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BPK 458 > Module 3: Pathophysiology of Cardiovascular Disease > Flashcards

Module 3: Pathophysiology of Cardiovascular Disease Flashcards

1
Q

describe the pathology, progression and health implications of atherosclerosis and hypertension.

A

a

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2
Q

analyze cardiac risk factors – definition, establishment, absolute risk, relative risk and basic statistical analysis.

A

a

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3
Q

Definition of atheriosclerosis

A

a generic term for arterial wall thickening and loss of elasticity.

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4
Q

What are the 3 general patterns of Atherosclerosis

A
  1. Hyaline arteriosclerosis
  2. Mönckeberg medial sclerosis
  3. Atherosclerosis
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5
Q

Arteriosclerosis which affects ______ and may result in an ischemic problem ____ to where the hardening is:

A
  1. small arteries and arterioles

2. distal

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6
Q

What is hyaline arteriolosclerosis

A

Thickening of the walls of arterioles

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7
Q

As the walls thicken, the lumen _____.

A

narrows

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8
Q

Thickening of the walls seems to be associated with leakage of serum proteins into the ______

A

subendothelial space.

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9
Q

hyaline arteriolosclerosis is related to _____ (3)

A

hypertension, aging, and diabetes mellitus.

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10
Q

There is a predisposition for arterioles in the _____ to have hyaline atheriosclerosis– can contribute to renal failure.

A
  1. kidney

2. renal failure

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11
Q

What is Mönckeberg medial sclerosis

A

Involves the MIDDLE layer of arteries with DESTRUCTION of MUSCLE and ELASTIC fibers and FORMATION of CALCIUM DEPOSITS

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12
Q

Mönckeberg medial sclerosis typically involve ____ sized arteries

A

large and medium-sized

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13
Q

At what age does Mönckeberg medial sclerosis typically occur

A

Over 50

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14
Q

What is the prevalance of Mönckeberg medial sclerosis

A

1%

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15
Q

What disorder is “senile” arteriosclerosis a nickname for

A

Mönckeberg medial sclerosis

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16
Q

What are the symptoms and prognosis of Mönckeberg medial sclerosis

A
  1. No prominent symptoms, usually discovered by chance

2. Is associated with a somewhat poorer prognosis, though this is not universally accepted

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17
Q

What is the term “atherosclerosis” derived from

A

from the Greek words for “gruel like” and “hardening”.

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18
Q

What are the 3 non-modifiable risk factors of arteriosclerosis

A
  1. Genetics
  2. Age
  3. Sex
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19
Q

Discuss the genetic risk factor of arteriosclerosis

A
  • Family history is one of the most important risk factors for atherosclerosis.
  • Hyperlipidemias account for a small % of cases.
  • Polygenic causes are more common in families where there is a well-established and additional risk factors such as hypertension and/or diabetes.
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20
Q

Discuss the age risk factor of arteriosclerosis

A

clinical manifestations usually occur between ages 40 and 60.

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21
Q

Discuss the genetic risk factor of arteriosclerosis

A

Pre-menopausal women are relatively protected against CVDs and complications of CVDs (compared to age-matched men and keeping other factors equal). Following menopause, the risk tends to increase and the risk exceeds that of men.

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22
Q

What are the modifiable risk factors of arteriosclerosis

A
  1. Hyperlipidemia
  2. Hypertension
  3. Smoking
  4. Diabetes Mellitus
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23
Q

Discuss the Hyperlipidemia risk factor of arteriosclerosis

A

Considered a MAJOR risk factor (which means that this risk factor can initiate a lesion on its own and even in the absence of other risk factors).

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24
Q

What is LDL and its fxn

A

Low Density Lipoprotein, LDL (aka bad cholesterol) is the major component of cholesterol responsible for the risk. LDL is responsible for delivering cholesterol to the peripheral tissue.

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25
Q

What is HDL and its fxn

A

Note that High Density Lipoprotein HDL (aka good cholesterol) has an opposite effect. It can take away cholesterol to the liver for excretion.

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26
Q

The level of LDL (bad cholesterol) can be targeted either through (2)

A

diet or pharmacological approaches.

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27
Q

Discuss the hypertension risk factor of arteriosclerosis

A

another major risk factor that can trigger atherosclerosis. Hypertension can increase the risk of Ischemic Heart Disease by about 60% when compared to individuals with normal blood pressure.

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28
Q

Discuss the smoking risk factor of arteriosclerosis

A

Another major risk factor and a very well-established factor in men and women. More years of smoking 1 pack of cigarettes or more lead to a doubling of the risk of death rate from Ischemic Heart Disease.

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29
Q

Smoking cessation results in reduction of the risk for coronary artery disease by ___% within a year following smoking and ____% after two years.

A
  1. 50%

2. 90%

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30
Q

What are 4 risk factors
considered for cardiovascular disease and they usually are found in individuals who lack the obvious risk factors (hypertension, smoking …. etc.):

A
  1. Inflammation
  2. Metabolic syndrome
  3. Lipoprotein
  4. Hyperhomocystinemia
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31
Q

Discuss the inflammation risk factor of arteriosclerosis

A

Inflammation is present during all stages of atherosclerosis and plays a role in the development of the PLAQUES.

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32
Q

Discuss the metabolic syndrome factor of arteriosclerosis

A

Associated with central obesity and manifest as dyslipidemia and insulin resistance.

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33
Q

Discuss the Lipoprotein a factor of arteriosclerosis

A

an ALTERED FORM of LDL and it can increase the risk of CHD

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34
Q

Discuss the Hyperhomocystinemia factor of arteriosclerosis

A

An inc blood levels of homocysteine correlates with inc risk of various forms of CVD including CHD

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35
Q

What 6 key players in “Response to Injury Hypothesis”

A
  1. Chronic inflammation
  2. Modified lipoprotein
  3. Macrophages
  4. T-lymphocytes
  5. Endothelial cells
  6. Smooth muscle cells of arterial wall
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36
Q

What is the step that is considered the cornerstone of how atherosclerosis develops.

A

Endothelial cell injury and dysfunction

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37
Q

How can the process of endothelial cell injury can be triggered

A

many mechanisms such as; hemodynamic forces, immune related mechanisms, chemicals and irradiation.

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38
Q

The exact mechanism in early development of atherosclerosis is not well understood but several risk factors have been linked to the initiation of atherosclerosis. These are: (4)

A
  1. Toxic substances from cigarette smoke,
  2. High homocysteine levels,
  3. Infectious agents (e.g. chlamydia)
  4. Cytokines such as Tumor Necrosis Factor (TNF).
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39
Q

The primary and most important factors for the development of Atherosclerosis are (2)

A

Hemodynamic Disturbances and Hypercholesterolemia.

40
Q

It has been shown in some in-vitro studies that nonturbulent (laminar) blood flow can lead an increase in an atheroprotective antioxidant called:

A

SOD: Super Oxide Dismutase

41
Q

Also, it has been documented that the risk of atherosclerosis tends to increase in the ____, along the ___ wall of the aorta and the openings of ____ vessels. All of which have disturbed blood flow patterns (turbulent in some capacity).

A
  1. branch points
  2. posterior
  3. exiting
42
Q

As far as Hypercholesterolemia, the evidence linking Hypercholesterolemia to atherosclerosis is suggested by: (8)

A
  1. Genetic defects in lipoprotein uptake and metabolism cause hypolipoproteinemia and accelerated atherosclerosis.
  2. Significant correlation btwn levels of cholesterol (including LDL) and severity of atherosclerosis.
  3. Lowering cholesterol thru diet or pharmacology slows rate of progression of atherosclerosis and this reduces the risk of cardiovascular events.
  4. Accumulation of lipoproteins.
  5. Adhesion of monocytes to the endothelium.
  6. Adhesion of platelets.
  7. Smooth muscle recruitment and proliferation.
  8. Lipid accumulation.
43
Q

It’s believed that the main instigator of inflammation is the

A

accumulation of cholesterol crystals

44
Q

Discuss the events that occur as a response to inflammation

A
  1. Proinflammatory cytokines e.g. IL-1 released, attracting additional blood cells e.g. monocytes (which become macrophages) and T-lymphocytes
  2. Eventually these macrophages and T-lymphocytes produce local cytokines that recruit and activate more inflammatory cell to region
  3. Activated macrophages may predispose to LDL oxidation because these macrophages produce reactive oxygen species (free radicals)
  4. Macrophages also produce growth factors that promote the proliferation of smooth muscle cells.
45
Q

Discuss the 5 steps in the Evolution of arterial wall changes in the response to injury hypothesis.

A

1, Normal.
2, Endothelial injury with monocyte and platelet adhesion.
3, Monocyte and smooth muscle cell migration into the intima, with macrophage activation.
4, Macrophage and smooth muscle cell uptake of modified lipids, with further activation and recruitment of T cells.
5, Intimal smooth muscle cell proliferation with extracellular matrix production, forming a well-developed plaque.

46
Q

LDL on own isn’t really bad. Initiator of all big problems is oxidation of LDL molecule. Oxidized LDL is what causes to pathogenesis of atheroscleross. LDL gets oxidized when exposed to free radicals. When oxidized loses electron from ApoB-100, creating a defective form of apoB-100 (ID badge for LDL receptor). LDL usually binds to its receptor and we bring it in and generate choesterol. But now no recognition btwn LDL receptor and LDL molecule so LDL wil remain outside. If we had 2 copies of apoB-100 then defecting one is still ok. But only have single copy of apoB-100. Now its floating around as foreign molecule. Anything foreign will be attacked by WBC. LDL molecule (oxidized) with defective apoB-100. Macrophage will recognize and bind to (thru scavenger receptor a/ SR-A on surface of macrophage) and phagocytose oxidized LDL. Lytic enzymes will break it down into building blocks like cholesterol. Over time the lvl of cholesterol will build up in macrophage. Over time size of macrophage will inc, and become foam cells (large, inflated). Macrophages now become useless and die to release the cholesterol inside of them. The cholesterol inside foam cells is hydrophobic so doesn’t work well with blood. So cholesterol will precipitate within tissues and blood vessels and attrack WBC like monocytes and t-lymphocytes thru cytokines e.g. IL-1. Once these cells arrive inflammation will follow. Due to inflammation response, plaque will form in size.

A

a

47
Q

Sequence of cellular interactions in atherosclerosis. Hyperlipidemia, hyperglycemia, hypertension, and other influences cause endothelial dysfunction. This results in platelet adhesion and recruitment of circulating monocytes and T cells, with subsequent cytokine and growth factor release from inflammatory cells leading to smooth muscle cell migration and proliferation as well as further macrophage activation. Foam cells in atheromatous plaques derive from macrophages and smooth muscle cells that have accumulated modified lipids (e.g., oxidized and aggregated low density lipoprotein [LDL]) via scavenger and LDL-receptor-related proteins. Extracellular lipid is derived from insudation from the vessel lumen, particularly in the presence of hypercholesterolemia, as well as from degenerating foam cells. Cholesterol accumulation in the plaque reflects an imbalance between influx and efflux; high-density lipoprotein (HDL) likely helps clear cholesterol from these accumulations. In response to the elaborated cytokines and chemokines, smooth muscle cells migrate to the intima, proliferate, and produce extracellular matrix, including collagen and proteoglycans. IL-1, interleukin-1; MCP-1, monocyte chemoattractant protein-1.

A

a

48
Q

Mild atherosclerosis composed of ____ plaques

A

fibrous

49
Q

Severe atherosclerosis with diffuse and complicated lesions including an _____ plaque and a lesion with overlying ____

A
  1. ulcerated

2. thrombus

50
Q

Histologic features of atheromatous plaque in the coronary artery. A, Overall architecture demonstrating fibrous cap (F) and a central necrotic core (C) containing cholesterol and other lipids. The lumen (L) has been moderately compromised. Note that a segment of the wall is plaque free (arrow); the lesion is therefore “eccentric.” In this section, collagen has been stained blue (Masson trichrome stain). B, Higher-power photograph of a section of the plaque shown in A, stained for elastin (black), demonstrating that the internal and external elastic laminae are attenuated and the media of the artery is thinned under the most advanced plaque (arrow). C, Higher magnification photomicrograph at the junction of the fibrous cap and core, showing scattered inflammatory cells, calcification (arrowhead), and neovascularization (small arrows)

A

a

51
Q

What are the Consequences/ Fate of Atherosclerosis (3)

A
  1. Rupture/fissuring, exposing highly thrombogenic plaque constituents
  2. Erosion/ulceration, exposing the thrombogenic subendothelial basement membrane to blood
  3. Hemorrhage into the atheroma, expanding its volume
52
Q

Discuss Rupture, ulceration, or erosion complication

A
  • Rupture, ulceration, or erosion of the intimal surface of atheromatous plaques exposes the blood to highly thrombogenic substances and induces thrombosis
  • > Stroke, myocardial infarction
53
Q

Discuss Hemorrhage into a plaque complication

A
  • Rupture of the overlying fibrous cap, or of the thin-walled vessels in the areas of neovascularization, can cause intra-plaque hemorrhage; a contained hematoma may expand the plaque or induce plaque rupture
  • > can occur in pre-existing abdominal aortic aneurysms
  • > can also narrow the lumen of a narrowed artery even further
54
Q

Discuss Atheroembolism complication

A
  • Plaque rupture can discharge atherosclerotic debris into the bloodstream, producing microemboli
  • > stroke, myocardial infarction
55
Q

Discuss Aneurysm formation complication

A
  • Atherosclerosis-induced pressure or ischemic atrophy of the underlying media, with loss of elastic tissue which leads to weakness resulting in aneurysmal dilation and potential rupture
  • > typical of abdominal aortic aneurysm
56
Q

Describe Vulnerable vs stable atherosclerotic plaque.

A

Vulnerable plaques have thin fibrous caps, large lipid cores, and greater inflammation. Stable plaques have thickened and densely collagenous fibrous caps with minimal inflam­mation and underlying atheromatous core.

57
Q

What is a sign of atherosclerosis

A

objectively measurable finding (i.e. carotid bruit).

58
Q

What is a symptom of atherosclerosis

A

subjective feeling described by patient (i.e. chest pain)

59
Q

Signs of Lower Limb Ischemia

A
  1. loss of leg hair
  2. skin discoloration
  3. coldness of leg
  4. thinned skin
  5. no pulse (complete blockage)
  6. gangrene (complete blockage)
60
Q

Signs of Cerebral Ischemia

A
  1. asymmetry in face (one side droops)
  2. loss of speech and mental functions
  3. trouble walking
61
Q

Signs of Mesenteric Ischemia

A
  1. gangrenous bowel
62
Q

Signs of Myocardial Ischemia

A
  1. cardiogram shows ST depression and then ST elevation as ischemia proceeds to infarction.
  2. arrhythmia may result from damage to cardiac conduction system.
63
Q

Symptoms of Lower Limb Ischemia

A
  • calf pain (“claudication”)
  • > partial blockage: goes away with rest
  • > complete blockage: severe, unrelenting
  • weak leg muscles
64
Q

Symptoms of Cerebral Ischemia

A
  • severe headache
  • sudden numbness or weakness of face, arm or leg on one side of body
  • trouble seeing
  • dizziness, loss of balance or coordination (AHA)
65
Q

Symptoms of Mesenteric Ischemia

A
  • abdominal pain
  • intensifies when eating because bowel needs more blood for digestion
  • diarrhea
  • blood in stool
66
Q

Symptoms of Myocardial Ischemia

A
  • chest discomfort: pressure, squeezing, pressure or pain
  • pain or discomfort in arms, back, neck, jaw or stomach
  • shortness of breath
  • sweating
  • nausea
  • lightheadedness (AHA)
67
Q

What are the 8 Clinical Investigation Techniques for Atherosclerosis

A
  1. Electrocardiography (ECG)
  2. Cardiac stress testing
  3. Coronary Artery CT scan
  4. Doppler study
  5. Magnetic resonance arteriography
  6. MIBI scan
  7. Ankle/Brachial Index (ABI)
  8. Arteriography
  9. Intravascular ultrasound
68
Q

What is an ECG

A

a procedure that measures the heart’s electrical impulses during a heartbeat. It is used to detect abnormal heart rate and rhythm or to see if previous heart damage has occurred.

69
Q

What is a cardiac stress test

A

patient exercises so that heart requires more blood; test can show if the blood supply in the coronary arteries is reduced. During test, patient’s heart rate, blood pressure, breathing, electrocardiography and fatigue level are monitored.

70
Q

What is a Coronary Artery CT scan

A

a CT scan of the coronary arteries, looking for calcium deposits.

71
Q

What is a Doppler study

A

an ultrasound using high frequency sound waves to detect blockage in the carotid artery. A simple Doppler study tells the vessel’s diameter while a more sophisticated test can tell what the flow is (i.e. what percentage of the artery is plugged).

72
Q

What is Magnetic resonance arteriography

A

MRI of an artery to look for blockage and calcium deposits

73
Q

What is a MIBI scan

A

radioactive material MIBI is injected into a vein during both rest and exercise, and used to take pictures of the heart. Parts of the heart that are not receiving enough blood can be detected.

74
Q

What is Ankle/Brachial Index (ABI)

A

a comparison of the blood pressure in the feet to that in the arms in order to diagnose peripheral arterial disease.
-> ABI = ankle systolic pressure / arm systolic pressure

75
Q

What is Arteriography

A

dye visible by X-ray is injected into the bloodstream. X-rays are then taken to see if arteries are damaged.

76
Q

What is

A

ultrasound of the arteries.

77
Q

Definition of hypertension

A
  • Persistent elevation of diastolic blood pressure (higher than 90mm Hg), systolic blood pressure (higher than 140mm Hg) or both.
  • measured on three separate occasions at least two weeks apart.
78
Q

What are the 2 classifications of hypertension

A
  1. Primary hypertension: idiopathic (95%)
  2. Secondary hypertension:
    renal disease, vascular disease, endocrine disorders, coarctation of the aorta, excessive alcohol intake, use of oral contraceptives, NSAIDs, corticosteroids, cocaine, pregnancy.
79
Q

In 2000, estimated that close to ___% of adult population is hypertensive.

A

25%

80
Q

____ million in US are on anti-hypertensive medications.

A

43

81
Q

What are the modifiable (6) risk factors and non-modifable (30 risk factors of hypertension

A

Modifiable:

  1. Diet
  2. Smoking
  3. Obesity
  4. High cholesterol
  5. Inadequate sleep
  6. alcohol

Non-modifiable:

  1. Genetics/ethnicity
  2. Sex
  3. Age
82
Q

What is the eqn for BP

A

(mean arterial) BP = cardiac output (CO) x total peripheral vascular resistance (TPR)

83
Q

Increased cardiac output (CO): can be affected by (4):

A
  1. Factors related to Blood Volume:
    - > Sodium,
    - > Mineralocorticoid effect (Can you name one type),
    - > Atrial Natriuretic Peptide (ANP).
  2. Factors related to the heart:
    - > Heart Rate (Can you predict which receptors?)
    - > Contractility.
  3. Increased peripheral vascular resistance (TPR): Can be affected by:
    - Humoral factors:
    - > Angiotensin II (C)*,
    - > Epinephrine and
    - > Norepinephrine (C),
    - > Thromboxane (C),
    - > Leukotriene (C),
    - > Prostaglandins (D)**,
    - > Nitric Oxide (D).
    - Neural factors:
    - > Alpha 1 receptor stimulation (C),
    - > Beta 2 receptor stimulation (D).
    - Local factors:
    - > Hypoxia,
    - > pH

*C: Constrictor (Constriction), D: Dilator (Dilation).

84
Q

What are the 4 Mechanisms that play a role in the pathogenesis of hypertension

A
  1. Abnormal sodium transport:
    - > More sodium is retained than normal, resulting in more fluid, resulting in higher pressures.
  2. Sympathetic nervous system stimulation:
    - > One hypothesis is that early on, activation of SNS and resultant vasoconstriction eventually results in “resetting” the normal range of blood pressure.
  3. Renin-angiotensin-aldosterone system:
    - > Vasoconstriction and sodium retention.
  4. Vasodilator deficiency.
85
Q

What Rare genetic defects are linked to rare types of hypertension.

A
  1. aldosterone synthase, 11β-hydroxylase, 17α-hydroxylase) - these lead to an increase in secretion of aldosterone.
  2. Mutations in sodium-transporting proteins in the kidney.
86
Q

A small proportion (__%) of those with pre-existing hypertension can exhibit a rapidly accelerating increase in blood pressures (Malignant Hypertension (a subtype of hypertension))

A
  1. 5%
87
Q

If malignant hypertension is not corrected, can cause:

A
  1. cause death within a few years,
  2. Severe hypertension,
  3. Rapid renal failure and retinal hemorrhages can occur – accompanied by many of the symptoms of acute, serious increases of blood pressure (headache, blurred vision, increased risk for stroke, polyuria).
88
Q

How is Hyperplastic Arteriolosclerosis related to malignant hypertension

A

This lesion occurs in malignant hypertension
- in malignant hypertension, they are accompanied by fibrinoid deposits and vessel wall necrosis (necrotizing arteriolitis), particularly in the kidney.

89
Q

What does hyperplastic arteriosclerosis look like

A
  • vessels exhibit “onion-skin lesions,” characterized by concentric, laminated thickening of the walls and luminal narrowing
  • The laminations consist of smooth muscle cells with thickened, reduplicated basement membranes; in malignant hypertension, they are accompanied by fibrinoid deposits and vessel wall necrosis (NEOCROTIZING ARTERIOLITIS), particularly in the kidney.
90
Q

Describe the early vs. late pathology of malignant hypertension

A

Early:

  1. None – the “silent killer”,
  2. Acute, exceptionally high inc in BP can result in severe headaches, blurred vision, confusion, and even hemorrhagic strokes.

Late:

  1. End-organ damage,
  2. Vessels of the heart, brain, kidneys, retina, extremities,
  3. Myocardium, leading to heart failure.
91
Q

How do the arterioles look like in hyaline arteriolar sclerosis (arteriolosclerosis)

A

Arterioles show homogeneous, pink hyaline thickening and luminal narrowing

92
Q

What causes the Arterioles show homogeneous, pink hyaline thickening and luminal narrowing in hyaline arteriolar sclerosis

A
  • from plasma protein leakage across injured endothelial cells, and increased smooth muscle cell matrix synthesis (similar findings in healthy elderly, but in those with hypertension the findings are more notable),
  • looks very similar to diabetic microangiography (due to hyperglycemic damage of endothelium),
  • In nephrosclerosis due to chronic hypertension, hyaline arteriosclerosis causes impairment of renal blood supply and causes glomerular scarring leads to poor kidney perfusion, renal failure.
93
Q

Is hypertension usually symptomatic or asymptomatic

A

Usually asymptomatic,

94
Q

When hypertension is symptomatic, why? And what are some

A
  • Symptomatic: - often acute, secondary causes of hypertension
    1. Headache,
    2. Vertigo,
    3. Flushed face,
    4. Blurred vision,
    5. Nocturia,
    6. Urinary frequency.
95
Q

Hypertension Treatments? (4)

A
  1. Quitting smoking
  2. Exercise & Weight reduction
  3. Diet
  4. Medications
96
Q

describe the pathology, progression and health implications of atherosclerosis and hypertension.

A

a

97
Q

analyze cardiac risk factors – definition, establishment, absolute risk, relative risk and basic statistical analysis.

A

a

BPK 458 (29 decks)

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