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LIFESCI 3AA3 > Atherosclerosis and Hypertension > Flashcards

Atherosclerosis and Hypertension Flashcards

1
Q

Hematocytopenia

A

Abnormally low number of red blood cells (RBCs) in the blood

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2
Q

Hemangioma

A

Benign tumor consisting of blood vessels

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3
Q

Cardioversion

A

Re-establishment of electrical activity in the heart by means of electrical shock

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4
Q

Hypertension

A

high blood pressure

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5
Q

How is HTN diagnosed

A

automated office blood pressure (AOBP)

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6
Q

What are the normal levels of AOBP?

A 
SBP = greater or equal to 135mmHg
DBP = greater or equal to 85mmHg
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7
Q

Systolic pressure

A

pressure exerted in the vessel by the blood during systole (i.e. contracting)

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8
Q

Diastole pressure

A

pressure exerted in the vessel by the blood during diastole (i.e. relaxing)

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9
Q

Are HTN rates increasing or decreasing?

A

HTN rates are increasing (they have increased by 60%).

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10
Q

Why are HTN rates increasing?

A

more awareness (more diagnosis), more risk factors associated with HTN (e.g., diabetes and obesity), and more women are getting diagnosed because possible of more doctor visits

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11
Q

Four consequences of HTN

A

peripheral vascular disease. retinopathy. hemorrhage, stroke. renal failure, proteinuria. LVH, CHD, CHF.

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12
Q

Can someone die because of HTN?

A

No. People don’t die directly because of HTN but die as a result of the consequences of HTN

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13
Q

Layers of a blood vessel

A

tunica intima/interna, tunica media, and tunica externa

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14
Q

Tunica intima/interna

A
  • closest to the lumen so direct contact with blood
  • composed of endothelium and connective tissue
  • releases endothelins which are vasoactive substances to constrict smooth muscles
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15
Q

Tunica media

A
  • composed of smooth muscle and connective tissue
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16
Q

Tunica Externa

A
  • composed of a sheath of connective tissue to keep the vessel in place
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17
Q

five variables affecting blood flow and pressure

A

compliance, cardiac output, volume of blood, viscosity, and blood vessel length and diameter

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18
Q

Compliance

A
  • Ability of the vessel to expand in response to degree of resistance and vascular tone
  • We want a good vascular tone and low degree of resistance so our heart doesn’t have to work so hard to pump the blood through the vessels
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19
Q

Vascular tone

A

ability of vessel to constrict and relax

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20
Q

cardiac output

A
  • Amount of blood in litres per minute that the heart will pump
  • Controlled by SNS
  • Beta receptors control the contractility
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21
Q

Volume of blood

A
  • greater volume, greater pressure
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22
Q

Why are some patients with HTN prescribed water pills or diuretics?

A

allow for increased passing of urine/water which means loss of water in the system and so a decrease of the amount of blood volume, and hence decrease in pressure.

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23
Q

Blood vessel length

A

longer the blood vessel, the greater the pressure

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24
Q

Blood vessel diameter

A

A slight increase/decrease in diameter results in a huge decrease/increase in resistance

25
Q

Describe the relationship between resistance and radius

A

resistance is inversely proportional to radius

changing radius by 2mm can change the resistance by 16x

26
Q

Atherosclerosis

A

narrowing and hardening of the arteries due to ‘plaque’ build-up

27
Q

Endothelial dysfunction

A

when the endothelium (i.e., endothelial cells lining the interna) doesn’t produce or respond to vasoactive substances

28
Q

What occurs due to endothelial dysfunction?

A

reduced NOS, increased ADMA, decreased vascular tone, and reduced responsiveness to vasoactive substances

29
Q

How does ADMA contribute to endothelial dysfunction?

A

ADMA levels increase. ADMA blocks the production of NO from L-arginine

30
Q

Atheromata

A

accumulation of debris (at arteries)

31
Q

Innate immunity

A

immune response that happens quickly in the body without previous exposure or “education”

32
Q

Adaptive Immunity

A

immune response that happens slowly after “education” or exposure to microbes

33
Q

Describe the events leading to atherosclerosis.

A
  1. LDL particles can slip between the already damaged endothelial cells lining the tunica interna.
  2. LDL is oxidized.
  3. Oxidized LDL particles bind to scavenger (CD36) receptor which is attached to the macrophage.
  4. Oxidized LDL causes a signal to be sent to the endothelial cells to start expressing more adhesion molecules which attract even more macrophages.
  5. Macrophages internalize LDL particles and turn into foam cells
34
Q

Cardiac output

A

heart rate and stroke volume

35
Q

What does RAAS stand for?

A

Renin Angiotensin Aldosterone System

36
Q

What is the overall goal of RAAS?

A

most important endocrine system controlling blood pressure, and is usually activated due to low blood pressure

37
Q

How is RAAS affected in people with HTN?

A

RAAS is overactive or uncontrolled

38
Q

Describe how RAAS works.

A

Renin substrate (secreted by the liver) is converted into angiotensin I by renin (secreted from the kidney).
Angiotensin converting enzyme (ACE) then converts angiotensin I to angiotensin II.
Angiotensin II causes three actions to occur, ultimately which all lead to an increase in blood pressure:
(1) Angiotensin II acts directly on the blood vessels and causes vasoconstriction (i.e. making blood pressure higher).
(2) Angiotensin II acts on the adrenal cortex causing secretion of a hormone called aldosterone (i.e., retains sodium in the body, which usually causes water to also be retained in the body (osmosis)).
(3) Angiotensin II acts on the pituitary gland causing secretion of antidiuretic hormone (ADH) (i.e., this allows water to be retained in the body which means increase in blood volume, which increases blood pressure).

39
Q

Why is renin normally released?

A

decrease of sodium in the blood (dehydration), decrease in blood pressure (hemorrhage), and SNS activation

40
Q

Why is it that individuals with HTN have more angiotensin II?

A

Physicians hypothesize that individuals with HTN have higher activity levels of ACE resulting in more angiotensin II.

41
Q

Does ACE only increase blood pressure by converting angiotensin I into angiotensin II?

A

no, ACE also breaks down bradykinin which decreases vasodilation, thereby increasing vasoconstriction which means high blood pressure

42
Q

Describe two ways in which SNS activation allows for increase in blood pressure/flow.

A
  1. SNS activation causes an increase in epinephrine and norepinephrine release. These two hormones cause activation of beta adrenergic receptors on the cardiac tissue of the heart, increasing contractility, and heart rate, thus increasing cardiac output. This increases blood going out.
  2. SNS activation causes renin release (in RAAS) causing an increase in PVR which is likely due to angiotensin II binding to receptors on blood vessels for vasoconstriction.
43
Q

List the four vasoactive susbtances

A

endothelin, bradykinin, nitric oxide (NO) and atrial natriuretic peptide (ANP)

44
Q

Endothelin

A
  • vasoconstrictor
  • salt-sensitive rise in BP (i.e., responsible for the rise in blood pressure due to high salt intake)
  • activator of RAAS
45
Q

Bradykinin

A
  • vasodilator

- inactivated by ACE

46
Q

Nitric oxide (NO)

A
  • vasodilator
  • made by endothelium
  • anti-hypertensive medication restores impaired NO production, but not smooth muscle response (NO resistance, irreversible)
47
Q

Atrial Natriuretic Peptide (ANP)

A
  • vasodilator
  • produced by atria when blood volume increases
  • increases sodium and water excretion
  • natural diuretic
48
Q

In people with HTN which vasoactive substances increase?

A

endothelin and ANP

49
Q

In people with HTN which vasoactive substances decrease?

A

NO, and bradykinin

50
Q

Why do ANP levels increase in people with HTN despite being a vasodilator?

A

because atria is expanding which increases blood volume which increases pressure

51
Q

Pulmonary HTN

A

mean pulmonary artery pressure exceeds 25mmHg

52
Q

Which vessel is involved in pulmonary HTN?

A

pulmonary artery leading from the right ventricle to the lungs

53
Q

How can pulmonary HTN lead to heart failure on the right side?

A

For people with pulmonary HTN the right ventricle has to work harder because the mean pressure is greater, it has to push against a higher resistance, which is why it can then lead to heart failure on the right side.

54
Q

Heart failure

A

hearts inability to pump blood to the rest of the body

55
Q

What are three things that can occur as a result of pulmonary HTN?

A

increase in left atrial pressure, diastolic dysfunction and mitral regurgitation

56
Q

What are the molecular mediators that could cause pulmonary HTN?

A

reduction in NO, increase in AMDA, increase in thromboxane, increase in endothelin-1, and activation of calcium channels on smooth muscles

57
Q

Why could an increase in thromboxane cause pulmonary HTN?

A

because thromboxane is a clotting factor that makes blood more viscous

58
Q

Why could activation of calcium channels on smooth muscles cause pulmonary HTN?

A

calcium is required on smooth muscles for contraction to take place

LIFESCI 3AA3 (4 decks)

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