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MD2 Pathology > Vascular Pathology > Flashcards

Vascular Pathology Flashcards

1
Q

What factors are related to risk of rupture of berry aneurysms?

A

Size

Episodes of HTN

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2
Q

What is the main site for a berry aneurysm?

A

AComm: 40%

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3
Q

What is the main site for a berry aneurysm?

A

AComm: 40%

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4
Q

What are Charcot-Bouchard aneurysms?

A

Aneurysms occurring in straight segments of small intracerebral arteries in basal ganglia, caused by chronic HTN

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5
Q

What is vasculitis?

A

Acute or chronic inflammation that results in structural damage to the vessel wall

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6
Q

What is vasculitis?

A

Acute or chronic inflammation that results in structural damage to the vessel wall

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7
Q

List 4 types of immune-mediated vasculitis

A

Henoch-Schonlein purpura
Cryoglobulinaemic vasculitis
Serum sickness
Connective tissue diseases

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8
Q

Direct Ab attack

A

Goodpastures’ syndrome

Kawasaki disease

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9
Q

ANCA associated

A

??

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10
Q

Unknown

A 
Giant cell (temporal) arteritis
??
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11
Q

Unknown

A 
Giant cell (temporal) arteritis
??
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12
Q

Unknown

A 
Giant cell (temporal) arteritis
??
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13
Q

How can you tell if there are small vessel changes?

A 
Retina
Kidney
Neuropathy
Purpuric rash that won't blanch, usually lower limbs more than upper limbs
GI bleeding and infarcts
Pancreatitis
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14
Q

How can you tell if there are small vessel changes?

A 
Retina
Kidney
Neuropathy
Purpuric rash that won't blanch, usually lower limbs more than upper limbs
GI bleeding and infarcts
Pancreatitis
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15
Q

Wegener’s

A

Respiratory tract and kidneys

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16
Q

Churg-Strauss

A

Granulomas

Eosinophils

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17
Q

Histological changes in small vessel vasculitis

A 
May be thrombus
Wall often dead with fibrinoid necrosis
Inflammation around vessel
Blood leaking out of vessel
May do other tests to assess whether there are e.g. Igs depositing in cell wall
Leukocytoclasis
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18
Q

Histological changes in small vessel vasculitis

A 
May be thrombus
Wall often dead with fibrinoid necrosis
Inflammation around vessel
Blood leaking out of vessel
May do other tests to assess whether there are e.g. Igs depositing in cell wall
Leukocytoclasis
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19
Q

Pathological process in small vessel vasculitis

A

Infiltrate of neutrophils causing vessel injury
Fibrin deposition (in lumen or vessel wall)
Leakage of RBCs
Lymphocytes and macrophages attract later to help in vessel repair
Fibrois of vessel wall
May progress direct to giant cell inflammation in giant cell vasculitis

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20
Q

List 7 small vessel vasculitides

A

Microscopic polyangitis
Wegener’s granulomatosis
Churg-Strauss syndrome
Henoch-Schonlein purpura (IgA deposition)
Cryoglobulinaemic vasculitis (test for cryoglobulins)
Serum sickness
Rheumatoid and lupus vasculitis (Rh factor, anti-dsDNA)

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21
Q

List 3 manifestations of small vessel vasculitis

A

Nephritis: usually a necrotising and crescentic GN
Pulmonary haemorrhage: haemorrhagic alveolar capillaritis, heals as interstitial fibrosis
Pulmonary-renal syndrome: in microscopic polyangitis and Goodpastures’ syndrome

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22
Q

Goodpasture’s disease

A

Anti-BM Abs

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23
Q

List 3 manifestations of small vessel vasculitis

A

Nephritis: usually a necrotising and crescentic GN
Pulmonary haemorrhage: haemorrhagic alveolar capillaritis, heals as interstitial fibrosis
Pulmonary-renal syndrome: in microscopic polyangitis and Goodpastures’ syndrome

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24
Q

Goodpastures’

A

Anti-BM Abs

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25
Q

List 3 manifestations of small vessel vasculitis

A

Nephritis: usually a necrotising and crescentic GN
Pulmonary haemorrhage: haemorrhagic alveolar capillaritis, heals as interstitial fibrosis
Pulmonary-renal syndrome: in microscopic polyangitis and Goodpastures’ syndrome
Skin: purpura
Abdominal pain: bowel necrosis, ulceration and haemorrhage, ??

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26
Q

List 3 manifestations of small vessel vasculitis

A

Nephritis: usually a necrotising and crescentic GN
Pulmonary haemorrhage: haemorrhagic alveolar capillaritis, heals as interstitial fibrosis
Pulmonary-renal syndrome: in microscopic polyangitis and Goodpastures’ syndrome
Skin: purpura (non-blanching, more common in lower limbs, rapid onset)
Abdominal pain: bowel necrosis, ulceration and haemorrhage, ??

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27
Q

List 3 manifestations of small vessel vasculitis

A

Nephritis: usually a necrotising and crescentic GN
Pulmonary haemorrhage: haemorrhagic alveolar capillaritis, heals as interstitial fibrosis
Pulmonary-renal syndrome: in microscopic polyangitis and Goodpastures’ syndrome
Skin: purpura (non-blanching, more common in lower limbs)
Abdominal pain: bowel necrosis, ulceration and haemorrhage, ??

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28
Q

List 3 manifestations of small vessel vasculitis

A

Nephritis: usually a necrotising and crescentic GN
Pulmonary haemorrhage: haemorrhagic alveolar capillaritis, heals as interstitial fibrosis
Pulmonary-renal syndrome: in microscopic polyangitis and Goodpastures’ syndrome
Skin: purpura (non-blanching, more common in lower limbs)
Abdominal pain: bowel necrosis, ulceration and haemorrhage, ??
Peripheral neuropathy, myalgia, arthralgia: involvement of small arteries and arterioles, may have elevated muscle enzymes

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29
Q

Goodpastures’

A

Anti-BM Abs

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30
Q

Pauci-immune vaculitis

A

??

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31
Q

Microscopic polyangitis

A

Necrotising systemic vasculitis affecting arterioles, capillaries and venules (and sometimes small and medium sized arteries)
Characterised by ??

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32
Q

Incidence of MP

A

1 in 1000

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33
Q

MP demographics

A

Slight M>F predominance

Mean age 50 years

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34
Q

Microscopic polyangitis

A

Necrotising systemic vasculitis affecting arterioles, capillaries and venules (and sometimes small and medium sized arteries)
Characterised by ??
Segmental vascular necrosis
Infiltrate of neutrophils and monocytes
May have leukocytoclasis - split neutrophils?, fibrin and haemorrhage
Thrombosis in small arteries causing infarction
Healing with fibrosis
Pseudoaneurysms may occur in medium sized arties)

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35
Q

MP demographics

A

Slight M>F predominance

Mean age 50 years

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36
Q

P-ANCA

A

MP

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37
Q

C-ANCA

A

??

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38
Q

C-ANCA

A

??

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39
Q

ANCA-positive

A

Probably pauci-immune?

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40
Q

ANCA-positive

A

Probably pauci-immune?

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41
Q

Wegener’s granulomatosis

A

Granulomatous inflammation, necrosis and vasculitis predominantly affecting respiratory tract
Variable renal involvement
Predominantly C-ANCA positive (75%)

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42
Q

Churg-Strauss syndrome

A 
Granulomatous inflammation
Peripheral blood eosinophilia
Can have asthmatic symptoms
60% P-ANCA, 10% C-ANCA, 30% negative
Systemic disease - may get kidney damage, may diagnose from biopsy
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43
Q

List 7 small vessel vasculitides

A

Microscopic polyangiitis
Wegener’s granulomatosis
Churg-Strauss syndrome
Henoch-Schonlein purpura (IgA deposition)
Cryoglobulinaemic vasculitis (test for cryoglobulins)
Serum sickness
Rheumatoid and lupus vasculitis (Rh factor, anti-dsDNA)

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44
Q

List 3 manifestations of small vessel vasculitis

A

Nephritis: usually a necrotising and crescentic GN
Pulmonary haemorrhage: haemorrhagic alveolar capillaritis, heals as interstitial fibrosis
Pulmonary-renal syndrome: in microscopic polyangiitis and Goodpastures’ syndrome
Skin: purpura (non-blanching, more common in lower limbs)
Abdominal pain: bowel necrosis, ulceration and haemorrhage, ??
Peripheral neuropathy, myalgia, arthralgia: involvement of small arteries and arterioles, may have elevated muscle enzymes

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45
Q

Microscopic polyangiitis

A

Necrotising systemic vasculitis affecting arterioles, capillaries and venules (and sometimes small and medium sized arteries)
Characterised by ??
Segmental vascular necrosis
Infiltrate of neutrophils and monocytes
May have leukocytoclasis - split neutrophils?, fibrin and haemorrhage
Thrombosis in small arteries causing infarction
Healing with fibrosis
Pseudoaneurysms may occur in medium sized arties)

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46
Q

Churg-Strauss syndrome

A 
Granulomatous inflammation
Peripheral blood eosinophilia
Can have asthmatic symptoms
60% P-ANCA, 10% C-ANCA, 30% negative
Systemic disease - may get kidney damage, may diagnose from biopsy
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47
Q

Henoch-Schonlein purpura

A

??

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48
Q

Medium-sized vasculitides

A

Polyarteritis nodosa

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49
Q

Polyarteritis nodosa

A

Ag often unknown (sometimes Hep B/C)

??

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50
Q

Microscopic polyangiitis vs PAN

A

??

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51
Q

Temporal artery - external carotid system - why blindness?

A

Potentially internal carotid system leading to retinal artery could also be affected

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52
Q

Temporal artery - external carotid system - why blindness?

A

Indicates that potentially internal carotid system leading to retinal artery could also be affected

53
Q

Temporal artery - external carotid system - why blindness?

A

Indicates that potentially internal carotid system leading to retinal artery could also be affected

54
Q

Temporal arteritis

A

Medical emergency - steroids?

55
Q

Temporal arteritis

A

Medical emergency - steroids?

56
Q

List ? causes of haemopericardium

A

?

57
Q

List ? causes of haemopericardium

A

?

58
Q

How does haemopericardium lead to death of a patient?

A

When the pericardial pressure exceeds the intra-chamber pressures, the chamber will collapse
CO and systemic BP drops

59
Q

What are the potential complications of aortic dissection?

A 
Cardiac tamponade
Aortic incompetence
MI
Aneurysm rupture
Regional ischaemia
Left arm ischaemia/vertebral steal
60
Q

What abnormalities of the vessel wall are seen in Marfan’s syndrome?

A

?

61
Q

List 5 causes of mitral valve incompetence

A

Infective endocarditis
Acute rheumatic fever
Ischaemic papillary muscle dysfunction or rupture
LV dilation
Myxomatous degeneration of leaflets or chordae

62
Q

How is Marfan’s syndrome inherited? What % of cases are sporadic?

A

AD

Up to 30%

63
Q

What is the abnormality in Marfan’s syndrome?

A

Defect in fibrillin-1 gene, a major building block of microfibrils and important in formation and maintenance of elastin in the ECM
Microfibrils also help regulated TGF-B availability, leading to aberrant activation in Marfan’s which is believed to have effects on the integrity of the ECM

64
Q

List ? manifestations of Marfan’s syndrome

A

Mitral valve prolapse/myxomatous degeneration
Cystic medionecrosis (cystic medial degeneration) of aorta
Spontaneous pneumothorax
Lens dislocation (ectopia lentis)

65
Q

List ? manifestations of Marfan’s syndrome

A

Mitral valve prolapse/myxomatous degeneration
Cystic medionecrosis (cystic medial degeneration) of aorta
OTHER?

66
Q

What are the main risk factors for aortic dissection?

A 
Marfan's syndrome
Ehlers-Danlos syndrome
Biscuspid aortic valve
Aortic atherosclerosis
Aortic dilation
Cardiac risk factors (HTN, dyslipidaemia, DM, smoking)
67
Q

List ? clinical manifestations of Marfan’s syndrome

A

Mitral valve prolapse/myxomatous degeneration
Cystic medionecrosis (cystic medial degeneration) of aorta
OTHER?

68
Q

How might mitral valve prolapse present?

A

Asymptomatic
Mitral incompetence +/- ruptured chordae
Arrhythmias and sudden death
Predisposition to infective endocarditis

69
Q

Diagnosis of vasculitis

A

Clinical features
Serology: ANCA, cryoglobulins, Hep B and C, complement, ANAs and rheumatoid factor
Pathology: biopsy if possible

70
Q

List some potential causes of sudden collapse and death in a young adult

A

?

71
Q

List ? causes of mitral (aortic??) valve incompetence

A

Marfan’s syndrome? dissecting aortic aneurysm?

72
Q

List ? causes of haemopericardium

A

?

73
Q

How does haemopericardium lead to death of a patient?

A

?

74
Q

What are the main risk factors for aortic dissection?

A

?

75
Q

What are the potential complications of aortic dissection?

A

?

76
Q

What abnormalities of the vessel wall are seen in Marfan syndrome?

A

?

77
Q

List ? causes of mitral valve incompetence

A

Marfan syndrome? dissecting aortic aneurysm?

78
Q

How is Marfan syndrome inherited? What % of cases are sporadic?

A

AD

Up to 30%

79
Q

What is the abnormality in Marfan syndrome?

A

Defect in fibrillin-1 gene, a major building block of microfibrils and important in formation and maintenance of elastin in the ECM
Microfibrils also help regulated TGF-B availability, leading to aberrant activation in Marfan’s which is believed to have effects on the integrity of the ECM

80
Q

What is the abnormality in Marfan syndrome?

A

Defect in fibrillin-1 gene, a major building block of microfibrils and important in formation and maintenance of elastin in the ECM
Microfibrils also help regulated TGF-B availability, leading to aberrant activation in Marfan’s which is believed to have effects on the integrity of the ECM

81
Q

List ? manifestations of Marfan syndrome

A

Mitral valve prolapse/myxomatous degeneration
Cystic medionecrosis (cystic medial degeneration) of aorta
OTHER?

82
Q

How might mitral valve prolapse present?

A

Asymptomatic
Mitral incompetence +/- ruptured chordae
Arrhythmias and sudden death
Predisposition to infective endocarditis

83
Q

List ? clinical manifestations of Marfan syndrome

A

Mitral valve prolapse/myxomatous degeneration
Cystic medionecrosis (cystic medial degeneration) of aorta
OTHER?

84
Q

How might mitral valve prolapse present?

A

Asymptomatic
Mitral incompetence +/- ruptured chordae
Arrhythmias and sudden death
Predisposition to infective endocarditis

85
Q

What are some of the possible sequelae of cystic medionecrosis?

A

Aortic dissection

Annuloaortic ectasia and aortic regurgitation

86
Q

What are the main risk factors for aortic dissection?

A

?

87
Q

List ? causes of mitral (aortic??) valve incompetence

A

Marfan syndrome? dissecting aortic aneurysm?

88
Q

Describe the likely pathogenesis of retinal flame haemorrhages

A

?

89
Q

Describe the likely pathogenesis of retinal flame haemorrhages

A

?

90
Q

What are the potential causes of systemic HTN in a 32 year old?

A

?

91
Q

What are the potential causes of systemic HTN in a 32 year old?

A

?

92
Q

What are the potential causes of a spontaneous SAH?

A

?

93
Q

What are the potential causes of a spontaneous SAH?

A

?

94
Q

How should a SAH be managed?

A

BP control
Analgesia
Find the cause, intervene neurosurgically

95
Q

What is the pathogenesis of vasospasm post-SAH? What can it cause?

A

?

96
Q

What are the 3 elements of the Cushing reflex?

A

HTN
Bradycardia
Irregular breathing

97
Q

What are the 3 elements of the Cushing reflex?

A

HTN
Bradycardia
Irregular breathing

98
Q

List ? causes of SAH

A

?

99
Q

What are the risk factors for formation of berry aneurysms?

A

?

100
Q

Where are the most common sites for berry aneurysms?

A

?

101
Q

What are the presenting clinical features of SAH?

A

?

102
Q

What are the complications of SAH?

A

?

103
Q

What proportion of patients with SAH die?

A

?

104
Q

Name 3 other types of aneurysms that may occur in vessels supplying the CNS

A

?

105
Q

List ? potential causes of renal and splenic infarction

A

?

106
Q

List 4 histological findings associated with vasculitis

A

Fibrinoid necrosis
Thrombosis
Perivascular haemorrhage
Leukocytoclasis

107
Q

What symptoms are consistent with vasculitis?

A

Range of clinical manifestations depending on affected organs
Constitutional symptoms of fever, LOW, malaise, arthralgias and myalgias

108
Q

List the 4 causes of vasculitis

A

Immune mechanisms (deposition of circulating immune complexes or in situ formation of immune complexes following previous seeding of Ag in the vascular bed)
Infection (direct invasion and immune-mediated)
Radiation
Toxins, drugs

109
Q

List the 4 causes of vasculitis

A

Immune mechanisms (deposition of circulating immune complexes or in situ formation of immune complexes following previous seeding of Ag in the vascular bed)
Infection (direct invasion and immune-mediated)
Radiation
Toxins, drugs

110
Q

List 2 vasculitides predominantly affecting large vessels

A

Giant cell arteritis

Takayasu arteritis

111
Q

List 2 vasculitides predominantly affecting medium vessels

A

Polyarteritis nodosa

Kawasaki disease

112
Q

List 3 ANCA-associated vasculitides predominantly affecting small vessels

A

Microscopic polyangiitis
Wegener’s granulomatosis
Churg-Strauss granulomatosis

113
Q

List 3 ANCA-associated vasculitides predominantly affecting small vessels

A

Microscopic polyangiitis
Wegener’s granulomatosis
Churg-Strauss granulomatosis

114
Q

List 4 immune complex vasculitides predominantly affecting small vessels

A

Anti-GBM disease (Goodpasture’s)
Cryoglobulinaemic vasculitis
IgA vasculitis (Henoch-Schonlein)
Hypocomplementemic urticarial vasculitis

115
Q

List 4 immune complex vasculitides predominantly affecting small vessels

A

Anti-GBM disease (Goodpasture’s)
Cryoglobulinaemic vasculitis
IgA vasculitis (Henoch-Schonlein)
Hypocomplementaemic urticarial vasculitis

116
Q

Distinguish between ANCA-associated and immune complex mediated vasculitides

A

ANCA-associated: few or no immune deposits, associated with ANCA specific for myeloperoxidase (APO-ANCA) or proteinase 3 (PR3-ANCA)
Immune complex mediated: moderate to marked deposits of Ig and/or complement in vessel walls

117
Q

Distinguish between ANCA-associated and immune complex mediated vasculitides

A

ANCA-associated: few or no immune deposits, associated with ANCA specific for myeloperoxidase (APO-ANCA) or proteinase 3 (PR3-ANCA)
Immune complex mediated: moderate to marked deposits of Ig and/or complement in vessel walls

118
Q

List 3 vasculitides associated with systemic disease

A

Lupus
Rheumatoid
Sarcoid

119
Q

List 3 vasculitides associated with systemic disease

A

Lupus
Rheumatoid
Sarcoid

120
Q

List 6 causes/associations of small vessel vaculitides

A 
AI
Associated with other systemic disease
Infections (e.g. hep B, hep C)
Malignancy
Drugs
Idiopathic/unknown
121
Q

List 6 causes/associations of small vessel vaculitides

A 
AI
Associated with other systemic disease
Infections (e.g. hep B, hep C)
Malignancy
Drugs
Idiopathic/unknown
122
Q

List 6 causes/associations of small vessel vaculitides

A 
AI
Associated with other systemic disease
Infections (e.g. hep B, hep C)
Malignancy
Drugs
Idiopathic/unknown
123
Q

Describe the likely pathogenesis of retinal flame haemorrhages

A

?

124
Q

List 4 potential causes of a spontaneous SAH

A

Saccular aneurysm rupture
AV malformations
Arterial dissections
Use of anticoagulants

125
Q

What is the pathogenesis of vasospasm post-SAH? What can it cause?

A

Believed to result from a delayed and reversible vasculopathy, impaired autoregulatory function and hypovolaemia
Can progress to cerebral infarction

126
Q

What are the presenting clinical features of SAH?

A 
Headache
Photophobia
Nausea/vomiting
Altered mental state
LOC
127
Q

What are the complications of SAH?

A 
Rebleeding
Acute hydrocephalus
Vasospasm
Pulmonary oedema
Hyperglycaemia
Seizure
Death
128
Q

What proportion of patients with SAH die?

A

Up to 50%

129
Q

Name 3 other types of aneurysms that may occur in vessels supplying the CNS

A

Fusiform
Dissecting/pseudo-aneurysm
Charcot-Bouchard (micro-) aneurysms

MD2 Pathology (28 decks)

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