lecture 19 hoffmann
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| signs of disorder of primary hemostasis | mucosal hemorrhages and petechiae, OJO - risk of CNS hemorrhage! failure to stop bleeding after initial injury, bleeding time is prolonged and plt # or morphology is abnormal
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| examples of primary hemostasis disorders | thrombocytopenia or plt dysfunction, qualitative plt disorders, vWF disorder, defects in vessel walls
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| pseudothrombocytopenia | artifactual clumping of certain individuals' plts in response to EDTA in certain collection tubes; must redraw using diff tube
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| information that mean plt volume (MPV) gives clinician | when MPV is high one infers that there is increased destruction of plts or the plts are very young. low MPV = decreased production
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| one cause of thrombocytopenia = bone marrow infiltration by leukemia/lymphoma, metastatic ca, TB, CMV/HIV infection, etc, which implies what about plts? | decreased production
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| reasons for increased destruction of plts, one cause of thrombocytopenia | immune thrombocytopenia (ITP) = Ab-mediated destruction, alloimmune from multiparous woman getting transfusion OR non-immune causes like DIC, TTP, HUS or vasculitis
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| causes of sequestration of plts or altered distribution | hypersplenism aka overactive spleen
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| schistocytes + thrombocytopenia suggest? | microangiopathic processes - there is RBC shearing by fibrin deposition within vessels as seen in DIC or TTP
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| dacrocytes/nucleated RBCs + thrombocytopenia suggest? | bone marrow infiltrative process
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| spherocytes + thrombocytopenia suggest? | autoimmune hemolytic anemia, immune thrombocytopenia; macrophages are biting off pieces of blood cells
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| macrocytes + thrombocytopenia suggest? | liver dz or alcoholism causing B12/folate deficiency and decreased thrombopoietin, which is made by the nl liver OR myelodysplasia
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| microcytes, hypochromia, aniso- and poikilocytosis + thrombocytopenia suggest? | signs of severe iron deficiency anemia
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| spur cell anemia | crenated RBCs due to excess chol in membrane
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| pharmacological agents that can induce thrombocytopenia | PCNs, cephalosphorins, sulfa drugs // heparin // furosemide, thiazides, methyldopa // carbamaszepine, Depakote // H2 receptor agonists, cocaine
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| most common cause of plt dysfunction | NSAID and ASA use
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| 2 functions of vWF | acts as a bridge btwn exposed vascular subendothelium and plt glycoprotein receptors (GPIb); acts as transport protein for VIII in blood, protects it from inactivation and increases its half-life
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| features of vW dz | most common bleeding disorder ~ 1% in population, easy bruisability and mucosal bleeding, bleeding time is prolonged, factor VIII levels may be low
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| lab diagnostic tools for vW dz | vwF antigen immunoassay, PFA-100, PTT, ristocetin cofactor assay to quantitatively measure vWF activity, ristocetin-induced plt aggregation (RIPA) to determine if it's actually a subtype that's hypersensitive
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| scurvy | disorder of vascular integrity: occurs in pts getting their calories from EtOH, characteristic perifollicular pattern of hemorrhage, looks like bruised chicken skin after feathers are plucked. vit C important for epithelial differentiation
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| leukocytoclastic vasculitis | type of disorder of vascular integrity: causes "palpable purpura" = hemorrhage appears as purple nodules or crusts that can be felt
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| Osler-Weber-Rendu dz aka hereditary hemorrhagic telangiectasia | AD disorder of vascular integrity characterized by multiple dermal, mucosal and visceral telangiectasias and freq epistaxis/mucosal bleeding. presumed mechanical fragility of abnormal vessels
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| clnical manifestations of pts with secondary hemostasis disorders | hemarthrosis (deep tissue and joint bleeding), delayed onset, deep hematomas in muscle compartments and retroperitoneum
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| PT extrinsic pathway (starting at VIIa), PTT intrinsic pathway (starting at XII) | vit K-dependent factors = 2, 7, 9, 10
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| the most warfarin-sensitive vit K-dependent factor | factor VII has shortest half-life in plasma
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| information that a 1:1 dilution of pt plasma with nl plasma tells you | if there is normalization deficiency is suggested; if failure to correct occurs then acquire inhibitor of factors is suggested
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| hemophilia A/B | caused by factors VIII/IX respectively, both X-linked recessive
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| TT or thromboplastin time | assesses levels of fibrinogen in blood, meaures clot formation in pt's plasma when thrombin is added
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| DDx when PT/INR and PTT are all abnormal | severe vit K deficiency, warfarin overdose, malabsorption of vit K/pt on TPN, DIC, liver dz, congenital factor I II V or X deficiencies
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| how to distinguish btwn liver dz and DIC when both cause PT/INR and PTT to be elevated | factor VIII is the only one NOT made in liver so in liver dz factor VIII will be nl but low in DIC
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| ** factor VII deficiency is the only one to cause an isolated prolongation of PT ** | b/c it turns over so quickly especially in liver dz
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| tx for ITP | IV Ig and prendnisone; Ig binds macrophages and distracts them from eating up plts until the prendnisone can work to decrease immune response
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