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TheBleedingPatient
lecture 19 hoffmann
| Question | Answer |
|---|---|
| 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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