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Terms in this set (100)

1. Inflammation contributes to the initiation, progression, and complications of atherosclerotic lesions. Normal vessels do not bind inflammatory cells. Early in atherogenesis, however, dysfunctional endothelial cells express adhesion molecules that promote leukocyte adhesion; vascular cell adhesion molecule-1 (VCAM-1), in particular, binds monocytes and T cells. After these cells adhere to the endothelium, they migrate into the intima under the influence of locally produced chemokines.

2. Monocytes differentiate into macrophages and avidly engulf lipoproteins, including oxidized LDL and small cholesterol crystals. Cholesterol crystals appear to be par ticularly important instigators of inflammation through activation of the inflammasome and subsequent release of IL-1. Activated macrophages also produce toxic oxygen species that drive LDL oxidation and elaborate growth factors that stimulate smooth muscle cell proliferation.

3. T lymphocytes recruited to the intima interact with the macrophages and also contribute to a state of chronic inflammation. It is not clear whether the T cells are responding to specific antigens (e.g., bacterial or viral anti- gens, heat-shock proteins [see further on], or modified arterial wall constituents and lipoproteins) or are nonspe- cifically activated by the local inflammatory milieu. Never- theless, activated T cells in the growing intimal lesions elaborate inflammatory cytokines (e.g., IFN-γ), which stimulate macrophages, endothelial cells, and smooth muscle cells.

4. As a consequence of the chronic inflammatory state, activated leukocytes and vascular wall cells release growth factors that promote smooth muscle cell proliferation and matrix synthesis.
1) Wavy myocardial fibers with brick-red color in HE stain; REVERSIBLE changes with mitochondrial swelling + relaxation of myofibrils

LM: few wavy myofibers at margin of infarct (these reflect the stretching and buckling of noncontractile dead fibers)

EM: IRREVESIBLE changes with sarcolemmal disruption and electron-dense mitochondrial deposits

Biochemical: Loss of ATP, increase in Lactate

3) same

4) Coagulation necrosis with loss of cross striations; contraction band necrosis, edema, hemorrhages; earliest neutrophils appear; increased eosinophilia of myofibers

- Continuing coagulation necrosis
- nuclear pyknosis, karyorrhexis, karyolysis
- cytoplasmic eosinophilia
- contraction band necrosis (reperfusion injury) at the periphery
- neutrophil infiltrate increases

*- Total loss of nuclei (karyolysis) and striations
- heavy neutrophilic infiltrates;
- fragmentation of neutrophil nuclei
- complete coagulation necrosis*

o Macrophages appear;
o early disintegration and phagocytosis of necrotic myofibers,
o loss of integrity of cardiac wall (danger of rupture);
o granulation tissue visible
o earliest fibrovascular response begins

8) Maximal phagocytosis; prominent granulation tissue in peripheral areas grows in from margins ; collagen deposition, angiogenesis

9) Most of necrotic tissue has been cleared away; maturing granulation tissue with fewer capillaries and more collagen; increased collagen deposition with decreased cellularity = organization

10) Fibrosis; dense collagenous scar