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lecture 19 hoffmann

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
examples of primary hemostasis disorders thrombocytopenia or plt dysfunction, qualitative plt disorders, vWF disorder, defects in vessel walls
pseudothrombocytopenia artifactual clumping of certain individuals' plts in response to EDTA in certain collection tubes; must redraw using diff tube
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
one cause of thrombocytopenia = bone marrow infiltration by leukemia/lymphoma, metastatic ca, TB, CMV/HIV infection, etc, which implies what about plts? decreased production
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
causes of sequestration of plts or altered distribution hypersplenism aka overactive spleen
schistocytes + thrombocytopenia suggest? microangiopathic processes - there is RBC shearing by fibrin deposition within vessels as seen in DIC or TTP
dacrocytes/nucleated RBCs + thrombocytopenia suggest? bone marrow infiltrative process
spherocytes + thrombocytopenia suggest? autoimmune hemolytic anemia, immune thrombocytopenia; macrophages are biting off pieces of blood cells
macrocytes + thrombocytopenia suggest? liver dz or alcoholism causing B12/folate deficiency and decreased thrombopoietin, which is made by the nl liver OR myelodysplasia
microcytes, hypochromia, aniso- and poikilocytosis + thrombocytopenia suggest? signs of severe iron deficiency anemia
spur cell anemia crenated RBCs due to excess chol in membrane
pharmacological agents that can induce thrombocytopenia PCNs, cephalosphorins, sulfa drugs // heparin // furosemide, thiazides, methyldopa // carbamaszepine, Depakote // H2 receptor agonists, cocaine
most common cause of plt dysfunction NSAID and ASA use
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
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
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
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
leukocytoclastic vasculitis type of disorder of vascular integrity: causes "palpable purpura" = hemorrhage appears as purple nodules or crusts that can be felt
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
clnical manifestations of pts with secondary hemostasis disorders hemarthrosis (deep tissue and joint bleeding), delayed onset, deep hematomas in muscle compartments and retroperitoneum
PT extrinsic pathway (starting at VIIa), PTT intrinsic pathway (starting at XII) vit K-dependent factors = 2, 7, 9, 10
the most warfarin-sensitive vit K-dependent factor factor VII has shortest half-life in plasma
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
hemophilia A/B caused by factors VIII/IX respectively, both X-linked recessive
TT or thromboplastin time assesses levels of fibrinogen in blood, meaures clot formation in pt's plasma when thrombin is added
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
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
** 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
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
Created by: sirprakes



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