Defense mechanisms used by the body to protect itself from any injurious agent may be specific or nonspecific. One nonspecific or general defense mechanism is the mechanical barrier such as skin or mucous membrane (often called the first line of defense) that blocks entry of bacteria or harmful substances into the tissues (Fig. 5-1). Associated with these mechanical barriers are body secretions such as saliva or tears that contain enzymes or chemicals that inactivate or destroy potentially damaging material.

The second line of defense includes the nonspecific processes of phagocytosis and inflammation. Phagocytosis is the process by which neutrophils (a leukocyte) and macrophages,” randomly engulf and destroy bacteria, cell debris, or foreign matter (see Fig. 5-2). Inflammation involves a sequence of events intended to limit the effects of injury or a dangerous agent in the body. Interferons are nonspecific agents that protect uninfected cells against viruses (see Chapter 6).

The third line of defense is the specific defense mechanism in the body (see Chapter 7). It provides protection by stimulating the production of unique antibodies or sensitized lymphocytes following exposure to specific substances. In recent years much effort has been expended on research on the immune system in an effort to increase understanding of the process of the immune response and to create ways to strengthen this defense mechanism.

An injury to capillaries and tissue cells will result in the following reactions:

When tissue injury occurs, the damaged mast cells and platelets release chemical mediators including histamine, serotonin, prostaglandins, and leukotrienes into the interstitial fluid and blood (Table 5-1). These chemicals affect blood vessels and nerves in the damaged area. Cytokines serve as communicators in the tissue fluids, sending messages to lymphocytes and macrophages, the immune system, or the hypothalamus to induce fever.

Although nerve reflexes at the site of injury cause immediate transient vasoconstriction, the rapid release of chemical mediators results in local vasodilation (relaxation of smooth muscle causing an increase in the diameter of arterioles), which causes hyperemia, increased blood flow in the area. Capillary membrane permeability also increases, allowing plasma proteins to move into the interstitial space along with more fluid (see Fig. 5-2). The increased fluid dilutes any toxic material at the site, while the globulins serve as antibodies, and fibrinogen forms a fibrin mesh around the area in an attempt to localize the injurious agent. Any blood clotting will also provide a fibrin mesh to wall off the area. Vasodilation and increased capillary permeability make up the vascular response to injury.

During the cellular response, leukocytes are attracted by chemotaxis to the area of inflammation as damaged cells release their contents. Several chemical mediators at the site of injury act as potent stimuli to attract leukocytes. Leukocytes and their functions are summarized in Table 5-2. First neutrophils (polymorphonuclear leukocytes [PMNs]) and later monocytes and macrophages collect along the capillary wall and then migrate out through wider separations in the wall into the interstitial area. This movement of cells is termed diapedesis. There the cells destroy and remove foreign material, microorganisms, and cell debris by phagocytosis, thus preparing the site for healing. When phagocytic cells die at the site, lysosomal enzymes are released and damage the nearby cells prolonging inflammation. If an immune response (see Chapter 7) or blood clotting occurs, these processes also enhance the inflammatory response.

The cardinal signs of inflammation are redness (rubor or erythema), heat, swelling, and pain:

Exudate refers to a collection of interstitial fluid formed in the inflamed area. The characteristics of the exudate vary with the cause of the trauma:

Fever or pyrexia (low grade or mild) is common if inflammation is extensive. If infection has caused the inflammation, fever can be severe, depending on the particular microorganism. However, high fever can be beneficial if it impairs the growth and reproduction of a pathogenic organism. Fever results from the release of pyrogens, or fever-producing substances (e.g., interleukin-1), from white blood cells (WBCs) or macrophages (Fig. 5-4). Pyrogens circulate in the blood and cause the body temperature control system (the thermostat) in the hypothalamus to be reset at a higher level. Heat production mechanisms such as shivering are activated to increase cell metabolism. Involuntary cutaneous vasoconstriction characterized by pallor and cool skin reduces heat loss from the body. Voluntary actions such as curling up or covering the body conserve heat. These mechanisms continue until the body temperature reaches the new, higher setting. Following removal of the cause, body temperature returns to normal by reversing the mechanisms.

5-3  

Think about

a. What are the physiologic changes that occur when the cause of a fever is removed?

b. Explain the differences among serous, fibrinous, and purulent exudates.

Leukocytosis (increased white blood cells in the blood), elevated serum C-reactive protein (CRP), an elevated erythrocyte sedimentation rate or ESR, and increased plasma proteins and cell enzymes in the serum are nonspecific changes (Table 5-3); they do not indicate the particular cause or site of inflammation. They provide helpful screening and monitoring information when a problem is suspected or during treatment. In patients with leukocytosis, there is often an increase in immature neutrophils, commonly referred to as “a shift to the left.” A differential count (the proportion of each type of WBC) may be helpful in distinguishing viral from bacterial infection. Allergic reactions commonly produce eosinophilia. Examination of a peripheral blood smear may disclose significant numbers of abnormal cells, another clue as to the cause of a problem. Increased circulating plasma proteins (fibrinogen, prothrombin, and alpha-antitrypsin) result from an increase in protein synthesis by hepatocytes.

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