1. WBC count values
  2. neutrophil
    • 5d, MPO in granules, secondary granules, lactoferrin.
    • lysosomes digest bacteria
    • phagocytois
    • ECM net
  3. basophils
    • granules release hsitomine, leukotrienes, cytokines
    • allergies and active inflammation
  4. Eosinophils
    • 8-12 hrs circulation
    • parasites and allergies
    • secrete cytokines
  5. lymphocytes
    mononuclear with round nucleus. T/B/NK cells
  6. monocytes
    horseshoe shaped- inflammation, phagocytosis, Ag presentation, complment pthway...vaculoles
  7. leukocytosis
    reactive infection or neoplastic
  8. dysfunction WBC
    congenital, or neoplastic
  9. leukopenia
    decreased production, increased destruction, splenic sequestration
  10. Neutopenia- decreased production
    • aplastic anemia
    • B12/folate deficieny
    • chemicals-arsenic
    • cogenital
  11. increased destruction
    • immune-mediated
    • chemotherapy
  12. neutropenia via sequestration
  13. neutropenia
    • infection and oral manesfestations
    • normal > 2000
    • severe< 500
  14. leukocytosis
    many reasons, infections, cancer, CML, tuberculosus,lupus, malaria, ulcerative colitis
  15. leukemoid reaction
    increased wbc count
  16. lymphocytosis
    • absolute lymphocytisus>5000
    • infectious mononucleosis

    • acute and chronic infecions
    • malignancy
  17. infecious mononucleosis
    • EBV fever, malaise, rash, sore throat, spleen, liver enlarged
    • EBV infects pharyngeal spithelium. and B lymphocytes carriers shed it sporadically. virus remains latent
  18. EBV dianogisis
    atypical lympocytes in blood
  19. plasma cells
    • B-cells that are terminally differentiated. Originated in bone marrow.
    • Normally do NOT ciculate in the peripheral bld
  20. Disease of plasma cells
    MM: CRAB (calcemia, renal failure, anemia, bone lesions)

    paraproteins cause kidney problems
  21. diagnosis of MM
    • M-protein in the serum/urine
    • bone marrow plasma cells clonal
    • rouleaux formation- stacks of rbcs
  22. platelets
    • cytoplasmic blebs from megakaryocyte(from myeloid stem cell)
    • 7-10 days
    • thrombopeotin from liver and kidney
  23. platelet derivation
  24. normal platelet count
    • most common in bld
    • 150-350,000
    • one mega gives rise to 1000
  25. formation of platlet plug
    • interplay b/t platlet memrane GP, vWF,
    • Factor 8
    • platelet granules also secrete substances
  26. collagen, vWF
    binds to endothelium
  27. causes thrmbocytopenia
    • DIC, TTP, thromboic thrombocytopenic purpura,
    • immune thrombocytopenu, aplastic anemia, alcohol
  28. cause thrombocythemia
    • primary pyrloproliferatice CML, PV, ET
    • acute bld loss
    • steroids
  29. <5k platelets
    • bad risk of GI, cerebral hemmmrge
    • spntaneous bleeding
    • bleeding w surgery
  30. detect increased platlets
    • bld smear
    • bone marrow look for increased megakaryocytes
  31. risk of clot formation
    • stroke, heart, pulmonary embolism,
    • reactive ususally resolved once primary cause is removed
  32. normal count but loss of bld function
    • renal failure
    • liver disease
    • aspriin
    • prosthetic values
    • congenital
  33. primary hemostasis vs secondary hemostatsis
    • vasoconstriction of damaged vessels and temp seal by platlets
    • formation of fibrin clot
  34. what causes anemia?
    • 1. blood loss
    • 2. RBC production
    • 3. destruction of RBCs
  35. tests for anemia
    • hematocrit
    • erythocyte count

    evaluating Hb
  36. types of anemia
    normocytic, microcytic, macrolytic
  37. normo
    • loss of bld, decrease in RBC production
    • inadequte iron absorption(small and paler cells)
    • deficiency in vitamin B12, folic acid , or both
  38. symptoms of iron deficient anemia:
    • pale color, tachy, fatigue.
    • sever cases, skin and musocal changes
  39. Intraoral sign of iron deficiency
    red appearing, sore, smsooth tongue,
  40. drugs for iron deficiency
    ferrous sulfate or deferoamine(acute iron toxicity)
  41. B12 vs folic acid deficiency
    no neurologic mnesfestation in folic acid (myelin synthesis)
  42. chronic exposure to nitrous oxide leads to
    megablastic anemia by inhibiting methionine synthase
  43. what drugs cause folic acid deficiency
    phenytoin, oral contraceptives, antimalarials
  44. cure for folic acid def
  45. inhibitor of clotting factor sythesis-warfin, heparin
    antiplatlet drugs-aspirin
    thrombolytic drugs
    what are antithrombics
  46. coagulation cascade extrinsic and intrinsic pathway mmeet at
    factor 10a
  47. heparin
    administered parenterally b/c rapidly hydrolyzed in GI tract. can cause muscle hematoma
  48. indirectly acting anticoagulants
    works on vitamin K (reduction) Vitakmin K is a cofactor in the clotting cascade
  49. indirect acting coagulants most toxic effect
    hemorrage but also interacct ith antimicrobials
  50. platlet inhibitos
    • aspirain
    • dipridamole
    • clopidogrel
  51. plasminogen activators for fibrinolysis
    • t-PA...liberates plasmin from plasminogen
    • Urokinase
    • streptokinase
    • anistreplase
  52. uses of plasmnogen activators
    • acute myocardial infarction
    • pulmonary embolism
    • deep vein thrombosis
  53. anticoagulant implication for dentistry
    • aspirin therapy-stop 5 days prior to therapy
    • coumarin therapy- risk of bleeding increase exponentiatlly with INR
    • heparin therapy- defer surgery 6 hrs
  54. general toxicities of antineoplastic agents
    immunosuppression, leucopenia, alopecia, oral mucositis
  55. chemo of head and neck cancer- 5 diff mechanisms
    • alkylating
    • antimetabolite
    • antitumor
    • alkaloids
    • taxoids
  56. alkylating agents
    form alkyl radicals; interact with DNA to cause substiution.(dacarbazine, cisplatin)
  57. antimetabolites
    inhivit enzymes involved in nucleic acid synthesis(puriine/pyradine analogues 5-Fu), methtrexate

    works during S-phase
  58. antitumor antibioticcs
    Strep species, cytotoxic properties.....bind to DNA and inhibit cell division

    • actinomycin D
    • doxorubicine
    • bleomycin- DNA scission/fragment: G2, M-phase
    • mitomycin
  59. Alkaloids/antimicotubule
    arrest cell divion in metaphase via tubulin (leukemia, lymphoma)
  60. taxanes
    • disrupts microtubule network via equilibrium of free tubulin
    • paclitaxel, docetaxel
  61. combination therapy at intermittent courses
    • ex: aternating non-cross resistant regimen for advanced Hodgkins disease
    • ultimate dose requires bone marrow transplation and peripheral stem cell reinfusion
  62. oral cancer egfr inhibitors
    gleevec, iressa, tarceva(erlotinib)
  63. philadephis chromocsome
    chr 22 and chr 9 exchange; BCR and ABL gene
  64. oral complications to cancer therapy
    • ooral mucositis
    • sailvary gland dysfunction
    • neurotoxcity
    • tempormandibular dysfuntion
    • dental and skeletal grwoth
  65. response to bld vessel damage
    • vasocontriction
    • clot via platelets
  66. secondary hemostatisis
    fibrin clot
  67. platelet seal
    ADP, thromboxane A2
  68. adherence to vessel endothelium ccurs via collagen and
  69. PG2
    inhibits platelet aggregation when vessel wall is NOT damaged
  70. plavix vs aspirin
    • blocks ADP
    • inhibits thromboxane A2 synthesis
  71. soft vs hear fibrin clost
    crosslinks b/t fibrin monomers via catalyst(thrombin)
  72. fibrinogen
    is cleaved to fibrin + 2A and 2B peptides
  73. liver
    synthesizes most factors for clotting
  74. intrinsic vs extrinsic pathway
    damamged surface vs trauma converge at Factor 10a
  75. extrinsic pathway requires
    • TF which is present in fibroblast membranes.
    • recombinant 7a used to speed clotting.
  76. classes of factors
    • serine protease
    • nonprotease activaots
    • stabilizer of factor 8
    • transamidase of fibrin crosslinks
    • nonprotein factors
  77. roles of thrombin
    • 1. cleave thrombin receptor on platlets to activate
    • 2. cleave 8 ad 10 to activate 8a and 10a
    • 3. limit clot formation by cleaving va and VIIIa
  78. platelets also
    release certain grwoth factos that facillitate healing of bld vessels
  79. coagulation factos need calcium to be active
    modification that binds to callicum requires vitamkin K
  80. glutamate residues modifies to
    GLA carbosygkutmate
  81. heparain vs coumadin
    IV vs oral
  82. dissolition of clot
    tpa helps break plasmiinogen into plasmin(which splits firbin into d-dimers. t-pa synthesized by vascular endothelium
  83. breakdown productos of firbinogen monomers via thrombin
  84. d-dimer levels are increased in
    • thromboembolism
    • infection
    • neoplasia
  85. lab tests of clotting function
    • bleeding time
    • prothrombin time
    • activated partial thromboplastin time(APTT)

    for APTT look at damaged surface at intrinsic pathway
  86. INR
    prothrombin time(clotting time in prescence of tissue factos) used to assess Warfin levels
  87. PTT
    • clotting time in prescence of added kaolin (used to assess heparin levels)
    • tissue factos of extrinsic pathway
  88. hypercoagulation disorders (thrombiphillia)
    • heriditary:
    • factor V mutation¬†
    • deficiency in protein C, protein S, or antithrombin.
    • use of oral contraceptives
  89. acquired thromphillia
    vascular injury and  inflmammation, severe trarum, cancer, obstretrical disorders, 

    autoimmune producion of antophospholipid antibodies
  90. cancer can induce expression of tissue factor
  91. DIC
    widespread thrombophillia; when both thrombi and bleeding occurs.

    treat with anticoagulants and treat underlying condition
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