Hematopoiesis flashcards

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Hematopoiesis flashcards
2010-10-06 19:46:01
hemostasis hematopoiesis anemia coagulation

NURS 501 Hematopoiesis lecture
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  1. What are the formed elements of blood?
    • RBCs
    • WBCs
    • Platelets
  2. What percentage of blood does plasma make up?
  3. What percentage of blood do RBCs make up?
  4. What is the buffy coat?
    Layer of Leukocytes and platelets in between plasma and erythrocytes in uncoagulated blood
  5. What are the functions of plasma?
    • Prevent blood loss
    • Carry RBCs that transport gases
    • Aid in body defenses
    • Transport nutrients, waste products, hormones
    • Facilitate exchange of body heat
  6. What is plasma made of?
    • Dissolved elements
    • Proteins
  7. Where are plasma proteins formed?
    In the liver
  8. What is the most abundant solute in plasma?
    Plasma proteins
  9. What are the major types of plasma proteins?
    • Albumins
    • Globulins
    • Fibrinogen
  10. What are the three types of globulin plasma proteins?
    • Alpha
    • Beta
    • Gamma
  11. What is the function of gamma globulins?
  12. What is the function of alpha globulins?
    Steroid and bilirubin transport
  13. What is the function of beta globulins?
    Iron and copper transport
  14. What is the lifespan of a RBC?
    ~120 days
  15. What percentage of blood is made up of WBCs?
  16. What is the difference between a macrophage and a monocyte?
    Monocytes circulate in blood and macrophages are found in tissues
  17. Where are blood cells formed?
    • Adult: bone marrow (some in liver/spleen)
    • Fetus: blood vessels, liver, spleen
  18. Which bones contain marrow that will produce blood cells?
    Flat bones of pelvis, ribs, sternum and vertebral bodies
  19. What are cytokines?
    Signaling molecules released by cell that acts on another cell
  20. What do cytokines do?
    Stimulate proliferation, differentiation and functional activation in bone marrow
  21. What does it mean when there are many mature blood cells?
    Equilibrium, no pathologic processes
  22. What does it mean when there are many immature blood cells?
    Mature cells are being lost somehow.
  23. What are Segs?
    Mature neutrophils
  24. What are Bands?
    Immature neutrophils
  25. What is erythrocyte sedimentation rate?
    The rate erythrocytes fall out of solution
  26. What does a high erythrocyte sedimentation rate indicate?
    • Infection
    • Inflammatory disease
    • Blood cancer
    • Metastasized cancer
  27. What are the five steps of hemostasis?
    • 1. Vessel spasm
    • 2. Platelet plug formation
    • 3. Formation of insoluble fibrin clot (coagulation cascade)
    • 4. Clot retraction
    • 5. Clot dissolution
  28. What is the lifespan of a platelet?
    8-9 days
  29. What is the lifespan of an RBC?
    ~120 days
  30. Which cytokine controls the production of platelets?
  31. What are non-cellular, cytoplasmic fragments of megakaryocytes have no DNA, no Nucleus and cannot reproduce?
  32. What promotes platelet adhesion?
    • Thromboxane A2 (TXA2)
    • Plasma Proteins
    • vonWillebrand factor
    • ADP
    • Calcium
  33. How long does vessel spasm last?
    ~1 minute
  34. What initiates vessel spasm?
    Endothelial injury
  35. What effect does prostacyclin have?
    Relaxes vessel endothelium and inhibits platelet aggregation
  36. What do platelets release that promotes vasoconstriction and spasm?
    Thromboxane A2
  37. What inhibits platelet adhesion?
  38. What is activation of the arachidonic acid pathway?
    Platelets release TXA2 and ADP
  39. What causes platelets to aggregate?
    Thromboxane A2
  40. What contributes to platelet plug stabilization?
    TXA2, ADP, Thrombin and Fibrin
  41. Why is fibrin important?
    It stabilizes the clot
  42. Where does the intrinsic pathway begin?
  43. Where does the extrinsic pathway begin?
    Trauma to tissues/vessels and release of a tissue factor
  44. What are the terminal steps of the coagulation cascade?
    • Activation of Factor X
    • Conversion of prothrombin to thrombin
    • Thrombin converts fibrinogen to fibrin
  45. What is fibrinolysis?
    Clot dissolution
  46. What is fibrinolysis regulated by?
    Thrombin and plasminogen activations
  47. What is the function of plasmin?
    It digests fibrin
  48. How long is plasmin’s half-life and why?
    Very short to keep the effect local
  49. Why do platelets contract and squeeze the serum from the clot and what stage of hemostasis does this occur?
    Drying increases stability of the clot during clot retraction
  50. What is the major purpose of clot retraction?
    Bring the edges of the broken vessel closer together
  51. What are the two types of thrombosis?
    • Increased platelet function
    • Accelerated Activity of coagulation
  52. What conditions are associated with increased platelet function?
    • atherosclerosis
    • Diabetes mellitus
    • Smoking
    • Increased lipids/cholesterol
    • Increased platelets
  53. What conditions are associated with accelerated activity of coagulation?
    • Pregnancy
    • Oral birth control
    • Postoperative
    • Immobility
    • CHF
    • Malignant dx
  54. What are three situations that increase probability of venous thrombosis and what is it called?
    • Virchow’s Triad
    • Stasis of blood
    • Increased blood coagulability
    • Vessel wall injury
  55. What is the function of all treatments for venous thrombosis?
    Increased venous flow
  56. What kinds of patients are likely to have thrombotic stroke?
    • Had a transient ischemic attack (TIA)
    • Previous thrombotic stroke
    • Likely to have clot formation in left heart (atrial fibrillation/heart valves)
  57. When are anticoagulants used?
    • For DVT
    • For patients with a likelihood or history of thrombotic stroke
    • For patients with hypercoagulability syndrome
  58. What is heparin?
    Polysaccharide made in our bodies that binds and activates antithrombin III
  59. What happens when antithrombin III is activated?
    It prevents the activation of factor X
  60. What does heparin do?
    Directly prevent the conversion of prothrombin to thrombin
  61. Why can’t heparin be given PO?
    Stomach acid destroys it
  62. What is aPTT?
    Activated Partial Thromboplastin Time
  63. Why is it important to know aPTT?
    It can indicate if there are factor deficiencies
  64. What is a healthy aPTT?
    1.5 to 2 times the normal value
  65. Can heparin be given during pregnancy?
  66. How do heparin and aPTT related?
    aPTT determines how much heparin is administered
  67. What is PT?
    Prothrombin Time
  68. What is INR?
    International Normalized Ratio
  69. What does the INR do?
    Adjusts the PT ratio to a value that takes into account the variability of lab reagents
  70. What is a target INR for basic blood-thinning needs?
    2.0 to 3.0
  71. What is a target INR for high risk of clot formation?
    2.5 to 3.5
  72. What is the treatment for heparin overdose?
    Stop infusion until the aPTT returns to the target level
  73. What is fractionated heparin?
    Low molecular weight heparin
  74. Why is fractionated heparin used?
    • It is safer
    • Doesn’t cause thrombocytopenia so monitoring not necessary
    • Can be given by caregiver at home
  75. How does fractionated heparin work?
    Inhibits Factor X, but not thrombin
  76. What is Warfarin’s MOA?
    Inhibits the synthesis of particular clotting factors (II, VII, IX, and X) by inhibiting vitamin K binding.
  77. What is the route of administration for Warfarin?
  78. Why is heparin continued when warfarin is started?
    Because warfarin has no effect on clotting factors that are already circulating, so they must be given time to leave the system
  79. What will effect the action of warfarin?
    Foods rich in vitamin K will inhibit warfarin, if Vitamin K is deficient warfarin will be too effective
  80. What are two examples of platelet drugs?
    Plavix and Ticlid
  81. What is the effect of Plavix and Ticlid?
    Cause irreversible inactivation of platelet aggregation
  82. What is the MOA of Plavix and Ticlid?
    Inhibit platelet aggregation
  83. What is TTP?
    Thrombocytopenic Thrombolytic purpura
  84. What drug is used as prophylaxis with 81 mg aspirin for atherosclerotic events or patients who are at risk for stroke or MI?
    Plavix and Ticlid
  85. What tests are used to monitor patients taking plavix and ticlid?
    CBC with differential for neutrophil count
  86. Which drug is active as taken, Plavix or Ticlid?
  87. Which drug is a prodrug, Plavix or Ticlid?
  88. What is the MOA of Glycoprotein Receptor Antagonists?
    Reversible blockade of platelet glycoprotein IIb/IIIa receptors, therefore inhibit the final step in aggregation
  89. What are glycoprotein receptor antagonists used for?
    To prevent ischemic events in patients with acute coronary syndromes, short-term
  90. What is the big benefit of using glycoprotein protein receptor antagonists over Ticlid or Plavix?
    It is reversible
  91. What is the action of thrombolytic drugs?
    Activate plasminogen to plasmin, which degrades fibrin and dissolve clot
  92. What are the indications/uses for tPA?
    Embolisms and MIs
  93. How can plasminogen activators be given?
    Itra-arterially into clotted vessel or by IV
  94. What are three causes of bleeding disorders?
    • Dysfunctional platelets or platelet action
    • Deficiency of Coagulation Factors
    • Poor Vascular Integrity
  95. What is purpura?
  96. What is petechia?
    Pinpoint hemorrhage
  97. What are the symptoms of thrombocytopenia?
    • Severe decrease in platelet count (10K-15K/ml)
    • Bleeding in small vessels
    • Petechia, purpura
    • Bleeding from nose/GI tract
  98. How do leukemia, HIV, radiation and chemotherapy cause platelet defects?
    • Decrease platelet counts
    • Decrease platelet production in bone marrow
  99. Where are 1/3 of platelets reserved in the body?
  100. What causes splenomegaly and what are the effects?
    Cirrhosis, portal hypertension and lymphomas, cause increased pooling of platelets in the spleen
  101. What is the end result of ITP and why?
    Fewer platelets because antibodies are produced against platelets.
  102. What is the difference between thrombocytopenia and thrombocytopathia?
    • Penia = fewer
    • Pathia = impaired function
  103. What are two causes of thrombocytopathia?
    • Inherited disorders of adhesion
    • Acquired defects
  104. What are three types of coagulation defects?
    • Defects in synthesis of factors
    • Inherited coagulation defects
    • Increased consumption of factors
  105. Which clotting factors are synthesized in the liver?
    • Prothrombin
    • Fibrinogen
  106. Why do patients with liver problems have increased risk of defective clotting factors?
    Because vitamin K is required for normal clotting activity and vitamin K needs bile salts to be absorbed from the intestines
  107. What causes Hemophilia A?
    A decrease in Factor VIII
  108. When is Hemophilia A diagnosed and how?
    • In childhood by severe and spontaneous bleeding
    • In adults through severe bleeding with mild trauma
  109. What causes Von Willebrand’s disease (VWF)?
    A decrease in platelet adhesion due to decreased VW factor
  110. When is Von Willebrand’s Disease diagnosed?
    Usually in adulthood
  111. What are two genetic diseases that cause coagulation defects?
    • Hemophilia A
    • Von Willebrand’s Disease
  112. What secondary disorder that is a paradox of widespread coagulation and bleeding involves systemic formation of fibrin, excessive clot formation and consumption of clotting factors?
    Disseminated Intravenous Coagulation (DIC)
  113. What are the other conditions that can occur with DIC?
    • OB complications
    • Cancer
    • Infections
    • Shock
    • Trauma
  114. What is the treatment for methemoglobin and carboxyhemoglobin?
    100% O2 gas
  115. What are 3 hemoglobin oxidation scenarios?
    • HbO2 (desirable)
    • Methemoglobin (low O2 affinity)
    • Carboxyhemoglobin (low O2 affinity)
  116. What causes methemoglobin?
    Chemicals, nitrates and smoking
  117. What causes carboxyhemoglobin?
    Carbon monoxide
  118. What will an iron deficiency do to Hb?
    Decrease hemoglobin in RBCs
  119. What does serum ferritin measure?
    Level of iron in liver and circulation
  120. Where does most of the iron reside in the body?
    Complexed to heme in hemoglobin (80%)
  121. What is the rate of RBC destruction?
    1% per day
  122. What happens to the components of hemoglobin when the RBCs are destroyed in the spleen, liver, bone marrow and lymph?
    • Amino acids and iron are recycled
    • Heme is converted to billirubin and excreted
  123. How long does it take for a reticulocyte to mature to an RBC?
    1-3 days
  124. How long does it take for a stem cell to mature to a reticulocyte?
    1 week
  125. What organ drives RBC production?
  126. What is the function of erythropoietin?
  127. What does Hct measure?
    Percent of RBCs in 100 ml of blood
  128. What does MCV measure?
    Size of RBCs
  129. What does MCHC measure?
    Color of RBC
  130. What does hypochromic indicate?
    Decrease in Hb concentration
  131. What are some causes of anemia?
    • Excessive blood loss
    • Destruction of RBCs
    • Decrease in RBC production
  132. What is defined as anemia?
    Abnormally low number of RBCs or hemoglobin (or both)
  133. What is hemolytic anemia caused by?
    Destruction of RBCs and Iron retention
  134. Where does destruction of RBCs occur in hemolytic anemia?
    Intravascularly or in spleen
  135. What causes hemolytic anemia?
    • Intrinsic: defect in cell membrane
    • Extrinsic: thing that destroy RBC (toxins, Abys, trauma, etc…)
  136. What are signs and symptoms of hemolytic anemia?
    • Fatigue
    • Lethargy
  137. What is the etiology of Sickle Cell Anemia?
    Abnormal substitution of one amino acid in Hb molecule
  138. How does sickle cell anemia lead to sickle cell crisis?
    Sickle cells are hyperadhesive and obstruct flow in circulation, leading to increased cell destruction from hypoxia
  139. What can chronic sickle cell anemia lead to?
    CVA, splenomegaly
  140. What can cause acquired hemolytic anemia?
    • Exogenous factors that destroy RBCs (drugs, chemicals, infection toxins)
    • Mechanical factors (heart valves, pumps)
    • Immune system (antibodies)
  141. What causes microcytic hypochromic anemia?
    Iron deficiency
  142. What causes megaloblastic normochromic anemia?
    • Folic acid deficiency
    • Vitamin B12 deficiency
  143. What causes pernicious anemia?
    Altered absorption of B12
  144. What causes aplastic anemia?
    Decrease in production of RBCs due to decreased number or function or bone marrow stem cells or radiation/chemotherapy
  145. Why does renal failure cause anemia?
    Decreased erythropoietin production
  146. What is pharmacologic erythropoietin?
    Epoetin alfa (recombinant protein)
  147. Why is darbepoetin preferred over epoetin alfa?
    It can be given less frequently
  148. Why is it important to monitor hematocrit and maintain iron levels when taking pharmacologic erythropoietin?
    To make sure healthy RBCs are being produced
  149. How is erythropoietin administered?
    SubQ and sometimes IV
  150. What is the target hematocrit when administering erythropoietin?
  151. What is leucopenia?
    Decrease in the absolute number of WBCs (neutrophils mostly)
  152. What causes neutropenia?
    • Decrease in production by bone marrow
    • Peripheral destruction
    • Shift from circulatory system to peripheral tissues
  153. What conditions can lead to neutropenia?
    • Complication of procedures
    • Diseases that interfere with blood cell formation
    • Infections which drain neutrophils from blood faster than they can be replaced
  154. What does G-CSF do?
    Promotes proliferation/maturation of granulocyte precursors
  155. In what circumstance will G-CSF not work?
    If the bone marrow has completely failed or if the bone marrow is functioning maximally
  156. What is Filgrastim?
    Recombinant protein with short half-life G-CSF drug
  157. What is pegfilgrastim?
    Filgrastim encased in protective substance
  158. What is febrile neutropenia a serious complication of?
  159. What are 2 G-CSF drugs?
    • Filgrastim
    • Pegfilgrastim
  160. Why does bone pain occur with treatment of leucopenia?
    Because of the bone marrow expansion
  161. How is Filgrastim administered?
    Daily IV or with SubQ injections
  162. How is Pegfilgrastim administered?
    One SubQ injection
  163. What does increase in neutrophils indicate when treating leucopenia?
    Decreased infection
  164. What is a platelet’s stem cell?
    Megakaryocyte stem cell
  165. Which cells do not come from myeloid stem cells?
    T cells and B cells
  166. What is the neutrophil’s stem cell?
    Granulocyte stem cell
  167. What is the erythrocyte’s precursor?
  168. What is the macrophage’s precursor?
  169. What is the monocyte’s precursor?