2. Course outline
Vascular Structure and Function
Vascular Anomalies
Vascular Wall Response to Injury
Hypertensive Vascular Disease
Atherosclerosis
Aneurysms and Dissection
Vasculitis
Veins and Lymphatics
Vascular Tumors
3. Vascular Structure and Function
All vessels except capillaries share a three-layered
architecture consisting of an endothelium lined
intima, a surrounding smooth muscle media, and
supportive adventitia, admixed with extracellular
matrix
The smooth muscle cell and matrix content of arteries,
veins, and capillaries vary according to hemodynamic
demands and functional requirements
4.
5. Based on their size & structural features, arteries are
divided into
Large or elastic arteries including , the aorta & its large
branches
Medium-sized or muscular arteries including coronary
& renal arteries
Small arteries & arterioles
The principal points of physiological resistance to blood
flow
6.
7. Vascular pathology results in disease via two principal
mechanisms:
Narrowing or complete obstruction of vessel lumina,
either progressively (e.g., by atherosclerosis) or
precipitously (e.g., by thrombosis or embolism)
Weakening of vessel walls, causing dilation and/or
rupture.
8. Response of Vascular Wall Cells to Injury
ECs and SMCs
• Main cellular components of the blood vessel walls
• Play central roles in vascular biology and pathology.
• The integrated function of these cells is critical for
vasculature to adapt to hemodynamic and biochemical
stimuli
9. Endothelial cell function is tightly regulated in both
the basal and activated states.
Various physiologic and pathophysiologic stimuli
induce endothelial activation and dysfunction that
alter the endothelial cell phenotype
Endothelial dysfunction is responsible for initiation of
thrombus formation, atherosclerosis & the vascular
lesions of hypertension
10.
11.
12. Injury to the vessel wall results in a stereotyped healing
response involving smooth muscle cell proliferation,
extracellular matrice deposition, and intimal expansion
The recruitment and activation of the smooth muscle cell
involves signals from cells (e.g.,endothelial cells, platelets,
and macrophages), as well as mediators derived from
coagulation and complement cascades.
Excessive thickening of the intima may result in luminal
stenosis and vascular obstruction.
14. Vascular Anomalies
Developmental or berry aneurysms
are small, spherical dilatations typically in the circle of Willis
can causes fatal intracerebral hemorrhage when rupture
Arteriovenous fistulas
are direct connections (usually small) between arteries and
veins that bypass the intervening capillary bed
16. Fibromuscular dysplasia
is a focal irregular thickening in medium and large
muscular arteries
results in luminal stenosis and reduces vascular flow
it can lead to renovascular hypertension in the renal
arteries
17.
18. Systemic and local tissue blood pressures must be
maintained within a narrow range
Low blood pressure (hypotension) results in
inadequate organ perfusion and can lead to tissue
dysfunction or death
High blood pressure (hypertension) can cause end-
organ damage and is one of the major risk factors for
atherosclerosis
19. Regulation of normal blood pressure
Blood pressure is a function of cardiac output and
peripheral vascular resistance, both of which are
influenced by multiple genetic and environmental
factors
20. Cardiac output is a function of stroke volume and
heart rate.
Peripheral resistance is regulated predominantly at
the level of the arterioles by neural and hormonal
inputs
21.
22. Factors released from the kidneys, adrenals, and
myocardium interact to influence vascular tone and to
regulate blood volume by adjusting sodium balance
About 98% of the filtered sodium is reabsorbed by
active sodium transporters
Small amount of remaining sodium is subject to
resorption by the epithelial sodium channel (ENaC),
which is tightly regulated by the renin angiotensin
system
23. The kidneys and heart contain cells that sense changes
in blood pressure or volume
Kidneys influence peripheral resistance and sodium
excretion/retention primarily through the renin-
angiotensin system (RAAS).
Myocardial natriuretic peptides are released from atrial
and ventricular myocardium inhibit sodium resorption
in the distal renal tubules
24.
25. Epidemiology of Hypertension
Sustained diastolic pressures ≥ 90 mmHg or sustained
systolic pressure ≥ 140 mmHg are associated with
increased risk of atherosclerotic disease
Approximately 25% of individuals in the general
population are hypertensive based on these criteria
26. Approximately 90% to 95% of hypertension is
idiopathic—so-called essential hypertension
Only 5-10% of patients have underlying cause –
secondary hypertension
Hypertension can cause cardiac hypertrophy and heart
failure (hypertensive heart disease), multi-infarct
dementia, aortic dissection, and renal failure
27. Malignant hypertension is characterized by
Severe hypertension (i.e., SBP ≥ 200 mm Hg, DBP≥ 120
mm Hg),
Renal failure, and
Retinal hemorrhages and exudates, with or without
papilledema
28. Pathogenesis of Hypertension
Hypertension is a disorder with multiple genetic and
environmental contributions
The vast majority (90% to 95%) of hypertension is
idiopathic
Most other causes fall under renal disease, including
renovascular hypertension (due to renal artery
occlusion)
Infrequently hypertension has an underlying
endocrine basis
31. Mechanisms of Essential Hypertension
Essential hypertension results from an interplay of
multiple genetic and environmental factors affecting
cardiac output and/or peripheral resistance
Reduced renal sodium excretion
Increased vascular resistance
Genetic factors
Environmental factors (life style and diet)
32. Vascular Pathology in Hypertension
Accelerates atherogenesis
Causes degenerative changes in the walls of large and
medium arteries that can lead to both aortic dissection
and cerebrovascular hemorrhage
Associated with two forms of small blood vessel
disease:
hyaline arteriolosclerosis and
hyperplastic arteriolosclerosis
33. MORPHOLOGY
Hyaline arteriolosclerosis
Associated with benign hypertension
Arterioles show homogeneous, pink hyaline thickening
with associated luminal narrowing
Hyperplastic Arteriolosclerosis
Occurs in severe hypertension
Vessels exhibit concentric, laminated (“onion-skin”)
thickening of the walls with luminal narrowing
Both are associated with luminal narrowing that may
cause downstream ischemic injury
37. Three general patterns with different clinical and
pathologic consequences
Arteriolosclerosis affects small arteries and arterioles
Mönckeberg medial sclerosis is characterized by
calcification of the walls of muscular arteries
Persons older than age 50 are most commonly affected
Usually not clinically significant
Atherosclerosis
the most frequent and clinically important pattern.
38. Atherosclerosis
Atherosclerosis is characterized by intimal lesions
called atheromas (also called atheromatous or
atherosclerotic plaques), that protrude into & obstruct
vascular lumens & weaken the vascular media
The constituents of the plaque include smooth muscle
cells, extracellular matrices, inflammatory cells, lipids
and necrotic debris
39. Epidemiology
Most prevalent among developed nations
Prevalence and severity of atherosclerosis and
ischemic heart disease among individuals and groups
are related to a number of risk factors (constitutional
and modifiable risk factors)
These risk factors have roughly multiplicative effect
40. Estimated 10-year rate of coronary artery disease in 55-year old men and
women as a function of established risk factors
42. Constitutional Risk Factors
Genetics
Family history is the most important independent risk factor
for atherosclerosis
Well -established familial predisposition to atherosclerosis
and ischemic heart disease is usually polygenic
Age
Between ages 40 and 60, the incidence of myocardial
infarction increases five-fold
Gender
Premenopausal women are relatively protected against
atherosclerosis
43. Modifiable Major Risk Factors
Hyperlipidemia and more specifically
hypercholesterolemia
Is a major risk factor for atherosclerosis
Even in the absence of other risk factors,
hypercholesterolemia is sufficient to initiate lesion
development
The major component of serum cholesterol associated with
increased risk is low-density lipoprotein (LDL) cholesterol
(“bad cholesterol”)
Higher levels of HDL (“good cholesterol”) correlate with
reduced risk.
44. Hypertension
can increase the risk for IHD by approximately 60%
Cigarette smoking
Smoking cessation reduces risk substantially
Diabetes mellitus
Induces hypercholesterolemia and markedly increases
the risk of atherosclerosis
Inflammation
45. Pathogenesis of Atherosclerosis
The “response to injury” hypothesis.
Atherosclerosis is a chronic inflammatory and healing
response of the arterial wall to endothelial injury
Lesion progression occurs through interaction of
modified lipoproteins, monocyte-derived
macrophages, and T lymphocytes with endothelial
cells and smooth muscle cells of the arterial wall
46. Atherosclerosis progresses in the following sequence:
Endothelial injury and dysfunction, causing
increased vascular permeability, leukocyte adhesion,
and thrombosis
Accumulation of lipoproteins (mainly LDL and its
oxidized forms) in the vessel wall
Platelet adhesion
Monocyte adhesion to the endothelium, followed by
migration into the intima and transformation into
macrophages and foam cells
47. Factor release from activated platelets, macrophages,
and vascular wall cells, inducing smooth muscle cell
recruitment, either from the media or from circulating
precursors
Smooth muscle cell proliferation, extracellular
matrix production and recruitment of T cells.
Lipid accumulation both extracellularly and within
cells (macrophages and smooth muscle cell)
48.
49.
50.
51.
52.
53. MORPHOLOGY
Fatty streaks.
Composed of lipid-filled foamy macrophages
Beginning as multiple minute flat yellow spots, they
eventually coalesce into elongated streaks 1 cm long or
longer
Not all fatty streaks are destined to progress to
atherosclerotic plaques
54.
55.
56. Atherosclerotic Plaque.
The key features of this lesion are intimal thickening
and lipid accumulation
White-yellow and encroach on the lumen of the artery
Superimposed thrombus over ulcerated plaques is red-
brown
Are patchy, usually involving only a portion of any given
arterial wall =>appear “eccentric” on cross section
57.
58.
59.
60.
61. The most extensively involved vessels are the lower
abdominal aorta, the coronary arteries, the popliteal
arteries, the internal carotid arteries, and the vessels of
the circle of Willis
Vessels of the upper extremities, mesenteric and renal
arteries, except at their ostia usually are spared
62. Atherosclerotic plaques have three principal
components:
(1) Cells (Smooth muscle cells, macrophages and T cells)
(2) Extracellular matrix including collagen, elastic fibers,
and proteoglycans and
(3) Intracellular and extracellular lipid
• The periphery of the lesions demonstrate
neovascularization
63.
64.
65. Atherosclerotic plaques are susceptible to the
following clinically important pathologic changes
Rupture, ulceration or erosion
Hemorrhage into a plaque
Atheroembolism
Aneurysm formation
66.
67. Consequences of Atherosclerotic Disease
Large elastic arteries and large and medium-sized
muscular arteries are the major targets of
atherosclerosis.
Myocardial infarction (heart attack), cerebral
infarction (stroke), aortic aneurysms, and peripheral
vascular disease (gangrene of the legs) are the major
consequences of atherosclerosis
68. The natural history, morphologic features, main
pathogenic events, and clinical complications of
atherosclerosis.
69. Atherosclerotic Stenosis
Atherosclerotic plaques can gradually occlude vessel
lumina, compromising blood flow and causing
ischemic injury
Critical stenosis is the stage at which the occlusion is
sufficiently severe to produce tissue ischemia
The effects of vascular occlusion ultimately depend on
arterial supply and the metabolic demand of the
affected tissue
70. Acute Plaque Change
Rupture/fissuring, exposing highly thrombogenic
plaque constituents
Erosion/ulceration, exposing the thrombogenic
subendothelial basement membrane to blood
Hemorrhage into the atheroma, expanding its
volume
71. The events that trigger abrupt changes in plaques and
subsequent thrombosis are complex and include both
intrinsic factors (e.g., plaque structure and
composition) and extrinsic factors (e.g., blood
pressure, platelet reactivity, vessel spasm)
Stable plaques tend to have a dense fibrous cap,
minimal lipid accumulation and little inflammation,
whereas “vulnerable” unstable plaques have thin
caps, large lipid cores, and relatively dense
inflammatory infiltrates.
72.
73.
74. Aneurysms and Dissections
Aneurysms are congenital or acquired dilations of the
heart or blood vessels that involve the entire thickness
of the wall
A “true” aneurysm
Involves an attenuated but intact arterial wall or thinned
ventricular wall of the heart
Eg. Atherosclerotic, syphilitic, and congenital vascular
aneurysms, as well as ventricular aneurysms that follow
transmural MI
75. A false aneurysm (pseudo-aneurysm)
A defect in the vascular wall leading to an extravascular
hematoma that freely communicates with the
intravascular space (“pulsating hematoma”).
Eg. ventricular rupture after myocardial infarction that is
contained by a pericardial adhesion, or a leak at the
sutured junction of a vascular graft with a natural artery
• An arterial dissection arises when blood enters a
defect in the arterial wall and tunnels between its
layers
76.
77. Aneurysms are classified by macroscopic shape and
size
Saccular aneurysms
• spherical outpouchings (involving only a portion of the
vessel wall)
• they vary from 5 to 20 cm in diameter and often contain
thrombi
Fusiform aneurysms
• involve diffuse, circumferential dilation of a long
vascular segment
• they vary in diameter (≤20 cm) and in length and can
involve extensive portions of the aortic arch, abdominal
aorta, or the iliacs
78.
79. Pathogenesis of Aneurysms
Aneurysms can occur when the structure or function
of the connective tissue within the vascular wall is
compromised
The intrinsic quality of the vascular wall
connective tissue is poor
The balance of collagen degradation and
synthesis is altered by inflammation and
associated proteases
The vascular wall is weakened through loss of
smooth muscle cells or the synthesis of
noncollagenous or nonelastic extracellular
matrix => cystic medial degeneration
80. The two most important causes of aortic aneurysms
are atherosclerosis and hypertension
Other causes include trauma, vasculitis, congenital
defects (eg. Berry aneurysm), and infections (mycotic
aneurysms)
81. Abdominal Aortic Aneurysm (AAA)
AAAs occur more frequently in men and in smokers,
rarely developing before age 50
Atherosclerosis is a major cause of AAA
82. MORPHOLOGY
Usually positioned below the renal arteries and above
the bifurcation of the aorta,
AAA can be saccular or fusiform,
Up to 15 cm in diameter, and up to 25 cm in length
There is severe complicated atherosclerosis with
destruction and thinning of the underlying aortic
media
The aneurysm frequently contains a bland, laminated,
poorly organized mural thrombus
83.
84.
85. Clinical Features
Most cases of AAA are asymptomatic
Rupture into the peritoneal cavity or retroperitoneal
tissues with massive, potentially fatal hemorrhage
The risk of rupture is directly related to the size of the
aneurysm
Obstruction of a vessel branching off from the aorta
resulting in ischemic injury to the supplied tissue
Embolism from atheroma or mural thrombus
Impingement on an adjacent structure
86. Thoracic Aortic Aneurysm
Most commonly associated with hypertension
These can present with signs and symptoms referable to
(1) respiratory difficulties due to encroachment on the
lungs and airways,
(2) difficulty in swallowing due to compression of the
esophagus,
(3) persistent cough due to compression of the recurrent
laryngeal nerves,
87. (4) Pain caused by erosion of bone (i.e., ribs and
vertebral bodies),
(5) cardiac disease as the aortic aneurysm leads to aortic
valve dilation with valvular insufficiency or narrowing
of the coronary ostia causing myocardial ischemia, and
(6) rupture
88. Aortic Dissection
Occurs when blood separates the laminar planes of the
media to form a blood-filled channel within the aortic
wall
Often ruptures outward, causing massive hemorrhage
89. Occurs principally in two groups of patients:
(1) Men aged 40 to 60 years with antecedent
hypertension (more than 90% of cases) and
(2) Younger adults with systemic or localized
abnormalities of connective tissue affecting the aorta
(e.g., Marfan syndrome).
90. Dissection is unusual in the presence of substantial
atherosclerosis or other cause of medial scarring
(medial fibrosis) such as syphilis
91. Pathogenesis
Hypertension is the major risk factor for aortic
dissection
Ischemic injury due to diminished flow through the
vasa vasorum causes degenerative changes of blood
vessels
Inherited or acquired connective tissue disorders with
defective vascular extracellular matrix
92. MORPHOLOGY
An aortic dissection usually initiates with an intimal
tear.
In the majority of spontaneous dissections, the tear
occurs in the ascending aorta, usually within 10 cm of
the aortic valve .
Such tears are typically transverse with sharp, jagged
edges up to 1 to 5 cm in length.
The dissection can extend retrograde toward the heart
as well as distally, sometimes into the iliac and femoral
arteries
Sometimes a new false vascular channel (“double-
barreled aorta”) created by second distal tear and
develop chronic dissections
93.
94. Clinical Features
The morbidity and mortality depend on part of the aorta
is involved
Accordingly, aortic dissections are generally classified into
two types
Type A (proximal) dissections
more common (and dangerous) lesions
involves the ascending aorta, either as part of a more
extensive dissection (DeBakey I) or in isolation (DeBakey
II)
Type B (distal or DeBakey III) dissections arise after the
take-off of the great vessels
95.
96. The classic clinical symptoms of aortic dissection are
the sudden onset of excruciating pain, usually
beginning in the anterior chest, radiating to the back
between the scapulae, and moving downward as the
dissection progresses; the pain can be confused with
that of myocardial infarction
The most common cause of death is rupture of the
dissection outward into any of the three body cavities
(i.e., pericardial, pleural, or peritoneal).
97.
98.
99. VASCULITIS
Vasculitis is a general term for vessel wall
inflammation.
The two most common pathogenic mechanisms of
vasculitis are
immune-mediated inflammation and
direct vascular invasion by infectious pathogens
100. Noninfectious Vasculitis
The main immunologic mechanisms underlying
noninfectious vasculitis are as follows:
Immune complex deposition
Anti-neutrophil cytoplasmic antibodies
Anti-EC antibodies
Autoreactive T cells
101. The systemic vasculitides are classified on the basis of
the size & anatomic site of the involved blood vessels ,
histologic characteristics of the lesion & clinical
manifestation.
101
102.
103. Giant-Cell (Temporal) Arteritis
a chronic inflammatory disorder, typically with
granulomatous inflammation,
principally affects large- to small-sized arteries in the
head
the temporal, vertebral and ophthalmic arteries, as
well as the aorta (giant-cell aortitis) are other common
sites of involvement
104. Clinical Features
• Rare before 50 years of age.
• Symptoms may be only vague and constitutional
• Facial pain or headache, most intense along the course
of the superficial temporal artery, which is painful to
palpation.
• Ocular symptoms abruptly appear in about 50% of
patients; these range from diplopia to complete vision
loss.
105. • Diagnosis depends on biopsy and histologic
confirmation.
• Treatment with corticosteroids is generally effective
105
111. Takayasu Arteritis
• A granulomatous inflammation of medium and larger
arteries characterized principally by ocular
disturbances and marked weakening of the pulses in
the upper extremities ( "pulseless disease").
share many of the clinical and histologic features of
giant cell aortitis
It occurs most frequently in women younger than 40
years of age.
111
112. • Takayasu arteritis manifests with transmural fibrous
thickening of the aorta-particularly the aortic arch and
great vessels-with severe luminal narrowing of the
major branch vessels.
• The cause and pathogenesis are unknown, although
immune mechanisms are suspected
112
114. Clinical Features
• Initial symptoms are usually nonspecific, including
fatigue, weight loss, and fever.
• With progression, vascular symptoms appear and
dominate the clinical picture.
• These include reduced blood pressure and weaker
pulses in the upper extremities relative to the lower
extremities, with coldness or numbness of the fingers;
• ocular disturbances, including visual defects, retinal
hemorrhages, and total blindness; and neurologic
deficits.
114
115. Polyarteritis Nodosa
• Polyarteritis nodosa (PAN) is a systemic vasculitis of
small or medium-sized muscular arteries
• typically involving renal and visceral vessels and spares
the pulmonary circulation.
• It is a segmental transmural necrotizing inflammation
• Kidney, heart, liver, and gastrointestinal tract vessels
are affected in descending order of frequency
115
117. Clinical Course
• PAN is a disease primarily of young adults, but it can
occur at all ages.
• The course can vary from acute to chronic but is
typically episodic, with long symptom-free intervals.
• The most common manifestations are malaise, fever,
and weight loss
117
118. A “classic” presentation involves involve some
combination
• hypertension, usually developing rapidly;
• abdominal pain and melena (bloody stool) caused by
vascular GI lesions;
• diffuse muscular aches and pains; and peripheral
neuritis, predominantly affecting motor nerves.
• Renal (arterial) involvement is common and a major
cause of death,
118
119. Wegener Granulomatosis (Granulomatosis With
Polyangiitis)
• is a necrotizing vasculitis characterized by a triad of
Acute necrotizing granulomas of the upper respiratory
tract (ear, nose, sinuses, throat) or the lower respiratory
tract (lung)
Necrotizing or granulomatous vasculitis affecting small
to medium-sized vessels (e.g., capillaries, venules,
arterioles, and arteries), most prominent in the lungs
and upper airways but affecting other sites as well
Renal disease in the form of focal necrotizing, often
crescentic, glomerulonephritis. 119
120. Pathogenesis
• Wegener granulomatosis probably represents some
form of cell-mediated hypersensitivity response,
possibly to an inhaled infectious or other
environmental agent
• c-ANCAs are present in up to 95% of cases; they are a
useful marker of disease activity, and may participate
in disease pathogenesis
120
121. Clinical Features
• Males are affected more often than are females, at an
average age of about 40 years.
• Classical features include persistent pneumonitis with
bilateral nodular and cavitary infiltrates (95%),
chronic sinusitis (90%), mucosal ulcerations of the
nasopharynx (75%), and evidence of renal disease
(80%).
• If untreated, the course of the disease is malignant;
80% of patients die within 1 year.
121
123. Thromboangiitis Obliterans (Buerger Disease)
Is characterized by segmental, thrombosing, acute and
chronic inflammation of medium- and small-sized
arteries,
Principally the tibial and radial arteries, with
occasional secondary extension into the veins and
nerves of the extremities
Occurs almost exclusively in heavy tobacco smokers
and usually develops before 35 years of age
123
124. Pathogenesis
• The strong relationship to cigarette smoking is
thought to involve direct toxicity to endothelium by
some tobacco products, or an idiosyncratic immune
response to the same agents
124
125. Clinical Features
• The early manifestations are a superficial nodular
phlebitis, cold sensitivity of the Raynaud type in the
hands, and pain in the instep of the foot induced by
exercise (so-called instep claudication).
• In contrast to the vascular insufficiency caused by
atherosclerosis, in Buerger disease the insufficiency
tends to be accompanied by severe pain, even at rest,
related undoubtedly to the neural involvement.
125
126. • Chronic ulcerations of the toes, feet, or fingers may
appear, perhaps followed in time by frank gangrene.
Abstinence from cigarette smoking in the early stages
of the disease often brings dramatic relief from further
attacks.
126
127. Infectious Vasculitis
• Localized arteritis may be caused by the direct
invasion of infectious agents, usually bacteria or fungi,
and in particular Aspergillus and Mucor species.
• Vascular invasion can be part of a more general tissue
infection (e.g., bacterial pneumonia or adjacent to
abscesses), or-less commonly-it may arise from
hematogenous spread of bacteria during septicemia or
embolization from infective endocarditis.
127
128. • Vascular infections can weaken arterial walls and give
rise to mycotic aneurysms or they can induce
thrombosis and infarction.
128
129. RAYNAUD PHENOMENON
• Results from an exaggerated cold-induced
vasoconstriction of digital arteries and arterioles.
• These vascular changes induce paroxysmal pallor or
cyanosis of the digits of the hands or feet; infrequently,
the nose, earlobes, or lips can also be involved.
129
130. • Characteristically, the involved digits show color
changes in the sequence white-blue-red , correlating
with vasoconstriction, cyanosis & vasodilation.
130
134. • Raynaud phenomenon may be a primary disease entity
or be secondary to a variety of conditions.
134
135. Primary Raynaud phenomenon
• Previously called Raynaud disease
• Reflects an exaggeration of central and local
vasomotor responses to cold or emotion
• Prevalence in the general population is 3% to 5% and a
predilection for young women.
135
136. Secondary Raynaud phenomenon
• refers to vascular insufficiency of the extremities in the
context of arterial disease caused by other entities
including SLE, scleroderma, Buerger disease, or even
atherosclerosis.
136
137.
138. Veins and Lymphatics
Varicose Veins
Varicose veins are abnormally dilated, tortuous veins
produced by prolonged, increased intraluminal
pressure leading to vessel dilation and incompetence
of the venous valves
10% to 30% of adults develop lower extremity
varicosities
Obesity and pregnancy increase risk by creating mass
effects that impede venous drainage
139.
140.
141. Clinical Features
Incompetence of the venous valves leads to stasis,
congestion, edema, pain, and thrombosis
Stasis dermatitis (also called “brawny induration”) and
ulcerations due to tissue ischemia
Poor wound healing and superimposed infections
142.
143. Thrombophlebitis and Phlebothrombosis
Venous thrombosis accompanied by inflammation
Involvement of deep leg veins accounts for more than
90% of cases
Virchow’s triad (venous stasis, systemic
hypercoagulability and turbulent blood flow) are
major risk factor of DVT
144. Congestive heart failure, neoplasia , pregnancy,
obesity, the postoperative state, and prolonged bed
rest or immobilization are the most important clinical
predispositions for deep vein thrombosis (DVT).
Genetic hypercoagulability syndromes can also be
associated with venous thrombosis.
145. Clinical features
Thrombi in legs tend to produce few, if any, reliable
signs or symptoms
Local manifestations, including distal edema,
cyanosis, superficial vein dilation, heat, tenderness,
redness, swelling and pain
Forced dorsiflexion of the foot (Homan sign) can elicit
pain in the calf muscle.
146.
147.
148. Vascular Tumors
Vascular neoplasms can be
Endothelial-derived
e.g. hemangioma, lymphangioma, angiosarcoma
Arise from cells that support or surround blood vessels
e.g. glomus tumor, hemangiopericytoma
149. Tumors of blood vessels and lymphatics range from
benign hemangiomas, to intermediate lesions that
are locally aggressive but infrequently metastatic, to
relatively rare, highly malignant angiosarcomas
Congenital or developmental malformations and non-
neoplastic reactive vascular proliferations (e.g.,
bacillary angiomatosis) can also present as tumor-like
lesions
152. Benign tumors
usually produce obvious vascular channels filled with
blood cells
lined by a monolayer of normal-appearing endothelial
cells
Malignant tumors
more cellular and more proliferative, and exhibit
cytologic atypia
they usually do not form well-organized vessels
153. Hemangioma
Constitute 7% of all benign tumors of infancy and
childhood
Localized lesions confined to the head and neck
Occasionally be more extensive (angiomatosis) and
can occur internally with nearly one-third being found
in the liver
Malignant transformation is rare
155. Capillary hemangiomas
the most common type
occur in the skin, subcutaneous tissues, and mucous
membranes of the oral cavities and lips, as well as in the
liver, spleen, and kidneys
Histologically, they are composed of thin-walled
capillaries with scant stroma
Juvenile (“strawberry type”) hemangioma
Occur in newborn and can be multiple
156. Cavernous hemangiomas
composed of large, dilated vascular channels
frequently involve deep structures
do not spontaneously regress
Pyogenic granulomas
are capillary hemangiomas
rapidly growing red pedunculated lesions on the skin,
gingival, or oral mucosa
Pregnancy tumor (granuloma gravidarum) is a pyogenic
granuloma that occurs in the gingiva of pregnant
women
157.
158. Lymphangiomas
benign lymphatic counterparts of hemangiomas
Simple (capillary) lymphangiomas
Cavernous lymphangiomas (cystic hygromas)
found in the neck or axilla of children, and in the
retroperitoneum
159.
160. Intermediate-Grade (Borderline) Tumors
Kaposi sarcoma (KS) is vascular neoplasm caused by
human herpes virus 8 (HHV8) that is highly associated
with acquired immunodeficiency syndrome (AIDS)
Four forms of KS are recognized, based on population
demographics and risks
Classic KS
Endemic African KS
Transplant-associated KS
AIDS-associated (epidemic) KS
161. Pathogenesis
All KS lesions are infected by human herpes virus 8
(HHV8)
Transmitted sexually and by poorly understood
nonsexual routes
HHV8 and altered T-cell immunity are likely required
for KS development
162. MORPHOLOGY
In classic KS (and sometimes in other variants), the
cutaneous lesions progress through three stages:
Patches
Plaques
nodular
163.
164. Malignant Tumors
Angiosarcoma is a malignant endothelial neoplasm
that primarily affects older adults
Occur at any site, but most often involves skin, soft
tissue, breast, and liver
Locally invasive and can readily metastasize
Editor's Notes
Saddle nose due to granulomatous distraction of nasal bones
