1

ARTERIOSCLEROSIS
SENILE ARTERIOSCLEROSIS
HYPERTENSIVE ARTERIOLOSCLEROSIS
● HYALINE ARTERIOLOSCLEROSIS
● HYPERPLASTIC ARTERIOLOSCLEROSIS
● NECROTISING ARTERIOLITIS
MÖNCKEBERG’S ARTERIOSCLEROSIS (MEDIAL CALCIFIC SCLEROSIS)
ATHEROSCLEROSIS

VASCULITIS
INFECTIOUS ARTERITIS
● ENDARTERITIS OBLITERANS
● SYPHILITIC ARTERITIS
● SYPHILITIC AORTITIS
● CEREBRAL SYPHILITIC ARTERITIS (HEUBNER’S ARTERITIS)
NON-SPECIFIC INFECTIVE ARTERITIS
NON-INFECTIOUS ARTERITIS
● POLYARTERITIS NODOSA
● HYPERSENSITIVITY VASCULITIS
● WEGENER’S GRANULOMATOSIS
● TEMPORAL (GIANT CELL) ARTERITIS
● TAKAYASU’S ARTERITIS (PULSELESS DISEASE)
● KAWASAKI’S DISEASE
● BUERGER’S DISEASE (THROMBOANGIITIS OBLITERANS)
MISCELLANEOUS HYPERSENSITIVITY VASCULITIS
● RAYNAUD’S DISEASE AND RAYNAUD’S PHENOMENON
ANEURYSMS
● ATHEROSCLEROTIC ANEURYSMS
● SYPHILITIC (LUETIC) ANEURYSMS
● DISSECTING ANEURYSMS AND CYSTIC MEDIAL NECROSIS
● FIBROMUSCULAR DYSPLASIA
 2

COMMON DISEASES OF VEINS

VARICOSITIES
● Varicose Veins
PHLEBOTHROMBOSIS AND THROMBOPHLEBITIS
Special Types of Phlebothrombosis
● THROMBOPHLEBITIS MIGRANS
● PHLEGMASIA ALBA DOLENS
● PHLEGMASIA CERULEA DOLENS
● SUPERIOR VENA CAVAL SYNDROME
● INFERIOR VENA CAVAL SYNDROME

DISEASES OF LYMPHATICS
LYMPHANGITIS
LYMPHOEDEMA

TUMOURS AND TUMOUR-LIKE LESIONS

BENIGN TUMOURS AND HAMARTOMAS
● HAEMANGIOMA
● CAPILLARY HAEMANGIOMA
● CAVERNOUS HAEMANGIOMA
● GRANULOMA PYOGENICUM
● LYMPHANGIOMA
● GLOMUS TUMOUR (GLOMANGIOMA)
● ARTERIOVENOUS MALFORMATIONS
● BACILLARY ANGIOMATOSIS AND PELIOSIS HEPATIS
INTERMEDIATE GRADE TUMOURS
● HAEMANGIOENDOTHELIOMA
MALIGNANT TUMOURS
● HAEMANGIOPERICYTOMA
● ANGIOSARCOMA
● KAPOSI’S SARCOMA
 3

Name/Definition Other information Etiology Pathogenesis Clinical features/Complication

MÖNCKEBERG’S an example of dystrophic age-related degenerative

ARTERIOSCLEROSIS
(MEDIAL CALCIFIC
SCLEROSIS)
calcification of the media of
large and medium-sized
muscular arteries, especially of
the extremities and of the
genital tract, in persons past the
age of 50.
calcification process
medial calcification also occurs
in some pathological states like
pseudoxanthoma elasticum and
in idiopathic arterial calcification
of infancy.
often an incidental finding in
X-rays.

ATHEROSCLEROSIS the most commonly affected Insudation hypothesis- SEQUELAE OR

thickening and hardening of
large and medium-sized
muscular arteries, primarily due
to involvement of tunica intima
and is characterised by
fibrofatty plaques or atheromas
are the aorta, the coronaries
and the cerebral arterial
systems.
Large arteries affected most
often are the aorta, renal,
mesenteric and carotids,
whereas the medium- and
small-sized arteries frequently
involved are the coronaries,
cerebrals and arteries of the
Major risk factors-
lower limbs.
1. Modifiable-
● Dyslipidaemias-
Abnormalities in plasma
lipoproteins.
hypercholesterolemia
has directly
proportionate
relationship with
atherosclerosis and
IHD.The atherosclerotic
plaques contain
cholesterol and
atherosclerosis is a form of COMPLICATIONS-
cellular proliferation of the 1. Heart (angina and myocardial
intimal cells resulting from infarction or heart attacks)
increased imbibing of lipids from 2. Brain (transient cerebral
the blood came to be called the ischaemia and cerebral infarcts
‘lipid theory’. Modified form of or strokes)
this theory is currently known as 3. Aorta—Aneurysm formation,
‘response to injury hypothesis’ thrombosis and embolisation to
other organs.
4. Small intestine—Ischaemic
Encrustation
bowel disease, infarction.
hypothesis- ​atheroma 5. Lower
represented a form of extremities—Intermittent
encrustation on the arterial wall claudication, gangrene.
from the components in
the blood forming thrombi
composed of platelets, fibrin
and leukocytes.
Reaction-to-Injury
Hypothesis-
original response to injury
theory→ endothelial injury →
 4
cholesterol esters, smooth muscle cell proliferation.
largely derived from the modified response-to-injury
lipoproteins in the blood. hypothesis- ​lipoprotein entry
Individuals with into the intima→ lipid
hypercholesterolaemia accumulation in macrophages
due to various causes (foam cells now)
such as in diabetes i) Endothelial injury-
mellitus, myxoedema, Caused mainly by→
nephrotic syndrome, von haemodynamic stress from
Gierke’s disease, hypertension and chronic
xanthomatosis and dyslipidemia.
familial ii) Intimal smooth muscle cell
hypercholesterolaemia proliferation-
have increased risk of Endothelial injury→ adherence,
developing aggregation and platelet release
atherosclerosis and IHD. reaction at exposed
a diet low in saturated subendothelial connective
fats and high in tissue→ infiltration of
poly-unsaturated fats inflammatory cells→ invading
and having omega-3 monocytes and macrophages
fatty acids (e.g. in fish, and activated platelets→ IL-1
fish oils etc) lowers the and TNF-a→ Proliferation of
plasma cholesterol intimal smooth muscle cells and
levels. familial production of extracellular
hypercholesterolaemia, Matrix AND local synthesis of
an autosomal growth factors-
codominant disorder, is @Platelet-derived growth factor
characterised by (PDGF) and fibroblast growth
elevated LDL cholesterol factor (FGF) stimulate
and normal triglycerides proliferation and migration of
and occurrence of smooth muscle cells from their
xanthomas and usual location in the media into
premature coronary the intima.
artery disease. It occurs @Transforming growth factor-β
due to mutations in LDL (TGF-β) and interferon (IFN)-γ
receptor gene. derived from activated T
● hypertension- doubles lymphocytes within lesions
the risk of all forms of regulate the synthesis of
cardiovascular disease. collagen by smooth muscle
 5
It acts probably by cells.
mechanical injury to the Endothelial cells→ nitric oxide
arterial wall due to and endothelin→ Smooth
increased blood muscle cell proliferation
pressure. Elevation of accompanied by synthesis of
systolic pressure of over matrix proteins—collagen,
160 mmHg or a diastolic elastic fibre proteins and
pressure of over 95 proteoglycans.
mmHg is associated with iii) Role of blood monocytes-
five times higher risk of Foam cell formation.(image
developing IHD below).
● diabetes mellitus- i​v) Role of dyslipidaemia-
association of type 2 may initiate endothelial injury
diabetes mellitus and dysfunction by causing
characterised by increased permeability.
metabolic (insulin hypercholesterolaemia with
resistance) syndrome increased serum concentration
and abnormal lipid profile of LDL promotes formation of
termed ‘diabetic foam cells
dyslipidemia’ is common v) Thrombosis-
and heightens the risk of Endothelial injury→ exposes
cardiovascular disease. subendothelial connective
Pathogenesis- tissue→ platelet aggregation→
endothelial dysfunction, smooth cell proliferation→ mild
increased aggregation of inflamatory reaction→ together
platelets, increased LDL with foam cells is incorporated
and decreased HDL. in the plaque.
● Smoking- due to lesions→ attaching fibrin and
reduced level of HDL, cells from blood→ enlarge→
deranged coagulation become part of plaque.
system and
accumulation of carbon Monoclonal
monoxide in the blood
Hypothesis-
that produces
based on the postulate that
carboxyhemoglobin and
proliferation of smooth muscle
eventually hypoxia in the
cells is the primary event and
arterial wall favouring
that this proliferation is
atherosclerosis.
monoclonal in origin similar to
2. Constitutional-
 6
increasing age(4th cellular proliferation in
decade and beyond), neoplasms.
male sex(high levels of Proliferated smooth muscle
oestrogen and cells→ have only one of the two
high-density lipoproteins forms of glucose-6-phosphate
in women), genetic dehydrogenase (G6PD)
abnormalities(Hereditary isoenzymes→ suggests
derangements of monoclonality. The monoclonal
lipoprotein metabolism), proliferation of smooth muscle
and familial and racial cells in atherosclerosis may be
predisposition. initiated by mutation caused by
Non-traditional emerging risk exogenous chemicals (e.g.
factors cigarette smoke), endogenous
1. environmental influences metabolites (e.g. lipoproteins)
2. Metabolic syndrome- and some viruses (e.g. Marek’s
obesity, insulin disease virus in chickens,
resistance, glucose herpesvirus).
intolerance, hypertension
3. exogenous hormones or
endogenous oestrogen
deficiency
4. Physical inactivity
5. Stressful lifestyle
6. Hypercystinaemia due to
elevated serum
homocysteine level from
low folate and vitamin
B12
7. Homocystinuria
8. Prothrombotic factors
and elevated fibrinogen
levels
9. infections, particularly of
Chlamydia pneumoniae
and viruses such as
herpesvirus and
cytomegalovirus
10. elevated C reactive
protein, an acute phase
 7
reactant
8

SYPHILITIC AORTITIS
WEGENER’S
GRANULOMATOSIS
another form of necrotising
vasculitis characterised by a
clinicopathologic triad consisting
of the following:
Syphilitic involvement of the
ascending aorta and the aortic
arch is the commonest
manifestation of cardiovascular
syphilis.
Preferential involvement of the
arch of aorta may be due to
involvement of mediastinal
lymph nodes in secondary
syphilis through which the
treponemes spread to
the lymphatics around the aortic
arch.
The lesions diminish in severity
in descending thoracic aorta
and disappear completely
at the level of the diaphragm
A limited form of Wegener’s
granulomatosis is the same
condition without renal
involvement.
Most commonly involved
organs are the lungs, paranasal
possibly the lesions occur due to
the presence of circulating
immune complexes. This is
supported by the observation of
subepithelial immuno globulin
deposits on the glomerular
9
a) Aortic aneurysm may result
from damage to the aortic wall .
b) Aortic valvular incompetence
used to be considered an
important sequelae of syphilis
but now-a-days rheumatic
disease is considered its more
important cause. The aortic
incompetence results from
spread of the syphilitic process
to the aortic valve ring.
c) Stenosis of coronary ostia is
seen may lead to progressive
myocardial fibrosis, angina
pectoris and sudden death.
Typical features include
pneumonitis with bilateral
infiltrates in the lungs, chronic
sinusitis, naso pharyngeal
ulcerations and renal disease.

i) Acute necrotising granulomas
of the upper and lower
respiratory tracts involving
nose, sinuses and lungs;
ii) focal necrotising vasculitis,
particularly of the lungs and
upper airways; and
iii) focal or diffuse necrotising
glomerulonephritis.
10
sinuses, nasopharynx and basement membrane and
kidneys. Other involved organs induction of remission by
are joints, skin, eyes, ears, immunosuppressive therapy.
heart and nervous system. The serum of these patients
Disseminated form of shows c-ANCA positivity.
Wegener’s granulomatosis
differs from a related entity,
idiopathic lethal midline
granuloma, in the sense that
the latter condition is highly
destructive and progressively
necrotic disease of the upper
airways.

RAYNAUD’S DISEASE
not a vasculitis but is a
functional vasospastic disorder
affecting chiefly small arteries
and arterioles of the extremities,
occurring in otherwise young
healthy females.
The disease affects most
commonly the fingers and
hands.
The ischaemic effect is
provoked primarily by cold but
other stimuli such as emotions,
trauma, hormones and drugs
also play a role.
probably occurs due to
vasoconstriction mediated by
autonomic stimulation of the
affected vessels.
Clinically, the affected digits
show pallor, followed by
cyanosis, and then redness,
corresponding to arterial
ischaemia, venous stasis and
hyperaemia respectively.
Long-standing cases may
develop ulceration and necrosis
of digits but occurrence of true
gangrene is rare.

RAYNAUD’S PHENOMENON differs from Raynaud’s disease

in having an underlying cause
e.g. secondary to
atherosclerosis, connective
tissue diseases like
scleroderma and SLE,
Buerger’s disease, multiple
myeloma, pulmonary
hypertension and ingestion of
ergot group of drugs.
also shows cold sensitivity but
differs from the latter in having
structural abnormalities in the
affected vessels.
 11

ANEURYSMS
permanent abnormal dilatation of a blood vessel occurring due to congenital or acquired
weakening or destruction of the vessel wall.
involve large elastic arteries, especially the aorta and its major branches.
Aneurysms can cause various illeffects such as thrombosis and thromboembolism, alteration in the flow of blood, rupture of the vessel and compression of
neighbouring structures.
CLASSIFICATION-
A. Depending upon the composition of the wall
1. True aneurysm composed of all the layers of a normal vessel wall.
2. False aneurysm having fibrous wall and occurring often from trauma to the vessel.
B. Depending upon the shape:
1. Saccular having large spherical outpouching.
2. Fusiform having slow spindle-shaped dilatation.
3. Cylindrical with a continuous parallel dilatation.
4. Serpentine or varicose which has tortuous dilatation of the vessel.
5. Racemose or circoid having mass of inter communicating small arteries and veins.
C. Based on pathogenetic mechanisms:
1. Atherosclerotic (arteriosclerotic) aneurysms are the most common type.
2. Syphilitic (luetic) aneurysms found in the tertiary stage of syphilis.
3. Dissecting aneurysms (Dissecting haematoma) in which the blood enters the separated or dissected wall of the vessel.
4. Mycotic aneurysms which result from weakening of the arterial wall by microbial infection.
5. Berry aneurysms which are small dilatations especially affecting the circle of Willis at the base of the brain

ATHEROSCLEROTIC most common form.
ANEURYSMS frequency increases after the
age of 50 year; more in males.
They are most common in the
abdominal aorta, so much so
that all forms of aneurysms of
the abdominal aorta (fusiform,
cylindrical and saccular) should
be considered atherosclerotic
until proved otherwise. Other
locations thoracic aorta, iliac
arteries and other large
systemic arteries.
severe atherosclerotic lesions
severe atherosclerotic
lesions→thinning and
destruction of the medial elastic
tissue → atrophy and
weakening of the wall.
In thoracic aorta medial
degenerative lesions may be
involved.
12
EFFECTS OR
COMPLICATIONS
1. Rupture
most serious and fatal
complication. Rupture of
abdominal aneurysm may occur
either into the peritoneum or
into the retroperitoneum
resulting in sudden and massive
bleeding. Occasionally, there
may be slow progressive leak
from the aneurysm. A ruptured
aneurysm is more likely to get
infected.
2. ​Compression
The atherosclerotic aneurysm
may press upon some adjacent
structures such as compression
of ureter and erosion on the
vertebral bodies.
3. Arterial occlusion

SYPHILITIC (LUETIC) Cardiovascular syphilis→
ANEURYSMS causes arteritis—syphilitic
aortitis and cerebral arteritis.
The predominant site of
involvement is the thoracic
aorta, especially in the
ascending part and arch of
aorta.
DISSECTING ANEURYSMS The most common site is the
AND CYSTIC MEDIAL aorta and is an acute
major complications of syphilitic
aortitis is syphilitic or luetic
aneurysm→ tertiary stage of
syphilis.
i) Hypertensive state
ii) Non-hypertensive cases
inflammatory infiltrate around
the vasa vasorum of the
adventitia→ endarteritis
obliterans→ ischaemic injury to
the media→ destruction of the
smooth muscle and elastic
tissue of the media→ scarring
weakened aortic media.
13
Atherosclerotic aneurysms of
the abdominal aorta may
occlude the inferior mesenteric
artery, or there may be
development of occlusive
thrombosis. However, collateral
circulation develops slowly and
is nearly always sufficient so as
not to produce effects of
ischaemia.
4. Thromboembolism​ is rather
common in abdominal
aneurysms.
1. Rupture
massive and fatal haemorrhage
into the pleural cavity,
pericardial sac, trachea and
oesophagus.
2. Compression
cause symptoms such as on
trachea causing dyspnoea, on
oesophagus causing dysphagia,
on recurrent laryngeal nerve
leading to hoarseness; and
erosion of vertebrae, sternum
and ribs due to persistent
pressure.
3. Cardiac dysfunction
When the aortic root and valve
are involved, syphilitic
aneurysm produces aortic
incompetence and cardiac
failure. Narrowing of the
coronary ostia may further
aggravate cardiac disease.
excruciating tearing pain in the
chest moving downwards.

NECROSIS
dissecting haematoma in which
the blood enters the separated
(dissected) wall of the vessel
and spreads for varying
distance longitudinally.
THROMBOPHLEBITIS
MIGRANS
multiple venous thrombi that
disappear from one site so as to
appear at another site.
catastrophic aortic disease.
In women, dissecting
aneurysms may occur during
pregnancy
migratory thrombophlebitis or
Trousseau’s syndrome
seen most often in disse mi
nated visceral cancers (e.g.
cancer of lungs, prostate,
female reproductive tract,
breast, pancreas and
gastrointestinal tract) as part of
paraneoplastic syndrome and
a) Marfan’s syndrome, an
autosomal dominant disease
with genetic defect in fibrillin
which is a connective tissue
protein required for elastic tissue
formation.
b) Development of cystic medial
necrosis of Erdheim, especially
in old age. c) Iatrogenic trauma
during cardiac catheterisation or
coronary bypass surgery.
d) Pregnancy, for some
unknown reasons.
14
Medial necrosis→ COMPLICATIONS-
haemodynamic factors cause 1. Rupture
tear in intima→ dissecting Haemorrhage from rupture of a
aneurysms. dissecting aneurysm in the
ascending aorta results in
mortality. Most often,
haemorrhage occurs into the
pericardium; less frequently it
may rupture into the thoracic
cavity, abdominal cavity or
retroperitoneum.
2. Cardiac disease
Involvement of the aortic valve
results in aortic incompetence.
Obstruction of coronaries
results in ischaemia causing
fatal myocardial infarction.
Rarely, dissecting aneurysm
may extend into the cardiac
chamber.
3. Ischaemia
Obstruction of the branches of
aorta by dissection results in
ischaemia of the tissues
supplied. Thus, there may be
renal infarction, cerebral
ischaemia and infarction
of the spinal cord.
 15
is also found in nonbacterial
thrombotic endocarditis.

CAPILLARY HAEMANGIOMA Haemangiomas are quite regress spontaneously within a

common lesions, especially in few years
infancy and childhood.
most common type.
Strawberry birthmarks and
‘port-wine mark’ are some good
examples. The common sites
are the skin, subcutaneous
tissue and mucous membranes
of the oral cavity and lips. Less
common sites are internal
visceral organs like liver, spleen
and kidneys.

CAVERNOUS HAEMANGIOMA
They are most common in the rarely involute spontaneously.
skin (especially of the face and
neck); other sites are mucosa
of the oral cavity, stomach and
small intestine, and internal
visceral organs like the liver
and spleen.

KAPOSI’S SARCOMA
malignant angiomatous tumors
frequent occurrence in patients
with HIV/AIDS.
CLASSIFICATION-
1. Classic (European)
Kaposi’s sarcoma
more common in men over 60
years of age. slow growing and
appears as multiple, small,
purple, dome shaped nodules
or plaques in the skin,
especially on the legs.
Involvement of visceral organs
rarely.
2. African (Endemic) Kaposi’s
opportunistic neoplasm in
immunosuppressed patients
which has excessive
proliferation of spindle cells of
vascular origin having features
of both endothelium and smooth
muscle cells:
i) ​Epidemiological studies
have suggested a viral
association implicating HIV and
human herpesvirus 8 (HSV 8,
also called Kaposi’s sarcoma-
associated herpesvirus or
KSHV).
largely confined to skin and the
course is generally slow and
insidious with long survival. →
classic forms
rapidly progressive course,
often with widespread
cutaneous as well as visceral
involvement, and high mortality.
→ endemeic and epidemic
sarcoma

sarcoma
found in younger age,
especially in boys and young
men and has a more
aggressive course than the
classic form. The disease
begins in the skin but grows
rapidly to involve other tissues,
especially lymph nodes and the
gut.
3. Epidemic
(AIDS-associated) Kaposi’s
sarcoma
30% cases of AIDS, especially
in young male homosexuals
than the other high-risk groups.
The cutaneous lesions are not
localised to lower legs but are
more extensively distributed
involving mucous membranes,
lymph nodes and internal
organs early in the course of
disease.
4. Kaposi’s sarcoma in renal
transplant cases
associated with recipients of
renal transplants who have
been administered
immunosuppressive therapy for
a long time.
Name Macroscopy
16
ii) Occurrence of Kaposi’s
sarcoma involves ​interplay of
HIV-1 infection, HHV-8
infection​, activation of the
immune system and secretion
of cytokines (IL-6, TNF-α,
GM-CSF, basic fibroblast factor,
and oncostain M). Higher
incidence of Kaposi’s sarcoma
in male homosexuals is
explained by increased
secretion of cytokines by their
activated immune system.
iii) ​Defective immune
regulation​ plays a role in its
pathogenesis is further
substantiated by observation of
second malignancy (e.g.
leukaemia, lymphoma and
myeloma) in about one-third of
patients with Kaposi’s sarcoma.
Microscopy Diagram

MÖNCKEBERG’S The deposition of calcium salts in the
ARTERIOSCLEROSIS media pro duces pipestem-like rigid
(MEDIAL CALCIFIC tubes without causing
SCLEROSIS) narrowing of the lumen.
ATHEROSCLEROSIS 1. FATTY STREAKS AND DOTS
on the intima by themselves are
harmless but may be the precursor
lesions of atheromatous plaques. They
are especially prominent in the aorta
and other major arteries, more often on
the posterior wall than the anterior wall.
the lesions may appear as flat or
slightly elevated and yellow. They may
be either in the form of small, multiple
dots, about 1 mm in size, or in the form
of elongated, beaded streaks
2. GELATINOUS LESIONS
in the intima of the aorta and other
major arteries in the first few months of
life. Like fatty streaks, they may also be
precursors of plaques. They are round
or oval, circumscribed grey elevations,
17
deposits of calcium salts in the media
without associated inflammatory
reaction while the intima and
the adventitia are spared.
May coexist with changes of
atherosclerosis.
Smooth muscle of media is replaced by
acellular hyalinised fibrous tissue.
Foci of dystrophic calcification are seen
in the media as basophilic coarse
granules.
1. FATTY STREAKS AND DOTS
fatty streaks lying under the
endothelium are composed of
closely-packed foam cells, lipid-
containing elongated smooth muscle
cells and a few lymphoid cells.
Small amount of extracellular lipid,
collagen and proteoglycans are also
present.
2. GELATINOUS LESIONS
gelatinous lesions are foci of increased
ground substance in the intima with
thinned overlying endothelium
3. ATHEROMATOUS PLAQUES
i) Superficial luminal part of the fibrous
cap is covered by endothelium, and is
composed of smooth muscle cells,
dense connective tissue and

about 1 cm in diameter.
3. ATHEROMATOUS PLAQUES-
also called fibrous plaque, fibrofatty
plaque or atheroma. It's a fully
developed atherosclerotic lesion.
Unlike fatty streaks, atheromatous
plaques are selective in different
geographic locations and races and are
seen in advanced age. These lesions
may develop from progression of early
lesions of atherosclerosis.
Most often and most severely affected
is the abdominal aorta, though smaller
lesions may be seen in descending
thoracic aorta and aortic arch.
white to yellowish-white lesions, varying
in diameter from 1-2 cm and raised on
the surface.
Cut section of the plaque reveals the
luminal surface as a firm, white fibrous
cap and a central core composed of
yellow to yellow-white, soft,
porridge-like material and hence the
name atheroma.
4. COMPLICATED PLAQUES- Various
pathologic changes that occur in
fully-developed atheromatous plaques.
Basically complications.
i) Calcification- especially in the aorta
and coronaries. The diseased intima
cracks like an egg-shell when the
vessel is incised and opened.
ii) Ulceration- The layers covering the
soft pultaceous material of an atheroma
18
extracellular matrix containing
proteoglycans and collagen.
ii) Cellular area under the fibrous cap is
comprised by a mixture of
macrophages, foam cells, lymphocytes
and a few smooth muscle cells which
may contain lipid.
iii) Deeper central softcore consists of
extracellular lipid material, cholesterol
clefts, fibrin, necrotic debris and lipid
laden foam cells.
iv) In older and more advanced lesions,
the collagen in the fibrous cap may be
dense and hyalinised, smooth muscle
cells may be atrophic and foam cells
are fewer.
v) Calcium salts are deposited in the
vicinity of necrotic area and in the lipid
pool deep in the thickened intima.
4. COMPLICATED PLAQUES-
i) Calcification- the calcium salts are
deposited in the vicinity of necrotic area
and in the soft lipid pool deep in the
thickened intima. This form of athero
sclerotic intimal calcification differs from
Mönckeberg’s medial calcific
arteriosclerosis that affects only the
tunica media
ii) Ulceration
iii) Thrombosis
iv) Haemorrhage- The haematoma
formed at coronary artery plaque after
rupture contains numerous
hemosiderin-laden macrophages.
v) Aneurysm formation-

may ulcerate as a result of
haemodynamic forces or mechanical
trauma. This results in discharge of
emboli composed of lipid material and
debris into the bloodstream, leaving a
shallow, ragged ulcer with yellow lipid
debris in the base of the ulcer. Causes
thromboembolic occlusion.
19
The changes in media include atrophy
and thinning of the media and
fragmentation of internal elastic lamina.
The adventitia undergoes fibrosis and
some inflammatory changes. These
changes cause weakening in the
arterial wall
resulting in aneurysmal dilatation.

iii) Thrombosis-The ulcerated plaque

and the areas of endothelial damage
are vulnerable sites for formation of
superimposed thrombosis. →
dislodged→ emboli; or organised→
mural thrombi→ occlusion→ may
recanalise.

iv) Haemorrhage- either from the blood

in the vascular lumen through an
ulcerated plaque, or from rupture of
thin-walled capillaries that vascu larise
the atheroma from adventitial vasa
vasorum.

v) Aneurysm formation-
advanced lesions are associated with
secondary changes in the media and
adventitia.

SYPHILITIC AORTITIS the affected part of the aorta may be
dilated, and its wall somewhat
thickened and adherent to the
neighbouring mediastinal structures.
Longitudinally opened vessels show
intimal surface studded with
pearly-white thickenings.
These lesions are separated by
wrinkled normal intima, giving it
characteristic tree-bark appearance.
i) Endarteritis and periarteritis of the
vasa vasorum located in the media and
adventitia.
ii) Perivascular accumulation of plasma
cells, lymphocytes and macrophages
that may form miliary gummas which
undergo necrosis and are replaced by
scar tissue.
iii) Intimal thickenings consist of dense
avascular collagen that may undergo

Cut section of the lesion shows more
firm and fibrous appearance than the
atheromatous plaques. However,
superimposed atherosclerotic lesions
may be present.
WEGENER’S
GRANULOMATOSIS
RAYNAUD’S DISEASE
RAYNAUD’S PHENOMENON
ATHEROSCLEROTIC They may be of variable size but are
ANEURYSMS often larger than 5-6 cm in diameter.
Atherosclerotic aneurysm is most
frequently fusiform in shape and the
lumen of aneurysm often contains
mural thrombus.
20
hyalinisation and calcification.
the characteristic feature of Wegener’s
granulomatosis is the presence of
necrotising granulo matous
inflammation of the tissues and
necrotising vasculitis with or without
granulomas:
i) The granulomas consist of fibrinoid
necrosis with extensive infiltration by
neutrophils, mononuclear cells,
epithelioid cells, multinucleated giant
cells and fibro blastic proliferation.
ii) The necrotising vasculitis may be
segmental or circumferential.
iii) The renal lesions are those of focal
or diffuse necrotizing
glomerulonephritis.
no pathologic changes are observed in
the affected vessels.
long-standing cases may show
endothelial proliferation and intimal
thickening.
segmental inflammation and fibrinoid
change in the walls of capillaries.
the wall of atherosclerotic aneurysm
loses its normal arterial structure.
Instead, there is a predominance of
fibrous tissue in the media and
adventitia with mild chronic
inflammatory reaction. The intima and
inner part of the media show remnants
 21
of atheromatous plaques and mural
thrombus.

SYPHILITIC (LUETIC) saccular in shape and usually 3-5 cm in
ANEURYSMS diameter. Less often, they are fusiform
or cylindrical.
The intimal surface is wrinkled and
shows tree-bark appearance.
When the aortic valve is involved, there
is stretching and rolling of the
valve-leaflets producing valvular
incompetence and left ventricular
hypertrophy due to volume overload.
This
results in massively enlarged heart
called ‘cor bovinum’.
The adventitia shows fibrous thickening
with endarteritis obliterans of vasa
vasorum.
The fibrous scar tissue may extend into
the media and intima.
Rarely, spirochaetes may be
demonstrable in syphilitic aneurysm.
Often, mural thrombus is found in the
aneurysm.

DISSECTING ANEURYSMS no significant dilatation. Therefore, it is characteristic features of cystic medial

AND CYSTIC MEDIAL currently referred to as ‘dissecting necrosis are found:
NECROSIS haematoma’. i) Focal separation of the fibromuscular
sharply-incised, transverse or oblique and elastic tissue of the media.
intimal tear, 3-4 cm long, most often ii) Numerous cystic spaces in the
located in the ascending part of the media containing basophilic ground
aorta. substance.
The dissection is seen most iii) Fragmentation of the elastic tissue.
characteristically between the outer and iv) Increased fibrosis of the media.
middle third of the aortic media so that
the column of blood in the dissection
separates the intima and inner two-third
of the media on one side from the outer
one-third of the media and the
adventitia on the other.
In about 10% of dissecting aneurysms,
a second intimal tear is seen in the
distal part of the dissection so that the
blood enters the false lumen through
the proximal tear and reenters the true
lumen through the distal tear. If the
 22
patient survives, the false lumen may
develop endothelial lining
and ‘double-barrel aorta’ is formed.
Two types:
1. Type A dissections: They have
proximal lesions involving either both
the ascending and descending aorta or
only the ascending aorta (types I and II
of the DeBakey classification). It is
more common but dangerous.
2. Type B dissections: They have distal
lesions which do not involve the
ascending part and usually begin distal
to the subclavian artery (DeBakey type
III).

CAPILLARY HAEMANGIOMA small or large, flat or slightly elevated,
red to purple, soft and lobulated lesions
well-defined but unencapsulated
lobules.
These lobules are composed of
capillary-sized, thin-walled, blood-filled
vessels.
These vessels are lined by single layer
of plump endothelial cells surrounded
by a layer of pericytes. The vessels are
separated by some connective tissue
stroma

CAVERNOUS HAEMANGIOMA single or multiple, discrete or diffuse,
red to blue, soft and spongy masses.
KAPOSI’S SARCOMA the lesions in the skin, gut and other
organs form prominent, irregular,
purple, dome-shaped plaques or
nodules.
23
composed of thin-walled cavernous
vascular spaces, filled partly or
completely with blood.
The vascular spaces are lined by
flattened endothelial cells.
They are separated by scanty
connective tissue stroma
changes are nonspecific in the early
patch stage- irregular vascular spaces
separated by interstitial inflammatory
cells and extravasated
blood and hemosiderin.
and more characteristic in the late
nodular stage- slit-like vascular spaces
containing red blood cells and
separated by spindle-shaped, plump
tumour cells. These spindle-shaped
tumour cells are probably of endothelial
origin.