Functions of blood
- Transport
- Regulation: ions/pH
- Defense: immune
- Hemostasis: prevent blood loss
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| Term | Definition |
|---|---|
| Functions of blood | - Transport - Regulation: ions/pH - Defense: immune - Hemostasis: prevent blood loss |
| Hematocrit | % of blood volume that is RBC's |
| Normal hematocrit | ~45% |
| Anemic hematocrit | Low (less RBC's = less oxygen) |
| Polycythemic hematocrit | High (adapted to low oxygen = increased RBC's) |
| Plasma Proteins: Albumins Source and Function? | Source: liver Function: colloid osmotic pressure (pulls water in) |
| Plasma Proteins: Globulins Source and Function? | Source: liver and lymphoid tissue Function: antibodies |
| Plasma Proteins: Fibrinogen Source and Function? | Source: liver Function: clotting |
| Plasma Proteins: Transferrin Source and Function? | Source: liver Function: iron transport |
| What is Serum? | fraction of plasma where fibrinogen and clotting factors are removed |
| What and where is hematopoiesis | - formation of blood cells - prenatal: happens in yolk sac, liver, spleen - postnatal: bone marrow |
| How is hematopoiesis regulated | cytokines: hormone-like - growth factors - Erythropoietin: produces RBC's - Thrombopoietin: produces platelet's |
| What makes CO inhalation fatal? | Hemoglobin can bind to it more easily than binding to oxygen |
| Essential factors for RBC production | - cytokine - dietary factors: iron, folic acid, B12 - intrinsic factor |
| Which cells are involved in recycling RBC's | macrophages |
| Where does recycling of RBC's happen | spleen |
| What is anemia? | decreased oxygen-carrying capacity bc of RBC/Hb deficiency |
| What cause anemia | - decreased RBC production in bine marrow - destruction of RBC's: hemolytic anemia - blood loss: hemorrhagic anemia - abnormal Hb production: sickle cell - lack of iron - lack of IF or B12: pernicious anemia - damage of bone marrow: aplastic anemia |
| Non-specific defenses: innate immunity | skin, enzymes, tears, mucus - granulocytes and monocytes/macrophages - no memory - fast - complement system |
| Specific defenses: acquired immunity | - lymphocytes - has memory - slow - antibodies |
| What kind of response is inflammation | non-specific |
| Vascular events of inflammation | 1. release histamine 2. vessels dilate 3. protein accumulation in extracellular spaces 4. inflammatory mediators released: bradykinin, prostaglandins (all cause pain) |
| Cellular events of inflammation | 1. macrophages kill pathogens and release chemical signal 2. WBC's move into infected area 3. phagocytosis of non-self agent |
| What is chemotaxis | ability of WBC's to move against conc gradient in response to chemotactic factors |
| How do phagocytes recognize bacteria | PRR: patter recognition receptors |
| What are opsonin's | speed up phagocytosis - produced by host body |
| Oxygen dependent killing | uses free radicals |
| Oxygen independent killing | - lysozymes - lactoferrin - defensins |
| What are complement proteins | - inactive proteins in plasma Function: OIL opsonization, inflammatory mediators, lysis (of bacteria) - MAC: forming a pore |
| Primary lymphoid tissue | source: bone marrow and thymus function: B/T cells developed here |
| Secondary lymphoid tissue | source: lymph nodes function: where B/T cells mature and activate |
| What 3 things must all lymphocytes be able to do | - recognize antigens - respond to antigens - remember the antigen |
| Active immunity | - acquired through exposure or vaccine - self-generated - takes weeks to acquire immunity - lasts years |
| Passive immunity | - acquired through placenta or mothers milk - preformed - immediate immunity - lasts weeks |
| Key steps of hemostasis | 1. vasoconstriction 2. primary hemostasis (platelet plug): white thrombus 3. secondary hemostasis (clotting): red thrombus |
| Where do platelets come from | Bone marrow/stem cells |
| T/F: platelets have a nucleus | False |
| Contents of platelet granules | 1. alpha granules: vWF, cytokines 2. dense granules: ADP, serotonin, Ca |
| Steps of the platelet plug | 1. adhesion: using vWF 2. activation: change shape 3. aggregation: stick together = plug |
| Why does the platelet plug not continuously expand | - signaling molecules (endothelial cells release chemical signal) |
| Aspirin: COX1 (platelets) | releases thromboxane A2: vasoconstriction, PRO hemostatic effect |
| Aspirin: COX2 (endothelial cells) | releases prostacyclin: vasodilation, ANTI hemostatic effect |
| Steps of blood clotting | prothrombin (active) uses prothrombinase = thrombin thrombin helps fibrinogen become fibrin |
| Intrinsic pathway | - internal trauma - cell injury, exposure to collagen, contact w/ foreign surfaces - factor XII in contact w. negatively charged surfaces In vivo: blood exposed w/ collagen In vitro: blood exposed w/ foreign surface |
| Extrinsic pathway | - external trauma: causes blood to leak out to surrounding tissues - exposure to TF Factor VII in blood encounter TF |
| What does thrombin do in clotting pathway | 1. activate platelets 2. fibrinogen -> fibrin 3. activate clotting factors 4. activate protein C (anticoag) |
| Clinical anticoags | Ca chelators, heparin, vitamin K antagonists |
| What is agglutination | surface antigens on RBC bound to antibodies to form clumps = blood types not meant together |
| T/F: Type A blood can donate to Type O | False, Type O has anti A and B antibodies |