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27 Cards in this Set
- Front
- Back
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Describe muscle structure and filaments
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Each muscle is multinucleate and behaves as single unit. It contains bundles of MYOFIBRILS, surrounded by SR and invaginated by T TUBULES
Each myofibril contains interdigitating THIN and THICK filaments arranged longitudinally in SARCOMERES Sarcomere runs from Z line to Z line |
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Thick filaments
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-present in A band in center of sarcomere
-contain MYOSIN -myosin has 6 polypeptide chains including one pair of HEAVY chains and two pairs of LIGHT chains -each myosin has two heads attached to single tail. Myosin heads bind actin and ATP, and are involved in cross bridge formation |
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Thin filaments
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-anchored at Z lines
-present in I bands -interdigitate with thick filaments in portion of A band -contain ACTIN, TROPOMYOSIN, TROPONIN |
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Troponin
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-regulatory protein that permits cross bridge formation when it binds Ca
-complex of 3 globular proteins |
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3 globular proteins of troponin
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Troponin T - attaches troponin complex to tropomyosin
Troponin I inhibits interaction of actin and myosin Troponin C - Ca binding protein, permits interaction of actin and myosin |
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T tubules
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-extensive tubular network, open to extracellular space, that carry depolarization from sarcolemmal membrane to cell interior
-located at junction of A and I bands -contain voltage sensitive protein |
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SR
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-internal tubular structure
-STORAGE SITE OF Ca -has TERMINAL CISTERNAE which are in contact with T tubules in triad arrangement -membrane contains Ca ATPase (pump) which transports Ca from intracellular fluid to SR interior,, keeping intracellular Ca low |
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This initiates depolarization of T tubules
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AP in cell membrane
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Describe excitation contraction coupling
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1. Action potential depolarizes T tubules
2. Depolarization of T tubules is sensed and causes conformational change, which opens Ca channels in SR, which causes release of Ca into intracellular fluid 3.Intracellular Ca increases 4.Ca binds to troponin C on thin filaments causing conformational change in troponin that moves tropomyosin out of the way allowing interaction of myosin and actin |
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Describe cross bridge cycle
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1. At first no ATP is bound to myosin, and myosin is tightly attached to actin. In rapidly contracting muscle this stage is brief. In absense of ATP, this stage is permanent (rigor mortis)
2.ATP then binds to myosin, which causes conformational change in myosin and myosin is released from actin 3.Myosin is displaced towards plus end of actin. There is hydrolysis of ATP to ADP and Pi. ADP is attached to myosin. 4.Myosin attaches to new site on actin which constitutes power generating stroke. ADP is then released returning myosin to rigor state 5. Cycle repeats as long as Ca is bound to troponin C, each cross bridge cycle "walks" myosin further along actin |
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Relaxation of muscle occurs when
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Ca is reaccumulated by SR Ca ATPase. Intracellular Ca decreases, Ca is released from troponin C and tropomyosin again blocks myosin-binding place on actin. As long as intracellular Ca is low, cross bridging can not occur
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Mechanism of tetanus
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A single action potential causes relase of standard amount of Ca from SR and produces single twitch. Of muscle is stimulated repeatedly, more Ca is released from SR and there is cumulative increase of Ca, extending time for cross bridge cycling. Muscle does not relax - tetanus
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Excitation contraction coupling in smooth muscle
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There is NO TROPONIN, instead Ca regulates myosin on thick filaments
Depolarization of cell membrane opens voltage gated Ca channels and Ca flows into cell down its electrochemical gradient, increasing intracellular Ca. Ca that enters cell causes release of additional Ca from SR. 3. Intraceelular Ca increases 4.Ca binds to CALMODULIN, this complex binds to and activates MYOSIN LIGHT CHAIN KINASE. When activated myosin light chain kinase PHOSPHORYLATES MYOSIN and allows it to binds actin. Contraction then occurs. 5. Decrease in intracellular Ca produces relaxation |
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Cardiac output of left heart equals
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cardiac output of right heart
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Cardiac output from left side is
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systemic blood flow
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Cardiac output from right side is
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pulmonary blood flow
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Direction of blood flow
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1. From lungs to left atrium via pulmonary veins
2.From left atrium to left ventricle through mitral valve 3.From left ventricle to aorta through aortic valve 4.From aorta to systemic arteries and systemic tissues 5. From tissues to systemic veins and vena cava 6.From vena cava to right atrium 7.From right atrium to right ventricle through tricuspid valve 8. From right ventricle to pulmonary artery 9.From pulmonary artery to lungs for oxygenation |
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P wave
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-represents atrial depolarization
-does not include atrial repolarization which is burid in QRS complex |
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PR interval
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interval from beginning of P wave to beginning of Q wave (initial depolarization of ventricle)
-varies with conduction velocity of AV node -decreased by stimulation of sympathetic nervous system (AV conduction velocity increased) |
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QRS complex
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depolarization of ventricles
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Qt interval
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entire period of depolarization and repolarization of ventricles
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ST segment
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Isoelectric
depolarization of ventricles |
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T wave
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Ventricular repolarization
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Resting membrane potential is determined by
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Conductance to K and is close to K equilibrium potential
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Inward current brings
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Depolarization
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Outward current brings
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Hyperpolarization
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Describe phases of AP in atria, ventricles and Purkinje fibers
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1. Phase 0 - UPSTROKE of AP, caused by transient increase in Na conductance, results in inward Na current that depolarizes membrane
Phase 1 - brief period of initial repolarization, caused by outward current, in part because of movement of K ions and in part because of decrease in Na conductance Phase 2 - PLATEAU phase, caused by transient increase in Ca conductance which results in inward Ca current and by increase in K conductance Phase 3 - repolarization, high K conductance Phase 4 - resting membrane potential, inward and outward currents are equal |
