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CVPR > CVPR Week 4: Atherosclerosis > Flashcards

CVPR Week 4: Atherosclerosis Flashcards

1
Q

What is arteriosclerosis?

A

hardening and thickening of artery walls

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2
Q

Types of arteriosclerosis

3 listed

A
  • Atherosclerosis
  • Medial calcification
  • Arteriolarsclerosis
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3
Q

What is atherosclerosis?

A
  • medium to large arteries
  • defined by intimal atheromas
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4
Q

What is medial calcification?

A

consequence of age

Calcium depositis in the media of the blood vessels

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5
Q

What is arteriolarsclerosis?

A

arteriosclerosis of small blood vessels less than 0.3 mm

2 different types

  • hyperplastic intimal thickening
  • Hyalin: acellular thickening (shown in this histologic section)
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6
Q

Atherosclerosis is defined by?

A

Intimal atheromas

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7
Q

What are Intimal atheromas?

A

a fatty collection within the blood vessel intima

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8
Q

Medial sclerosis AKA

A

Monckeberg’s sclerosis

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9
Q

What is this?

A

medial sclerosis

has calcium deposits in the muscular media of the blood vessel

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10
Q

What is this?

A

hyalin type arteriolarsclerosis

where there is acellular thickening in the intima of the very small blood vessel secondary to endothelial dysfunction

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11
Q

What is this?

A

Hyperplastic type Arteriolarsclerosis

where the intima thickening due to intima hyperplasia

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12
Q

hyalin type arteriolarsclerosis is associated with?

A

essential or common type HTN

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13
Q

Hyperplastic type Arteriolarsclerosis is associated with

A

malignant HTN or extremely high BPs

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14
Q

Atherosclerosis vessels that can be affected?

8 listed

A
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15
Q

Identify

A
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16
Q

What is this a depiction of?

A

gross view of atherosclerosis in the abdominal aorta, these brown spots are all ulcerating atherosclerotic plaques within the aorta

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17
Q

microscopic pathophysiology of atherosclerosis

8 listed

A

defined by intimal plaques

muscular media changes

  • loss of smooth muscle cells
  • increase of collagen fibers
  • increase of ground substance

Adventitia changes

  • fibrous thickening
  • mild inflammation
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18
Q

What is this

A

atherosclerotic intimal plaque

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19
Q

Identify

A
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20
Q

How are atheromatous plaques initiated and formed

A
  • atherosclerotic plaques are thought to arise from an initial endothelial dysfunction or injury
  • the risk factors explain how the endothelial injury or dysfunction can arise such as high BP
  • the endothelial dysfunction or injury allow monocytes migrate to the intima and become macrophages
  • leukocytes and monocytes recruit smooth muscle cells from the media layer and these move into the intima and form a fibrous cap
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21
Q

What is this?

A

atherosclerotic plaque and fibrous cap

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22
Q

What is this?

A

lipids in atherosclerotic plaque and fibrous cap

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23
Q

what is the weakest part of the atherosclerotic plaque

A

the shoulder of the fibrous cap… this is important because

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24
Q

Atherosclerosis risk factors

10 listed

A
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25
Q

unchangeable atherosclerosis risk factors

A
  • age
  • sex
  • genetics
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26
Q

Major reversible atherosclerosis risk factors

4 listed

A
  • smoking
  • diabetes
  • HTN
  • HLD
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27
Q

Minor reversible atherosclerosis risk factors

3 listed

A
  • Obesity
  • lifestyle
  • personality
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28
Q

Pathogenesis of atherosclerosis

A
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29
Q

Clinical effects of atherosclerosis

4 listed

A
  • arterial narrowing - organ ischemia or injury
  • Thrombus if the plaque ruptures
  • embolize if the plaque ruptures
  • aneurysm formation from the weakening of blood vessels
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30
Q

Arterial narrowing causes

3 listed

A

shoulder regions are prone to rupture

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31
Q

Thrombosis cause by?

A

acute changes in plaque

  • erosion or ulceration
  • plaque hemorrhage
  • plaque rupture
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32
Q

What is this?

A

arterial narrowing due to

  • shown is atherosclerotic plaque
  • huge Calcium deposit
  • and the hemorrhage of into atheroma
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33
Q

Plaques most vulnerable to rupture

3 listed

A
  • moderate luminal narrowing like 50% stenosis
  • Lipid rich center
  • Thin fibrous cap
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34
Q

What is this?

A

Thrombus in blood vessel from ruptured plaque

call lines of Zohn which are alternating fibrin and RBCs

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35
Q

What is this?

A
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36
Q

Embolism initiation, origin and destinations?

A
  • rupture or erosion of plaque
  • most from the aorta
  • most go to kidneys, pancreas and spleen or the lower limbs and cause dry gangrene
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37
Q

What is this?

A

dry gangrene from an embolus

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38
Q

What is an aneurysm?

A
  • an excessive localized enlargement of an artery caused by a weakening of the artery wall.
  • Abnormal dilation of a blood vessel
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39
Q

Aneurysm Types

2 listed

A
  • Atherosclerotic
  • Dissecting
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40
Q

What is this?

A

gross histological image of an atherosclerotic aneurysm of the abdominal aorta

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41
Q

Atherosclerotic aneurysm common location

A
  • abdominal aorta below the renal arteries
  • Iliac arteries
42
Q

Atherosclerotic aneurysm common in?

A
  • Men > women
  • >60 years old
43
Q

Atherosclerotic aneurysm

A
44
Q

Atherosclerotic aneurysm size?

A

becomes clinically significant when > 5cm in diameter

45
Q

Dissecting aneurysm risk factors

A
  • HTN
  • Genetics: connective tissue disease such as (Marfan Syndrome)
46
Q

Dissecting aneurysm types

A
  • HTN or genetic such as marfans
  • Both types have cystic medial degeneration
47
Q

Dissecting aneurysm location

A

commonly starts in the arch of the aorta

48
Q

What is this?

A

Aortic dissection gross histological image

49
Q

What is this?

A
  • outside relatively normal muscularis media
  • inside cystic medial degeneration
  • starts of an aneurysm
50
Q

Marfan Syndrome Cause

A

Autosomal dominant mutation in FBN1 gene (Fibrillin-1 gene)

51
Q

Marfan Syndrome epidemiology

A

1 in 5000

25% are new mutations

52
Q

FBN1 description & pathology

3 listed

A
  • Marfans Syndrome
  • is an important component of the ECM
  • normally affects these organ systems cardiovascular, ocular and skeletal system
  • it provides scaffolding for elastic fibers in medium and large blood vessels
53
Q

Marfan’s Syndrome diagnostic criteria

A
54
Q

What is this?

A
  • Marfan’s Syndrome
  • Pectis caranadum (pigeon-beaked chest)
55
Q

What is this?

A
  • Marfan’s Syndrome
  • Pectis excavitum (cavitated chest)
56
Q

Hand signs of Marfan’s Syndrome

A
57
Q

Marfan’s torso

A

Scoliosis of >20* is characteristic of Marfan’s Syndrome

58
Q

What is this?

A

hyper or hypo elbow extension is common in Marfans

59
Q

What is this?

A

Pes planus (flat feet) common in Marfans

60
Q

Major skeletal system features of Marfan’s Syndrome

7 listed

A
61
Q

What is this?

A

ectopia lentis (lense dislocation) is common in marfans

62
Q

What is this?

A

Aortic root dilation in Marfan’s

63
Q

What is this?

A

aortic dissection from a dilated aortic root which is common in Marfan’s

64
Q

Major cardiovascular features of Marfans

A
65
Q

Minor pulmonary features of Marfans

A

High risk for spontaneous pneumothorax absence of vascular markings on the left in this

apical blebs

66
Q

Skin and integument features of Marfans

A
  • lumbosacral dural cysts
  • this is an expansion in the lumbosacral area
67
Q

Marfan’s family history

2 listed

A

Major part of the diagnostic criteria

68
Q

Pathology of Marfans

A
  • Fibrillin-1 forms microfibers in the cardiovascular system and connective tissue
  • makes up microfibrils in the ECM and helps to form the scaffolding for the elastic fibers
  • Elastic fibers are one the main contributors of integrity to blood vessels
69
Q

Fibrillin-1 mutations

A
70
Q

Main coronary arteries

3 listed

A

Left coronary artery

Right coronary artery

circu?

71
Q

Identify

A
72
Q

Myocardial ischemia is a deficit in?

A

Amount of coronary blood flow

73
Q

Causes of defect in amount of coronary flow

A
  • Size/narrowing of coronary arteries
  • hypotension
  • development of the collateral circulation
  • arrhythmias
74
Q

Defects that can cause myocardial oxygen requirements

A
  • Anemia
  • Exercise/Excitement/fever/hyperthyroidism
75
Q

MI concerns and contributing factors

6 listed

A
76
Q

Identify grade of occlusion of coronary artery

A

grade 0

77
Q

Identify grade of occlusion of coronary artery

3 listed

A
  • grade 1
  • 25% occlusion
  • minimal occlusion
78
Q

Identify grade of occlusion of coronary artery

4 listed

A
  • grade 2
  • 50% occlusion
  • highest risk for plaque rupture
  • Mild occlusion
79
Q

Identify grade of occlusion of coronary artery

3 listed

A
  • Grade 3
  • 75% occlusion
  • moderate occlusion
80
Q

Identify grade of occlusion of coronary artery

3 listed

A
  • Grade 4
  • 90% occlusion
  • marked occlusion
81
Q

Identify grade of occlusion of coronary artery

A
  • Grade 6 complete occlusion
  • Complete occlusion
82
Q

What is this?

A

moderate occlusion that ruptured grade 3 occlusion rupture at shoulder region

83
Q

Main coronary arteries and areas perfused

3 listed

A

LAD: Anterior wall, apex, septum

Right Coronary: posterior base and posterior septum

Left circumflex: Lateral wall

84
Q

What is this?

A

coronary artery thrombus

85
Q

importance and consequences of developing collateral circulation

A

collaterals developed between right and left coronary artery collateral problem is if you get a thrombus in the right you may also get ischemia on the other side as well

86
Q
A
87
Q

Infract size and location

A
  • the more proximal the infarct is then more likely to cause a large territory infarct
  • if distal it is much more likely to cause a small area infarct
  • also dependent upon the adequacy of collateral circulation
88
Q

Recent thrombus and larger coronary artery typically

A

transmural large-territory infarct

89
Q

Thrombus of an already narrowed artery typically

A

subendocardial infarct

90
Q

What is this?

A

?

91
Q

Sequela of infarct

5 listed

A
  • death from arryththmia or CHF
  • if survive
  • Healing
  • can result in an aneurysm commonly seen in apex and commonly involve LAD
  • myocardial rupture can occur (most vulnerable 3-7 day window)
  • postmyocardial syndrome (Dressler’s Syndrome)
92
Q

Healing sequelae of MI

A
  • first 12 hours neutrophils grow in density 1-3 days
  • 3-7 days clean-up phase macrophages clean up dead neutrophils and myocytes
  • 7-14 days repairative phase deposition of granulation tissue
  • 2-8 weeks deposition of scar tissue
93
Q

Most common postmyocardial syndrome

A

Dressler’s Syndrome

94
Q

Dressler’s Syndrome description

A
  • an immune-mediated event after underogoing a MI
  • occurs 10-14 days after large-territory MI
  • main manifestation (pericarditis or inflammation of pericardium)
  • pericarditis can be Dx by EKG and signs and symptoms
95
Q

What is this?

A
  • most people that suffer cardiac sudden death don’t present with coronary artery thrombi
  • they instead have multiple severe stenotic atherosclerotic lesions of the coronary arteries which precipitated an MI from which they died in minutes
96
Q

What is this?

A
  • large apical aneurysms following a large-territory MI
  • can create thrombi which can cause end-organ damage
97
Q

what is this?

A

large intramural thrombus in the left ventricle in an area of thrombus

thrombi develop here because aneurysms are akinetic and blood pools within the aneurysms

98
Q

Infarct healing

A
99
Q

Sudden Cardiac Death

A
100
Q

Summary

A

CVPR (93 decks)

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