1. Home
  2. Flashcards
  3. Preview

Heme

The flashcards below were created by user ariadne9 on FreezingBlue Flashcards.

  1. Where do all blood cell types originate from?
    pluripotent hematopoietic stem cells
  2. When would you tend to see a high number of reticulocytes?  What does this mean?
    • In an anemic pt.
    • The immature cells are coming out of the BM earlier than normal as a compensatory mechanism.
  3. What is the most important regulator of RBC production?
    Tissue oxygenation.  RBC function is to carry O2 attached to Hgb.
  4. Normal RBC value for men.
    • 4.7 - 6.1 million cells / microliter
    • Avg= 5.2 million
  5. Normal RBC value for women.
    • 4.2 - 5.4 million cells / microliter
    • Avg= 4.7 million
  6. What is MCV?
    mean corpuscular volume, aka avg RBC size
  7. What is MCH?
    mean corpuscular Hgb, avg amount (mass) of Hgb in a RBC
  8. What is MCHC?
    mean corpuscular Hgb concentration
  9. Microcytic anemia
    reduced MCV
  10. Macrocytic anemia
    Increased MCV (often from nutritional anemias from B12 and folate deficiency)
  11. Hypochromic anemia
    characterized by decreased MCH
  12. In low O2 states, ______ will stimulate the production of RBCs.
    Erythropoietin
  13. Where is erythropoietin made (2 sites)
    • 90% in the kidney
    • 10% in the liver
  14. T or F, in kidney failure the liver can compensate to produce enough erythropoietin for adequate RBC production?
    F
  15. What substances will stimulate erythropoietin  production?
    NE, epi, and prostaglandins
  16. Glycoprotein hormone
    stimulates erythropoietin production in the kidney
  17. Anemia
    Decreased O2 carrying capacity from any cause
  18. Do RBCs have a nucleus?
    NO!
  19. Avg RBC lifespan?
    120 days
  20. Carbonic anhydrase
    RBCs carry a large amount of this enzyme.  It catalyzes the reaction of CO2 and water to form carbonic acid.  This allows the blood to carry large amounts of CO2 in the form of bicarb ion from the tissues to the lungs.  Then it gets converted back to CO2 and is exhaled.
  21. Major buffer found in whole blood?
    RBCs, Hbg is a protein, and like other proteins, is a really good buffer.
  22. Avg H+H for a male
    45 / 15
  23. Each gram of Hgb can carry about ____ ml of O2.
    1.34
  24. An individual can carry about ___ ml of O2 per 100 ml of _____.
    20, blood
  25. G6PD deficiency
    • Glucose-6-phosphate dehydrogenase is an enzyme in the glycolytic pathway.  
    • A deficiency in G6PD will disrupt the glycolytic pathway that's needed for RBC metabolism.  
    • Hemolytic anemia results (G6PD is needed for the stability of the RBC, so without it, RBCs have decreased life span).  
    • Genetically transmitted.
  26. Hct
    fractional volume of RBC mass
  27. Major blood components
    • RBCs- 45%
    • "Buffy coat"- WBCs and Plts- 1%
    • Plasma- 54%
  28. Hct= ____ x 3
    Hgb
  29. stimulation to produce erythropoietin
    hypoxia
  30. Optimal erythropoiesis occurs when there is sufficient ____, _____, and ____.
    B12, iron, and folate.
  31. T or F, SCD is AD?
    F, AR
  32. SCD involves substitution of ____ for ____ in the beta globulin subunit, making it Hgb S.
    valine, glutamic acid
  33. What type of anemia is SCD?
    hemolytic
  34. What factors will cause Hgb S to sickle?
    hypoxia (PO2< 40 mmHg), acidosis, dehydration, hypothermia
  35. What issues are r/t sickling of cells?
    • Cells get stiff clog vessels, organ infarction can occur
    • Blood sequestration in the liver and spleen
  36. Is SCD usually the homo or heterozygous form?
    homozygous
  37. Sickle cell trait
    • Heterozygous form
    • Have 1 Hgb A (normal) and 1 Hgb S (SCD)
    • Carrier of SCD 
    • Rare clinical manifestations
  38. SCD
    -Onset?
    -Type of anemia?
    -Associated issues?
    • Early in life
    • Severe hemolytic
    • Vaso occlusive disease involving the bone marrow, liver, spleen, kidneys, and CNS
  39. Most common cause of M+M in SCD?
    Pulm and neuro complications
  40. How does SCD affect the oxyHgb dissociation curve?
    • Right shifted, O2 is given up more easily to the tissues.
    • Normal P50 = 27, in SCD it's 31 mmHg
  41. P50
    PO2 at which the Hgb is 50% saturated
  42. What surgeries are considered low risk for SCD pts?
    Inguinal hernia repair, extremity surgeries (except hips)
  43. What surgeries are considered moderate risk for SCD pts?
    chole, abd surg
  44. What surgeries are considered high risk for SCD pts?
    • intracranial or intrathoracic
    • hip surgery
  45. What are peri-op risk factors for SCD pts?
    • age
    • frequency of hospitalizations or transfusions
    • prior organ damage
    • concurrent infections
  46. T or F, heterozygous SCD is associated with increased peri-op M+M?
    F, homozygous SCD is associated with increased peri-op M+M
  47. Goal pre-op Hct for SCD pts
    30%
  48. What should be avoided intra-op with SCD pts?
    • Dehydration (1.5 x maint fluid req. for 12h)
    • Acidosis
    • Hypothermia
    • Hypoxemia (minimize pre-op sedation, full reversal at case end, supplemental O2 x 12-18h)
    • Hypotension and low flow situations
  49. Acute chest syndrome
    • May develop post-op in pts with SCD
    • Need aggressive oxygenation, analgesia, and blood transfusions
  50. Why should N20 be avoided in pts with megaloblastic anemias
    N20 inhibits methianone synthetase and may worsen the anemia (further impairs B12 activity)
  51. Macrocytic anemias
    • Due to folate (alcoholism) or vit B12 deficiency
    • Deficiency causes BM to be affected
    • RBC precursors in the BM become large and can't complete cell division
    • These large RBCs are released into the circulation
    • Possible neuro issues (peripheral neuropathy, gait disturbances, bilateral paresthesias)
    • Tx= replacement of vitamins parenterally
  52. Microcytic anemia
    • Due to iron deficiency
    • Small RBCs
    • Tx= iron replacement
  53. Thalassemia
    • Inherited defect in globin chain synthesis
    • Type of microcytic anemia
    • Beta form common in Africa and the Mediterranean
    • Alpha form common in SE Asia
  54. Types of thalassemia
    • minor- Hgb 10-14
    • intermedia
    • major- severe and life threatening anemia during the 1st few months of life, require LT transfusion therapy
  55. Anesthesia considerations for thalassemia minor
    Chronic compensated anemia, therefore no big considerations.
  56. Anesthesia considerations for thalassemia major
    Pts may have splenomegaly, hepatomegaly, CHF, R sided HF, cirrhosis, or various encrinopathies
  57. Methehemoglobinemia
    • Decreased O2 affinity, left shifted oxyHgb dissociation curve
    • Little O2 delivery to the tissues
    • MetheHgb formed when Fe2+ is oxidized to Fe3+
    • Due to mutations or certain drugs
  58. Normal amt of methehemoglobin
    1%
  59. Methehemoglobin concentration < 30% of total Hgb
    No compromise in oxygenation
  60. Methehemoglobin concentration 30-50% of total Hgb
    Pts start to show signs of decreased oxygenation
  61. Methehemoglobin concentration > 50% of total Hgb
    Coma and death may result
  62. Methehemoglobinemia treatment
    • Methylene blue 1-2 mg / kg IV as 1% solution over 3-5 minutes
    • Requires G6PD to be effective
  63. RBC hypoproliferation
    -what is it?
    -causes?
    • decreased RBC production
    • causes can include- aplastic anemia due Fanconi's syndrome or drug or radiation induced
  64. Aplastic anemia
    decreased production of all blood cell types
  65. Fanconi's anemia
    • type of aplastic anemia
    • AR
    • exhibits as pancytopenia
  66. Chemo drugs and radiation can produce BM damage associated anemia- is this reversible?
    Yes, in most cases
  67. T or F, infectious diseases such as Epstein Barr, HIV, TB, and viral hepatitis can cause BM damage leading to aplastic anemia?
    T, usually reversible however
  68. Polycythemia
    • erythrocytosis or elevated Hct or RBC count
    • may be a compensatory response to prolonged hypoxia
  69. Tissue oxygenation is optimal at a Hgb of ____g/dl
    11-12
  70. Why is O2 delivery decreased in polycythemia?
    Blood viscosity increases, flow decreases, and hence less O2 is delivered to the tissues
  71. At what Hct do effects of polycythemia begin to be seen?  What s/sx?
    • Hct > 50%
    • Decreased blood flow to brain and other key organs, may see easy fatigability 
  72. At what Hct is polycythemia life threatening?
    • Hct > 60%
    • Brain is particularly susceptible to decreased perfusion
    • Risk arterial and venous thrombosis
  73. What's the difference between primary and secondary polycythemia?
    • Primary- due to a stem cell d/o
    • Secondary- due to physiologic response to hypoxia, chronic exposure to high altitude, or increased erythropoietin (tumor)
  74. T or F, its with polycythemia vera are at increased risk of both thrombosis and hemorrhage peri-op?
    T, increased risk for peri-op hemorrhage due to acquired vWD
  75. Polycythemia anesthesia considerations
    • Pre-op phlebotomy
    • O2 therapy
    • Increased risk for both thrombosis and bleeding
  76. What WBC subtype makes up the majority of WBCs
    • neutrophils (PMNs- polymorphonuclear neutrophils)
    • 60%
  77. What are band cells?  Normal % of WBCs?
    • Immature neutrophils
    • 0-3%
  78. When might an increase in band cells be seen?  What is this called?
    • With infection, BM putting out younger (immature) neutrophils to try to fight off infection
    • Left shift
  79. When might an increase in eosinophils be seen?  Normal % of WBC count?
    • Allergies or parasitic infections
    • 1-4 %
  80. WBC subtype making up the smallest %?
    • Basophils
    • 0.5-1%
  81. WBC normal count
    5-10K
  82. Leukemia
    uncontrolled WBC production
  83. Common issues associated with leukemia
    • Bleeding
    • Infection
    • Anemia
    • Fatigue (cancerous cells using all the nutrients and energy)
    • All due to non functional leukemic cells displacing the BM (so functional cells can't be made)
  84. What are the 2 subtypes of leukemia?
    • Lymphogenous (generated in lymph tissues or nodes)
    • Myelogenous (generated in the BM)
  85. Leukemia treatment
    Chemo - bleomycin and doxyrubicin

    BM transplant
  86. General SE of chemo drugs
    • Susceptibility to infection or bleeding due to BM suppression
    • Tumor destruction increases uric acid load so arthritis and nephropathies can develop
  87. Doxyrubicin SE
    cardiotoxic, even up to 5 years later
  88. Bleomycin
    • Pulm toxic, causes pulm fibrosis
    • PF worsens with increased concentrations of O2, so keep FiO2 < 30%
  89. Vinca alkaloids SE
    • chemo agents
    • ex: vinchristine, vinblastine
    • SIADH or peripheral neuropathy
    • paresthesias of the hand
  90. Time to engraphment with BM transplant
    • Time for new cells to take hold in the BM
    • 10-28 days, pt must be in isolation during this time
  91. Anesthesia considerations for pts with leukemia
    • Coagulopathies
    • Volume status- N/V
    • Use of chemo agents that could have SE (cardiac or pulm)
  92. AIDS
    • viral infection kills helper T cells
    • HIV belongs to a retrovirus family
  93. As AIDS occurs, a _____ in the CD4 T cells is seen and a ____ in the viral load, because the virus uses those cells (CD 4 T cells) to gain entry into the T cells.
    decrease, increase
  94. What CD 4 T cell count is associated with an increased M+M?
    < 200 cells / ml
  95. T or F, up to 90% of pts with HIV have an abnormal cardiac echo and pericardial effusion?
    • F, 50% have abn echo
    • 25% have pericardial effusions
  96. Pneumocystis carinii (PCP)
    • PNA associated with HIV
    • Occurs when CD 4 count < 200 cells / ml
  97. SE of PCP
    • Night sweats
    • Wt loss
    • SOB
  98. HAART
    • Highly active anti-retroviral therapy
    • 3 agents
    • goal is to have undetectable viral load by 24 weeks
  99. In what bodily fluids can HIV be found?
    Tears, saliva, blood, semen, vaginal secretions, CSF, urine, breast milk
  100. How long can HIV live for outside of the host?
    7-10 days
  101. Is immunosuppression from GA of concern to a pt with HIV?
    • Yes
    • Immunosuppression occurs within 15 mins of induction and may persist for as long as 3-11 days.  
  102. T or F, autonomic neuropathy may be associated with HIV?
    T
  103. Why should succ be avoided in HIV pts?
    HIV pts may have myopathy or peripheral neuropathy making succ dangerous
  104. Following a hollow needle stick with high risk fluid, how soon should post-exposure prophylaxis be started?
    • Within 1-2 hours, but can be as long as 1-2 weeks after.  
    • You can treat beyond this time frame, but in this case you are limiting the severity, not preventing infection.  
  105. What causes VC of the vessel to occur?
    BV injury that causes disruption of the normal endothelial lining
  106. What events occur to cause VC of a BV
    • 1) Disruption of the endothelial lining of the BV causes endothelin (VC) to be released
    • 2) There is also a myogenic spasm (local)
    • 3) Thromboxane A-2 (VC) is released from Plts
  107. What is the primary goal of primary hemostasis
    Plt plug formation
  108. Plt half life
    8-12 days
  109. Plts are fragments of _____ and have no nucleus.
    megakaryocytes
  110. What role do glycoproteins play in Plt action?
    • Glycoproteins activate the Plts and cause them to stick onto the exposed endothelial surface when there's a BV breach
    • Also prevent Plts from sticking to normal endothelial cells
  111. ____ of Plts are sequestered in the spleen
    1/3
  112. What 3 factors are needed for formation of a Plt plug (hint- A)?
    • Adhesion
    • Activation
    • Aggregation
  113. What are some characteristics of Plts that enable them to form clots?
    • Contractile proteins (actin & myosin filaments, thrombosthenin)
    • Calcium stores (golgi)
    • Mitochondria (ATP)
  114. What 2 molecular interactions cause Plts to adhere to the sub-endothelium (collagen)?
    • 1) GP1b and VWF (VWF is secreted by activated Plts and injured sub-endothelium)
    • 2) GPVI

    both attach to collagen
  115. What happens during Plt activation?
    • granules are released
    • Plts change their shape and get contractile and form pseudopods
  116. In what 2 ways can Plt activation occur?
    • 1) exposure of sub endothelial collagen
    • 2) Tissue factor (called thromboplastin in clotting cascade)
  117. T or F, the membranes of the activated Plts are really important to a number of critical reactions in the clotting cascade including conversion of prothrombin to thrombin?
    T
  118. What 3 factors mediate Plt aggregation?
    • Thromboxane A2
    • ADP
    • Collagen
  119. What receptors are essential to Plt aggregation?
    • ADP (P2Y1 and P2Y)
    • GP2b3a
  120. What drugs inhibit the GP2b3a receptor?
    Integrillin, reopro, aggrastat
  121. What receptor do the anti-Plt drugs plavix, prasugrel, and ticlopidine affect?
    P2Y ADP receptor
  122. Essential pieces to the coagulation mechanism
    • Prothrombin activator causes prothrombin to be converted to thrombin (need Ca++)
    • Presence of thrombin (an enzyme) causes fibrinogen to convert to fibrin
    • Thrombin causes activation of fibrin stabilizing factor, cross linked fibrin fibers are formed
  123. What is the rate limiting step in the coagulation process?
    • Formation of prothrombin activator
    • Formed in response to a damaged BV
  124. Where is fibrin stabilizing factor released from?
    Plts
  125. What is the significance of fibrin stabilizing factor?
    • Without FSF the fibrin fibers are held loosely together by H+ bonds
    • With FSF the fibrin fibers are held more tightly b/c the H+ bonds become covalent bonds
  126. After how long does clot retraction occur?
    20-60 mins
  127. What is needed for clot retraction to occur?
    Adequate Plts
  128. What does clot retraction do?
    • Serum is expressed from the clot
    • Helps to bring the sides of the vessel together to help in healing
  129. Primary hemostasis
    Secondary hemostasis
    • 1- Plt plug
    • 2- clotting cascade
  130. Factors I-IV of the clotting cascade
    • I- fibrinogen
    • II- prothrombin
    • III- tissue factor (thromboplastin)
    • IV- calcium ion
  131. What does an "a" mean after a clotting factor roman numeral?
    activated
  132. What 3 mechanisms lead to formation of prothombin activator?
    • 1) trauma to vessel wall or other tissues
    • 2) trauma to blood itself
    • 3) contact between blood and damaged endothelial cells
  133. prothombin activator purpose
    convert prothrombin to thrombin
  134. In what 2 ways can prothombin activator be formed?
    intrinsic or extrinsic pathway
  135. Major events of the extrinsic pathway
    • Tissue factor (thromboplastin) released due to vessel wall surrounding tissue trauma 
    • Factor X is activated
    • prothombin activator is formed
  136. Why is thrombin so important to the extrinsic pathway?
    Thrombin activates factor V which speeds up the process of converting prothrombin to thrombin 
  137. What is the goal of both the intrinsic and extrinsic pathways?
    Formation of prothrombin activator
  138. How is the intrinsic pathway initiated?
    • By damage to the blood
    • Contact of the blood with collagen
  139. T or F, calcium is critical to all steps of the intrinsic pathway except steps 1 and 2
    T
  140. Activation of factor ___ begins the intrinsic pathway.
    XII
  141. Trigger for extrinsic pathway to be initiated
    Tissue factor released by damaged BV
  142. How quickly can clotting occur in the extrinsic pathway?
    15 seconds
  143. How quickly can clotting occur in the intrinsic pathway?
    1-6 mins
  144. Do the extrinsic and intrinsic pathways occur simultaneously?
    Yes
  145. Hemostasis purpose
    • allow vessel to remain patent
    • restricted to the site of injury
  146. How is hemostasis achieved by the vessel?
    • Balance of pro-coag and anti-coag factors
    • Anti-coag factors are secreted by the endothelium (TPA, prostacyclin, anti-thrombin III, proteins C & S)
    • Procoag factors tend to be localized to the site of injury
  147. Thrombocytopenia
    Plt count < 150 K
  148. Does Plt count give qualitative or quantitative assessment of primary hemostasis?
    Quantitative, only tells you how many, not how well they're working
  149. Intra-op bleeding can be severe if Plt count is between ___ - ____.
    40K- 70K
  150. What tests can be used to evaluate qualitative Plt function
    • Ivy bleeding time
    • Clot retraction
  151. Does Plt aggrenometry provide qual or quant info?
    quant
  152. What info can a thromboelastogram (TEG) provide?
    Quantitative info about clot retraction
  153. What parameters does a TEG assess?
    • R- rxn time, how long it takes for a clot to begin to form (thrombin required)
    • K- clot formation time, time after R for clot to reach 20 mm width
    • Alpha angle- speed of clot formation
    • F- rate of fibrinolysis
    • MA- max amplitude, strength of fully formed clot
  154. If thrombin were decreased what might be seen on TEG?
    • Increased K 
    • Decreased alpha angle
    • Due to increased clot formation time
  155. Do aPTT, TT, ACT, and PT measure primary or secondary hemostasis
    Secondary
  156. T or F, factors must be decreased by 30% before PT or PTT is prolonged
    T
  157. PT is most sensitive to a decrease in what factor?
    What about PTT?
    • PT- 7
    • PTT- 8 & 9
  158. With heparin therapy, the ___ will be prolonged
    PTT
  159. With coumadin therapy, the ___ will be prolonged
    PT or INR
  160. What does TT (thrombin time) measure?
    Ability of thrombin to convert fibrinogen to fibrin
  161. Which is more common, hemophilia A or B?
    A
  162. Hemophelia A is a deficiency in factor ___.  
    Hemophelia B is a deficiency in factor ___.  
    • A- 8
    • B- 9
  163. What are the 2 parts to factor 8?
    Coagulant factor 8 and VWF
  164. T or F, hemophelia is sex linked and occurs mostly in males?
    T
  165. Pts with hemophilia A usually have normal amounts of ___ and decreased levels of ____.
    • VWF
    • 8C
  166. Hemophelia A tx
    • factor 8
    • -replaced to 25% if pt is bleeding
    • -replaced to 50-100% of normal for elective surgery
  167. What's the difference (clinically) in the presentation of hemophilia A and B?
    Clinically indistinguishable
  168. Infusion guidelines of factor 8c for hemophilia A pts
    • Initial infusion: 50-60U/ kg 
    • Then: 25-30U/kg q 8-12 hours
  169. Factor 8c halflife
    • 12 hours
    • (decreased to ~6 hours in peds)
  170. For each U / kg of factor 8 given, plasma factor 8 concentration increases by _____.
    2%
  171. How long is factor 8 replacement therapy continued post-op to prevent bleeding that would interfere with wound healing?
    What about with bone and joint surgery?
    • 2 weeks
    • Bone and joint: 4-6 weeks
  172. Peri-op, what should be avoided with hemophilia pts?
    • Nasal intubations
    • IM injections
    • Regional anesthesia
    • NSAIDs
Author
ariadne9
ID
251454
Card Set
Heme
Description
Heme
Updated
Show Answers

  1. Home
  2. Flashcards
  3. Preview