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Cardio II: Exam 2 > Blood Vessel Pathology > Flashcards

Blood Vessel Pathology Flashcards

1
Q

atherosclerosis

A

mainly elastic and muscular aa. (Abdominal AA)

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2
Q

HTN

A

= mostly small muscular arteries and arterioles (and vaso vasorum) – (Thoracic AA)

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3
Q

prostacyclin

A

elaborated by eptihelial cells

inhibits platelet aggregation and vasodilates

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4
Q

vascular injury

A

results in intimal thicekening –> may impede vascular flow

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5
Q

berry aneurysms

A
  1. Developmental (congenital, berry) aneurysms:
    a. seen in 2% of autopsies
    b. most involve circle of Willis
    c. saccular type aneurysm arising in an artery with a developmental wall abnormality
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6
Q

AV fistulas

A
  1. Arteriovenous fistulas:
    a. rare abnormal communications between arteries and veins
    b. most congenital; some produced (rupture of an arterial aneurysm into adjacent vein, injuries that pierce walls of artery and vein, or inflammatory necrosis of adjacent vessels)
    c. short-circuit blood and cause heart to pump additional volume (high-output cardiac failure can ensue)
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7
Q

fibromuscular dyplasia

A

– focal irregular medial and intimal hyperplasia with thickening of walls of medium and large muscular arteries which occurs more commonly in young women – see “string of beads” appearance

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8
Q

Benign (essential) hypertension

A

(95%) –controlled hypertension with no short term problems

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9
Q

HTN urgency

A

Hypertensive urgency - systolic >220 mm Hg or diastolic >120 mm Hg with no evidence of target organ damage

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10
Q

HTN emergency

A

Hypertensive emergencies
• Accelerated hypertension- significant increase in B. P. associated with target organ damage (flame-shaped hemorrhages or exudates of fundus, renal failure, headache, angina, etc.)
• Malignant hypertension- as above + papilledema

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11
Q

Secondary HTN?

A

(~10% of cases):
• Renal: GN, CKD, Polyciistic disease, Renal aa. stenosis, renal vasculitis, renin tumors
• Endocrine: Adrenocortical hyperfunction (Cushing syndrome, primaryaldosteronism, congenital adrenal hyperplasia, licorice ingestio) Pheochromocytoma, Contraceptives, hypothyroidism, hyperthyroidism
• Cardiovascular: Coarctation of aorta, polyarteritis nodosa, increased intravascular volume, increased CO, rigid aorta
• Neurologic: psychogenic, increased intracranial pressure, sleep apnea, acute stress, surgery

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12
Q

Liddle syndrome

A

moderately severe salt sensitive hypertension due to increased distal tubular reabsorption of Na+ with aldosterone stimulation
• ENaC channel is overresponsive to aldosterone!!!

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13
Q

Monckeberg medial calcific sclerosis

A

: in muscular arteries of >50 y. o. with no vessel lumen narrowing (can ossify) – hardening of mm. media

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14
Q

arteriolosclerosis

A

arteriosclerosis (hardening) of small arteries and arterioles

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15
Q

atherosclerosis

A

Atherosclerosis (atheromas=atheromatous plaques=fibrofatty plaques) develops primarily in elastic arteries and muscular arteries (primarily occurs in medium to larger arteries)

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16
Q

hyaline arteriolosclerosis

A
  • Protein deposition (hyalinized)
  • Seen in
  • aging
  • diabetes mellitus
  • benign nephrosclerosis (hypertension)
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17
Q

hyperplastic arteriolosclerosis

A
  • Cell death (onion-skinning)
  • +/-necrotizing arteriolitis
  • Seen in:
  • malignant HTN
  • necrotizing arteriolitis
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18
Q

atherosclerotic plaques

A

• turbulent flow and low shear stress areas are prone to atherosclerosis
o laminar flow → endothelial trauma and dysfunction → increased risk of developing plaques
o inflammation of endothelial cells → increased risk of atherosclerotic plaque
Atheromatous plaque consists of raised lesion with soft core of lipid covered by a fibrous cap

  • Stable plaques tend to have dense fibrous cap, minimal lipid accumulation and little inflammation,
  • “vulnerable” plaques have thin caps, large lipid cores and dense inflamm. infiltrates
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19
Q

CRP

A

acute phase reactant that is a risk factor for atherosclerosis

see elevated CRP protein

a. CRP: acute phase reactant synthesized primarily by liver
b. strongly and independently predicts the risk of MI, stroke, PAD, sudden cardiac death

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20
Q

risk factors of atherosclerosis?

A

↑LDL, ↓ HDL and ↑Lp(a) associated with ↑ atherosclerosis

hyperlipidemia
HTN
cigartetes
DM

CRP protein
hyperhomocysteinemia
central obesity
lipoprotein A (an altered form of LDL)
elevated plasminogen activator inhibitor
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21
Q

atherosclerosis pathogenesis?

A

• Endothelial injury and dysfunction: causes increased vascular permeability, leukocyte adhesion, thrombosis
o hemodynamic disturbances= often due to turbulence
o hypercholesterolemia /hyperlipidemia: see LDL foam cell macrophages
o Inflammation: triggered by accumulation of cholesterol crystalsand FFAs in macrophages and other cells
o infection
• Accumulation of liporporteins: mostly LDL to vessel wall
• Monocyte adhesion to the endothelium: followed by migration into intima and transformation into macrophages and foam cells
• Platelet Adhesion and Activation
• Factor release: induces smooth mm. recruitment from media or from circulating precursors
• Smooth mm. cell proliferation: smooth mm. cell proliferation and extracellular matrix deposition convert a fatty streak into a mature atheroma and contribute to the progressive growth of the lesion
• Lipid accumulation

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22
Q

infections contributing to atherosclerosis?

A

Chlamydia pneumoniae, herpesvirus, cytomegalovirus

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23
Q

morphology of atherosclerosis

A

• Fatty Streaks: composed of lipid-filled foamy macrophages- begin as flat yellow spots and slowly can evolve into plaques
• Atherosclerotic plaques: see intimal thickening and lipid accumulation → encroach on the lumen of artery
o most often seen in: lower ab. aorta, coronary aa, popliteal aa, internal carotid aa, circle of willis
o can result in rupture, ulceration/erosion which may lead to thrombosis
o hemorrhage into a plaque, atheroembolism, aneurysm formation

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24
Q

familial hypercholesterolemia

A
  • Due to mutations in the LDL receptor (Type IIa)
    • Impair the intracellular transport and catabolism of LDL
    • Causes elevated LDL cholesterol in the plasma
    • Forces oxidized LDL receptors to take over – done by monocytes, macrophages and smooth mm. endothelial cells → cholesterol in macrophages (xanthoma), oxidized LDL is cytotoxic to endothelial SMC’s → Atherosclerosis

Autosomal Dominant Familial Hypercholesterolemia:
• heterozygotes have 2-3x plasma elevation, homozygotes have 5x plasma elevation
• Develop severe atherosclerosis, mitral valve stenosis, corneal arcus and xanthomas
• die from complications as children or young adults

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25
Q

aneurysm

A

= localized abnormal dilation of blood vessel or of the wall of the heart

Atherosclerosis = AAA ; HTN = Thoracic AA

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26
Q

mycotic aneurysm

A

due to infections
• embolization of septic embolus = infective endocarditis
• extension of adjacent suppurative process or deposition of circulating organisms in arterial wall

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27
Q

saccular aneurysm

A

Saccular aneurysm (B): appears rounded

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28
Q

fusiform aneurysm

A

Fusiform aneurysm (C): involves long segment of artery and is not rounded

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29
Q

False aneurysm

A

False aneurysm: hematoma secondary to transmural rupture

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30
Q

Arterial dissection

A

arises when blood enters a defect in the arterial wall and tunnels between its layers

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31
Q

AAA

A

• usually occurs below the renal aa. and above bifurcation of aorta
• can involve the renal aa. and lead to renal complications
• M>F; smokers, age of 50 years+
1. Inflammatory AAA: see rich lymphocytes, plasma cells, macrophages, giant cells – occurs at younger age
2. Mycotic AAA: atherosclerotic AAs that have become infected – Salmonella gastroenteritis

Clinical Consequences?
• can result in rupture into peritoneum or retroperitoneal tissue
• if aneurysm is 5cm or greater, it is usually surgically repaired
• can obstruct vessel → ischemic injury
• Embolism from atheroma or mural thrombus
• Can impinge on adjacent structures
• presents as an abdominal mass that is often pulsating

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32
Q

Syphilitic (Luetic) Aneurysm:

A
  • see obliterative endarteritis in tertiary stage of syphilis involving the vasa vasorum of the thoracic aorta → results in ischemic injury of media → loss of medial elastic fibers and mm. cells
  • can lead to aneurysmal dilation that can include the aortic annulus → aortic valve incompetence
  • tree barking: repeated bouts of scarring of the vaso vasorum → contraction of fibrous scars with intervening segments of intima
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33
Q

tree barking

A

: repeated bouts of scarring of the vaso vasorum → contraction of fibrous scars with intervening segments of intima

syphilitic aneurysm

34
Q

TAA

A
  • most often due to HTN
  • results in respiratory difficulties due to encroachment on lungs, difficulty swallowing, persistent cough, pain caused by erosion of bones, aortic valvular insufficiency
35
Q

Aortic dissection

A
  • occurs when blood separates the laminar planes of the media to form a blood-filled channel within the aortic wall
  • may or may not occur with aneurysm
  • 90% occur in men aged 40-60 with HTN (Arteriolosclerosis → smooth mm. loss)
  • in younger pt. usually due to CT disorder (Marfan, Ehlers-Danlos, Vit. C deficiency)
  • often occurs secondary to Vasa Vasorum rupture
  • Must decrease the BP in order to keep the dissection from getting larger

Clinical presentation:
• Sudden onset of excruciating pain, usually involves anterior chest, radiating to the back, and moving downward as the dissection progresses
• Most common cause of death is rupture into the body cavities

** Dissection is unusual in substantial atherosclerosis or other cause of medial scarring such as syphilis

36
Q

Marphan syndrome

A

= Loss of function mutation in fibrillin
• mutations in FBN1 gene
• 75% are autosomal dominant pattern, the rest are sporadic
• results in decreased fibrillin1 and increased TGF-B activity
• fibrillin is involved in inactivating TGF-B, which enhances collagen production and ECM remodeling
• this leads to overgrowth of bones and myxomatous changes in mitral valve
• increased aneurysm and dissection of thoracic aorta

Clinical presentation:
• Skeleton: Slender with abnormally long legs, arms, and fingers (arachnodactyly); high-arched palate; hyperextensibility of joints; spinal deformities (kyphoscoliosis); pectus excavatum or pigeon-breast
• Eyes: Bilateral dislocation (subluxation) of lens from weakness suspensory ligaments (ciliary zonules holding lens are made up exclusively of fibrillin)
• Cardiovascular system: Aneurysmal dilation and aortic dissection; dilation of the aortic valve ring (aortic incompetence); mitral and tricuspid valve floppy valve syndrome giving rise to congestive cardiac failure

**Death from aortic rupture may occur at any age and is the most common cause of death (less commonly, cardiac failure is the terminal event)

37
Q

FBN1 gene

A

fibrillin = loss results in marphan syndrome

38
Q

Loeys-Dietz syndrome:

A
  • similar to Marphan, however there is not an increased arm span
  • due to TGF-B receptor mutation
39
Q

large vessel vasculitis

A

Giant cell arteritis, takayasu arteritis

40
Q

Giant-cell (temporal) arteritis

A

Granulomatous inflammation; also frequently involves the temporal artery.

Usually occurs in patients older than age 50 and is associated with polymyalgia rheumatica

see intimal thickening with reduced luminal diameter

  • painful to palpation, facial pain/h/a, ocular sx, fever, fatique, w/l
  • age >50, often assoc .w/ polymyalgia rheumatica
  • ophthalmic arterial involvement → diplopia and permanent blindness
41
Q

Takayasu arteritis

A

Granulomatous inflammation usually occurring in patients younger than age 50

• marked by ocular disturbances and marked weakened pulses in upper extremities = “pulseless disease”
• transmural fibrous thickening of the aorta
Morphology
• most often affects aortic arch, pulmonary aa, coronary and renal aa.
Clinical features:
• seen in patients younger than 50
• fatigue, w/l, fever
• reduced BP and weak pulses in carotids
•

42
Q

Medium vessel vasculitis

A

polyarteritis nodosa, kawasaki disease

43
Q

small vessel vasculitis

A

microscopic polyangiitis, wegener granulmatosis, churg-strauss syndrome,

44
Q

Polyarteritis nodosa

A

Necrotizing inflammation typically involving renal arteries but sparing pulmonary vessels

  • NO associated w/ ANCA
  • 30% of pt. w/ PAN have Hep B

Clinical:
• young adults (and geriatrics)
• renal arterial involvement → death
• Hep B surface Ag/Ab complexes
• no GN
• Malaise, fever, w/l, rapidly accelerated HTN
• abdominal pain and melena, muscular aches/pains, ulcers, infarcts, peripheral neuritis
• Treatment: steroids and cyclophosphamide (cured in 90% of cases)

45
Q

Kawasaki disease

A
  • acute febrile, usually self-limited illness of infancy/childhood
  • assoc. w/ arteritis affecting large to medium or small vessels
  • see anti-endothelial cell and smooth mm. autoantibodies

** if coronary aa involved → acute MI → #1 cause of acquired heart disease in children

Clinical:
• conjunctival and oral rash/blistering = “strawberry tongue”
• edema of hands and feet
• erythema of plasma and soles and desquamative rash
• cervical lymph node enlargement
• treatment: IV IgG’s and aspirin

46
Q

Wegener granulomatosis

A

= “granulomatosis with polyangitis”

Associated with PR3-ANCAs

  • nectorizing granulomas of UR tract (ear, nose sinus throat lung)
  • necrotizing or granulomatous vasculitis (capillaries, arterioles, veins) mostly affecting lungs, upper airways, eyes and skin
  • focal crescentic glomerulonephritis → renal disease

Clinical triad: coughing up blood, kidney failure, lesions in the nose/UR tract

  • affects males around 40 years
  • Persistent pneumonitis
  • Chronic sinusitis in 90%
  • Mucosal ulcerations of the nasopharynx in 75%
  • Renal disease in 80%
  • Skin rashes, mm pains, fever
  • If left untreated, 80% of pt. die w/in year. Tx = immunosuppression
47
Q

Churg-Strauss syndrome

A

Eosinophil-rich, allergic granulomatous

Associated with asthma, allergic rhinitis, lung infiltrates and blood eosinophilia.

Associated with
MPO-ANCAs

Clinical:
• coronary arteritis and eosinophilic myocarditis are principal causes of morbity and mortality
• renal disease is uncommon
• palpable purpura, GI tract bleeding

48
Q

Microscopic polyangitis

A

Necrotizing small-vessel vasculitis with few or no immune deposits;

Associated with MPO-ANCAs (P ANCAS)

unlike PAN, all lesions of microscopic polyangiitis tend to be of same age

Clinical:
• palpable purpura of skin
• Necrotizing glomerulonephritis in 90% of pt.
• pulmonary capillaritis
• hemoptysis, arthralgia, ab pain, bleeding, hematuria, proteinuria, hemorrhage, mm. pain, weakness

49
Q

MPO ANCA

A

p-ANCA = MPO ANCA = microscopic polyangitis and Churg Strauss syndrome

50
Q

PR3-ANCA

A

c-ANCA = PR3-ANCA = Wegener Granulomatosis

51
Q

Behcet disease

A

• small to medium vessel neutrophilic vasculitis
• associated w/ HLA-B51
• can have positive pathergy test (exaggerated rxn to sterile pinpcirck)
Clinical:
• Triad: oral apthous ulcers, genital ulcers, uveitis (inflamm. of eye, pus in anterior chamber)

52
Q

Buerger disease

A

Thromboangiitis Obliterans = “Buerger Disease”
• segmental, thrombosing, acute and chronic inflammation of medium and small arteries (tibial and radial aa.) – extends into vv. and nn. of extremities
• ofen leads to vascular insuff. in extremities
• CIGARETTE SMOKING
Clinical
• begins before age 35
• ulceration in toes, feet, fingers, gangrene
• pain at rest due to nerve involvement

53
Q

infectious vasculitis

A
  • Sometimes from direct invasion of bacteria (pseudomonas) or fungi (Aspergillus and mucormycosis)
  • Can frequently accompany bacterial pneumonia
  • Can occur adjacent to caseous tuberculous abscesses
  • Can occur in superficial cerebral vessels in meningitis
  • Can be secondary to septic emboli
  • May result in a mycotic aneurysm or induce thrombosis and infarction
54
Q

• Vasoconstriction involving nose, ears, hands, feet

A

frostnip

55
Q
  • Nonfreezing temperatures and damp conditions

* Chronic, recurrent vasculitis with red raised lesions

A

chilblain or “perniosis”

56
Q
  • Feet have been wet, but not freezing
  • May not heal, chronic pain, edema and blotchy discoloration
  • Often produces a superficial, moist, liquefaction gangrene
A

Immersion (trench) foot – water draws heat out of tissue

57
Q
  • Sudden sharp drops in temperature that are persistent
  • Vasoconstriction and increased viscosity of the blood
  • Hyperemia and edema, large, clear blisters, vesicles filled with hemorrhagic fluid to complete gangrene
  • usually dry gangrene, nice clean necrosis, nothing should be done when you see these patients
A

frostbite

58
Q

• see “red, white and blue” pallor or cyanosis of digits of hands/feet/nose ears

A

Raynaud Phenomenon:
• see “red, white and blue” pallor or cyanosis of digits of hands/feet/nose ears
• Primary Raynaud: cold or emotion enduced vasoconstriction
• Secondary Raynaud: Arterial insufficiency caused by SLE, systemic sclerosis, atherosclerosis or Buerger Disease

59
Q

thrombophlebitis

A

= when blood clot blocks vv.

  • 90% come from deep leg veins
  • Cardiac failure, pregnancy, obesity, prolonged immobilization, estrogen therapy, oral contraceptives
  • migratory thrombophlebitis → + Trousseau syndrome → pain elicited on squeezing the calf mm.
  • Homan sign = forced dorsiflexion of the foot
  • PE is associated with complication
  • Plemasia alba dolens – “painful white leg” – iliofemoral venous thrombosis in pregnant women
  • periprostatic vv in men, or pelvic venous plexus in women
60
Q

SVC syndrome

A

swllen arms
• Usually neoplasm compresses or invades with cyanosis and dilation of the veins of the head, neck, and arms
• If pulmonary vessels also compressed have respiratory distress

61
Q

IVC syndrome

A
  • Neoplasm compresses or penetrates (renal, hepatic or adrenal cortex carcinomas) or a thrombus propagates upward with leg edema, distention of lower abdomen superficial collateral veins
  • With renal vein involvement massive proteinuria
62
Q

lymphangitis vs. lymphadenitis

A

Lymphangitis - Infections involving lymphatics with red streaks
• (Group A beta hemolytic streptococci)
• in severe cases produces cellulitis or focal abscesses

Acute lymphadenitis - red streaks with painful enlarged regional lymph nodes

63
Q

milroy disease

A

primary lymphedema due to genetics

64
Q

lymphedema praecox

A

age 10 to 25 years, usually female, unknown cause with edema starting in the feet and slowly accumulating throughout life (extremity may swell to many times its normal size and the process may extend to the trunk)

65
Q

Hemangiomas:

A

common tumors with rare malignant transformation
- constititue 7% of all benign tumors of childhood – most often seen in skin and liver
- due to increased number of normal/abnormal vessels filled with blood in the tumors
may regress spontaneously

66
Q
  1. Capillary hemangioma:
A

a. most common vascular tumor usually skin, subcutaneous tissues, and mucous membranes, but can be in any organ with a vascular supply
b. lumina may be thrombosed, rupture of vessels causes scarring (hemosiderin pigment occasionally found)

67
Q
  1. Juvenile Hemangiomas
A
  1. Juvenile Hemangiomas: “strawberry type” capillary hemangioma of the skin of newborns (1 in 200 births), grows rapidly in the first few months, and regresses by age 7 in 75% to 90%
68
Q

cavernous hemangioma

A

a. Larger, less circumscribed, and more frequently involves deep structures than capillary hemangiomas
b. May be locally destructive
c. No tendency to regress
d. Intravascular thrombosis with associated dystrophic calcification
e. Hemangiomas of the brain threatening since cause pressure symptoms or rupture

NOTE: cavernous hemangiomas are one component of Von Hippel-Lindau disease: see hemangioblastomas angiomatous lesions of cerebellum, brainstem, eye, cystic neoplasms in pancreas and liver

69
Q

pyogenic granuloma

A

“lobular capillary hemangioma”

b. polypoid capillary hemangioma
c. rapidly growing red nodule
d. skin or gingival or oral mucosae
e. bleeds easily and is often ulcerated
f. 1/3 develop after trauma
g. edema and inflammatory infiltrate
h. (resemble exuberant granulation tissue)
Granuloma Gravidarum = pyogenic granuloma that is seen in 1% of pregnant women = pregnancy tumor

70
Q

lymph angiomas

A
  1. Simple (capillary) lymphangioma
    a. small lymphatic channels
    b. tend to occur subcutaneously in the head and neck and in axilla
    c. absence of luminal erythrocytes
  2. Cavernous Lymphangioma (cystic hygroma)
    a. in children in the neck or axilla and, rarely, retroperitoneum
    b. massively dilated, cystic lymphatic spaces
    c. cystic hygromas (lymphangioma colli) of the neck occur in Turner syndrome
71
Q

Turner syndrome

A

Cavernous Lymphangioma (cystic hygroma) - occur in the neck

72
Q

“Glomangioma

A

Glomus tumor = “Glomangioma”
• Benign often painful tumor, when squeezed
• From modified cells of the glomus body (arteriovenous anastomosis involved in thermoregulation)
• Most commonly distal digit
o Small slightly elevated, rounded, red-blue, firm nodules
o minute foci of fresh hemorrhage if under the fingernails
• Specialized glomus cells (modified smooth muscle cells on electron microscopy) arranged around vessels

73
Q

vascular ectasia

A

= localized dilation of pre-existing vessels
- Telangiectasia - congenital anomaly or acquired permanent exaggeration of preformed vessels
• composed of prominent capillaries, venules, and arterioles

74
Q

nevus flammeus

A

= birthmark, light pink/purple composed of dilated vessels

a. “port wine stain” = thickened Nevus that does not fade with time
b. Sturge-Weber syndrome = port wine stain on trigeminal nn. distribution – also see mental retardation, seizures, hemiplegia and skull radio-opacities

75
Q
  1. Spider telangiectasia
A

(arterial spider): nonneoplastic vascular lesions that look like a spider, contain pulsatile arrays of dilated subcutaneous arteries that blanch with pressure

a. seen often with pregnant women and cirrhosis
b. usually face, neck or upper chest

76
Q

Osler-Weber-Rendu Disease

A
  1. Hereditary hemorrhagic telangiectasis (Osler-Weber-Rendu Disease): autosomal dominant disorder caused by mutations in TGF-Beta pathway – see lesions on mucous membrane that can spontaneously ruptrure causing epistaxis, GI bleeding or hematuria
    a. congenital malformations of dilated capillaries and vv.
    b. see hemangiomas on lips, tongue, bucal mucosa
77
Q

Bacillary angiomatosis

A
  • Opportunistic infection of immunocompromised persons by gram-negative bacilli of the Bartonella family (first described in AIDS)
  • Skin, bone, brain, and other organs
  • Domestic cat is the reservoir of B. henselae and cat flea its vector (cause of cat-scratch disease)
  • Human body louse in infection due to B. quintana (cause of trench fever)
78
Q

Kaposi sarcoma

A

Human herpesvirus 8 [HHV-8]

  • Classic KS = disorder of older men of Mediterranean / middle eastern descent – not assoc. w/ HIV (see multiple red-purple skin plaques or nodules in lower extremities)
  • Endemic African KS: most common tumor in central Africa – occurs in younger individuals and follows more aggressive course – involves lymph nodes
  • AIDS-associated (epidemic) KS: most common HIV-related malignancy

Stages of KS:
1. Patch stage- pink to purple solitary or multiple macules
• Dilated angulated blood vessels and chronic inflammatory cells (lesions difficult to distinguish from granulation tissue)
2. Plaque stage- larger, violaceous dermal jagged vascular channels lined by plump spindle cells with occasional mitoses with RBC extravasation
3. Nodular stage – raised nodular lesions
• often accompanied by involvement of lymph nodes and of viscera
• sheets of spindle cells with mitotic figures and slit-like spaces that often contain rows of red cells

79
Q

Hemangioendothelioma•

A

• Epithelioid hemangioendothelioma
• vascular tumor occurring around medium and large veins in the soft tissue of adults
• inconspicuous well-defined vascular channels and tumor cells are plump and often cuboidal
• most cured by excision but
• 40% recur
• 20% to 30% metastasize
15% die from metastases

80
Q

angiosarcoma: 3 types?

A
  • Malignant and vary from differentiated (hemangiosarcoma) to anaplastic
  • More often in older adults, anywhere in the body
  • Most commonly skin, soft tissue, breast, and liver
  • Have local invasion and metastatic spread (5 year survival 30%)
  • Can be induced by radiation and may be associated with foreign material introduced into the body
  • Immunohistochemistry; CD31, CD34, Factor VIII or vWF
  1. Cutaneous angiosarcoma:
    • small, red nodules
    • eventually become large, fleshy pale/gray, with central softening and hemorrhage
  2. Hepatic angiosarcomas:
    • associated with carcinogens: [arsenic, Thorotrast and vinyl chloride]
    • Many years between exposure and tumors
  3. Lymphangiosarcoma:
    • Arise in chronic lymphedema (approximately 10 years following radical mastectomy)
81
Q

Hemangiopericytoma

A
  • Believed to be derived from pericytes (myofibroblasts)
  • Some fibroblastic tumors previously incorrectly included in this category
  • Fleshy or spongy consistency
  • Slowly growing in pelvic retroperitoneum or lower extremities (especially thigh) of middle aged women
  • Thin-walled branching (“staghorn”) vascular pattern
  • 1/2 act benign and 1/2 malignant
  • Necrosis, high mitotic rate, and nuclear pleomorphism, associated with aggressive behavior

Cardio II: Exam 2 (7 decks)

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