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CARDIOVASCULAR
SYSTEM
The cardiovascular system includes the heart,
arteries, veins, capillaries as well as lymphatic.
The function of cardiovascular system is essential in
maintaining life and health through providing of nutrients, oxygen etc to the
tissues as well as removal of waste products from them
Congenital
cardiovascular anomalies
Definition
Congenital
anomalies of heart and great vessels simply defined as an abnormality present
from birth. Animals with severe defects are unable to survive in utero, while those of the mildest lesions may have no
clinical signs. However, the intermediate lesions show gradually developing
signs of cardiac failure. A range of congenital developmental anomalies may
occur affecting the muscle valves and
vessels.
Frequency and etiology
• Cardiovascular anomalies are reported in all
species of animals, but most frequent in dog, cat and cattle.
• In most cases there is no identifiable cause. Many
cases result from action of many teratogens in the
first trimester of pregnancy as drugs and toxins.
Classification
Cardiac anomalies can divided into the following:
1) Complete absence of the organ.
It's called acardius
amorphous means absence of the heart. It's occur in incomplete twining in
catties
2-Defet that allow shunting of blood from
right to left
•Persistent truncus arteriosus resulting from failure of aorta and pulmonary
artery and persisting as a single blood vessel.
• Transportation of great arteries as aorta and
pulmonary artery (Fig.1 ).
Fig.1:
Heart showing gross picture of Transportation of great arteries as aorta
and pulmonary artery.
3- Left to right shunt
•
Patent ductus arteriosus
(blood shunt from aorta to pulmonary artery) (Fig.2).
•
Arterial septal defect (persistent foramen ovale between the two atria). This foramen is closed
directly after birth (at 3 month of life).
•
Ventricular septal defect.
Fig. 2:
Heart showing patent
ductus arteriosus .
4- Defect that lead to obstruction of
blood flow
•
Subaortic stenosis.
•
Coarctation (narrowing) of aorta.
•
Pulmonary stenosis.
5- Valvular
defects that may lead to obstruction or regurgitation
• Valvular stenosis.
• Vulvular insufficiency.
6- Abnormal arterial and venous
connection
• Persistent right aortic arch
• Double aortic arch.
7- Malpositions
of the heart “Ectopia cordis”
It is a rare condition in which the entire heart lies outside the thorax as ectopia
cordis cervicals where
the hart displaced in to the neck.
Heart
The heart is a conical muscular organ composed of
four chambered pumps with four valves.
The heart wall consists of three layers. The outer
layer is lined by the visceral pericardium. The endocardium
is the inner layer of the heart and is lined by endothelial cell lying on
thin layer of connective tissue. The third layer is the myocardium which is
the prominent muscular layer of the heart and composed of cardiac muscle. The
myocardial thickness is related to the pressure present in each chamber. The
atria are thin and the ventricles are thick.
Regeneration and repair
• Regeneration of cardiac muscle cells is generally
not occur. Rarely in very young animals especially avian limited myocytes
regeneration occurs.
• Necrosis of cardiac muscle is followed by leukocytic invasion and fibroblastic proliferation.
Cardiac failure
Definition
The
term heart failure indicate that the inability of cardiac output to maintain
adequate circulation sufficient to meet the requirements of the body tissues.
Circulatory failure could result from heart disease or peripheral circulatory
failure as blood vessel disease and shock.
Causes
A. Primary causes
• Congenital anomalies.
•Valvular diseases
(congenital and acquired) as stenosis and
insufficiency.
• Infectious myocarditis
• Nutritional deficiencies and certain poisons.
• Pericarditis.
B. Precipitating causes
• Infectious disease.
• Anemia.
• Hyperthyroidism.
Pathogenesis
The various condition resulted in
decrease cardiac output through damaged myocardium, or through increased resistance
to blood flow as in pulmonary hypertension or through in adequate ventricular
filling as in case of valvular diseases and through
inability of heart to expand and fill as in case of pericarditis.
• Compensatory mechanisms
1- In acute heart failure the animal may be die without compensatory mechanisms.
2- However, when animal is survive
the initial insult, several mechanisms help to maintain adequate cardiac
output.
a) Cardiac dilatation lead
to increase diastolic volume.
b) Generalized vasoconstriction as a result of
increase secretion of renin and angiotensin.
c) Increase blood volume due to release of aldosterone which cause increase tubular reabsorption of water and sodium.
Classification of heart failure
I. Acute heart failure
Definition
It is sudden cessation of effective cardiac
contraction leading to brain death.
Causes
• Acute myocarditis.
• Cardiac tamponade.
•Sudden occlusion of pulmonary artery or aorta.
•Severe electrolytes imbalance and certain poisons.
Lesions
1- Dilated ventricles.
2- Pulmonary and systemic congestion without edema.
II. Chronic heart failure (congestive
heart failure)
It is the failure of the heart to maintain adequate
circulation, which persist for long time due to diminished output (forward failure)
or backing up of blood (back failure). The chronic heart failure divided
into:
a) Left side heart failure
Cause
The cause present in heart as damaged myocardium, valvular diseases, anomalies and hypertension.
Lesions
• Dilatation and hypertrophy of left ventricle.
• Alveolar hemorrhage with presence of heart failure
cells.
• Thickening of alveolar wall and hypertrophied of
alveolar lining cells.
• Hydrothorax and ascites.
b) Right side heart failure (Core pulmonale, high altitude or Brisket disease)
Cause
• Pulmonary diseases as emphysema, pulmonary
embolism, chronic fibrosing pneumonia.
• Disorders in tricuspid and pulmonary valves.
Lesions
• Chronic passive congestion of viscera (liver
spleen, intestine).
• Edema especially subcutis,
ascites, hydrothorax due to increase hydrostatic
pressure.
N.B.: The right and left cardiac failure lead to
other and lead to total heart failure.
Pericardial
diseases
The pericardial
cavity may contain excess serous fluid, blood or inflammatory exudate. Sudden distension of the pericardial sac results
in pressure on atria, especially the right, and prevents cardiac expansion
due to pressure from outside. The condition is termed as cardiac tamponade.
I. Accumulation of non inflammatory fluid in pericardial sac
1- Hydropericardium
(pericardial effusion)
It is the accumulation of fluid in pericardial sac. Serous
fluid (hydropericardium) may
accumulate in the pericardial sac in case of congestive cardiac
failure, in anemia or toxemia and may occur with a mesothelioma.
N.B. Normally there is about 30-50 ml
fluid in human pericardial sac.
The fluid may be serous, serosanguineous
or chylous.
Causes
1. Diseases lead to generalized edema as congestive
heart failure, pulmonary hypertension, renal
failure.
2. Associated with some systemic diseases as heart
water disease in cattle, African horse sickness in equine.
Sequelae
1. Hydropericardium of
rapid onset lead to cardiac tamponade.
2. The one with slow onset is usually without clinical
signs.
3. If the cause removed, prognosis favorable.
2. Hemopericardium
It is
the accumulation of whole blood in pericardial sac.
Cause
Hemopericardium is uncommon but
is a result of hemorrhage resulted from traumatic perforation of heart spontaneous
atrial rupture in dog, Intrapericardial
rupture in horse and from hemangiosarcoma
affecting the right atrium, in older dogs particularly German shepherd dogs.
Sequelae
Death occurs due to cardiac tamponade.
II. Metabolic alteration
1. Visceral gout in birds and snakes.
2. Focal melanosis in sheep
and goat.
3. Serous atrophy of fat (Fig.3).
Fig. 3: Pericardium showing serous atrophy of
fat. H&E.
III. Inflammation (pericarditis)
Infection of the pericardial sac may
occur as part of systemic infection in any species. It may also be an
extension of infection/inflammation of the pleura.
A range of types can occur
including serous, fibrinous or fibrino-purulent;
the latter are only common in farm species. Primary pericarditis
is rare. It is usually secondary to disorders in or about the heart.
Classification of pericarditis
1-Serous pericarditis
It is characterized by accumulation of protein rich
fluid (inflammatory fluid) in pericardial sac.
Microscopic appearance
-Hyperemia of pericardial vessels.
-Serous exudate
mixed with inflammatory cells were seen.
Sequelae
• If cause remove, reabsorption of exudate and
regeneration occurs.
• It occurs slowly and therefore rarely produce pressure upon the heart.
2-Serofibrinous and fibrinous
pericarditis
It is the most encountered forms in animal. It is
usually hematogenous infection and associated with
diseases as pasteurellosis, bovine pleuropneumonia and feline peritonitis
.
Macroscopic appearance
The pericardial sac filled with serous and fibrin exudate (Fig.4). Moreover, yellowish fibrin deposits
covered the pericardial surface leading to adherence of visceral and parietal
layers (bread and butter heart).
Microscopic appearance
Eosinophilic granular fluid mixed with fibrin and neutrophils lies over congested pericardium (Fig.ures 5&6 ).
Fig. 4: Pericardium showing gross picture fibrinous
pericarditis. The pericardial sac become thickened and grayish white in
color.
Fig. 5: Pericardial sac filled
with serous and fibrinous exudate
which infiltrated with inflammatory cells.
The myocardium showing hyaline degeneration. H&E.
Fig. 6: Pericardial sac filled
with serofibrinous exudates and infiltrated with neutrophils. Some fibrin threads showing hyaline
degeneration. H&E.
3-Fibrino -purulent pericarditis
Purulent
and fibrin exudate fills the pericardial space (Fig.
7). Healing by organization resulting in constrictive fibrosing
pericarditis. In cattle, pericarditis
is particularly associated with traumatic reticulitis
and large amounts of pus, fibrin and gas develop.
4. Constrictive pericarditis
It is chronic inflammation accompanied by extensive
fibrous proliferation and adhesion between the two layers of pericardium.
Sequelae
It lead to congestive heart failure.
Fig.
7: Pericardium microscopic picture showing replacement of myocardial sac
with fibrinopurulent exudate. H&E.
Myocardium
Myocardial degeneration
Degeneration (or
necrosis) of myocardial muscle (Figs 8 & 9)
may occur along with similar changes in other tissues or other muscle. The
response to many non specific causes. Myocardial
degeneration including hydropic degeneration, fatty
change and atrophy occurs in variety of systemic diseases especially with
fever, anemia and toxemia.
Hyaline
degeneration due to vitamin E or selenium deficiency is common in young
animals where the muscle appears pale (white muscle disease).
Fig. 8:
Gross picture of heart showing cardiac
degeneration. The degenerated muscles appear grayish in color.
Fig. 9: Myocardium showing hyaline degeneration
represented microscopically by hyaline degeneration of some muscle
fibers. H&E.
Infiltration
•
Fatty infiltration is the increased numbers of adipocytes
interposed between myocardial muscles fibers. It is associated with obesity.
•
Glycogen infiltration in diabetic dogs.
Necrosis and mineralization
Focal to massive
myocardial necrosis is a common lesion in necropsy material (Fig.10). The
necrosis may be the outcome of a wide variety of causes of injury including:
Fig.
10: Heart showing necrosis of some muscle fibers.
H&E.
1-Nutrional
deficiencies. Dystrophic calcification may occur of degenerate heart muscle
associated with vitamin E or selenium deficiency.
2-Infectious
diseases as foot and mouth disease in calves, piglets and lamb, tuberculosis
and ovine caseous lymphadenitis (Fig.11).
Fig.11:
Myocardium showing
necrosis (necrotic myocarditis). The necrotic muscle fibers are infiltrated
with lymphocytes. H&E.
3-Chemical
and plant toxins. Moreover, Metastatic
calcification due to Vitamin D toxicity and may be caused by ingestion of
plants containing vitamin D analogues.
4-Physical
injuries as trauma and shock.
5-Ischemic necrosis as in case of coronary
embolism.
Disturbances in
circulation
1-Infarction
It occurs in coronary embolism, disseminated intravascular
coagulation and in inflammatory vascular diseases as periarteritis
nodosa.
Macroscopic picture
The affected area appear pale first and may be
progress to prominent yellow to white dry gritty area of dystrophic
calcification (Fig.12).
Fig. 12:
Myocardial
infarction represented by pale grayish areas.
Microscopic picture
1. In recent necrosis fibers appear swollen and hypereosinophilic
beside indistinct striations and pyknotic nuclei.
2. Necrotic areas are infiltrated by inflammatory cells, mainly macrophages and
few neutrophils, by 24 to 48 hours after injury.
3. The healing phase is characterized by interstitial fibroblast proliferation
and deposition of collagen fibers (scars).
Sequelae
• If the necrotic area is small, it replaced by
granulation tissue and healing occur.
• If large area, it lead to aneurysm or rupture.
2. Active hyperemia
It associated with septicemic
diseases.
3. Passive hyperemia
It associated with general passive hyperemia.
4. Hemorrhage. It is often occurs in pig
leading to the term “mulberry heart” disease (Fig.13 )
5. Edema. Perivascular edema
is seen in heart associated with several pathological changes (Fig.14).
Fig.13: Myocardium showing
hemorrhage represented by extravasations of erythrocytes among muscle
fibers. H&E.
Fig.14: Myocardium showing perivascular edema H&E.
Myocarditis
•
Myocarditis is a common pathologic lesions associated with several systemic
diseases. It is usually secondary but it is rarely primary. Inflammation of
heart muscle (myocarditis) may be caused by a range of organisms.
•
The infection occurs either by direct extension from inflammatory lesions of endocardium and pericardium or through hematogenic rout in many infectious diseases.
•
A wide range of myocarditis including suppurative,
necrotizing, hemorrhagic, lymphocytic and eosinophilic inflammation are
seen.
1. Suppurative myodocarditis
It occurs due to localization of pyogenic
bacteria as Listeria monocytogens
and Actinobacillus equli.
Macroscopically, pale disseminated lesions are seen.
Microscopically, neutrophilic infiltration and monocytes necrosis to form abscess are seen.
2. Eosinophilic myocarditis
The cause usually unknown but in some cases is
associated with degenerated sarcocyst.
3. Hemorrhagic myodocarditis
It occurs with blackleg disease
4. Lymphocytic myodocarditis
It is usually of viral infection. The heart is flabby
with numerous grayish white foci and streaks. Microscopically, interstitial lymphocytic aggregation with
degeneration of monocytes are noticed.
Fibrosis are seen in chronic cases (Figs. 15 & 16).
Fig.15: Myocardium showing lymphocytic
myocarditis represented by infiltration of
myocardium by lymphocytes. H&E.
Fig.16: Myocardium showing lymphocytic
myocarditis represented by infiltration of
myocardium by lymphocytes. H&E.
5. Parasitic myocarditis
Several parasites, tend to
localize in myocardium or in the course of their migration especially if they
migrating in an abnormal host, produce myocarditis. Toxicara
larvae (Fig.17), Sarcocystis, cysticerci
of Taenia ovis,
T. saginata and T. solium, Trichinella
spiralis and Echinococcus
granulosa.
Fig.17 Myocardium
showing Toxicara larvae surrounded by eosinophils and
macrophage (Parasitic myocarditis). H&E.
Cardiopathy
The term cardiopathy used
to describe any disease of the heart. The primary or
idiopathic
cardiomyopathy is used to describe primary
myocardial dysfunction of unknown causes. Secondary cardiomyopathy
is used to describe myocardial diseases with known causes and those secondary
to other cardiovascular disorders. Three forms of cardiomyopathy
are recognized:
1- Dilated cardiomyopathy
(congestive cardiopathy)
It is characterized by dilatation of the four
chambers of the heart due to failure of ventricle to empty with some degree
of atrophy or hypertrophy (Fig.18).
Fig.
18: Heart showing dilated ventricle.
Microscopic picture:
The picture are non
specific. There is progressive fibrosis.
Sequelae
It leads to heart failure
2. Hypertrophic
cardiopathy
It is characterized by marked hypertrophy of
myocardium without dilatation and with resistance to diastolic filling (Fig.
19).
Cardiac hypertrophy is a response to increased work
load over a long period. All four chambers may be hypertrophic
or may be asymmetric, hypertrophy.
Irregular selective hypertrophy of septum which lead to obstruction of left ventricle outflow called
obstructive cardiopathy.
Fig. 19. Heart showing
hypertrophy of left ventricle.
Microscopic picture
Hypertrophied and disarranged
myocytes
to produce interweaving rather than parallel arrangement (Fig. 20).
Interstitial fibrosis and various degenerative alteration in myocytes also may
be present.
Fig.
20: Myocardium showing hypertrophy and
disarranged myocytes to produce interweaving
rather than parallel arrangement . H&E.
3- Restrictive cardiomyopathy
A disease in which restriction to ventricular filling
occurs and may results from amyloidosis or endocardial fibrosis resulting in encroachment of lumen.
Endocardium
A. Degenerative lesions
1. Subendocardial
fibrosis
• It may be acquired or congenital, focal or diffuse.
• Diffuse subendocardial
fibrosis is seen associated with prolonged dilated ventricle or atrium.
• Localized Subendocardial
fibrosis is seen associated with valvular
disorders. It is observed chiefly in atria.
2- Subendocardial
mineralization
• It is common in dogs that have recovered from
ulcerative endocarditis.
• Also, it occurs in lambs suffer from nutritional myopathy.
• It may accompany endocardial
fibrosis.
• It is appear as opaque layers of mineralization.
3- Endocardiosis
in dogs
• It is the most common cardiovascular lesions in
dogs.
• In advanced cases lead to left side heart failure
(Fig.21).
Fig. 21:
Gross picture of endocardiosis
in dog.
B. Degenerative lesions
It is usually observed with septicemic
diseases or after killing animals for necropsy.
C- Endocarditis
1-
Infectious endocardiosis
• Inflammatory lesions of endocardium
usually infections .
• The lesions most common on the valves (valvular endocarditis) (Fig.
22)
, but less frequent on the wall of atrium or ventricles (mural endocarditis) (Fig. 23)
.
• Valvular endocarditis is more frequent on left side of heart than
right except in bovine where the right more affect than left.
• It is an infection associated with formation of
vegetation on the endocardial surface.
Fig.
22 :
Endocardium
showing valvular endocarditis.
Fig.
23 Endocardium
showing gross picture of mural endocarditis.
H&E.
Causes
Most microorganism may cause
endocarditis, some are recorded more than other.
In horse: Streptococcus equi
and Acrinobacillus equuli.
In cattle: Actinomyces
pyogenes.
In dogs: Streptococcus, Staphylococcus spp. and E. coli.
In swine: Streptococcus spp.
and Erysipelthria rhusiopathiae.
Pathogenesis and lesions
1. Infection arise from
adhesion of microorganism to endocardium or their
adherence thrombi that have developed on an endocardium
damage for other reasons.
2. Highly virulent strain can adhere to normal
endothelium.
3. In most cases, the infectious endocarditis is
associated with cardiac anomalies, which are predisposing cause for endocarial injury and sterile thrombus formation.
4. By the help of agglutinating antibodies and
bacterial adhesion factors, the bacterial clumps adhere to endothelium.
5. Damaged endothelium and superficial connective
tissue with hyperemia and leukocytic infiltration
(simple endocarditis) are resulted from bacterial
adhesion. It may follow by extensive endocardial
destruction (ulcerative endocarditis) (Fig.24).
6. On the surface left by destructed endothelium, a
thrombus forms with proliferating bacterial colonies (vegetative endocarditis) (Fig.25).
Fig. 24: Endocardium showing vegetative
endocarditis.
Fig.
25: Gross picture of vegetative endocarditis.
Sequelae
1. Extension of infection can lead to formation of abscesses in adjacent tissue.
2. Necrosis and rupture of chordae tendiae.
3. Organization of the thrombus by granulation tissue, which mature to fibrous
connective tissue. In some cases the surface covered by endothelium.
4. When the infectious endocarditis is valvular, it lead to valvular stenosis (Fig.26) impaired function of valve which lead
to congestive heart failure.
5. Detached thrombi containing microorganisms entered
the systemic circulation lead to abscesses or infection especially in lung,
kidneys, spleen and joints.
Fig.
26 : Valve showing valvular stenosis.
The
Vascular System
Normal morphology
The vascular system divided into: arterial system,
microcirculation, venous system and lymphatic system.
Arteries are divided to three categories:
1.
Large or elastic arteries including aorta.
2.
Medium sized or muscular arteries (carotid, coronary, etc).
3.
Small arteries (usually less than 2 mm in diameter).
• All arteries posses three
coats, a tunica intema, media and adventitia.
• Microcirculation consists
of vessels less than 100 µm in diameter namely, arterioles,
terminal arterioles, capillaries, post capillary venules
and venules.
• Veins are divided into small, medium and large
veins have thin wall in relation to lumenal size. The adventitia is the
thickest layer valves are present to prevent back flow of blood.
• Lymphatic capillaries: they contain lymph rather
than blood. All vessels lined by endothelium lying over a basal lamina.
Arterial diseases
1. Aneurysm and rupture
It is a localized dilatation or outpuching
of a thinned and weakness portion of vessel.
Causes
1. Most causes are idiopathic.
2. Copper deficiency “copper need for normal elastic
tissue”.
3. Verminous aneurysm as one associate with Spirocerca lupi infection (Fig.ure
27).
4. A complication of atherosclerosis.
aneurysm may be classified
on basis of gross appearance into berry, saccular, fusiform of dissecting.
Fig. 27: Artery showing
verminous aneurysm.
Dissecting aneurysm
It characterized by entering the blood into the wall
of blood vessel through an intemal tear and creates
activity within the arterial wall.
Rupture
It may follow sever trauma or a complication of
aneurysm. It lead to death due to internal
hemorrhage or from cardiac tamponade due to rupture
of ascending aorta covered by pericardium.
2. Arterial thrombosis
Frequently observed in animals include posterior
aortic thrombi in dogs with cardiomyopathy and
thrombosis of pulmonary arteries with Dirofilariasis
and in aortic-iliac thrombosis in horse.
3. Arterial hypertrophy
Hypertrophy may affect one or all component of
arterial wall as in case of high altitude disease of cattle which show
pulmonary arterial constriction and hypertrophy, which lead to pulmonary
hypertension and right heart failure (core pulmonale)
(Fig.28 )
Fig. 28: Arterial hypertrophy
characterized by thickened muscular layer. H&E.
4) Inflammation (Arteritis)
It
is inflammation of artery (Fig.29).
Fig.
29:
Vasculitis represented by infiltration of the blood vessel wall by
inflammatory cells. H&E
N.B.: Vasculitis
is
term applied to inflammation of all types of vessels.
Causes of arteritis
1. Infection by direct endothelial injury or by
extension from inflammation adjacent to vessel wall.
2.
In the course of some systemic diseases as in case of
equine viral arteritis.
3.
In some parasitic infestation as
Spirocerca lupi strongylus
valgaris (Fig.30).
4. Immune mediated reaction as in polyarteritis
nodosa in dogs.
Fig.
30: Artery showing parasitic
arteritis due to Spirocerca
lupi parasite.
Fig.
31: Aorta showing microscopic picture of parasitic arteritis characterize by
presence of spirocerca lupi. H&E.
5. Amyloidosis
Amyloidosis is often deposited
in vessels with chronic diseases.
6. Equine intemal
bodies
Mineralized hyaline bodies are frequent finding in
the intema of arterioles of horse. They are round
to oval pleomorphic densely stained bodies in sub endothelial space.
Arteriosclerosis
Definition:
Arteriosclerosis means hardening of the arteries or
it refer to group of disorders characterized by
thickening and loss of elasticity of arterial wall. Arteriosclerosis are
three different forms:
1) Atherosclerosis
It is the disease of large and medium size muscular
and elastic arteries characterized by formation of atheromatous
plaque.
It is most frequent in human and is the leading cause
of death through myocardial infarction, cerebral
infarction and aortic aneurysm.
Causes
1. Hypertension: it is the most important risk
factor.
2. Cigarette smoking: it is due to presence of
factors such as carbon monoxide that cause endothelial injury.
3. Diabetes mellitus: it is due to coexistence of other
factors as hypertension, obesity and hyperlipidemia.
4. Hyperlipidemia as
increase total serum cholesterol, increase total plasma triglycerides,
increase low density lipoprotein/cholesterol, low high density
lipoprotein/cholesterol and abnormal apoproteins.
Pathogenesis
•Endothelial injury or increase permeability to lipid
due to exposure to previous causes lead to deposition of fat droplets in intema.
•Adhesion of monocytes to
vessel wall and activity enter the intema and
become macrophage which secret free radicals that oxidize LDL which produce
more endothelial injury. The injured endothelium lead
to platelets adhesion and fibrin deposition forming microthrombus.
•Macrophages and platelets secret various factors as
platelets derived growth factor (PDGF), TNF, fibroblast growth factor (FGF)
and IL1, which has been identified as mitogenic
causing migration of smooth muscle into the intema
and proliferation there in.
•IL1 and TNF are chemotactic
factors causing leukocytic adhesion and migration
to the intema.
•Macrophages and smooth muscle in the intema have phagocytic capacity
and engulf the lipid droplets and changed to foam cells.
Macroscopic and microscopic pictures
a. Early yellowish fatty streaks are seen in intema. They consist of macrophages and smooth muscle
cells which there cytoplasm filled with lipid (foam cells).
b. The fibrous atheromatous
plaque, which is white to yellowish plaques protruded to the lumen. It consist histologically from
three layers (Figs. 32& 33).
1. Fibrous cap under endothelium which consist of
smooth muscle, dense fibrous connective tissue and few leukocytes.
2.
Cellular areas consist of macrophages and smooth
muscle cells containing fat droplets (foam cells).
3. Basal zone consist of
necrotic areas with cholesterol cleft.
c) Complicated plaque
• Thrombosis which lead to infarction.
• Dystrophic calcification.
• Aneurysm.
Fig.
32: Gross picture of arteriosclerosis.
Fig.
33: Microscopic picture of arteriosclerosis.
Sequelae
1. Thrombus occluding blood vessels leading to infarction.
2. Thromboemboli.
3. Aneurysm and hemorrhage.
Monckeberg medial sclerosis
or calcification
• It involves the medium-sized muscular arteries.
• It is associated with advancing age but not
necessarily with hypertension.
• It produced experimentally in dog with excessive
administration of adrenaline.
Lesions
• Hyaline and fatty degenerative changes occur in the
muscular tissue of the media
• Necrosis and calcification are seen.
• Rarely ossification occur
in vessel wall.
N.B.: extensive calcification of aorta
and thoracic arteries (media only) has been seen in slaughtered young cattle.
III. Arteriolosclerosis
• It much more common in human than animals.
• It divided into 2 forms:
Hyaline arteriolosclerosis
It characterized by replacing of the arteriolar wall
by homogenous eosinophilic
hyaline material with narrowing of its lumen (Fig. 34).
Fig. 34: Hyaline
arteriosclerosis. The wall of blood vessels is transformed into homogenous
more eosinophilic structureless substance. H&E.
Hyperplastic
arteriolosclerosis
It characterized by smooth muscle proliferation, which
lead to onion skin like concentric laminating thickening of blood vessel
wall.
Veins
Phlebitis, thrombophlebitis
Definition
It is the inflammation of vein and it is usually
accompanied by thrombosis.
Phlebitis occurs usually within the inflamed and infracted
area, or due to spread of inflammatory process. Phelipolith
is the deposition of calcium in the necrotic tissue (Fig.35
).
More specific causes of phlebitis include feline
infectious peritonitis and Schistosomiasis.
Fig. 35: Phelipolith characterized by the deposition of calcium in the
necrotic tissue.
Varicose vein
Definition
It is markedly and elongated vein, thus hold an
abnormal amount of blood which tend to become static
Local anoxia, malnutrition and pain are noticed
Lymph vessels
Lymphangectasia
It is dilatation of lymphatic is frequently associated with inflammatory and
neoplastic diseases that obstruct normal lymphatic
flow
Lymphangitis
It is inflammation of lymph vessel.
Neoplasms of vessel
Hemangiomal capillary and
cavernous, hemangiosarcoma, lymphangioma
and lymphangiosarcoma are recorded.
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