2350 Exam 2 SG PDF

Module 4 OBJECTIVE: Describe normal hematopoiesis and factors influencing this process Components of the blood (~5L in body): o Plasma: antibodies, nutrients to tissue & carries wastes away o Red Blood Cells (rBCs) – erythrocytes ▪ carry O2 to and CO2 from ti...

Module 4 OBJECTIVE: Describe normal hematopoiesis and factors influencing this process Components of the blood (~5L in body): o Plasma: antibodies, nutrients to tissue & carries wastes away o Red Blood Cells (rBCs) – erythrocytes ▪ carry O2 to and CO2 from tissues low O2 can lead to clubbing --> “Moon Man Fingers” ▪ iron + hemoglobin = oxygen carrying capacity ▪ hemoglobin formation: heme part is synthesized in the mitochondria and the cytosol of immature red blood cells; globin protein parts are synthesized by ribosomes in the cytosol. ▪ Hematocrit (HCT) - the volume of packed red blood cells (RBC) relative to whole blood ▪ erythropoiesis – production of RBC in bone marrow ▪ specialized kidney cells produce hormone erythropoietin (EPO) that triggers erythropoiesis o White Blood Cells (WBCs) – leukocytes ▪ inflammatory & immune response ▪ produced in the bone marrow Agranular o Lymphocytes: T cells, B bells and NK cells o Monocytes Granular = BEN o Basophils o Eosinophils o Neutrophils (first, most abundant) hematopoiesis - the formation of blood cellular components o Platelets – thrombocytes ▪ produced in Bone marrow ▪ essential to clotting ▪ constricts/plugs damaged vessels  Hemostasis - Normal Clotting Mechanism o Coagulation is the transformation of fluid blood into a solid state to seal breaks in the vascular system. o The coagulation process involves vasoconstriction, platelet aggregation to form a plug, and intrinsic and extrinsic clot formation to plug any breaks in the system. ▪ Intrinsic --> produces clot on the inside vessel ▪ Extrinsic --> produces clot on the outside o The conversion of prothrombin to thrombin, which results in insoluble fibrin threads, is the final step of clot formation. o To prevent the occlusion of blood vessels and the denying of blood to the tissues, a formed clot must be dissolved. o The base of the clot-dissolving system is the conversion of plasminogen to plasmin (fibrinolysin) by several factors, including Hageman factor. Plasmin dissolves fibrin threads and resolves the clot. Pathways o Intrinsic – activated by contact with inside vessel tissue o Extrinsic – activated by contact with damaged outside vessel tissue activated o Common – conversion of the intrinsic/extrinsic pathways --> both converge onto factor X OBJECTIVE: Describe the etiology and common manifestations of select bleeding disorders Thrombocytopenia: Decreased platelet counts, high risk for bleeding Monitor for blood in patient’s stool, urine and vomit Avoid IVs and injections when possible o If not possible, make sure to hold prolonged pressure over area to ensure patient stops bleeding Hemophilia: In most cases of hemophilia, there is a decreased amount or function in one or more clotting factors, which makes secondary hemostasis less active and allows more bleeding to occur o Steps leading up to fibrin reinforcement of the platelet plug makeup process is called secondary hemostasis and results in the hard clot at the site of the injury Is a hereditary recessive x-linked chromosomal disorder Deficiency is FVIII of FIX Prolonged bleeding after a minor or major cut or scrap o Dangerous complication is bleeding into the brain, which can cause a stroke or increased intercranial pressure. o Severity of the symptoms depends on the severity of the underlying mutation, which determines the activity of the factor. o Since factors 8 & 9 (IX & VIII) are part of intrinsic pathway prothrombin time is normal and partial thromboplastin time is prolonged in hemophilia A and B. o In order to confirm hemophilia A and B, tests to look at specific factor activities and mutation testing of the genes and encoding them can be done. Deep Vein Thrombosis (DVT) Clotting happens via coagulation which forms thrombus (clot) Symptoms: asymmetrical edema, calf swelling, calf pain, acute chest pain Treatment: anticoagulants (heparin/warfarin) or prophylaxis (compression, physical activity) Virchow’s Triad: 3 factors that contribute o Hypercoagulability (or thrombophilia) - the increased tendency of blood to thrombose (clot) (e.g. oral contraceptives, inherited disorders, pregnancy) o Injury to the vessel wall – endothelial injury (e.g. trauma, medication-related) o Venous stasis – decreased blood flow or return (e.g. age, immobility) Stages: o Propagation: clot growing along with vessel o Organization: within vessel layer o Recanalization: holes form in thrombus o Embolism: dislodged thrombus Medical emergency when a thrombus dislodges (embolus) and travels to the heart or lungs (pulmonary embolism) Antiplatelets - decrease the formation of the platelet plug by decreasing the responsiveness of the platelets to stimuli that would cause them to stick and aggregate on a vessel wall. Aspirin o Indication: MI, CVA o MOA: antiplatelet - Inhibits prostaglandin and thromboxane synthesis resulting in inhibition of platelet aggregation. o Contraindications: surgery, surgery/invasive procedures, chicken pox/influenza o Side Effects/Adverse Events: Acute aspirin toxicity with hyperpnea, tinnitus Clopidogrel (Plavix) o Clopidogrel is an irreversible inhibitor of the platelet P2Y12 adenosine diphosphate receptor. Inhibition of this receptor prevents the downstream activation of the glycoprotein IIb/IIIa receptor complex, which leads to reduced platelet aggregation. Plavix is metabolized in liver to its bioactive form. o Indication: lowers risk for ischemic events; Hx: MI, peripheral artery disease, CVA, CAD o MOA: antiplatelet o Route: PO w/loading dose o Contraindications: boxed warning for people who poorly metabolize the liver enzyme CYP2C19 – medication is not effective without metabolism to bioactive form. o Side Effects/Adverse Events: bleeding Anticoagulants: Heparin- Intrinsic o Glycosaminoglycans – inactivates clotting factors o Subcutaneous as preventative or IV for known issues o If IV monitor by aPTT every 6 hours o Indication: DVT prevention, blood clot, PE, Cardiac disorders o MOA: anticoagulant - blocking the conversion of prothrombin to thrombin and fibrinogen to fibrin o Contraindications: active bleed/bleeding disorders, thrombocytopenia (