how is each treated? a. easily bruise. Pre-transfusion nursing considerations: i. active clotting disorders. bruises. Usually given IVP when fibrinogen level <100 mg/dL 2. Check blood product (pt ID. and post-transfusion? a. Infuse over 15-30 minutes iii. Hemophilia—hereditary bleeding disorder resulting from deficiencies in clotting factors i.deficiency of factor IX (20%) b. Best if ABO compatible b. Hemophilia A (classic). Meds to inhibit platelet clumping. during. Fresh Frozen Plasma—replace blood volume. Type and cross match iii. Vital signs taken immediately prior to transfusion.5 times normal 1. transplantation of tissue (require ABO and Rh antigen compatibility check ii. stroke. Platelets-.<10. Indications of blood transfusions: active bleeding i. alprostadil (Prostin) 19. leading to MI. or abrasions (from abnormal platelet function). During transfusion: i. Infuse over 30-60 minutes iv. Hemophilia B (Christmas). expiration date) vi. 20 gauge IV and tubing with blood filter iv. Sex-linked disease (X-linked recessive trait) ii. ABO. Rh. presence of von Willebrand’s factor 1. and renal failure. Pooled from donors: don’t need same blood type as patient 2. Assessment: excessive bleeding from minor cuts. Verify order/ get consent ii. Cryoprecipitate— product derived from plasma. Discuss when various types of blood component therapy would be indicated.aspirin.deficiency of factor VIII (80%) iii. scheduled for invasive surgery 1.000 thrombocytopenia with active bleeding. PRBCs—usually for Hgb <8g/dL or hypoxemic. What are important nursing consideration pre. Plasmapheresis and the infusion of fresh frozen plasma 2.

Irradiation destroys T-cells and their cytokine products. Most common with whole blood transfusions or when the patient receives multiple transfusions. Antigen-antibody complexes that destroy transfused cells and start inflammatory response. Bacterial—occur as a result of infusion of contaminated blood products. dyspnea. hypotension. N/V. Older adults most at risk for this. Prevent this reaction by giving the patient washed RBCs e. S&S. chills. ii. Host disease—immunosuppressed patients. restlessness. and recurrent infection ii. onset is quick d. and tachypnea b. i.chills. or anaphylaxis ii. raise in temperature v.7 ii. S&S. 1 unit= 2 hours minimum. distended jugular veins. SOB. itching. why each may occur. tachycardia. bronshospasm. Hemolytic—caused by blood type or Rh incompatibility i. Manage and prevent this complication by monitoring intake and output. confusion ii. Allergic—occurs up to 24 hours post transfusion. Assess for chills. c. After transfusion: i. and shock. Document 21. Graft vs. Manifestations occur within 1-2 weeks and include thrombocytopenia. chronic hepatitis. hypotension. i. i. Discuss the several types of transfusion reactions. bounding pulse. and giving diuretics (doses of Lasix in between transfusions) f. S&S: urticaria (hives).tachycardia. a situation that can develop after multiple transfusions. Fluid overload is a potential complication of rapid infusion iv. fever. hives. 80-90% mortality rate but can be prevented by using irradiated blood products. infusing blood products more slowly. Circulatory overload—occurs when a blood product is infused too quickly. S&S: HTN. Discontinue infusion and dispose of the bag and tubing properly ii. itching. Reaction may be mild with fever and chills or life threatening with disseminated intravascular coagulation (DIC) and circulatory collapse. and relevant nursing considerations a. most often in patients with history of allergies i. weight loss. 4 hours maximum (blood contaminated after 4 hours) d. donor T-cell lymphocytes attack host tissues. anorexia. . fever. i. Febrile—occurs most often in the patient with anti-WBC antibodies. Stay with patient for at least 15-30 minutes iii.