Cadiac Output, Blood Pressure Topic 2-3
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| Stenosis | *a narrowed valve
*BC more pressure must eject blood thru valve-->
1. Increased residual bl. vol. in a chamber
2. Cardiac cell hypertrophy
3. Low PP
*Usually assoc w/ calcification of valve
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| Incontinence | *valve that does not close properly, can lead to—>
1. Backward blood flow
2. Increased bl. vol. in affected chamber
3. Low PP
*Associated w/ valve leaflets "billowing" backwards
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| Heart Murmers | turbulent blood flow, that can be caused by stenosis restricting opening of heart valve
turbulent blood flow, that can be caused by stenosis restricting opening of heart valve
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| Cardiac Output | *Volume of blood ejected by each ventricle per MINUTE
*SV x HR
*@ rest 5 L/min.
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| Stroke volume | *Volume of blood ejected by each ventricle per BEAT
*about 70 ml/beat
*Diff. btw EDV and ESV
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| Heart Rate | *# of times the heart beats/min.
*ave. cardiac cycles/min.
* about 75/min.
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| Cardiac Reserve | *difference btw resting and maximal cardiac output
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| End Diastolic Volume | *Volume of blood that fills a ventricle during diastole *about 120 ml.
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| End Systolic Volume | *Volume of blood remaining in a ventricle after systole
*about 50 ml.
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| SV | SV= EDV-ESV
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| SV Factors | 1. Preload
2. Contractility
3. Afterload
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| Remember | Diastole= heart FILLING + Systole= heart EMPTYING
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| Ejection Fraction | *Volume ejected
* SV/EDV *average 70%, >50%= cardiac failure could occur, athletes=up to 90%
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| Preload | *degree to which cardiac muscle fibers are stretched prior to contraction
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| Frank-Starling Law of Cardiac Muscle | *If cardiac muscle sarcomeres are stretched w/in limits—> contract more forcibly
*Recall length-tension relationship
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| Preload Factors | *Factors that increase preload
1. Increased venous return
2. Increased time for filling (length of diastole)
3. increased muscle activity
4. increased inspiration
5. vasoconstriction
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| Contractility | *any change in muscle contractile strength=independent of EDV & sarcomere length
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| Positive Ionotropic Effects | *Increase Contractility
1. Autonomic Nerv. Sys.: SNS (Fight-or-Flight)
2. Chemicals: Epinephrine, Norepineprhine, Excess Ca2+, Glucagon, Thyroxine, Digitalis
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| Negative Ionotropic Effects | *Decrease Contractility
1. Autonomic Nerv. Sys.: PNS
2. Chemicals: Acetylcholine Excess H+, Excess K+, Calcium channel blockers (like used in high blood pressure)
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| Afterload | *Pressure that ventricles must overcome to eject blood into arteries
*> arterial pressure= harder for ventricles to eject blood—> reduced SV
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| Corrective Response-Elevated | Aortic&Carotid pressoreceptors stimulated—>afferent impulse across Glossopharyngeal/Vagus nerve to Medulla—>Cardiacinhibotory center activated/Cardioaccelatory Center inhibited—>Efferent message to SA node via Vagus nerve—>HR decreases, BP decreases
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| Corrective Response- Reduced | Aortic/Carotid pressorecptors=NOT stimulated—>reduced messaged to medulla—>CAC activated/CIC inhibited—>Efferent messsage to SA node via cardiac sympathetic nerves—> HR/BP increases
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| Congestive Heart Failure | heart's weak pumping action causes a buildup of fluid called congestion in lungs and other body tissues
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| Causes of CHF | *High BP *Irregular heart beat
*Heart valve disease
*Cardiomyopathy *
Congenital heart defects
*Alcohol/drug use
*Previous heart attacks
*Coronary heart disease
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| Symptoms of CHF | *Fatigue, weakness, swelling, edema of lung tissue, shortness of breath
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| Continuous Capillaries | *endothelial cells joined by tight junctions-->maybe interrupted in some places by intercellular clefts
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| Fenestrated Capillaries | *Like continuous cap. BUT endothelial cells have pores (fenestrations) covered by thin membranes-->more PERMEABLE than continuous cap.
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| Sinusoids | *Leaky Cap. w/ large lumens & usually fenestrated *few tight jxns + intercellular clefts
*Found: liver, bone marrow, lymphoid tissues, + some endocrine organs
*Examples: spleen/liver sinusoids lined with macrophages = Kupffer Cells
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| Arteriosclerosis | *Hardening/loss of elasticity of medium/large arteries
*Cause: aging, hypertension, diabetes, smoking, hereditary factors, elevated cholesterol
*Smooth muscle cells/collagen fibers migrate-->tunica MEDIA
*Lumen-->narrowed
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| Atherosclerosis | *Thickening of artery wall due to accumulation of fatty materials (cholesterol)
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| Varicose Veins | *Damage to one or more valves in VEIN -->swollen, twisted veins due to abnormal collection of blood
*Venous distention/pooling of blood-->become tangible/palpable/tortuous--> surrounding tissue may become--edematous
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| Aneurysm | *Localized dilation/outpouching of blood vessel or cardiac chamber
*Arterial walls= weakened, may rupture
*Common sites: ab. aorta, renal arteries, cerebral arteries
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| Phlebitis | *Inflammation of vein usually due to infection or trauma
* May lead to pooled blood & edema
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| Thrombophlebitis | *Inflammation of a vein associated with a blood clot
*Redness, heat, swelling, pain in affected area--> clot may break off= embolus that blocks smaller vessels
*Examples: occur after using intravenous line or trauma to vein
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| Blood Flow | *Volume of blood following thru a vessel/organ/circulation in a given time pd.
*Flow=cardiac output
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| Blood Flow Equation | (Pressure in Arteries-Pressure in Veins) / Resistance
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| Mean Arterial Pressure | *Blood pressure changes in elastic arteries (high systolic pressure, lower diastolic pressure)
*Diastolic pressure + (Pulse Pressure/ 3)
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| Blood Pressure | *Force per unit area exerted on a vessel wall by blood
*Pressure diff. drives--> BLOOD FLOW
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| Pulse Pressure | *The difference btw. systolic & diastolic pressure
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| Resistance | *Opposition to blood flow
*Opposition to blood flow
*Systemic resistance= peripheral resistance
*3 Factors
1: Blood Vessel Length
2. Viscosity
3. Vessel Radius
***RADIUS=BIGGEST DETERMINANT
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| Resistance Formula | (Length x Viscosity) / radius^4
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| Systolic Arterial Pressure | *Pressure in artery @ PEAK of ventricular SYSTOLE *about 120 mmHg
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| Pulse Pressure Factors | *Pressure in artery @ END of ventricular DIASTOLE
*Blood= moving from elastic arteries--> smaller vessels
*Recoil of arterial wall
*about 80 mmHg
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| Capillary Pressure | 1. Dispensability of Artery: how well artery can expand to receive SV 2
2. Amount of SV
*Strongest in arteries closest to heart + can be felt in any elastic artery positioned close to surface of bone and over firm tissue
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| Venous Pressure | *Venous return= enhanced by respiratory movements and external pressure of contracting skeletal muscle
*Normally 0-20 mmHg
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| MAP | MAP= CO x R
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| Short-Term Controls of Bl. Volume & Resistance | *Negative feedback
1. Vasomotor Center
2. Vasomotor Tone
3. Baroreceptors
4. Chemoreceptors
5.Higher brain centers
6. Chemicals + Hormones
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| Vasomotor Center | *Sympathetic neurons in medulla oblongata that control resistance by stimulating vasoconstriction *works w/ cardiac center
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| Vasomotor Tone | *State of partial arteriolar constriction that helps to maintain normal MAP
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| Baroreceptors | *Blood pressure receptors in carotid sinuses + aortic arch
*Activated by increased MAP
* THINK BS-Barorecepoors in bodies
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| Chemoreceptors | *Receptors (carotid + aortic bodies) in aortic arch + carotid sinuses that monitor blood pH, plasma O2, and CO2 concentrations
*THINK CB-chemo in bodies
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| Higher Brain Centers | The cerebral cortex + hypothalamus can modify mean arterial pressure by acting thru medulla oblongata
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| Velocity | *Inversely related to Total Cross Sectional Area of blood vessels
* Velocity= 1/ total cross sectional area
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| Autoregulation | *automatic adjustment of blood flow to tissues based on their changing needs
*Controlled by:
1. Local, NOT systemic factors (CO, Volume factors)
2. Altered by change in Arteriolar Diameter a & O
opening/closing precapillary sphincters
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| Autoregulation Mechanisms | 1. Myogenic Controls
2. Metabolic Controls
3. Angiogenisis (LT controls)
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| Myogenic Controls | *Reduced Arteriolar PressureArteriolar Dilation
*Increased Arteriolar PressureArteriolar Constriction
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| Metabolic Controls | *Elevated MRarteriolar dilation & relaxation precapillary sphincters (blood flow increased)
*Reduced MR arteriolar constriction & contraction of precapillary sphincters (blood flow decreased)
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| Reactive Hyperemia | *Increased tissue blood flow in response to a period of ischemia
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| Active Hyperemia | *Increased tissue blood in response to elevated MR
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| Vasomotion | *the intermittent, slow flow of blood thru capillaries based on the opening/closing of precapillary sphincters
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| Angiogenesis | *growth of new blood vessels into an area
*stimulated by periods of hypoxia, or by growth factors, interleukins or colony stimulating factors (CSF’s)
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| Hydrostatic Pressure (HP) | *Pressure exerted by a fluid in an enclosed space
*Amount of pressure depends on amt. of fluid & size of space
*Filtration OUT= HP
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| Osmotic Pressure (OP) | * the “pulling pressure” that a hypertonic solution exerts on a hypotonic solution
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| Hydrostatic Capillary Pressure (HPc) | *pressure that blood exerts on wall of capillary
*Tends to favor fluid OUT of cap…diff. pressures on arterial vs. venous ends
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| Hydrostatic Fluid Reabsorption (HPif) | *Hydrostatic pressure f interstitial fluid, ranges from slightly negative-slightly positive (0)
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| Capillary Osmotic Pressure (OPc) | *Presence of large, nondiffusable proteins in blood plasma exerts osmotic pressure on tissue fluid
*favors reabsorption
*26 mmHg
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| Interstitial Fluid Osmotic Pressure (OPif) | *Proteins in the interstitial fluid exert osmotic pressure on the plasma
*Pulls things out, doesn’t change unless disease present
*1 mmHg
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| Net Filtration Pressure (NFP) | Net Pressure Out- Net Pressure In
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| Functions of Lymphatic System | 1. Return protein w/ fluid interstitial fluid back to blood
2. Transport fat & fat soluble vitamins (D,A,K,E) from GIblood
3. Protect and defend body
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| Lymph | *fluid that enters lymph cap. from interstitial fluid
*similar to blood plasma with LESS PROTEIN
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| Lymph Capillary | *Collects lymph from interstitial spaces and deliver to lymphatics
*Made of: single layer of overlapping endothelial cells..NO basement membrane ..creates valve to allow lymph in not out
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| Lymphatic Collecting Vessels | *Afferent: deliver lymph to lymph node
*Efferent: carries lymph away from lymph node
*Counterintuitive
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| Lymphocytes | *arise in red bone marrow then migrate to other tissues to become immunocompetent
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| B-Lymphocytes | *produce antibody secreting plasma cells
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| T-Lymphocytes | *fight antigens directly and regulate the immune response
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| Macrophages | Phagocytize foreign antigens and help to activate T-cells
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| Dendritic cells | *Antigen presenting cells found in mucosal membranes and in the skin
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| Reticular Cells | Connective tissue cells that produce reticular fibers for the stroma that supports other lymphoid cells in lymphoid organs
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| Lymphoid Tissue | *Made of network of reticular fibers (STROMA) + lymphoid cells (macrophages + lymphocytes)
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| Diffuse Lymphatic Tissue | Small areas of unencapsulated lymphatic tissue found in most organs + lamina propria of mucous membranes
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| Lymphoid Follicles | *Greater density of fibers than diffuse lymphatic tissue
* Lymph nodules: Peyer’s patches + appendix
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| Mechanisms of Lymph Movement | 1. Contraction of skeletal muscles (near lymph. Vessels)
2. Pressure changes during ventilation
3. Presence of valves
4. Pulsations f large elastic arteries adj. to lymphatic vessels
5. Contraction of smooth muscle in walls of lym. Ducts/trunks
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| Lymph Nodes | *Macrophages filter lymph + activate immune cells
*Nodes scattered w/in connective tissue, assoc. w/ lymph. Vessels
*Cluster in some areas (intuitive: inguinal, cervical, axxilary, mediastinal, mesenteric, etc.)
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| Spleen | 1. Lymphocytes production
2. Fetal RBC production
3. Stores plateletls
4. Contains macrophagesdegrade RBCS + platelets
5. Stores iron
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| Spleen Pulps | 1. White Pulp: lymphocytes attached to reticular fibers
2. Red Pulp: remaining tissue: venous sinuses & splenic cords (macrophages)
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| Thymus Gland | * Thymic cells secrete Thymopoitin + thymosisntrigger differentiaon of lymphocytes into immunocomeptent T lymphocytes
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| Tonsils | • Gather and remove pathogens from tissue fluid
• Palentine, Lingual (tongue), Pharyngeal
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| Peyer’s Patches | *Consists of nodules w/ germinal centers surrounded by lymphocytes
*Located in intestinal wall
* remove pathogens from absorbed material + site of antibody production
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| Non-Specific Systems (Innate) | *Response Time: immediate
* Targets: effective against range of targets
*Examples: Barriers (skin, mucous membranes), chemical systems like salt in tears/lysosomes in saliva, cells (phag., NK)
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| Specific Systems (Adaptive) | *Response Time: some delay
*Targets: selective, adaptive response to each target
*Examples: B + T lymphocytes, Antigen Presenting Cells
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| Non-Specific Resistance | *Intact skin: 30-50 rows of stratified keratinized squamous epithelium, pH3-5
*NA+ +Cl- in sweat
*Skin secretions: lysozymes and fatty acids
*Normal flora
*Mucous Membranes: acidic, may have cilia etc.
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| Phagocytes | *Macrophages (monocytes), neutrophils, eosinophils, mast cells
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| Mechanisms of Phagocytosis |
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| Other Phagocytosis Mechanisms |
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| For Phagocytosis to Occur: |
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| Natural Killer Cells |
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| Perforins |
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| Granzyme B |
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| Antimicrobial Proteins |
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| Interferons |
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| Complement |
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| Activation of Complements |
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| Mechanism of Complements |
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| Onsonizaton |
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| C Reactive Protein |
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| Inflammation |
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| Symptoms of Inflammation |
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| Mechanism of Inflammation |
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| Vascular Changes |
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| Vasodilation |
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| Increased Capillary Permeability |
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| Pain |
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| Phagocyte Mobilization |
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| Remember COLI |
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| Diapedesis/ chemotaxis |
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| Immune Response Characteristics |
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| Two types of Cell Immunity |
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| Humoral Immunity |
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| Cell-Mediated Immunity |
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| PLAN-OP |
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| Neutralization |
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| Agglutination |
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| Precipiation |
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| Cells of Adaptive Immune Responses |
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| APCs |
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| B Lymphocytes |
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| T Lymphocytes |
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| Immunogens (Antigens) |
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| Incomplete Antigen (Hapten) |
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| Antigenic Determinant (Epitopes) |
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| Major Histocompatibility Antigens |
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| MHC Class 1 Antigens |
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| MHC Class II Antigens |
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| MHC 1 Class Antigens can be Stimulated By: |
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| Autoimmunity |
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| Self Tolerance |
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| Loss of Immunologic Tolerance |
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| Immunodeficiency |
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