pathology of vascular system for medical students in asian counties such as Philippines. The chapter is seen in Robbins Pathologic bases of disease

1. PATHOLOGY OF
BLOOD VESSELS
Angel R Reyes Jr, RMT, MD, FPSP, CHA DipHLM

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.

3. 3

4. 4
Arteries
• Large arteries are elastic (conducting) arteries
– pressure reservoirs
• Medium arteries are muscular (distributing)
arteries – more smooth muscle
• Contraction or relaxation of muscle changes
the size of the lumen, and so controls the
blood pressure in the vessel.

5. 5

6. 6
Capillaries
• Only a single layer of endothelium and a
basement membrane
• Connect arterioles and venules
• Functional part of system
• True capillaries begin at a precapillary
sphincter which controls blood flow through
the capillary

7. 7

8. 8
Veins
• Relatively thin; less elastic
• Larger in diameter than arteries
• Have valves to prevent backflow of blood
• Flow to heart is assisted by contraction of
skeletal muscles

9. 9

10. 10

11. 11

12. 12
Control of systemic circulation
• Nervous control – innervated by sympathetic
nervous system ONLY
• Cardiac control center (primarily in medulla
oblongata)
• Heart has both Sympathetic and
Parasympathetic innervations.

13. 13
• Baroreceptors and chemoreceptors:
– Monitor pressure
– Monitor blood levels of O2, CO2 and H+
– Send information to cardiovascular center, which
responds

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

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

16. 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

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

18. 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

20. 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.

21. 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.

22. 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) .

23. 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.

24. 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.

25. • 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.

26. • 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.

27. 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.

28. • 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).

31. 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,

32. m

35. • 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

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

37. 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.

38. 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.

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

40. 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

41. • 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).

42. 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.

44. 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.

46. 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

47. • 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)

48. S

49. • 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

50. • 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

51. 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

52. • 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

53. • 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

54. 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 )

55. • 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.

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

57. • 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

58. • 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

59. Classification of dissections

60. 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 .

61. 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

62. • 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.

63. • 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.

65. • 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

67. 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)

68. • 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)

69. • 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

70. • 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).

71. • 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

72. 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.

73. • 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.

74. 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

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

76. 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).

77. 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).

78. • 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

79. • 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)

80. • 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).

81. 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

82. • 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

83. • 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

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

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

86. • THANK YOU