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ClinicianWho applies knowledge and skill to
1. Maintain the state of health of human body
2. Restore the healthy state, if the person is sick
(AL-QANOON)
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Organs
stomach
Tissues
Epithelial,
connective,
Muscle
Cells
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CellThing which can cause injury to cell
Defect in cell function ~tissue ~ organ ~ system
Injurious agents
Ischemia
Chemical agents
Physical agents
Nutritional imbalances
Microbial agents
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Cells
Tissues
Epithelial,
connective,Muscle
Organs
Heart
Blood vessels
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Human body
Systems
CVS,
Blood cell disorders
Respiratory,
GITEndocrine
renal
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Blood vesselsBlood flow
Nutrients (healthy material) towards cells
Waste (toxic) material away from cells
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Blood vessels
Narrowing or complete obstruction ofvessel lumen
Weakening of the vessel wall
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ATHEROSCLEROSIS
Why should we study atherosclerosis ?
What should be studied in atherosclerosis ?
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Transmural myocardial
infarction
Thin fibrous wall
Thin band of collagen
Reduced stroke volume
Aneurysm
Thrombosis
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There has been a previous extensive transmural
myocardial infarction involving the free wall of the
left ventricle.The thickness of the myocardial wall is normal
superiorly, but inferiorly is only a thin fibrous wall.
The infarction was so extensive that, after healing,the ventricular wall was replaced by a thin band of
collagen, forming an aneurysm.
Such an aneurysm represents non-contractile tissue
that reduces stroke volume and strains the remainingmyocardium.
The stasis of blood in the aneurysm predisposes to
mural thrombosis.
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Here is a large remote cerebral infarction. Resolution of the
infarction has left a huge cystic space encompassing much
of the cerebral hemisphere in this neonate.
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This is a normal coronary artery. The lumen islarge, without any narrowing by atheromatous
plaque. The muscular arterial wall is of normal
proportion.
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Causes or risk factors ?
Pathogenesis ?
Components ?Macroscopic & microscopic appearance ?
Clinical significance / complications ?
Prevention ?
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Intima
Media
Adventitia
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Intima
Media
Adventitia
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Properties & Functions of
endothelial cellsMaintenance of permeability barrier
controls the transfer of molecules into the vessel wall
Maintenance of non thrombogenic bloodtissue interface
prostacyclins, thrombomodulins, plasminogen activater
Elaboration of prothrombotic molecules
von willebrand factor, Tissue factor, plasminogen
activater inhibitor
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Properties & Functions of
endothelial cellsExtracellular matrix production
collagen and proteoglycans
Modulation of blood flow
vasoconstrictors Endothelin
vasodilators NO, Prostacyclin
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Properties & Functions of
endothelial cellsRegulation of inflammation and immunity
IL-1, IL-6, IL-8
adhesion molecules
histocompatibilty antigens
Regulation of cell growthplatelet derived growth factor PDGF
fibroblast growth factor FGF
transforming growth factor beta TGF-b
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Properties of smooth muscle
cellsVasoconstriction
Vasodilation
Synthesis of collegan, elastin, proteoglycans
Migration to intimaProliferation after vasculer injury
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Normal to Abnormal
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PATHOGENESIS
Atherosclerosis is considered to be
a chronic inflammatory response ofthe arterial wall initiated by some
form of injury to the endothelium.
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PATHOGENESIS
Injurious agent
endothelial cells
Inflammatory response
atherosclerosis
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Chronic endothelial injury
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chronic endothelial injury - endothelial dysfunction
increased permeability with adhesion of monocytes
and platelets
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PATHOGENESIS
chronic endothelial injuryendothelial dysfunction
increased permeability
insudation of lipoproteins
adhesion of monocytes and platelets
release of factors from platelets and
macrophages
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PATHOGENESIS
Migration of smooth muscle cells from media to
intima
Proliferation of smooth muscle cells
Elaboration of extracelluler matrix
Accumulation of lipids in the cells macrophages
and smooth muscle cells as well as
extracellulerly
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Migration of monocytes into the intima and
their transformation into Macrophages and
Foam cells
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Proliferation of smooth muscle cells in the intima and
elaboration of extracellular matrix, leading to
accumulation of collagen and proteoglycans
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Release of factors from activated platelets,
macrophages, or vascular cells that cause migration
of smooth muscle cells from media into the intima
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Role of Lipid
Increased LDL Cholesterol
Decreased HDL Cholesterol
Increased level of abnormal
lipoproteins
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Role of Lipid
Major lipids in atheroma are
plasma derived
cholesterol
cholesterol esters
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Chronic hyperlipidemia
Impair endothelial cell function
increased production of oxygen free radicals
deactivate nitric oxide ( endothelial relaxing factor)
Lipoprotein accumulate in the intima
thickening of intima
Free radicals generated by macrophages
oxidized LDL
taken by macrophages and form foam cell
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Macrophages
Dysfunctional endothelial cells
Expression on adhesion molecules
Adherence of macrophages
Migration to intima
Foam cell formation
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figure
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Thank youFor your kind attention &
Listening