Human Physiology Test 3 Study Guide
Human Physiology Test 3 Study Guide BIOL 3160
Popular in Human Physiology
Popular in Biological Sciences
80887 - BIOL 3150 - 001
verified elite notetaker
This 41 page Study Guide was uploaded by MBattito on Monday March 28, 2016. The Study Guide belongs to BIOL 3160 at Clemson University taught by Dr. Tamara McNutt-Scott in Fall 2015. Since its upload, it has received 120 views. For similar materials see Human Physiology in Biological Sciences at Clemson University.
Reviews for Human Physiology Test 3 Study Guide
Great notes!!! Thanks so much for doing this...
Report this Material
What is Karma?
Karma is the currency of StudySoup.
You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!
Date Created: 03/28/16
Human Physiology Test 3 Study Guide Chapter 12: Mechanisms of Contraction and Neural Control • Ability to use chemical energy to produce force and movement is present to a limited extend in most cells o In muscle cells it has become dominant • Force generation and movement by muscle can be used in a variety of ways in the human body o Movement within external environment (skeletal muscle) o Regulate internal environment (smooth muscle) o Speech o Drawing a picture o Twiddling your thumbs o Typing these notes • As long as you have a contractile protein, you an have movement of the cell Structure of Skeletal Muscle • Origin: attachment to immovable bone • Insertion: attachment to moveable bone o Insertion moves toward origin when contracted • Epimysium: outer sheath formed by fibrous connective tissue fibers within tendon extending around muscle • Fascicles: subdivisions of the muscle body formed by the epimysium extending into it o Perimysium: connective tissue sheath surrounding each fascicle o Myo-‐fibers: muscle fibers that each fascicle is composed of o Sarcolemma: plasma membrane surrounding the myo-‐fibers o Endomysium: thin connective tissue layer enveloping the sarcolemma of each myo-‐fiber § Basement membrane – or basal lamina • Connective tissue of tendons, epimysium, perimysium and endomysium are all continuous à therefore muscle fibers do not normally pull out of the tendon when contracted • Fascia: connective tissue between major organs • Skeletal muscle fibers are multinucleate • Most distinctive feature if their striated appearance produced by alternating dark and light bands o A bands: dark bands o I bands: light bands § Z lines: thin dark lines seen in the middle of the I bands • Myofilaments make up myofibrils à myofibrils makes up muscle fibers (surrounded by endomysium and sarcolemma) à muscle fibers make up fascicles (surrounded by perimysium) à fascicles make up muscle (surrounded my epimysium) Motor End Plate and Motor Unit • Motor end plate: specialized region of the sarcolemma of the muscle fiber at the neuromuscular junction o Motor neuron stimulates the muscle fiber to contract by liberating acetylcholine at the junction • End plate potential: depolarization at the motor end plate that causes action potential o Depolarization of a motor axon terminal causes exocytosis of ACh into the synaptic cleft à bind to several thousand nicotinic ACh receptors on the motor end plate à binding causes ACh receptor ion channels to open à end plate potential • Motor unit: each somatic motor neuron with all of the muscle fibers that it innervates • Graded contractions: varied number of motor units activated o Activated by rapid, asynchronous contractions for smooth, sustained contraction • Smaller motor unit allows for a finer control of skeletal muscle contraction • Smaller motor unit are activated first and stimulated by lower level excitatory input than larger motor units o Smaller motor units are used most often o Recruitment: process of activating larger and larger motor units à used when contractions of greater strength of required • Two processes occur when you gradually increase the force of a muscle contraction: o Motor units involved are stimulated asynchronously at a greater frequency à summation of contractions o Recruitment of additional larger motor units § Can occur at the same time § Increase the force of contraction Mechanisms of Contraction • Cross bridges between thick and thin filaments cause sliding of the filaments – thus muscle tension and shortening o Activity of the cross bridges is regulated by calcium availability o Availability of calcium is increased by action potentials produced by the sarcolemma • Myofibrils: subunits that compose each muscle cell o ~1 micrometer in diameter o Extend in parallel rows o So densely packed that other organelles are restricted to the narrow cytoplasmic spaces between adjacent myofibrils • Dark A and light I bands are seen within each myofibril and stacked vertically from one side of the muscle fiber to the other o Individual myofibrils are not visible with an ordinary light microscope à entire muscle fiber seems to be striated • Myofilaments: small structures contained in each myofibril o A bands: thick filament § Primarily composed of myosin § H band in the center § M line in the center of the H band o I bands: thin filament § Primarily composed of actin § Z-‐lines in the center of each I band o I bands overlap A bands at the edges – causes outside of A band to appear darker § H bands: the center lighter region of A bands that contains only thick filament • Sarcomere: smallest contractile unit of muscle o Subunits from Z line to Z line o M line in the center of the sarcomere is produced by protein filaments at the center of the thick filament § Serve to anchor the thick filaments so they stay together during contraction o Titin: largest protein in the human body § Each protein has its terminal end in a Z disc – spring-‐like portion running through the I band and a longer portion bound to the M line § The spring-‐like portion is highly folded and unfolds when the sarcomere is stretched § Contributes to their elastic recoil à allows muscle to return to resting length when relaxed • Contraction: refers to the activation of force–generating sites within muscle fibers Sliding Filament Theory of Contraction 1. A myofiber with its myofibrils shortens by movement of the insertion toward the origin of the muscle 2. Shortening of the myofibrils is caused by shortening of the sarcomeres 3. Shortening of the sarcomeres is accomplished by sliding of the myofilaments – the length of each myofilament remains constant 4. Sliding of the filaments is produced by asynchronous power strokes of myosin cross bridges, which pull the thin filaments (actin) over the thick filaments (myosin) 5. The A bands remain the same length during contraction, but are pulled toward the origin of the muscle 6. Adjacent A bands are pulled closer together as the I bands between them shorten 7. The H bands shorten during contraction as the thin filaments on the sides of the sarcomeres are pulled toward the middle Interaction between thin and thick filament • Cross bridges are part of the myosin proteins that extend from the axis of the thick filaments to form “arms” that terminate in globular “heads” • Myosin has 2 globular heads that serve as cross bridges on either side o Each head is oriented opposite of each other so when actin is attached on either side it can pill the actin from each side toward the center • Each myosin head contains an ATP-‐binding site closely associated with an actin-‐binding site o Each head functions as a myosin ATPase enzyme o ATP must be split into ADP and P before the myosin heads can bind to actin o The position of the myosin head changes and now has the potential energy required for a contraction • Once the myosin head forms a cross bridge with actin, myosin is dephosphorylated o Causes a conformational change and the cross bridge produces a power stroke – the force that pulls the thi filament toward the center of the A band • After the power stroke, ADP is released and a new ATP is attached so myosin can detach from actin • The cycle will repeat itself to reach required overall contraction • During contraction, only a portion of cross bridges are attached at any given time – thus, power strokes are not in synchrony • Force produced by each power stroke is constant, but when the muscle’s load is greater, the number of cross bridges engaged in power strokes is increased to generate more force Regulation of Contraction: • Regulation of cross bridge attachment to actin is a function of 2 regulatory molecules associated with the thin filament o Tropomyosin: lies within groove between G-‐actin monomers § Covers binding site for myosin in relaxed muscle o Troponin: 3 protein complex: § TnT: binds to tropomyosin § TnI: inhibits the binding of cross bridges to actin § TnC: binds calcium § Responsible for moving tropomyosin – requires interaction of troponin with calcium • F-‐actin: actin filament that is a polymer formed of 300-‐400 G-‐actin subunits arranged in a double row and twisted into a helix • Troponin and tropomyosin work together to regulate attachment of cross-‐ bridges to actin o Serve as a “switch for muscle contraction/relaxation – Calcium is what initiates contraction • Calcium binds to troponin – troponin moves tropomyosin – tropomyosin allows myosin to bind to actin Role of Calcium in Muscle Contraction • In a relaxed muscle calcium concentration in the sarcoplasm is very low o Sarcoplasm: cytoplasm of muscle cell • When a muscle cells is stimulated to contract, calcium concentrations quickly rise in the sarcoplasm o Some of the calcium binds to the troponin causing a conformational change that moves it and tropomyosin out of the way à allows actin to bind to the cross bridge • Calcium is the go signal for contracting – highly regulated • Calcium is only released when a signal is given through a neuromuscular junction • Other reasons to keep calcium levels low: o Signal transduction o Promotes the breakdown of glycogen within the muscle cell so there is glucose for ATP o Calcium and phosphate form crystals that make your bone too hard • Calcium is tightly regulated – observe regulation by 2 intracellular proteins: o Calsequestrin within the sarcoplasmic reticulum o Calmodulin within sarcoplasm Excitation-‐Contraction Coupling: • Muscle contraction begins when sufficient intracellular calcium levels are reached • Relaxation is produced by active calcium transport out of sarcoplasm and into the sarcoplasmic reticulum o Sarcoplasmic reticulum: modified endoplasmic reticulum consisting of interconnected sacs and tubes that surround each myofibril within the muscle cell • Terminal cisternae: expanded portions of the sarcoplasmic reticulum where most of the calcium is stored in relaxed muscle fibers • Calcium release channels (Ryanodine receptor): membrane channels from the sarcoplasmic reticulum into the sarcoplasm o 10x larger than voltage-‐gated Ca2+ channels permitting a very high rate of calcium diffusion • Transverse tubules (T tubules): narrow membranous tunnels formed from and continuous with sarcolemma o Open to the extracellular environment through pores in the cell surface and are able to conduct action potentials • Skeletal muscle fibers are electrically activated by the release of ACh from axon terminals at the motor end plate • End plate potentials are produced and generate action potentials • T tubules contain voltage-‐gated calcium channels (DHP receptors) o Respond to membrane polarization • DHP receptors change shape when T tubules conduct action potentials à direct coupling between these channels on the T tubules and the calcium release channels in the sarcoplasmic reticulum o The channels on the T tubules directly causes the calcium release channels to open à releases calcium into cytoplasm and stimulating contraction • Excitation-‐contraction coupling: process by which action potentials cause contractions o Electromechanical release mechanism: excitation-‐contraction coupling mechanism in skeletal muscle § Voltage gated calcium channels are the calcium release channels are physically (mechanically) coupled § DHP is voltage gated § Ryanodine is mechanically gated • Calcium induced calcium release channels: calcium release channels on the membrane of the sarcoplasmic reticulum that open in response to a rise in calcium concentration in the cytoplasm o Most calcium that is released is from these channels • To stop cross-‐bridge cycle, the production of action potentials must cease o SERCA pumps: sarcoplasmic/endoplasmic reticulum calcium ATPase pumps § Active transport pumps that accumulate calcium so that it is sequestered from the cytoplasm § Prevents calcium from binding to troponin – tropomyosin blocks actin binding site § Requires ATP • Two absolutes you must have for contraction: o Calcium o ATP – not only needed for contraction, but also relaxation in the form of making sure the pumps are running Mechanics of Skeletal Muscle • Skeletal contractions typically produce bone movement at joints, which act as levers to move load against which the muscle tension is exerted o Tension: the force exerted on an object (the load) by the contracting muscle o Load and tension are opposing forces o Load > tension = no movement § Isometric contraction (constant length) – does not mean there is no tension being generated; the cells are still contracting just not sliding o Tension > load = movement § Isotonic contraction (constant tension) • Concentric • Eccentric: lengthening • Series-‐elastic component: during contraction, non-‐contractile parts of muscle and connective tissue of tendon are being pulled – have elasticity – when distending force released, then “spring back” to resting lengths • Absorb some of the tension as muscle contractions Muscle Twitch: • Mechanical response of a muscle to a single action potential/electrical stimulus • Muscle contractions are graded responses o In general, muscle contraction can be grades in 2 ways § Changing the strength of the stimulus • Threshold stimulus: weakest stimulation at which motor unit is stimulated to contract • Maximal stimulus: strongest stimulus to recruit all motor units to contract § Changing frequency of stimulation • Latent period: time it takes for the action potential to go from the motor neuron to activate the dhp and get contraction started • Period of contraction: when actin and myosin are interacting with each other • Period of relaxation: point where calcium is being taken off – vacuuming up extra calcium Incomplete and Complete Tetanus: nd • If 2 identical stimuli are delivered to a muscle in rapid succession, the 2 twitch will be stronger than the first à wave summation o Occurs because subsequently induced contractions occur before muscle can relax à summing the contractions • With increasingly faster rate of stimulation, muscle relaxation is shorter and increases calcium – leading to incomplete tetanus • When a “fusion frequency” of stimulation is reached with no visible relaxation between successive twitches complete tetanus is attained Treppe: • Warming up period à make the muscles ready to work • Staircase pattern observed when muscle fibers first stimulated to contract o Stimulus strength constant • Due to: o Increasing amounts of calcium available in sarcoplasm o Heat generated from muscle work increases enzyme efficiency in muscle o Muscle more pliable • Seen in a muscle that is warming up Force-‐Velocity Curve: • Lighter objects are moved faster than heavier objects o Inverse relationship between force opposing muscle contraction and velocity of muscle shortening o Lighter object: steep slope o Heavier object: less steep slope • What does this curve represent physiologically? o Actin and myosin interactions cause muscles to move – the shortening velocity is determined by the rate of the cross-‐bridges undergoing their cycling activity • As we increase the load and add resistance, the velocity shortening takes longer à as load increases, velocity decreases Length-‐Tension Relationship • Muscle contraction strength can be influenced by a variety of factors o Fiber numbers activated, stimulus frequency, muscle fiber thickness, length of muscle fiber at rest • An “ideal” resting length for striated muscle fibers that results in maximum force generation • Force generation about how actin and myosin interact with each other o Force is actually generated between the sliding within the sarcomere – the more distance you have to slide, the more strength that you can generate • Muscle stretched across a joint is always set at their optimal length – where they can generate the most force Energy Requirements for Skeletal Muscle: • Skeletal muscle cannot store ATP, so it must have metabolic mechanisms in place to meet demand once contractile activity begins • Metabolism of Skeletal Muscle: o Skeletal muscles metabolize anaerobically for the first 45-‐90 seconds of moderate to heavy exercise o Aerobic respiration contributes the major portion of the skeletal muscle energy requirements following the first 2 minutes of exercise • Oxygen is important for ATP generation in a working muscle • Observe maximal capacity for aerobic exercise in an individual – dependent on the maximum rate of oxygen consumption by the body à maximal oxygen uptake or aerobic capacity • Lactate threshold: also defines intensity of exercise o Percentage of the maximal oxygen uptake at which a significant rise in blood lactate levels occurs • Oxygen Debt: o Includes oxygen that was withdrawn from savings deposits – hemoglobin in blood and myoglobin in muscle – the extra oxygen required for metabolism by tissues warmed during exercise, and the oxygen needed for the metabolism of the lactic acid produced during anaerobic metabolism o Repaid by the heavy breathing following exercise • Skeletal muscle has 3 options – it can use creatine phosphate, glycolysis or oxidative phosphorylation o Oxidative phosphorylation gets a lot more ATP à best option Muscle Fatigue: • Defined as any exercise-‐induced reduction in the ability of muscle to generate force/power (reversible) o Observe increase in extracellular potassium concentration during maximal contraction o Reduces membrane potential, thus interferes with ability to generate action potentials • Causes (due to exercise type): o Depleting of muscle glycogen o Reduced ability of sarcoplasmic reticulum to release calcium o “Others” – increase in phosphate, decrease in ATP • In humans, fatigue is experienced before muscles fatigue o Central fatigue: muscle fatigue caused by changes in the central nervous system rather than by fatigue of the muscles themselves § Don’t want to be completely unable to move a muscle • Muscle fatigue has 2 major components: o Peripheral component: fatigue in the muscles themselves o Central component: fatigue in the CNS that causes reduced activation of muscles by motorneurons Types of Skeletal Muscle Fibers: • Skeletal muscle is classified on the basis of contraction speed o Fiber types: § Slow-‐twitch (type I fibers): suited for prolonged contractions • Red fibers § Intermediate fibers § Fast-‐twitch (type II fibers): suited for rapid, intense movements • Fatigue quickly • White fibers • Fibers differ in mechanical and metabolic characteristics • Human muscles are a mixture of fiber types o Gives muscle a range of contraction speed, varying resistance levels to fatigue and performance • Muscles are a mixture of all muscle fiber types o All muscles associated with one motor unit are the same type • Want slow and fast twitch – not intermediate à mixture helps with muscle having a range of contraction speeds • Number of muscle fibers you have generally determines how many fast and slow twitches • Resistance to fatigue: o Slow twitch: § High resistance § Use aerobic respiration § Found in long distance runners o Fast twitch § Low resistance § Use anaerobic – use up the source much quicker § Larger diameter § Found in sprinters Muscle Damage and Repair • Observe resident stem cells in skeletal muscle o Satellite cells: § “Leftover” from embryological development § Located outside muscle fibers o Permits some degree of repair and regeneration • Ability declines with age o Sarcopenia: loss of muscle tissue as a normal part of the aging process • Myostatin: transforming growth factor – Beta family, also know as GDF-‐8 o Paracrine regulator inhibits satellite cells and muscle growth (myokine) o May be used therapeutically to treat muscle wasting diseases (muscular dystrophy for example) Neural control of skeletal muscle and reflexes: • Muscle tone: state of tension in resting muscle • Gamma motor neuron activity maintained to keep muscle spindle under proper tension • Two type of muscle o Extrafusal: § muscle fiber innervated by an alpha motor neuron o Intrafusal: muscle in muscle spindle § Innervated by a gamma motor neuron § Only contracts on the ends § Has sensory neuron wrapped around it • You contract the ends of the muscle spindle so you can use gamma motor neuron activity to maintain the proper tension à alpha-‐gamma co-‐activation o So sensory neuron can register the degree of stretch/tension of muscle fiber • Reciprocal innervation: cause one set of muscles to contract and the other set to relax • When muscle spindle is stretched, have antagonistic muscle contractions • Withdraw reflex: synapse onto a variety of elements Cardiac Muscle • Striated, short branched muscle fibers • Electrically coupled via gap junctions in the intercalated disc o Electrical impulse conducted along axis from cell to cell o Functional syncytium: behave as a single functional unit o Contract to fullest extent • Pacemaker cells o Spontaneously depolarize o Set contractile rate o Modified by autonomic innervation • Excitation-‐contraction coupling o Calcium induced calcium release § Different from skeletal muscle – no “direct” interaction between T tubules and sarcoplasmic reticulum § Slower process • Striated = sarcomeres are present • Have voltage gated sodium and potassium channels on sarcolemma • Down T tubules – have voltage gated calcium channels – no direct interaction between T tubule and sarcoplasmic reticulum à slower process • First need to open voltage gated calcium channels—calcium flows to activate Ca release channels on sarcoplasmic reticulum – sodium flows out to move troponin, which moves myosin o Calcium ATPase pump stops as calcium levels fall Smooth Muscle • Non-‐striated o No sarcomeres but actin and myosin are present § Thin filaments are long § Dense bodies • Sites of attachment for thin filaments • Connected by intermediate filaments § Thick filaments vertically stacked § Sliding can occur along entire length of thin filament • Advantage to arrangement and ability to slide whole length of thin filament? o Gives the ability to contract even when greatly stretched • Sarcoplasmic reticulum is less development in smooth muscle and only accounts fro beginning phase of contraction • No T-‐Tubules • Extracellular fluid calcium enters via voltage gates channels and provides calcium for contraction o Ca binds to calmodulin à Ca-‐Calmodulin complex activates MLCK à MLCK phosphorylates myosin so we can now contract o Contraction responds in a graded manner § Greater depolarization, greater Ca channels open = greater contraction • To relax, still have Ca ATPase transport pumps found in sarcoplasmic reticulum and on plasma membrane that run continuously o Get rid of calcium and inactive MLCK and enzyme myosin phosphatase (dephosphorylates myosin) • Latch state: slow and sustained contractions o Allows smooth muscle to maintain contraction without using a lot of ATP to it can keep the contraction Chapter 13: Blood, Heart and Circulation • Circulatory System o Functional term o Prefer the use of cardiovascular system • Blood o Function divided into 3 broad areas: § Transportation – moving oxygen and wastes, hormones, clotting factors, etc. § Regulation – body temperature for example § Protection – antibodies Composition of Blood: • Blood is the only fluid tissue of the human body • Arterial Blood: blood leaving the heart o Bright red because of high oxyhemoglobin concentration • Venous Blood: blood returning to the heart o Darker red because of less oxygen • Plasma: fluid portion o Liquid of water and dissolved solutes, plus varied organic molecules à sodium makes up the largest percentage o 55% of blood composition • Cellular component: (Table 13.2) o Suspended in plasma o 45% of blood composition o Platelets: also called thrombocytes § Smallest of formed elements that are actually fragments of large cells found in bone marrow § Lack nuclei but are capable of movement through the capillaries § Survive for 5-‐9 days before being destroyed by liver and spleen § Important in blood clotting § Release serotonin (causes vasoconstriction) and growth factors (maintain integrity of blood vessel) o Erythrocyte § Function to transport oxygen and carbon dioxide § Lack nuclei and mitochondria § Circulating life span of about 120 days § Contain 280 million hemoglobin à give blood its red color • Hemoglobin molecule = 4 globin protein chains bound to one heme molecule – the iron group in heme is able to combine with oxygen in the lungs an release it in the tissues § Transferrin: protein that carries iron in the blood tot the bone marrow § The iron is recycled from old red blood cells by phagocytes in the liver and spleen o Leukocyte: § Different from erythrocytes because they have nuclei and mitochondria and can move through capillary walls • Diapedesis or Extravasation: movement of leukocytes through capillary walls to reach sites of infection • Aids in defense against infections by microorganisms § Granulocytes: survive 12 hours-‐3 days • Neutrophils: o 2-‐5 lobes o 54-‐62% of WBC o Phagocytic • Eosinophil: o Bilobed o 1-‐3% of WBC o Detoxify foreign substances, secrete enzymes that dissolve clots, fight parasitic infection • Basophil: o >1% of WBC o Release anticoagulant heparin § Agranulocytes: Survive 100-‐300 days • Monocytes: o 3-‐9% of WBC o phagocytic • Lymphocytes: o Nucleus nearly fits cell o 25-‐33% of WBC o provides specific immune response (includes antibodies) Hematopoiesis • Occurs in red bone barrow • Influence by cytokines and other regulatory molecules o Thrombopoietin and erythropoietin regulate the pathway of what the stem cells produce • Hemacytoblast: pluripotent hematopoietic stem cell o Forms lymphoid stem cell à produces lymphocyte o Forms myeloid stem cellà forms erythropoietin and interleukins, CSFs § Erythropoietin produces erythrocytes, neutrophil and monocyte § Interleukins produce eosinophil, basophil and megakaryocyte Erythrocytes: Red Blood Cells • Supply of iron, vitamin B12 and folic acid needed for proper red blood cell production • Regulated by EPO o Produced by kidney o Looks at oxygen carrying capacity (oxygen level) – if oxygen level is too low à makes more erythrocytes • Lover, spleen and bone marrow remove aged cells, recycle iron and globin • Erythropoiesis is a very active process – requires iron and myoglobin • Ferroportin channels in enterocytes – regulate iron concentration levels • Transferrin (plasma protein) in plasma • Role of HEPCIDIN (poly peptide hormone produced by the liver) o Promotes cellular storage of iron and lower blood iron concentration, does so by working through Ferroportin channels • Blood type result of distinguishing antigens displayed on cell surface o Genetically determined o Immune system exhibits tolerance to body’s red blood cells • Longevity ~ 120 days Blood Clotting: • Homeostasis: cessation of bleeding • Effective in dealing with injury to small vessels but little help for middle to large vessels • Observe 3 separate but overlapping homeostatic mechanisms o Vascular spasm o Formation of platelet plug o Clot forming Vascular Phase: • Function: close off vessels, reduce blood loss and allow time for other processes to stop bleeding in larger vessels • Vasocontrictive event: immediate response to injury o Occurs in smooth muscle of vessel walls – inherent in smooth muscle itself • Vascular spasm: occurs in vascular wall o Makes the lumen smaller by contracting to reduce blood flow/loss and gives time for other process Platelet Phase: • Platelet Plug: o Positive feedback event o Organizes for blood clot formation o Platelets activate clotting factors o Temporary fix – must be stabilized • Platelets repelled from each other and endothelium • Prostacyclins/Prostaglandins and NO – vasodilators and inhibit platelet aggregation • CD39: enzyme that breaks down ADP à promotes platelet aggregation • Degranulate • Platelet release reaction o Exposure of collagen and VWF activate platelets o More platelets activated and recruited Coagulation Phase: • Blood Clot – initiating the process of transforming blood from a liquid to a gel • Represents the transformation of blood from a liquid to a gel that results in the formation of a clot • Conversion of fibrinogen (soluble plasma protein) into fibrin (insoluble fibrous protein) o Fibrin stabilizes the clot Clotting Pathways • Extrinsic Pathway: o Chemical released by damaged tissue – tissue thromboplastin o Activator tissue factor activates VII à activates X à activates common pathway § VII complex: VII, tissue factor, calcium, phospholipids à require calcium and phospholipids from platelets • Intrinsic Pathway o Contact pathway: initiated by negatively charged structures – collagen, phosphates and NETS o Initial activation factors activate XII à activates XI à activates IX (forms VIII complex)à activates X à activates common pathway § VIII complex: VII, activated IX, calcium and phospholipids from platelets) • Common Pathway o Activate factor 10: Stewart Brower factor o Activated X forms V complex § V complex: V, X activated, calcium and phospholipids (from platelets) o Activate factor 10 activates thrombin from prothrombin à thrombin activates fibrinogen into fibrin which is polymerized by factor XIII à blood clot is formed • Intrinsic is slower than Extrinsic • Many clotting factors are synthesized in the liver o Deficiency of vitamin K can lead to clotting problems and dysfunction in the liver • Clot retraction: contraction within platelet mass to form more compact and effective plug – serum (plasma-‐lacking clotting factor) • Vitamin K: important in the synthesis of the clotting factor produced in the liver o Problems in people that take a lot of antibiotics because it kills the bacteria hat provides vitamin K à leads to problems in clotting Clot Dissolution • Plasminogen activators turns plasminogen into plasmin à produces soluble fibrin fragments from fibrin (breaks down some of the clot) o Kallikrein: main plasminogen activator in humans – tears down the clot • 3 mechanisms that oppose clot formation: o Tissue factor pathway inhibitor – TFPI § From endothelium; blocks clotting o Thrombomodulin: § Receptor for thrombin – becomes inactive upon binding protein C (natural anticoagulant) activator o Antithrombin III: § Inactivates thrombin and other clotting factors • Function: limit clot formation so that the clot does not get too large – does not completely inhibit • Balance between clot formation and elements that are depressing the clotting process Circulation Circuits and the Heart: • Pulmonary: out of the right side of the heart à lungs à drop CO2 and add O2 à back to the left side of the heart through the aorta • Systematic: pick up CO2 out of the left side of the heart and brings oxygen to the tissues • Equal blood flow in circuits – prevents fluid accumulation in lungs and oxygenated blood delivery to the body • Side-‐by-‐side pumps: right and left side feed different circulatory circuit o Right side serves pulmonary circuit o Left side serves systematic circuit o In general: blood flows from right side of heart à lungs à left side à body tissue à back to right side (constant cycle) o More resistance in the systematic circuit so the wall of the left ventricle is thicker than the right • Valves: direct blood flow in the heart o Atrioventricular valves: direct blood from the atria to the ventricles § Valves between atria and ventricles • Tricuspid valve: has 3 flaps on the right side of the heart • Bicuspid valve: has 2 flaps on the left side o Semilunar valves: direct flow from atria to aorta or pulmonary trunk but do not allow backflow from the ventricles to the atria § Allow blood from the heart out to the circulation circuits – oppose blood back into the heart from circuits § Located at the origin of the pulmonary artery and aorta • Fibrous Skeleton: layer of dense connective tissue found between the atria and the ventricles o Serves as an attachment site for the myocardium of the ventricles o Structurally and functionally separates the atria from the ventricles o Provides support for the valves Cardiac Cycle • Repeating pattern of the contraction and relaxation of the heart o Systole: contraction phase § Isovolumetric contraction phase and ejection phase o Diastole: relaxation phase § Isovolumetric relaxation phase, rapid filling phase and atrial contraction phase o Diastole and systole partitioned differently – diastole is longer • Occurs in both the atria and the ventricles • Ventricles are power pumps – generate force to push blood through circuits • Atria primary job is to fill up ventricles • Isovolumetric contraction: all valves are c
Are you sure you want to buy this material for
You're already Subscribed!
Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'