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27 Cards in this Set
- Front
- Back
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Arteries - layers, whats thicker and why, diameter
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go from heart to tissue, thicker wall and have elastic. Adventitia, thicker media, interna with elastic membrane. smaller diameter, more resilient and under pressure.
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Veins - layers, diameter, structures
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adventia thicker, thinner media, simple intima, larger diameter, less resilient, has valves. less pressure.
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Capillaries - purpose, diameter, layers
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blood exchange, one cell thick endothelium, diameter is one RBC, delicate w/o media and externa.
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Atherosclerosis - what?
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hardening of the arteries, become stiff and thickened due to deposition of fibro-fatty plaques called atheroma between tunica media and intima
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Risk Factors for Atherosclerosis - Age and Gender
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Age: increase with each decade, early stages in young children, 40-60 5x more myocardial infarction
Gender: M>W, 35-55 white women 1/5 risk to white men, menopause equals it out in 60's-70s |
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Atherosclerosis risk factors: Familial and Big 4
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Family: risk for hypertension and diabetes, hyperlipidemia
Big 4: diet hyperlidipemia, hypertension, cigarette smoking, diabetes mellitus |
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Hyperlidpidemia - what and numbers
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high total cholestoerl levels increase risk for atherosclerosis. unsual for <150mg/dL. <200 good. 200-240 borderline, >240 is high risk
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Different types of cholesterol - name and what it does
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LDL - low density lipoprotiens, bad, mobilizes lipid in blood
HLD - high density lipoprotiens good; mobilize lipid in cells and plaques to liver for excretion in bile |
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High LDL and significance
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strong indicator of risk of coronary and atheroscleroctic disease. also result in endothelial dysfunction
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HDL - what raises and lowers
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prevent or delay atherosclerosis, exercise increases and obesity and smoking decrease
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Hypertension and Atherosclerosis
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after 45 - more important than hypercholesterolemia.
M: 45-62 with BP>160/95 have 5x more risk than men with BP < 140/90 |
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Smoking and Atherosclerosis
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1+ pack a day = increase death rate by 200%
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Diabetes mellitus and Atheorsclerosis
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diabetes induces hypercholesterolemia. MI 2x in diabetics. Increased risk for stroke. 100x for atherosclerosis induced gangrene in lower extremities
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Other factors for atherosclerosis
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Insufficient physical activity, Type A life style, oral contraceptives,
Atherosclerosis can appear in absence of risk factors |
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Chronic Endothelial Injury - what is it and happens step one
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allows LDL to accumulate in the T. Intima and become oxidized. Injuries are from: hyperlipidemia, hypertension, smoking, immune reactions, hemodynamic factors, toxins
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Oxidized LDL
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more readily digested by macrophages, chemotactic to circulating monocytes, inhibits motility of macrophages to lesions, stimulates release of chemical mediators of inflammation, cytotoxis to endothelial and smooth muscle cells, antioxidents help protect against.
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2. Endothelial dysfunction
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monocytes adhere and migrate between endothelial cells and engulf LDL to become foam cells. increased permeability, leukocyte adhesion, monocyte adhesion and emigration.
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3. Smooth muscle emigration...
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migrate towards intima from meida and proliferate and macrophage activation.
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4. Macrophages/Smooth muscle cells engulf lipid
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the accumulation of foam cells show up as fatty streaks and induce inflammatory response.
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5. Smooth muscle proliferation, collagen deposition..
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collagen and elastin are produced by the smooth muscle cells forming fibrous plaque. ECM deposition, extracellular lipid. called fibrofatty atheroma
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Further progression of atherosclerosis
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plaque can ulcerate resulting in bleeding. platelets become adhered and forming thrombi or thromboemboli. calcium deposits on lesion. fissure, rupturing and ulceration of plaque form cholesterol emboli. tx anitplatelet or thombolytic drugs
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Consequences of Plaque Formation: Atherosclerotic Occlusions
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small vessels: coronary arteries, cerebral arteries
partial or total vascular occlusion - ischemia |
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Consequence of Atherosclerosis: atherosclerotic aneurysms
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large vessels: aorta, lumen doesn't occlude but aneurysm can develop. increased blood pressure will push plaque formation outward and increase wall tension leading to aneurysm
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Consequences of Atherosclerosis: atherosclerotic thrombi
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may form over the top of a lesion, cause infarction. called complicated lesions or atheroma blood clot. chronic lesions with acute crisis
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Clinical consequences based on location of atherosclerosis
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Coronary Arteries: major factor in myocardial infarction
Cerebral arteries: stroke Renal arteries: hypoperfusion of kidneys, renin system activated, hypertension |
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Clinical consequences location based continued
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Intestinal Arteries: chronic ischemia causes nonspecific gastrointestinal problems. acute occlusion causes massive intestinal infarction.
Extremities: chronic ischemia: underperfusion - cramps sudden occlusion - leads to gangrene |
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Summary in Pathogenesis of Atherosclerotic Lesions
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1) chronic endothelial injury initiates - thrombogenic
2) hemodynamic disturbances, turbulent flow, often at bifurcations 3) adverse effect of hypercholesterolemia 4)smoking increases LDL oxidation 5)endothelial toxins such as homocysteine |
