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Blood
| Question | Answer |
|---|---|
| Cardiovascular System consists of: | 1. A pump (the heart) 2. A conducting system (blood vessels) 3. A fluid medium (blood) –Specialized fluid connective tissue containing cells suspended in a fluid matrix |
| Hematology | the study of blood and blood disorders |
| Blood Functions | 1) Transportation of dissolved substances - O2, CO2, hormones, immune cells, nutrients, and waste 2) Regulation of pH and ions (homeostasis) 3) Restriction of fluid losses at injury sites (hemostasis) 4) Defense against toxins and pathogens – travelin |
| Three General Characteristics of Blood | 1. 38C (100.4F) is normal temperature 2. High viscosity 3. Slightly alkaline pH (7.35–7.45) •Average adult has 5 liters of blood |
| Blood = Plasma + Formed Elements | Plasma, Buffy Coat, and Hematocrit |
| Erythrocytes (RBCs) | Hemoglobin, RBC structure and life cycle, Erythropoiesis, Recycling |
| Characteristics of Erythrocytes (RBCs) | Biconcave –Disc shape with sunken center for large surface area for gas diffusion •No nucleus or DNA –Cannot replicate •Live 120 days |
| Structure of the Erythrocyte | •Biconcave disc with thin center and thick margins/borders 1. Large surface area-to-volume ratio –Greater total surface area means faster O2 exchange 2. RBCs can stack like dinner plates and not stick together –Rouleaux (roo-LO) –Easier to pass throu |
| Life Cycle of the Erythrocyte | •120 day circulation –Die, break apart, and recycled by spleen and liver phagocytes –Body must make new RBCs constantly to replace the old (1% daily) •Erythropoiesis –Making new RBCs –Maintained via a negative feedback loop •Erythropoietin (EPO) – |
| Erythropoiesis occurs in Myeloid Tissue | •Production of new erythrocytes (RBCs) •Takes 3-5 days •Occurs only in myeloid tissue (red bone marrow) in adults •Stem cells mature to become erythrocytes •Hemocytoblasts –Blood stem cells –Divide to become either RBCs, platelets, or WBCs |
| Stages of Erythrocyte Maturation | 1. Hemocytoblast 2. Myeloid stem cell 3. Proerythroblast 4. Erythroblast 5. Reticulocyte 6. Mature erythrocyte (RBC) |
| Reticulocytes are Immature RBCs | •Increase in number –If blood loss (hemorrhage) or patient moves to higher altitude, blood doping/EPO, dehydration (polycythemia) •Decrease in number –Due to certain anemias or bone marrow disorders. Anemia interferes w/ oxygen delivery to peripher |
| Hemoglobin (Hgb) – the Red Pigment | •More than 95% of the proteins inside a RBC are Hgb •Each Hgb has two alpha chains and two beta chains of polypeptides (each of the four chains is a globular subunit) •Oxyhemoglobin – blood carrying oxygen bound to Fe+2 in one of the four subunits |
| Breakdown of RBCs | •Macrophages in spleen, liver, and red bone marrow ingest and old RBCs •Hemolysis – the rupture of RBCs at the end of 120 days Two products recovered from hemoglobin: 1. Globin –Amino acids released for use by cells 2. Heme (bilirubin + iron) –Biliv |
| Lab Values for CBC | Hemoglobin, WBC, platelets, and information about RBC size, shape, and number |
| Lab Values for Normal Blood | •How much O2 blood carries depends of quantity of RBCs and hemoglobin •CBC panel includes normal values of the following: 1. Hematocrit: F 37-48%, M 45-52% 2. Hemoglobin (Hgb): F 12-16 g/dL, M 13-18 g/dL 3. RBC count: F 4.2-5.4 million/mm3, M 4.6-6 |
| Iron Requirements | •Dietary iron is required for hemoglobin synthesis •Need 5-20 mg iron from food per day to restore normal loss •Women of reproductive age have higher dietary requirement for iron, B12, folic acid, and vitamin C due to menstruation –Average blood loss |
| Selected Blood Disorders | Sickle Cell Disease, Polycythemia, and Anemia |
| Blood in the Urine | •Hemoglobinuria –Red or brown urine –Due to abnormally large numbers of RBCs breaking down in the bloodstream •Hematuria –Presence of INTACT RBCs in the urine –Due to kidney damage or damage to vessels along urinary tract |
| Sickle Cell Disease | •Inherited RBC disorder –Mutation of beta chain amino acid sequence –Causes defective Hgb to stick to other Hgb molecules •Stiff, curved cells –Can’t fold and recover – fragile –Sharp, sickle shape –Clump and block small blood vessels, cutting of |
| Sickle Cell Population Facts from the NIH | •In the United States, most people with sickle cell disease are of African ancestry or identify themselves as black. •About 1 in 13 black or African American babies is born with sickle cell trait, which is protective against malaria! • About 1 in ev |
| Polycythemia | •More new RBCs being created than destroyed causes imbalance in blood viscosity (thickness) •Polycythemia vera –Overproduction of RBCs due to cancer or other disease •Secondary polycythemia –Overproduction due to compensation for lack of O2 like smo |
| Anemia | •Fatigue, shortness of breath, pallor, low blood viscosity = faster heart rate, lower BP •Deficiency of iron or hemoglobin 1. Iron-deficiency anemia MC – insufficient supply of iron from diet 2. Pernicious anemia - lack of Vitamin B12 from lack of |
| Leukocytes (White Blood Cells) | Leukopoiesis, Granulocytes vs. Agranulocytes |
| White Blood Cells/Leukocytes | •Leukopoiesis- making WBC's •Fewest of the formed elements but are the body’s defense against infectious pathogens •All WBCs have a nucleus •Granules –Presence or absence of these structures when stained in a lab setting –Granulocytes have obviou |
| WBC Disorders | •Leukopenia –Inadequate numbers of WBCs –Virus ex: HIV/AIDS •Leukocytosis –Too many WBCs –Due to infection (normal) or leukemia (pathological) |
| WBCs: Granulocytes | •Neutrophils (polymorphonuclear - PMNs) –Most common, 60-70% of all WBCs –Called band or stab cells due to appearance; live in blood vessels until needed in tissues against infection –Aggressive, mobile phagocytes – first responders! –Main component |
| WBCs: Agranulocytes | •Lymphocytes –Second MC, 25-33% of all WBCs, Smallest –Long-term immunity 1. Natural Killer cells of innate (inherited) immune system 2. T-lymphocytes (Cytotoxic Ts attack cancer and viruses and Helper Ts help all Ts and Bs) 3. B-lymphocytes (Plasma |
| Platelets | The children of Megakaryocytes, a large red bone marrow (myeloid) cell |
| Thrombocytes (platelets) and Hemostasis | •Thrombocytopoiesis •Key role in stopping of bleeding (hemostasis) •Platelets are fragments of megakaryocytes •Live about 7 days •Thrombocytopenia •Thrombocytosis |
| Hemostasis | Blood Clotting has 3 Phases: Vasoconstriction, Platelet Plugging, and Coagulation |
| Three Phases of Hemostasis | •Hemostasis –Cessation of bleeding –Natural process that stops blood loss when vessel injured 3 phases of Hemostasis: 1. Vascular phase 2. Platelet phase 3. Coagulation phase |
| 3 Phases of Hemostasis d/t Injury | 1. Vascular (Vasospasm + Vasoconstriction) Phase –Injured endothelial cells release endothelin, the strongest vasoconstrictor known –Collagen is exposed, drawing platelets to adhere 2. Platelet (Plug Formation) Phase –von Willebrand factor binds to |
| 3rd Phase: Coagulation (Clot Formation) | •Clotting factors –Proteins called from either outside the blood vessel (extrinsic) or inside the blood vessel (intrinsic) –Final step: must convert floating fibrinogen into fibrin •Both pathways result in formation of Factor X, after which the clot |
| Fibrinolysis | •Dissolution of a blood clot •The clot cannot remain as it interferes with normal blood flow •Gradual dissolution of clot •Vessel heals and series of small chain reactions occurs –Plasminogen (inactive plasma protein) converted to Plasmin (active) –P |
| Preventing Blood Clots | 1. Smooth endothelium –Vessel lining is smooth so platelets usually don’t stick 2. Normal blood flow –Small amt of thrombin (pro-clot enzyme) is usually circulating and diluted by normal flow of blood –Pooling blood due to sitting long periods or ly |
| Vitamin K and Gallstones | •Liver synthesizes most clotting factors – abnormal liver fcn interferes with clotting •Gallstones can interfere with clotting due to lack of vitamin K –Vitamin K necessary for clotting factors –Absorbed into blood from intestine but is only lipid so |
| Blood Clotting Disorders | •Thrombus –Unwanted blood clot inside a vessel that is in place •Embolus –Broken off piece of thrombus that is now circulating through blood –Tx: heparin injection to block thrombin; coumadin to block vitamin K in liver (less prothrombin from liver |
| Blood Types and Reactions | A, B, AB, O and Rh |
| Blood Types Overview | •Blood Types –Are genetically determined –Blood is typed based on which antigen is present on surface of RBCs •A, B, O, and Rh factor is called D •Antigens (agglutinogens) •Antibodies (agglutinin) •Transfusion reaction/cross reaction causes clumpin |
| RBC Antigens & Antibodies | •Surface Antigens (agglutinogens) –RBC surface proteins that identify cells to immune system –Normal cells are ignored and foreign cells attacked •Antibody (agglutinin) –Protein in the blood plasma against the antigen of the other blood types •C |
| Antigen and Antibody Locations | –Type A has A antigens on surface of RBC •Type B antibodies in plasma –Type B has B antigens on surface of RBC •Type A antibodies in plasma –Type AB has both A and B antigens on surface of RBC •No antibodies in plasma at all –Type O has no antigens |
| Antigens: Proteins on the Surface of RBCs | 1. A (surface antigen A) 2. B (surface antigen B) 3. AB (antigens A and B) 4. O (neither A nor B) |
| Cross-Reactions/Transfusion Reaction | •Cross-reactions in transfusions –Also called transfusion reaction •Plasma antibody meets its specific surface antigen (enemy) •Blood will agglutinate and hemolyze •Occur if donor and recipient blood types not compatible •A cross-match tests donor an |
| Rhesus (Rh) Factor | •Rh positive blood contains Rh antigen •Rh negative blood does not have Rh antigen •Most blood is Rh-positive –85% white Americans and 95% African Americans •Blood does not normally contain anti-Rh antibodies –Remember: during lab class experiments |
| Two Ways to Develop Sensitization (Anti-Rh Antibody Development) | 1. Transfusion route –Rh neg person receives Rh pos blood during transfusion and recipient’s body interprets Rh pos as a threat, creates anti-Rh antibodies. If next transfusion is Rh pos again, the recipient’s new anti-Rh antibodies will attack the b |
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tarich5z
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