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Pathology > 3.1b Blood Vessels 2 > Flashcards

3.1b Blood Vessels 2 Flashcards

0
Q

Mechanisms of vasculitis (2)

A
  1. Direct injury to vessels (invasion of vascular walls by infectious pathogens)
  2. Immune-mediate inflammation
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1
Q

What is vasculitis?

A

Vessel wall inflammation

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2
Q

Classification of vasculitis acc to size of blood vessels (4)

A
  1. Large vessel vasculitis: aorta, large branches to extremities, head, neck
  2. Medium vessel vasculitis: main visceral arteries and their branches
  3. Small vessel vasculitis (ANCA +)
  4. Small vessel vasculitis (ANCA -)
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3
Q

Examples (diseases) of large vessel vasculitis (2)

A

Giant cell arteritis

Takayasu arteritis

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4
Q

Examples (diseases) of medium vessel vasculitis (2)

A
  1. Polyarteritis nodosa

2. Kawasaki disease

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5
Q

Examples (diseases) of small vessel vasculitis ANCA+ (3)

A
  1. Wegener’s granulomatosis
  2. Microscopic polyangitis
  3. Churg Strauss syndrome
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6
Q

Examples (diseases) of small vessel vasculitis ANCA- (4)

A
  1. Henoch Schonlein purpura
  2. Cryglobulinaemic vasculitis
  3. Cutaneous leukocytoclastic vasculitis
  4. Anti-GBM disease
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7
Q

Classification of vasculitis based on Pathogenesis of blood vessels (3)

A
  1. Direct infection (ie. fungal infection of vessel wall)
  2. Immunologic (more common)
  3. Idiopathic (ie. giant cell arteritis)
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8
Q

Example of immunologic vasculitis (4)

A
  1. Immune-complex mediated: SLE, drug induced
  2. ANCA-mediated: Wegener’s granulomatosis
  3. Direct Ab attack: Goodpasture syndrome, Kawasaki disease
  4. Cell-mediated: organ rejection
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9
Q

What are the main mechanisms that initiate noninfectious vasculitis? (3)

A
  1. Immune complex deposition
  2. ANCA (antineutrophil cytoplasmic antibodies)
  3. Anti-endothelial cell antibodies
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10
Q

This immunological mechanism induces in-situ vasculitis formation due to Ab-Ag complex

A

Immune complex deposition

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11
Q

This immunological mechanism is a heterogenous group of autoantibodies directed against constituents of neutrophil primary granules, monocytes, lysosomes, endothelial cells

A

ANCA

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12
Q

What are the staining patterns of ANCA? Describe each (2)

A
  1. c-ANCA: cytoplasmic location of immunofluorescence stain

2. p-ANCA: perinuclear location of IF stain

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13
Q

This immunological mechanism that initiate noninfectious vasculitis states that antibodies to endothelial cells may predispose certain vasculitides

A

Anti-endothelial cell antibodies

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14
Q

Name the common types of vasculitis (7)

A
  1. Giant cell/Temporal arteritis
  2. Takayasu arteritis
  3. Polyarteritis nodosa (PAN)
  4. Microscopic polyangitis
  5. Kawasaki disease
  6. Wegener granulomatosis
  7. Thromboangitis obliterans (Buerger Disease)
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15
Q

Chronic granulomatous inflammation of SMALL and MEDIUM sized arteries in head and neck, especially TEMPORAL arteries

A

Giant-cell/Temporal Arteritis

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16
Q

Giant-cell/Temporal arteritis also affects which arteries? (2)

A
  1. Vertebral arteries

2. Ophthalmic arteries –> may lead to permanent blindness

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17
Q

Giant-cell arteritis sad a therapeutic response to what?

A

Corticosteroids (may help prevent blindness)

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18
Q

Diagnostic procedure for Giant-cell arteritis

A

Temporal artery biopsy (2-3cm of artery is needed)

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19
Q

Pathogenesis of Giant-cell arteritis (3)

A
  1. T-cell mediated immunologic reaction: Ab are directed vs unknown Ag
  2. Pro-inflammatory cytokines (TNF)
  3. Anti-endothelial cells
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20
Q

Predilection of Giant-cell arteritis (3)

A
  1. Elderly
  2. Females
  3. Single vascular site
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21
Q

The ff are clinical features of?
1. Headaches, facial pain, ocular symptoms (range from diplopia to complete loss of vision)

  1. Unilateral throbbing headache (esp. Along superficial temporal artery - painful with palpation)
  2. Temporal ophthalmic arteries most commonly affected
  3. Systemic manifestations: joint pains, myalgia, muscle pains
A

Giant-cell/Temporal arteritis

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22
Q

Which disease is characterize by the ff:

  1. Granulomatous thickening of inner portions of ECA
  2. Tender temporal arteries
  3. Physical exam and labs are nonrevealing
A

Giant-cell/Temporal arteritis

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23
Q

What is the gross morphology of Giant-cell/Temporal arteritis?

A

Nodular intimal thickening of the artery upon palpation

  • diameter of lumen is reduced
  • rope-y consistency (looks like a worm on your temples)
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24
Q

What are the histologic feature of Giant-cell/Temporal arteritis? (3)

A
  1. Granulomatous inflammation with giant cells, T-cells, macrophages –> elastic lamina fragmentation
  2. Thromboses may be present
  3. Nonspecific mononuclear inflammation
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25
Q

Describe the old lesions seen in Giant-cell/Temporal arteritis? (2)

A
  1. Fibrosis

2. Thickening

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26
Q

Describe the healing stage in Giant-cell/Temporal arteritis (3)

A
  1. Medial scarring
  2. Intimal thickening
  3. Residual elastic tissue fragmentation
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27
Q

What is the defining diagnostic finding in Giant-cell/Temporal arteritis?

A

Granulomatous inflammation with giant cells

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28
Q

Granulomatous vasculitis of MEDIUM and LARGE arteries (aorta)

A

Takayasu arteritis

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29
Q

It is associated wit

  1. Fibrous thickening and obliteration of the aorta (aortic arch, great vessels)
  2. Luminal narrowing of major branch vessels

Characterized by

  1. Ocular disturbances
  2. Marked weakening of pulses in upper extremities :. aka Pulseless Disease
A

Takayasu arteritis

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30
Q

It is aka Pulseless Disease

A

Takayasu arteritis

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31
Q

It has a predilection for female, younger than 50 years old

A

Takayasu arteritis

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32
Q

The ff are clinical features of which disease?

  1. If brachiocephalic is affected –> secondary head disturbances, headache, pain
  2. Ocular disturbance
  3. Weakened pulses in upper extremities (UL: feeble, LL: full, bounding)
  4. Neurological deficits
  5. Pulmonary HPN
A

Takayasu arteritis

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33
Q

What are the gross characteristics of Takayasu arteritis? (3)

A
  1. Irregularly thickened intima (hyperplasia)
  2. Fibrous aortic wall
  3. Narrowed lumen
    = weakened peripheral pulses
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34
Q

What are the histologic characteristics of Takayasu arteritis? (4)

A
  1. Adventitial and medial mononuclear inflammation
  2. Granuloma with giant cell (similar to temporal arteritis but involves aorta and its branches)
  3. Perivascular cuffing of vasa vasorum
  4. Necrosis of media of aorta
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35
Q

SYSTEMIC vasculitis of SMALL/MEDIUM muscular arteries (but not arterioles, capillaries, venues) typically involving RENAL and VISCERAL vessels

A

Polyarteritis Nodosa (PAN)

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36
Q
  1. It is 30% associated with positive Hepa B antigen

2. Part of connective tissue disease

A

Polyarteritis Nodosa (PAN)

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37
Q

It has a predilection for males, young adult, branch point of vessels

A

Polyarteritis Nodosa (PAN)

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38
Q

Its clinical feature include the ff:

  1. Fever of unknown origin
  2. Peripheral neuritis
  3. Malignant HPN - important clinical feature
  4. Renal arterial involvement - prominent; major cause of death
A

Polyarteritis Nodosa (PAN)

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39
Q

What is the histology of Polyarteritis Nodosa (PAN)? (4)

A
  1. Segmented transmural necrotizing inflammation
  2. Involves full thickness inflammation –> weakened arterial wall –> rupture/aneurysm
  3. Sharply segmental in distribution (affected and unaffected blood vessels may be seen together)
  4. Blood vessel involvement: kidneys > heart > liver > GIT
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40
Q

What treatment is give on for Polyarteritis Nodosa (PAN)? (2)

A

Corticosteroids

Cyclophosphamide

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41
Q

What are the stages in Polyarteritis Nodosa (PAN)? (3)

A
  1. Acute: transmural neutrophilic inflammation with fibrinoid necrosis, mixed infiltrate (neu, eosi, mononuclear cells)
  2. Healing (late stage): start of fibrous thickening of vessel wall, mononuclear inflammation, nodular thickening of vessels (rosary bead)
  3. Healed: marked fibrosis, obstruction to blood flow may lead to scarring
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42
Q

T/F: all stages in Polyarteritis Nodosa (PAN) can co-exist in differ vessels or same vessels, suggesting ongoing and recurrent insults

A

True

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43
Q

What happens in the acute stage of PAN? (2)

A
  1. Transmural neutrophilic inflammation with fibrinoid necrosis
  2. Mixed infiltrate (neu, eosi, mononuclear cells)
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44
Q

What happens in the healing stage ore PAN? (3)

A
  1. Start of fibrous thickening of vessel wall
  2. Mononuclear inflammation
  3. Nodular thickening of vessels (rosary bead)
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45
Q

What happens in the healed stage of PAN? (2)

A
  1. Marked fibrosis

2. Obstruction to blood flow may lead to scarring

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46
Q
  1. It is also called hypersensitivity vasculitis or leukocytoclastic vasculitis
  2. It’s usual manifestation in post-capillary venues is infiltrating and fragmenting neutrophils
  3. Necrotizing vasculitis
  4. ANCA+ in most cases
  5. Necrotizing glomerulonephritis and pulmonary capilliritis are common
  6. Associated with drug hypersensitivity
A

Microscopic polyangitis

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47
Q

What are the distinguishing features of Microscopic polyangitis vs. PAN? (2)

A
  1. Vessels affected: arterioles, capillaries, venules
    (PAN: small to medium sized arteries)
  2. All lesions are of the same histologic age
    (PAN: multiple stages at the same time)
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48
Q

Pathogenesis of Microscopic polyangitis (2)

A
  1. Antibody response to antigens such as:
    - drugs (ie. penicillin)
    - microorganisms (ie. strep)
    - heterologous proteins
    - tumor proteins

–> immune complex deposition / tigger secondary immune response

  1. Pauci-immune (devoid of immune complexes): recruitment and activation of neutrophils –> disease manifestations
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49
Q

The ff are clinical features of?

  1. Hemoptysis
  2. Hematuria
  3. Proteinuria
  4. Bowel pain or bleeding
  5. Muscle pain or weakness
  6. Palpable cutaneous purpura
A

Microscopic polyangitis

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50
Q

In Microscopic polyangitis, what induces remission and improves long term survival (except for cases of widespread renal or brain involvement)? (2)

A
  1. Cyclophosphamide

2. Steroid immunosuppression

51
Q

Describe the histology of Microscopic polyangitis (2)

A
  1. Segmental fibrinoid necrosis of the media with focal transmural necrotizing lesions
  2. Little or no immunoglobulin aka pauci-immune injury
52
Q
  1. Arteritis of LARGE and MEDIUM sized arteries associated with mucocutaneous syndrome
  2. Leading cause of acquired heart disease in children
  3. Results from delayed hypersensitivity reaction of T-cells
A

Kawasaki disease

53
Q

Pathogenesis of Kawasaki disease (2)

A
  1. T-cell stimulation –> cytokines production, macrophage activation
  2. Polyclonal B-cell stimulation –> form autoAb to endothelial and smooth ms cells –> acute vasculitis
54
Q

Predilection of Kawasaki disease (2)

A
  1. Young children

2. Infants

55
Q

An important characteristic in Kawasaki disease (1)

A

Coronary artery involvement –> aneurysms –> rupture or thrombose –> acute MI

56
Q

What is another name for Kawasaki disease?

A

Mucocutaneous lymph node syndrome

57
Q

What are the clinical features of Kawasaki disease? (2)

A
  1. Mucocutaneous LN syndrome

2. Fever

58
Q

Manifestations of Mucocutaneous lymph node syndrome (5)

A
  1. Conjunctival and oral erythema and erosion
  2. Erythema of palms and soles
  3. Edema of hands and feet
  4. Desquamative rash
  5. Cervical lymphadenopathy
59
Q

Describe histology of Kawasaki Disease (2)

A
  1. Segmental, fibrinoid, necrotizing panarteritis

2. Inflammation affecting entire thickness of vessel wall

60
Q
  1. Segmental, thrombosing, acute and chronic inflammation of MEDIUM and SMALL arteries (tibial and radial arteries)
  2. Associated with heavy cigarette smoking
A

Thromboangiitis Obliterans aka Breuger Disease

61
Q

Pathogenesis of Thromboangiitis Obliterans (2)

A
  1. Direct endothelial cell toxicity
  2. Idiosyncratic immune response

Both to some component of tobacco

62
Q

Thromboangiitis Obliterans has a predilection for:

A

Male, middle age, with history of heavy cigarette smoking

63
Q

Its early manifestations include:

  1. Superficial modular phlebitis
  2. Cold sensitivity of the Raynaud type (hands)
  3. Pain in instep of foot induced by exercise (instep claudication)
A

Thromboangiitis Obliterans

64
Q

What are the clinical features of Thromboangiitis Obliterans? (2)

A
  1. Severe pain even at rest (neural involvement)

2. Chronic ulcerations (toes, feet, fingers) –> gangrene

65
Q

Gross manifestation of Thromboangiitis Obliteransm (1)

A

Gangrene of distal arteries

66
Q

Describe the histology of Thromboangiitis Obliterans (3)

A
  1. Thrombus (contains microabscess composed of neutrophils surrounded by granulomatous inflammation)
  2. Inflamed/scared neurovascualar bundles
  3. Neutrophils adjacent to epithelial giant cells deep inside thrombi
67
Q

Granulomas are present on which diseases? (4)

Hint: TuTuBoW and granuloma

A
  1. Temporal arteritis
  2. Takayasu arteritis
  3. Buerger disease
  4. Wegener’s granulomatosis
68
Q

Pathogenesis of varicose veins (2)

A

Prolonged intra luminal pressure and loss of vessel support –> abnormally dilated, tortuous veins –> increased venous pressure –> VENOUS STASIS, PEDAL EDEMA

69
Q

Pathogenesis of varicose veins in normal veins (1)

A

Simple orthostatic edema

70
Q

It clinical features include:
1. Stasis, congestion, edema, pain, thrombosis (d/t incompetent venous valves leading to dilation)

  1. Stasis dermatitis, ulcerations (d/t persistent edema in extremity, ischemic skin changes)
  2. Chronic varicose ulcers (d/t poor wound healing, soup imposed infections)
  3. Gastro-esophageal varices, hemorrhoids, capture medusa
A

Varicose veins

71
Q

Primary disorders of this are extremely rare, secondary processes are more frequent and develop in association with inflammation or malignancies

A

Disease in the lymphatics

72
Q

It is acute inflammation due to bacterial infection –> dilated lymphatics with exudate of neutrophils and monocytes –> CELLULITIS, FOCAL ABSCESS

A

Lymphangitis

73
Q

It is due to an isolated congenital defect (familial Milroy disease)

A

Primary lymphedema

74
Q

It is due to blockage of a previously normal lymphatic, which may result from:

  1. Malignant tumors
  2. Post-irradiation fibrosis
  3. Filariasis/elephantiasis
A

Secondary/Obstructive lymphedema

75
Q

In obstructive lymphedema, what causes increased interstitial fluid accumulation?

Hint: recall mechanism of arterioles-venules

A

Increased hydrostatic pressure

76
Q
  1. Reactive vascular proliferations
  2. Usually produce obvious vascular channels filled with blood cells or lymph
  3. Lined by a layer of normal-appearing endothelial cells
A

Benign tumors

77
Q

(4) types of benign tumors

A
  1. Hemangioma
  2. Lymphangioma
  3. Glomangioma
  4. Vascular ectasias
78
Q

Of the benign tumors

  1. It is the most common vascular tumor
  2. Called angiomatosis if it involves large portions of the body
  3. Represents 7% of all benign tumors in infancy and childhood
A

Hemangioma

79
Q

What are the morphological variants of Hemangioma? (3)

A
  1. Capillary hemangioma
  2. Cavernous hemangioma
  3. Pyogenic granuloma/lobular capillary hemangioma
80
Q

Which variant of hemangioma is described by the ff:

  1. Common site: skin, subQ, mucous membranes of oral cavities and lips
  2. “Strawberry type” or juvenile hamangioma

Hint: most common variant

A

Capillary hemangioma

81
Q

What is the gross morphology of capillary hemangioma? (3)

A
  1. Red to blue
  2. Flat/elevated/pedunculated
  3. Intact overlying epithelium
82
Q

This variant of hemangioma has the ff histologic characteristics:

  1. Lobular proliferation of closely packed, thin-walled blood filled capillaries
  2. Flattened endothelial lining
  3. Scant connective tissue stroke
  4. May or may not have lumen thrombosis
A

Capillary hemangioma

83
Q

This type of hemangioma possess the ff characteristics:

  1. Larger, deeply situate, dilated vascular channels
  2. Locally destructive
  3. Associated with von Hippel-Lindau disease (systemic hemangiomas in the cerebellum, brain stem, eye, pancreas, liver)
  4. Intra vascular thrombosis with associated dystrophic calcification is common
A

Cavernous hemangioma

84
Q

Which variant of hemangioma has the ff histologic characteristics?

  1. Widely dilated lumen
  2. Mass is sharply defined but not encapsulated
  3. Composed of large, cavernous, blood-filled vascular spaces
  4. Separated by modest connective tissue stroma
A

Cavernous hemangioma

85
Q

Which variant of hemangioma has the ff characteristics:

  1. Rapidly growing pedunculated red nodule one the skin, gingival or oral mucosa
  2. Develops after trauma
  3. Accompanied by extensive edema with acute chronic infiltrate
A

Pyogenic granuloma/Lobular capillary hemangioma

86
Q

This is seen in the gingiva of pregnant women and regresses after delivery or undoes fibrosis

A

Granuloma gravidarum/pregnancy tumor

87
Q

Which type of benign tumor is described?

  1. Lymphatic analogues of blood vessel hemangioma
  2. Occurs subcutaneously, head, neck, axilla
  3. Slightly elevated, filled with milky lymph fluid
  4. Vascular network of endothelium-lined lymph spaces WITHOUT RBC
A

Lymphangioma

88
Q

What are the types of lymphangioma? (2)

A
  1. Simple (capillary) lymphangioma

2. Cavernous lymphangioma (Cystic hygroma)

89
Q

Type of lymphangioma:

  1. Pedunculated lesions of small lymphatic channels (head, neck, axillary sibQ tissues)
  2. Networks of endothelium-lined spaces WITHOUT ERYTHROCYTES
A

Simple/Capillary Lymphangioma

90
Q

Type of lymphangioma:
1. Found in neck (common in Turner’s Syndrome) or axilla of children

  1. Tumors
    - composed of massively dilated lymphatic spaces lined by endothelial cells
    - separated by intervening connective tissue stroma containing lymphoid aggregates
A

Cavernous Lymphangioma (Cystic Hygroma)

91
Q
  1. Benign, very painful tumor
  2. Origin: modified smooth ms cells of glomus body, an atriovenous structure associated with thermoregulation
  3. Commonly sub-ungal in location (under fingernails)
A

Glomangioma (Glomus Tumor)

92
Q

Describe gross morphology of glomangioma (1)

A

Small, round, red-blue nodules

93
Q

Describe histologic morphology of glomangioma (1)

A
  1. Aggregates, nests, masses of specialized glomus cells intimately associated with branching vascular channels
  2. Within a connective tissue stroma
94
Q

This benign tumor is NOT a true tumor and is characterized by local dilations of blood vessels

A

Vascular ectasias

95
Q

What are the types of Vascular ectasias? (4)

A
  1. Nevus Flemmus (birthmark)
  2. Port-wine stain
  3. Spider Telangiectasia/Arterial Spider
  4. Hereditary Hemorrhagic Telangiectasia/Osler-Weber-Rendu Disease
96
Q

Type of Vascular ectasias:

  1. Most common
  2. Usually located in head and neck
A

Nevus Flammeus

97
Q

Describe the gross morphology of Nevus Flammeus (2)

A
  1. Flat

2. Light pink to purple

98
Q

Describe the histologic morphology of Nevus Flammeus (1)

A

Dilatation of vessels in the dermis

99
Q

Type of Vascular Ectasias:

  1. It is a special form of Nevis Flammeus
  2. May be associated with Sturge-Weber Syndrome (SWS, enchephalotrigeminal angiomatosis) with distribution along trigeminal nerve
  3. Venous angiomatous masses in the leptomeninges and cortex
  4. Angiomas in the brain and leptomeninges associated with mental retardation, seizures, hemiplegia, radio-opacities in the skull
A

Port-wine stain

100
Q

Type of Vascular Ectasias:

  1. Radial pulsatile network do dilated subcutaneous arteries which BLANCHES ON PRESSURE at the center
  2. Usual location: face, neck, upper chest
  3. Associated with pregnancy and cirrhosis
  4. Hyperestrinism plays a role in its histiogenesis
  5. In males, liver cirrhosis increases circulating levels of estrogen leading to this disorder
A

Spider Telangiectasia/Arterial Spider

101
Q

Describe the gross morphology of Spider Telangiectasia (1)

Hint: Imagine anatomy of a spider

A

Small, red, dilated capillary channels (legs of spider) emanating from a core (body of spider)

102
Q

Type of Vascular Ectasias:

  1. Congenital, autosomal dominant
  2. Genetic malformations associated with dilate capillaries and veins
  3. Widely distributed: skin, mucous membranes of oral cavity, lips, respiratory tract, GIT, UT
A

Hereditary Hemorrhagic Telangiectasis

103
Q

What are the (2) intermediate (borderline) malignancies?

A
  1. Kaposi Sarcoma

2. Hemangiothelioma

104
Q

It is the most common AIDS-associated cancer

A

Kaposi Sarcoma

105
Q

Pathogenesis of Kaposi sarcoma (2)

A
  1. Herpes virus (HHV-8, KS-Associated Herpes Virus)

2. KSHV Effect

106
Q

What is the KSHV Effect? (2)

A
  1. Disruption of normal control of cellular proliferation

2. Prevent apoptosis of endothelial cells (through production of p53 inhibitors and a girls homologue of cyclin D)

107
Q

It has a predilection for MSM and is present in 1/3 of AIDS patients

A

Kaposi sarcoma

108
Q

Its gross characteristics include:

  1. Multiple red, purple, patch, plaque and macules in the extremities
  2. Affects the ff viscera: liver, spleen, mucosal
A

Kaposi Sarcoma

109
Q

Histologic manifestation of Kaposi Sarcoma (1)

A

Lymph node infiltration

110
Q

The ff are histologic features of:
1. Dilated irregular endothelial cell-lined vascular spaces with interspersed lymphocytes, plasma cells, macrophages, making it difficult to distinguish from granulation tissue

  1. With time: lesions become larger and form raised plaques on the skin, with dilated, jagged vascular channels surrounded by spindle cells
  2. Eventually: lesions become nodular and more neoplastic, sheets of plump proliferating spindle cells in the dermis or subQ tissue
A

Kaposi Sarcoma

111
Q

Types of Kaposi Sarcoma (4)

A
  1. Chronic/European KS
  2. ENDEmic/Lymphadenopathic/African KS
  3. Transplant-/Immunosuppression-Associated KS
  4. AIDS-Associated/EPIdemic KS
112
Q

This type of KS is not associated with HIV and has 10% visceral involvement

A

Chronic/European KS

113
Q

This type of KS:

  1. Local or generalized lymphadenopathy
  2. Sparse skin lesions
  3. Aggressive clinical course
  4. Dr. Yanez: associated with HIV
  5. Robbins: not associated with HIV
A

ENDEmic/Lymphadenopathic/African KS

114
Q

Type of KS:

  1. Occurs following organ transplant with recipient receiving high doses of immunosuppressive therapy
  2. Aggressive
  3. Involves lymph nodes, mucosa, visceral organs
A

Transplant-/Immunosuppression-Associated KS

115
Q

Gross morphology of which KS?

  1. Large, pearly, red, hemorrhagic lesions on the skin
  2. Malignant vascular proliferation on the skin
A

Transplant-/Immunosuppression-Associated KS

116
Q

This type of KS:

  1. Originally found in 1/3 of AIDS patients (males)
  2. Antiretroviral therapy has lowered its incidence to
A

AIDS-Associated/EPIdemic KS

117
Q

Type of Intermediate (borderline) Malignancy:

  1. Wide spectrum of vascular neoplasms
  2. Clinical behaviors intermediate between benign, well-differentiated hemangiomas and highly malignant angiosarcomas
A

Hemangiothelioma

118
Q

It is a vaulter tumor do adults occurring around medium-sized and large veins

A

Epitheloid hemangioendothelioma

119
Q
  1. Its tumor cells are plump, cuboidal (resembling epithelial cells)
  2. Well defined vascular channels are inconspicuous
  3. Clinical behavior is variable: most cure by excision, some recur, others metastasize
A

Epitheloid hemangioendothelioma

120
Q

Types of malignant tumors (4)

A
  1. Lymphangiosarcoma
  2. Hemangiosarcoma
  3. Angiosarcoma
  4. Hemangiopericytoma
121
Q

Which malignant tumor is describe by the ff:

  1. Malignant vascular tumor
  2. Adults
  3. Common site: skin, soft tissue, breast, liver
  4. Clinical behavior: local invasion, distal metastasis, poor outcome (high mortality rate), aggressive
A

Angiosarcoma

122
Q

Etiogenesis of malignant tumors (2)

A
  1. Carcinogens
    - arsenic (pesticides)
    - thorotrast (radioactive contrast agent)
    - polyvinyl chloride (widely use plastic)
  2. Chronic lymphedema (Lymphangiosarcoma)@
    - radiation
    - foreign body
123
Q

The ff gross characteristics ddescribe what?

  1. Start out small, sharply demarcated,a symptomatic, multiple red nodules
  2. Eventually become large, fleshy masses of red-tan to gray-white tissue
  3. Margins blend with surrounding structures
  4. Central areas of necrosis and hemorrhage
A

Malignant tumors

124
Q

The ff histologic characteristics ddescribe what?

  1. All degrees of differentiation can be seen
  2. Plump, anaplastic but recognizable endothelial cells producing Vascular channels to wildly undifferentiated tumors with spindle cell appearance without definite blood cells
  3. Endothelial cell origin can be demonstrated by staining CD31 or vWF
  4. Vascular channels containing RBC are prominent
  5. Atypical cells with hyperchromatic nuclei
A

Malignant tumors

125
Q
  1. Malignant vascular tumor with characteristic thin-walled branching vascular pattern
  2. Histiogenesis: pericytes
  3. Common in lower extremities especially thigh and retroperitoneum
A

Hemangiopericytoma

126
Q

Its histologic features of malignancy include:

  1. (+) necrosis
  2. High mitotic rate
  3. Nuclear pleomorphism
  4. Larger size
A

Hemangiopericytoma

Pathology (10 decks)

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