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(OMS2) CPR II Exam 1 > Chapter 11/Lecture 1: Vascular Anomalies, HTN, Atherosclerosis, Aneurysms/Dissections > Flashcards

Chapter 11/Lecture 1: Vascular Anomalies, HTN, Atherosclerosis, Aneurysms/Dissections Flashcards

1
Q

In which layer of vessels will you find nerve fibers and the vasa vasorum (“vessels of the vessels”)?

A

Adventitia

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2
Q

Which type of vessel has an endothelial cell lining, no media, and variable number of pericytes?

A

Capillaries

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3
Q

In most inflammatory rxns, vascular leakage and leukocyte exudation occur via what vessels?

A

Post-capillary venules (veins)

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4
Q

All vessels except _______ share a 3-layered architecture consisting of an endothelium lined intima, a surrounding smooth m. media, and supportive adventititia.

A

Capillaries

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5
Q

Large or multiple AV fistulas may shunt blood from arterial or venous circulation, forcing the heart to pump additional volume and lead to what clinically significant event?

A

High-output cardiac failure

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6
Q

Fibromuscular dysplasia is a focal thickening in which arteries (size and type)?

A

Medium and large muscular arteries (i.e, renal, carotid, splanchnic, and vertebral)

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7
Q

Is there a genetic association with fibromuscular dysplasia and who is most often affected?

A
  • First-degree relatives have ↑ incidence
  • Most frequently in young women (NO assoc. w/ OC’s or ↑ estrogen)
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8
Q

Which layers of the vessel wall undergo hyperplasia and fibrosis in fibromuscular dysplasia?

A

Media and intima

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9
Q

Fibromuscular dysplasia of renal arteries can be a cause of?

A

Renovascular HTN

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10
Q

Endothelial dysfunction refers to an alteration in endothelial what?

Often has what 2 characteristics?

A
  • Phenotype
  • Often both proinflammatory and prothrombogenic
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11
Q

Alteration of endothelial phenotype seen in endothelial dysfunction is responsible for the initiation of what changes seen in pathological processes?

A

Initiation of thrombus formation, atherosclerosis, and vascular lesions of HTN

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12
Q

Vascular smooth m. cells have the capacity to proliferate when appropriately stimulated and can also synthesize what?

A
  • Collagen
  • Elastin
  • Proteoglycans
  • Elaborate cytokines and GF’s
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13
Q

What is the stereotypical response of the vessel wall to any insult?

A

Intimal thickening

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14
Q

Turbulent flow, HTN, cytokines, complement, bacterial/lipid prods., advanced glycation end-products, hypoxia, acidosis, viruses and cigarette smoke may cause endothelial activation which leads to increased/altered expression of what?

A
  • Procoagulants, adhesion molecules, and pro-inflammatory cytokines
  • Altered expression of chemokines, cytokines, and GF’s
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15
Q

Describe the 3 events in the stereotypical response to vascular injury.

A
  1. Recruitment of smooth m. cells or smooth m. precursor cells to intima
  2. Smooth m. cell mitosis
  3. Elaboration of extracellular matrix = intimal thickening
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16
Q

Secondary HTN is a result of an underlying disease in which organs?

A
  • Renal –> renal a. stenosis
  • Adrenal = 1’ aldosteronism, Cushing syndrome or pheochromocytoma, pregnancy induced
  • CV = coarctation of aorta, polyarteritis nodosa
  • Neuro = sleep apnea, acute stress, psychogenic
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17
Q

Which systolic and diastolic BP characterize malignant HTN?

A

>200/>120

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18
Q

Malignant HTN is often superimposed on what?

A

Pre-existing “benign” HTN

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19
Q

What are 5 cardiovascular causes of secondary HTN?

A
  • Coarctation of aorta
  • Polyarteritis nodosa
  • Increased intravascular volume
  • Increased cardiac output
  • Rigidity of aorta
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20
Q

What are 4 neurologic causes of secondary HTN?

A
  • Sleep apnea
  • ↑ ICP
  • Sleep apnea
  • Acute stress, including surgery
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21
Q

Blood pressure is a product of _______ x________

A

Cardiac output x Peripheral Resistance

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22
Q

The most important determinant of stroke volume is what?

Regulated by?

A
  • Filling pressure
  • Regulated thru Na+ homeostasis (mineralocorticoids and ANP) and its effect on blood volume
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23
Q

How is cardiac output calculated?

A

CO = SV x HR

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24
Q

List the 5 humoral factors which are constrictors and have an effect on peripheral resistance?

A
  • Angiotensin II
  • Catecholamines
  • Thromboxane
  • Leukotrienes
  • Endothelin
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25
Q

Peripheral resistance is regulated predominantly at the level of which vessels?

By which inputs?

A
  • Arterioles
  • Neural and hormonal inputs
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26
Q

What 2 relaxing substances are produced by the kidney to counterbalance the vasopressor effects of angiotensin?

A
  • NO
  • Prostaglandins
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27
Q

Explain the effects of renal artery stenosis and how they contribute to renovascular HTN?

A
  • ↓ pressure in afferent arteriole = ↓ GFR
  • ↑ Renin secretion = RAAS system activation = ↑ vascular tone and blood volume
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28
Q

Liddle syndrome is due to gain-of-function mutations in which protein and leads to what?

A
  • ENaC protein
  • Causes ↑ Na+ reabsorption in response to aldosterone
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29
Q

Gene defects in which enzymes involved in aldosterone metabolism lead to primary hyperaldosteronism and in turn secondary HTN?

A
  • Aldosterone synthase
  • 11β-hydroxylase
  • 17α-hydroxylase
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30
Q

HTN is associated with what 2 forms of small blood vessel disease?

A

1) Hyaline arteriolosclerosis
2) Hyperplastic arteriosclerosis

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31
Q

Homogenous pink hyaline thickening with associated luminal narrowing is characteristic of?

A

Hyaline arteriosclerosis

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32
Q

What type of arteriosclerosis is associated with severe HTN and is often a component of malignant HTN?

A

Hyperplastic arteriosclerosis

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33
Q

Vessels exhibiting concentric, laminated (“onion-skin”) thickening of the walls with luminal narrowing is characteristic of?

A

Hyperplastic arteriosclerosis

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34
Q

Nephrosclerosis due to chronic HTN is a form of what type of arteriosclerosis?

A

Hyaline arteriosclerosis

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35
Q

What type of arteriosclerosis is a common feature of diabetic microangiography?

A

Hyaline arteriosclerosis

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36
Q

The laminations of hyperplastic arteriosclerosis are accompanied by what other morphological changes in malignant HTN?

A
  • Fibrinoid deposits
  • Vessel wall necrosis (necrotizing arteriolitis)
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37
Q

What do the laminations of hyperplastic arteriosclerosis consist of?

A

Smooth muscle cells w/ reduplicated BM

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38
Q

Monckeberg medial sclerosis most often occurs in which age group and is characterized by what?

Clinically significant?

A
  • >50 yo
  • Calcification of walls of muscular arteries, typically internal elastic membrane
  • No narrowing of lumen and no clinical significance
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39
Q

What is the most frequent and clinically important pattern of arteriosclerosis?

A

Atherosclerosis

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40
Q

The likelihood of atherosclerosis is determined by the combination of which acquired and inherited risk factors?

A
  • Acquired = cholesterol levels, smoking and HTN
  • Inherited = LDL receptor gene mutations
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41
Q

What are in the intimal lesions seen in atherosclerosis and describe their morphology?

A
  • Atheroma = atheromatous = atherosclerotic plaque
  • Raised lesion w/ a soft grumous core of lipid covered by fibrous cap
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42
Q

Besides obstructing blood flow, atherosclerotic plaques can rupture leading to what?

A

Catastrophic obstructive vascular thrombosis

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43
Q

Which country is known to have the highest ischemic heart disease-associated mortality?

A

Soviet Union

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44
Q

What are the 5 major modifiable risk factors for atherosclerosis?

A
  1. Hyperlipidemia
  2. HTN
  3. Cigarette smoking
  4. Diabetes
  5. Inflammation
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45
Q

How do multiple risk factors present act in concert to increase risk of atherosclerosis?

A

Have a multiplicative effect = Synergism

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46
Q

Woman of which age are somewhat protected from atherosclerosis?

May due to effect of?

A
  • Pre-menopausal woman
  • Effect of estrogen
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47
Q

Atheroprotective effects of estrogen therpay seem to be related to what factor?

A

Age at which therapy is initiated –> younger postmenopausal woman are more protected

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48
Q

What is a major risk factor for atherosclerosis even in the absence of other factors and is sufficient to initiate lesion development?

A

Hypercholesterolemia

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49
Q

What are 2 activities which raise HDL levels?

A
  • Exercise
  • Moderate consumption of ethanol
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50
Q

Which disease causes a 100x ↑ risk for atherosclerosis-induced gangrene of LE’s?

A

Diabetes mellitus

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51
Q

Which circulating marker of inflammation associated wth ischemic heart disease is one of the easiest to measure and one of the most sensitive?

A

CRP

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52
Q

Expression of CRP is increased by a number of inflammatory mediators, especially what?

A

IL-6

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53
Q

What is a useful serum marker to gauge the effects of risk reduction measures, such as smoking cessation, weight loss, exercise, and statins?

A

CRP

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54
Q

Serum homocysteine levels correlate with risk for what 4 vascular pathologies?

A
  • Coronary atherosclerosis
  • Peripheral vascular disease
  • Stroke
  • Venous thrombosis
55
Q

Metabolic syndrome associated with central obesity is characterized by what dysfunctions?

A
  • Insulin resistance
  • HTN
  • Dyslipidemia
  • Hypercoagulability
  • Pro-inflammatory state
56
Q

The systemic hypercoagulable and proinflammatory state associated with metabolic syndrome contribute to what 2 pathological processes?

A
  • Endothelial dysfunction
  • Thrombosis
57
Q

What is lipoprotein A [Lp(a)]?

Increases risk for what?

A
  • Altered form of LDL –> contains ApoB-100 portion of LDL linked to ApoA
  • Associated w/ coronary and cerebrovascular disease risk, independent of total cholesterol or LDL levels
58
Q

Elevated plasminogen activator inhibitor 1 is a potent predictor of?

A

Risk for major atherosclerotic events, including MI and stroke

59
Q

What are the 2 most important causes of endothelial dysfunction leading to atherosclerosis?

A
  1. Hemodynamic disturbances = turbulence
  2. Hypercholesterolemia
60
Q

Where do plaques seen in atherogenesis most commonly occur?

A
  • Openings of exiting vessles
  • Branch points
  • Posterior wall of the aorta
61
Q

Which genetic disorder is associated with defective LDL receptors and inadequate hepatic LDL uptake which can precipitate MI before the age of 20?

A

Familial hypercholesterolemia

62
Q

Chronic hypercholesterolemia can directly impair endothelial cell function by increasing the production of what?

A

ROS = membrane/mitochondrial damage + accelerated NO decay

63
Q

With chronic hyperlipidemia, lipoproteins accumulate where in the vessel and undergo what?

A
  • Intima
  • Aggregate and are oxidized by free radicals –> modified LDL
64
Q

What occurs to the modified LDL that aggregates in the intima of vessels?

A
  • Phagocytosed and accumulates in macrophages = FOAM CELLS
  • Smooth m. cells can also transform into lipid-laden foam cells
65
Q

What is the lesion caused by the accumulation of foam cells in the intima of vessels called?

Stimulates what?

A
  • Fatty streak
  • Lead to ↑ cytokine, ↑ GFs and ↑monocyte recruitment + activation
66
Q

Chronic inflammation which contributes to the initiation and progression of atherosclerotic lesions is triggered by what?

Leads to activation of the inflammasome and secretion of what?

A
  • Accumulation of cholesterol crystals and FFA’s in macrophages
  • Secretion of IL-1
67
Q

Secretion of IL-1 assoc. w/ chronic inflammation in atherosclerotic lesions leads to the recruitment and activation of what?

A

More macrophages + T lymphocytes = ↑ cytokines/chemokines which recruit and activate more inflammatory cells

68
Q

Intimal smooth m. cell proliferation + extracellular matrix deposition convert fatty streaks into what?

A

Mature atheroma

69
Q

Which GF’s are implicated in smooth muscle proliferation associated w/ atherogenesis?

A
  • PDGF
  • FGF
  • TGF-α
70
Q

Smooth m. cells stimulated by GF’s in atherogenesis synthesize what that stabilizes atherosclerotic plaques?

A

Extracellular matrix (notably collagen)

71
Q

Atheromas are dynamic lesions consisting of what 4 cell types?

A
  1. Dysfunctional endothelial cells
  2. Proliferating smooth m. cells
  3. T lymphocytes
  4. Macrophages
72
Q

Fatty streaks are a normal finding in which subset of pts?

A
  • Aorta of infants
  • Virtually all adolescents
73
Q

How do atherosclerotic plaques appear grossly inside of a vessel?

A
  • White, yellow and patchy, only portion of wall involved
  • Eccentric appearance
74
Q

In descending order of frequency/severity of involvement list the 5 vessels most extensively affected by atherosclerotic plaques.

A
  1. Lower abdominal aorta
  2. Coronary arteries
  3. Popliteal arteries
  4. Internal carotid arteries
  5. Vessels of circle of Willis
75
Q

The extracellular matrix of atherosclerotic plaques consist of what 3 components?

A
  • Collagen
  • Elastic fibers
  • Proteoglycans
76
Q

What is found deep to the fibrous cap of atherosclerotic plaques?

A
  • Necrotic core containing lipids (primarily cholesterol and cholesterol esters)
  • Debris from dead cells + Foam cells + Fibrin
77
Q

What is seen morphologically at the periphery of atherosclerotic plaques?

A
  • Neovascularization
  • May also see calcification over time
78
Q

Rupture, ulceration or erosion of the surface of atherosclerotic plaques exposes what and leads to?

A
  • Exposes highly thrombogenic substances
  • Leads to thrombosis
79
Q

Rupture of the overlying fibrous cap, or of the thin-walled vessels in the area of neovascularization of atherosclerotic plaques can lead to what?

A
  • Hemorrhage into the plaque (intraplaque hemorrhage)
  • Contained hematoma may expand the plaque or induce plaque rupture
80
Q

Atherosclerotic plaque rupture can discharge atherosclerotic debris where and lead to what?

A
  • Into the bloodstream
  • Producing micoemboli
81
Q

Atherosclerosis-induced pressure or ischemic atrophy of the underlying media, with loss of elastic tissue, causes weakness and potential rupture due to formation of a?

A

Aneurysm

82
Q

What are the 4 major consequences of atherosclerosis?

A
  1. MI (heart attack)
  2. Cerebral infarction (stroke)
  3. Aortic aneurysms
  4. Peripheral vascular disease (gangrene of the legs)
83
Q

The stage at which occlusion of a vessel is sufficiently severe to produce ischemia is known as?

A

Critical stenosis

84
Q

What % decrease in luminal cross-section area is considered critical stenosis?

A

70%

85
Q

Critical stenosis of the arterial lumen may lead to chronic ischemia where?

A
  • Myocardium
  • Bowel (mesenteric ischemia)
  • Brain (ischemic encephalopathy)
  • Extremities (intermittent claudication)
86
Q

Critical stenosis of the coronary artery can lead to chest pain w/ exertion, known as?

A

Stable angina

87
Q

Acute plaque change falls into what 3 general categories?

A
  1. Rupture/fissuring
  2. Erosion/ulceration
  3. Hemorrhage into the atheroma
88
Q

What are the characteristics of “vulnerable plaques” in terms of the fibrous cap, foams cells, and smooth m. cells?

A
  • Contain large areas of foam cells/extracellular lipids
  • THIN fibrous caps
  • Few smooth m. cells + dense clusters of inflammatory cells
89
Q

What is the major structural component of the fibrous caps of atherosclerotic plaques and what produces this structural component?

A
  • Collagen
  • Produced by smooth m. cells
90
Q

What are 2 influences extrinsic to plaques which contribute to acute plaque change?

A
  • Adrenergic stimulation: ↑ BP + ↑ vasoconstriction= ↑ stress on plaque —> seen with wakening and rising in the AM
  • Intense emotional stress: ↑ BP = ↑ stress on plaque
91
Q

Spherical outpouchings involving only a portion of the vessel wall describes what type of aneurysm?

A

Saccular

92
Q

Diffuse, circumferential dilation of long vascular segments defines what type of aneurysm?

A

Fusiform aneurysms

93
Q

Defect in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space (“pulsating hematoma”) defines what?

A

False aneurysm (aka pseudo-aneurysm)

94
Q

Defective synthesis of the scaffolding protein fibrillin leading to aberrant TGF-β activity and weakening of elastic tissue leading to aneurysms underlies what disease?

A

Marfan syndrome

95
Q

Mutations in TGF-β receptors causing defective synthesis of elastin and collagens I and III and potential aneurysms is associated with what disorder?

A

Loeys-Dietz Syndrome

96
Q

Weak vascular walls due to defective type III collagen synthesis is a hallmark of the vascular forms of which syndrome?

A

Ehlers-Danlos Syndrome

97
Q

There is a nutritional basis for aneurysm formation in people with which vitamin deficiency?

A

Vitamin C (scurvy)

98
Q

Increased expression of what by macrophages in atherosclerotic plaques or in vasculitis may contribute to aneurysm formation?

A

MMP

99
Q

The release of elastolytic MMP from macrophages is stimulated by what cytokines and is often seen in AAA’s?

A

IL-4 and IL-10

100
Q

Systemic HTN can cause significant narrowing of arterioles of the vasa vasorum, which causes ischemia of which part of the vessel?

A

Outer medial ischemia

101
Q

Loss of vascular wall elastic tissue/ineffective elastic synthesis, with disrupted and disorganized elastin filaments and increased ground substance (glycosaminoglycan) gives what hallmark histological finding?

A

Cystic medial degeneration

102
Q

What is a final common result of different conditions, including ischemic medial damage and Marfan syndrome?

A

Cystic medial degeneration

103
Q

Which finding characteristic of late stage tertiary syphillis is a cause of aortic aneurysms?

Predilection for which vessels?

A
  • Obliterative endarteritis
  • Predilection for small vessels, including those of vasa vasorum of the thoracic aorta
104
Q

The obliterative endarteritis of late-stage tertiary syphillis leads to what vascular/heart complications?

A
  • Ischemic injury of the aortic media and aneursymal dilation
  • Sometimes involving the aortic valve annulus (aortic valve regurgitation)
105
Q

The 2 most important causes of aortic aneurysms are what?

Which is a greater factor in AAA’s and which for ascending aortic aneurysms?

A
  1. Atherosclerosis = AAA’s
  2. HTN = ascending aortic aneurysms
106
Q

Mycotic aneurysms can originate via what 3 ways?

A
  1. Embolization of a septic embolus (usually as complication of infective endocarditis)
  2. Extension of an adjacent suppurative process
  3. Circulating organisms directly infecting arterial walls
107
Q

AAA’s occur in the abdominal area most typically where?

A

Below the renal arteries and above bifurcation of the aorta

108
Q

AAA’s are characterized by severe atherosclerosis of the aorta, and are frequently covered by what?

A

Bland, laminated, poorly organized mural thrombus

109
Q

AAA is often accompanied by smaller aneurysms in which arteries?

A

Iliac arteries

110
Q

Which type of AAA is more common in younger patients and presentation includes back pain and elevated inflammatory markers?

A

Inflammatory AAA

111
Q

Inflammatory AAA’s are characterized by what type of inflammation and inflammatory infiltrate?

A

Abundant lymphoplasmacytic inflammation w/ many macrophages (and even giant cells)

112
Q

Which variant of AAA is associated with aortitis and periaortitits that weakens the wall and may also have sx’s associated with affected pancreas, bilirary system, and salivary glands?

A

IgG4-related disease

113
Q

Why is recognition of IgG4-related disease as a variant cause of AAA important?

A

Responds well to steroid therapy

114
Q

Which variant of AAA is due to lodging of circulating microorganisms in the wall w/ suppuration further destroying the media, potentiating rapid dilation and rupture?

A

Mycotic AAA

115
Q

AAA’s of which size are usually managed aggressively via surgery?

A

5cm or >

116
Q

What are 4 potential complications of an AAA?

A
  • Rupture into peritoneal cavity or retroperitoneal tissues w/ hemorrhage
  • Obstruction of vessel branching off of aorta (iliac, renal, mesenteric, or vertebral as.)
  • Embolism from atheroma or mural thrombus
  • Impingement on adjacent structure (i.e., compressed ureter or erosion of vertebra)
117
Q

Thoracic aortic aneurysms are most commonly due to what?

May also be caused by what congenital defects?

A
  • Most common = HTN
  • Also seen in Marfan syndrome and Loeys-Dietz syndrome
118
Q

What are some of the major signs/sx’s of thoracic aortic aneurysms due to their location?

A
  • Impingement –> Resp. difficulties or Dysphagia or Persistent cough (recurrent laryngeal n.)
  • Pain due to erosion of bone (ie ribs and vertebral bodies)
  • Aortic valve dilation w/ valve insufficiency or narrowing
  • RUPTURE!
119
Q

Most patients with syphilitic aneurysms die of?

A

Heart failure 2’ to aortic valvular incompetence

120
Q

Aortic dissection occurs principally in what 2 groups of patients?

A
  • Men aged 40-60 yo w/ HTN
  • Younger adults w/ disorders of CT affecting the aorta (i.e., Marfan)
121
Q

Sudden onset of severe chest pain (usually beginning in anterior chest), radiating back between the scapulae and moving downward is the classic presentation of what?

A

Aortic Dissection

122
Q

Aortic dissections can be catastrophic if what occurs?

A

Rupture through the adventitia –> massive hemorrhage into adjacent spaces (i.e., thoracic or abdominal cavities) or cardiac tamponade (hemorrage into pericardial sac)

123
Q

What is the major risk factor for aortic dissection?

A

HTN

124
Q

Aortas of patients with HTN have what type of hypertrophy and degenerative changes associated with loss of what?

A
  • Medial hypertrophy of the vasa vasorum
  • Degenerative changes w/ loss of medial smooth m. cells + disorganized ECM
125
Q

What is the most frequent pre-existing histologically detectable lesion in aortic dissections?

Inflammation?

A

Cystic medial degeneration and inflammation is absent

126
Q

Most aortic dissections arise where?

Initiates via what type of tear?

A

- Ascending aorta within 10cm of the aortic valve

- Via an intimal tear

127
Q

If a dissecting hematoma from an aortic dissection re-enters the lumen of the aorta through a 2nd distal intimal tear, creates a new false vascular channel known as?

Over time these false channels can be endotheliazed to become recognizable as?

A
  • “Double-barreled aorta”
  • Chronic dissections
128
Q

The more common (and dangerous) aortic dissections, type A dissections involve what?

A
  • Boththeascendinganddescending aorta
  • Or just the ascending aorta
129
Q

Aortic dissections which extend into and involve the spinal arteries can cause what?

A

Transverse myelitis

130
Q

Most common cause of death from aortic dissections is due to what?

A

Rupture into the pericardial, pleural, or peritoneal cavities

131
Q

Retrograde dissection into the aortic root can lead to what?

A

Dilation of aortic valve –> aortic valve insufficiency

132
Q

How are type A dissections dealt with at clinical presentation?

A
  • INTENSIVE anti-hypertensive therapy
  • Surgical repair of intimal tear
133
Q

How are type B dissections managed clinically?

A

Conservatively; with surgery or anti-hypertensive therapy

(OMS2) CPR II Exam 1 (23 decks)

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