hematology patho 4

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mthompson17
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hematology patho 4
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2013-04-02 03:00:03
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hematology nursing
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hematologic disorders for patho in nursing
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  1. neutrophil
    granulocyte that is usually first on scene of inflammation/infection and releases enzymes that kill microbes
  2. eosinophil
    granulocytes that are released in response to allergies and parasites
  3. basophils
    granulocytes that respond in allergic/inflammatory reactions

    • release histamine = vasodilation
    • release heparin = thin blood
  4. hematopoiesis?
    formation of blood cells
  5. HgB?
    oxygen transport protein of the RBC
  6. Hct?
    % of RBC in the blood
  7. methemoblobin
    form of HgB where iron in the heme groups is in the ferrous state (Fe3+) instead of ferrous state (Fe2+) that is naturally produced in the body

    cannot bind oxygen
  8. Anemia?
    decreased RBC's or HgB in the blood
  9. Polycythemia?
    increased proportion of RBC for blood volume
  10. Pancytopenia?
    reduced amount of RBC, WBC, and platelets
  11. Granulocytopenia?

    What are the 3 granulocytes?
    decrease in amount of granulocytes

    neutrophils, eosinophils, and basophils
  12. Megaloblasts?
    unusually large erythroblast
  13. erythroblast?
    nucleated precursor cell for RBC
  14. microcytic?
    small RBC's
  15. hypochromic?
    RBC's are paler than normal due to decreased HgB of the cell
  16. reticulocyte count?

    Why may it rise?
    measures how fast RBC are made by the bone marrow and released into the blood

    will rise anytime negative feedback shows the need for more RBC:  hypoxia, RBC destruction, hemorrhage, etc
  17. epistaxis
    nosebleed
  18. acrocyanosis
    blue fingers and toes
  19. hematology
    study of blood and blood forming tissues
  20. 4 major organs of blood formation and their functions?
    • 1. bone marrow - blood forming organ
    • 2. spleen - filters micro-org from blood; RBC destruction
    • 3. lymph system - maturation of T lymphocytes
    • 4. liver - formation of plasma proteins
  21. Composition of the blood?
    45% cells, 55%plasma
  22. platelets AKA?
    thromocytes
  23. How much blood is in the body?
    5-6L
  24. Composition of plasma?
    mostly water with plasma proteins and inorganic compounds
  25. Normal RBC count?
    4.2 - 6.2 million/mm3
  26. 2 functions of RBC?
    • 1. transport O2 and CO2
    • 2. assist in maintaining acid-base balance
  27. Normal WBC count?
    5000-10,000/mm3
  28. 2 functions of WBC?
    • 1. phagocytosis
    • 2. immune antibody formation
  29. 2 types of neutrophils?
    bands and segs
  30. Bands?
    baby neutrophils - indicates acute bacterial/viral infection
  31. Segs?
    old neutrophils
  32. 2 types of agranulocytes?
    monocytes and lymphocytes
  33. What is different about lymphocytes from all other blood cells?
    come from a diff stem cell from other blood cells
  34. Normal platelet count?
    150,000 - 400,000
  35. Where are non-circulating platelets stored?
    spleen
  36. What causes the release of platelets?
    damage to the capillary endothelium

    form a platelet plug
  37. Where are plasma proteins formed?
    mainly in the liver
  38. 3 plasma proteins that contribute to colloid osmotic pressure and blood pressure?

    How does this occur
    albumin, serum globulin, fibrinogen

    they hold water in the vascular space due to colloid osmotic pressure
  39. Serum albumin function?

    AKA?
    essential to maintain blood volume and pressure
  40. Serum globulin functions to transport ____, ____, _____, ____, & _____ in the plasma and contains _______molecules.
    bilirubin, lipids, steroids, iron, and copper

    antibody
  41. Fibrinogen?
    inactive precursor of fibrin whih forms the framework for blood clots
  42. Where does hematopoiesis occur in embyo?
    liver and spleen
  43. Where does hematopoisis occur in adults?
    in the red bone marrow
  44. 3 serum globulin fractions?
    alpha, beta, and gamma
  45. 2 stages in hematopoiesis?
    • 1. mitosis
    • 2. maturation/differentiation
  46. When and how does mitosis of hematopoiesis occur?
    immature stem cells undergo mitosis when stimulated by a biochemical signal that is released when the number of circulating cells is decreased
  47. 2 functions of erythropoeitin?
    1. stimulates maturation/differentiation of blood cells in adults

    2. stimulates marrow conversion from yellow to red
  48. What type of hematopoiesis is abnormal in adults?
    extramedullary (outside bone marrow
  49. Lymphopoiesis?
    differentiation of immature lymphoid stem cell into mature lymphocytes
  50. Why might an adult have extramedullary hematopoiesis?
    long-term chronic anemia overworks the bone marrow and it cannot meet demands of the body so spleen and liver start performing hematopoiesis
  51. Lymphocytes differentiate into ____ & _____.
    b cells and t cells
  52. Erythropoiesis?
    RBC production
  53. What controls erythropoiesis?
    amnt of HgB in the blood
  54. Why does HgB level affect erythropoiesis?
    decreased O2 transport stimulates increased RBC production
  55. What stimulates the release of erythropoietin?
    renal hypoxia
  56. Renal hypoxia -> release of erythropoieting ->_____.
    RBC production is stimulated
  57. hemolysis?
    RBC destruction
  58. Where does hemolysis occur?
    spleen and liver
  59. Broken down RBC's ae removed from the circulation by _____.
    the spleen
  60. When hemolysis occurs what happens to HgB?
    • 1. broken down to heme and globin
    • 2. heme is converted to bilirubin -> transported to liver by serum globulin and albumin -> liver excretes bilirubin into intestine as part of bile -> bacteria in intestine convert bilirubin to urobiligen ->excreted in feces and some in urine
  61. 2 parts of HgB?
    heme and globin
  62. What is necessary for the production of HgB?
    iron
  63. 67% of body's iron is ______, 30% is bound to ____, ____, and ___ _____, and 3% is ____.
    bound to heme in RBC and muscle cells

    stored bound to ferritin, some macrophages, and hepatic cells

    lost daily in urine, sweat, and via intestines
  64. heme = _____.
    Fe
  65. Why does liver dysfunction cause jaundice?
    bilirubin (yellow - colored) builds up in the body b/c it is normally excreted into the intestines by the liver as part of bile
  66. What is O2 sat a reflection of?
    % of HgB that is saturated with oxygen
  67. Normal Hct in men and women?
    men - 45%

    women - 42%
  68. Normal relationship of Hct to HgB?
    Hct usually HcT usually 3X that of HgB
  69. Normal HgB?
    15
  70. If a pt has a severely depleted H&H with O2 sat of 100% are they OK?

    What would be a more accurate reflection?
    no, because they don't have much HgB so even if all of it is saturated with O2 they don't have enough O2 either way

    PaO2 - amount of O2 in the blood (on ABG)
  71. Anemia?
    defecit of RBC's that is not a disease but a manifestation of a pathologic process
  72. Pt with decreased RBC has decreased _______ and can have ______ and tissue ______.
    O2-carrying ability

    hypoxemia, and hypoxia
  73. 3 reasons for anemia?
    • 1. decreased RBC production
    • 2. blood loss
    • 3. increased RBC desruction
  74. Main concern with a pt with anemia?
    decreased O2 carrying capacity of blood
  75. Manifestations of anemia stem from _____ and include _____.
    decreased O2 carrying capacity of the blood

    mech to compensate for tissue hypoxia
  76. First manifestations of anemia?
    fatigue, weakness
  77. Second S/S of anemia?
    due to compensation - tachycardia, DOE, pallor, vasoconstriction, shunting of blood flow to vital organs (AWAY from skin and kidneys)
  78. S/S of severe anemia?
    chest pain, fainting, and possible heart murmur
  79. Why chest pain with severe anemia?
    infarction of heart tissue due to hypoxia from anemia
  80. Major complication of severe anemia?
    MI due to hypoxia
  81. Why have a heart murmur with anemia?
    severe anemia - tachycardia and increased CO due to compensation causes murmur
  82. Iron deficiency anemia?
    lack of iron necessary for HgB synthesis
  83. 2 main causes of iron deficiency anemia in men and women?
    • men - GI bleed
    •  
    • women - menorrhagia
  84. 2 causes of Fe deficiency anemia?
    decreased intake or absorption by the duodenum or loss via hemorrhage
  85. Labs for iron de
    decreased H&H, RBC, serum Fe,

    RBC are small and pale

    MCV, MCH, MCHC are decreased
  86. RBC indices?
    part of CBC with differential

    description of size, weight, and width of the RBC
  87. S/S of iron deficiency anemia?
    • 1. most assymptomatic
    • 2. may display general s/s of anemia
    • 3. classic clinical manifestations:  glossitis (smooth red tongue), chelitis (dry, cracked lips), PICA
  88. glossitis?
    smooth, red tongue
  89. Chelitis?
    dry, cracked lips
  90. Treatments of iron deficiency anemia?
    • 1. treat underlying causes
    • 2. iron replacement (ferrous SO3 PO, IV replacemtn for severe cases)
    • 3. dialysis pt should have optimal serum iron and ferritin levels
  91. Why do dialysis pt need good Fe and ferritin levels?
    give dialysis pt procrit (synthetic erythropoiten) - if there is no Fe or ferritin to carry Fe then RBC will be produced but they will not contain HgB
  92. Ferritin?
    itracellular protein that stores and transports Fe in the body
  93. Thalassemia major?
    genetic disorder most prevalent among Asians and ethnic groups near Mediterranean sea that causes anemia
  94. Patho of thalassemia major?
    insufficient production of normal HgB due to inherited problem with either the alpha or beta globin protein fraction - mutant gene replaces normal fraction -> the non-effected globin protein is over-produced and the RBC are oddly shaped and prone to hemolysis
  95. labs with thalassemia major?
    • 1. very low HgB
    • 2. MCV, MCH, MCHC are all decreased - RBC are small and pale due to lack of HgB
  96. Thalassemia minor?
    carrier only
  97. S/S of thalassemia major?
    • 1. S/S of anemia
    • 2. splenomegaly - r/t excessive filtering of deformed RBC's
    • 3. hepatomegaly - r/t Fe overload
    • 4. down's syndrome appearance
    • 5. bone deformities due to overworked bone marrow - bone marrow will overgrow
  98. Tx of thalassemia major?
    • 1. blood tranfusions to maintain accetable H&H in children
    • 2. bone marrow transplantation
    • 3. chelation/vitamin C for Fe overload
  99. Chelation?
    therapy to remove heavy metals from the blood
  100. Why is it necessary to maintain acceptable blood levels with blood transfusions in thalassemia?
    RBC are being destroyed
  101. Why does Fe build up in thalassemia major?
    RBC destruction releases iron and causes overload
  102. Only way to cure thalassemia?
    bone marrow transplantation
  103. Who does thalassemia major present in most?
    children
  104. Why is it necessary to ONLY get blood levels to acceptable levels?
    will stifle their body's own RBC production if get levels too high
  105. Aplastic anemia?
    genetic stem cell disorder that causes all blood cell types to be decreased
  106. 2 causes of aplastic anemia?
    congenital or acquired
  107. 4 possible causes of acquired aplastic anemia?

    EX 2 drugs that can cause it?
    radiation, toxins, drugs, and infection

    tegretol/carbamazepine and anti-neoplastics
  108. Labs in aplastic anemia?
    pancytopenia on CBC
  109. S/S of aplastic anemia?
    • 1. general S/S of anemia
    • 2. bacterial infections
    • 3. signs of bleeding:  epistaxis, increased bruising, increased menstrual flow, retinal hemorrhage)
  110. 2 major concerns in aplastic anemia?
    • prone to infection
    • prone to bleeding

    r/t reduced WBC and platelets
  111. 6 Tx for aplastic anemia
    • 1. Tx the underlying cause
    • 2. prevention and management of infection
    • 3. immunosuppresive therapy if caused by autoimmune disorder
    • 4. maintain acceptable levels of HgB and platelets
    • 5. bone marrow transplatation with umuunosuppresive therapy is curative
    • 6. vit B12 or folate deficiency
  112. Tx for prevention and management of infection in aplastic anemics?
    neupogen
  113. ______ medications can cause aplastic anemia?
    anti-convulsants
  114. What is the result of anemia caused by deficiencies in folate and B12?
    disrution of DNA synthesis of blast cells of the bone marrow -> funky shaped RBC's
  115. 3 causes of folate and B12 deficiencies?
    • 1. dietary deficiency
    • 2. lack of intrinsic factor produced by parietal cells of the stomach (gastrectomy)
    • 3. possibly a genetic, autoimmune disease causing antibodies against intrinsic factor
  116. Functions of B12?
    mylenation and DNA synth of blast cells in bone marrow
  117. What is necessary for B12 absorption?
    intrinsic factor
  118. Pernicious anemia?
    classic B12 deficiency anemia caused by lack of intrinsic factor
  119. Labs in pernicious anemia?
    • 1. large RBC
    • 2. decreased H&H
    • 3. decreased serum cobalamin/B12
  120. 2 diagnostic tests for pernicious anemia?
    1. + Schilling test - indicates low levels of excretion of radioactive vit B12

    2. gastric acid analysis - may be negative for HCL acid
  121. Why is gastric acid low in pt with pernicious anemia?
    because parietal cells that produce intrinsic factor also produce HCL acid
  122. Problem that occur in gastric bypass?
    low levels of intrinsic factor = pernicious anemia
  123. 2 Tx gastric bypass ppl have to do for life
    intrinsic factor replacement and B12 supplements
  124. Schilling test?
    diagnostic test for pernicious anemia IM injection of B12 and oral B12 that is radioactive then test urine for B12
  125. S/S of pernicious anemia?
    • 1. general S/S of anemia
    • 2. neuromuscular S/S:  weakness, parethesias, reduced position sense, impaired thought processes
  126. Why are there neuromuscular S/S with pernicious anemia?
    B12 is involved in nerve myelination
  127. Tx of pernicious anemia?
    • 1. IM B12 injections + oral folate until cause is ID'd
    • 2. blood transfusions may be necessary for elderly pt
    • 3. manage possible hypokalemia associated with early B12 therapy
  128. 2 effects of deficient B12?
    anemia and neuromuscular effects
  129. Major concern when pt is taking B12 supplements?
    hypokalemia
  130. Sickle cell anemia?
    autosomal recessive genetic disorder with abnormal form of HgB produced - HgB S
  131. What occurs in sickle cell anemia?
    RBC become deformed and crescent shaped when O2 levels are low
  132. Approx. _____ African Americans are carriers of sickle cell anemia.
    1 in 10
  133. Prognosis for sickle cell anemia?
    incurable - often fatal by middle age form renal and pulmonary failure
  134. Labs with sickle cell anemia?
    • 1. severe anemia
    • 2. sickled cells on blood smears
    • 3. increased serum bilirubin due to high rates of RBC hemolysis
  135. S/S of sickle cell anemia are all r/t what?

    Results of this?
    all r/t sickled shape of HgB

    sickled cells cannot pass through blood vessels and may get stuck and occlude vessels causing thrombosis and/or sickled cells are damaged by running into vessel walls which causes increased RBC hemolysis in spleen and causes severe anemia
  136. Sickle cell crisis?
    mass sickling of RBC
  137. 2 S/S of sickle cell crisis?
    • 1. vaso-occlusion anywhere
    • 2. severe pain
  138. 7 factors that can cause sickle cell crisis?
    • 1. hypoxia of RBC
    • 2. lung infection
    • 3. dehydration (cells clog vessels more)
    • 4. high altitudes
    • 5. emotional/physical stress
    • 6. surgery & blood loss
    • 7. extreme cold
  139. S/S of sickle cell anemia?

    mainly s/s are caused by what?
    • S/S mainly caused by clots due to clogging of vessels:
    • 1. retinopathy
    • 2. cardiomegaly -> congestive heart failure
    • 3. renal infarcts -> hematuria
    • 4. bone marrow hyperplasia
    • 5. aseptic bone necrosis -> osteomyelitis
    • 6. CVA -> mental retardation
    • 7. pulmonary embolism -> pneumonia
    • 8. splenomegaly -> splenic atrophy
    • 9. infarcts of extremities
    • 10. vaso-occlusion
    • 11. ulcers (on legs)
    • 12. severe pain
  140. Tx of sickle cell anemia?
    • 1. oxygen
    • 2. pain meds
    • 3. bed rest
    • 4. IV fluids
    • 5. blood transfusion if needed
    • 6. bone marrow transplant
    • 7. teaching
  141. Why is pain a big priority with sickle cell anemia?
    pain is severe and can cause stress that increase crisis
  142. Teaching for sickle cell anemia?
    • 1. avoid high altitudes
    • 2. adequate fluid intake
    • 3. prevent/treat infections:  vaccines important
  143. ASA and tylenol is sickle cell anemia?
    avoid ASA - salicylic acid - acidity can lead to crisis

    tylenol can increase liver probs that can occur in sickle cell
  144. Acquired hemolytic anemia?
    caused by abnormal breakdown of RBC due to physical trauma, immune disorders, or infections/toxins
  145. 4 EX of physical traumas that could cause acquired hemolytic anemia?
    hemodialysis, CPB, prosthetic heart valves, burns
  146. 3 EX of infections/toxins that can cause acquired hemolytic anemia?
    malaria, arsenic or lead poisoning, snake venom
  147. Anemia of acute blood loss?
    present after major trauma or secondarty to a disease process such as a GI bleed
  148. Effect of anemia of acute blood loss?
    rapidly decreases overall blood volume
  149. Anemia caused during cardiac bypass surgery?
    heart and lung machine used during cardiac bypass surgery that pumps blood through the machine and acts as artificial heart - can destroy RBC
  150. Clinical manifestations of anemia of acute blood loss?
    • 1. 10% loss - asymptomatic
    • 2. tachycardia/hypotension with exercise, cold/clammy skin at rest
    • 3. 50% loss - shock and death
  151. Tx for anemia of acute blood loss?
    • 1. Stop blood loss
    • 2. replace lost volumes:  IV fluids (crystalloids and colloids) - usually NS initially
    • 3. replace blood volume with blood transfusions
  152. Polycythemia?
    too many RBC
  153. Polycythemia results?
    blood circulation may be impaired by hypervolemia and hyperviscosity of blood
  154. 2 types of polycythemia?
    primary - polycythmia vera

    secondary polycythemia
  155. Polycythemia vera cause?
    caused by chromosomal mutation of a single stem cell into an abnormal cell which multiples at very high rates
  156. When does polycythemia vera start?
    aroung age 60
  157. Development of polycythemia vera?
    dev slowly and follows a chronic course
  158. Labs in polycythemia?
    increased RBC, WBC, and platelets

    O2 sat is normal
  159. Secondary polycythemia cause?
    hypoxia due to an outside process
  160. Some conditions that can cause secondary polycythemia?
    COPD, anything that causes chronic hypoxia
  161. Why does hypoxia cause polycythemia?
    not enough O2 will increase RBC production
  162. Labs in secondary polycythemia?
    increased RBC, O2 sat will be reduced
  163. Clinical manifestations and potential complications of polycythemia?
    • 1. CVA due to thrombosis
    • 2. thomboses
    • 3. hypertension
    • 4. angina/CHF
    • 5. pronounced pruritis
    • 6. hemorrhage r/t destruction of vessels due to excess blood volume
    • 7. hepatomagaly and splenomegaly
  164. Most serious complication of polycythemia?
    CVA due to thrombosis
  165. Tx for polycythemia?
    • phlebotomy to keep Hct at around 48%
    • 2. hydration
    • 3. ROM to prevent clots
    • 4. possibly myelosuppresive therapy to suppress bone marrow
  166. Hemostais?
    arrest of bleeding/ prevention of blood loss
  167. How is hemostasis achieved/dysfunctional?
    acheived through interactions between vessel wall, platelets, and plasma coagulation proteins

    if any of the 3 are dysfunctional will alter hemostasis
  168. Labs for coagulation disorders?

    What will occur is the pt has thinner blood/ blood that is not clotting normally?
    • 1. PT- prothrombin time
    • 2. INR - international normalized ratio
    • 3. aPTT - activated partial thromboplastin time

    increases in these values mean "thinner" blood that will take longer to clot than normal
  169. PT?

    PT normal?

    Drug?
    prothrombin time

    10-14 seconds

    coumadin
  170. INR?

    INR normal?

    Drug?
    international normalized ratio

    0.8 -1.2

    coumadin
  171. aPTT?

    aPTT normal?

    Drugs?
    activated partial thromboplastin time

    35-45 seconds

    heparin and lovenox
  172. What would you expect the aPTT to look like for a person on heparin?
    should be higher than normal

    therapeutic - 55 to 75
  173. What should be monitored if pt is taking the drugs heparin and lovenox?
    aPTT
  174. What should be monitored in pt taking coumadin?
    PT & INR
  175. 3 drugs where increased clotting time/ thinness of blood is expected and desired?
    coumadin, lovenox, and heparin
  176. Thrombocytopenia?
    platelet count < 100,000
  177. #1 reason ppl are on coumadin?
    atrial fibrilation
  178. S/S of thrombocytopenia?
    no S/S until gets < 50,000

    < 50,000 - increased bruising/prolonged bleeding after minor trauma

    <20,000 spontaneous hemorrhage
  179. HITS?
    heparin induced thrombocytopenia
  180. 4 causes of thrombocytopenia?
    1. idiopathic thrombocytopenic purpura - immune mediated thrombocytopenia

    2. drugs - heparin (allergic reaction), digoxin, thiazide diuretics, dilantin, tegretol

    3. alcohol intake

    4. radiation/chemotherapy
  181. Why does everyone put on heparin have to have a baseline CBC?
    have to have baseline platelet level to monitor for HITS - will be cut in half after admin of heparin
  182. EX of a drug that can cause thrombocytopenia?
    lopressor
  183. S/S of thrombocytopenia?
    • 1. bleeding most common - epistaxis
    • 2. petechia, purpura, ecchymosis
    • 3. bleeding into joints, retina, brain
    • 4. s/s of internal bleeding
  184. Contraindication if a pt is on heparin or has severely low platelet levels?
    IM injections will cause bleeding
  185. Petechiae?
    flat, pinpoint, non-blanching red or purple spots caused by capillary hemorrhages in the skin and MM's
  186. Purpura?
    petechiae that occur in groups or patches
  187. Ecchymosis?
    bruise
  188. Hematoma?
    raised bruise
  189. Thrombocytosis?
    platelet count >400,000 that is usually a secondary response to hemorrhage, inflammatory disease, trauma, malignancy, infection, hemolysis (anything that causes bleeding and increases platelet production)
  190. Meds that can cause thrombocytosis?
    estrogen/oral contraceptives
  191. Tx for thrombocytosis?
    treat with antiplatelet drugs
  192. Antiplatelet drugs?


    How do they work?
    ASA, plavix, hydroxyurea, agrylin

    ASA and plavix prevent platelet aggregation

    agrylin inhibits maturation of platelets
  193. What is aspirin used for in the hospital?

    Not used for?
    used as anticoagulant med

    not for pain or fever
  194. Hemophilia and von willebrand disease?
    inherited disorders of coagulation where pt is lacking a clotting factor
  195. What clotting factors are deficient in hemophilia A, hemophilia B, and von willebrand disease?
    hemophilia A - Facor VIII and fibrinogen

    hemophilia B - Factor IX and fibrinogen

    vwd - deficiency of von Willebrand coagulation protein
  196. Clinical manifestations of hemophilia A&B and von Willbrand disease?
    • 1. prolonged bleeding from even minor injuries
    • 2. uncontrolled bleeding after dental procedures
    • 3. hematuria
    • 4. GI bleeding
    • 5. ecchymoses and hematomas
    • 6. hemarthrosis
    • 7. hemophilia and von willebrand disease
  197. Hemarthrosis?

    Where does it occur most?
    bleeding into joints causes pain and possible deformitiy

    mostly in knees, ankles, elbows, shoulders, and hips
  198. Tx/prevention of hemophilia A&B and von Willebrand disease?
    • 1. replacement of deficient clotting factor with FFP
    • 2. avoidance of aspirin
    • 3. joint bleeding controlled with immobilization and ice
    • 4. prophylaxis before dental procedures
    • 5. DDAVP (desmopressin)
  199. DDAVP?

    What does it do?
    desmopressin

    stim release of clotting factors from endothelial cells
  200. How is coumadin toxicity treated?
    FFP
  201. FFP?
    fresh frozen plasma
  202. DIC?
    disseminated intravascular coagulation  - life-threatening syndrome in which clotting and bleeding occur simultaneously
  203. 2 triggers of DIC?
    1. anything that causes damage to vascular wall and initiates the inflammatory response

    2. clotting response is initiated by presence of pro-coagulation substances in the blood or stagnant blood flow
  204. Patho of DIC?
    coagulation cascade is initiated by inflammatory response or presence of pro-coagulation substances in blood or stagnant blood flow -> accelerated clotting is initiated -> clotting factors are depleted and the fibrinolytic system is over-activated to break down the clots -> bleeding
  205. #1 cause of DIC?
    sepsis
  206. 2 EX of things that cause DIC through inflammation?
    sepsis, burns
  207. 3 things that can cause DIC through pro-coagulation substances?
    snake venom, malignancy, incompatible blood tranfusion
  208. EX of a condition that causes DIC through stagnant blood flow?
    shock
  209. 6 potential causes of DIC?
    sepsis, burns, snake venom, milignancy, incompatile blood transfusion, shock
  210. What is the ultimate result of DIC?
    massive hemorrhage
  211. Clinical manifestations of DIC?
    clotting and bleeding issues

    • 1. clot to any organ:  MI, kidneys and lungs are mainly affected
    • 2. hemorrhagic:  bleeding may occur from various sources:  petechiae, bruising, internal bleeding
  212. How would the nurse recognize if DIC has caused renal failure?
    Hct, daily weights, I&O, BUN
  213. How would the nurse recognize if DIC has caused pulmonary infarct?
    • 1. dyspnea
    • 2. decreased O2 sat
    • 3. anxiety
  214. Labs for DIC?
    + D dimer and elevated anti-thrombin complex

    1 of them positive does not indicate DIC but if both are postivie it is indicitive of DIC
  215. D-dimer?
    specifically measures excessive fibrinolysis
  216. anti-thrombin complex
    small protein that inactivates several enzymes of the coagulation system
  217. Tx of DIC?
    • 1. removal of underlying cause and support of major organs
    • 2. replacement of depleted clotting factors
    • 3. anti-fibrinolytics for life=threatening hemorrhage
    • 4. controversial - begin heparin drip on at risk pt to prevent clots from ever forming
  218. How are clotting factors replaced for DIC?
    FFP, PRBC's
  219. Amicar?
    anti-fibrinolytic that is used in DIC to treat life-threatening hemorrhage

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