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BIO 204 Exam 2
Cadiac Output, Blood Pressure Topic 2-3
| Question | Answer |
|---|---|
| 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 |
| 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 |
| 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 |
| Cardiac Output | *Volume of blood ejected by each ventricle per MINUTE *SV x HR *@ rest 5 L/min. |
| Stroke volume | *Volume of blood ejected by each ventricle per BEAT *about 70 ml/beat *Diff. btw EDV and ESV |
| Heart Rate | *# of times the heart beats/min. *ave. cardiac cycles/min. * about 75/min. |
| Cardiac Reserve | *difference btw resting and maximal cardiac output |
| End Diastolic Volume | *Volume of blood that fills a ventricle during diastole *about 120 ml. |
| End Systolic Volume | *Volume of blood remaining in a ventricle after systole *about 50 ml. |
| SV | SV= EDV-ESV |
| SV Factors | 1. Preload 2. Contractility 3. Afterload |
| Remember | Diastole= heart FILLING + Systole= heart EMPTYING |
| Ejection Fraction | *Volume ejected * SV/EDV *average 70%, >50%= cardiac failure could occur, athletes=up to 90% |
| Preload | *degree to which cardiac muscle fibers are stretched prior to contraction |
| Frank-Starling Law of Cardiac Muscle | *If cardiac muscle sarcomeres are stretched w/in limits—> contract more forcibly *Recall length-tension relationship |
| 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 |
| Contractility | *any change in muscle contractile strength=independent of EDV & sarcomere length |
| Positive Ionotropic Effects | *Increase Contractility 1. Autonomic Nerv. Sys.: SNS (Fight-or-Flight) 2. Chemicals: Epinephrine, Norepineprhine, Excess Ca2+, Glucagon, Thyroxine, Digitalis |
| 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) |
| Afterload | *Pressure that ventricles must overcome to eject blood into arteries *> arterial pressure= harder for ventricles to eject blood—> reduced SV |
| 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 |
| 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 |
| Congestive Heart Failure | heart's weak pumping action causes a buildup of fluid called congestion in lungs and other body tissues |
| Causes of CHF | *High BP *Irregular heart beat *Heart valve disease *Cardiomyopathy * Congenital heart defects *Alcohol/drug use *Previous heart attacks *Coronary heart disease |
| Symptoms of CHF | *Fatigue, weakness, swelling, edema of lung tissue, shortness of breath |
| Continuous Capillaries | *endothelial cells joined by tight junctions-->maybe interrupted in some places by intercellular clefts |
| Fenestrated Capillaries | *Like continuous cap. BUT endothelial cells have pores (fenestrations) covered by thin membranes-->more PERMEABLE than continuous cap. |
| 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 |
| 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 |
| Atherosclerosis | *Thickening of artery wall due to accumulation of fatty materials (cholesterol) |
| 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 |
| Aneurysm | *Localized dilation/outpouching of blood vessel or cardiac chamber *Arterial walls= weakened, may rupture *Common sites: ab. aorta, renal arteries, cerebral arteries |
| Phlebitis | *Inflammation of vein usually due to infection or trauma * May lead to pooled blood & edema |
| 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 |
| Blood Flow | *Volume of blood following thru a vessel/organ/circulation in a given time pd. *Flow=cardiac output |
| Blood Flow Equation | (Pressure in Arteries-Pressure in Veins) / Resistance |
| Mean Arterial Pressure | *Blood pressure changes in elastic arteries (high systolic pressure, lower diastolic pressure) *Diastolic pressure + (Pulse Pressure/ 3) |
| Blood Pressure | *Force per unit area exerted on a vessel wall by blood *Pressure diff. drives--> BLOOD FLOW |
| Pulse Pressure | *The difference btw. systolic & diastolic pressure |
| 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 |
| Resistance Formula | (Length x Viscosity) / radius^4 |
| Systolic Arterial Pressure | *Pressure in artery @ PEAK of ventricular SYSTOLE *about 120 mmHg |
| Pulse Pressure Factors | *Pressure in artery @ END of ventricular DIASTOLE *Blood= moving from elastic arteries--> smaller vessels *Recoil of arterial wall *about 80 mmHg |
| 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 |
| Venous Pressure | *Venous return= enhanced by respiratory movements and external pressure of contracting skeletal muscle *Normally 0-20 mmHg |
| MAP | MAP= CO x R |
| 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 |
| Vasomotor Center | *Sympathetic neurons in medulla oblongata that control resistance by stimulating vasoconstriction *works w/ cardiac center |
| Vasomotor Tone | *State of partial arteriolar constriction that helps to maintain normal MAP |
| Baroreceptors | *Blood pressure receptors in carotid sinuses + aortic arch *Activated by increased MAP * THINK BS-Barorecepoors in bodies |
| Chemoreceptors | *Receptors (carotid + aortic bodies) in aortic arch + carotid sinuses that monitor blood pH, plasma O2, and CO2 concentrations *THINK CB-chemo in bodies |
| Higher Brain Centers | The cerebral cortex + hypothalamus can modify mean arterial pressure by acting thru medulla oblongata |
| Velocity | *Inversely related to Total Cross Sectional Area of blood vessels * Velocity= 1/ total cross sectional area |
| 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 |
| Autoregulation Mechanisms | 1. Myogenic Controls 2. Metabolic Controls 3. Angiogenisis (LT controls) |
| Myogenic Controls | *Reduced Arteriolar PressureArteriolar Dilation *Increased Arteriolar PressureArteriolar Constriction |
| Metabolic Controls | *Elevated MRarteriolar dilation & relaxation precapillary sphincters (blood flow increased) *Reduced MR arteriolar constriction & contraction of precapillary sphincters (blood flow decreased) |
| Reactive Hyperemia | *Increased tissue blood flow in response to a period of ischemia |
| Active Hyperemia | *Increased tissue blood in response to elevated MR |
| Vasomotion | *the intermittent, slow flow of blood thru capillaries based on the opening/closing of precapillary sphincters |
| 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) |
| 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 |
| Osmotic Pressure (OP) | * the “pulling pressure” that a hypertonic solution exerts on a hypotonic solution |
| 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 |
| Hydrostatic Fluid Reabsorption (HPif) | *Hydrostatic pressure f interstitial fluid, ranges from slightly negative-slightly positive (0) |
| Capillary Osmotic Pressure (OPc) | *Presence of large, nondiffusable proteins in blood plasma exerts osmotic pressure on tissue fluid *favors reabsorption *26 mmHg |
| 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 |
| Net Filtration Pressure (NFP) | Net Pressure Out- Net Pressure In |
| 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 |
| Lymph | *fluid that enters lymph cap. from interstitial fluid *similar to blood plasma with LESS PROTEIN |
| 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 |
| Lymphatic Collecting Vessels | *Afferent: deliver lymph to lymph node *Efferent: carries lymph away from lymph node *Counterintuitive |
| Lymphocytes | *arise in red bone marrow then migrate to other tissues to become immunocompetent |
| B-Lymphocytes | *produce antibody secreting plasma cells |
| T-Lymphocytes | *fight antigens directly and regulate the immune response |
| Macrophages | Phagocytize foreign antigens and help to activate T-cells |
| Dendritic cells | *Antigen presenting cells found in mucosal membranes and in the skin |
| Reticular Cells | Connective tissue cells that produce reticular fibers for the stroma that supports other lymphoid cells in lymphoid organs |
| Lymphoid Tissue | *Made of network of reticular fibers (STROMA) + lymphoid cells (macrophages + lymphocytes) |
| Diffuse Lymphatic Tissue | Small areas of unencapsulated lymphatic tissue found in most organs + lamina propria of mucous membranes |
| Lymphoid Follicles | *Greater density of fibers than diffuse lymphatic tissue * Lymph nodules: Peyer’s patches + appendix |
| 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 |
| 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.) |
| Spleen | 1. Lymphocytes production 2. Fetal RBC production 3. Stores plateletls 4. Contains macrophagesdegrade RBCS + platelets 5. Stores iron |
| Spleen Pulps | 1. White Pulp: lymphocytes attached to reticular fibers 2. Red Pulp: remaining tissue: venous sinuses & splenic cords (macrophages) |
| Thymus Gland | * Thymic cells secrete Thymopoitin + thymosisntrigger differentiaon of lymphocytes into immunocomeptent T lymphocytes |
| Tonsils | • Gather and remove pathogens from tissue fluid • Palentine, Lingual (tongue), Pharyngeal |
| 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 |
| 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) |
| Specific Systems (Adaptive) | *Response Time: some delay *Targets: selective, adaptive response to each target *Examples: B + T lymphocytes, Antigen Presenting Cells |
| 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. |
| Phagocytes | *Macrophages (monocytes), neutrophils, eosinophils, mast cells |
| Mechanisms of Phagocytosis | |
| Other Phagocytosis Mechanisms | |
| For Phagocytosis to Occur: | |
| Natural Killer Cells | |
| Perforins | |
| Granzyme B | |
| Antimicrobial Proteins | |
| Interferons | |
| Complement | |
| Activation of Complements | |
| Mechanism of Complements | |
| Onsonizaton | |
| C Reactive Protein | |
| Inflammation | |
| Symptoms of Inflammation | |
| Mechanism of Inflammation | |
| Vascular Changes | |
| Vasodilation | |
| Increased Capillary Permeability | |
| Pain | |
| Phagocyte Mobilization | |
| Remember COLI | |
| Diapedesis/ chemotaxis | |
| Immune Response Characteristics | |
| Two types of Cell Immunity | |
| Humoral Immunity | |
| Cell-Mediated Immunity | |
| PLAN-OP | |
| Neutralization | |
| Agglutination | |
| Precipiation | |
| Cells of Adaptive Immune Responses | |
| APCs | |
| B Lymphocytes | |
| T Lymphocytes | |
| Immunogens (Antigens) | |
| Incomplete Antigen (Hapten) | |
| Antigenic Determinant (Epitopes) | |
| Major Histocompatibility Antigens | |
| MHC Class 1 Antigens | |
| MHC Class II Antigens | |
| MHC 1 Class Antigens can be Stimulated By: | |
| Autoimmunity | |
| Self Tolerance | |
| Loss of Immunologic Tolerance | |
| Immunodeficiency |
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