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LIFESCI 3AA3 > TOPIC TWO: HYPERTENSION AND ATHEROSCLEROSIS > Flashcards

TOPIC TWO: HYPERTENSION AND ATHEROSCLEROSIS Flashcards

1
Q

What is tachycardia

A

High heart rate

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2
Q

What is hypernatremia

A

high sodium in the blood

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3
Q

What is normal sodium levels

A

125 - 135 mmol/L

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4
Q

What is hypertension

A

High blood pressure

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5
Q

What is the systolic and diastolic blood pressure indicative of hypertension

A

Systolic: ≥ 135mmHg
Diastolic: ≥ 85mmHg

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6
Q

What were the old standards to diagnose hypertension

A

140/90

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7
Q

What is diastolic pressure

A

Pressure exerted on the inside of the blood vessels by the blood when the heart is in relaxation

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8
Q

What is systolic pressure

A

Pressure exerted on the inside of the blood vessels by the blood when the heart is in systole (contracting)

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9
Q

What is the device used to diagnose HTN

A

Automated blood pressure cuff

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10
Q

Do people always have symptoms of HTN

A

NO! It can be asymptomatic, but the damage is already done - silent killer

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11
Q

What does primary/essential HNT mean and what % of HTN fall under this category

A

Unknown cause

90-95% of patients

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12
Q

What does secondary HNT mean and what % of HTN fall under this category

A

High blood pressure caused by something else (disease, medication etc.)

5-10%

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13
Q

How much of an increase in HTN has there been over time

A

60%

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14
Q

Why has there been an increase in hypertension

A

More awareness - more people are being tested, more people are being diagnosed

More risk factors - diabetes, obesity, sedentary behaviour

Women are more likely to visit the doctor therefore more likely to be diagnosed

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15
Q

What are some consequences of HTN (6)

A

Heart disease

  • Left ventricular hypertrophy
  • Coronary heart disease
  • Heart failure
Kidney failure
Peripheral Vascular Disease
Retinopathy
Hemorrhage and stroke
- Could possibly lead to dementia
Impotence (in men)
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16
Q

Do people die from HTN?

A

NO
People die from what HTN causes

  • MIs
  • Heart failure
  • Ischemic heart disease
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17
Q

Anatomy of a Vessel

What are the three layers

A

Tunica intima/Interna

Tunica media

Tunica externa (adventitia)

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18
Q

Anatomy of a Vessel

Where is the tunica intima located

What is it made of

A

The most internal part of the blood vessel, closest to the lumen

Made of endothelium and connective tissue that makes direct contact with the blood

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19
Q

Anatomy of a Vessel

What is the lumen

A

Open space where the blood flows through

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20
Q

Anatomy of a Vessel

What does the tunica intima release

A

Endothelins

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21
Q

Anatomy of a Vessel

What are endothelins

A

Vasoactive substance

Vasoconstrictor that acts on the smooth muscle in the tunica media to cause vasoconstriction

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22
Q

Anatomy of a Vessel

Where is the tunica media located

What is it composed of

A

The middle layer

Composed of smooth muscle and connective tissue

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23
Q

Anatomy of a Vessel

Where is the tunica external located

What is it composed of

A

Outer layer

Sheath of connective tissue keeping the vessel in place

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24
Q

What variables affect blood flow and pressure (5)

A 
Compliance (most relevant)
Cardiac output
Volume of blood
Viscosity
Blood vessel length and diameter
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25
Q

How does compliance affect blood flow and pressure

What is the definition

A

Compliance is the ability to expand and the degree fo resistance, vascular tone (ability for the vessel to constrict and react)

We want a good vascular tone and a low degree of resistance so that the blood can flow easily and the heart does not have to work as hard to pump the blood

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26
Q

How does cardiac output affect blood flow and pressure

What is the definition

What receptors control it

What activates it

A

Cardiac output is the amount of blood pumped by the heart (L/min)

The beta receptors on the heart control the degree of contractility

The beta receptors are activate by the SNS

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27
Q

How does volume of blood affect blood flow and pressure

A

Greater the volume of blood, the greater the pressure

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28
Q

What is a diuretic

A

A water pill which deceases blood volume by decreasing H2O in the blood

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29
Q

How does viscosity affect blood flow and pressure

A

The more viscous, the greater the pressure exerted on the vessel wall

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30
Q

How does blood vessel length affect blood flow and pressure

A

The longer the vessel, the greater the resistance and the lower the flow

The farther away from the heart (longer the vessel) means higher resistance and lower flow

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31
Q

What is the relationship between resistance and pressure

A

When you increase resistance, you increase pressure

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32
Q

What is the relationship between vessel diameter and resistance

A

Resistance is inversely proportional to diameter

A slight decrease in diameter leads to a huge increase in resistance

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33
Q

What is the formula for resistance related to radius

A

Resistance = 1/radius^4

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34
Q

What is Atherosclerosis

A

Narrowing and hardening of the arteries due to plaque build up

Blood flow is significantly changed when there is narrowing of the vessel (increased resistance)

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35
Q

What is endothelial dysfunction

A

When the endothelium doesn’t produce or respond to vascoactive substances

There is decreased vascular tone and responsiveness to vasoactive substances. Therefore the blood vessel cannot constrict and dilate in a healthy manner which can lead to hypertension over time

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36
Q

Where are the endothelial cells and what do they do

A

The endothelial cells line the intima

Normally produce or respond to vasoactive substances

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37
Q

What are vasoactive substances

A

Substances that act on the smooth muscle of the blood vessels to cause construction and dilation

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38
Q

What type of vasoactive substance is Nitric Oxide (NO)

A

Vasodilator

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39
Q

What type of vasoactive substance is endothelin

A

Vasoconstrictor

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40
Q

What type of vasoactive substance is prostacyclin

A

Vasodilator

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41
Q

How does endothelial dysfunction work

A

Stiff vessels (that are not responding/producing to vasoactive substances) lead to increased blood pressure and increases sheer stress which results in endothelial dysfunction

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42
Q

What is the results of endothelial dysfunction (NO)

A

There is a reduction in nitric oxide synthase which results in less NO production

NO is a vasodilator therefore there is more constriction

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43
Q

What is the result of endothelial dysfunction and ADMA

What does ADMA usually do

A

There is an increase in asymmetric dimethylarginine (ADMA)

ADMA blocks the production of NO from L-arginine

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44
Q

Is atherosclerosis a static or dynamic process

A

Dynamic

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45
Q

What are the other bodily processes involved in atherosclerosis

A

The immune system + inflammation

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46
Q

What is the mediator of atheromata formation (general)

A

Immune cells

There are many immunes cells involved and some are located in the atheromata as well

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47
Q

What is an atheromata and where is it located

A

Accumulation of debris under the intima layer of blood vessel

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48
Q

What is innate immunity

A

Immune response that happens quickly in the body without previous exposure or education

Happens right away

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49
Q

What is adaptive immunity

A

Immunes response that occurs after “education” or exposure to microbe

Slower

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50
Q

What are leukocytes

A

White blood cells

Immune cells

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51
Q

What are the immune cells of interest here

A

Macrophages
Dendritic cell
Mast cell

52
Q

Atherosclerosis formation

Step One

A

The LDL particle (previously traveling through the blood) slips between two endothelial cells which line the intima

53
Q

Atherosclerosis formation

Step Two

A

The LDL particle becomes oxidized by 8-10 chemical reactions

54
Q

Atherosclerosis formation

Step Three

A

The oxidized LDL particles are binding to the CD 36 scavenger receptor on the macrophage/monocyte

This is a spark of the reaction

55
Q

Atherosclerosis formation

Step Four

A

Binding of the oxidized LDL causes a cascade of events

The monocyte/macrophages engulf the LDL - foam cell

There is a signal sent to the endothelial cells toe start expressing more adhesion cells to attract more monocytes to that particular spot

There is also an increase in adhesion of smooth muscle cells to macrophages and foam cells in plaque

There is movement of the smooth muscle cells from the media compartment to the intima compartment and they start to adhere to the immune cells

56
Q

Atherosclerosis formation

Step Five

A

There is the development of foam cells when the macrophage engulfs the oxidized LDL particle

This is the key cell type found in atherosclerosis

57
Q

Where is the atheroma forming

A

In the intima layer

58
Q

What is in the atheroma

A

Smooth muscle cells have moved from the media to the intima

Macrophages, white blood cells and foam cells are here

The small intima compartment has now grown and is encroaching on the lumen

There is proliferation and movement of cells form the media to the intima

The blood vessel is remodelling in a detrimental way

59
Q

Role of monocytes

When are they involved in atherosclerosis

A

Very early during lesion formation and later in the established lesion

60
Q

Role of monocytes

What are they attached to and how

A

The endothelial cells via surface adhesion molecules

61
Q

Role of monocytes

What doe they do

A

Cause inflammation, cause the production of cytokines and ROS, suppress NO and have an effect on TNF alpha and IL 1

Causes a cytokine storm

62
Q

Role of monocytes

What do cytokines do

A

Direct monocytes to the intima, which continues as the lesion progresses

63
Q

Role of monocytes

What do monocytes express that are essential for the SPARK of atherosclerosis

A

CD36 receptors

Oxidized LDL binds to CD36 receptors

64
Q

Role of monocytes

What do TLR do and what cells express them

A

Monocytes and macrophages have toll like receptors (TLR) that trigger pro inflammatory cytokine cascade (TNF, IL-1 increase)

65
Q

Role of monocytes

How do activated monocytes lead to more tissue damage

A

Produce Matrix metalloprotienases (MMP) and ROS

66
Q

Role of monocytes

What do MMP do

A

Enzymes that break down cellular matrix molecules like collagen

This is bad.

If a plaque forms, we want to keep it in one spot. Breaking down the collagen will allow the plaque to break off and move around. This can cause other diseases like stroke heart attack etc.

WE WANT THE PLAQUE TO STAY IN PLACE ONCE IT FORMS

67
Q

Role of monocytes

What can ROS do to further damage the vessel

A

ROS can cause cellular and molecular damage

68
Q

What are the most important immune cells for developing atheromatas

A

Monocytes/macrophages

69
Q

Role of Dentritic cells

A

Present antigens (HLA) to T cells

Promotes a greater immune response

Crosstalk between the innate and adaptive immune system

70
Q

Role of Mast Cells

A

Release vasoactive histamine and leukotrienes which increase vascular permeability (more LDL can slip through)

Causes an increase in IL-6 which enhances inflammatory cascade

IL-6 levels are generally higher in individuals with vascular disease

71
Q

Role of Platelets

A

Secrete pro inflammatory cytokines and myeloid related protein (MRP)
- leads to endothelial cell apoptosis and thrombosis (blood clotting)

Platelet aggregation via platelet derived growth factors (PDGF), transforming growth factor (TGF-beta)

  • This can lead to increased blood viscosity
  • This coupled with the decreasing radius of the blood vessel results in the perfect storm of CVD
72
Q

Does cardiac output contribute to HTN

A

yes

73
Q

What NS contributes to cardiac output and how

A

SNS contributes to cardiac output through activation of the beta receptor which causes contractions

More contraction leads to greater cardiac output which can lead to HTN because volume is related to pressure

74
Q

How does the SNS relate to peripheral vascular resistance (PVR)

How to PVR related to atherosclerosis

How does it all related to endothelial dysfunction

A

SNS also acts on the peripheral vascular resistance (PVR) by increasing the amount of intracellular calcium that the smooth muscles have causing more contraction and increased resistance
- PVR is one of the main contributors to essential HTN

Atherosclerosis contributes to PVR

Endothelial dysfunction is a part of atherosclerosis which can feedback on PVR and increase resistance

75
Q

What does RAAS stand for

A

Renin angiotensin aldosterone system

76
Q

What type of system is RAAS

A

Endocrine

77
Q

What is the RAAS system really important for controlling

A

Blood pressure

78
Q

What is the RAAS system in HTN patients

A

Overactive or uncontrolled

79
Q

In healthy individuals, when is renin released

A

When there is decreased Na in the blood (dehydration)

When there is a decrease in BP (maybe due to hemorrhage)

SNS activation (fight or flight)

80
Q

What organ secretes the renin substrate

A

The liver

81
Q

What organ secretes renin

A

The kidney

82
Q

What does renin do

A

Causes the conversion of renin substrate to angiotensin I

83
Q

What converts angiotensin I to angiotensin II

A

Angiotensin converting enzyme (ACE)

84
Q

What does angiotensin II control

A

Blood pressure

85
Q

How does angiotensin II regulate BP (3 ways)

A

Acts directly on the blood vessels to cause vasoconstriction

Acts on the adrenal cortex causing secretion of a hormone called aldosterone

Causes secretion of antidiuretic hormone from the pituitary gland

86
Q

Why does angiotensin II help when you have low BP

A

When you have low BP, you want your blood vessels to constrict, you want to retain water, and you want to retain Na

87
Q

What does anti-diuretic hormones do

A

Retain water

88
Q

What does aldosterone do

A

Retains Na at the level of the kidney (water retain via osmosis)

89
Q

In health individuals what happens when you have increased salt in your diet (wrt angiotensin II)

A

There is reduced angiotensin II to maintain BP

Regardless of sodium intake, the BP should stay relatively the same by reducing angiotensin II

90
Q

In HTN individuals what happens when you have increased salt in your diet (wrt angiotensin II)

A

Angiotensin II levels do not decrease, and BP therefore increases

Graph shifted to the right

91
Q

In treated HTN individuals what happens when you have increased salt in your diet (wrt angiotensin II)

A

In individuals treated for hypertension, the graph is shifted to the left

Individuals BP increases, but not to the level of someone with HTN and is not treated with medication

Angiotensin blocker works so that the body still has some control on BP but the regulation is not as tight as normal individuals

Graph shifted to the left

92
Q

What is causing the higher levels of angiotensin II in HTN patients

A

It is not really known

93
Q

HTN and angiotensin II

Related to ACE

A

There is increased ACE activity in HTN patients, which would give rise to more angiotensin II

94
Q

What is Bradykinin

What breaks down bradykinin

A

Bradykinin is involved in vasodilation

ACE breaks down bradykinin which means more vasconstriction and higher BP

95
Q

What is the ANS composed of

A

The sympathetic and parasympathetic NS

96
Q

What part of the ANS is often involved when talking about BP

A

The sympathetic NS

97
Q

What happens when there is SNS activation (wrt epi and norepi)

A

There is increased release of epi and norepinephrine from the adrenal glands

98
Q

What does epi and norepinephrine cause

A

Cause the beta receptors on the cardiac tissues to be activated

99
Q

What happens when beta receptors are activated

A

Increased contraction and cardiac output

Increased blood leaving the heart

100
Q

What is cardiac output the product of

A

Heartbeat and stroke volume

101
Q

What else is released in response to SNS activation

What does this cause

A

Renin release

Will lead to PVR likely by angiotensin II binding to receptors on vessels causing vasoconstriction

102
Q

What happens when patients are treated with Beta blockers

A

Reduced BP

103
Q

What is endothelin

What does it cause a __ sensitive rise in ___

What is it an activator of

A

A vasoconstrictor

Responsible for the salt sensitive rise in BP

Angiotensin II should decrease in response to more salt, however if the blood Na stay high for a long time, endothelin is probably playing a larger role than the reduction of angiotensin II

Activator of RAAS

104
Q

What is bradykinin

What is it inactivated by

What does ACE inhibitors do

A

Vasodilator

Inactivated by ACE

Increase bradykinin by presventin ACE and increasing bradykinin release

105
Q

What is Nitric Oxide

What is it made by (cells)

What does anti-hypertensive medications do to the vessel

A

Vasodilator

Made by endothelium

Anti-hypertensive medication restores impaired NO production, but not smooth muscle response (NO resistance, irreversible)
- There is some damage that can be reversed, but there is part of endothelial dysfunction that is not reversible

106
Q

What is atrial natriuretic peptide (ANP)

What is it produced by and when

What does it do

A

Vasodilator

Produced by the atria when blood volume increases

Increases Na and water excretion

It is a natural diuretic

107
Q

What is the pressure for diagnosis of pulmonary hypertension (PHTN)

A

Mean pulmonary artery pressure >25 mmHg

108
Q

Recall

Where is the pulmonary artery

A

Leaving the right ventricle

The afterload (resistance) that is pushing against is higher

109
Q

What heart failure results from PHTN

A

Heart failure on the right side

110
Q

What is heart failure

A

When the heart cannot pump to the rest of the body

111
Q

What is PHTN a complication of

A

Left heart disease (left ventricular hypertrophy, hearth failure)

Could be a biomarker of underlying CVD

Could have a role of estrogen

Could be a role of infection

112
Q

Is there a higher PHTN in men or women

A

Women

113
Q

Where is there increased pressure in PHTN

Does PHTN cause diastolic dysfunction and what it is

What related to the mitral valve occurs

A

Increased left atrial pressure

Diastolic dysfunction (inability for the heart to relax)

Mitral valve regurgitation (when there is increased left arterial pressure, there can be increase in left ventrical pressure and the blood can flow the wrong way)

114
Q

Is PHTN progressive and fatal?

A

Yes

115
Q

Flow of PHTN

A

First there is vasoconstriction in the pulmonary artery making it harder for the right side of the heat to work and can lead to right side heart failure which can lead to total heart failure

116
Q

Molecular mediators of PHTN (5)

A

Decrease NO

Increased ADMA (blocks NO) - less vasodilation

Increase thromboxane (clotting factor) - might make the blood more viscous

Increased endothelin 1 - Vasoconstrictor

Activation of Ca channels on SMC - more Ca therefore more contraction and vast constriction

117
Q

COVID

What does the COVID spike protein bind to

What does this cause

A

Interacts with the lunge ACE2

Increase in the presence of ACE which will lead to vasoconstriction by angiotensin II

118
Q

What type of association is there between angiotensin II and COVID severity

A

Linear relationship

Also with the RAAS system

119
Q

COVID can cause… (5)

A

Endothelial dysfunction

Inhibition of NO

Microvascular disease

Dysfunction of ACE and ACE pathway - there is more Ace than ACE receptors which can lead to PHTN

Associated with cytokine storm (inflammatory response) - can lead to endocardial ischemia (lack of blood flow to the endocardium) which can lead to PHTN and right ventricle heart failure

120
Q

How much BP reduction is associated with _% risk reduction in major cardiac events

A

Reduce systolic BP by 5 mmHg reduce your risk of major cardiac event by about 50%

121
Q

Diet and BP

A

DASH diet include a low intake of fat and Na, high intake of vegetables
(Dietary approaches to stop hypertension)

There was a decrease in about 5 mmHg in BP in those that adhered the best compared to those that only adhere a little to the diet (#1)

122
Q

Exercise and BP

Decrease in BP associated with a single session

Decrease in BP associated with several sessions

A

Exercise is a great tool to use to prevent the risk of many different chronic diseases

There is even a benefit of exercising once!

A single session of aerobic exercise results in a reduction of systolic BP between 5-8mmHg for about 11 hours

There is a reduction from 5-15 mmHg following several sessions

People mostly want to reduce systolic BP

The greatest change results from aerobic exercise and following a Mediterranean diet

123
Q

What does exercise to direct on BP (6)

A

Improves artery compliance due to NO production

Improved renal function and fluid balance

Down-regulates renin and angiotensin II (beneficial for people with HTN)

Reduces PVR (mby through NO production)

Increases tissue perfusion (circulation)

Longterm: decrease SNS activity (less epi and Norepi (which bind to Beta receptors causing increase HR and contractility)

124
Q

Exercise and BP

How does artery compliance relate

A

Artery compliance: the ability of the vessel to contract and dilate in response to vasoactive substances

Here we are talking specifically vasodilation in response to NO production

We increase the production of NOS (NO synthase) when we exercise, leading to more NO production

125
Q

Exercise and BP

Here does Renal function relate

A

Better regulated fluid balance. Therefore we do not have high BV leading to high BP - we are better able to regulate the fluid in out body

126
Q

Exercise and CVD

Benefits (3)

A

Improved glucose sensitivity

Lower LDL

Decrease weight

127
Q

What is the recommended exercise

A

150 minutes per week

LIFESCI 3AA3 (6 decks)

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