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Samenvatting van alle colleges - MG: Circulatory Tract (WBFA040-05)
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  • MG: Circulatory Tract (WBFA04005)
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  • Rijksuniversiteit Groningen (RuG)

Summary of all MG circulatory tract courses (WBFA040-05) at the University of Groningen. All medications you need to learn before the exam are marked in red in the summary, making them easier to learn!!

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  • September 14, 2024
  • 41
  • 2023/2024
  • Summary

Subjects

  • circulatory tract

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  • Rijksuniversiteit Groningen (RuG)
  • Farmacie
  • MG: Circulatory Tract (WBFA04005)
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MG: Circulatory Tract
Lecture 1: The cardiovascular system

Heart  arteries (oxygenated blood)  capillaries (exchange)  veins (deoxygenated blood) 
heart.

Heart Anatomy
- Inferior vena cava and superior vena cava brings deoxygenated blood into right atrium 
right to ventricle  pulmonary artery  lungs.
- Heart (and veins) has valves prevent blood flowing back.

Diastole  relaxes and fills with blood.
Systole  atria and ventricles contract.

Coronary artery system
- Supplies the heart itself with blood.
- Coronary flow  heart has a large metabolic need, however one of the most poorly perfused
tissue in the body.
- Coronary flow only occurs during diastole.

Heart rhythm cycle
1. Late diastole  relaxed heart, valves are open, atrium and ventricle can fill. Valve towards
pulmonary artery is closed.
2. Atrial systole  heart starts to contract to transport some blood to ventricles.
3. Isovolumetric ventricular contraction  pressure increases, pushes AV valves closed.
Semilunar valves not open yet, so volume in ventricles stays the same.
4. Ventricular ejection  semilunar valves open and blood goes to aorta and pulmonary artery.
5. Isovolumetric ventricular relaxation.  relaxation so heart can fill with blood again.

Left ventricular pressure
A. Diastole  all valves open, no increase in pressure,
increase in volume.
B. End-diastolic volume (EDV) reached  atria will
contract, little bit more blood in ventricles.
C. Isovolumetric contraction  increase ventricular
pressure, no difference in volume, when pressure is high
enough the valves open where pressure increases but
volume decreses.
D. Ventricular ejection, end-systolic volume (ESV) is
reached  pressure ventricle drops completely, going
back to diastole.

Electrical conduction in the heart (pacemaker cells)
- Most important pacemaker cells are in the sinoatrial (SA) node in the right atrium.
- Pacemaker cells have an unstable membrane potential  they are automatically depolarised
and produce an electrical impulse.
- Cardiomyocytes do the contraction of the heart  have intercalated disks with gap junctions
that guide the pulse over the atria and then ventricles so they contract.
- When SA node is damaged  also pacemaker cells in the atrioventricular (AV) node, bundle
of his and Purkinje fibres.

1

,Action potential of pacemaker cells
The resting potential of pacemaker cells it -60 mV, this will spontaneously move up to -40 mV =
pacemaker potential. This is due to the funny channels  influx of sodium. This leads to the influx of
calcium = the action potential.

Action potential of contractile cells (myocytes)
- Resting potential is -90 mV.
- They are depolarized by neighbour myocytes.
- Potential goes to -70 mV  sodium influx  when at peak, sodium channels close and
calcium and potassium channels open  decrease in potential again.
- Opening of calcium channels makes the repolarisation slow  plateau phase.

Electrical conduction of the heart
SA depolarises  guides its electrical impulse to the AV node (here the impulse delays so that the
atria can contract before the ventricles, so they are empty)  depolarisation moves rapidly to the
apex of the heart  wave spreads upwards from apex  contraction of ventricles.




The main difference between the action potential (AP) of a pacemaker cell and a contractile cell
(cardiomyocyte) is that there is no plateau phase with pacemaker cells.

Heart beat per minute (BPM)  normally around 70 BPM.
SA node normally fires about 100 times a minute, but this is controlled by the sympathetic and
parasympathetic nervous system. When the SA node is damaged, the AV node can take over but the
frequency is slower (40-60) Also the Purkinje fibres can take over, but this is even slower (30-40).

Refractory period
Period that ion channels are inactive, so no new action potential can be generated  no
accumulation. To protect the heart from muscle cramps, only new action potential when contraction
is finished. Heart has a much longer refractory period than the skeletal muscles.

Types of muscle
Different muscle tissues differ in action potential mechanism and contraction mechanism.
- Skeletal muscle cells  large fibres, multinucleated, striated, have sarcomeres, act
independent of one another, fastest contraction speed. Via Na+ entry.
- Cardiac muscle cells  small fibres, uni-nucleated, striated, have sarcomeres, cells
are in contact via intercalated disks and gap junctions. Via Na+ entry.
- Smooth muscle cells  small, uni-nucleated, not striated, not well organised, no
sarcomeres, some are independent some are linked via gap junctions, slowest
contraction speed. Via Ca+ entry.

Skeletal muscle
- Composed of several bundles that are composed of fibres.
- Fibres have a large sarcoplasmic reticulum with calcium needed for contraction.
- Myofibrils are present in the fibres which are composed of sarcomeres.
- In sarcomeres there is interaction between myosin and actin  slide along each other 
contraction.

2

,  Myosin  thick filaments with head and tail.
 Actin  thin filaments which contain
- Tropomyosin is present in actin  prevents interaction myosin head with actin.

Skeletal muscle contraction
- Somatic motor neurons release Ach  binds to nicotinic receptors.
- Resting potential is -70 mV.
- Nicotinic receptors = ligand gated ion channel  Ach binds and channel opens  sodium
(Na+) influx  action potential generated and transported over the muscle via T-tubules 
open the DHP calcium channels which are coupled to RyR (ryanodine receptor-channel)
channels in the SR  calcium release from SR  binds to troponin  calcium-troponin
complex pulls tropomyosin away from actin  inorganic phosphate of myosin head detaches
 actin filaments move towards centre of sarcomere  muscle contraction.

Effect of filament overlap on tension development
- Little overlapping  difficult to generate force.
- No overlapping  cannot generate force.
- Overlapping  good force. Can be enhanced by stretching the system a little bit.


Excitation-contraction coupling smooth muscle cell
1. Calcium enter cell and calcium is released from SR.
2. Calcium binds to calmodulin (CaM).
3. Calcium-CaM complex activated the myosin light chain kinase (MLCK).
4. MLKC phosphorylates light chains in myosin heads and increase
myosin ATP activity. ATP is hydrolysed into ADP and inorganic
phosphate resulting in a weak interaction with actin. When inorganic
phosphate is released we get cocking of the myosin head.
5. Movement of actin  contraction.
Relaxation  inhibition of MLCK or activation MLC phosphatase
(dephosphorylation).




In cardiac muscle cells  Desmosomes cause contraction, gap junctions transmit the signal and T-
tubules are for conduction of the action potential.


Excitation-contraction mechanism cardiac muscle
1. Action potential enters from another cell.
3

, 2. Opening of the L-type voltage gated calcium channels  Ca2+ enters the cell.
3. Calcium induces release of calcium by SR by activation of Ryr receptor.
4. Calcium spark.
5. Create a calcium signal.
6. Calcium binds troponin  same as in skeletal muscle.
Relaxation  calcium unbinds troponin, tropomyosin binds actin again, calcium is transported back
to SR, calcium is pumped out of the cell by Ca2+/Na+ exchanger (NCX antiporter).




Autonomic nervous system
- Sympathetic and parasympathetic.
- They control cardiac muscle, smooth muscle and exocrine/endocrine glands.
- The heart beats on it own because of the pacemaker cells, the nervous system influence the
frequency, force and velocity conductance.

Sympathetic stimulation  increase heart rate
- Together with adrenaline cause depolarization of the autorhythmic cell and speeding up the
depolarization rate  increase in heart rate.
- Causes increase in frequency of action potentials in pacemaker cells. Also increase force by
increase contractile cells.
- E.g. via Gs coupling  adenylyl cyclase  cAMP  PKA  phosphorylate L-type calcium or
MLCK = increase contraction. cAMP can also open ion channels = increase heart rate.
 The heart has beta-1 and beta-2 receptor which are both Gs coupled.

Inotropy  contraction force.
Chronotropy  heart rate.

Parasympathetic stimulation  decrease heart rate
- Hyperpolarizes the membrane potential of the autorhythmic cell and slows down
depolarization  decrease in heart rate.
- Increased potassium permeability and reduced calcium permeability  firing frequency
pacemaker cells decrease.
- Activation by Ach.
- Mainly M2 receptor  Gi coupled  adenylyl cyclase inhibited  less cAMP  less sodium
influx.
 Atropine is a M2 receptor antagonist  increase heart rate.




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