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34 Cards in this Set
- Front
- Back
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hematocrit
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the cellular portion of the blood
formed elements 45% of the total blood volume |
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globulin
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alpha and Beta globulins = carry lipid hormones through the blood plasma...carry all fats or anything lipid soluble. trap fats inside to transport them. (HDLS/LDLS = lipoproteins)
Gamma globulin = antibodies |
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gasses dissolved in the blood plasma
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CO2
O2 N2 |
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Hemoglobin
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About 280 Hb molecules per RBC
Hb consists of a protein globin, and an iron containing pigment called heme. The heme group binds the oxygen. |
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Heme:
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iron-containing pigment of Hemoglobin.
binds the oxygen. Carries Iron in the middle Iron can be oxidized/reduced. grabs ahold of oxygen. Each Heme carries 4 oxygen. breaks down into Bilirubin and Iron. Iron bound to Transferin molecule, transferrin transfers iron back to bone marrow to make more RBCs. Iron is recycled so we dont need much in our diet. Bilirubin is conjugated with a carrier molecule and returned to the intestines and blood (by products give wastes their color) |
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Erythropoiesis
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Stem cell/erythroblasts: undergo mitosis.
Normoblast: has a nucleus and starts to make Hb (expels nucleus to become a Reticulocyte). Reticulocyte: the nucleus is absent, but still can make Hb (destroys its mitochondria to become erythrocyte). Erythrocyte: has no nucleus, can no longer make Hb, is put inot the blood; JUSt carries oxygen |
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Factors necessary for erythropoiesis
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Hormone Erythropoietin: mitosis of erythroblasts
Vitamin B12 - Cayanocobalamin: final maturation of RBCs Folic Acid: synthesis of purines and pyrimidines (DNA) Iron - Fe: essential component of Hb |
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Prostacyclin
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PGI2
a type of prostaglandin produced by the endothelial cells of blood vessels. Causes platelets to be repelled from each other and from the endothelial lining of the BV, in the absence of BV damage. |
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Nitric Oxide
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secreted by the endothelial cells of blood vessels.
Acts as a vasodilator and... Acts on platelets to inhibit aggregation IN THE ABSENCE OF DAMAGE TO BV |
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CD39
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Enzyme contained in the plasma membrane of endothelial cells of blood vessels.
Located on the apical surface of the cells, with the active site sticking into the lumen. Takes ADP from the lumen of a healthy vessel and breaks it down into AMP and Pi. --> ADP can cause platelets to aggregate. |
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Sequence of events leading to Platelet Aggregation
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1) blood vessel injured
2) exposure of collagen fibers (CT) beneath endothelium 3) damaged endothelial cells secrete a protein (von Willebrand factor) which coats the exposed collagen fibers 4) Platelets stick to these coated collagen fibers. 5) Stuck platelets release granules in their cytoplasm. Granules contain: ADP - makes platelets sticky Serotonin - local acting neurotransmitter, stimulates vasoconstriction Thromboxane A2 (TxA2, prostaglandin) - stimulates vasoconstriction and makes other platelets sticky The substances released from platelets function in vasoconstriction and formation of a platelet plug |
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Fibrin Proteins
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Insoluble stringy protein fibers from Fibrinogen.
Fibrinogen made by Liver. Fibrin: makeup fibrin clot, strenthening the platelet plug. |
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Intrinsic Pathway
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Exposed collagen fibers (in vivo) and glass (in vitro) (a negatively charge surface):
Factor 12 is activated. Factor 12 activates Factor 11. Factor 11 activates Factor 9. Factor 9 forms Factor 8 Complex along with Factor 8 ( VIII, IX, Ca, phospholipid on platelet membrane) Factor 8 complex initiates the common pathway. |
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Common Pathway
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Factor X is activated either by Factor 8 complex from the Intrinsic Pathway or by Factor 7 Complex from the Extrinsic pathway.
Factor X forms a complex with Factor V: Factor V Complex includes Factors 10 and 5, Ca, phospholipid of platelets membrane) Factor 5 Complex activates prothrombin --> thrombin thrombin activates Fibrinogen --> Fibrin Thrombin activates Factor 13. Fibrin can polymerize in the presence of activated Factor 13. Forms a meshwork of Fibrin proteins (goes from soluble to insoluble) called a Fibrin polymer |
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Extrinsic Pathway
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The formation of a fibrin clot can occur more rapidly this way.
Damaged tissue releases tissue Thromboplastin or Factor III Factor III initiates the Extrinsic Pathway Factor VII is activated. Factor 7 forms Factor 7 Complex (phospholipid on platelet membrane, Cal, Thromboplastin, and VII) Factor 7 COmplex activates Factor 10. Active Factor 10 initiates Common Pathway ultimately leading to Fibrin polymer. |
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Clot Retraction
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The platelets trapped in the clot send out pseudopods and then contract them.
This condenses the fibrin by pulling the fibrin proteins together, squeezing out the serum (plasma without the fibrinogen) The clot is strengthened, the vessel walls are pulled together so they can adhere. Stitching helps this process. |
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Vitamin K in blood clotting
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Vita K is essential because it is required for the synthesis of prothrombin and Factors VII, IX, and X.
Vitamin K is produced by microbes in your gut. Its needed to convert glutamate into Gamma Carboxyglutamate, which binds Calcium and makes the clotting complexes (Factor Complex) |
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Atherosclerosis
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buildup of plaques (clots on inside of BV walls)
unrepaired: fats stick to the clots, smooth muscle starts to feed on the fat, muscle cells start to divide in that spot The lumen becomes smaller Increased BP |
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Dissolution of Clots
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As BV wall is repaired:
Active Factor XII promotes the conversion of Prekallikrein (found in plasma) into Active Kallikrein. Active Kallikrein catalyzes the conversion of Plasminogen into Plasmin, then Plasmin digests the fibrin, dissolving the clot. Active Kallikren also simultaneously promotes the conversion of Kininogen (from endothelial cells of BVs) into Bradykinin. Bradykinin causes vasodilation. |
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heparin
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activates a plasma protein called Antithrombin III which combines with and inactivates thrombin.
Green top Heparin is naturally found in the body, produced by the WBCs. (Basophils = mast cells) Keeps you bleeding --> pressure forces the bacteria in the opposite direction of the infection |
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Coumarins
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Prevent blood clotting by competing with Vitamin K which is needed for the synthesis of prothrombin VII, IX, X.
Slow acting. Warfarin, Dicumarol. |
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Aspriin
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Inhibits prostaglandin production, resulting in defective platelet release reaction.
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Tissue Plasminogen Activator = Streptokinase
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Streptokinase = naturally found in bacteria
Tissue Plasmenogen Activator = emergency medicine, a product of human genes introduced into bacteria. Both Breaks down clots and can reduce damage to heart from blood clots. Can be administered to a heart attack patient to stop formation of clots. Its the clots that kill, not the actual attack. BOTH activate Plasminogen inot Plasmin (plasmin breaks down clots) |
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Inflammatory Response
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The body's response to damaged tissue.
1) Injury to tissue 2) Vasodilation increases blood flow to the damaged areas and brings the blood cells and important proteins to the area. 3) Increased tissue permeability permits the cells and proteins into the damaged area. 4) Phagocyte migration *within an hour phagocytes appear *the first line of defense is the neutrophils, then the monocytes follow. Neutropils will stick to the endothelium of the BV = Margination The Neutrophils will the squeeze between the endothelial cells and enter the tissue space = Diapedesis Once inside the tissue space, the cells will move by ameboid motion to the site of tissue damage |
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Phagocytosis
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4 Phases:
1. Chemotaxis: the chemical attraction of phagocytes to microorganisms ***Chemicals include: components of WBCs, damaged tissue cells, complement proteins 2. Adherence: the attachment of the phagocyte plasma membrane to the surface of the microorganism or other foreign material. 3. Ingestion: the plasma membrane of the phagocyte extends pseudopods that engulf the microbe...microbe is taken into the cell as a phagosome. 4. Digestion: the phagosome fuses with primary lysosome. Contents take 10-30 mins to kill many bacteria. What cannot be digested reamains as residual body. ***Some toxins from Staphylococci can kill phagocytes (blows them up from inside) ***Mycobacterium tuberculosis can multiply within the phagolysosome and destroy it. ****Other microbes can remain dormant in phagocytes for years! |
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Histamine
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Found mainly in mast cells, basophils and platelets.
Release of histamine fro mast cells occurs: 1) when microbes cause tissue damage which mechanically disrupts the mast cells, releasing histamine (as its dying) 2) with the activation of complement proteins which cause the release of histamine by mast cells 3) when tissue damage attracts neutrophils to the area and neutrophils will secrete chemicals which cause the release of histamine for the mast cells. Histamine causes vasodilation of BVs It increases permeability to proteins and fluid into the tissue space (makes Diapedesis easier). Swelling of tissue in response to Histamine stimulates pain receptors to briain. |
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Kinin
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generated in Plasma from a cascade of activations
Small polypeptide Microbes cause tissue damage which activates a protein called the Hageman Factor. Active Hageman Factor activates prekalllikrein to active Kallikrein. Active Kallikrein activates Kininogen to form Kinin. Function in inflammatory Response: vasodilation of BVs increased permeability to proteins and fluid inot the tissue. Chemotaxis (attraction of the neutrophils) Stimulation of pain receptors |
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Complement Proteins Pathways
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Made by liver and found in blood
20 plasma protiens Cascade of activation occurs from C1, C4, C2, C3, C5, C6, C7, C8,C9 Can Perform various functions as theyre activated. The nonspecific/alternate pathway: the polysaccaride contained in the cell walls of certain bacteria and fungi interact with the proteins of the Properdin system, which includes Properdin, Factor B, and Factor D. These proteins then activate C3 and the rest of the cascade. The Specific/Classical pathway: initiated by the binding of antibodies to antigen, which initiates the C1 protein. C1 then activates the rest of the cascade of proteins. C1 binds to the "c" region/tail of Antibody. |
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Functions of Complement Proteins
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1) release of histamine from the mast cells (C3a and C5a)
2) activation of Kinin via activation of Kallikrein 3) increased vasodilation of the BVs 4) increased permeability of the proteins and fluid into the tissue (kinins) 5) Chemotaxis (C5a) 6) enhancement of phagocytosis by coating the microbe and promoting the attachment of the phagocyte to the microbe. (C3b) --> Opsonization - C1-C3 are activated 7) Cytolysis: direct destruction of the microbe: ***involves activated C5-C9: Membrane Attack Complex (MAC) ***the MAC produces cellular lesions, called Trans-Membrane Channels that lead to the loss of ions and eventually cytolysis (due to osmotic imbalance) ***This is called Complement Fixation |
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Interferons
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Small proteins with molecular weights between 15,000 and 30,000
Produced by fibroblast in CT, by lymphocytes and by other leukocytes Are host cell specific but not virus specific. Entry of a virus into a host cell induces interferon synthesis by the host cell. Once synthesized, interferon released from cell, diffuses to uninfected cells and causes them to synthesize ANTIviral Protein (AVP) Antiviral Proteins inhibit Viral multiplication. Interferon has no effect on viral replication in the cells that are already infected by viruses. Only effective for a short time Interferon stimulates cytotoxic T lymphocytes and natural killer cells and so clinical trials are being conducted to determine the anti-cancer effects of interferon Inhibit: cell division, tumor growth, maturation of adipose cells and erythrocytes ...if you treat someone w/interferon it can lead to anemia =( |
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3 types of Interferon
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alpha interferon - produced by most body cells
beta interferon - produced by most body cells gamma interferon - certain T Lymphoctes and Natural Killer Cells only produce these |
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Antibody
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Produced by the body in response to an antigen and capable of combining specifically with that antigen
Composed of 4 interlinked polypeptide chains There are 2 long chains: heavy chains there are 2 short chains: light chains The polypeptide chains are joined by disulfide bonds Fab portion of the antibody contains variable amino acid sequences and is the area where the antigen binds. Combinations of 3 regions of DNA allow for more than 1 billion Antigen types Fc portion: Crystallizable Frangment - contains constant amino acid sequence and this is where the C1 proteins bind. Antibodies belong to proteins called Immunoglobulins. |
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Immunoglobulins
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Involved in Humoral Specific Immune Response.
Contain Antibodies IgG: most abundant, crosses the walls of BVs and enters tissue, passive immunity from mother to fetus IgM: first ones to appear in initial exposure to an antigen, involved in agglutination, pentamer IgA: protects mucosal membranes from the attachment of pathogens, monomers or dimers, found in secretions, passive immunity from mother to baby. IgD: functions unknown IgE: bind tightly by their Fc portions to receptors on mast cells and basophils and cause release of histamine, increases in concentration during allergies or parasitic infections, IgEs are a problem in Inflammatory Diseases (Lupus, Fibromyalgia, allergies) |
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Lymphokine
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Released by the cytotoxic T Lymphocyte when it combines with the Antigen.
One Lymphokine is a chemotactic stimulus which attracts neutropils but mainly monocytes to the areas which can then phagocytize the cell with the Ag. One lymphokine is a migration inhibitory factor, which keeps the macrophages in the area. One lymphokine is a macrophage activation factor which activates macrophages and makes them more efficient. One lymphokine is a cytotoxin which is able to kill the target cells directly without phagocytosis! |
