Ch 42 bio

• a.v. - b/t atrium and ventricle
•    - on right side called tricuspid valve
•    - left side bicuspid valve/mitral valve
• semi - b/t ventricle + aorta/pulmonary artery

A break in the blood vessel wall exposes proteins that attract platelets and initiate coagulation, the conversion of liquid components of blood to a solid clot. The coagulant, or sealant, circulates in an inactive form called fibrinogen. In response to a broken blood vessel, platelets release clotting factors that trigger reactions leading to the formation of thrombin, an enzyme that converts fibrinogen to fibrin. Thrombin also activates a factor that catalyzes the formation of more thrombin, driving clotting to completion through positive feedback.

This is the hardening of arteries by accumulation of fatty deposits. 

• 1. Lipoproteins such as LDL enter the lining of the artery and aggregate, leading to engulfment by immune cells called macrophages. Uptake of these lipoproteins by macrophages leads to the generation of lipid-rich foam cells.
• 2. Secretion of extracellular matrix components increase lipoprotein aggregation. T lymphocytes enter the growing plaque, causing chronic inflammation. Smooth muscle cells from the lining of the artery also enter the plaque.
• 3. Smooth muscle cells form a fibrous cap separating the plaque from the blood. Within the plaque, foam cells die, releasig cellular debris and cholesterol. If the plaque ruptures, a blood clot can form within the artery. 
• 4. If the plaque continues to grow but does not rupture, the artery becomes increasingly obstructed.

Intercostals