Samenvatting Casussen voor The downhill slope

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Samenvatting - Casussen voor The downhill slope

  • 4.1 Structure of heart muscle

  • What are the three types of cardiac muscles that make up the heart?
    Atrial muscle
    Ventricular muscle
    - both the above muscle will contract in the same way that the normal skeletal muscle cells contract, except the duration of the contraction is longer. 
    Excitatory (contractile) and conductive muscle fibres- are involved in the normal heart beat
    -      the conductive muscle fibres are responsible for controlling and coordinating the heart beat
    - the contractile muscle fibres are responsible for causing the contraction that will propel the blood through the heart.
  • What is the difference between the contraction of the atrial, ventricular and the conductive muscle fibres?
    The atrial and ventricular muscle fibres contract similarly to the skeletal muscle cells, except that they do so for longer. 
    The conductive and contractile muscle fibres contract feebly, as they only have a few muscle fibres, however their main role is to produce action potential, or allow the conduction of the action potentials that will stimulate the heart to beat.
  • What are the contractile muscle fibres of the heart?
    Cardiomyocytes
  • What are the intercalated discs within the cardiomyocytes?
    The dark bands shown in histology slides. 
    The are the membranes that separate one cardiomyocyte from another. Therefore, cardiac muscle fibres are made up of a series of cardiomyocytes that are connected together and run parallel to each other.
  • How can the excitation of a single cardiomyocyte lead to all cardiomyocytes that make up a cardiac muscle fibre to contract simultaneously?
    The intercalated disks are the points in where one cardiomyocyte has fused with another. The cells have fused in such a way that they have formed gap junctions and desomosomes. These structures allow the passage of free ions through from one cell to another- one action potential can travel from one cardiomyocyte to another through these gap junctions.
  • What is a syncytium?
    A multinucleated cell that results from the fusion of many unicellular cells- the cardiac muscle fibres are syncytium- as they are formed due to the fusion of multiple cardiomyocytes.
  • What is the structure of a gap junction?
    Made up of 6 elements called connexins that contain a hollow tube that allow for the passage of ions. 
    Span the 2-4nm intracellular gap between fused cells.
    Allow simultaneous excitation of the cells.
  • What is the structure of the desmosomes?
    -provide structural attachment- filled with glycoproteins called cadherins
    - made up of desmin filaments
    - span the wider intracellular gaps- that are too wide for the gap junctions.
  • What is the essential contractile unit of a cardiomyocyte?
    Sarcomere- sarcomeres extend down the cardiomyocye. They are responsible for the striated appearance that is characteristic of a cardiomyocyte cell.
  • What is a t-tubule and what is its function?
    Extensions of sarcomeres deep into the cell. They allow for the conduction of the signal into deeper layers of the heart muscle, despite the fact that the signal is mainly contracted along the surface of the external membrane.
  • 4.2 Action potentials in cardiac muscle

  • What is the process that regulates the concentration of Ca2+?
    Excitation-contraction coupling
  • What are the different phases in the action potential of the cardiac muscle?
    phase 0: rapid depolarisation- influx of Na+ ions
    phase 1: initial repolarisation- K+ switch on and off- allows some K+ to enter exit cell. 
    phase 2: plateau- normal refractory period- Efflux of K+ and influx of Ca2+ through slow opening channels.
    The plateau phase is different for different cells of the heart e.g. the cells of the SAN do not contain a plateau phase. 
    phase 3: slow repolarisation
    phase 4: return to normal resting potential- Ca2+ close and intracellular Ca2+ pumped out of cell. K+ ion channels open. Efflux of K+ leads to return of the membrane potential.
  • What happens during excitation-contraction coupling?
    - Action potential passes through the T-Tubules. 
    - Causes the L-type calcium channels (LTCC) on the membrane of the t-tubules to open and allow the influx of calcium channels - channels are slow opening.
    - Influx of ca2+ cause the intracellular concentration of Ca2+ to increase. Lead to the opening of the ryanodine receptor (RyR)  on the membrane of the SR- leads to the release of ca2+ from the SR into the cell.
    - Peak ca2+ cause muscle contraction= bind to the troponin complex of actin (bind to TnC- changes conformation of TnI- exposes the myosin binding site of actin- leads to contraction).
  • What is the important of the ca2+ that enter through the t-tubules?
    Without this extra influx of ca2+, the contraction of the cardiac muscle would be weak
  • What is the importance of the concentration of the Ca2+ ?
    The concentration of the ca2+ will determine the strength of the contraction of the cardiac muscle cell. 
    The concentration is dependent on the concentration of ca2+ in the extracellular fluid- because the t-tubules open into the extracellular spaces that surround the cardiomyocyte.
  • How is Ca2+ pumped out of the cell?
    - SERCA ATPase and associated PLB protein (on SR)
    - PMCA and NCX (on cell membrane)
  • How is the action potential affected after an MI?
    - Remodelling of the gap junctions- dysregulated cadherins in the infarcted tissue
    - T-tubules number decrease following an MI
  • How is the action potential affected in a patient who has congenital heart failure?
    The intracellular concentration of ca2+ decreases- does not peak as high as it should. Additionally, it takes longer for the membrane potential to return to normal.
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Laatst toegevoegde flashcards

What is the difference between compensated heart failure and decompensated heart failure?
compensated heart failure: when the cardiac output increases to the point where the kidneys output returns to normal= fluid retention decreases. 
decompensated heart failure: when the cardiac output is not enough for the kidneys excrete fluid= oedema and enlargement of the heart- complete heart failure.
What happens to the cardiac reserve after an acute heart failure?
The cardiac reserve decreases- this means that as long as the person remains in a rested state, their cardiac output has returned to normal. If they exercise, their heart may not have recovered enough to increase the cardiac output to cope with the extra demands, and so they may suffer from another attack.
What happens to the renal output when the cardiac output returns to normal?
Renal output returns to normal and so there is no more fluid retention- the fluid retention remains from before.
What are the consequences of severe fluid retention?
- severe fluid retention without appropriate intervention can have an effect on the excretion of salt and water by the kidneys. the excess fluid volume can:
 1. cause excessive muscle hypertrophy of the heart- enlarged heart can affect the conductance of signals therefore affecting heart beat.
 2. increased workload can get too much for the heart
 3. increased right atrial pressure can lead to pulmonary oedemas, which can affect gas exchange and can reduce the amount of oxygen in the blood.
4. excessive oedemas can form systemically.
How can fluid retention of the kidneys increase cardiac output?
Fluid retention can increase cardiac output by:
- increasing the mean systemic filling pressure, so that venous return increases and more blood flows into the right atrium.
- distends the veins so that venous resistance can decrease.
What happens after the first few minutes of an acute heart attack?
Prolonged semichronic state:
 - retention of fluid in the kidneys:
- a low cardiac output will affect the ability of the kidneys to produce urine- fluid retention can lead to a low urine output/
What happens during acute heart failure?
Cardiac output and venous return temporarily decrease.
Sympathetic activity counteracts this by activating beta1-adrenergic receptors.
Sympathetic activity will also increase arterial resistance= increasing mean systemic filling pressure=increases venous return= increases cardiac output.
Therefore, the hypoeffectiveness of the heart during acute heart failure is short lived.
What does the test show?
Small amounts of troponin I and T may be normally present in the blood stream- but in very small quantities. Following damage to the heart, they are released into the blood stream, where they can be detected. 
 
Released within 3-4 hours of damage and can remain in the blood stream for 10-14 days.
What is the troponin T-test?
Muscle fibres contain troponin- C, I and T. 
Skeletal troponin is different from cardiac troponin. 
When there is damage to the heart, e.g. heart attack, troponin I and T are released into the blood stream.
How does increase blood volume affect the cardiac output?
Increases- increased blood volume will increase the systemic filling pressure= increases atrial pressure= increases the venous return= increases the cardiac output.
 
Eventually, the cardiac output returns to normal:

1. blood volume returns to normal- increase in blood volume increases the capillary pressure- leads to fluid leaking out
2. increase in blood volume= distends the veins and decreases the resistance
3. autoregulation will cause the venous return to come back to normal