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D&T3 Cardiology > Norton Vascular Diseases > Flashcards

Norton Vascular Diseases Flashcards

1
Q

What are the components of the adventitia?

A
  1. CT
  2. Nerves
  3. Vasa Vasorum
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2
Q

Which arteries have media rich in elastic fibers that expand in systole and recoil in diastole?

A

Aorta and Large Branches (Elastic Arteries)

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3
Q

Which arteries have media rich in smooth muscle cells?

A

Muscular arteries (branches off of aorta- coronary arteries, renal arteries)

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4
Q

What is the main contribution to resistance to blood pressure?

A

Arterioles

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5
Q

Which layer(s) of vasculature are present in capillaries?

A

Intima only

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6
Q

What is the function of lymphatics?

A

To reduce edema

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7
Q

What factors can loosen the endothelial tight junctions?

A
  1. Hypertension

2. Vasoactive Agents (Histamine)

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8
Q

What is endothelial cell activation and what are the results?

A
  • Expression of inducible properties of the endothelium in response to a specific factor:
    1. Exp of Adhesion Molecules
    2. Production of Cytokines and Chemokines, Vasoactive Molecules and Pro/Anticoagulants
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9
Q

What is endothelial dysfunction?

A

A potentially reversible response that results in the alteration of gene expression and protein synthesis leading to an impairment of vasoreactivity

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10
Q

What are potential results of endothelial dysfunction?

A
  1. Thrombus Formation
  2. Initiation of atherosclerosis
  3. Vascular effects
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11
Q

Describe the vasculature’s response to injury

A

Intimal Thickening: Endothelial cells migrate into the intima from adjacent uninjured areas or from circulating precursors. SMCs also migrate in, proliferate and synthesize new ECM

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12
Q

What is the potential risk to intimal thickening?

A

Stenosis or occlusion of small and medium sized vessels

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13
Q

What is arteriolosclerosis?

A

Injury to small arteries and arterioles; especially renal

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14
Q

What are the mechanisms and causes of arteriolosclerosis?

A
  1. Hyaline Arteriolosclerosis (HTN and diabetes)

2. Hyperplastic Arteriolosclerosis (Malignant HTN –> onionskin thickening)

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15
Q

What is Monckeberg Arteriosclerosis?

A

Calcifications in the media of muscular arteries (ulnar and radial)

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16
Q

Where is atherosclerosis typically seen?

A

Elastic and Muscular Arteries

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17
Q

What are the risk factors for Atherosclerosis? (10)

A
  1. Age
  2. Gender
  3. Genetics
  4. Hyperlipidemia
  5. HTN
  6. Cigarette Smoking
  7. Diabetes
  8. Inflammation
  9. Hyperhomocystinemia
  10. Metabolic Syndrome
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18
Q

What lifestyle behaviors can decrease LDL levels?

A

Exercise and moderate Alcohol consumption

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19
Q

Describe the Pathogenesis of Atherosclerosis (7 Steps)

A
  1. Endothelial Injury (from HTN or Hypercholesterolemia) that causes increased permeability, leukocytee adhesion and Thrombosis
  2. Lipoproteins (LDL) move into vessel wall
  3. Monocytes stick to damaged endothelium, migrate into sub endothelium and transform to macrophages and foam cells
  4. Platelets stick to damaged endothelium
  5. Factors (platelets, macrophages and endothelium) stimulate SMC recruitment
  6. SMCs proliferate and lay down new ECM
  7. Lipid accumulates extracellularly and in cells
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20
Q

What is the first morphological finding of atherosclerosis?

A

Fatty Streak (or dots)

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21
Q

Where are fatty streaks often found?

A

The ostia of branch vessels

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22
Q

Which arteries are most susceptible to atherosclerosis?

A
  1. Abdominal Aorta
  2. Coronary Arteries
  3. Popliteal Arteries
  4. Internal Carotid Arteries
  5. Vessels of the Circle of Willis
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23
Q

What is seen in atherosclerotic plaques?

A
  1. SMC
  2. Macrophages/ Foam Cells
  3. T Cells
  4. ECM
  5. Lipids
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24
Q

What makes up the necrotic center (lipid core) of plaques?

A
  1. Cell debris
  2. Cholesterol Crystals
  3. Foam Cells
  4. Calcium
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25
Q

What makes up the fibrous cap of atherosclerotic plaques?

A
  1. SMC

2. Collagen

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26
Q

How can atherosclerosis cause an aneurysm?

A

Plaque weakens the underlying vessel wall

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27
Q

What are the primary effects of atherosclerosis?

A
  1. Ischemic Heart Disease
  2. Stroke
  3. Ischemic Bowel
  4. Peripheral Vascular Occlusive Disease
  5. Renal Artery Ischemia
  6. Aneurysm
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28
Q

What is critical stenosis?

A

When the occlusion limits flow to the point the oxygen demand exceeds supply

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29
Q

What are the three acute plaque changes?

A
  1. Rupture/Fisuring –> exposure of thrombogenic constituents
  2. Erosion/Ulceration –> exposure of thrombogenic basement membrane
  3. Hemorrhage into the plaque –> increase in size
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30
Q

What characterizes a vulnerable plaque?

A
  1. Thinner fibrous cap

2. Larger liid core

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31
Q

What is a false aneurysm?

A

An extravasation hematoma (that is pulsating); caused by a defect in vascular wall
**True Aneurysms are thinning of the vascular wall and do not result in blood outside of the circulatory system

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32
Q

What is the main cause of an abdominal aortic aneurysm?

A

Atherosclerosis

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33
Q

What is the main cause of an ascending aortic aneurysm?

A

HTN

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34
Q

What conditions may result in weak CT in the vascular wall and lead to aneurysms?

A
  1. Marfan Syndrome
  2. Ehlers-Danlos Syndrome
  3. Vitamin C Deficiency
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35
Q

Describe the two processes which have been associated with the pathogenesis of aneurysm formation

A
  1. Inflammation and MMPs change the balance of collagen degradation/synthesis
  2. Cystic Medial Degeneration- Caused by ischemia to the vessel wall (inner media from atherosclerosis; outer media from thinning of vasa vasorum due to HTN)
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36
Q

What are the results of Cystic Medial Degeneration?

A
  1. Loss of SMCs
  2. Scarring and loss of elasticity
  3. Inadequate ECM synthesis
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37
Q

In addition to atherosclerosis, what are other risk factors in developing an abdominal aortic aneurysm?

A
  1. Age > 50
  2. Men
  3. Smokers
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38
Q

Where will most abdominal aortic aneurysms be located?

A

Below the renal arteries and above the bifurcation

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39
Q

Describe the morphology of an abdominal aortic aneurysm

A

The intima will show severe atherosclerosis with destruction of the underlying aortic media

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40
Q

Mural thrombus and atheromatous ulcers may be seen in what condition?

A

Abdominal Aortic Aneurysm

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41
Q

In addition to hemorrhage, what clinical consequences may occur from an abdominal aortic aneurysm?

A
  1. Obstruction of branch vessels –> ischemia

2. Embolism from atherosclerotic plaque (atheroma) or mural thrombus

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42
Q

What condition presents with a palpating abdominal mass?

A

Abdominal Aortic Aneurysm

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43
Q

The clinical features of a thoracic aortic aneurysm are caused by what?

A

Compression of local structures:

  1. Lungs/air way- breathing difficulties
  2. Esophagus- swallowing problems
  3. Ribs/Vertebral Bodies- pain from bone erosion
  4. Cardiac Disease/aortic valvular incompetence
  5. Rupture
44
Q

What condition is associated with aortic dilation?

A

Aortic Dissection

45
Q

Which patient groups are most likely to get aortic dissections?

A
  1. Men 40-60 with HTN

2. CT Disease Pts (Marfan)

46
Q

Where is the intimal tear seen in aortic dissections?

A

Within 10cm of the aortic valve

47
Q

Where does the aortic dissection extend?

A

Between the middle and outer third of the media

48
Q

What are the consequences of an aortic dissection?

A
  1. Rupture –> Hemorrhage (hemothorax, cardiac tamponade)

2. Creation of a new vascular channel

49
Q

What is the most commonly detected lesion in aortic dissection?

A

Cystic Medial Degeneration

50
Q

What is Type A classification for an aortic dissection?

A

A proximal lesion in the ascending +/- descending aorta- more common and more dangerous (DeBakey I or II)

51
Q

What is Type B classification for an aortic dissection?

A

A distal lesion that does not involve the ascending aorta (DeBakey III); **begins distal to the subclavian artery

52
Q

What condition may present as sudden onset of excruciating pain in the anterior chest that radiates to the back?

A

Aortic Dissection

53
Q

What would be the consequences of a retrograde aortic dissection?

A
  1. Disruption of the aortic valve
  2. Cardiac Tamponade
  3. Aortic Insufficiency
  4. MI
54
Q

What are the non-specific vasculitis symptoms?

A
  1. Fever
  2. Myalgias
  3. Arthralgias
  4. Malaise
55
Q

What are the mechanisms of vasculitis?

A
  1. Invasion of vessel wall by infectious agents

2. Immune Mediated Inflammation

56
Q

Common causes of Immune Complexes that damage vessels include what?

A
  1. Drug resistance (Penicillin)

2. Viral Infections (Hep B)

57
Q

What are the two types of antineutrophil cytoplasmic antibodies?

A
  1. Anti-MPO ANCA

2. Anti-PR3 ANCA

58
Q

In which conditions do you see MPO-ANCA?

A

Microscopic Polyangiitis and Churg Strauss

59
Q

In which condition do you see PR3-ANCA?

A

Wegner Granulomatosis

60
Q

What are the types of large vessel vasculitities?

A
  1. Giant Cell Arteritis

2. Takayasu Arteritis

61
Q

Which age group is affected by Giant Cell Arteritis?

A

Elderly

62
Q

Which vessels are affected by Giant Cell Arteritis?

A

Temporal, Vertebral and Ophthalmic

63
Q

Which vasculitis is associated with granulomatous inflammation, nodular intimal thickening, elastic lamina fragmentation and giant cells?

A

Giant Cell Arteritis

64
Q

Which condition is seen in half of patients with giant cell arteritis?

A

Polymyalgia rheumatica

65
Q

What are the symptoms of GCA, and what is the most significant risk?

A

Risk- Blindness

Symptoms- HA, facial pain, jaw claudication

66
Q

What is the treatment for Giant Cell Arteritis?

A

Corticosteroids

67
Q

What are the Medium Sized Arteritities?

A
  1. Polyarteritis Nodosa

2. Kawasaki Disease

68
Q

Which vasculitis is associated with Chronic Hep B?

A

Polyarteritis Nodosa (PAN)

69
Q

Which vasculitis is segmental, affects branching points/bifurcations, and affects the kidneys, heart, liver, GI but NOT the lungs?

A

PAN

70
Q

What vasculitis causes destruction of arterial media and internal elastic lamina causing aneurysmal nodules?

A

PAN

71
Q

What is the acute and later stages of morphological changes associated with PAN?

A

Acute- Transmural inflammation (PMNS, Eos, Mononuclear Cells) –> Fibrinoid Necrosis
Later: Fibrous thickening
**Both stages can be present at same time

72
Q

Which demographic is affected by PAN?

A

Young adults

73
Q

What are the symptoms of PAN?

A
  1. Non-specific vasculitis sx
  2. Kidney involvement
  3. GI- abdominal pain, melena
  4. MSK- myalgia, arthralgia
  5. Peripheral Neuritis
74
Q

What is the treatment for PAN?

A

Corticosteroids and Cyclophosphamide

75
Q

What condition linked with PAN must also be treated for a good prognosis?

A

HTN

76
Q

What arteries are affected in Kawasaki disease?

A

Coronaries

77
Q

What is the morphological change associated with Kawasaki disease?

A
  1. Fibrinoid Necrosis

2. Intimal Lesions and severe transmural destruction

78
Q

What may occur after the acute inflammatory phase of Kawasaki Disease?

A

Aneurysms –> rupture/thrombosis –> MI

79
Q

What are the sx of Kawasaki Disease?

A
  1. Conjunctivitis
  2. Rash
  3. Adenopathy (Cervical nodes)
  4. Strawberry Tongue (and lips/oral mucosa)
  5. Hands and Feet- edema
    BURN- fever
80
Q

Describe the levels of severity regarding the cardiovascular sequelae of Kawasaki Disease?

A
  1. Asx Vasculitis of the Coronaries
  2. Giant Coronary Aneurysm
  3. MI or Sudden Death
81
Q

What is the treatment for Kawasaki Disease?

A

Aspirin, IVIg

82
Q

What are the Small Vessel Vasculitities?

A
  1. Microscopic Polyangiitis
  2. Churg-Strauss
  3. Wegener’s Granulomatosis
83
Q

What arteries are affected in microscopic polyangiitis?

A

Arterioles, capillaries and venules

84
Q

Which vasculitis presents with lesions all the same age?

A

Microscopic Polyangiitis

85
Q

What is typically present in Microscopic Polyangiitis?

A

MPO-ANCA

86
Q

The immune complex deposition or secondary immune response (MPO-ANCAs) seen with Microscopic Polyangiitis may be triggered by what?

A

Ab response/hypersensitivity to:

  1. Drugs (penicillin)
  2. Microorganisms (Strep)
  3. Heterologous Proteins
  4. Tumor Antigens
87
Q

Most lesions in microscopic polyangiitis are pauci-immune, meaning what?

A

There is no immune complex deposition

88
Q

What is the key finding of microscopic polyangiitis?

A

Fibrinoid necrosis of the media of small vessels

89
Q

In which vasculitis may you see infiltrating and fragmenting neutrophils?

A

Microscopic Polyangiitis

90
Q

What are potential symptoms of microscopic polyangiitis?

A
  1. Lung- Hemoptysis
  2. Kidney- Hematuria and Proteinuria
  3. GI- Bowel pain and bleeding
  4. Muscle- Weakness and Pain
  5. Skin- Palpable purpura
91
Q

What is the treatment for microscopic polyangiitis?

A

Immunosuppression

92
Q

What is a small vessel necrotizing vasculitis that is associated with allergic rhinitis, asthma and eosinophil infiltration?

A

Churg-Strauss Syndrome

93
Q

What is the main morphological feature of Churg Strauss?

A

Granulomas

94
Q

In what condition are only 50% positive for MPO-ANCA?

A

Churg Strauss

95
Q

What is the triad associated with Wegener’s Granulomatosis?

A
  1. Respiratory Tract Involvement with granulomas of the upper (ENT) and lower (lung) part of tract
  2. Focal Necrotizing or Granulomatous vasculitis **especially in lungs
  3. Renal Disease (focal necrotizing glomerulonephritis)
96
Q

Which vasculitis has a high correlation with PR3-ANCA?

A

Wegener’s Granulomatosis

97
Q

Which vasculitis involves small arteries and has adjacent granulomatous inflammation with epitheliod cells and giant cells?

A

Wegener’s Granulomatosis

98
Q

What is the clinical presentation of Wegener’s Granulomatosis?

A
  1. Persistent Pneumonitis with bilateral nodular and cavitary infiltrates
  2. Sinusitis
  3. Mucosal ulceration of the nasopharynx
  4. Evidence of renal disease
99
Q

What is the treatment for Wegener’s Granulomatosis?

A
  1. Immunosuppressives

2. Cyclophosphamide

100
Q

Which condition is characterized as a segmental thrombosing and inflammation of medium and small arteries; especially the tibial and radial arteries?

A

Thromboangiitis obliterans

101
Q

What demographic is affected by Wegener’s?

A

Men- age 40

102
Q

What demographic is affected by thromboangiitis obliterates?

A

Heavy Smokers

103
Q

What is the pathogenesis of Thromboangiitis obliterates?

A

Vascular insufficiency caused by hypersensitivity to tobacco extracts in patients

104
Q

Describe the thrombus associated with thromboangiitis obliterates

A

Contains a micro abscess with neutrophils surrounded by granulomatous inflammation

105
Q

Which vasculitis is associated with ulceration of the extremities followed by gangrene?

A

Thromboangiitis obliterans

D&T3 Cardiology (7 decks)

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