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Physiology > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

0
Q

Does the heart contain valves?

A

Yes

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1
Q

The heart is what kind of pump?

A

dual pump?

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2
Q

How are muscle cells connected in the heart?

A

via gap junctions

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3
Q

What type of cells muscle cells does the conduction system have?

A
  • non contractile muscle cells (SA and AV node)

- contractile muscle cells (myocardium ventricles)

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4
Q

What are these non-contractile muscle cells modified to do?

A

to initiate and distribute impulse throughout the heart

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5
Q

what are the parts of the conduction system?

A
  • sinoatrial node (SA)
  • atrioventricular node (AV)
  • bundle of his (AV bundle)
  • purkinje fibres
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6
Q

Describe the sinoatrial node? (SA) What is it’s rate?

A
  • it’s the pacemaker because it depolarizes faster than other areas which generates AP faster.
  • 100 APs/min which is modified by the Parasympathetic NS to become 75APs/min
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7
Q

Where is the sinoatrial node found?

A

right atrium

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8
Q

where is the atrioventricular node found?

A

right atrium

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9
Q

what is the rate of contraction at the AV node

A

50 APs/min

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10
Q

Describe the the Bundle of His. Where does it originate?

A
  • originates from the AV node
  • it’s the only route of electrical activity to go from the atria to the ventricles and bundle branches on left and right of the heart
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11
Q

Describe the Purkinje fibres. What is the rate of impulse?

A
  • they are terminal fibres which stimulate the ventricles myocardium
  • 30APs/min
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12
Q

Describe the electrical activity in the heart. Use diagram from notes page 1

A
  • did you get it right?
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13
Q

What happens if the SA node is damaged?

A

the next fastest pacemaker takes over which is the AV node

- as a result, the atria might not contract and the ventricles might contract at AV speed which is 50APs/min

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14
Q

what are artificial pacemakers?

A

they are devices which stimulate the the hearts if SA node or AV node are damaged.

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15
Q

Describe the cells in the SA & AV nodes?

A
  • they are non contractile autorhythmic cardiac muscle cells which are self-excitable
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16
Q

What threshold is needed to fire up an AP in SA and AV nodes?

A

-40 mv

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17
Q

Do SA and AV nodes have a resting potential?

A

no

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18
Q

What are the phases of pacemaker activity?

A
  • Pacemaker Potential
  • AP depolarization
  • AP repolarization
  • Na+ channels open at -60mv
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19
Q

Describe the pacemaker potential.

A
  • There is low K+ permeability because K+ voltage gates are closed
  • There is slow inward leak of Na+ because Na+ voltage gates are open
    = which causes slow depolarization towards the threshold (-40mv)
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20
Q

Describe the AP depolarization

A
  • slow inward of leak of Na+ due to open Na+ voltage gates
  • Ca2+ voltage gates open which allows Ca2+ to move in = this causes the depolarization which causes AP
  • during depolarization, the Na2+ voltage gates close
  • Ca2+ voltage gates close at the peak
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21
Q

Are Na+ voltage gates involved in Depolarization?

A
  • no
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22
Q

When do the Ca2+ voltage gates close down?

A

when peak is reached.

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23
Q

describe the AP repolarization

A

at the peak, the K+ voltage gates open to let K+ diffuse out

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24
Q

When do the Na+ voltage gates open up again?

A
  • as soon as -60mv is reached, the Na+ voltage gates open up and pacemaker potential is established once again.
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25
Q

What type of cells are present in the ventricular myocardium?

A
  • contractile cardiac muscle
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26
Q

what is the AP called in the ventricular myocardium?How does it travel?

A
  • Ventricular myocardial AP

- from cell to cell via gap junction

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27
Q

what is the resting membrane potential in the ventricular myocardium?

A

-90mv

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28
Q

What are the phases of ventricular myocardial AP?

A
  • depolarization
  • plateau
  • repolarization
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29
Q

Describe the depolarization phase of ventricular myocardal AP

A
  • the Na+ voltage gates (same gates as neurone, skeletal muscle) open VERY fast
  • This allows +30mv to be reached
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30
Q

Describe the plateau phase of the ventricular myocardial AP?

A
  • Na+ voltage gates begin to close and get inactivated which causes slight drop in membrane potential
  • Ca2+ voltage gates however, open, maintaining the depolarization
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31
Q

What happens during repolarization?

A
  • Ca2+ channels being to close
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32
Q

What is the absolute refractory period of ventricular myocardial AP?

A
  • long inactivation of Na+ voltage gates until MP is close to -70mv
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33
Q

Explain the excitation-contraction coupling in myocardial cells.

A
  • when AP is reached, the Ca2+ voltage gates open which causes increase of cytosolic Ca2+ from the ECF
  • this causes the Ca2+ chemical gates to open in the sarcoplasmic reticulum which increases cytosolic Ca2+ which then binds to the troponin which leads to contraction
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34
Q

What happens in the contraction in myocardial cells?

A
  • the sliding filament mechanism
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35
Q

When does contraction begin and end in contractile myocardial cells

A
  • a few msec after AP begins and ends when AP is over.
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36
Q

What is the duration of AP and twitch?

A
  • about 250 msec

- about 300 msec

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37
Q

Is there summation (which causes tetanus contraction) in cardiac muscles?

A
  • no there is an alternation of contraction and relaxation
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38
Q

The cardiac cycle’s electrical activity can be measured by what?

A
  • Electrocardiogram (ECG)
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39
Q

The small currents due to depolarization and repolarization of the heart move through?

A

salty body fluids

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40
Q

Potential differences on body surface is are measured via?

A

electrodes also known as lead

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41
Q

The recorded waves seen in the electrocardiogram represent what?

A

the sum of all electrical activity of all myocardial cells not an AP

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42
Q

What are the different waves in an ECG?

A
  • P, Q, R, S, T waves
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43
Q

What does the P wave represent?

A
  • atrial depolarization followed by contraction
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44
Q

What does the QRS wave complex represent?

A
  • the ventricle depolarization followed by contraction
  • this is also the atrial reporalization. It’s just masked by larger ventricle electrical event due to larger muscle mass
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45
Q

What does the T wave represent?

A
  • ventricle repolarization followed by relaxation
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46
Q

What does the PQ or the PR ECG interval imply?

A

that the the atria has contracted and signals are passing through the AV node

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47
Q

What does the S-T ECG interval imply?

A
  • the ventricles has contracted and atria is relaxed
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48
Q

What does the T-P ECG interval represent?

A
  • the heart at rest
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49
Q

What is Tachycardia?

A

when resting heart rate is over 100 beats per minute

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50
Q

When resting heart rate is less than 60 beats per minute, what abnormality is this called?

A

Bradycardia

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51
Q

What is a heart block?

A
  • slowed conduction through AV node which increases the P-Q interval
  • ventricles may not contract after atrial contraction.
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52
Q

What is a 3rd degree heart block?

A
  • when there is no conduction at AV node so atria and the ventricles fire at their own will
  • atria fire at SA node rate which is about 75 APs/min and the ventricle fire at the bundle/perkinje rate which is about 30 APs/min
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53
Q

What are two main events of mechanical activity in the cardiac cycle?

A
  • systole

- diastole

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54
Q

What does systole refer to?

A
  • the contraction and emptying
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55
Q

What does the diastole refer to?

A

the relaxation and filling

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56
Q

systole and diastole are initiated by what activity?

A

-electrical activity

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57
Q

In terms of systole and diastole, what is equivalent to one heart beat?

A

systole + diastole of the atria AND systole + diastole of the ventricle

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58
Q

What is the average heart rate?

A

75 beats per minute

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59
Q

1 cardiac cycle is equivalent to how many seconds per beat. How do you calculate this number?

A
  1. 8/beat

- 60sec/beat divided by 75 beats/min

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60
Q

What is happening in the atria within that 0.8second/beat aka 1 cardiac cycle

A

at time 0, atrial contraction occurs so it is in systole for 0.1 sec and 0.7 in diastole

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61
Q

What is happening in the ventricles within 0.8sec/beat or 1 cardiac cycle

A

ventricle enters systole after atria (0.1 sec delay at the AV)

  • ventricle enters systole as soon as atrium enters diastole,
  • ventricles are in systole for 0.3 sec and 0.5 sec in diastole
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62
Q

Blood flow is due to?

A

1) emptying pressure changes (high pressure to low pressure)
2) valves
4) myocardial contraction which increases pressure

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63
Q

Describe the blood flow in the heart. Using diagram on page 5 of the notes.

A

Did you get it right?

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64
Q

What does venous return refer to?

A

blood returns to the heart

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65
Q

during ventricular systole, what causes the atrioventricular valves to close shut

A
  • the higher pressure in the ventricles causes the atrioventricular valves to close shut.
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66
Q

what gives the heart it’s first sound (“LUB” sound)?

A
  • the turbulence of blood after the atrioventricular valves are shut
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67
Q

when does the first heart sound begin?

A

shortly after the QRS waves start during the ventricular systole

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68
Q

what causes the pulmonary semilunar valves to open during ventricular systole

A
  • the higher pressure in ventricles than the pulmonary trunk/aorta
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69
Q

During ventricular diastole, the semilunar valves close shut. What causes this event?

A
  • at this point the pressure in the ventricles decreases

- therefore, the higher pressure in the aorta/pulmonary trunk causes the semilunar valves to close shut

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70
Q

What causes the second heart sound “DUB”? when does this occur?

A
  • the turbulence of blood after semilunar valves close shut.
  • ventricular diastole
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71
Q

At what point do the AV valves open during ventricular diastole?

A
  • when the pressure in the ventricles is lower and we can conclude that the pressure in the atria is higher.
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72
Q

what type of blood flow causes heart sounds?

A
  • turbulent flow
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73
Q

what type of blood flow does not cause heart sounds?

A
  • laminal flow
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74
Q

How does the turbulent flow cause heart sounds?

A
  • it makes noises due to blood turbulence when the valves close shut
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75
Q

What is the korotkoff sounds?

A
  • the turbulence heard in the brachial artery during blood pressure measurement
  • due to cardiac cycle events
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76
Q

In terms korotkoff sounds, what implied the beginning and end?

A
  • beginning = systolic pressure

- end = diastole pressure

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77
Q

What is the cardiac output?

A
  • the volume of blood ejected by each ventricle in 1 min (ml/min)
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78
Q

What is the formula for cardiac output?

A
  • Heart rate (beats/min) x Stroke Volume (mL/beat)
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79
Q

What is the stroke volume?

A
  • the volume of blood ejected by each ventricles within one beat (ml/beat)
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80
Q

What is the formula for stroke volume?

A

End Diastolic Volume (EDV) - End Systolic Volume (ESV)

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81
Q

What is the end diastolic Volume (EDV)

A
  • the volume of blood in each ventricle after ventricle diastole (preload
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82
Q

What is the max volume of blood at EVD?

A

about 120 mL

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83
Q

What is the End Systolic Volume?

A
  • the volume that’s left in each ventricle at the end of systole?
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84
Q

About how much blood volume is left at ESV?

A
  • about 50 mL
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85
Q

What is the ideal Stroke Volume then?

A

SV = EDV - ESV
= 120 - 50
SV = 70 mL

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86
Q

What is the ideal Cardiac output then?

A

CO = Heart rate (75beats/min) x Stroke Volume (70mL/beat)
= 5250 mL/min per ventricle
= 5.25 L/min per ventricle

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87
Q

What is the total blood Volume in the body? What does this say about Cardiac output?

A
  • There is about 5 L of blood volume in our body

- therefore, the total blood volume passes through each ventricle (both circuits) within one minute

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88
Q

During exercise, the Cardiac output can increase to what?

A

5x or more

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89
Q

What does the Cardiac output control?

A
  • Heart Rate

- Stroke Volume

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90
Q

What controls or sets the basic rate of heart rate?

A
  • the SA Node
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91
Q

What is an intrinsic control of the heart ? Give an example

A
  • built in control in heart (originates from the heart)

- the SA node

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92
Q

What is the extrinsic control of the heart? Give an example

A
  • external controls or controls originating outside of the heart
  • these are the heart rate modifiers
  • change in pacemaker potential (AP does not change)
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93
Q

What are the types of extrinsic control?

A

Neural, Hormonal, ions, fever, age, fitness

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94
Q

In terms of neural extrinsic control, how does the Sympathetic nervous system affect the heart rate?

A
  • Under emotional and physical activity, The SNS (thoracic nerves) open up Na+ channels wider at the SA node which increases its permeability. Thus increasing the slope of the pacemaker potential.
  • as a result, threshold is reached faster which increases the heart rate
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95
Q

In terms of neural extrinsic control, how does the parasympathetic nervous system affect the heart rate?

A
  • during resting conditions, the PSNS (vagus nerves) keeps the resting heart rate lower than the pace set by the SA node alone by sending continuous impulses
  • the PSNS (vagus nerves), increases the permeability of K+ at the SA Node, thus allowing a more -ve repolarization
  • as a result, it takes longer for threshold to be reached which decreases heart rate.
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96
Q

In terms of Hormonal extrinsic control, how do epinephrine and norepinephrine affect the heart rate?

A
  • epinephrine and norepinephrine increases the heart rate under SNS
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97
Q

In terms of hormonal extrinsic control, how does thyroid hormone affect hear rate>

A
  • it directly increases heart rate though it’s a slow procedure that takes days
  • it also increases the number of epinephrine receptors which leads to epinephrine sensitivity
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98
Q

In terms of ionic extrinsic control, how does high levels of K+ affect heart rate?

A
  • High levels of K+ ions (meaning not a lot of K+ are leaving) in the ISF can cause a more +ve than normal which causes the Na+ channels from not opening
  • high levels of K+ ions in the ISF can prolong repolarization which causes low heart rate that may lead to cardiac arrest
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99
Q

In terms of ionic extrinsic control, how do low levels of K+ affect heart rate?

A
  • lower levels of K+ than normal in the ISF (means too much K+ are diffusing out) can cause Membrane potential to be too -ve which decreases heart rate
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100
Q

What causes feeble beat, abnormal rhythm?

A
  • low levels of K+ in the ISF
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101
Q

Is the heart rate lower or higher in the presence of fever?

A

Higher

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102
Q

do newborns have lower or higher heart rates?

A

higher

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103
Q

How does fitness affect heart rate?

A
  • Increased fitness = lowers heart rate

- decreased fitness = increases heart rate

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104
Q

How is stroke volume increased in terms of intrinsic control?

A
  • an increased venous return, increases the End Diastolic Volume, which increases the heart stretch, which increases force of contraction (because at rest, cardiac fibres are not in their optimal lengths unlikes skel. muscle)
  • therefore, stretching allows cardiac fibres to reach its optimal length
  • as a result, more cross bridges are form which increases form and in the end, there is an increase of stroke volume within physiological limits
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105
Q

Explain the relationship between the EDV and SV

A
  • we use Frank-Starling’s Law of the Heart
  • it states that the force of ejection is directly proportional to the length of ventricular contractile fibres.
  • stretching the cardiac muscles cells can produce a higher EDV which causes an increase of stroke volume or contraction force
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106
Q

What causes an increase in venous return?

A
  • exercise increases the speed of venous return

- and low heart rate increases the volume of venous return because it has more time to fill up

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107
Q

How does the SNS affect the stroke volume in terms of extrinsic control?

A
  • SNS stimulation increases the opening of Ca2+ channels which increases the Ca2+ movement into the cytosol which forms more crossbridges, increasing the force of contraction, which leads to a higher stroke volume
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108
Q

SNS also increases heart rate which reduces the time of ventricle filling which causes reduced EDV, how can stroke volume still be maintained at a hight heart rate?

A
  • The increased force caused by the SNS, decreases the ESV (it compensates for the decreased EDV)
  • meaning ESV is still going to be lower than EDV which at least maintains the stroke volume in a high heart rate
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109
Q

In terms of extrinsic control, how do hormones such as Epinephrine, norepinephrine and thyroid hormone affect stroke volume?

A
  • Epi and NE increases force under SNS

- Thyroid hormone increases force and number of epi receptors

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110
Q

What other factors increase the force of stroke volume

A

1) digitalis drugs increases Ca2++ inside which increases stroke volume
2) Increase of external Ca2++

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111
Q

What other factors decrease stroke volume?

A
  • acidosis, increase of external K+ and Ca2++ channel blockers like verapamil.
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112
Q

What drugs increase and decrease stroke volume?

A

1) digitalis increase stroke volume

2) verapamil decreases stroke volume

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113
Q

What is blood flow?

A
  • the volume of blood flowing through any tissue per minute (mL/min)
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114
Q

How is blood flow in a vessel determined?

A
  • by change in pressure/resistance
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115
Q

Resistance is defined as?

A
  • friction of blood rubbing against vessel walls

- opposes blood flow

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116
Q

Resistance depends on what factors?

A
  • vessel length
  • blood viscosity
  • radius of arterioles (major resistance vessel)
117
Q

Arterioles which are major resistance vessels are controlled by?

A
  • smooth muscle innervated by the SNS.
118
Q

What is the major resistance vessel?

A

arterioles

119
Q

How does vasodilation affect radius of arterioles?

A

in increases radius which decreases resistance but increases flow

120
Q

How does vasoconstriction affect radius of arterioles?

A
  • it decreases radius, therefore resistance is increases and flow is decreased
121
Q

Blood flow to organs is controlled by?

A

vasoconstriction and vasodilation

122
Q

How does vasoconstriction affect blood flow to organ?

A
  • it reduces radius, therefore increases resistance and decreases blood flow
  • the pressure in the artery is higher (backs up)
  • the pressure in the organ is lower because less blood flows into the organ capillaries
123
Q

How does vasodilation affect blood flow to organs?

A
  • it increases radius which decreases resistance and increases blood flow
  • pressure in the artery is lower
  • pressure in the organ is higher
124
Q

If vasoconstriction/vasodilation is local (ie. one organ) what happens to systemic blood pressure?

A
  • no change
125
Q

If vasoconstriction/vasodilation is systemic, what happens to systemic blood pressure?

A

there will be changes

126
Q

In terms of intrinsic control, what affects vasoconstriction and vasodilation of arteriole radius???

A
  • myogenic regulation

- hormonal regulation

127
Q

How does myogenic regulation, an intrinsic control, affect vasoconstriction and vasodilation of arteriole radius?

A
  • when smooth muscle are stretched they constrict
  • therefore, increase in systemic blood pressure results to vasoconstriction of arterioles
  • decrease in systemic blood pressure results to vasodilation of arterioles
128
Q

What is the myogenic mechanism?

A
  • how the arterioles and arteries react to changes of blood pressure to keep blood flow constant
129
Q

when standing up, what is the state of blood pressure in the feet? How does the blood pressure influence the radius of arterioles and blood flow?

A

blood pressure is high in the feet, this causes vasoconstriction of arterioles which decreases flow to the organ capillaries

130
Q

When standing up, what is the state of blood pressure to the brain? how does this affect the radius of the arterioles and their blood flow?

A
  • blood pressure to the brain is low which causes vasodilation of arterioles which causes increased blood flow to organ capillaries.
131
Q

How does metabolism, an intrinsic control, affect the radius of arterioles?

A
  • low O2, high CO2, low pH = increased metabolism. This causes endothelial cells and hemoglobin to release nitric oxide which causes vasodilation = as a result, blood flow is high towards the organ
  • high O2, low CO2, high pH = decreased metabolism. This causes endothelial cells to releases endothelins which causes vasoconstriction = as a result, there is a decreased blood flow to the organ.
132
Q

Blood gases & pH levels are important to skel muscle, heart and brain. What maintains these?

A

myogenic regulations and metabolic regulations

133
Q

What affects the radius of the arterioles in terms of extrinsic control?

A

SNS of the nervous system and the hormones of the endocrine system

134
Q

How does the SNS, an extrinsic control, affect radius of arterioles

A
  • SNS can trigger vasoconstriction of arterioles except in the brain, that’s an intrinsic control
  • decreased SNS signals can cause vasodilation (PSNS can also cause arteriole vasodilation of penis/clitoris)
  • SNS also causes venoconstriction or vein constriction
135
Q

What causes arteriole vasodilation of penis and clitoris?

A

-PSNS

136
Q

decreased signals of SNS causes what in arterioles?

A

vasodilation

137
Q

how does epinephrine, an extrinsic hormonal control, affect the radius of arterioles?

A
  • it can cause vasoconstriction in the skin and viscera which reinforces the SNS
  • it can cause vasodilation in the heart, skel. muscle and liver which opposes the SNS
138
Q

How does angiotensin II and ADH affect radius of arterioles?

A
  • vasoconstriction
139
Q

How does histamine affect radius of arterioles?

A
  • vasodilation
140
Q

What is blood pressure?

A

the hydrostatic pressure exerted by blood on the wall of vessel (clinically on the wall of arteries)

141
Q

Blood pressure results when?

A

flow is opposed by resistance

142
Q

How is systolic pressure produced

A

when the ventricular contraction go against vascular resistance

143
Q

How is diastolic pressure produced?

A

when elastic arteries go against vascular resistance (when ventricles are at rest)

144
Q

normal blood pressure?

A

120/80

145
Q

What does the top number in a blood pressure reading represent?

A

systolic pressure

146
Q

What does the bottom number in a blood pressure reading represent?

A

diastolic pressure

147
Q

What is pulse pressure?

A

the difference between systolic pressure and diastolic pressure

148
Q

What is the mean arterial pressure?

A

The average blood pressure within one cardiac cycle

149
Q

How to measure MAP? why is it measured this way?

A

MAP = diastolic pressure + 1/3(pulse pressure)

- because the diastolic pressure is longer than systole

150
Q

How is pressure calculated?

A

P = Flow x Resistance

151
Q

How is MAP calculated?

A 
MAP = diastolic pressure + 1/3(pulse pressure) 
MAP = Cardiac Output x Total Peripheral Resistance
  • Total Peripheral Resistance refer to the resistance in all arterioles
  • Cardiac Output = heart rate x stroke volume
152
Q

Pressure = MAP - Venous pressure? True or False

A

True

153
Q

what is the venous pressure? What is its rate?

A

pressure in veins

- about 0

154
Q

MAP is regulated by controlling?

A

1) Cardiac Output
2) Total Peripheral Pressure in the arteriole radius
3) Blood Volume (affects venous returns, therefore SV affects MAP as well)

155
Q

In terms of extrinsic control, what neuronal factors affect MAP?

A
  • baroreceptor reflexes

- chemoreceptor reflexes

156
Q

What are baroreceptor reflexes?

A

one of the body’s homeostatic mechanisms to maintain blood pressure

157
Q

When do baroreceptor reflexes act up?

A

in short term changes such as standing

158
Q

In terms of baroreceptor reflexes, what receptor monitors MAP?

A
  • stretch receptors
159
Q

Stretch receptors of _________ monitors the blood pressure.

A

carotid sinus

160
Q

stretch receptors of ________ monitors the systemic blood pressure.

A

aortic arch

161
Q

When a stretch receptor (baroreceptor) identifies an increase in MAP, what happens?

A
  • an increase of baroreceptor impulse –> impulses stimulates medulla —> which triggers the SNS & the PSNS

** The SNS impulses decrease–> lowers epinephrine secretion, lowers vasoconstriction, lowers venoconstriction which decreases venous return which decreases stroke volume therefore CO is decreased, –> lowered MAP

**The PSNS impulses increase –> decrease CO –> lowered MAP

162
Q

What happens baroreceptors identify decrease in MAP

A

decrease in MAP –> increased baroreceptor impulses —> stimulates the medulla –> affects SNS & PSNS

** SNS impulses increases –> increased secretion of epinephrine, increased vasoconstriction, increased vesoconstriction –> increased venous return —> increased stroke Volume –> increased CO –> increased MAP

** PSNS impulses decrease –> increased CO –> increased MAP

163
Q

What are the receptors of chemoreceptor reflex?

A

peripheral chemoreceptors

164
Q

Peripheral chemoreceptors respond to?

A
  • O2, CO2, pH levels
165
Q

Where are peripheral chemoreceptors found?

A

carotid sinus and aortic arch

166
Q

How do chemoreceptor reflexes affect blood pressure?

A
  • low O2, high CO2, low pH(high metabolism) –> increases chemoreceptor impulses –> stimulates the medulla cardiovascular centre –> increases SNS and epinephrine release –> increased vasoconstriction, increased Total Peripheral Resistance, increased heart rate, force of contraction which increases CO –> MAP increases
167
Q

What is the relevance of Renin-Angiotensin System?

A

it creates angiotensin II which affects MAP

168
Q

List the steps of angiotensin II production

A

Plasma angiotensinogen –> combines with renin (enzyme + hormone) –> angiotensin I –> combines with angiotensin-converting-enzyme (ACE) –> angiotensin II

169
Q

How does angiotensin II, an extrinsic hormonal control, affect MAP

A
  • it increases vasoconstriction, and venoconstriction which increases MAP
  • it increases aldosterone and ADH which increase renal Na+ and H2O absence leading to thirst which increases blood volume. As a result, there is an increase in MAP
170
Q

How does atrial natriuretic peptide (ANP), an external hormonal control, affect MAP

A
  • it decreases renin production which decreases production of angiotensin II which decreases aldosterone which decreases ADH which increases urine production which decreases blood volume
  • it decreases vasoconstriction
  • overall, it decreases MAP
171
Q

Capillary exchange is between?

A
  • blood and ISF
172
Q

solutes enter and leave capillaries by:

A

1) diffusion
2) vesicular transport = transcytosis
3) mediated transport

173
Q

In terms of solutes movements in and out of capillaries, does diffusion happen in the brain?

A
  • no
174
Q

Where does diffusion happen in terms off solute movements in and out of the capillaries?

A
  • major routes
175
Q

What is diffused in and out of the capillaries?

A
  • CO2, O2, ions, hormones, amino acids, glucose etc
176
Q

What kind of solute moves in and out of the capillaries via vesicular transport?

A

large proteins like antibodies

177
Q

How do large proteins like antibodies move in and out of the capillaries in a vesicular transport?

A
  • via transcytosis

- where endocytosis from blood into endothelial cells and exocytosis from endothelial cells into ISF

178
Q

What does mediated transport need in terms of solute movement in and out of the capillaries?

A

carrier protein

179
Q

Where does mediated transport happen in terms of solute capillary exchange?

A

brain

180
Q

How does fluid enter (absorption) and leave (filtration) the capillaries?

A

by:
1) osmosis
2) bulk flow

181
Q

What causes bulk flow?

A
  • due to pressure differences
182
Q

What are the four pressures involved in bulk flow?w

A

1) hydrostatic blood pressure = blood pressure
2) blood osmotic pressure = due to plasma proteins
3) ISF hydrostatic pressure = 0mmHg
4) ISF osmotic pressure - due to ISF proteins

183
Q

Blood osmotic pressure is due to?

A

plasma proteins

184
Q

ISF Osmotic pressure is due to?

A

ISF proteins

185
Q

Blood Hydrostatic pressure causes fluid to move in or what of the cell?

A

move out

186
Q

ISF osmotic pressure (IFOP) causes fluid to move in and out of the cell?

A

out?

187
Q

Blood osmotic pressure causes fluid to move in and out of the cell?

A

move in

188
Q

ISF hydrostatic pressure (IFHP) causes fluid to move in and out of the cell?

A

move in

189
Q

In terms of bulk flow, what type of pressures causes fluid to move out of the capillaries?

A
  • blood hydrostatic pressure (BHP)

- ISF Osmotic pressure (IFOP)

190
Q

In terms of bulk flow, what types of pressure causes fluid to move in to the capillaries?

A
  • Blood Osmotic Pressure (BOP)

- ISF hydrostatic pressure (IFHP)

191
Q

What is the Net Filtration Pressure?

A

It is the summary of hydrostatic pressure and osmotic pressure acting on a capillary.

192
Q

How do you calculate NFP?

A

NFP = filtration - absorption
aka.
NFP = (BHP+IFOP) - (BOP+IFHP)

193
Q

Which way does blood flow in a capillary? From the arteriole end to the venous end? OR From the venous end to the arteriole end?

A
  • arteriole end to venous end
194
Q

Where is Net Filtration Pressure Higher? arteriole end or the venous end

A

Arteriole end?

195
Q

In an arteriole end? Do you get filtration or absorption? Why

A

filtration because it has a higher BHP which causes a higher NFP

196
Q

In the venous end of the capillary, do you get filtration or absorption? Why?

A

Absorption because it has a lower BHP which causes a lower or a negative NHP.

197
Q

How do you get the overall net filtration pressure across a capillary?

A

Total NHP = NHP at the arteriole end + NHP at the venous end

198
Q

In the body, about how many percentage of filtered fluid is reabsorbed in the blood?

A

90%

199
Q

In the body, how many percentage of fluid enter the lymph?

A

10%

200
Q

Does ISF volume remain constant?

A

yes

201
Q

What is Edema?

A

accumulation of fluid in the issue (ISF) which causes swelling

202
Q

What is the accumulation of fluid in tissue that causes swelling called?

A

edema

203
Q

What causes Edema?

A
  • Increased blood pressure which increases BHP
  • leakage of plasma proteins in the ISF which causes inflammation which causes increased IFOP
  • decreased plasma proteins which causes decreased BOP , malnutrition and burns
  • obstruction of lymph vessels which causes elephantiasis (surgery is needed)
204
Q

What is circulatory shock?

A
  • inadequate blood flow which causes low O2 and nutrients in cells
205
Q

What are the types of circulatory shock?

A

1) Hypovolemic shock

2) Vascular shock

206
Q

What is a hypovolemic shock?

A
  • the state of decreased blood volume due to blood loss, severe burns, diarrhea and vomiting
207
Q

What is vascular shock?

A
  • the state where blood volume is normal but vessels are expanded
208
Q

Vascular shock is due to?

A
  • system vasodilation of blood vessels which causes decreased blood pressure
209
Q

what are the different types of vascular shock?

A

1) anaphylactic shock
2) septic shock
3) cardiogenic shock

210
Q

What is anaphylactic shock and what is it due to?

A
  • allergic reactions

- due to lots of histamine released from the mast cells

211
Q

What causes septic shock?

A

bacterial toxins

212
Q

What is cardiogenic shock?

A
  • failure in pumping which causes decreased CO which prevents the heart from sustaining blood flow
213
Q

What are the stages of shock?

A

1) Compensatory stage
2) Progressive stage
3) Irreversible stage

214
Q

What happens in the compensatory stage of circulatory shock?

A
  • the mechanisms maintain homeostasis themselves. This involves baroreceptors, chemoreceptors and ischemia (lack of O2) in the medulla
215
Q

Compensatory stage of circulatory shock trigger SNS to do what?

A
  • increases heart rate which generalizes vasoconstriction and increases blood pressure
216
Q

What does the SNS do during compensatory stage when blood flow to the kidney is low?

A
  • it triggers the release of renin which creates angiotensin II, which increases aldosterone production, which releases ADH which establishes vasoconstriction, increased Na+ and H2O retention (to maintain blood volume) which increases thirst
217
Q

What happens in the progressive stage of circulatory shock?

A
  • the mechanism is too inadequate to sustain homeostasis therefore, intervention is needed.
  • The CO is decreased which causes blood pressure in cardiac circulation to go down. Therefore CO activity is decreased
  • The blood to the brain is decreased which decreases cardiovascular control
  • the low blood flow causes damage to viscera, especially the kidneys which causes renal failure.
218
Q

What causes renal failure in the progressive stage of circulatory shock?

A
  • low blood flow to kidneys
219
Q

What happens in the irreversible stage of circulatory shock?

A
  • the decreased CO pretty much leads to low blood flow to the heart which decreases CO even more
  • at this point, it is a self-perpetuating cycle which leads to deah
220
Q

What does blood contain?

A

Plasma and formed elements

221
Q

The plasma component of the blood contain what?

A
  • H2O
  • Proteins
  • electrolytes
  • nutrients, gases, wastes and hormones
222
Q

Water makes up _______ of plasma?

A

90.5

223
Q

Proteins make up ______ % of the plasma

A

7

224
Q

What makes up 90.5% of the plasma

A

water

225
Q

What makes up 7% of the plasma

A

proteins

226
Q

What are the different proteins present in the plasma?

A

albumins, globulins fibrinogens

227
Q

What makes up 58% of the proteins present in the plasma?

A

albumins

228
Q

The albumins make up _____% of the the plasma proteins?

A

58%

229
Q

What makes up 38% of the proteins in the plasma?

A

globulins

230
Q

What makes up 4% of the proteins in the plasma?

A
  • fibrinogens
231
Q

The globulins make up what percentage of the proteins in the plasma?

A
  • 38%
232
Q

The fibrinogen makes up _____% of the proteins in the plasma?

A

4%

233
Q

What do the proteins present in the plasma usually do?

A
  • they produce osmotic pressure, especially the albumins
  • they buffer pH (7.35-7.45) - prevents it from fluctuating
  • clot formation
  • Y (gamma) globulins = make antibodides
  • A & B globulins = transport lipids, metal ions and hormones
234
Q

Which protein makes antibodies?

A
  • Y(gamma) globulins
235
Q

Which protein transport lipids, metal ions, and hormones?

A
  • A & B globulins
236
Q

Electrolytes or ions are also part of the plasma. What do they do?

A
  • they are there for membrane excitability

- buffer HCO3-

237
Q

The formed elements present in the blood consist of?

A
  • red blood cells

- white blood cells

238
Q

What does the red blood cells do?

A
  • transport O2 on iron to of hemoglobin and CO2 on globin
  • buffer - the globin binds to the H+ reversibly
  • Carbonic anhydrase - which imp. CO2 transport in blood
239
Q

Hemoglobin, a component of the red blood cells, consists of two things. What are they?

A

4 hemes + 4 globins (protein)

240
Q

How much iron is present in a hemoglobin?

A
  • 4

- 1 Fe/heme

241
Q

What breaks down hemoglobin?

A

macrophages

242
Q

Macrophages break down hemoglobin to its original components. What are they?

A

heme & globin

243
Q

What happens with the iron stored in the hemoglobin when its broken down?

A
  • its taken away from the heme and stored in liver, muscle and spleen
244
Q

Aside from the liver, spleen and muscle, where else does the Fe go after its been taken away from the heme during hemoglobin breakdown? What does it do there?

A
  • redbone marrow to produce more heme which makes more red blood cells
245
Q

Where does the non-iron of heme go after hemoglobin breakdown?

A
  • it becomes bilirubin which gets excreted in bile from liver
246
Q

What is jaundice?

A
  • the excess bilirubin in blood
  • blockage of bile excretion
  • liver dysfunction (neonates —> liver immature)
247
Q

what happens to the globin component of hemoglobin after hemoglobin breakdown

A
  • gets converted into amino acids which gets recycled
248
Q

Do red blood cells contain nuclei or mitochondria?

A

no

249
Q

does rbc facilitate anaerobic respiration?

A

yes

250
Q

What are the two major categories of white blood cells?

A

1) granulocytes

2) agranulocytes

251
Q

What are the types of granulocytes?

A
  • neutrophils
  • eosinophils
  • basophils
252
Q

What do the neutrophils do?

A
  • they are the 1st to enter an infected area of the body (immune response)
253
Q

What does the eosinophils do?

A
  • attack parasites

- break down chemical released in allergic reactions

254
Q

What do basophils do?

A
  • secrete histamine which promotes inflammation

- secrete heparin which inhibits local clotting

255
Q

What are the different types of agranulocytes?

A
  • monocytes
  • lymphocytes
  • platelets
256
Q

What do monocytes do?

A
  • enter tissues, become enlarged to become macrophages
257
Q

Give examples of lymphocytes

A
  • T lymphocytes
  • B lymphocytes
  • Natural Killer cells
258
Q

What are some types of T lymphocytes?

A
  • T helper cells (Th)

- Cytotoxic T lymphocytes (CTL)

259
Q

When B lymphocytes are activated, what do they do?

A
  • give rise to plasma membranes which makes antibodies
260
Q

What are platelets?

A
  • a type of lymphocytes which are cell fragments from megakaryocytes
261
Q

What do platelets do?

A
  • form platelet plug to prevent blood loss

- they contain granules which contain coagulating factors (these are proteins and chemicals involved in clotting)

262
Q

What do platelets contain? What do they do

A

granules - which contain coagulating factors like proteins and chemicals involved in clotting

263
Q

What is hemostasis?

A

process of stopping bleeding

264
Q

What are the processes involved in hemostasis?

A

1) vascular spasm
2) platelet plug formation
3) clotting formation
4) clot repair + fix
5) fibrinolysis

265
Q

What happens in vascular spasm?

A
  • vasoconstriction = which decreases blood flow for mins to hours
266
Q

What happens in platelet formation?

A

platelets stick to the damaged blood vessel where chemicals (factor) are released which causes:

1) more platelets to stick (therefore a positive feedback mechanism)
2) promote clotting
3) begins healing
- neighbouring healthy endothelial cells secrete chemicals that prevent the plug from spreading

267
Q

what do healthy neighbouring endothelial cells contribute to platelet plug formation?

A
  • they release chemicals which prevent plug from forming
268
Q

what does plug formation require? And what inhibits it?

A
  • prostaglandin

- aspirin

269
Q

What are the 3 stages that occur during clot formation?

A

1) production of prothrombin activator by
2) conversion of prothrombin to thrombin
3) conversion of fibrinogen to fibrin

270
Q

How are prothrombin activators created?

A

extrinsic pathway = caused by factors released by damaged tissues
intrinsic pathway = caused by factors contained in the blood

271
Q

when producing prothrombin activators, do extrinsic and intrinsic pathways occur together?

A

yes usuay

272
Q

So combing intrinsic and extrinsic pathways, what does the body need to create prothrombin activators?

A
  • Ca2+, platelets, tissue, and or plasma factors
273
Q

What happens in prothrombin conversion?

A
  • the prothrombin activators convert prothrombin to thrombin
274
Q

What happens in fibrinogen conversion?

A
  • fibrinogen gets converted to fibrin by thrombin and Ca2++
275
Q

what does the fibrin do in clot formation?

A

it forms webs of threads on the plug to trap formed elements

276
Q

is the production of thrombin a positive or negative feedback?

A
  • positive as it creates more thrombin
277
Q

About how many factors are involved in clot formation?

A

about 2 dozen

278
Q

In general, where are these required factors from?

A
  • diet, liver (plasma proteins), platelets, damaged tissue
279
Q

What vitamin is required to create 4 required factors in clot formation?

A

Vitamin K

280
Q

What happens in the clot retraction + fixation process?

A
  • during retraction, the blood vessel edges are pull together
  • during fixation, the fibroblasts create new CT, and endothelial cells to repair lining
281
Q

In the last stage of hemostasis which fibrinolysis, what happens?

A
  • clot dissolution happens by:
  • producing plasmin (a fibrin digesting enzyme) from plasminogen = the plasmin breaks down the clot
  • and then the phagocytes clean up the clot in clumps
282
Q

What cleans up the clot in clumps during fibrinolysis?

A
  • phagocytes
283
Q

What breaks down the clot in fibrinolysis?

A

plasmin

284
Q

What is thrombus?

A

a stationary clot in an undamaged blood vessel

285
Q

What is an embolus?

A

a free floating clot

286
Q

What is a stationary clot in an undamaged vessel called?

A

thrombus

287
Q

What is a free floating clot called?

A
  • embolus
288
Q

what is hemophilia

A

lack of clotting mechanism or abnormal clotting mechanism

289
Q

what percentage of people have Type A hemophilia?

A

83%

290
Q

What is missing in Type A hemophilia?

A
  • clotting factor VIII

Physiology (11 decks)

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