61338
Beschreibung
Karteikarten von alexlpeart, aktualisiert more than 1 year ago
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Erstellt von alexlpeart
vor mehr als 11 Jahre
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| Frage | Antworten |
| low levels of physical activity are associated with.... | Higher levels of mortality |
| What is the greatest cause of death? | Cardiovascular disease |
| What level of exercise is more likely to be continued? | Moderate to low level |
| What level of exercise is more likely to be continued? | Moderate to low level |
| What is Athrosclerosis | The build up of cholesterol blocking and artery. |
| Give 2 atherogenic molecules and one anti-atherogenic. give the defining features of each molecule, | VLDL- atherogenic, TAG rich LDL - atherogenic, Cholesterol rich HDL - Anti-atherogenic, Protein and phospholipid rich |
| Describe the process of plaque creation in atherosclerosis. | Physical or infection damage to vascular endothelium. Cytokines release attracts WBCs. high cytokine conc=monocytes pulled between endothelium cells (called diapedesis). Monocyte matures into macro-phage which along with platelet and endothelium cells releases cytokines (PDGF). The cytokines promote smooth muscle cell movement from the media to the intima. Macrophage, engulfs modified cholesterol forming a foam cell. Macrophage releases protein degrading chemicals which destabilizes the plaque (cellular cytoxicity). The plaque may rupture and travel to the heart or brain. |
| Where is the biggest benefit of physical activity seen in terms of inactive, moderately active highly active? | Between least active and moderately active. |
| Explain why branch points are common places for athersclerotic plaques to form? Explain why? | Branch points of arteries, because the blood flow causes eddies where the flow is slower, meaning less eNOS (endothelial derived nitric oxide synthase) which normally prevents white blood cells sticking but when it is low WBCs can stick more easily forming plaques. |
| Normal cells ____ the production of _____ when they have high levels of LDLs. Macrophage cells don't do this because .... | inhibit, LDL receptors. Macrophages see the modified cholesterol as damaged cells so it enguphs them and forms foam cells. |
| Explain how HDL molecules are anti-atherogenic. | They inhibit the expression of the adhesion molecule preventing monocytes from sticking to the endothelium. HDLs also prevent LDL oxidation so we don't have modified LDLs and the macro-phages don't engulf them meaning no foam cells are formed. HDLs promote LDL efflux from the intima to the blood. |
| Explain the role of LCAT in the production of HDLS | Free cholesterol must be converted to a cholesterol ester before it can be placed into the core of a HDL, LCAT allows this to happen turning an immature HDL cell into a mature HDL cell. |
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