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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
What makes up the fibrous cap of atherosclerotic plaques?
1. SMC | 2. Collagen
26
How can atherosclerosis cause an aneurysm?
Plaque weakens the underlying vessel wall
27
What are the primary effects of atherosclerosis?
1. Ischemic Heart Disease 2. Stroke 3. Ischemic Bowel 4. Peripheral Vascular Occlusive Disease 5. Renal Artery Ischemia 6. Aneurysm
28
What is critical stenosis?
When the occlusion limits flow to the point the oxygen demand exceeds supply
29
What are the three acute plaque changes?
1. Rupture/Fisuring --> exposure of thrombogenic constituents 2. Erosion/Ulceration --> exposure of thrombogenic basement membrane 3. Hemorrhage into the plaque --> increase in size
30
What characterizes a vulnerable plaque?
1. Thinner fibrous cap | 2. Larger liid core
31
What is a false aneurysm?
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
32
What is the main cause of an abdominal aortic aneurysm?
Atherosclerosis
33
What is the main cause of an ascending aortic aneurysm?
HTN
34
What conditions may result in weak CT in the vascular wall and lead to aneurysms?
1. Marfan Syndrome 2. Ehlers-Danlos Syndrome 3. Vitamin C Deficiency
35
Describe the two processes which have been associated with the pathogenesis of aneurysm formation
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)
36
What are the results of Cystic Medial Degeneration?
1. Loss of SMCs 2. Scarring and loss of elasticity 3. Inadequate ECM synthesis
37
In addition to atherosclerosis, what are other risk factors in developing an abdominal aortic aneurysm?
1. Age > 50 2. Men 3. Smokers
38
Where will most abdominal aortic aneurysms be located?
Below the renal arteries and above the bifurcation
39
Describe the morphology of an abdominal aortic aneurysm
The intima will show severe atherosclerosis with destruction of the underlying aortic media
40
Mural thrombus and atheromatous ulcers may be seen in what condition?
Abdominal Aortic Aneurysm
41
In addition to hemorrhage, what clinical consequences may occur from an abdominal aortic aneurysm?
1. Obstruction of branch vessels --> ischemia | 2. Embolism from atherosclerotic plaque (atheroma) or mural thrombus
42
What condition presents with a palpating abdominal mass?
Abdominal Aortic Aneurysm
43
The clinical features of a thoracic aortic aneurysm are caused by what?
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
What condition is associated with aortic dilation?
Aortic Dissection
45
Which patient groups are most likely to get aortic dissections?
1. Men 40-60 with HTN | 2. CT Disease Pts (Marfan)
46
Where is the intimal tear seen in aortic dissections?
Within 10cm of the aortic valve
47
Where does the aortic dissection extend?
Between the middle and outer third of the media
48
What are the consequences of an aortic dissection?
1. Rupture --> Hemorrhage (hemothorax, cardiac tamponade) | 2. Creation of a new vascular channel
49
What is the most commonly detected lesion in aortic dissection?
Cystic Medial Degeneration
50
What is Type A classification for an aortic dissection?
A proximal lesion in the ascending +/- descending aorta- more common and more dangerous (DeBakey I or II)
51
What is Type B classification for an aortic dissection?
A distal lesion that does not involve the ascending aorta (DeBakey III); **begins distal to the subclavian artery
52
What condition may present as sudden onset of excruciating pain in the anterior chest that radiates to the back?
Aortic Dissection
53
What would be the consequences of a retrograde aortic dissection?
1. Disruption of the aortic valve 2. Cardiac Tamponade 3. Aortic Insufficiency 4. MI
54
What are the non-specific vasculitis symptoms?
1. Fever 2. Myalgias 3. Arthralgias 4. Malaise
55
What are the mechanisms of vasculitis?
1. Invasion of vessel wall by infectious agents | 2. Immune Mediated Inflammation
56
Common causes of Immune Complexes that damage vessels include what?
1. Drug resistance (Penicillin) | 2. Viral Infections (Hep B)
57
What are the two types of antineutrophil cytoplasmic antibodies?
1. Anti-MPO ANCA | 2. Anti-PR3 ANCA
58
In which conditions do you see MPO-ANCA?
Microscopic Polyangiitis and Churg Strauss
59
In which condition do you see PR3-ANCA?
Wegner Granulomatosis
60
What are the types of large vessel vasculitities?
1. Giant Cell Arteritis | 2. Takayasu Arteritis
61
Which age group is affected by Giant Cell Arteritis?
Elderly
62
Which vessels are affected by Giant Cell Arteritis?
Temporal, Vertebral and Ophthalmic
63
Which vasculitis is associated with granulomatous inflammation, nodular intimal thickening, elastic lamina fragmentation and giant cells?
Giant Cell Arteritis
64
Which condition is seen in half of patients with giant cell arteritis?
Polymyalgia rheumatica
65
What are the symptoms of GCA, and what is the most significant risk?
Risk- Blindness | Symptoms- HA, facial pain, jaw claudication
66
What is the treatment for Giant Cell Arteritis?
Corticosteroids
67
What are the Medium Sized Arteritities?
1. Polyarteritis Nodosa | 2. Kawasaki Disease
68
Which vasculitis is associated with Chronic Hep B?
Polyarteritis Nodosa (PAN)
69
Which vasculitis is segmental, affects branching points/bifurcations, and affects the kidneys, heart, liver, GI but NOT the lungs?
PAN
70
What vasculitis causes destruction of arterial media and internal elastic lamina causing aneurysmal nodules?
PAN
71
What is the acute and later stages of morphological changes associated with PAN?
Acute- Transmural inflammation (PMNS, Eos, Mononuclear Cells) --> Fibrinoid Necrosis Later: Fibrous thickening **Both stages can be present at same time
72
Which demographic is affected by PAN?
Young adults
73
What are the symptoms of PAN?
1. Non-specific vasculitis sx 2. Kidney involvement 3. GI- abdominal pain, melena 4. MSK- myalgia, arthralgia 5. Peripheral Neuritis
74
What is the treatment for PAN?
Corticosteroids and Cyclophosphamide
75
What condition linked with PAN must also be treated for a good prognosis?
HTN
76
What arteries are affected in Kawasaki disease?
Coronaries
77
What is the morphological change associated with Kawasaki disease?
1. Fibrinoid Necrosis | 2. Intimal Lesions and severe transmural destruction
78
What may occur after the acute inflammatory phase of Kawasaki Disease?
Aneurysms --> rupture/thrombosis --> MI
79
What are the sx of Kawasaki Disease?
1. Conjunctivitis 2. Rash 3. Adenopathy (Cervical nodes) 4. Strawberry Tongue (and lips/oral mucosa) 5. Hands and Feet- edema BURN- fever
80
Describe the levels of severity regarding the cardiovascular sequelae of Kawasaki Disease?
1. Asx Vasculitis of the Coronaries 2. Giant Coronary Aneurysm 3. MI or Sudden Death
81
What is the treatment for Kawasaki Disease?
Aspirin, IVIg
82
What are the Small Vessel Vasculitities?
1. Microscopic Polyangiitis 2. Churg-Strauss 3. Wegener's Granulomatosis
83
What arteries are affected in microscopic polyangiitis?
Arterioles, capillaries and venules
84
Which vasculitis presents with lesions all the same age?
Microscopic Polyangiitis
85
What is typically present in Microscopic Polyangiitis?
MPO-ANCA
86
The immune complex deposition or secondary immune response (MPO-ANCAs) seen with Microscopic Polyangiitis may be triggered by what?
Ab response/hypersensitivity to: 1. Drugs (penicillin) 2. Microorganisms (Strep) 3. Heterologous Proteins 4. Tumor Antigens
87
Most lesions in microscopic polyangiitis are pauci-immune, meaning what?
There is no immune complex deposition
88
What is the key finding of microscopic polyangiitis?
Fibrinoid necrosis of the media of small vessels
89
In which vasculitis may you see infiltrating and fragmenting neutrophils?
Microscopic Polyangiitis
90
What are potential symptoms of microscopic polyangiitis?
1. Lung- Hemoptysis 2. Kidney- Hematuria and Proteinuria 3. GI- Bowel pain and bleeding 4. Muscle- Weakness and Pain 5. Skin- Palpable purpura
91
What is the treatment for microscopic polyangiitis?
Immunosuppression
92
What is a small vessel necrotizing vasculitis that is associated with allergic rhinitis, asthma and eosinophil infiltration?
Churg-Strauss Syndrome
93
What is the main morphological feature of Churg Strauss?
Granulomas
94
In what condition are only 50% positive for MPO-ANCA?
Churg Strauss
95
What is the triad associated with Wegener's Granulomatosis?
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
Which vasculitis has a high correlation with PR3-ANCA?
Wegener's Granulomatosis
97
Which vasculitis involves small arteries and has adjacent granulomatous inflammation with epitheliod cells and giant cells?
Wegener's Granulomatosis
98
What is the clinical presentation of Wegener's Granulomatosis?
1. Persistent Pneumonitis with bilateral nodular and cavitary infiltrates 2. Sinusitis 3. Mucosal ulceration of the nasopharynx 4. Evidence of renal disease
99
What is the treatment for Wegener's Granulomatosis?
1. Immunosuppressives | 2. Cyclophosphamide
100
Which condition is characterized as a segmental thrombosing and inflammation of medium and small arteries; especially the tibial and radial arteries?
Thromboangiitis obliterans
101
What demographic is affected by Wegener's?
Men- age 40
102
What demographic is affected by thromboangiitis obliterates?
Heavy Smokers
103
What is the pathogenesis of Thromboangiitis obliterates?
Vascular insufficiency caused by hypersensitivity to tobacco extracts in patients
104
Describe the thrombus associated with thromboangiitis obliterates
Contains a micro abscess with neutrophils surrounded by granulomatous inflammation
105
Which vasculitis is associated with ulceration of the extremities followed by gangrene?
Thromboangiitis obliterans

D&T3 Cardiology (7 decks)

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