HNN227 Study Guide - Final Guide: Prostaglandin, Cardiac Muscle, Corticosteroid
1 Jun 2018
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The inflammatory response can be divided into a vascular response, a cellular response, formation of
exudate and healing.
VASCULAR RESPONSE
After cell injury, local arterioles briefly undergo transient vasoconstriction. After release of histamine and
other chemicals by the injured cells, the vessels dilate. Both vasodilation and increased capillary
permeability are responsible for redness, heat and swelling at the site of injury. Swelling is a result of the
capillaries becoming leaky and allowing fluid to leave the intravascular space and enter the surrounding
tissues (or capillary permeability).
As the plasma protein fibrinogen leaves the blood, it is converted to fibrin by the products of the injured
cells. Fibrin strengthens a blood clot formed by platelets. In tissue the clot functions to prevent further
blood loss, trap bacteria, prevent their spread and serve as a framework for the healing process. Platelets
release growth factors that start the healing process.
CELLULAR RESPONSE
Neutrophils and monocytes move from circulation to the site of injury.
Neutrophils
Neutrophils are the first leucocytes to arrive at the injury site (within 6-12 hours). They phagocytose
(engulf) bacteria, and other foreign material and damaged cells. With their short life span (24-48 hours),
dead neutrophils soon accumulate. In time a mixture of neutrophils, digested bacteria and other cell debris
accumulates as a creamy substance termed pus.
To keep up with demand for neutrophils, the bone marrow releases more neutrophils into circulation,
which results in elevated WBC count.
Monocytes
Monocytes are the second type of phagocytic cells that migrate from circulating blood. They are attracted
to the site by chemotactic factors and usually arrive within 3-7 days after the onset of inflammation. On
entering the tissue spaces, monocytes transform into macrophages. Together with the tissue
macrophages, these newly arrived macrophages assist in phagocytosis of the inflammatory debris.
Macrophages have a long life span; they can multiple and may stay in the damaged tissues for weeks. They
are important in the healing process.
Macrophages can accumulate and fuse to form a giant cell. The giant cell is then encapsulated by collagen,
leading to the formation of granuloma. The granuloma formed consists of an aggregate of active
macrophages around the infecting agent and often shows necrosis.
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Document Summary
The inflammatory response can be divided into a vascular response, a cellular response, formation of. After cell injury, local arterioles briefly undergo transient vasoconstriction. After release of histamine and other chemicals by the injured cells, the vessels dilate. Both vasodilation and increased capillary permeability are responsible for redness, heat and swelling at the site of injury. Swelling is a result of the capillaries becoming leaky and allowing fluid to leave the intravascular space and enter the surrounding tissues (or capillary permeability). As the plasma protein fibrinogen leaves the blood, it is converted to fibrin by the products of the injured cells. Fibrin strengthens a blood clot formed by platelets. In tissue the clot functions to prevent further blood loss, trap bacteria, prevent their spread and serve as a framework for the healing process. Platelets release growth factors that start the healing process. Neutrophils and monocytes move from circulation to the site of injury.
