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Physiology Test 2

Tri 2

Immune Rxns of Blood a reaction is caused by antigenicity. There are antigens on the membranes and antibodies in the plasma. There are over 300 different rare Ag on blood cells. TRANSFUSION RXNXS can happen as a delay, or immidiate causing death
ABO Blood Groups A Ag has Type A agglutinogens. AB Ag have AB agglutinogens. H Ag have O agglutinogens. B Ag have B agglutinogens. People with no ABO blood group Ag are the Bombay phenotype and produce Ab to all three blood types. A and B are inherited
O Blood Type recessive, parents both had O. They have H Ag on cells and produce Ab to A and B. These are the universal donor
genotype what was recieved from parents (OO, OA, AA, AB, BO, BB)
phenotype expressed blood type (O, A, B, Oh)
Agglutinins antibodies found in the plasma. At birth you have none, Ab begin dvlping 2-8 mnths. By age 10 you have max titer, which declines with age. You are exposed by environment and form gamma globulins, mostly IgM and IgG
Foward Typing When you take the Pt cells and test for Ab present. You use a known serum
Reverse Typing When you take Pt serum and test against known cells
Rh Blood group agglutinins form with exposure, (D, C, E, d, c, e) D is the most reactive and is the Rh factor. Rh is short for rhesus. Rh- has no D Ag (dd). Rh+ has the D Ag (DD or Dd)
Erythroblastalis Fatalis Hemolitic disease of the newborn. There is agglutination and phagositosis of the RBC. The mother must be Rh- and the dad Rh+. Mom forms Rh+ Ab that are IGg and crross the placenta on subsequent pregnancies.
Kernicterus This is when an Rh rxn causes the baby problems when there is more than 20 mg/dl of biliruben(from the lysed cells) that cross the blood brain barrier. Jaundice, mental retardation, and death can occur.
Transfusion Reactions There can be an immidiate rxn, a delayed rxn, and kidney failure can occur. Also circulation shock, renal tubules blocked, or death.
Transplantation Four types of grafts, autograph, isograph, allograft, xenograft.
Autograft transplant from and into same animal
Isograft from one identical twin to another
Allograft same species
xenograft from one species to another
HLA Complex of antigens most imp causing graft rejection, only six are present on the cell surface, 150 diff types, on WBC and tissue cells,
Prevention of graft rejection supress immune system ( T cells), glucocorticoid hormones, drugs toxic to lymphoid tissue, cyclosporine-inhibitory to helper T cells
Hemostasis components are blood platelets, endothelial cells, and plasma coag. factors
Events of Hemostasis compression and vasoconstriction, formation of platelet plug, blood coagg., clot retractiom and hrombus dissolution.
Hemostasis and vascular spasm The walls of the vessel contract reducing blood flow and blood loss, caused by nervous reflexes(pain), local myogenic spasm(in small vessels) and local humoral factors
Formation of platelet plug Adherence, aggregation, secretion
Adherence activated by plasma substance and initiated by cell substances. Receptor platelets bind to vascular surface and change with exposure to collagen..Swell and assume irregular forms with pseudopods. Contractile proteins contract and release granules
Aggregation platelets stick to the collagen fibers and the subendothelial matrix is exposed. Collagen and laminin support platelet adherence. Von Willebrand Factor(V111) adn thrombin are used
Secretion releases ADP, thromboxane, collagen. Other platelets are also activated, and stickiness is increased
Blood clot formation begins 15-20s after severe trauma, 1-2 min after micro trauma. Initiated by activator substances from wall and platelets and blood protiens. Clot forms 3-6 minutes.
Fibrous tissue growth clot retraction occurs within 20 min to 1 hour. After formation of clot..clot becomes invaded by fibroblasts which form connective tissue(1-2 weeks) or clot simply dissolves.
Platelets round to oval discs, 2-4 micrometers, formed by megakaryocytes in the bone marrow. 150-300,000/microliter. Half life 8-12 days. Eliminated by tissue macrophage system, mostley in spleen. No nuclei, cannot reproduce
Platelets Cytoplasm cytoplasm has actin and myosin molecules, thrombosthenin causes contraction, There are still residuals of RER and golgi(synthesize enzymes and store large calcium ion). They have mitochindria(ATP and ADP). They synthesize prostaglandins
Platelets Cytoplasm 2 Hva Fibrin stabilizing factor, and growth factor.
Platelets Cell Membrane has surface coat glycoproteins that help avoid adherence to endothelium and to adhere to injury. Phospholipids
Blood Coaggulation there are more than 50 substances involved. requires more than a dozen blood coag factore net result is prothrombin activator
Precoaggulants promote coagulation
anticoaggulants inhibit coag
Prothrombin activator catalyzes conversion of prothrombin to thrombin. Ca2++
Prothrombin plasma protein, alpha2-globulin 68,700 MW, FORMED IN LIVEER, VIT K DEPENDANT
Thrombin converts fibrinogen into fibrin fibers
Fibrinogen high MW (340,000), protein formed in liver, seldom leaks into interstitial fluid
Clot retention expressed fluid, fluid=serum, platelets necessary, contraction accelerated by thrombin and Ca+
Coagulation Cascade formation of prothombin activator, extrinsic pathway, intrinsic pathway, phospholipids, common pathway
Extrisic Pathway trauma to vascular wall, release of tissue factor
Intrinsic pathway begins in the blood, clotting factors, vit K dependant(prothrombin, factor 7, factor 9, factor 10, protein C
Phospholipids necessary for both pathways
Clot Retraction and Fibrinolysis (blank)
Prostacyclin (PGI2) endothelial cell metabolite, inhibts platelet function, generated by arachodonic acid
tissue plasminogen activator (TPA) released by activated endothelial cells, converts plasminogen to plasmin
Plasmin protein, hydrlyses fibrin, limits clotting
thrombin binds to thrombomodulin on surface of endothelial cells, converts protein C to active protease
Protein C and cofactor protein S restrain coag. by proteolysis of factors 5a and 8a, activated protein C augmets fibrinolysis by blocking inhibitor of TPA
anthrombin III potent inhibitor of proteases, activity accelerated by heparin
heparin mucopolysaccharide in many cells
thrombotic disordes deficiencies or abnormalities in proteins that regulate or constrain coagulation, leads to sever consequences
Excessive bleeding vit K def., hemophilia, thrombocytopenia.
Thromboembolic Conditions (blank)
thrombus abnormal clot that develops in blood vessel
emboli free flowing clot
Causes of thromboembolis conditions roughened endothelial surfaces, slow flowing blood, DIC-disseminated intravascular coagulation
Anticoagulants heparin, coumarins
coumarins depress liver, lower levels of prothrombin, competes with vit K
Blood Coag. Tests bleeding time, clotting time, prothrombin time
Simple Diffusion atoms or molecules intermingle in a random pattern due to the motion produced by their thermal energy
Simple Diffusion 2 through lipd bilayer-requires diffusion of particle through water, then lipid, then water again
Facilitated Difusion movement across cell membrane utilizing a hole opened by an integral membrane protein
Active transport mvmnt against concentration gradients-requires energy
Concept of Simple Diffuison the higher the concentrationthe higher the rate of diffusion, the higher the temperature the faster the molecules move, higher molecular weight=slower mvmnt, random,
Fick's Law J=-DAdc/dx
J net rate of diffusion
A area of plane where diffusion occurs
dc/dx concentration gradient of particles
D diffusion constant
Protein Transporters there are channels and carrier proteins
Channel proteins there is voltage gated, ligand gated, random opening, Aquaporins
Voltage gated open and close in response to change in the electrical state of the membrane
Ligand gated open and close in response to the binding of a chemical agent to the allosteric site
Random opening due to mechanical manipulation
Aquaporins water channels, provide exchange of water between cell interior and extracellular space
Regulation of channel proteins by size(bore), by gates
Carrier protiens transporter molecule must bind to the carrier protein to undergo transport through the membrane, opening is a shape change.
Characeristics of Protein transporters species specific, saturation kinetics, competitive for transport, obligative coupling of fluxes, higher flux rate than Fick's Law predicted
Saturation Kinetics the time to cycle, number of transporters on the cell, J=Number of transporters/cycle time
Competition for transport Competitive Inhibition and Non-cometitive Inhibitor SEE GRAPHS
Competitive Inhibition usually not transported but blocks access to the transporter for the transport molecule
Non competitive inhibitor binds to the allosteric site changing the shape of the transport protein preventing its normal function usually for lomg periods
Obligative Coupling of Fluxes In central protein transporters two or more transport species are moved. The number o feach molecule moved is always exact and tied to the movement of the other transport species.
Factore affecting Net Rate of Diffusion Membrane permiablity, Diffusion Coefficient, Concemtration difference, Electrical Potential, Pressure difference
Membrane Permiability Membrane thickness, lipid solubility, number of transporters, Temp (high temp=faster), mol weight
Diffusion Coefficient D=PxA where P=membrane permiability
flux rate of diffusion J=D([x]o-[x]i) Whatever thhis means!!
Osmosis moves form high concentration to low concentration
Tonicity concentration that does not move through membrane. Water movement into and out of a cell determines state of TONE (how full the cell is by coparison to normal)
Van't Hoff's Law pie=iRT[x]
pie osmotic pressure
i ionization constant
R ideal gas constant
T Temperature
[x] concentration of dissolved solute
Osmotic presure one mole of solute dissolves ina solution yields an aosmotic pressure of 19600 mmHg=1 Osmole
Isotonic equal
Hypotonic cell swells, outside has less solutes so it flows into cell
Hypertonic cell crenates, outside has more solutes.
Electrical potential there is an electrical charge on the cell b/c the flow into and out creates an electrical current
Nernst Potential The point of electrical and concentration gradient equivelancy. EMF=61 log {[x]I/[x]o} NO MORE MVMT
Principles of electricity potential difference determined by difference in charge b/tw 2 points
Voltage msrd b/tw 2 points
Current flow of electrical charges from one point to another. A movemt from outside to inside changes the factor X2
Ohm's Law I=E/R, R=resistance I=current flow, E=electrical potential
Cell Aqueous solution and good conductor
Lipid membrane high electrical resistance-good insulator
ECF and ICF low electrical resistance
Resting Membrane Potentail ECF=zero
Leak channels open all time, slow leak of ions. Sodium, potassium and chlorine. The membrane is 75% more permiable to potassium than sodium. These channels account for 95% of resting membrane potential
NA=K=ATPase Pump Unequal transport of positive ions makes the ICF more negative. 2 K+ inside and 3 Na+ outside. Accounts for 5% resting membrane potential
Electrochemical gradient chemical concentration gradient and electrical concentration gradient
Resting Membrane Potential inside is neg., membrane potential usually -40 to -90, these cells are polarized, both inside and outside are electrically neutral
Inside Membrane Potential NA-14, K-140, Cl-4
Outside Membrane Potential Na-140, K-4, Cl-108
Selecxtive membrane permiablity at rest more permiable to Na, 75 times more permiable to K, and freely permianble to CL
Cl no contribution to membrane potential
Nernst Eq. -61mV log inside/outside
Goldman Eq gives resting membrane potentail. Em=[gNa/(gNa+gK+gCl)ENa
Excitable cells nerve and muscle cells, must be less than -40mV, musthave a large change in membrane pot,
Graded potential short distance, subthreshold electricla stimuli that does not produce a true action potential, but does generate electrical signals. Stimuli may be electrical or mechanical. Could create local potentials called recepotor or generator potentials. `
Action Potential long distance,
Graded Potential, local response across a leaky channel, die out quickly
Types of graded potential Receptor potentials, pacemaker potential, poststnaptic membrane potential, EPP end plate potential,
Created by: hwhite