athrosclerosis
Terms
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- The first stage of fatty streak formation involves some type of _____. This often times occurs in artery __________ for many reasons (e.g., as a result of too many lipids or because of a virus)
-
injury
branch points - In the second stage of fatty streak formation, ______ project from the endothelium and grab hold of monocytes undergo diapedesis to enter the intima
- VCAMs (vascular cell adhesion moleuces)—
- During the (3rd) migration stage of fatty streak formation cytokines are released from ______. These cytokines cause monocytes to become _____ and ______ to migrate from the media to the intima.
-
T-cells
macrophages
smooth muscle - During the oxidation stage of fatty streak formation, _______ receptors on the macrophages bind to ______LDL molecules and engulf them to become ______ that accumulate to form _______.
-
scavenger
oxidized
foam cells
fatty streaks - Many studies involve the use of vitamens __ & __ (anti-oxidants) in hopes of halting the formation of fatty streaks.
- A E
- _______ and ________forces on endothelial cells promote the formation of VCAMs at branch points, whichs sets in motion the cascade of effects in fatty streak formation
-
Cholesterol
hemodynamic - T cells produce cytokynes (____ & ______) which induces a change in monocytes. The monocyte developes scavenger receptors which attach to oxidized low-density lipoprotiens. It also releases growth factors which results in the proliferation of ______
-
TNF-alpha & y-IFN
smooth muscle and macrophages - Dietary fat is integrated into the intestinal cell, it is transported in the bloodstream by _____.
- chylomicrons
- Lipoprotien lipase frees the ________ from the chylomicron and packages them in adapose and muscle tissue.
- triglycerides
- The chylomicron reminant travels to the ____.
- liver
- In the liver cholesterol synthesis is taking place. Cholesterol is packaged for the bloodstream in a ____.
- VLDL
- Lipoprotien lipase frees some of the cholesterol and turns the VLDL into an ___.
- IDL
- Lipoprotien does the same thing to turn an IDL into a ___.
- LDL
- Exchange reactions occur between HDL & ____ or _____.
- LDL or VLDL
- LDL can be ______ and when it is it is engulfed by either a macrophage or a smooth muscle cell. Both are cells of atherosclerotic lesions.
- oxidized
- Lipoprotien a is a _____ like componant that is inacive and competes with the real protease. It contributes to clot formation and contributes to the development of atherosclerosis.
- Plasminogen
- ideally Genetically engineered dna could translate for healthy protiens that form normal ___ receptors.
- LDL
- Often a patient with familial hypercholesterolemia (type II)will present with _____ at an early age. They may have a family history of coronary artery disease. On PE you may find _____. Their lab results may show a very high ______ & _____
-
chest pain
Xanthomas
cholesterol
LDL - Describe the stages of fatty streak formation.
-
The first stage of fatty streak formation involves some type of injury. This often times occurs in artery branch points for many reasons (e.g., as a result of too many lipids or because of a virus)
In the second stage of fatty streak formation, VCAM (vascular cell adhesion moleuces)— project from the endothelium and grab hold of monocytes undergo diapedesis to enter the intima
During the (3rd) migration stage of fatty streak formation cytokines are released from T-cells. These cytokines cause monocytes to become macrophages and smooth muscle to migrate from the media to the intima.
During the oxidation stage of fatty streak formation, scavenger receptors on the macrophages bind to oxidized LDL molecules and engulf them becoming foam cells that accumulate to form fatty streaks. Many studies involve the use of vitamens A & E (anti-oxidants) in hopes of halting the formation of fatty streaks. - Describe the effects of cholesterol and hemodynamic forces on endothelial cells.
- Cholesterol and hemodynamic forces on endothelial cells promote the formation of VCAMs at branch points, whichs sets in motion the cascade of effects in fatty streak formation
- Describe how a monocyte transforms into a lipid-ingesting macrophage.
- T cells produce cytokynes (TNF-alpha & y-IFN which induces a change in monocytes. The monocyte developes scavenger receptors which attach to oxidized low-density lipoprotiens. It also releases growth factors which cause the proliferation of smooth muscle and more macrophages.
- Integrate lipoprotein metabolism with atherosclerosis
- Dietary fat is integrated into the intestinal cell, it is transported by chylomicrons, lipoprotien lipase frees the triglycerides from the chylomicron and packages them in adapose and muscle tissue. The chylo micron reminant travels to the liver. In the liver cholesterol synthes is taking place where it is packaged in a VLDL. Lipoprotien lipase frees some of the cholesterol and turns the VLDL into an IDL. Lipoprotien does the same thing to turn an IDL into a LDL. Exchange reactions occur between HDL & LDL & VLDL. LDL can be oxidized and when it is it is engulfed by either a macrophage or a smooth muscle cell. Both are cells of atherosclerotic lesions.
- Describe the role of Lipoprotein (a) in the development of atherosclerosis.
- Plasminogen like componant that is inacive and competes with regular plasminogen.
- Identify your patient with familial hypercholesterolemia
- Often a patient with familial hypercholesterolemia (type II)will present with chest pain at an early age. They may have a family history of coronary artery disease. On PE you may find Xanthomas. Their lab results may show a very high cholesterol & LDL