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18 Cards in this Set
- Front
- Back
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What % composition |
55% plasma Buffy coat - WBC, and platelets Formed elemesnts - RBC |
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plasma composition |
7% proteins - Albumins, globulins, fibrinogen(clot) 91% water 2% other- gases, waste, ions, nutrients |
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the seven things that make up plasma |
Water Proteins Ions Nutrients Waste products Gases Regulatory Substances |
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Allformed elements derived from single population- |
Hemacytoblast-is astem cell the becomes – proerythroblasts, myeloblasts, lymophblasts, monoblasts, megakaryoblasts |
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–Proerythroblasts: –Myeloblasts: Lymphoblasts: Monoblasts: Megakaryoblasts: |
–Proerythroblasts: Develop into red blood cells –Myeloblasts: Develop into basophils, neutrophils,eosinophils(are granulocytes) –Lymphoblasts: Develop into lymphocytes –Monoblasts: Develop into monocytes –Megakaryoblasts: Develop into platelets |
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Neutrophils- Eosinphil- Basophil- Lyphocytes- Monocytes- |
Neutrophils-firstrespond to infection, phagocytize microorganism Eosinphil-allegric reaction to worm Basophil- release heparin and histome-blood thinner and dilation of blood vessels Lyphocytes-immunity Monocytes-transform into macrophages, type of phagocyte |
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Erythropoietin Blood doping |
Erythropoietin - hromone that sitmulates RBC production, produced by kidneys in response to low blood O2. EPO, lance armstrong Blood doping - take blood out, centrifuge RBC's out, the put RBC back into blood,c changes viscosity of blood. |
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Bilirubin- Jaundice- |
Bilirubin- waste product of RBC Jaundice- Hyperbilirubinemia, too much bilirubin, turn slightly yellow, warning sign of kidney failure |
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Von willenbrand factor- |
Vonwillenbrand factor-casuesa bridge between collegen andplatelets |
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•Eicosanoids(prostaglandins, thromboxane, etc.) involved in platelet aggregation •Producedthrough cyclooxygenase(COX).•Aspirin is aCOXI inhibitor,therefore decreases action of platelets (makes less sticky) -> petechiation(small hemorrhages) •Plavix: blocks ADP receptors on platelets. |
Aspirin+ Plavix + warfarin + Heparin– stopclotting |
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Extrinsitc clotting pathway |
1- damaged tissue release tissue factor (TF;Factor III) -When Ca is present, forms factor VII, which activates factor X 2-Prothrombinase converts prothrombin to thrombin 3- thrombin converts fibriogen to bribrin -thrombin activates XIII, which stabilizes cloth |
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Anticoagulants |
antirhombin- stop creation of thing that makes them stick Heperain and psotazuylin- wont let them stick |
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% of each blood type |
O- 47% A- 41% B- 9% AB-7% AB minus - RAREST Only 1% |
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ErythroblastosisFetalis |
Momdoesn’t have RH, baby has RH -> childbirth causes exchange ofblood -> has RH antigen given to momSecond pregnancy, mom is RHpositive now but second child could also have RH positive RhoGam-drug that stops |
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WBC percentages |
–Neutrophils:60-70% –Lymphocytes:20-30% –Monocytes:2-8% –Eosinophils:1-4% –Basophils:0.5-1% |
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Anemia 1)Sickle cell anemia 2)aplastic anemia 3)Hemeragic anemia-lack of blood for any reason, hemerage. pale fatigue 4)hemolytic anemia- abnormall short life span |
anemia- too few RBC 1)Sickle cell- cells are prone to clotting 2)Aplastic anemia- not making enough RBC 3)Hemorrhagic anemia-lack of blood for any reason, hemorrhage. pale fatigue 4)hemolytic anemia- abnormal short life span |
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Eurthrocytosis- h Leukopenia- Leukocytosis- Polycythiema- Acute Leukemia- Chronic leukemia- |
Eurthrocytosis- higher than normal # RBC Leukopenia- lower then normal # of WBC Leukocytosis- higher than normal WBC # Polycythiema- too much RBC produced, usually other things high too Acute Leukemia- cancer of Red bone marrow, when immature blood cells aggressively divide Chronic leukemia- mature cells become cancerous |
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hemophylia- ---------------- Type A- ---------------- Type B- Infectous mononucleousis- |
hemophylia- lacks clotting factors VIII and IX -----------------Type A- deficnecy of factor VIII -----------------------Type B- defiency of facotr IX Infectous mononucleousis- caused by espen bar virus, takes incubation, 10 days to 2 weeks |
