M103 T3 L3 Flashcards

1
Q

What stresses cause a blood vessel to burst?

A

internal stresses
Turbulent flow
Large diameter - high wall tension
Low compliance - when the blood vessel is stiff or not stretchy enough

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2
Q

What damage can cause a blood vessel to burst? (TAD)

A

Trauma
Atherosclerosis
Diabetes

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3
Q

What is the relationship between diameter and wall tension in a blood vessel?

A

The larger the vessel, the greater the wall tension

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4
Q

What is the difference between low and high compliance vessel graphs?

A

high - has a more vertical slope with a positive gradient

low - has a more horizontal slope with a positive gradient

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5
Q

What does a double arrow in a low / high compliance vessel graph represent?

A

the pulse pressure between systole and diastole turbulence

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6
Q

What is a feature of laminar flow?

A

flow is slow at the edges

most of the fluid molecules travel in a straight line

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7
Q

What causes turbulent flow?

A

if the vessel is branching
if the blood has low viscosity
high speed flow
obstacles (e.g. atherosclerosis)

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8
Q

How does the endothelium lining blood vessels control blood vessel tone?

A

the inner endothelial surface layer cells monitor the blood vessel
the ends of these cells secrete nitric oxide for vasodilation and also control vasoconstriction
lets them regulate perfusion in the local area

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9
Q

What activities does the endothelium regulate?

A
blood vessel tone
fluid filtration
haemostasis
white cell recruitment
angiogenesis
hormone tracking
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10
Q

How is the endothelium responsible for fluid filtration?

A

bc it helps make different secretions via fluid filtration

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11
Q

What are the effects of acute myocardial infarction?

A

reduces the capacity of the heart to pump
if there is one large or many small infarct(s), can lead to heart failure where the pump of the heart is functioning suboptimally - doesn’t pump out enough blood
can be fatal - can trigger arrhythmia and HF

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12
Q

What are the symptoms of atherosclerosis?

A

asymptomatic but can lead to other disorders

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13
Q

What is atherosclerosis caused by?

A

hyperlipidaemia
immune action
unknown aetiology

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14
Q

What are the symptoms and primary cause of coronary artery disease?

A

Angina or asymptomatic

atherosclerosis

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15
Q

How is coronary artery disease treated?

A

drugs for hyperlipidaemia, angina or hypertension
stenting
surgically replacing clogged vessels

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16
Q

Are atheromas dangerous?

A

they are relatively safe, even if they occlude 50% of a vessel.
However, if plaque rupture occurs in a coronary artery, a thrombus or embolism - myocardial infarction

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17
Q

How is the sympathetic NS involves with MI’s?

A

releases adrenaline and noradrenaline in response to pain and to haemodynamic abnormalities
can help compensate for HF - increases heart rate, contractibility strength
increases peripheral resistance - can make it harder for the heart to pump out blood but powerful resistance can also help to maintain pressure
can lead to an increase in arrhythmia - can lead to sudden death

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18
Q

What are the two forces that act on water in a capillary?

A

Hydrostatic and Osmotic pressure

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19
Q

What is the usual osmotic pressure in a capillary?

A

25 mmHg bc there’s usually more water and protein on the inside

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20
Q

How does hydrostatic pressure vary through a capillary?

A

the arterial end will have a higher hydrostatic pressure than the venous end
in the arterial end the net pressure is driving the fluid out because the hydrostatic pressure is greater than that of the osmotic pressure
the opposite is true for the venous end

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21
Q

What happens to fluid moved out of capillaries’ arterial end by hydrostatic pressure?

A

leaks out of the vessel
finds its way to lymphatics
travels in the same direction to the blood vessel
the blood vessel will draw the liquid back out of the lymphatic further down the line

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22
Q

How does a Pulmonary Oedema occur?

A

fluid going out of the blood vessels
not brought by a lymphatic so it doesn’t return to the blood vessel
leads to net fluid accumulation in the tissue outside of the blood vessel

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23
Q

What effect does Pulmonary Oedema have on gas exchange?

A

impaired gas exchange bc the extra oedema fluid in the lungs prevents the newly breathed oxygen from getting to the blood vessels buried inside of the lung
the O2 diffusion path is lengthened

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24
Q

What is the most common cause of pulmonary oedema?

A

left heart failure - there is a net damning of blood - it can’t go into the left heart
this build up of blood in the left heart causes the blood to move back into the pulmonary vasculature / the lungs
causes a net increase in hydrostatic pressure inside the pulmonary circulation
results in a net fluid leak outward

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25
Q

What are the symptoms of pulmonary oedema? (DOH)

A

dyspnoea and / or orthopnea

both can lead to hypoxia

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26
Q

What are the effects of peripheral oedema?

A

often associated with gravitational effects

the swelling of tissues, especially the ankles

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27
Q

What is the main cause of peripheral oedema?

A

chronic low output HF

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28
Q

Is compensation beneficial?

A

it’s normal - it’s what you want to occur
If there’s a problem with a physiological function, you compensate
this prevents that there being a shortfall of something else
HOWEVER
cardiac remodelling is initially compensatory but later on, they become pathological - they cause risks to the person’s health and life

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29
Q

How is HF compensated for?

A

plasma volume is increased, which increases sympathetic activity
pressure increases, as does the net amount of pumping out of the heart

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30
Q

How will a patient with decompensated HF present and why?

A

patient will present with “not being able to breathe” usually due to the fact that there is water inside the lungs

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31
Q

What is cardiac modelling caused by?

A

injury such as MI or long term hypertension or valvular disease
occurs in response to an increase in preload or afterload

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32
Q

What two forms of cardiac modelling are there?

A

hypertrophy

changes shape

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33
Q

What is a consequence of Takotsubo cardiomyopathy?

A

weakens the heart muscle and means it doesn’t pump blood as well as it should

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34
Q

What treatment inhibits cardiac remodelling?

A

ACE inhibitors and spironolactone

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35
Q

From where is ADH secreted from and what type of molecule is it? (PPG)

A

the posterior pituitary gland

a peptide

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36
Q

What is the effect of aldosterone on the kidneys?

A

theyl’ll reabsorb more NaCl and water

directly decreases natriuresis which goes on to decrease diuresis

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37
Q

From where is aldosterone secreted from and what type of molecule is it?

A

the adrenal cortex

a steroid

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38
Q

What is the relationship between diuresis and blood pressure?

A

Decreased diuresis leads to higher bp

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39
Q

What does angiotensin II have an effect on?

A

vasoconstriction - increases bp
increased fluid retention
contributes to ventricular hypertrophy and heart remodelling

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40
Q

How does angiotensin II increase fluid retention?

A

more ALDOSTERONE < NA+ RETENTION
more ADH

it increases aldosterone secretion from the adrenal cortex which increases sodium retention
it increases ADH secretion from the posterior pituitary

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41
Q

When might cardiac hypertrophy be beneficial or dangerous?

A

beneficial - athlete and pregnancy

disadv - heart failure

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42
Q

What are the effects of ACE?

A

is extremely active and it will go to the adrenal cortex and affect reabsorption of water and salt, & compensation
LOWERS bp

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43
Q

What is the survival rate for Chronic low output heart failure?

A

a poor five year survival rate

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44
Q

What causes congestive HF?

A

the patient only have left HF failure, but not right
the right heart pumps blood into the lungs as usual, but the left atrium is too full
suddenly there is the amassing of hydrostatic pressure in the pulmonary circulation (left) because there’s damming of the blood
the blood goes into the lungs, but it can’t leave because the left heart isn’t pumping sufficiently
in the extreme, fluid starts leaking out of the blood vessels and into the lungs
leads to respiratory problems / symptoms

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45
Q

What happens in the case of right HF, but not left HF?

A

in a normal heart, a normal central venous pressure pushes blood into the right heart, but the right heart isn’t pumping out blood
causes a backup of blood
the central venous pressure will build up fluid, but there will be no place for it to go because it can’t return to the heart because the right heart isn’t empt
causes an increase in central venous pressure

46
Q

What systemic symptoms could right HF lead to?

A

potentially peripheral oedema

ascites

47
Q

What are the symptoms of HF? (Fat People oD)

A

Fatigue
Peripheral Oedema
Dyspnoea

48
Q

Why is fluid retention a feature of all forms of HF?

A

initially compensatory / homeostatic
leads to Dyspnoea, Ascites, Ankle oedema
retains too much fluid - volume overload

49
Q

How does cardiogenic shock progress?

A

there is insufficient perfusion of tissues, especially in the heart, so it will beat less and pump with reduced strength
ends up pumping even less blood out, so the originally insufficient profusion of the heart becomes even worse
this is how insufficient perfusion progresses by positive feedback

50
Q

How is cardiogenic shock treated?

A

Aggressive IV fluid AND Oxygen and the airway must be maintained

51
Q

What are chronic HF treatments? (ADB)

A

ACE Inhibitors, Diuretics and Beta blockers

52
Q

What is the aim that chronic HF treatments are trying to achieve?

A

to reverse the body’s homeostatic response to HF which are dangerous / damaging in the long term

53
Q

What leads to the kidney accumulating fluid?

A

the normal, homeostatic response to low cardiac output

54
Q

Why does the kidney accumulate fluid?

A

the kidney can’t recognise the difference between a haemorrhage and HF
Prehistorically, haemorrhages were much more common than HF, which only happens in people around 50 years old and many didn’t survive until that age
the kidney detects low pressure and assumes it is a haemorrage - loss of fluid - and so decides to retain fluid to try and stop the haemorrage
However, in the case that this is HF, it backfires and is dangerous

55
Q

When the kidney increases plasma volume, what does it lead to?

A

fluid overload

the heart is already damaged so it’s unable to pump this fluid

56
Q

What happens when the heart is unable to pump out extra fluid?

A

Fluid damming leads to increased venous hydrostatic pressures
Increased back pressure further damages heart
this positive feedback loop leads to rapid detioration

57
Q

What processes occur during decompensated heart failure?

A

the kidney increases plasma volume
the heart is unable to pump out extra fluid
the capillaries leak fluid into the tissues
the lungs have fluid and so can’t exchange o2 and co2

58
Q

What are the three treatment goals for low output HF?

A

prevent acute decompensated HF
counteract cardiac remodelling
minimize symptoms

59
Q

What is another terms for a stroke?

A

cerebrovascular accident

60
Q

What does RAAS stand for?

A

renin-angiotensin-aldosterone system

61
Q

What does ACE stand for?

A

angiotensin converting enzyme

62
Q

What is ADH otherwise known as?

A

vasopressin

63
Q

What are the criteria for shock?

A

systolic bp > 90 mmHg

usually 125 mmHg

64
Q

What is the role of renin?

A

to convert angiotensin I into II

65
Q

What is an example of a diuretic drug?

A

thiazimide

66
Q

What is the role of thiazide-like drugs?

A

to block reabsorption at the DCT

67
Q

What are internal stresses caused by?

A

high pressures from high bp or downstream blockages

68
Q

What does Low compliance describe?

A

if the blood vessel is stiff or not stretchy enough

69
Q

What is an example of trauma that could cause a blood vessel to burst?

A

Transluminal procedures

70
Q

What can pulmonary oedema lead to?

A

ascites

71
Q

What is an example of a Transluminal procedure?

A

PCI

72
Q

What are examples of dyspnoea that appear in HF?

A

orthopnoea, paroxysmal nocturnal dyspnoea

73
Q

How do ACE Inhibitors work to treat chronic HF?

A

stops the heart from trying to remodel itself and become larger

74
Q

How do Diuretics work to treat chronic HF?

A

stops the heart from trying to increase its ability to maintain fluid

75
Q

How do Beta blockers work to treat chronic HF?

A

stops the heart from trying to increase pressure via heart rate and contractibility

76
Q

What do murmers signify?

A

the improper closing of valves

77
Q

What age group is Degenerative valvular disease common in?

A

in the elderly of the UK

78
Q

Where is rheumatic fever seen globally?

A

not seen in the UK but in areas of poverty in 3rd world countries

79
Q

What is Rheumatic valve disease caused by?

A

rheumatic fever

80
Q

What is the most common valve disease in EU?

A

aortic stenosis

81
Q

How are the leaflets of the bicuspid valve made?

A

often two of the other leaflets will be fused together making one, so instead of a tri leaflet valve, they’ll have a bi-leaflet valve

82
Q

What is aortic regurgitation otherwise known as?

A

incompetence

83
Q

What is an Early diastolic murmur caused by?

A

aortic regurgitation

84
Q

What is a fulminant pulmonary oedema caused by?

A

when pressure is pushed back from the left side of the heart onto the vasculature very quickly without the body being able to accommodate

85
Q

What happens during Mitral valve prolapse?

A

Initially valve shuts during the early part of systole but then, either because the leaflet is too ‘baggy’ or because of abnormal sub-valvar apparatus the leaflet prolapses back into the left atrium potentially allowing though a jet of regurgitation

86
Q

What are other terms for Mitral valve prolapse?

A

click-murmur syndrome
Barlow’s syndrome
floppy valve syndrome

87
Q

How does a Systemic emboli form a pulmonary embolism?

A

it always impacts in the lungs after passing through the right side of the heart

88
Q

What are mechanical valves?

A

metallic valves

89
Q

What are biological valves?

A

prosthetic valves

90
Q

What is the normal pulse pressure?

A

approximately 40 mmHg

91
Q

What sound is made for the duration of the systole and for mitral regurgitation?

A

pan-systolic murmur

92
Q

Why does HF need to be compensated for?

A

needs to maintain cardiac output - can’t because of damage

93
Q

What leads to the kidney accumulating fluid?

A

decreased GFR
increased Central Venous Pressure
increased Venous Return
increased preload in the right ventricle

94
Q

What is the criteria for ascites?

A

more than 25 ml of fluid in the peritoneal cavity, although volumes greater than one liter may occur

95
Q

Why is flow slow at the edges in laminar flow?

A

friction is created from the fluid moving against a non-moving surface - slows them down

96
Q

What fluids is the endothelium responsible for creating via filtration?

A

the BBB, CSF and GI secretions (in the glomerulus in the kidney)

97
Q

What is the role of the endothelium in the BBB?

A

it filters most molecules out of the BBB

98
Q

What are examples of catecholamines?

A

dopamine

norepinephrine and epinephrine

99
Q

What did epinephrine used to be known as?

A

adrenalin or adrenaline

100
Q

What is the main hormone secreted by the adrenal medulla?

A

Adrenaline

101
Q

When is epinephrine released?

A

when the brain perceives danger and the ANS is activated

102
Q

By what process is the flight or fight response stimulated?

A

amygdala triggers the hypothalamus < activates the ANS < adrenal gland secretes epinephrine < fight or flight

103
Q

In what conditions is epinephrine released?

A

low bp and stress

104
Q

What are the effects of norepinephrine on the body?

A

vasoconstriction < increased bp
increased heart rate
increased blood sugar levels

105
Q

Where is adrenaline made?

A

almost exclusively in the adrenal medulla

106
Q

Where is noradrenaline made?

A

Predominantly in the symp NS

107
Q

What type of biological substance is adrenaline?

A

acts mainly as a hormone and is released primarily by the adrenal medulla into the bloodstream

108
Q

What type of biological substance is noradrenaline?

A

acts mainly as an NT at the synapse between neurons when released from symp neurons (stored in vesicles).
is released in small concs as a hormone in the blood circulation by the adrenal medulla

109
Q

What is adrenaline synthesised from?

A

noradrenaline

110
Q

What is noradrenaline synthesised from?

A

dopamine

111
Q

When is adrenaline released?

A

at a stressful moment such as a fight/flight situation

during stress

112
Q

When is noradrenaline released?

A

continuously as a hormone in the blood circulation at a low dose