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Year 1: LSS 1 > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

1
Q

What level does the descending aorta pierce the diaphragm?

A

Aortic hiatus

T12

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2
Q

What are the branches off the aortic arch?

A

The bracheocephalic trunk which branches off to form the right common carotid and right subclavian artery
left common carotid
left sublclavian

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3
Q

What do the subclavian arteries supply?

A

The upper limbs

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4
Q

What do the common carotid arteries supply?

A

The head and neck

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5
Q

What returns blood from the upper left and right sides of the body?

A

Two brachiocephalic veins which join to form the superior vena cava

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6
Q

What drains the head and neck and upper limbs?

A

Head and neck- internal jugular vein
Limbs- Left subclavian
Both join the brachiocephalic veins

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7
Q

What are the names of the atrioventricular valves?

A

Left- mitral

Right -tricuspid

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8
Q

What are the cusps of the pulmonary valve?

A

Left
Right
anterior

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9
Q

What are the cusps of the aortic valve?

A

Left
Right
Posterior

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10
Q

Where do coronary arteries arise from?

A

Aortic sinuses

Left and right cusps of the aortic valve

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11
Q

How are antrioventricular valves joined to the heart?

A

Attached to papillary muscles by chordae tendinae.

Muscles are located on the inner surface of the ventricles

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12
Q

How is the heart drained of blood?

A

The heart is drained by coronary veins
Great cardiac vein on left
Small cardiac vein on right
Drain into coronary sinus which drains into the right atrium

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13
Q

What is cardiac muscle?

A

Specialised muscle tissue made up of cells that are not in synctium like skeletal muscle
Made up of cardiomyocytes which are connected via intercalated discs that allow the pasage of action potentials

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14
Q

What is the sinoatrial node?

A

Group of cardiomyocytes that can initiate a heart beat

Located in right atrium, near entrance of superior vena cava

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15
Q

What is the appearance of ventricular cells?

A

100x15 um

Rectangular appearance

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16
Q

What is the purpose of t-tubule?

A

Carrying the wave of depolarisation from the surface to the cell

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17
Q

How is cardiac muscle contraction initiated.

A

Action potentials travel through cardiomyocytes through the intercalated discs. Carried by t-tubules to L type calcium channel causing an influx of calcium into the cell. This calcium activated the sarcoplasmic reticulum calcium channel initiating an influx of calcium which binds to troponin. This allows tropomyosin to bind to the myosin head and form cross linkages. At the same time the action of Ca2+ Atpase actively transports calcium back into the sarcoplasmic reticulum and the Na+/ca2+ anti porter on t-tubule surface will restore calcium ions extracellularly

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18
Q

What is the difference between active force and passive force?

A

Active force relies on cross bridge formation and linking

Passive force is more to do with elastic property

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19
Q

Why does active force decrease after a certain muscle length?

A

Muscle has stretch too much

Number of cross bridges formed has decreased

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20
Q

What is isometric contraction?

A

No shortening of muscle fibres but a force is generated

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21
Q

What is preload?

A

The force that stretches the heart muscle before it contracts.
The passive force that is generated whilst the ventricles are filled with blood

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22
Q

How can preload be measures?

A

End diastolic volume
End diastolic pressure
Right atrial pressure

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23
Q

What is after load?

A

The force that needs to be overcome to cause contraction

Afterload is not seen in the resting state

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24
Q

What is after load more dependant on?

A

Diastolic arterial blood pressure as the pressure of the left ventricles is higher than the right

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25
Q

What is the Frank-Starling relationship?

A

Increased diastolic fibre length results in increased ventricular contraction

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26
Q

What are the two properties of myofilaments that effect the Frank-Starling relationship?

A

Changes in the number of myofilament cross bridges

Calcium sensitivity

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27
Q

Why are less actin-myosin cross bridges formed at lower lengths of actin molecules?

A

At lower lengths, the actin molecules double up on them selves, but at longer lengths they pull apart and expose the overlapped region

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28
Q

At greater sarcomere lengths, why is less calcium required to produce a given force?

A

At greater lengths, the affinity of troponin C for calcium increases

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29
Q

What is stroke work?

A

The work done by the heart to eject blood under pressure into the aorta and pulmonary artery
Stroke volume x pressure

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30
Q

What influences stroke volume?

A

Preload and afterload

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31
Q

Why must stroke volume remain the same for both ventricles?

A

If the amount of blood to the tissues is imbalanced it will result in odeoma.

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32
Q

What is the law of Laplace?

A

If the pressure in a cylinder is constant, the tension in its walls will increase with increased radius length

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33
Q

Why is there lower pressure in dilated cardiomyopathy?

A

Dilation leads to thinner walls and a larger radius leading to larger wall stress being generated

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34
Q

How is the slope of pre-potential affected by the sympathetic and parasympathetic nervous system?

A

Sympathic- steeper

Parasympathetic- shallower

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35
Q

Why is there a reduction in outward potassium ion flow in the sinoatrial node cell?

A

They is net movement of Na+ but the cell has low permeability to K+

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36
Q

Why do ventricles have a long action potential?

A

Due to the inward movement of calcium ions due to voltage dependent calcium channels

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37
Q

Which drugs affect calcium?

A

Digoxin- increases calcium

Verapamil- decreases calcium

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38
Q

What is the P wave?

A

Atrial depolarisation

Atria Contract

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39
Q

What is the QRS complex?

A

Ventricles contract

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40
Q

What is the T wave?

A

Ventricular repolarisation

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41
Q

What is the mean frontal plane axis?

A

The general direction of an impulse of the heart

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42
Q

What is the name given to three connected limb leads?

A

Einthoven’s triangle

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43
Q

What is the reference point when using standard limb leads?

A

The right foot

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44
Q

How are the limb leads connected?

A

Lead 1- right arm to left arm
Lead 2- right arm to left foot
Lead 3- left arm to left foot

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45
Q

Which are the theoretical leads?

A

AvR- connects the right arm to the mid point between the left arm and left foot
AvF- connects the left arm to the mid point between the right arm and left foot
AvL- connects the left foot to the mid point between the right arm and left foot

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46
Q

Which is the isoelectric lead?

A

The most flat lead?

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47
Q

What happens if an ECG shows no upward or downward deflection?

A

The wave of depolarisation is travelling directly between the electrodes of the lead

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48
Q

What is the normal range for the mean frontal plane axis?

A

-30 and +90 degrees

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49
Q

What is left axis deviation?

A

A mean frontal plane axis of less than -30 and is a result of aortic stenosis and when the left ventricle thickens

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50
Q

What is right axis deviation?

A

A mean frontal plane axis of above 90 degrees and is due to pulmonary pathophysiologies

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51
Q

What is the difference between the six standard limb leads and the chest leads?

A

Limb leads look at the coronal plane

Chest leads look at the axial plane

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52
Q

What is the diameter of a capillary?

A

7um

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53
Q

What are the different types of capillaries?

A

Fenestrated
Discontinuous
Continuous

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54
Q

Give an example of a continuous capillary

A

The blood brain barrier is a modified form with no gap junctions

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55
Q

Where do discontinuous capillaries exist?

A

Bone marrow to let through red blood cells

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56
Q

How is flow calculated?

A

pressure gradient/vascular resistance

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57
Q

How is pressure gradient determined?

A

The gradient between the maximum pressure in the arterioles and the pressure in the capillaries

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58
Q

What is resistance?

A

The hindrance to blood flow as a result of the friction between the moving blood and the stationary wall vessels

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59
Q

What affects flow?

A

Blood viscosity
Vessel radius
Vessel length

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60
Q

What is the mean arterial pressure?

A

93mmHg

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61
Q

What is the pressure in the capillaries

A

37 mmHg

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62
Q

What is vascular tone?

A

A state of partial constriction

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63
Q

Why is the radius of blood vessels adjusted?

A

To supply blood flow depending on the metabolic needs of the tissue
To regulate arterial blood pressure

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64
Q

What undertakes the neural control of the blood pressure?

A

Cardiovascular centre in the medulla by the sympathetic nervous system

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65
Q

What mediates the sensitivities to change in flow in the brain and heart?

A

Brain- alpha receptors

Heart- beta receptors

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66
Q

What is bulk flow?

A

A volume of protein free plasma that filters out of the capillaries and mixes with the surrounding interstitial fluid and is then reabsorbed

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67
Q

What are the starling forces?

A

Hydrostatic pressure which forces fluid out of the capillaries.
Oncotic pressure which causes fluid to be reabsorbed as the result of the osmotic pressure exerted by the proteins

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68
Q

Which end of the capillary does ultrafiltration occur?

A

Arteriolar end

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69
Q

Which end of the capillary does reabsorption occur?

A

Venous end

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70
Q

How does oncotic and hydrostatic pressure change throughout the capillary?

A

Hydrostatic pressure decreases further down the capillary.

Oncotic pressure remains constant

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71
Q

Why are lymphatic capillaries blind ended?

A

They have no loop.
They are unidirectional.
Only purpose is to return net loss of fluid from the blood back to the heart

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72
Q

How does lymph return to the heart?

A

Drain into the right lymphatic duct and thoracic duct which drain into the left and right subclavian veins

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73
Q

How much lymph is returned per day?

A

3L

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74
Q

What is elephantiasis?

A

A parasitic infection which results in the blockage of the lymph vessels

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75
Q

What is the cardiac cycle?

A

The mechanical and electrical events which result in volume changes, pressure changes and sounds that are associated with a heart beat

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76
Q

What is end diastolic volume?

A

The amount of blood in the ventricles at the end of atrial systole

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77
Q

What is end systolic volume?

A

The amount of blood in the ventricles at the end of ventricular systole

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78
Q

What is stroke volume?

A

The amount of blood that has been ejected out of the heart in one heart beat

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79
Q

How can stroke volume be calculated?

A

Find the difference between end diastolic and end systolic volume

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80
Q

What is the ejection fraction?

A

Stroke volume/End diastolic volume

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81
Q

What are the stages of the cardiac cycle?

A 
Atrial systole 
Isovolumic contraction 
Rapid ejection 
Reduced ejection 
Isovolumic relaxation 
Rapid filling 
Reduced filling
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82
Q

What happens when the atria contract?

A

The ventricles are topped off with any blood remaining in the atria

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83
Q

What is the cause of the first wave in the jugular venous pulse?

A

When the ventricles are being filled with blood, some blood pushes back against the jugular vein

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84
Q

What heart sound may be heard during atrial systole due to problems?

A

S4

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85
Q

What is the cause of the heart sound S4?

A

Pulmonary embolism, congestive heart failure, tricuspid incompetence

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86
Q

What causes the atrioventricular valves to close?

A

The ventricular pressure exceeds atrial pressure

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87
Q

Which sound correlates to the closure of the atrioventricular valves?

A

S1

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88
Q

What causes the opening of the semilunar valves?

A

The ventricular pressure exceeding the aortic pressure

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89
Q

What causes reduced ejection?

A

The semilunar valves begin to close as the pressure gradient between the aortic and ventricular pressure begin to decrease.

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90
Q

Which stage in the cardiac cycle marks the end of systole?

A

Isovolumic relaxation

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91
Q

What is the dichrotic notch due to?

A

Rebound pressure on the aortic valve as a result of the relaxation of the distended aortic wall

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92
Q

What causes the second jugular pulse?

A

Blood pushing against the tricuspid valve as the atria fill with blood

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93
Q

If S3 is heard, what stage of the cardiac cycle will it be present?

A

Rapid ventricular filling

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94
Q

What does S4 correspond to?

A

Mitral incompetence
Turbulent filling
Severe hypertension

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95
Q

What else can reduced ventricular filling be called?

A

Diastasis

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96
Q

What are the standard systolic/diastolic pressures for the left and right side of the heart?

A

120/80 mmHg

25/5 mmHg

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97
Q

When may PAWP be increased?

A

Left ventricular failure

Mitral stenosis

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98
Q

What do the points of the pressure volume loop correspond to?

A

1- end diastolic volume
2- Aortic pressure has been encountered
3- end systolic pressure
4- opening of atrioventricular valves

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99
Q

What do the stages between the points correspond to?

A

1 & 2 - isovolumic contraction
2&3 - ejection
3&4 - isovolumic relaxation
4&1 - filling of the ventricles

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100
Q

What represents preload on the flow volume loop?

A

Point 1

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101
Q

What represents after load on the flow volume loop?

A

Between points 2 and 3

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102
Q

What does the horizontal distance between isovolumic contraction and relaxation represent?

A

Stroke volume

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103
Q

How can the contractility of the heart be measured?

A

Using the ejection fraction

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104
Q

What is the duration and amplitude of the P wave

A
  1. 11 seconds

2. 5 mm in lead II

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105
Q

How long is the PR interval

A

0.12-0.2 seconds

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106
Q

How long is the QRS complex?

A

0.12 seconds
R wave in V6 - 25 mm
R wave and S wave in V1 - 35 mm

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107
Q

How long is the QT interval?

A

0.38-0.42 seconds

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108
Q

In which leads can the T wave be inverted without being abnormal?

A

lead III, avr, v1, v2

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109
Q

How would you calculate heart rate from an ECG?

A

Divide 300 by the number of large squares between the QRS segments

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110
Q

What is bradycardia?

A

A heart rate less than 60 beats per minute

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111
Q

What is tachycardia?

A

A heart rate more than 100 beats per minute

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112
Q

What is a sinus rhythm?

A

Each P wave is followed by a QRS complex

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113
Q

What may cause an occasional extra QRS complex?

A

Ectopic beat

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114
Q

What does the QRS complex tell you about the heart?

A

Its orientation within the chest wall
The thickness of the ventricular muscle
Abnormalities in the direction of ventricular depolarisation

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115
Q

How does the ECG show first degree heart block?

A

If the PR interval is prolonged but still followed by the QRS complex
This is due to delayed conduction through the AV node

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116
Q

How does the ECG show second degree heart block type 1?

A

If successive PR waves get successively longer until one is not followed by a QRS complex and then the pattern returns to normal
Wenkebach’s phenomenon

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117
Q

How does the ECG show second degree heart block type 2?

A

If the PR intervals are constant but occasionally not followed by the QRS complex

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118
Q

How does the ECG show complete heart block?

A

There is no relationship between the PR intervals and QRS complex as the atria and ventricles depolarise separately

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119
Q

Why may a PR interval appear to be shorter than usual?

A

An accessory pathway is present which causes electrical activity to be conducted from atria to ventricles more rapidly than usual

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120
Q

What may an increased amplitude of the QRS complex suggest?

A

Left ventricular hypertrophy

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121
Q

What may a reduced amplitude of the QRS complex suggest?

A

Obesity
Chronic airways disease
Pericardial effusion
Hyperinflated lung

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122
Q

What may cause ST depression?

A

Drugs
Myocardial ischaemia
Ventricular hypertrophy

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123
Q

What may an elevated ST segment suggest?

A

Acute myocardial infarction

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124
Q

What may cause a prolonged QT interval?

A

Drugs
Hypocalcaemia
Ramano- Ward syndrome

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125
Q

What can T wave inversion suggest?

A

Previous infarction
Myocarditis
Hypertrophy

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126
Q

What is the ECG appearance of sinus tachycardia?

A

Absent P waves replaced by f waves

350-600 beats per minutes

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127
Q

How may atrial fibrillation lead to thrombus?

A

It is irregular beating of the atria
Irregular flow of blood
Stasis of blood
Thrombus

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128
Q

What causes atrial flutter?

A

Premature electrical impulse arising from the atria

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129
Q

What are general symptoms of heart block?

A

Syncope
Lightheadedness
Palpitations

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130
Q

What are blocks that occur below the AV node?

A

Infra-hisian blocks

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131
Q

What are blocks that occur in the fascicles of the left bundle branch?

A

hemiblocks

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132
Q

How is flow achieved?

A

By the action of the muscular pump of the heart which generates a pressure gradient that propels blood through a series of tubes

133
Q

How far is a cell from a capillary?

A

10um

134
Q

What acts as a reservoir for blood volume?

A

Veins and venules

135
Q

What act as dampening vessels?

A

Large arteries

136
Q

What is ohms law?

A

Voltage = flow x resistance

137
Q

How does blood flow?

A

Laminar flow

138
Q

What is laminar flow?

A

Fluid flows in layers or is streamlines

139
Q

What is shear rate?

A

The viscosity gradient at any point?

140
Q

What is shear stress?

A

Sheer rate x viscosity

141
Q

How does velocity of layers of blood increase as you move away from the wall?

A

Increases

142
Q

What does high shear stress promote?

A

Cell survival
Cell alignment with direction of flow
Secretion of substances that promote vasodilation and anticoagulation

143
Q

What is transmural pressure?

A

Pressure in the wall of the vessel

144
Q

What is the Windkessel effect?

A

Dampening the magnitude of pressure change

145
Q

Why is most blood volume stored in the veins?

A

Veins are more compliant at low pressures than arteries

146
Q

What problems does standing up pose?

A

The effect of gravity increases pressure in lower limbs.
Veins are compliant so the volume of blood in veins increases.
Volume of blood returning to the heart decreases so cardiac output and blood pressure could fall.

147
Q

How are the problems that could be caused as a result of standing up solved?

A

Sympathetic nervous system is activated
Venous smooth muscle constriction- to stiffen the veins
Constriction of the arteries- increase resistance and maintain blood pressure
Increase contractility of the heart and heart rate
Myogenic vasoconstriction
Use of muscle and respiratory pumps

148
Q

What are varicose veins?

A

Dilated superficial veins

149
Q

Which layer is present in ever blood vessel in the body?

A

Vascular endothelium

150
Q

What are the functions of the vascular endothelium

A 
Vascular tone management 
Thrombostasis 
Absorption and secretion 
Growth 
Barrier
151
Q

Which mediators have an effect on vascular tone?

A 
Nitric oxide- vasodilation 
Prostacyclin - vasodilation
Thromboxane- vasoconstriction
Endothelin 1- vasoconstriction and vasodilation 
Angiotensin II- vasoconstriction
152
Q

Which mediators have an effect of platelet aggregation

A

Nitric oxide- inhibits
Prostacyclin- inhibts
Thromoxane- activates

153
Q

Which two mediators can arachidonic acid form?

A

Thromboxane A2

Prostacyclin

154
Q

How is prostacyclin formed?

A

COX enzyme converts arachidonic acid into PGH2, which is a precursor and then it is converted into prostacyclin using prostacyclin synthase

155
Q

What is the alternative route for arachidonic acid?

A

Form leukotrienes

156
Q

What is the prostacyclin pathway?

A

Leave the cell on the luminal cell
On the basolateral membrane bind to prostacyclin receptors on smooth muscle cells which activate adenylyl cyclase and protein kinase A

157
Q

How is endothelin 1 produced?

A

From the nucleus of endothelium cells

158
Q

Which endothelin 1 receptors of found on smooth muscle cells?

A

ETA and ETB

159
Q

which endothelin receptors are found on endothelium cells?

A

ETB

160
Q

How does endothelin produce a vasodilatory response?

A

It up regulates eNOS which stimulates NO release

161
Q

Give an example of an angiotensin receptors inhibitor

A

Candestartan

162
Q

Give an example of an ACE inhibitor

A

Ramripil

163
Q

Give an example of a calcium channel blocker

A

Amlodipine

164
Q

What is the precursor of nitric oxide?

A

L-arginine

165
Q

What is the secondary messenger of nitric oxide?

A

Guanylyl cyclase

166
Q

What is the receptor for prostacyclin?

A

IP1

167
Q

Which postganglionic neurones secrete acetyl choline?

A

Sweat gland,

Ach acts on sweat receptors

168
Q

What does sympathetic innervation to the adrenal medulla result in?

A

Secretion of adrenaline and some noradrenaline

169
Q

Why doe sympathetic innervation to the heart increase cardiac output?

A

Exerts a ionotropic effect on the cardiac muscle- increasing the force of contractility of the heart- increasing stroke volume
Exerts a positive chronotopic effect, increase heart rate

170
Q

Which blood vessels vasodilator when sympathetically innervated?

A

Ones which have
Cholinergic fibres
B adrenergic fibres

171
Q

How is noradenaline synthesised?

A

Amino acid tyrosine is converted into DOPA using tyrosine hydroxylase
DOPA is converted into Dopamine using DOPA decarboxylase
Dopamine is stored in secretory vesicle with Dopamine Beta hydroxylase which converts it into noradrenaline

172
Q

How is over transmission of noradrenaline prevented?

A

On post synaptic neurones- Converted into an inactive form using catecholamine-O- methyltransferase (COMT)
on pre synaptic neurone - taken up by secretory granules to be used as neurotransmitter using ATP
broken down into metabolites using mitochondria using monoamine oxidase A MAO- A

173
Q

Where are alpha 1 adreno receptors found?

A

Post synaptic neurones

174
Q

Where are alpha 2 adreno receptors found?

A

Pre synaptic neurones

175
Q

Where are B1 adrenoreceptors found?

A

cardiac muscle and smooth muscle of GI tract

176
Q

Where are B2 adrenoreceptors found?

A

Uterine, bronchial and vascular smooth muscle

177
Q

Where are B2 adreno receptors found?

A

Fat cells

178
Q

Which receptors does adrenaline react with?

A

All receptors

179
Q

Which receptors does noradrenaline react with?

A

Alpha

Beta 1

180
Q

Which receptors does dopamine react with?

A

Alpha 1

Beta 1

181
Q

Which receptors does isoprenaline react with?

A

Beta receptors

182
Q

Where is renin secreted from?

A

Kidney

183
Q

What stimulates renin release?

A

Low blood pressure
Low sodium level
Sympathetic innervation of B1 adrenoreceptors

184
Q

Where is ACE secreted from?

A

Epithelial cells of the lung

185
Q

What are the functions of angiotensin II?

A

Potent vasoconstrictor
Enhances action of peripheral noradenaline
Increase sympathetic discharge
Catecholamine release from adrenal response

186
Q

What type of receptor is the AT 1 coupled receptor?

A

G1 and Gq protein coupled receptor

187
Q

Where are AT 1 receptors located?

A

Kidneys
Bood Vessels
Brain
Heart

188
Q

What is auto regulation?

A

The intrinsic capacity to compensate for any perfusion changes sensed

189
Q

What are the two theories of auto regulation?

A

Metabolic

Myogenic

190
Q

What is the metabolic theory?

A

As blood flow changes, the concentration of metabolites changes therefore the radius of vessels changes to accommodate the metabolites. This can be in response to c02, adenosine, protons and potassium ions.
For example, if the blood flow is lower, metabolites will accumulate so the radius increases

191
Q

What is the myogenic theory?

A

As blood flow increase, pressure rises and causes a stretch of the smooth muscles. Muscles respond to the stretch by undergoing vasoconstriction.

192
Q

Which mediator from platelets causes constriction?

A

Serotonin

193
Q

Where does vasopressin come from?

A

Neurohypophysis

194
Q

What do the sympathetic and parasympathetic nervous system control?

A

Sympathetic- circulation

Parasympathetic- heart rate

195
Q

What does the sympathetic nervous system not innervate?

A

Capillaries
Precapillary spincters
Metarterioles

196
Q

How does noradrenaline cause vasoconstriction?

A

Binds to alpha 1 receptors

197
Q

What receptors does adrenaline preferentially bind to?

A

Beta 2

198
Q

How can adrenaline bring about vasodilation?

A

Massive stimulation of the sympathetic nervous system can lead to increase concentration of adrenaline and some will bind to a receptors causing vasodilation

199
Q

What does the vasomotor centre consist of?

A

Pressor area
Depressor area
Cardioregulatory inhibitory centre

200
Q

How does the vasomotor centre transmit impulses?

A

Distally through the spinal chord

201
Q

How do vessels receive sympathetic innervation?

A

Via post ganglionic neurones

202
Q

How does the vasomotor centre stimulate vasoconstriction and vasodilation

A

Pressor area stimulates sympathetic nervous system

Depressor inhibits sympathetic nervous system

203
Q

How does adrenaline lead to increased contractility?

A

Adrenaline binds to beta 1 receptors on the heart which activates the cAMP pathway which causes a cascade effect. Upregulates calcium ATPase and the sarcoplasmic reticulum calcium channel

204
Q

Which extrinsic factors increase the contractility of the heart?

A

Increased sympathetic action

Adrenaline

205
Q

Which intrinsic factor increase the action of the heart?

A

Increased venous return which increases end diastolic volume

Increased respiratory movements lead to a decreased inter-thoracic pressure leading to lower end diastolic volume

206
Q

How do baroreceptors feed back to the brain from the carotid sinus and aortic arch

A

Carotid sinus- glossopharyngeal nerve

Aortic arch - vagus nerve

207
Q

What is the most sensitive range of the baroreceptor reflex?

A

90-100mmHg

208
Q

By which mechanism is the baroreceptor reflex controlled?

A

Recipricol innervation

209
Q

How does reciprocal innervation work?

A

Afferent input via the parasympathetic nervous system is coupled with an inhibitory sympathetic neurone.
Therefore blood pressure is decreased two ways.
Parasympathetic stimulation and inhibited sympathetic innervation decrease heart rest
Inhibited sympathetic innervation decreases stroke volume

210
Q

Why does gravity increase pressure in the foot?

A

Due to the hydrostatic pressure of the blood vessels

211
Q

Why may standing cause stroke volume to decrease?

A

Increased gravity causes hydrostatic pressure of the blood vessels to increase. This causes more blood to pool in the veins as veins are more compliant.
The increase in hydrostatic pressure can also cause blood to be driven out of the arteries which could result in oedema.
As a result of venous distension that is a reduction of circulating blood volume which decreases blood pressure and end diastolic volume and ultimately stroke volume.
The hypotension is transient

212
Q

What are the compensatory mechanisms for standing?

A

Baroreceptors sense a drop in pressure and relay this back to the vasomotor centre which release sympathetic discharge to the heart.
Disinhibition occurs where activation of the parasympathetic nervous system is halted alongside the inhibition of the sympathetic nervous system.
The sympathetic nervous system exhibits a chronotopic and ionotropic affect on the heart.
Vasoconstriction also allows less blood to be pooled in compliant veins and increases resistance. More blood enters the circulation, increasing end diastolic volume and stroke volume

213
Q

How does the sympathetic nervous system allow the kidneys to release renin?

A

Causes vasoconstriction of the sphlancic and renal beds

214
Q

What does the problems posed by haemorrhage differ from change in posture?

A

Haemorrhage results in an actual reduction in the volume of circulating blood

215
Q

What are the compensatory mechanisms for haemorrhage?

A

Hydrostatic pressure everywhere falls
Colloid osmotic pressure increases slightly due to fluid loss so solute concentration increases.
Autotransfusion occurs.
Low renal blood flow activates the renin-angiotensin system
Angiotensin II allows more renin to be released
Aldosterone increases sodium retention and water retention
Vasopressin increases water retention
Urinary output is decreased
More fluid is able to be kept in the body

216
Q

What is auto transfusion?

A

The net reabsorption of fluid from the interstitial fluid into the blood.
Erythrocytes are not replaces.

217
Q

How much blood loss can the compensatory mechanisms for haemorrhage cope with?

A

10%

218
Q

What is the challenge that exercise presents?

A

Maintaining blood pressure whist keeping blood flow at a high rate

219
Q

During exercise, which areas receive increased sympathetic output?

A

Gi tract

Kidneys

220
Q

During exercise which area received decreased sympathetic output?

A

Skin

221
Q

What negative things occur during exercise?

A

Increased capillary pressure across muscle leads to fluid loss
Salt and water is lost in sweat

222
Q

During exercise, why is there a net increase in cardiac output?

A

Increase sympathetic innervation and decreased parasympathetic innervation to the heart leads to increased stroke volume
Skeletal muscle pumps lead to increased venous return

223
Q

What is primary haemostasis?

A

Due to the release of chemical mediators from the endothelium, the vessel constricts which confines injury to one place.
Platelet aggregation causes the formation of an unstable plug

224
Q

What is secondary haemostasis?

A

The unstable plug formed into primary haemostasis is stabilised with fibrin.
The clot is dissolved in a process called fibrinolysis

225
Q

What are glycoproteins gp1a and gp1b?

A

Integrins that are present on the surface of platelets

226
Q

Describe platelet adhesion

A

After a vessel has been damaged, collagen is exposed.
This causes the binding of circulating von Willebrand factor.
Platelet will bind to this via GpIb
Platelets will bind directly to this via GpIa
Platelets that activate will undergo a morphological change and project filopodia

227
Q

What initiates platelet aggregation?

A

ADP and prostaglandins from the activated platelets which will cause circulating platelets to bind and become activated.

228
Q

Why is calcium required for the binding of further platelets?

A

Fibrinogen causes the binding of adjacent platelets via gpIIa and gpIIb
Fibrinogen needs calcium

229
Q

What is released during platelet activation?

A

Thromoxane
Prothrombin
Coagulation factor IIa

230
Q

Why are clotting factors formed?

A

Liver- many clotting factors
Endothelial cells- von Willebrand factor
Megakaryocytes- precursors of platelets

231
Q

How is inappropriate coagulation prevented?

A

Coagulation factors are kept separate from the initiators of coagulation

232
Q

How can coagulation be initiated?

A

Vessel damage- intrinsic pathway

Trauma- extrinsic pathway

233
Q

Explain the intrinsic pathway

A

The exposed collagen allows the first coagulation factor to bind
Factor XII is converted to Factor XIIa
Factor XIIa converts XI to XIa
Factor XIa converts IX to IXa
In the presence of factor VIIIa and PI, factor IXa converts X to Xa which activates the common pathway

234
Q

Describe the extrinsic pathway

A

Trauma causes the conversion of Factor VII to VIIa under the influence of a tissue factor
Tissue factor and VIIa combine to form the complex TF-VIIa
TF-VIIa causes Factor X to be converted to Xa, activating the common pathway
TF-VIIa also contributes to the intrinsic pathway by converting IX to IXa

235
Q

Describe the common pathway

A

Father Xa converts Factor II (prothrombin) to IIa in the presence of Va and PI
IIa (thrombin) converts fibrinogen into insoluble fibrin
IIa also converts XIII into XIIIa
IIa activates more platelets

236
Q

What is the role of Factor XIIIa

A

Allows cross linkages between the fibrin molecules leading to the formation of the fibrin plug

237
Q

What causes plasminogen and plasminogen activating factor to bind?

A

The presence of the fibrin clot to form active plasmin

238
Q

What is the purpose of plasmin?

A

To degrade the fibrin clot, leaving being fibrin degradation products

239
Q

How is coagulation inhibited?

A

Direct - antithrombin

Indirect- protein C

240
Q

What does antithrombin inhibit?

A

Factors IXa, Xa, XIa

Thrombin

241
Q

Why is heparin given for immediate anticoagulation in venous thrombosis and pulmonary embolism?

A

It accelerates the action of antithrombin

242
Q

Explain indirect inhibition of coagulation

A

The endothelium expresses thrombomodulin which thrombin binds to.
Protein C binds to this and causes activated protein C.
Activated protein C break down Factors Va and VIIIa

243
Q

Which genetic variation process causes coagulation to be more prominent?

A

Factor Va Leiden cannot be broken down by protein C and protein S

244
Q

What are the risk factors of thrombosis?

A

Antithrombin deficiency
Protein S deficiency
Protein C deficiency
Factor Va Leiden

245
Q

What can defects in primary haemostats exist?

A

Absent collagent
Lack of von Willebrand factor
Lack of platelets

246
Q

What increases the lack of collagen?

A

Steroid use

Age

247
Q

What causes lack of platelets?

A

Aspirin

Thrombocytopenia

248
Q

What are the characteristics of defects in primary haemostasis

A 
Bleeding is immediate 
Easy bruising 
Prolonged epistaxis
Menorrhagia 
Petechiae
Bleeding after trauma or surgery 
Prolonged gum bleeding
249
Q

What is an example of a defect in secondary haemostasis?

A

Haemophilia

250
Q

What is diluted coagulapathy?

A

Dilution of blood by transfusion leads to there not being enough coagulation factors

251
Q

What is dissemated intravascular coagulapathy?

A

Excessive protein consumption
Small clots form throughout the body using up the clotting factors and normal coagulapathy being disrupted
Being activated monocytes and macrophages can express tissue factor on their surface

252
Q

How may dissemated intravascular coagulapathy lead to organ failure?

A

Formation of many micro clots means fibrynolisis is activated a lot using up fribinogen. Fibrinogen can deposit fibrin and block up organs

253
Q

What are the characteristics of secondary haemostatic defects?

A

Delayed bleeding
Deeper bleeding in joints and muscles
Nosebleeds are rare
Bleeding occurs after trauma or surgery after intramuscular injections

254
Q

What can cause clot instability?

A

Excess plasmin
Excess plasminogen activating factor
Deficient antiplasmin

255
Q

What can arterial thrombi cause?

A

Myocardial infarction
Limb ischaemia
Strokes

256
Q

What can venous thrombi cause?

A

Oedema

Pain

257
Q

What are risk factors for venous thrombosis?

A

Age
Previous illness and events
Genetics

258
Q

What is Virchow’s triad?

A

Blood stasis
Hypercoagulability
Endothelial injury

259
Q

What type of thrombi can blood stasis cause?

A

Venous

260
Q

What type of thrombi can hyper coagulability cause?

A

Arterial and venous

261
Q

What type of thrombi can endothelial injury cause?

A

Arterial

262
Q

What are foam cells?

A

Macrophages that migrate to the endothelium and uptake lipids that have been deposited

263
Q

Where do LDLS deposit in the endothelium?

A

Under the tunica intima and bind to matrix proteoglycans

264
Q

What oxidises the LDL’s?

A

Free radicals

265
Q

What do oxidised LDLs release?

A

Aldehydes

266
Q

How is cholestrol released from LDL’s?

A

Products of LDL oxidation bind to apoproteins on the surface of LDL’s

267
Q

Why do scavenger receptors on macrophages keep on uptaking modified LDL’s?

A

They have no negative feedback system

268
Q

Why may inflammation occur as a result of foam cells?

A

They secret inflammatory mediators

269
Q

How do foam cells forms a plaque?

A

They undergo atoptsis

More monocytes are recruited which also secrete inflammatory mediators

270
Q

How do vascular endothelial cells aid the development of lesions?

A

Act as a barrier site to leukocytes and allow them through

Function as leukocyte recruitment in response to inflammatory mediators causing more inflammation

271
Q

How do platelets aid the development of lesions?

A

Important in thrombus formation
Release cytokines to recruit other platelets
Release growth factors

272
Q

How do monocytes/macrophages aid the development of lesions?

A

Become foam cells
Secrete cytokines and growth factors
Source of free radicals leading to oxidation of LDL’s and more foam cells being formed
Secrete mettaloproteinases which break down extracellular matrix and allow more clots to form and LDL’s to bind

273
Q

How do vascular smooth muscle cells aid the development of lesions?

A

Allow migration of cells and LDL’s
Required for collagen synthesis
Required for formation of fibrous cap

274
Q

How do T-lymphocytes aid the development of lesions?

A

Important in activating macrophages

275
Q

Why are areas where arteries bifurcate prone to plaque formation?

A

Disruption of laminar flow
Mini-reversals of flow of blood
More turbulent
More vulnerable to damage

276
Q

What is plaque erosion?

A

Breakdown of the endothelial lining of the plaque without full rupture of the fibrous plaque

277
Q

What is plaque rupture

A

Rupture of the fibrous cap which separates the plaque from the blood

278
Q

What factors predispose to an instable plaque?

A 
Lipid rich core 
Thin fibrous cap 
Low collagen 
Low vascular smooth muscle cells 
Infiltrative macrophages 
Neurovascularisation
279
Q

What degrades collagen?

A

Macrophages

280
Q

What will transient ischaemic attack in the eye cause?

A

Amaurosis fugax

281
Q

What initiates the formation of the vasa vasorum?

A

Vascular endothelial growth factor

282
Q

Where are vasa vasorum located?

A

Tunica adventitium

283
Q

What is the function of the vasa vasorum?

A

Supplied larger blood vessels with smaller vessels

Recruits monocytes

284
Q

Why can the vasa vasorum cause haemorrhage?

A

Extra blood supply is weak and prone to rupture

285
Q

What is stenosis?

A

The gradual narrowing of arteries

286
Q

What are the main types of cell involved in development of atherosclerosis?

A

Vascular endothelial cells
White blood cells
Platelets
Vascular smooth muscle cells

287
Q

What do the three layers of the vascular endothelium consist of?

A

Tunica intima- endothelium
Tinica media- smooth muscle cells
Tunica adventitia - vasa vasorum, nerves

288
Q

What are the functions of the endothelium?

A

Vascular tone and permeability
Haemstasis and thrombosis
Inflammation
Angiogenesis

289
Q

What is angiogenesis?

A

When new blood vessels sprout from currently existing ones

290
Q

What is the Janus paradox?

A

The fact that in atherosclerosis, angiogenesis has both beneficial and harmful benefits.
Will vascularise the plaque therefore promote its growth
Will also reach areas occluded by the plaque and therfore prevent damage post ischaemia

291
Q

What is senescence?

A

The limited proliferative capacity of human cells in culture

292
Q

What is the cause of senescence?

A

The shortening and dysfunction of telomeres

293
Q

What can induce senescence?

A

Cardiovascular risk factors eg.
Smoking
Oxidative stress

294
Q

Which chemical in red wine has beneficial effects in preventing atherosclerosis?

A

Resveratrol

295
Q

What is hermatic action?

A

Beneficial at low doses

Cytotoxic at high doses

296
Q

Where are endothelial progenitor cells derived from?

A

Circulating bone marrow CD34+ stem cells

297
Q

What causes the mobilisation of EPC’s?

A

Ischaemia
Pro-angiogenic factors
Statins

298
Q

Why may EPC’s be injected at the site of ischaemia?

A

Migrate to site and contribute to re-endothilisation and angiogenesis

299
Q

What is hypertension?

A

A persons blood pressure is constantly over 140/90 mmHg

The level of blood pressure above which investigation and treatment could do more good than harm

300
Q

What influences primary hypertension?

A

Genetics

Environment

301
Q

Give example of monogenic causes of hypertension

A

Liddle’s syndrome

Mineralcorticoid excess

302
Q

What are the environmental factors of hypertension?

A 
Dietary salt 
Alcohol Consuption 
Obesity 
Pre natal environment 
Pregnancy
303
Q

What are the causes of secondary hypertension?

A 
Renal disease (renal artery stenosis 
Tumours secreting catecholamines 
Tumours secreting aldosterone 
Conn's sydrome 
Oral contraceptive pill
304
Q

What is phaoechromacytoma?

A

Tumours secreting catecholamines

305
Q

What is Conn’s sydrome?

A

Tumours secreting aldosterone leading to hyperaldosteronism.
More fluid retention and greater blood volume

306
Q

What are the risks associated with hypertension?

A 
Coronary heart disease
Atrial fibrillation
Stroke 
Retinopathy 
Heart failure
307
Q

How can hypertension call chambers to become smaller?

A

Causes left ventricular hypertrophy causing cardiac remodelling to compensate for the higher blood pressure

308
Q

What can coronary artery disease present with?

A

Arrhythmia
Acute coronary syndrome
Coronary artery death
Heart failure

309
Q

What is angina pectoris marked by?

A

Discomfort in shoulders, chest, arms, jaw and back

310
Q

How is angina relieved?

A

Rest

Nitroglycerin within 5 minutes

311
Q

What are the treatments for angina?

A

Improving blood supply by revascularisation
Reducing demand for metabolic oxygen by reducing heart rate
Preventing development of atherosclerosis

312
Q

What is myocardial infarction?

A

Cell death arising from interrupted blood flow to the heart

313
Q

Which cardiac protein can be used to detect necrosis of cardiac tissue?

A

Troponin

314
Q

Which of Virchow’s triad has the most dominant influence in arterial thrombosis?

A

Endothelial injury

315
Q

Which thrombi are common in arterial thrombosis?

A

White thrombi - platelet rich

316
Q

Which thrombie are common in venous thrombosis?

A

Red thrombi- fibrin rich

317
Q

What is the nature of white infarcts?

A

Anaemic

318
Q

What is the nature of red infarcts

A

Haemorrhagic

319
Q

What type of organs to red and white infarctions affects?

A

White- kidney and spleen (solid)

Red- lung (loose)

320
Q

What are the characteristics of red infarctions?

A

Occlusion of a vein
Loose tissues that allow blood to collect in the infarcted zone
Tissues with dual circulatory system
Reperfusion of previous ischaemic tissue

321
Q

What occurs after an infarction

A

There is cardiac remodelling
Infarction replaced with fibrous tissue
Infarct is expanded, thinned and elongated
Left ventricle dilates to reduce wall tension and maintain cardiac output
Non infarcted tissue undergoes electrical recoupling

322
Q

What are the adverse affects of remodelling?

A

Increased mixed venous oxygen
Ventricular arrhythmia’s and fibrillation
Mitral regurgitation
Decreased myocyte shortening
Increase systolic and diastolic wall tension

323
Q

What is given to reduce affects of remodelling?

A

ACE inhibtors

Beta blockers

324
Q

What is reperfusion injury?

A

Increased damage to heart tissue. Restored blood flow reintroduces oxygens in cells which damages cellular proteins, DNA and plasma membrane

325
Q

How is reperfusion injury reduced?

A

Cardioprotection

326
Q

What is the acute management of thrombotic burden?

A

Thomboectomy and giving drugs

327
Q

What is the recurrent management of thrombotic burden?

A

Anti-coagulants and anti-platelets

328
Q

How are plaques stabilised?

A

Put in a stent

Give statins and ACE inhibitors

Year 1: LSS 1 (3 decks)

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