ROBBINS PATHOLOGY

1. PATHOLOGY OF BLOOD VESSELS
By Dr. Martins

2. 1.NORMAL VESSELS
• 3 concentric layer; intima, media & adventitia.
 Intima; internal elastic lamina
 Media;external elastic lamina
 Adventitia; vasa vasorum
• Arteries;
 Elastic(large): aorta, innominate, subclavian,
 Muscular(medium-sized): renal and coronary
 Small arteries and arterioles
• Capillaries
• Veins;
 post-capillary venules, collecting venules, veins.

4. Vascular organization
• Large elastic arteries > medium-sized arteries
> small arteries >arterioles > capillaries > post-
capillary venules > collecting venules > veins

5. Lymphatics
• Endothelium-lined channels that drain excess
interstitial tissue fluid, eventually returning it
to blood via the thoracic ducts.

6. 2.VASCULAR WALL CELLS AND THEIR
RESPONSE TO INJURY
• Endothelial cells;
Elaboration of Anticoagulant, Antithrombotic,
Fibrinolytic Regulators
Elaboration of Prothrombotic Molecules
Extracellular Matrix Production (Collagen,
Proteoglycans)
Modulation of Blood Flow and Vascular Reactivity
Regulation of Inflammation and Immunity
Regulation of Cell Growth
Oxidation of LDL

7. Ctd
• Vascular Smooth Muscle Cells
proliferate when appropriately stimulated
synthesize ECM collagen, elastin, and proteoglycans
elaborate growth factors and cytokines
vasoconstriction or vasodilation

8. Response of Vascular Wall Cells to
Injury
• Endothelial injury contributes to a host of pathologies
including thrombosis, atherosclerosis, and
hypertensive vascular lesions.
• Injury to the vessel wall results in a healing response,
involving intimal expansion by proliferating SMCs and
newly synthesized ECM.
• The recruitment and activation of the SMCs in this
process involves signals from cells eg ECs, and
mediators derived from coagulation and complement
cascades.
• Therefore, intimal thickening is a stereotyped
Response to Vascular Injury

10. 3.CONGENITAL ANOMALIES
• Rarely symptomatic;
Developmental (berry) aneurysms occur in cerebral
vessels.
Arteriovenous fistulas are direct connections between
arteries and veins that bypass the intervening
capillaries.
Fibromuscular dysplasia is a focal irregular thickening
of the walls of medium and large muscular arteries.

11. 4.ARTERIOSCLEROSIS
• Arterial wall thickening and loss of elasticity.
Arteriolosclerosis affects small arteries and arterioles with
two anatomic variants hyaline and hyperplastic.
Mönckeberg medial calcific sclerosis; calcific deposits in
muscular arteries.
Atherosclerosis.

12. 5.ATHEROSCLEROSIS
• General descriptions;
intimal lesions called atheromas (also called
atheromatous or atherosclerotic plaques), that
protrude into vascular lumina.
plaque consists of a raised lesion with a soft, yellow,
grumous core of cholesterol (esters) covered by a firm,
white fibrous cap.
obstructs blood flow & weaken the underlying media
and rupture, causing acute catastrophic vessel
thrombosis.
causes ischemic heart disease (IHD) .

13. Epidemiology
• Causes more morbidity and mortality (roughly
half of all deaths) in the Western world than any
other disorder.
• The mortality rate for IHD in the United States is
among the highest in the world and is
approximately five times higher than that in
Japan.
• Japanese who immigrate to the United States and
adopt American lifestyles and dietary customs
acquire the same predisposition to
atherosclerosis as the homegrown population.

14. Major Constitutional Risk Factors for
IHD
• Nonmodifiable factors;
Age; between ages 40 and 60, the incidence of myocardial
infarction in men increases fivefold.
Gender; premenopausal women are relatively protected
against atherosclerosis and its consequences compared with
age-matched men.
Genetics; well-established familial predisposition to
atherosclerosis and IHD is multifactorial:such as hypertension
or diabetes, familial hypercholesterolemia, that result in
excessively high blood lipid levels.

15. • Major Modifiable Factors;
 Hyperlipidemia; esp. hypercholesteremia i.e. LDL cholesterol
has an essential physiologic role delivering cholesterol to
peripheral tissues while mobilizes cholesterol from developing
and existing atheromas.
Hypertension; increase the risk of IHD by approximately 60%
in comparison with normotensive populations.
Cigarette Smoking; Prolonged (years) smoking of one pack of
cigarettes or more daily increases the death rate from IHD by
200%.
Diabetes Mellitus; induces hypercholesterolemia, the
incidence of myocardial infarction is twice as high in diabetic
as in nondiabetic individuals.

16. • Additional Factors;
Inflammation as marked by C-reactive protein.
Hyperhomocystinemia.
Lipoprotein a.
Factors Affecting Hemostasis.
Other Factors; like lack of exercise; competitive, stressful
lifestyle ("type A" personality); and obesity.

17. Pathogenesis
• Response-to-injury hypothesis;
Atherosclerosis as a chronic inflammatory response of the
arterial wall to endothelial injury.
Lesion progression occurs through interactions of modified
lipoproteins, monocyte-derived macrophages, T lymphocytes,
and the normal cellular constituents of the arterial wall.

18. • Central tenets of the hypothesis;
 Chronic endothelial injury, with resultant endothelial
dysfunction, causing (among other things) increased
permeability, leukocyte adhesion, and thrombosis.
 Accumulation of lipoproteins (mainly LDL and its oxidized forms)
in the vessel wall.
 Monocyte adhesion to the endothelium, followed by migration
into the intima and transformation into macrophages and foam
cells.
 Platelet adhesionFactor release from activated platelets,
macrophages, and vascular wall cells, inducing
 SMC recruitment, either from the media or from circulating
precursors.
 SMC proliferation and ECM production.
 Lipid accumulation both extracellularly and within cells
(macrophages and SMCs).

21. Morphology
• Fatty Streaks; composed of lipid-filled foam cells but are not significantly raised,
begin as multiple minute yellow, flat spots that can coalesce into elongated
streaks,
• Atherosclerotic Plaque; a.k.a fibrous or fibrofatty plaques impinge on the lumen of
the artery and grossly appear white to yellow; thrombosis superimposed over the
surface of ulcerated plaques is red-brown in color.
• Atherosclerotic plaques have three principal components: (1) cells, including
SMCs, macrophages, and T cells; (2) ECM, including collagen, elastic fibers, and
proteoglycans; and (3) intracellular and extracellular lipid.
• Parts of the plaque(on cross-section):
 Superficial fibrous cap is composed of SMCs and relatively dense collagen.
 “Shoulder”- beneath and to the side of the cap = more cellular area containing macrophages,
T cells, and SMCs.
 Necrotic core; deep to the fibrous cap, containing cholesterol (esters), debris from dead cells,
foam cells (lipid-laden macrophages and SMCs), fibrin, variably organized thrombus, and other
plasma proteins; the cholesterol content is frequently present as crystalline aggregates that
are washed out during routine tissue processing and leave behind only empty "clefts.“
 Neovascularization at the periphery of the lesions,

22. m

25. • Plaque changes;
Rupture, ulceration, or erosion; exposes the bloodstream to
highly thrombogenic substances and induces thrombus
formation and occlude the lumen and lead to downstream
ischemia.
Hemorrhage into a plaque
Atheroembolism; plaque rupture can discharge debris into
the bloodstream, producing microemboli composed of
plaque contents.
Aneurysm formation; Atherosclerosis-induced pressure or
ischemic atrophy of the underlying media, with loss of
elastic tissue, causes weakness of the vessel wall and
development of aneurysms that may rupture

26. Natural History of Atherosclerosis
• Preclinical and clinical phase.

27. Prevention of Atherosclerotic Vascular
Disease
• Primary prevention programs; cessation of cigarette
smoking, control of hypertension, weight loss, exercise,
and lowering total and LDL blood cholesterol levels
while increasing HDL (e.g., by diet or through statins)
• Secondary prevention programs; use of aspirin (anti-
platelet agent), statins, and beta blockers (to limit
cardiac demand), as well as surgical interventions (e.g.,
coronary artery bypass surgery, carotid
endarterectomy). These can successfully reduce
recurrent myocardial or cerebral events.

28. 6.HYPERTENSIVE VASCULAR DISEASE
• General description;
Elevated blood pressure is called hypertension.
Remains asymptomatic until late in its course.
Contributes to the pathogenesis of coronary heart
disease and cerebrovascular accidents, causes cardiac
hypertrophy and heart failure, aortic dissection, and
renal failure.

29. Regulation of Blood Pressure
• BP= CO X PR
• RAA System
• Vasodilators
• Adrenal aldosterone
• ANP

30. Pathogenesis of Hypertension
• 90% to 95% of hypertension is idiopathic (essential
hypertension), which is compatible with long life, unless a
myocardial infarction, cerebrovascular accident, or other
complication supervenes.
• Most of the remainder of "benign hypertension" is
secondary to renal disease or, less often, to narrowing of
the renal artery, usually by an atheromatous plaque
(renovascular hypertension).
• Accelerated or malignant hypertension, the clinical
syndrome is characterized by severe hypertension (diastolic
pressure over 120mmHg), renal failure, and retinal
hemorrhages and exudates, with or without papilledema

31. • Essential Hypertension;
 alterations in renal sodium homeostasis and/or vessel wall tone or
structure underlie essential hypertension.
 interplay of multiple genetic and environmental factors affecting
cardiac output and/or peripheral resistance.
• Secondary Hypertension;
 Renal: acute glomerulonephritis, chronic renal disease, polycystic
disease, renal artery stenosis, renal vasculitis, renin-producing tumors.
 Endocrine: Adrenocortical hyperfunction, Exogenous hormones,
Pheochromocytoma, Acromegaly, Hypo/hyperthyroidism, Pregnancy-
induced.
 Cardiovascular: Coarctation of aorta , polyarteritis nodosa increased
intravascular volume , increased cardiac output , rigidity of the aorta.
 Neurologic: psychogenic , increased intracranial pressure , sleep apnea,
acute stress (surgery).

32. Vascular Pathology in Hypertension
• Accelerating atherogenesis
• Potentiate both aortic dissection and
cerebrovascular hemorrhage
• Two forms of small blood vessel disease
Hyaline Arteriolosclerosis: a homogeneous pink hyaline
thickening of the walls of arterioles with loss of underlying
structural detail and with narrowing of the lumen
 Hyperplastic Arteriolosclerosis. Related to acute or severe
elevations of blood pressure, characteristic of malignant
hypertension , associated with "onion-skin," concentric,
laminated thickening of the walls of arterioles with luminal
narrowing ,the laminations consist of SMCs and thickened,
duplicated basement membrane.

34. 7.ANEURYSMS AND DISSECTIONS
• General description;
aneurysm is a localized abnormal dilation of a blood vessel
or the heart
 "true" aneurysm.
 false aneurysm (pseudoaneurysm): pulsating hematoma.
arterial dissection arises when blood enters the wall of the
artery, as a hematoma dissecting between its layers.
 Causes; atherosclerosis and cystic medial degeneration of
the arterial media, wall-weakening factors like include
trauma, congenital defects (e.g., berry aneurysms), infections
(mycotic aneurysms), or syphilis, and vasculitis.
 Mycotic aneurysms can originate (1) from embolization of a
septic thrombus, usually as a complication of infective
endocarditis; (2) as an extension of an adjacent suppurative
process; or (3) by circulating organisms directly infecting the
arterial wall.

36. Abdominal Aortic Aneurysm
• Definition
Out pouching of the aorta, most commonly in
abdominal aorta, following
atherosclerotic destruction of the aortic media,
leading to vessel wall weakness

37. • Morphology
 Big fusiform or sacular bulge out the side of the
abdominal aorta of varying width and length below the
renal arteries and above the bifurcation of the aorta.
 Often contains atheromatous ulcers with thrombi (source
of atherothrombotic origin)
 May be so large that it compresses nearby vessels or the
thrombus causes occlusion syndromes
Special Variants
• Inflammatory AAA = Macrophages, Giant Cells, Lymphocytes,
Plasma cells, AAA
• Mycotic AAA = Supuritic lesions with organisms hiding inside
(salmonella)

38. S

39. • Pathogenesis
 Atherosclerosis is number 1 cause
Cystic Medial Degeneration = Collagen. Aneurysms
come from abnormal collagen
(Marfan’s) or an abnormality of collagen remodeling
(increased degradation decreased
synthesis caused by an immune reaction) resulting in
an inherently weakened aortic wall

40. • Clinical Course
 Rupture is often fatal. Hemorrhage occurs into the
peritoneum. ↑size = ↑risk
 Obstruction of a vessel (mesenteric, renal, vertebral)
leading to ischemic injury
 Direct Compression of the ureter or of the vertebrae
(casing vertebral erosion)
 Embolism from the thrombus that’s sitting inside
 Tumor = AAA is a palpable mass that may

41. Syphilitic Aneurysm
• Cause
obliterative endarteritis characteristic of the tertiary
stage of syphilis can involve small vessels in any part
of the body.
Syphilis (stage 3) has a vascular predilection for
small vessels, especially of the aorta
Infection with subsequent Inflammation of the vasa
vasorum leads to obstruction, inducing ischemia
and obliterative endarteritis of the aorta, causing
death of muscle and elastic tissue, called syphilitic
aortitis

42. • Morphology
Starts in the adventitia with vessels with
inflammation reactions in adventitia.
syphilitic aortitis.
Muscle that dies is replaced with fibrous scar
tissue in the media, contraction of which
causes the “tree‐barking” appearance
Effects thoracic aorta with possible dilation
of aortic valve leading to insufficiency

43. • Presentation
All causes by the encroachment on
mediastinal tissues
• Crush the lungs = Dyspnea Pain from
rib and vertebral erosions Death from
rupture
• Crush the esophagus = Dysphagia,
Cardiac Disease from valve
involvement Aortic Regurgitation

44. Aortic Dissection
• Definition
blood splays apart the laminar planes of the media to
form a blood-filled channel within the aortic wall
ruptures through the adventitia and into various
spaces, where it causes either massive hemorrhage or
cardiac tamponade (hemorrhage into the pericardial
sac).
men aged 40 to 60 years, with antecedent
hypertension (> 90% of cases ), and younger patients
with systemic or localized abnormalities of connective
tissue affecting the aorta ( Marfan’s )

45. • Morphology
A single intimal tear cuts into but not through the
media of the ascending aorta creating a blood filled
pocket within the aorta, between layers
Dissection can continue in both direction (towards the
heart and towards the femoral)
Usually rupture outwards, but can rupture back
inwards
– Outward = hemorrhage = fatal
– Inward = second intimal tear back into the normal lumen, forming
a new vascular channel (“double‐barrel Aorta”) which can, over
time, endothelize and become a permanent vessel.

46. No distinguishing histology except for warning
signs = elastic tissue fragmentation and medial
degeneration

47. • Pathogenesis
HTN is primary causative agent, if you see HTN pick
Dissecting Hematoma
Medial weakening is not required for dissection, but
cystic medial necrosis from
Marfan’s or Ehler’s Danlos (weak elastic layer)
predisposes dissection
If you have a dissection, pick HTN. If HTN isn’t there,
pick Marfans
Once dissection has happened, arterial blood pressure
favors hematoma

48. • Clinical Course
If the dissection is Proximal subclavian/carotid (type A
= bad), if distal (type B = better)
Pain in the chest radiating to the back is a tell tale sign
Death usually results from rupture
If dissection involves aortic root, you can get valve
problems (regurgitation, murmur

49. Classification of dissections

50. 8.VASCULITIS
• General description;
Inflammation of vessel walls.
2 mechanisms: immune-mediated inflammation and
direct invasion of vascular walls by infectious
pathogens.
Noninfectious Vasculitis.
Infectious Vasculitis.
Vasculitis Associated with Other Disorders .

51. Non-infectious Vasculitis.
• Classification;
Large-Vessel Vasculitis
» Giant-cell (temporal) arteritis
» Takayasu arteritis
Medium-Vessel Vasculitis
» Polyarteritis nodosa
» Kawasaki disease
Small-Vessel Vasculitis
» Wegener granulomatosis
» Churg-Strauss syndrome
» Microscopic polyangiitis

52. • Pathogenesis;
 immune complex deposition; Antibody and complement are
typically detected in vasculitic lesions, DNA-anti-DNA
complexes(SLE) and drug hypersensitivity.Can be 2ndary to
viral infections.
antineutrophil cytoplasmic antibodies (ANCAs); circulating
antibodies that react with neutrophil cytoplasmic antigens.
Cytoplasmic localization (c-ANCA) >>proteinase-3 (PR3) and
Perinuclear localization (p-ANCA) >>myeloperoxidase (MPO).
anti-endothelial cell antibodies; Antibodies to ECs may
predispose to certain vasculitides, for example Kawasaki
disease.

53. • Giant-Cell (Temporal) Arteritis
Most common form of Vasculitis, especially in Elderly Women
affects the arteries in the head-esp. the temporal arteries-but
also the vertebral and ophthalmic arteries & the aorta (giant-
cell aortitis).
T cell-mediated immune response to an unknown vessel wall
antigen.
nodular intimal thickening with reduction of the lumen and
occasional thrombosis.
granulomatous inflammation within the inner media
centered on the internal elastic membrane.
fragmentation of the internal elastic lamina
Head pain, vision disturbances /blindness(ophthalmic artery
involved)
Responds well to steroids.

55. • Takayasu Arteritis
"pulseless disease“
transmural fibrous thickening of the aorta-
particularly the aortic arch and great vessels.
severe luminal narrowing of the major branch
vessels- loss of pulse.
in women younger than 40 years of
age(Japanese population)
intimal hyperplasia and irregular thickening of
the vessel wall

57. adventitial mononuclear infiltrates >>
mononuclear inflammation in the media >>
granulomatous inflammation(giant cells and
patchy medial necrosis)
reduced blood pressure and weaker pulses in
the upper extremities with coldness or
numbness of the fingers; ocular disturbances,
and neurologic deficits. Claudication of the
legs(distal aorta involved); pulmonary
hypertension(PA involved). Narrowing of the
coronary ostia >>MI, systemic
hypertension(renal arteries involved)

58. • Polyarteritis Nodosa
Involves renal and visceral vessels but not the pulmonary
circulation.
segmental transmural necrotizing inflammation of small to
medium-sized arteries
part of the vessel circumference involved, with a
predilection for branch points.
weakens the arterial wall >>aneurysms or even rupture.
Impaired perfusion >>in the distribution of affected vessels
transmural inflammation >>fibrinoid necrosis >>fibrous
/nodular thickening of the vessel wall that can extend into
the adventitia(which may coexist)

59. • Kawasaki Disease
self-limited illness of infancy and childhood (80% of patients
are younger than 4 years)
coronary arteritis >>aneurysms that rupture or thrombose,
causing AMI.
leading cause of acquired heart disease in children.
delayed-type hypersensitivity -T cells to uncharacterized
vascular antigen.
pronounced inflammation affecting the entire thickness of the
vessel wall.
Clinical Course: mucocutaneous lymph node syndrome with
conjunctival & oral erythema and erosion, edema of the hands
and feet, erythema of the palms and soles, a desquamative
rash, and cervical lymph node enlargement

60. • Microscopic Polyangiitis
• necrotizing vasculitis that affects capillaries , arterioles and
venules.
• hypersensitivity vasculitis or leukocytoclastic vasculitis.
• necrotizing glomerulonephritis (90% of patients) and pulmonary
capillaritis present.
• an antibody response to antigens such as drugs (e.g., penicillin),
microorganisms (e.g., streptococci), heterologous proteins, or
tumor proteins.
• segmental fibrinoid necrosis of the media- with focal transmural
necrotizing lesions
• granulomatous inflammation is absent.
• infiltrating and fragmenting neutrophils- in postcapillary venules.
• little or no immunoglobulin can be seen in most lesions (so-called
"pauci-immune" injury).

61. • Wegener Granulomatosis
Triad
– Acute necrotizing granulomas of the upper respiratory tract
– Necrotizing or granulomatous vasculitis
– Renal disease in the form of focal necrotizing, often crescentic,
glomerulonephritis.
cell-mediated hypersensitivity response, possibly to an
inhaled infectious or other environmental agent.
The upper respiratory tract lesions range from
inflammatory sinusitis with mucosal granulomas to
ulcerative lesions of the nose, palate, or pharynx, rimmed
by granulomas with geographic patterns of central necrosis
and accompanying vasculitis
renal lesions

62. Clinical Features
• persistent pneumonitis with bilateral nodular and cavitary
infiltrates
• chronic sinusitis (90%),
• mucosal ulcerations of the nasopharynx (75%), and evidence
of renal disease (80%).
• Other features include rashes, muscle pains, articular
involvement, mononeuritis or polyneuritis, and fever
• Allergic granulomatosis and angiitis (Churg-Strauss
syndrome) has association with allergic rhinitis, bronchial
asthma, and peripheral eosinophilia; p-ANCAs are present in
roughly half the patients.

63. • Thromboangiitis Obliterans
Buerger Disease
segmental, thrombosing acute and chronic
inflammation(tibial and radial arteries)
exclusively in heavy smokers of cigarettes, usually beginning
before age 35.
direct toxicity to endothelium by some tobacco products, or
an idiosyncratic immune response to the same agents
sharply segmental acute and chronic vasculitis of medium-
sized and small arteries, predominantly of the extremities.
superficial nodular phlebitis, cold sensitivity of the Raynaud
type in the hands, and instep claudication.

64. Vasculitis Associated with Other
Disorders
• Disorders; rheumatoid arthritis, SLE,
malignancy, or systemic illnesses such as
mixed cryoglobulinemia, antiphospholipid
antibody syndrome and Henoch-Schönlein
purpura
• Rheumatoid vasculitis
• Lupus vasculitis

65. Infectious Vasculitis
• Direct invasion of infectious agents;
Aspergillus and Mucor species
mycotic aneurysms
can induce thrombosis and infarction.

66. 9.RAYNAUD PHENOMENON
• Results from an exaggerated vasoconstriction
of digital arteries and arterioles
• Two types;
Primary Raynaud phenomenon; exaggeration of
central and local vasomotor responses to cold or
emotion(common in young women)
Secondary Raynaud phenomenon; vascular
insufficiency of the extremities due to arterial disease
from other entities (SLE, scleroderma, Buerger disease
or atherosclerosis).

67. 10.VEINS AND LYMPHATICS
• Varicose Veins
Superficial veins (usually of the legs) become
distended, more cosmetic than anything else
Obesity, jobs with legs dependent (barber,
surgeon), and pregnancy are disposing factors
Stasis of blood, rupture of valves, or thinning of walls
allows distention
May cause ulceration, but are generally asymptomatic
(do not cause emboli)
Can also be in the esophagus (esopheal varices) and in
the anus (hemorrhoids).

68. • Thrombophlebitis and Phlebothrombosis
Aka Deep Vein Thrombosis, DVT.
The distinction between thrombosis of the vein
(phlebothrombosis) and inflammation of the
Vein with thrombosis (thrombophlebitis) is not
relevant, they are all DVTs
Presents with pain in the calf with red, tender lesions,
with a positive Homan’s Sign(dorsiflexion induces pain)
Risk increases with Estrogen, Birth Control, Smoking,
Age, Hypercoagulability
Can result in pulmonary embolism or edema

69. • Superior and Inferior Vena Caval Syndromes
Something blocks these large veins (invasive neoplasm,
mural thrombosis) that causes a back up distally,
without a failure of the heart
Massive edema inferiorly for IVC (ankle, ascites, pelvis)
or superiorly for SVC (face, neck, arms)

70. • Lymphangitis and Lymphedema
Infection gets into the lymph nodes.
Red streaks from site of penetration, follows along
lymph tract, finished at lymph node.
Lymphadenopathy is present with PMNs and
Lymphocytes infiltrating site of infection.
Caused by Cancer or Virulent Bacteria (Staph).

71. 11.TUMORS
• Classification of Vascular Tumors and Tumor-like Conditions
 Benign Neoplasms, Developmental and Acquired Conditions
– Hemangioma
– Capillary hemangioma
– Cavernous hemangioma
– Pyogenic granuloma Lymphangioma
– Simple (capillary) lymphangioma
– Cavernous lymphangioma (cystic hygroma)
– Glomus tumor
– Vascular ectasias
– Nevus flammeus
– Spider telangiectasia (arterial spider)
– Hereditary hemorrhagic telangiectasis (Osler-Weber-Rendu disease)
– Reactive vascular proliferations
– Bacillary angiomatosis
 Intermediate-Grade Neoplasms
– Kaposi sarcoma
– Hemangioendotheliom
 Malignant Neoplasms
– Angiosarcoma
– Hemangiopericytoma

72. • Benign Tumors and Tumor-like Conditions
Hemangioma
– Capillary Hemangioma
– Cavernous Hemangioma
– Pyogenic Granuloma
Lymphangioma
– Simple (Capillary) Lymphangioma
– Cavernous Lymphangioma (Cystic Hygroma)
 Glomus Tumor (Glomangioma)
Vascular Ectasias
– Nevus Flammeus
– Spider Telangiectasia
– Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu Disease)
Bacillary Angiomatosis

73. • Intermediate-Grade (Borderline Low-Grade
Malignant) Tumors
Kaposi Sarcoma
– Chronic KS
– Lymphadenopathic KS (also called African or endemic KS)
– Transplant-associated KS
– AIDS-associated (epidemic) KS
Hemangioendothelioma
– Epithelioid hemangioendothelioma

74. • Malignant Tumors
Angiosarcoma
 Hepatic angiosarcomas
 Lymphangiosarcoma
Hemangiopericytoma

75. 12.PATHOLOGY OF VASCULAR
INTERVENTION
• Endovascular Stenting
• Vascular Replacement