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Lecture 3

Lecture 3 Inflammation and Repair Part 1 NTC (2).docx

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Department
Pathology
Course
PATH 300
Professor
Edith Zorychta
Semester
Winter

Description
Lecture 3 PATH 300 Jan 14 Lecture 3 - Inflammation and Repair: Part 1  Inflammation is the reaction of living tissues to injury.  Injured tissue releases mediators that cause changes in the local microcirculation providing the injured tissue. o Microcirculation consists of an arteriole, a capillary bed, a venule, and then connects back to circulation.  Changes are in the vessel properties  The 4 classical signs have long been known as: o Redness, hot, swelling, and pain. A 5 sign might apparent if the inflammation is serious enough, and it would be a loss of function. Acute inflammation (fast onset and mild) delivers leukocytes and plasma proteins to sites of injury. The two major components are: 1. Vascular Changes:  Specific hemodynamic changes include changes in pressure and flow of blood due to hydrostatic pressure. Entrance to the capillary bed is through the arterioles which are surrounded by smooth muscle. The smooth muscle can contracts or relax. (FIG) This controls the amount of blood that flows through the vessel. o When smooth muscle relaxes, there is increased blood flow into the microcirculation resulting in vasodilation. The area becomes red and hot. o Hyperemia results from a greater than normal flow of blood ( it's the opposite to ischemia)  Some fluid flows past cells on the arteriole side and enters back on the venous side. As it's going through the tissue it delivers gases and nutrients and takes away metabolic waste products. Fig 1 - Schematic of the microcirculation and the leaving fluid Lecture 3 PATH 300 Jan 14  There are two main different forces acting on the fluids. The first main pushing force is hydrostatic pressure. It's highest on arteriole side so fluid can flow out into the tissue. The force acting to keep fluid inside the vessels or draw it in is the osmotic pressure. o Not all of the fluid that exits the microcirculation comes back on the venous side. Some excess fluid is drained in the lymphatic system.  If the fluid flowing out is protein-free it is called transudate. Under acute inflammation you lose some of the plasma proteins and the fluid is then called exudate (2-4). Tissue with exudate is much more swollen Proteins leave the vasculature via spaces between the endothelial cells. This is a normal process that happens under injury. However the more serious the injury is to the endothelial cells, the more destructive it is and the spaces become too big and many components leak out. Contraction of endothelial cells increases the spaces between them and is the due to the action of vasoactive mediators. Fig 3 - Schematic of the exudate and transudate  Net flow out increases on the venous side during  Mild inflammation: only the venule will contract and increase in permeability takes place.  Mast cells are located right next to blood vessels and release vasoactive mediators. One of them is histamine o Histamine acts on both sides of capillary bed. It causes vasodilation of arterioles (the area becomes red) and contraction of endothelial cells in venules so you get swelling.  During extensive inflammation all of the microcirculation dilates.  The transient permeability of the microcirculation is minor and due to mast cells. In sustained injury the swelling lasts longer, but there's a delayed prolonged reaction. The cause of the injury doesn't cause swelling right away but the synthesis of more mediators which are released later on, so you don't get redness and pain during injury. You don't Lecture 3 PATH 300 Jan 14 know you are being damaged. For example, you don't turn red from a sunburn right away but when you get home. 2. Cellular: accumulation of leukocytes  At the capillary level, the flow of cells is such that smaller cells flow in the middle and larger against the vessel walls. During inflammation, different mediators cause the larger cells stick to the endothelial cells and eventually get out into the tissue.  RBCs and platelets stay in circulation while leukocytes enter tissue  Normal laminar flow means leukocytes are in contact with the endothelial cells. As inflammation begins and fluid flows out, the concentration of cells increase together and leukocytes are pushed more firmly against the walls. Leukocytes interact with endothelial cells with selectins  Selectins stick to the endothelial cells with their extensions. This interaction is not very strong so they detach often. The results in them trolling along the endothel
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