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Atherosclerosis
ATHEROSCLEROSIS IS THE CHRONIC DISEASE WITH THE LIPID AND PROTEIN ABNORMAL METABOLISMS, WITH THE DISTRUCTION OF LARGE ARTERIES AND AORTA, AND WITH A FORMATION OF ATHEROSCLEROTIC PLAQUES.
ATHEROSCLEROTIC PLAQUE
Atherosclerosis
COMMON
1 2 3 4
Atherosclerosis
POTENTIAL CONTROLLABLE RISK FACTORS ARE 1 HYPERLIPIDEMIA 2 HYPERTENTION 3 DIABETES MELLITUS 4 CIGARETTE SMOKING
Atherosclerosis
OTHER
1 OBESITY
2 PHYSICAL INACTIVITY
3 STRESS 4 POSTMENOPOUSAL ESTROGEN DEFICIENCY
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Atherosclerosis
OTHER RISK FACTORS ARE 5 HIGH CARBOHYDRATE INTAKE
6 LIPOPROTEINS
7 HARDENED UNSATURATED FAT INTAKE 8 CHLAMYDIA PNEUMONIA
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Pathogenesis of Atherosclerosis
According
considers atherosclerosis to be a chronic inflammatory Response of the arterial wall initiated by injury:
to injury hypothesis
Pathogenesis of Atherosclerosis
chronic endothelial injury 2 insudation of lipoproteins [LDL] 3 modification of lipoproteins by oxidation 4 adhesion of blood monocytes 5 adhesion of platelets
Pathogenesis of Atherosclerosis
6 migration of smooth muscle cells from the media into the intima 7 proliferation of smooth muscle cells in the intima 8 enhanced accumulation of intra and extra cellular lipids
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ATHEROSCLEROTIC PLAQUE
The
change of the large arterial intima is called atherosclerotic plaque or atheroma atherosclerotic plaque is the intimal thickening with lipid accumulation
atherosclerotic plaque
It has three principle components: 1 cells smooth muscle cells, macrophages other leukocytes 2 Extra cellular matrix- collagen, elastic fibers, proteoglycans 3 Intra cellular and extra cellular lipids
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atherosclerotic plaque
vulnerable 2 stable
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atherosclerotic plaque
1 vulnerable 2 STABLE
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Lipid strips
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calcinosis
FORMS OF ATHEROSCLEROSIS
CEREBRAL
ARTERIES INJURY CARDIAC ARTERIES INJURY RENAL ARTERIES INJURY AORTA INJURY INTESTINAL ARTERIES INJURY EXTREMITY ARTERIES INJURY
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ISCHEMIC INFARCTION
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heart disease refers to a group of closely related syndromes caused by an imbalance between the myocardial oxygen demand and the blood supply.
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A PICK INCIDENCE IS AFTER 50 YEARS IN MEN AND 60 YEARS IN WOMEN 90% OF ALL INCIDENCES ARE CAUSED BY CORONARY ARTERY NARROWING
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Classification is followed
Acute 1 2
types:
stenocardia (angina pectoris) sudden cardiac death 3 acute coronary insufficiency 4 myocardial infarction
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is followed
Chronic
types are as follow 1 gross post infarction cardiosclerosis 2 diffused atherosclerotic cardiosclerosis
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1 ATHEROSCLEROTIC STENOSIS 2 CORONARY ARTERY THROMBOSIS 3 CORONARY ARTERY EMBOLISM 4 CORONARY ARTERY SPASM FOR A LONG TIME
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reduction blood suplay is followed by atherosclerotic plaque in the lumen of coronary arteries.
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Occlusive thrombus
2 mural thrombus on atherosclerotic plaque of aortic sinus closed to coronary artery mouth
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of the myocardium leads to added perfuse as reversible then irreversible lesions of the myocardium. Increased myocardial oxygen demand with functional overexertion may also contribute to the development of myocardial ischemia.
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3 scarring
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MYOCARDIAL INFARCTION
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MYOCARDIAL INFARCTION
This
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MYOCARDIAL INFARCTION
The granulation tissue seen here is most prominent from 2 to 3 weeks following onset of infarction.
1 primary 2 reccurent (within 6 weeks after primary) 3 second (after 6 weeks from primary)
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According to the location: 1 anterior and apical left ventricle 2 anterior intraventricle septum 3 posterior wall and posterior third of the intraventricle septum 4 lateral wall 5 papillary muscles 6 enlarge infarct with lesion two or more wall and even right ventricle lesion.
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1 2 3 4
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muscle dysfunction 2Papillary muscle rupture 3External rupture of the infarction 4Rupture of the ventricle septum 5Mural thrombosis 6Acute fibrinous pericarditis 7Ventricle aneurisms (acute, chronic)
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Cardiac arrhythmias 2 Cardiogenic shock 3 Left ventricle failure 4 Rupture of wall, septum, papillary muscle 5 Thromboembolism within artery blood stream
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Chronic aneurism
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THE END
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