NURS 324 Coagulation and Anemias acquired platelet defects caused by ANS drugs that inhibit TXA2 synthesis thereby inhibiting platelet aggregation ASA and some NSAIDS all cells are derived from ANS a small population of pluripotent stem cells allogenic stem cells ANS stem cells from another person anemia secondary to acute blood loss ANS sudden drop in blood volume GI bleed trauma surgery identify source and stop the bleeding anticoagulants ANS counter mechanism to clotting keeps blood in fluid state arterial thrombi ANS from conditions that produce turbulent flow endothelial damage autologous stem cells ANS stem cells from BM peripheral blood umbilical cord blood coagulation ANS process when fibrin strands create a meshwork that cements blood components together blood components ANS 1 plasma 55 2 leukocytes and platelets 1 3 erythrocytes 45 body iron ANS 80 complexes to heme in Hb 20 stored in BM liver spleen dietary iron helps maintain stores comes from meat bone marrow biopsy ANS full evaluation of hematopoiesis posterior iliac crest pressure on puncture site for 5 10 min causes of accelerated activity of coagulation ANS pregnancy oral birth control immobility CHF causes of folic acid deficiency anemia ANS poor nutrition malabsorption alcohol abuse anorexia hemodialysis causes of increased platelet function ANS atherosclerosis DM smoking increased lipids cholesterol increased platelets causes of iron deficiency anemia ANS 1 inadequate dietary intake or malabsorption 2 blood loss causes of pernicious anemia ANS 1 autoimmune disease 2 Gastrectomy small bowel resection Crohn s disease causes of platelet defects ANS leukemia HIV radiation treatment chemo splenomegaly immune thrombocytopenic purpura drugs that destroy platelets quinidine sulfa heparin causes of vit k deficiency ANS parenteral nutrition combined with antibiotics destruction of normal gut flora changes in hematocrit ANS hydration status increases when volume goes down but number of RBCs stay the same decreases when volume goes up and number of RBCs stay the same characteristics of spleen ANS LUQ size of fist fragile highly distensible clot dissolution ANS plasminogen activators activate plasmin plasmin digests fibrin plasma is rapidly inactivated to keep the effect local clot dissolution regulated by ANS thrombin and plasminogen activators clot retraction ANS large numbers of platelets join the edges of the vessel platelets contract and squeeze the serum from the clot edges of the broken vessel are then joined clotting studies ANS PT APTT partial thromboplastin time INR international normalized ratio bleeding time seconds CO poisoning ANS CO has a higher affinity to Hb than O2 CO binds with Hb reducing Cobalamin deficiency anemia ANS vitamin B12 defective intrinsic factor production of gastric mucosa cobalamin can t be absorbed cobalamin deficiency anemia CBC ANS macrocytic elevated MCV normochromic MCH normal serum levels low cobalamin deficiency anemia treatment ANS IM cobalamin injections for life larger doses initially then monthly for life nasal sprays also available cobalamin normally absorbed in ANS the distal ileum components of a CBC ANS Hb weight dL Hematocrit MCV size MCH weight WBC count total WBC differential specific WBC type platelet count DIC treatment ANS prevent further clotting replace clotting components dietary iron absorption ANS only 5 10 of what is ingested is absorbed absorbed in duodenum Disseminated Intravascular Coagulation DIC ANS paradox of widespread coagulation and bleeding in vasculature usually a complication of a condition sepsis bleeding oozing from puncture sites effects of aging ANS decreased stem cells decreased ability to compensate for illness Hb levels decrease ability to raise WBC count in response to infection may be diminished effects of hemolytic anemias ANS defects of the RBC sickle cell disease enzyme deficiencies RBC membrane abnormalities Erythrocyte sedimentation rate ANS rate at which RBCs fall in anticoagulated blood affected by changes in plasma proteins non specific test erythropoiesis ANS production of erythrocytes RBCs move through a series of divisions each producing a smaller cell erythropoietin ANS hormone synthesized and released by kidneys in response to cellular hypoxia extrinsic clotting factors ANS injured tissue extrinsic coagulation pathway ANS faster process activated when blood is exposed to tissue extracts fate of Hb after RBC destruction ANS AA s and iron are recycled bulk of heme is converted to bilirubin and excreted fibrin ANS acts as glue to stabilize the clot folic acid deficiency anemia ANS megaloblastic slow onset needed for DNA and RNA synthesis within maturing RBCs folic acid deficiency anemia treatment ANS 1 5mg QD folic acid PO function of spleen ANS filters RBCs stores 30 of platelets rich supply of lymphocytes and monocytes produces RBCs during fetal development functions of plasma ANS prevent blood loss carries RBCs that transport gases aids in body defenses transports nutrients waste products hormones facilitates exchange of body heat gamma globulins ANS antibodies body defense hematocrit components ANS leukocytes and platelets plus erythrocytes the formed elements hemoglobin ANS protein iron compound that transports oxygen Hemophilia A ANS inherited defect a decrease in factor 8 therefore problem with the coagulation cascade shows up in childhood with severe and spontaneous bleeding Heparin MOA ANS binds to antithrombin III which inactivates thrombin factor 10 and others this suppresses the formation of fibrin Homan s sign ANS calf pain with dorsiflexion of foot sign of possible venous thrombosus hypercoagulability states ANS hemostasis exaggerated leads to thrombosis increased platelet function accelerated activity of coagulation impaired hemostasis ANS defective synthesis Vit K deficiency required for the synthesis and regulation of prothrombin impaired hemostasis liver disease ANS impairment in production of clotting factors plasminogen and thrombopoietin leads to impaired clotting and low platelet count intrinsic clotting factors ANS endothelial injury intrinsic coagulation pathway ANS slow process initiates with blood coming in contact with collagen in vessel walls iron deficiency anemia findings ANS micryocytic small low MCV hypochromic pale low MHC increased TIBC iron loss ANS 1mg is lost daily in GI tract sweat and urine labs for RBCs ANS 1 RBC RBCs in blood 2 reticulocytes rate of RBC production 3 Hb content 4 Hct RBCs