Kaplanphysiomuscle.txt

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Author:
arimoses
ID:
118790
Filename:
Kaplanphysiomuscle.txt
Updated:
2011-11-24 11:19:14
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Kaplan Physiology
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Description:
Striated and Cardiac muscle
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  1. A myofibril is a part of, is comprised by?
    • Muscle fiber
    • Sarcomeres.
  2. Sarcomeres are made of, demarked by?
    • Myosin: Thick Filaments
    • Actin: Thin filaments
    • Z lines.
  3. How does contraction change the sarcomeres?
    • No change in A band (length of myosin filament)
    • Shortening of I band (end of one myosin to end of other myosin(of next sarcomere))
    • Shortening of H zone (end of one actin to the other(within same sarcomere)).
  4. Where is most Ca stored in muscle?
    Terminal Cisternae of Sarcoplasmic reticulum, near the T-tubular system.
  5. What proteins make up the thin filaments?
    • Actin: structural component, contains attachements for cross-bridges
    • Tropomyosin: covers attachement sites, moves to allow cross-bridging
    • Troponin: binds calcium to move troponin-tropomyosin complex.
  6. What three subunits make up troponin?
    • Troponin-T: binds tropomyosin
    • Troponin-I: Inhibits myosin binding to actin
    • Troponin-C: binds calcium.
  7. When is contraction terminated?
    When Ca is removed from troponin.
  8. What protein makes up the thick filaments?
    • Myosin
    • Possesses cross bridges, which have ATPase activity.
  9. What causes dissociation of the cross bridge?
    Binding of ATP.
  10. Cross-bridge cycling will continue until?
    • Withdrawal of Ca: normal resting muscle
    • Depletion of ATP: Rigor Mortis.
  11. Which two ATPases are involved in contraction?
    • Myosin ATPase: energy for mechanical contraction
    • SERCA: Sarcoplasmic endoplasmic reticulum calcium-dependent ATPase - provides energy for termination of contraction by pumping Ca back into depot.
  12. How is tetanus reached?
    There is sufficient free Ca for continuous cycling of all cross-bridges.
  13. What is summation?
    • Increased frequency of APs --> increased Ca released --> increased magnitude of response
    • Possible because of very short refractory period.
  14. What are the two types of tension on a muscle?
    • Passive: Preload
    • Active: contraction.
  15. Preload on a muscle increases what?
    • Stretch
    • Passive tension.
  16. What does the magnitude of developed active tension depend on?
    Number of cross-bridges that cycle.
  17. What are the characteristics of white muscle?
    • Large mass, short term use
    • High ATPase activity (fast)
    • High capacity for anaerobic glycolysis
    • Low myoglobin.
  18. What are the characteristics of red muscle?
    • Small mass, long term use
    • Low ATPase activity (slow)
    • High capacity for aerobic metabolism (mitochondria)
    • High myoglobin (red color).
  19. What are the two direct indices of ventricular preload?
    • LVEDV: Left ventricular end-diastolic volume
    • LVEDP: Left ventricular end-diastolic pressure.
  20. What are the three indirect indices of ventricular preload?
    • Left Atrial pressure
    • Pulmonary Venous pressure
    • Pulmonary capillary wedge pressure (swan-ganz).
  21. Acute changes in contractility are usually due to?
    Changes in intracellular dynamics of Calcium.
  22. Increased sympathetic activity to the heart will produce?
    • Decreased systolic interval: contractility effect
    • Decreased diastolic interval: heart rate effect.
  23. What would result in a loss in preload?
    Hemorrhage.
  24. Loss in contractility?
    CHF.
  25. Increase of contractility?
    • Excersise
    • Increased sympahtetics.
  26. Increase of preload?
    Volume loading.
  27. What determines Cardiac Output (CO), venous or arterial parameters?
    Venous parameters.
  28. Stroke Volume (SV)=?
    SV= EDV-ESV.
  29. Ejection Fraction (EF)=?
    EF= SV/EDV.
  30. Cardiac Output (CO)=?
    CO= SV x HR.
  31. what is systolic dysfunction?
    Abnormal reduction in ventricular emptying (increased afterload).
  32. What is diastolic dysfunction?
    Abnormal ventricular filling (stiffened ventricular wall s/p MI).
  33. What is, causes concentric hypertrophy?
    • Chronic pressure overload
    • Dramatic Increase in wall thickness, decrease in chamber diameter
    • Consequence: decreased ventricular compliance -> diastolic dysfunction, eventually systolic dysfunction.
  34. What is, causes eccentric hypertrophy?
    • Chronic Volume overload (eg. MR, AR, PDA)
    • Modest increse in wall thickness, no change in chamber diameter
    • Consequence: systolic dysfunction -- compliance of ventricle uncompromised.
  35. What are the three types of cardiomyopathies?
    • Dilated: Dilation without compensation in wall thickness
    • Restrictive: Decreased ventricular compliance
    • Hypertrophic: most common assymmetric hypertrophy of septum.

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