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Block 9 Week 1 > Vascular Pathology-Fung > Flashcards

Vascular Pathology-Fung Flashcards

1
Q

Where do developmental (berry) anuerysms occur? Why do they commonly occur? These are called congential anomalies, but is this truly congenital?

A
  • cerebral vessels
  • Majority are sporadic, some are genetic
  • No, not present at birth, develops over time
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2
Q

What are some genetic causes of developmental (berry) anuerysms?

A
  • AD polycystic disease
  • Ehler-Danlos syndrome
  • NF1
  • Marfan syndrome
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3
Q

What are the risk factors for Developmental (Berry) aneurysms?

A

cigarette smoking and HTN

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4
Q

What are AV fisutlas?

Why do they occur?

A

Small direct connections between arteries and veins that bypass capillaries

Occur due to:

  • Developmental defects
  • Rupture of arterial aneurysm into an adjacent vein
  • Penetrating injuries that pierce arteries and veins
  • Inflammatory necrosis of adjacent vessels
  • Iatrogenic
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5
Q

What is this:
Focal irregular thickening of the walls of medium and large muscular arteries

What will this result in?
Who does it mostly occur in?

A

Fibromuscular dysplasia

Luminal stenosis

Can occur at any age but most frequent in young women

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6
Q

What is this:
localized abnormal dilation of a blood vessel or the heart

Is it congenital or acquired?

What are the 2 shapes of aneurysms?

What are the 2 types?

A

Aneurysm

  • Could be either
  • Saccular or fusiform
  • True aneurysm or false aneurysm
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7
Q

What is this:
a spherical outpouching involving only a portion of the vessel
How big is it?

A

Saccular true aneurysm

between 5 and 20 cm in diameter

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8
Q

What is this:
Diffuse, circumferential dilation of a long vascular segment

How big is it?

What parts of the aorta does it affect?

A

Fusiform true aneurysm

up to 20cm in diameter

extensive portions of the aortic arch, abdominal aorta, iliac arteries

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9
Q

How do you get an aneurysm?

A

any process that weakens vessel wall

  • Sporadically
  • HTN
  • CT disease
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10
Q

What are the CT diseases that cause weakening of the vessel wall that can result in anuerysm?

A
  • Marfan syndrom (defect in fibrillin)
  • Ehlers-Danlos syndrome (defect in the synthesis or structure of fibrillar collagen)
  • Vit C deficiency (altered collagen cross-linking)
  • Loeys-Dietz syndrome- Defect in elastin, collagen I and III
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11
Q

How can inflammation cause aneurysms?

How can you get loss of smooth muscle cells or proliferation of non-collagneous/non elastic ECM that causes aneurysm?

A
  • inflammation alters the balance of synthesis and destruction of collagen (increased matrix metalloprotease MMP that degrade the ECM)
  • Cystic degeneration (thickening of intima decreases diffusion of oxygen and nutrients to the media)
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12
Q

What are the 2 most important predisposing factors for aneurysm? Which type is associated with each?

A

HTN (ascending aortic aneurysm)

atherosclerosis (abdominal aortic aneurysm)

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13
Q

What are the clinical consequences of abdominal aortic aneurysm?

A

Rupture with potential fatal hemorrhage
Obstruction of branch vessel
Embolism from atheroma or mural thrombus
Impingement on adjacent structures

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14
Q

What are the signs and symptoms of thoracic aneurysm (most commonly associated with HTN)?

A
  • Encroachment on mediastinal structures, lungs and airways, and esophagus
  • Cough due to pressure on recurrent laryngeal nerve
  • Bone pain
  • TAA leads to aortic valve dilation with insufficiency
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15
Q

What is this:
Blood splays apart the laminar planes of the media to form a blood filled channel within the vessel wall
May or may not be associated with vessel dilation

A

Dissection

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16
Q

Who do dissections occur?

A
  • men 40-60 years with HTN
  • younger patients with system and localized abnormalities of the aorta
  • iatrogenic
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17
Q

T or F

Dissection is not usually seen with atherosclerosis

A

T

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18
Q

Why is HTN the major risk factor for dissection?

A

Medial hypertrophy of the vasa vasorum with degenerative changes of the media

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19
Q

(blank) is the most freuqent histologically detectable lesion in dissection

A

cystic medial degeneration

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20
Q

What is a Debakey Type I dissection?
Debakey Type II?
Debakey Type III?

A
  • Proximal lesion involves ascending and descending aorta
  • proximal lesions involving just the ascending aorta
  • Distal lesions beginning distal to the subclavian artery and not involving ascending aorta
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21
Q

What is stanford type A dissection?

type B?

A

A- Debakey type I and II (involving any part of the ascending aorta)
B- Debakey type III
(descending)

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22
Q

What is this:

General term for vessel wall inflammation

A

vasculitis

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23
Q

What are the pathogenic mechanisms of vasculitis?

A
  • immune-mediated inflammation

- direct invasion of vascular walls by infectious pathogens

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24
Q

What are the large vessels that get vasculitits? What are the 2 types of large vessel vasculitis?

A

aorta and large branches to extremities, head and neck

  • Giant cell (temporal) arteritis
  • Takayasu arteritis
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25
Q

What are the medium vessels that get vasculitis? What are the 2 types of medium vessel vasculitis?

A
  • Main visceral arteries and their branches
  • polyarteritis nodosa
  • Kawasaki disease
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26
Q

What are the vessels that get small vessel vasculitis?

A
  • arterioles
  • venules
  • capillaries
  • small arteries
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27
Q

What are the types of small vessel vasculitis?

A
  • Wegener granulomatosis
  • Churg-Strauss syndrome
  • Microscopic polyangiitis
  • Immune complex vasculitis
  • Anti-GBM disease
  • Cryoglobulinemic vasculitis
  • IgA vasculitis
  • Hypocomplementemic urticarial vasculitis
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28
Q

What are the types of vasculitis that effect all vessels?

A

Behcet’s disease

Cogan’s syndrome

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29
Q

Which is a granulomatous disease, Takayasu arteritis or giant cell arteritis?

A

BOTH!

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30
Q

Which medium vessel vasculitis is a immune complex mediated one?

A

Polyarteritis nodosa

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31
Q

Which medium vessel vasculitis is a anti-endotheial cell antibody disease?

A

Kawasaki disease

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32
Q

Which small vessel vasculitis presents without asthma or granulomas?

A

microscopic polyangitis

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33
Q

Which small vessel vasculitis presents with granulomas and NO asthma?

A

Wegener granulomatosis

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34
Q

Which small vessel vasculitis presents with eosinophilia, asthma, and granulomas?

A

Chrug-Stauss syndrome

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35
Q

What are the immune complex mediated small vessel vasculitis?

A
  • SLE Vasculitis
  • IgA Henoch schonlei purpura
  • Cryoglobulin vasculitis
  • goodpasture disease
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36
Q

What are the three types of non-infectious vasculitis?

A

Immune-complex deposition
Anti-neutrophil cytoplasmic antibodies
Anti-endothelial cell antibodies
-Predispose to vasculitis (Kawasaki disease)

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37
Q

What are some examples of immune complex associated vasculitis?

A

-Systemic lupus erythematosus
-Polyarteritis nodosa
-Drug hypersensitivity vasculitis
Antibody, complement and antigen-antibody complexes detected

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38
Q

What is ANCA?

A

Anitneutrophil cytoplasmic antibodies that circulate and attack neutrophils, monocyte lysosomes, and endothelial cells.

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39
Q

What are the 2 major types of antineutrophil cytoplasmic antibodies?

A
  • Anti-myeloperoxidase (MPO-ANCA)

- Anti-proteinase-3 (PR3-ANCA)

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40
Q

What is MPO? what will MPO-ANCA do to it? Where will it accumulate? What will cause this? What diseases will you see it in?

A
  • Lysosomal granule constituent
  • Kill the the lysosomal granules
  • Perinuclear
  • Therapeutic agents (propylthiouracil)
  • Microscopic polyangitis and Churg-Strauss syndrome
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41
Q

What is PR3?
What will Anti-proteinase-3 (PR3-ANCA) do?
Why does PR3-Anca happen?
What disease will you see it in?

A
  • A neutrophil azurophilic granule consituent
  • mess this up
  • homology with microbial peptides
  • Wegener granuomatosis
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42
Q

What are the 2 mechanisms for vasculitis with ANCA?

A
  • Drugs or cross-reactive microbe (antigens) induce ANCA formation
  • neutrophil release MPO/PR3 and cause ANCA formation in a susceptible host
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43
Q

Explain while release of MPO/PR3 can cause ANCA formation?

A
  • Host release cytokines (TNF) that cause expression of MPO/PR3 on neutrophils or other cell types.
  • ANCA react and directly induce endothelial cell injury or activation of other neutrophils
  • ANCA-activated neutrophils degranulate and release reactive oxygen species further injuring endothelial cells
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44
Q

What does C-ANCA look like?

What does P-ANCA look like?

A

green with black holes

green with white spots

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45
Q

What is this:
Most common vasculitis among elderly individuals (50 years and older)
Chronic, granulomatous inflammation of large to small-sized arteries

A

Giant cell arteritis

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46
Q

What arteries does Giant cell arteritis typically affect?

A

principally arteries of the head:

temporal artery, vertebral artery, opthalmic artery and aorta

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47
Q

Is Giant cell arteritis a medical emergency and why?

A

yes, because it affects the ophthalmic artery which can lead to blindness

48
Q

What is the pathogenesis behind Giant cell arteritis?

A

T-cell lymphocytic immune response against an unknown antigen.
TNF and anti-endothelial cell humoral immune responses also contribute

49
Q

What is the histology of Giant cell arteritis?

A
  • Discontinuous involvement of the vessel (multiple biopsies)
  • Intimal thickening
  • Medial granulomatous inflammation with giant cells
  • elastic lamina fragmentation
50
Q

What is this:
granulomatous arteritis of medium or larger arteries characterized by ocular disturbances, and marked weakening of the pulses in the upper extremities (pulseless disease).

A

Takayasu arteritis

51
Q

What is considered the “pulseless disease”?

A

Takayasu arteritis

52
Q

What does the aorta look like in Takayasu arteritis?

Who typically gets it?

A
  • fibrous thickening of the aorta

- patients less than 50 years old

53
Q

What is this:
systemic vasculitis of small or medium-sized muscular arteries
-affects renal vessels, visceral vessels (heart, liver, GI tract)
-SPARES pulmonary circulation and does not involve arterioles, capillaries or venules

A

Polyarteritis nodosa

54
Q

What is polyarteritis nodosa associated with?

A

associated with chronic hep B

HbsAg-Hbs-Ab complexes in vessels (immune complex mediated

55
Q

What is the cause of polyarteritis nodosa?

A

unknown in majority of cases

56
Q

What is this:

  • Segmental transmural necrotizing inflammation (neutrophils, eosinophils, and lymphocytes)
  • Affect the vessel circumferentially and prefer vessel branch points
  • Inflammatory process can weaken vessel and cause aneurysms
  • acute inflammatory infiltrate is replaced by (blank) thickening of the vessel wall
A

Polyarteritis nodosa

57
Q

In polyarteritis nodosa, lesions coexist in (Blank) stages

A

different (recurrent and ongoing insults)

58
Q

What is this:
acute febrile, self-limited illness of infancy and childhood affecting large to medium sized and small vessels
Is a mucocutaneous lymph node syndrome

A

Kawasaki disease

59
Q

What are some clinical characteristics of Kawasaki disease?

A
  • conjunctival and oral erythema and erosion
  • edema of hands and feet
  • erythema of palms and soles
  • desquamative rash
  • cervical lymph node enlargement
60
Q

Why is Kawasaki disease clinically significant?

What can happen that can result in MI?

A
  • because of coronary artery involvement

- aneurysms that rupture and thrombose resulting in MI

61
Q

What is the vasculitis in Kawasakis’ disease thought to be due to?

A

from a delayed hypersensitivity reaction of T cells to an uncharacterized antigen (possibly infectious agents)

62
Q

Explain the delayed type hypersensitivity reaction seen in Kawasakis disease?

A
  • cytokines are produced and B-cells are activated leading to auto-antibody production
  • auto-antibodies to endothelial and smooth muscle cells
63
Q

What does the vessel wall look in Kawasaki’s disease?
Does it have more or less fibrinoid necrosis than PAN?
What will healed lesions look like?

A
  • Marked inflammation affecting the entire thickness of the vessel wall
  • less fibrinoid necrosis
  • healed lesions may have obstructive intimal thickening
64
Q

What is this:
segmental fibrinoid necrotizing vasculitis that affects capillaries, arterioles, and venules
Resembles PAN but affects smaller vessels
Hypersensitivity vasculitis (leukocytoclastic vasculitis)
All lesions are in the same stage at the same time

A

Microscopic polyangitis

65
Q

What type of ANCA is microscopic polyangitis?

A

MPO-ANCA

66
Q

What does microscopic polyangitis affect?

A 
Skin (palpable cutaneous purpura)
Mucous membranes
Lungs (hemoptysis)
Brain
Heart
Gastrointestinal tract (bowel pain, bleeding)
Kidney (hematuria, proteinuria)
Muscle (muscle pain, weakness)
67
Q

What does microscopic polyangitis occur with?

A
  • Henoch-Schonlein purpura
  • Essential mixed cryoglobulinemia
  • Vasculitis associated with CT disorders
68
Q 
What is this:
small vessel necrotizing vaculitis associated with 
-asthma
-allergic rhinitis
-lung infiltrates
-peripheral hypereosinophilia
-extravascular necrotizing granulomas

What is another name for it?

A

Churg-Strauss syndrome

Allergic granulomatosis

69
Q

What does Churg-Strauss syndrome look like histologically?

A

resembles PAN or microscopic polyangitis but has granulomas and eosinophils

70
Q

What kind of ANCA is sometimes present in Churg-Strauss syndrome?

A

MPO-ANCAs

71
Q

What are the clinical manifestations of Churg-strauss syndrome?

A
  • Palpable purpura
  • GI tract bleeding
  • Focal and segmental glomerulosclerosis
72
Q

What is this:

  • acute necrotizing granulomas of the upper respiratory tract and/or lower respiratory tract
  • necrotizing granulomatous vasculitis affecting small to medium sized vessels
  • focal necrotizing, crescentic glomerulonephritis
A

Wegener granulomatosis

73
Q

Wegener granulomatosis clinically resembles polyarteritis nodosa except has (blank) involvement

A

respiratory

74
Q

What causes Wegener granulomatosis?

What ANCA is present?

A

T-cell mediated hypersensitivity reaction to an inhaled infectious agent
-Anti-PR3 (C-ANCA)

75
Q

What is thromboangiitis obliterans?

A

Buerger disease

-segmental thrombosing acute and chronic inflammation of medium and small sized arteries

76
Q

What does thromboangiitis obliterans lead to?

Who is it seen in and why?

A

vascular insufficiency principally in the tibial and radial arteries (sometimes veins and nerves)

  • Exclusively seen in heavy smokers before 35
  • cigarettes are directly toxic to endothelial cells or an immune response to cigarette
77
Q

What are the clinical features of thromboangiitis obliterans?

A
  • Superficial nodular phlebitis
  • Raynaud type cold sensitivity
  • Instep claudication
  • Severe pain at rest in the extremities
78
Q

What is infectious vasculitis?
What types of fungus does this?
What may this lead to?

A
  • direct invasion of infectious agents (bacteria, fungus) due to hematogenous seeding during sepsis or embolization
  • Mucor, Aspergillus
  • mycotic aneurysms
79
Q

(blank) results from exaggerated constriction of digital arteries and arterioles.

A

Raynaud phenomenon

80
Q

What are the symptoms of raynaud phenomenon?

A

paroxysmal pallor and cyanosis of digits of hands and feet

81
Q

What is this:

exaggeration of the central and local vasomotor responses to cold or emotional stress

A

Primary Raynaud phenomenon

82
Q

What is this:

Vascular insufficiency of the extremities secondary to arterial disease caused by ….. (blank X 4)

A
  • SLE
  • Scleroderma
  • Buerger disease
  • Atherosclerosis
83
Q

What is this:
abnormally dilated, tortuous veins produced by prolonged increased intraluminal pressure and loss of vessel support
What does it affect?
Why does this result in esophageal varices and hemorrhoids?

A
  • Varicose Veins
  • Superficial veins of upper and lower leg
  • Due to portal HTN
84
Q

Why is esophageal varices scary?

A

cuz they can rupture and cause fatal hemorrhage

85
Q

What do you call venous thrombosis and inflammation?

A

thrombophlebitis or phlebothrombosis (interchangeable words)

86
Q

Where do you typically get thrombophlebitis?

What can it result in?

A 
deep leg veins (90%)
(prolonged immobilization predisposes)
Periprostatic venous plexus
Pelvic venous plexus
Large veins of the skull
Dural sinuses

-Pulmonary embolism

87
Q

(blank) predisposes to thrombophlebitis

A

Systemic hypercoagulability

88
Q

(blank) syndromes can cause migratory thrombophlebitis

A

paraneoplastic

89
Q

What is this:

Caused by neoplasms (bronchogenic carcinoma, mediastinal lymphoma) that compress or invade the SVC

A

SVC syndrome

90
Q

What is this:
Caused by neoplasms that compress or invade the IVC (Heptaocellular Carcinoma, Renal cell carcinoma)
Thrombus from hepatic, renal or LE veins

A

IVC syndrome

91
Q

What is this:

acute inflammation due to bacteria (group A Beta hemolytic streptococci)

A

lymphangitis

92
Q

What causes primary lymphedema?

A
  • congenital defects

- familial agenesis or hypoplasia

93
Q

What causes secondary lymphedema?

A 
Tumors
Dissection of lymph nodes
Post-irradiation fibrosis
Filariasis
Post-inflammatory thrombosis and scarring
94
Q

Are primary tumors of large vessels rare or common?

A

rare

95
Q

Where are neoplasms of vessels derived from?

A
  • endothelium derived

- cells that support blood vessels

96
Q

(blank) produce well formed vascular channels lined by normal endothelium

A

Benign tumors

97
Q

(blank) do not produce well formed vascular channels and exhibit cytologic atypia

A

Malignant tumors

98
Q

What is this:

common tumors with increased numbers of blood vessels filled with blood.

A

Hemangioma/pyogenic granuloma

99
Q

What is this:
closely packed thin walled capillaries
What is this:
large dilated vascular channels

A

Capillary hemangioma

Cavernous hemangioma

100
Q

What is a pyogenic granuloma?

A

a form of capillary hemangioma

101
Q

What is this:

benign lymphatic analogues of BV hemangioma

A

Lymphangioma

102
Q

What is a simple capillary lymphangioma?

A

small lymphatic channels

103
Q

What is this:

massively dilated lymphatic channels with lymphocytes in the CT

A

Cavernous lymphangioma (cystic hygroma)

104
Q

What is the cause of Kaposi Sarcoma? What does it present as?

A

Human herpes virus 8 (HHV-8)

Skin lesions

105
Q

Who does chronic KS occur in?

A

Older Eastern European/Mediterranean men.

106
Q

Where does Lymphadenopathic KS occur? What does it present as?

A

areas of Africa

lymphadenopathy

107
Q

What is transplant associated KS? How does it present?

A
  • occurs in settings of organ transplantation and immunosuppresion
  • with nodal, mucosal, and visceral involvement. Aggressive.
108
Q

What is AIDS associated KS?

What does it present with?

A

occurs in the setting of HIV/AIDS. Most prevalent malignancy in AIDS patients.
Lymph node and visceral involvement

109
Q

What is this:

malignant endothelial neoplasm that range from well differentiated to anaplastic.

A

Angiosarcoma

110
Q

Hepatic angiosarcoma arises in the setting of (blank, blank, and blank). What other settings can you get angiosarcoma?

A

arsenic
thorotrast
polyvinyl chloride

-lymphedema and post-radiation

111
Q

What is this:

benign tumors arising from modified smooth muscle cells of the glomus body (thermoregulation)

A

glomus tumor

112
Q

What is this:

common lesions, not true neoplasms. Local dilation of pre-existing vessels.

A

Vascular ectasia

113
Q

What are examples of vascular ectasia?

A
  • nevus flammeus (birthmarks, port-wine stain, sturge-weber syndrome)
  • spider telangiectasia
  • hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease)
114
Q

What are some kinds of nevus flammeus?

A

birthmarks
port-wine stain
Sturge-weber syndrome

115
Q

What is bacillary angiomatosis?

A

bartonella bacteria causes a vascular proliferation

116
Q

What is hemangiopericytoma?

A

rare tumor derived of pericytes

117
Q

(bank) is a rare tumor that both clinically and histologically is intermediate between angiosarcoma and hemangioma

A

hemangioendothelioma

Block 9 Week 1 (7 decks)

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