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Cardiovascular > 04.08 - Aneurysms, PVD (Nichols) > Flashcards

04.08 - Aneurysms, PVD (Nichols) Flashcards

1
Q

Vasculitis Cause of AA

A

Giant Cell Arteritis

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2
Q

1/3 of PAN patients have what infection

A

Chronic Hep B

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3
Q

2 Age groups for Aortic Dissection

A

40-60 w antecedent HTN; younger pts with CT disorders

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4
Q

2 common features of Microscopic Poly

A

Necrotizing Glomerulonephritis and Pulmonary Capillaritis

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5
Q

2 Immune Axes in GCA

A

TH1: IL-12 - IFN-gamma; TH17: IL-1 - IL-23

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6
Q

2 most common pathogenic mechanisms of vasculitis

A

Immune-mediated inflammation, Direct Vascular Invasion by Infectious Pathogens

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7
Q

2 Most important causes of Aortic Aneurysms

A

Athersclerosis and HTN

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8
Q

2nd most commonly affected vessels in Takayasu

A

Pulmonary in 50% of cases

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9
Q

3 Major CV Sequelae of Kawasaki if untreated

A

Coronary Artery Aneurysms, MI, SCD

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10
Q

4 Top Presentations of Wegener’s

A

Bilateral Pneumoitis, Chronic Sinusitis, Mucosal ulcerations of Nasopharynx, Renal disease

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11
Q

A patient with AAA is at significantly increased risk for what other events

A

IHD and Stroke

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12
Q

Ab’s in PAN

A

Characteristically has none

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13
Q

Ab’s present in Wegener’s

A

PR3-ANCAs

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14
Q

Ab’s to Endothelial cells =

A

Kawasaki Disease

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15
Q

Abundant Basophilic Debris (Nuclear Dust) + Geographic Pattern Necrosis is called

A

Pathergic Necrosis

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16
Q

Acute Arterial Occlusion is often a __ emergency

A

Surgical

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17
Q

Acute Arterial Occlusion is usually due to thromboemboli from

A

Heart (mural > LA)

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18
Q

Affect of ANCA’s on neutrophils

A

Can directly activate them

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19
Q

Age group of Kawasaki

A

Usually self-limited illness of infancy and childhood

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20
Q

Age group of PAN

A

Young adults

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21
Q

ANCA titers generally mirror

A

Clinical severity

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22
Q

Aneurysms of what size are managed surgically

A

5cm or larger

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23
Q

Anti-myeloperoxidase =

A

p-ANCA

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24
Q

Anti-proteinase 3 =

A

C-ANCA

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25
Q

Antibodies usually associated with PAN

A

None

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26
Q

Arteries involved in Giant Cell Arteritis

A

Temporal and Ophthalmic, Thoracic Aorta

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27
Q

Atheroembolization is associated with

A

Peripheral Blood Eosinophilia

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28
Q

Bluish Myxoid Ground Substance =

A

Young

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29
Q

Buerger Disease is aka

A

Thromboangiitis Obliterans

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30
Q

Buerger disease occurs almost exclusively in

A

heavy tobacco smokers, usually develops before age 35

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31
Q

C-ANCA =

A

Anti-proteinase 3

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32
Q

Cause of ischemia in GCA

A

Nodular intimal thickening and occasional thromboses

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33
Q

Classic Clinical Symptom of Aortic Dissection

A

Sudden onset of excrutiating tearing or stabbing pain, usually beginning in the anterior chest, radiating to the back between the scapulae, and moving downward

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34
Q

Clinical course of PAN is typically

A

episodic (long symptom-free intervals)

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35
Q

Clinical Significance of Kawasaki

A

Involvement of Coronaries

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36
Q

Culprit immune cell in GCA

A

T Cell-mediated response against unknown vessel wall antigen

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37
Q

Cystic Medial Degeneration

A

Fibrosis, Inadequate ECM synthesis, Accumulation of Amorphous Proteoglycans

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38
Q

Decreased TIMP expression tips balance toward

A

Net ECM degradation

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39
Q

Demographic of Giant Cell Arteritis

A

Elderly white females of Northern European descent

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40
Q

Distinct type of AAA characterized by dense periaortic fibrosis containing abundant lymphoplasmacytic inflammation with mac’s and giant cells

A

Inflammatory AAA

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41
Q

Distinction between GCA and Takayasu is made largely on basis of

A

patient age (50 is cutoff)

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42
Q

Dx of Giant Cell Arteritis is based on

A

High ESR and + Bx

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43
Q

Ectasia vs Aneurysm

A

Ectasia is not discrete and localized

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44
Q

Exception of Vasculitis that also affects veins

A

G w P (Wegener’s)

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45
Q

Fever, Fatigue, Weight Loss, Pain in side of head, Ocular Symptoms

A

GCA

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46
Q

Fibrinoid Necrosis is most common in

A

PAN

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47
Q

Fibrosis, Inadequate ECM synthesis, Accumulation of Amorphous Proteoglycans

A

Cystic Medial Degeneration

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48
Q

Findings in Wegener’s

A

Triad: Granulomas, Vasculitis, Glomerulonephritis

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49
Q

G w/ P: Granulomatous vasculitis of both arteris and veins in lungs will cause

A

Areas of pathergic Necrosis –> Nodules –> Central Cavitation

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50
Q

G w/ P: Patient will likely have

A

Granulomatous Vasculitis and Glomerulonephritis

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51
Q

GCA is associated with what rheumatic disease

A

Polymyalgia Rheumatica

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52
Q

GCA takes the form of

A

Chronic, typically granulomatous, inflammation of large to small arteries (mainly head)

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53
Q

GCA: increased IFN-g correlates with production of

A

VEGF and PDGF –> Lumen stenosis

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54
Q

GCA: what induces mac’s to for multinucleated giant cells

A

IFN-gamma

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55
Q

GCA: what leads to lumen stenosis

A

IFN-g –> VEGF and PDGF

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56
Q

Granulomas, Vasculitis, Glomerulonephritis

A

Triad of Findings in Wegener’s

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57
Q

Granulomatosis with Polyangiitis affects which primary 3 parts of body

A

(1) Lungs; (2) Kidney; (3) Nasopharynx

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58
Q

Granulomatous Vasculitis with Eosinophilia

A

Churg-Strauss

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59
Q

heavy tobacco smokers, usually develops before age 35

A

Buerger disease occurs almost exclusively in

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60
Q

IL-12 and IL-18 in GCA upregulate release of what from T cells

A

IFN-gamma; CCL19 and CCL21

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61
Q

In Marfarn, defective synthesis of Fibrillin leads to

A

abnormal sequestration of TGF-beta

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62
Q

In up to 30% of patients with PAN, vasculitis is attributable to

A

Immune complexes to Hep B

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63
Q

In whom is PAN most common

A

Middle-aged males

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64
Q

Inflammation in Aortic Dissection

A

Characteristically absent

65
Q

Inflammatory Giant Cells indicated

A

TH1’s secreting IFN-gamma

66
Q

Kawasaki Disease is AKA

A

Mucocutaneous Lymph Node Syndrome

67
Q

Leukocytoclastic Vasculitis is aka

A

Microscopic Poly

68
Q

Luminal thrombosis with small microabscesses

A

Buerger Disease

69
Q

Major cause of death in PAN patients

A

Renal involvement (renal arteries most likely to be affected)

70
Q

Major Determinant of AA Rupture

A

Diameter

71
Q

Major risk factor for Aortic Dissection

A

HTN

72
Q

Manifestation of TAA

A

(1) Encroachment on mediastinal structures; (2) Persistent cough; (3) Pain from bone erosion; (4) Cardiac disease

73
Q

Microscopic Poly is characterized by

A

Segmental fibrinoid necrosis of media with focal transmural necrotizing lesions

74
Q

Morphology of Kawasaki resembles

A

PAN

75
Q

Most cases of Microscopic Poly are associated with

A

MPO-ANCA

76
Q

Most common clinical manifestation of immune complex dep

A

Skin Lesions

77
Q

Most common form of vasculitis among elderly in developed countries

A

GCA

78
Q

Most common symptom in GCA

A

Headache

79
Q

Most frequent histologically detectable lesion in Aortic Dissection

A

Cystic Medial Degeneration

80
Q

Most lesions in Microscopic Poly are

A

Pauci-Immune

81
Q

MPO-ANCA is fka

A

P-ANCA

82
Q

MPO-ANCA’s (fka P-ANCA) are associated with

A

Microscopic Polyangiitis, Churg-Straus

83
Q

Multifocal necrotizing granulomatous vasculitis with a surrounding fibroblastic proliferation

A

Wegener’s

84
Q

Mutations in TGF-beta or down-stream signaling pathways result in

A

Defective Elastin and Collagen synthesis –> Aneurysms

85
Q

Mycotic AAA’s occur when

A

Circulating microorganisms seed the aneurysm wall or associated thrombus

86
Q

Necrosis seen in PAN

A

Fibrinoid

87
Q

Necrotizing Glomerulonephritis and Pulmonary Capillaritis

A

2 common features of Microscopic Poly

88
Q

Necrotizing vasculitis that generally affects capillaries, as well as small arterioles and venules

A

Microscopic Polyangiitis

89
Q

Ocular disturbances and marked weakening of pulses in upper extremities

A

Takayasu Arteritis is characterized principally by

90
Q

Other name of Kawasaki

A

Mucocutaneous Lymph Node Syndrome

91
Q

p-ANCA =

A

Anti-myeloperoxidase

92
Q

Pathergic Necrosis

A

Abundant Basophilic Debris (Nuclear Dust) + Geographic Pattern Necrosis is called

93
Q

Pathogenesis of AA involves increased

A

Matrix Metalloproteinases

94
Q

Pathology of PAN

A

Segmental transmural necrotizing vasculitis of Small, Medium Arteries with Fibrinoid Necrosis (and lesions at diff stages)

95
Q

Pauci-immune =

A

Vascular lesions do not typically contain demonstrable Ab and Complement

96
Q

PR3-ANCA (fka C-ANCA) is associated with

A

Wegener Granulomatosis

97
Q

PR3-ANCA fka

A

C-ANCA

98
Q

Primary associated disease with C-ANCA

A

Granulomatosis with Polyangiitis (Wegener’s)

99
Q

Primary associated disease with P-ANCA

A

Microscopic Polyangiitis

100
Q

PVD: Pain at rest, ulcers =

A

Severe disease

101
Q

Rising ANCA titers usually predict

A

Disease Relapse

102
Q

Segment fibrinoid necrosis of the media with focal transmural necrotizing lesions

A

Microscopic Poly

103
Q

Segmental transmural necrotizing inflammation of small to medium-sized arteries

A

PAN

104
Q

Segmental transmural necrotizing vasculitis of Small, Medium Arteries with Fibrinoid Necrosis (and lesions at diff stages)

A

Pathology of PAN

105
Q

Sharply segmental acute and chronic transmural vasculitis of medium and small arteries

A

Buerger Disease (thromboangiitis obliterans)

106
Q

Signature cytokine of Th1 cells

A

IFN-gamma

107
Q

Signs and Symptoms of Acute Arterial Occlusion

A

Pain, Pallow, Paralysis, Paresthesia, Pulselessness (Poikylothermia)

108
Q

Steroid tx cannot affect expansion of which population in GCA

A

TH1 cells

109
Q

Striking infiltration of vessels and perivascular tissues by eosinophils

A

Churg-Strauss

110
Q

Sudden onset of excrutiating tearing or stabbing pain, usually beginning in the anterior chest, radiating to the back between the scapulae, and moving downward

A

Classic Clinical Symptom of Aortic Dissection

111
Q

Systemic manifestation of Giant Cell Arteritis

A

Fever

112
Q

Systemic manifestations of GCA are most responsive to

A

Reduction of TH17 but prednisone

113
Q

T/F: All cases of GCA have granulomas and giant cells

A

False, 25% do not

114
Q

T/F: ANCA autoantibodies make up most of the immune complex deposition

A

FALSE

115
Q

T/F: In PAN, all lesions are at same level of progression

A

False, characteristically all stages of activity coexist, indicating ongoing and recurrent pathogenic insults

116
Q

T/F: Kawasaki disease is usually fatal

A

False, usually self-limited of infancy and chilhood

117
Q

T/F: Recognizable medial damage is prereq for Aortic Dissection

A

FALSE

118
Q

T/F: Takayasu has giant cells

A

TRUE

119
Q

TAA’s are most commonly associated with

A

HTN and Marfan Syndrome

120
Q

Takayasu Arteritis classically affects

A

Aortic Arch and Arch Vessels

121
Q

Takayasu Arteritis is characterized principally by

A

Ocular disturbances and marked weakening of pulses in upper extremities

122
Q

Takayasu Arteritis manifests with

A

Transmural scarring and thickening of the aorta - with severe luminal narrowing of major branch vessels

123
Q

Three Steps of Mycotic Aneurysms

A

(1) Embolization of septic embolus; (2) Extension of an adjacent suppurative process; (3) Direct infection of aterial wall

124
Q

Triad of Findings in Wegener’s

A

Granulomas, Vasculitis, Glomerulonephritis

125
Q

Tx of Giant Cell Arteritis

A

Steroids

126
Q

Tx of Kawasaki

A

IV IG and Aspirin

127
Q

Tx of Wegener’s

A

Cyclophosphamide, Corticosteroids

128
Q

Type B Aneurysm means

A

Below Aortic Arch

129
Q

Typical Wegener’s patient

A

40 year old male

130
Q

Unlike in PAN, all lesions in Microscopic Poly

A

tend to be of same age

131
Q

Upper Respiratory Tract Ulcerations =

A

Granulomatosis with Polyangiitis

132
Q

Vascular lesions of Churg-Strauss differ from PAN and Micro Poly by presence of

A

Granulomas, Eosinophils

133
Q

Vasculitis w/ Eosinophilia, Asthma, and Granulomas

A

Churg-Straus

134
Q

Vasculitis w/ Granulomas but no Asthma

A

Wegener’s

135
Q

Vasculitis w/out Asthma or Granulomas

A

Microscopic Polyangiitis

136
Q

Vessels affected in Microscopic Poly

A

Capillaries and small vessels

137
Q

What causes Cystic Medial Degeneration

A

Luminal narrowing of aortic vasa vasorum leading to ischemia of outer media

138
Q

What initiates the immune response in Giant Cell Arteritis

A

Dendritic Cells

139
Q

What is a rare cause of Obliterative Endarteritis of Aortic Vasa Vasorum

A

Tertiary Syphillis

140
Q

What is absent in Microscopic Poly

A

Granulomatous inflammation

141
Q

What is attacked in Giant Cell Arteritis

A

Calcified Int Elastic Lamina in arteries (Calcified Atrophic T Media of Thoracic Aorta)

142
Q

What is characterized by focal acute and chronic inflammation of medium-sized and small arteries, especially tibial and radial, associated with thrombosis

A

Buerger Disease

143
Q

What is likely causing endothelial cell injury in vasculitis

A

ANCA-activated neutrophils

144
Q

What is produced and released by Dendritic Cells in GCA

A

IL-12 and IL-18

145
Q

What molecules are mediators of matrix degeneration, intimal hyperplasia, and luminal narrowing in GCA

A

MMP-2 and -9

146
Q

What regulates SM cell proliferation and matrix synthesis

A

TGF-beta

147
Q

What size vessels do GCA affect

A

Large

148
Q

What size vessels does Churg-Straus affect

A

Small

149
Q

What size vessels does Kawasaki affect

A

Medium

150
Q

What size vessels does PAN affect

A

Medium

151
Q

What size vessels does Takayasu affect

A

Large

152
Q

What size vessels does Wegener’s affect

A

Small

153
Q

What vessels does PAN commonly affect

A

Medium Muscular: Renal and Visceral (spares pulmonary)

154
Q

Which cells are circulating systemically in GCA

A

TH17

155
Q

Which has better prognosis: Type A or B Aortic Dissection?

A

Type B

156
Q

Which Type of Aortic Aneurysm can be managed more conservatively

A

Type B

157
Q

Why is Giant Cell Arteritis almost exclusively in the eldery

A

Prereq of Arterial Calcification

158
Q

With progression of Takayasu, ___ signs and symptoms dominate clinical picture

A

Vascular: Reduced UE BP/Pulse, Neurologic, Ocular disturbances

Cardiovascular (18 decks)

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