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Summary Medical Biochemistry and Pathophysiology: Pathophysiology Section - Biomedical Sciences, minor Patient-Oriented Research, University of Amsterdam $4.88   Add to cart

Summary

Summary Medical Biochemistry and Pathophysiology: Pathophysiology Section - Biomedical Sciences, minor Patient-Oriented Research, University of Amsterdam

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Summary of lectures of Medical Biochemistry and Pathophysiology, part Pathophysiology. Biomedical Sciences, minor Patient-Oriented Research, University of Amsterdam. The summary is written in English, since the entire course is taught in English and the exam is also in English.

Last document update: 8 year ago

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  • October 27, 2016
  • October 28, 2016
  • 94
  • 2016/2017
  • Summary

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By: jessicazincken • 6 year ago

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Molecular Pathophysiology



Atherosclerosis, metabolism and nuclear receptors – De Vries




Atherosclerosis = formation of lesion (=plaque) in blood vessels, consisting of dead cells, cholesterol,
cholesteryl esters, triglycerides, macrophages, smooth muscle cells, crystallized calcium > narrowing
vessels

Atherosclerosis is the underlying pathology of myocardial and cerebral infarction

When there are high LDL levels in the blood circulation:

- Monocytes are attracted by endothelial cells to clean up LDL
- Monocytes (in blood) go into tissue and become macrophages (=monocytes in tissue)
- LDL is a little oxidized by radical oxygen species (ROS)
- Macrophages can take up oxidized LDL
- Macrophages cannot handle all the LDL and become ‘foam cells’
- Macrophages secrete cytokines > inflammation and attraction of more monocytes
- Macrophages also secrete growth factors > smooth muscle cells (SMCs) differentiate and can
now migrate to endothelial cells > enlarge the lesion

, Multi-factorial disease and treatment:

- Environment: smoking, diet, lack of exercise > can be prevented
- Risk factors:
 High cholesterol (LDL) > statins (to decrease cholesterol synthesis and upregulate LDL
receptors)
 Low HDL
 Hypertension > multiple drugs
 Diabetes > insulin (in Diabetes type I)
- Genetic components
 Familiar Hypercholesterolemia (FH) > LDL receptor gene mutation
 Tangier disease > ABCA1 receptor defect
 ‘Genetic predisposition’ > multiple genes

Acute myocardial infarction: atherosclerosis in coronary artery > plaque rupture > formation of
thrombus that can obstruct the coronary artery, which results in decreased or no blood flow = infarction




Cells involved in atherosclerosis: monocytes/macrophages, T cells, endothelial cells, smooth muscle
cells

Treatment of atherosclerosis: stent in coronary artery > metal thing in which a balloon can be pumped
up to widen narrowed or obstructed vessels (angioplasty) (stent ensures that the vessel remains open)

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