Ch 19 set 2
Terms
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- Hormones that regulate the differentiation and proliferation of particular progenitor cells
- Hemopoeitic Growth Factors
- Increases the number of RBC precursors
- Erythropoietin / EPO
- Hormone produced by the liver that stimulates formation of platelets from megagaryocytes
- Thrombopoietin / TPO
- Small glycoproteins that are produced by red bone marrow cells, leukocytes, macrophages, fibroblasts, and endothelial cells that regulate develpment of different blood cell types
- Cytokines
- Important families of Cytoikines
- Colony Stimulating Factors (CSF's) and Interleukins
- Component of Hemoglobin, Composed of four polypeptide chains
- Globin
- Component of Hemoglobin, four non-protein pigments
- Hemes
- Beginning of RBC Production
- Red bone marrow with a precursor cell called a proerythroblast
- RBC Production
- Proerythroblast divides several times, producing cells that begin to sythensize hemoglobin. Ultimtely, a cell near the end of the development sequence ejects it nucleus an becomes a reticulocyte.
- Cell near the end of the RBC development sequence that loses it's nucleus
- Reticulocyte
- Cellular Oxygen Defficiency, occurs if too little oxygen enters the blood
- Hypoxia
- Cells that contain a nucleus but no hemoglobin
- White Blood Cells (WBC's) / Leukocytes
- Classification of WBC's
- Granular and Agranular
- Chemical filled cytoplasmic vesicles in WBC's
- Granules
- Types of Granule Leukocytes
- Neutrophils, Eosinophils, and Basophils
- Types of Agranular WBC's
- Lympphocytes and Monocytes
- An increase in the number of WBC's for protective response to stresses such as invading microbes, strenous exercise, anesthesia, and surgery
- Leukocytosis
- Abnormally low level of WBC's
- Leukopenia
- Leave the bloodstream and collect at points of pathogenic invasion or inflamation, never return
- Granulocytes and Monocytes
- Continually recirculate from blood to interstitial spaces of tissues to lymphatic fluid back to blood
- Lymphocytes
- Process by which WBC's leave the bloodstream, roll along the endothelium, stick to it, and then squeeze between endothelial cells
- Emigration
- Molecules that help WBC's stick to endothelium
- Adhesion Molecules
- Active in Phagocytosis, ingest bacteria and dispose of dead matter
- Neutrophils and mactophages
- Process by which several different chemicals releaed by microbes and inflamed tissues attract phagocytes
- Chemotaxis
- WBC's that respond most quickly to destruction by bacteria
- Neutrophils
- Proteins released by Neutrophis that exhibit a broad range of antibiotic activity against bacteria
- Defensins
- WBC's that arive to sight of infection later than neutrophis, but arive in larger numbers and destroy more microbes
- Monocytes
- WBC's that leave the capillaries and enter the tissue fluid, release enzymes such as histaminase, phagocytize antigen antibody complexes
- Eosinophils
- Often indicates an allergic condition or parasitic infection
- High Eosinophil Count
- WBC's that leave the capillaries, enter tissues, and liverate heparin, histamine, and serotonin at sites of inflamation
- Basophils
- Types of Lmyphocytes
- B cells, T cells and Natural Killer Cells
- Effective in destroying bacteria and inactivating their toxins
- B Cells
- Attack viruses, fungi, transplaned, cells, cancer cells, and some bacteria
- T Cells
- Attack a wide variety of infectious microbes and certian spontaneously arising tumor cells
- Natural Killer Cells
- Ordered by a physician to detect infection or inflammation, determine the effects of possible poisoning by chemicals or drugs.
- Differential White Blood Cell Count
- Myeloid stem cells deveolp into megakaryocyte colony forming ells that, in turn, develp into precursor cells called megakaryoblasts.
- Thrombopoetin
- Enclosed by a piece of the plasma membrane breakes off from the magakaryocytes in red bone marrow an then enters the blood circulation
- Platelet
- Function of platelets
- Help stop blood loss from damaged blood vessels by forming a platelet plug. Contain granules that when released help clot
- Valuable test that screens for anemia and varoius infections
- Complete Blood Count
- Sequence of responses that stops bleeding
- Hemostasis
- 3 Mechanisms that reduce blood loss
-
1. Vasuclar Spasm
2. Platelet Plug Formation
3. Bloot clotting (Coagulation) - When arteries or arterioles are dmaged, the circularily arranged smooth muscle in their walls contract immediately
- Vascular Spasm
- Chemicals in the vesicles of platelets that form blood clots
- Thromboxane A2, a prostoglandidn: fibrin-stabilizing factor.
- Hormone in platelets that can cause proliferation of vascular endothelial cells, vascular smooth muscle fibers, and fibroblasts to help repair damaged blood vessel walls.
- Platelet derived growth factor (PDGF)
- Platelets contact and stick to parts of a damaged blood vessel, such as collogen fibers of the connective tissue inderlying the damaged endothelial cells.
- Platelet Adhesion
- Once platelets have adhered, they extend many projections that enable them to contact and interact with one another, and they liverate the contents of their vesicles.
- Platelet Release Reaction
- Gathering of new platelets to old platelets becasue of ADp
- Platelet Aggregation
- Plasma minus clotting proteins
- Serum
- Gel in blood that consists of a network of insoluble protein fibers called fibrin in which the formed elements of blood are trapped
- Clot
- Clotting of undamaged blood vessels
- Thrombosis
- Extrinsic Blood Clotting occurs
- Rappidly, Faster than Intrinsic
- Tissue protien that comes from outside the blood vessel involved in Extrinsc Pathway
- Tissue Factor / Thromboplastin
- Thromboplastin / Tissue Factor is a mixture of
- Lipoproteins and phospholipids released from the surface of damaged cels
- Once X factor is activated
- It combines with Factor V in the presence of Ca to form the active enzyme prothrombinase, completing the Extrinsic Pathway
- Vitamin K is necesary for
- Formation of Clotting factors by hepatocytes: Factors II (prothrombin), VII, IX, and X
- Soluablity of VitaminK
- Fat Soluable
- Dissolves small, inappropriate clots
- Fibronolytic System
- A clot does not extend beyond a wound site becasuse
- Fibrin abslorbs thrombin into the clot, and dispersal of some of the clotting factors by the blood, their concentrations are not high enough to bring about widespread clotting
- Powerful inhibitor of platelet adhesion, opposes the actions of Thromboxane A2, produced by endothelial cells and WBC's
- Prostacyclin
- Antithrombin, Heparin, Activated Protein C
- Anticoagulants
- Blocks the Action factors of XII, XI, IX, X, and II
- Antithrombin
- Produced by mast cells and basophils, combines with antrithrombin and increases it's effectiveness in blocking thrombin
- Heparin
- Inactivates factors V and VIII, the two major clotting factors not blocked by antirthrombin, and enhances activity of plasminogen activators
- Activated Protein C
- Clotting in an unbroken blood vessel
- Thrombosis
- Blood clot, bubble of air, fat from broken bones, or a piece of debris that is transported by the blood stream
- Embolus
- Inhibits vaoconstriction and platelet aggregation by blocking synthesis of thromboxane A2
- Aspirin
- The surface of erythrocytes contain a genetically determined assortment of glycoproteins and glycolipids that can act as antigens
- Isoantigens or Agglutinogens
- Blood type is based on the display of
- Antigens on RBC's
- To react with isoantigens, blood plasma contains
- Isoantibodies or Agglutinins