Fishbein3.txt

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emm64
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Fishbein3.txt
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2012-02-13 00:59:40
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Fischbein 3
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  1. TYPES OF ARTERIOSCLEROSIS
    • 1. Atherosclerosis
    • Most common and important type of arteriosclerosis, generally affecting large & medium-sized arteries
    • 2. Medial calcific (Mönckeberg) arteriosclerosis
    • 3. Arteriolosclerosis
  2. Medial Calcific Arteriosclerosis
    • Left panel is a low power photomicrograph of medial calcific arteriosclerosis of a muscular artery in which there are calcific deposits within the vessel wall beginning at the internal elastic lamina. The calcific deposits encroach upon the media. Note that there is no luminal encroachment.
    • Right panel is a higher power photomicrograph showing calcification of the internal elastic lamina (arrow) with extension into the media.
    • -left: lumen is wide open; vessel is patent
    • Fatty Streak
    • arterial Plaque
    • Begin as yellow, flat spots (<1 mm="" br="">Coalesce into elongated streaks (>1 cm)
    • Consist of lipid-laden macrophages, smooth muscle cells, few lymphocytes, and little extracellular lipid in fine meshwork of fibrous and elastic tissue
    • FIBROUS PLAQUE
    • AKA raised plaque
    • Consist of smooth muscle cells, macrophages, & other leukocytes in connective tissue stroma composed of collagen, elastic tissue, & proteoglycans, with intra- & extracellular lipid present
    • COMPLICATED PLAQUE
    • Fibrous plaque + Calcification
    • Ulceration
    • Hemorrhage
    • Thrombosis
    • Only type of plaque that is clinically significant
    • Upper panel is a gross photograph of an aorta with complicated atherosclerosis due to ulcerations.
    • Lower panel is a gross photograph of an aorta with complicated atherosclerosis due to calcifications and ulcerations with superimposed thrombi.
    • -this type of plaque can completely occlude an artery; these plaques can also rupture, causing thrombosis- if in a large artery, these plaques can embolize
    • when this happens in a small artery, more likely to get an occlusion- often found in pts w myocardial infarction
    • -in complicated plaques, as pts get older, there is more scarring; but lipid is still always found
  3. AtheroGenesis
    • Chronic endothelial injury
    • Endothelial dysfunction – increased permeability, leukocyte adhesion, and thrombotic potential
    • Insudation of lipoproteins into vessel wall (mainly LDLs)
    • Oxidation of lipoproteins
    • Adhesion, emigration, & transformation of monocytes to macrophages & foam cells
    • Platelet adhesion & activation
    • Migration of SMCs from media to intima
    • Proliferation of SMCs with elaboration of ECM and accumulation of collagen and proteoglycans
    • Enhance accumulation of intra- and extracellular lipids
  4. IHD Divisions
    • IHD can be divided as follows:
    • Angina pectoris
    • Myocardial infarction
    • Sudden cardiac death
    • Chronic IHD with heart failure
    • angina pectoris- crushing chest pain; can migrate down into left arm, jaw, back, ear; a reversible form- will go away if stop exercise
    • myocardial infarction- demand for oxygen so far exceeds supply, that the tissue dies
    • major thrust of therapy- to open up a vessel as soon as possible, after occlusion
    • sudden cardiac death- abt 40-50% of the time, when the artery occludes, it causes arrhythmia, which can be fatal
    • chronic IHD w heart failure- surviving a heart attach leaves scars; if enough muscle is damaged, the heart fails as a pump (heart failure)
  5. 3 types of angina:
    • Stable angina (most common)
    • Due to diminished coronary perfusion to critical level such that supply does not meet increased demand during physical activity or emotional excitement
    • Usually associated with stable atherosclerotic plaques
    • Unstable angina
    • Increased in frequency, pain, and duration, or of new and recent onset
    • Due to disruption of unstable atherosclerotic plaque with superimposed nonocclusive thrombus
    • Often precursor to myocardial infarction
    • Prinzmetal variant (uncommon)
    • Occurs at rest and is due to coronary artery spasm
  6. MI Pathogenesis
    • Initial event = disruption of unstable plaque (erosion/ulceration, intraplaque hemorrhage, or rupture)
    • Exposure to thrombogenic subendocardial collagen and necrotic plaque contents results in platelet adhesion, aggregation, activation, and release of potent aggregators
    • Platelet aggregation and release of mediators stimulates vasospasm
    • Complete occlusion of coronary artery by thrombus resulting in anoxia of downstream myocardium
    • Myocardial coagulative necrosis occurs if coronary artery is not re-opened within 20 to 30 minutes
    • Athermatous Plaque
    • Photomicrograph of a Masson trichrome-stained section of a coronary artery with an atheromatous plaque exhibiting intraplaque hemorrhage and luminal thrombosis.
    • -this is the underlying lesion in 75% of acute coronary events
  7. Transmural
    • Ischemic necrosis involves full or nearly full thickness of ventricular wall in distribution of single coronary artery
    • Usually associated with coronary atherosclerotic disease, rupture of unstable plaque, and superimposed occlusive thrombus
    • 10% of transmural MIs are not due to disrupted unstable plaque with superimposed thrombus
    • Isolated, intense, and relatively prolonged vasospasm (e.g. cocaine use)
    • Emboli from left ventricle or atrium
    • Paradoxical embolization from right ventricle or atrium
    • Vasculitides, hematologic disorders, coronary artery dissection
    • affecting 50% or more of the ventricular wall thickness
    • paradoxical embolization- clot from a vein can go through defect in atrial septum, to get into the arterial system
  8. Subendocardial
    • Ischemic necrosis limited to inner third to half of ventricular wall
    • May extend beyond perfusion territory of single coronary artery
    • Usually due to sufficiently prolonged and severe reduction of BP in the setting of severe coronary atherosclerosis
    • May also be due to plaque disruption with superimposed thrombus which becomes lysed before full thickness necrosis occurs
    • usually the inner third or half of ventricular wall
    • usually due to hypotension- when BP/oxygen goes down, there is shift of blood from subendocardium to myocardium, so that subendocardium dies first; there is wavefront phenomenon, with tissues dying in a wave- we try to stop this ischemic wavefront
    • pump function may not be as bad, but still at risk for arrhythmias
  9. Which tissues are most susceptible to necrosis in MI?
    • Subendocardial myocardium is the area most susceptible to ischemic injury and will become necrotic first
    • Due to fact that this area is furthest away from the blood supply
    • Endocardium itself is perfused by the blood in the heart chambers
  10. Myocardial Necrosis after MI
    • Septal or free wall perforation with associated pericardial tamponade
    • Left panel illustrates a free wall myocardial rupture (arrow) from mechanical weakening that occurs in necrotic and inflamed myocardium. This is the most common type of myocardial rupture and can result in hemorrhage into the pericardial cavity (pericardial tamponade).
    • Upper right panel shows a myocardial rupture of an interventricular septum (arrow). This can lead to a left-to-right shunt with volume overload of the right ventricle and pulmonary hypertension.
    • Lower right panel shows a heart exhibiting pericardial tamponade with blood filling the pericardial cavity. This can potentially be fatal especially if this were to occur acutely.
    • -ruptured heart; blood in pericardial sac (bottom right)- blood in pericardial sac compresses heart, doesn’t let it fill (cardiac tamponade) > almost always causes death
    • LV aneurysm-
    • wall is ballooned and thinned; aneurysm is a part of the heart is not contracting, a site of potential clot formation; also a common source of arrhythmias
    • scar tissue and normal tissue mixed together increases the risk of arrythmia
  11. SUDDEN CARDIAC DEATH
    • Rapid, unexpected death (in < 24 hrs) without obvious cause when body found
    • Most cases of sudden death in Western world due to heart disease
    • Accounts for ~300,000 deaths per year in U.S. and for 50% of all cardiovascular deaths
    • Most common cause of sudden cardiac death is ischemic heart disease
    • 50% of ischemic heart disease patients present with sudden death as initial manifestation
    • Chronic ischemia predisposes myocardium to development of lethal ventricular arrhythmias, usually ventricular fibrillation
  12. CHRONIC ISCHEMIC HEART DISEASE
    Development of progressive congestive heart failure due to long-term ischemic myocardial injury
    • Metastatic neoplasms
    • Much more common than primary cardiac tumors
    • May occur in up to 10% of pts with disseminated cancer
    • Usually involve pericardium, but can involve myocardium
    • Most common tumors that metastasize to heart
    • Carcinomas of lung & breast
    • Malignant melanoma
    • Lymphomas and leukemias
    • CARDIAC MYXOMA
    • Most common primary tumor in adults
    • 90% located within atria (L:R = 4:1)
    • Thought to derive from differentiation of primitive multipotential mesenchymal cells
    • Carney syndrome
    • 10% pts with myxomas
    • AD inheritance
    • Multiple cardiac & extracardiac myxomas, spotty pigmentation, & endocrine overactivity
    • AV valve obstruction by “ball-valve” mechanism or embolization may occur
    • Surgical removal is usually curative
    • Photomicrograph of a cardiac myxoma with scattered globular/stellate myxoma cells embedded with an abundant myxoid stroma. The black arrow is pointing to a blood vessel.
  13. CARDIAC ANGIOSARCOMA
    Most common primary malignant cardiac tumor

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