NURS 6501: Advanced Pathophysiology

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Huether: Understanding Pathophysiology, 6th Edition Chapter 6: Innate Immunity: Inflammation and Wound Healing Innate Immunity 1. Neonates often have transiently depressed inflammatory function, particularly neutrophil

chemotaxis and alternative complement pathway activity. 2. Elderly persons are at risk for impaired wound healing, usually because of chronic illnesses. 3. There are three layers of human defense: barriers; innate immunity, which includes the

inflammatory response; and adaptive (acquired) immunity. 4. Physical barriers are the first lines of defense that prevent damage to the individual and

prevent invasion by pathogens; these include the skin and mucous membranes. 5. Antibacterial peptides (cathelicidins, defensins, collectins, and mannose-binding lectin) in

mucous secretions, perspiration, saliva, tears, and other secretions provide a biochemical barrier against pathogenic microorganisms.

6. The skin and mucous membranes are colonized by commensal or mutualistic microorganisms that provide protection by releasing chemicals that facilitate immune responses, prevent colonization by pathogens, and facilitate digestion in the gastrointestinal tract.

7. The second line of defense is the inflammatory response, a rapid and nonspecific protective response to cellular injury from any cause. It can occur only in vascularized tissue.

8. The macroscopic hallmarks of inflammation are redness, swelling, heat, pain, and loss of function of the inflamed tissues.

9. The microscopic hallmarks of inflammation are vasodilation, increased capillary permeability, and an accumulation of fluid and cells at the inflammatory site.

10. Inflammation is mediated by three key plasma protein systems: the complement system, the clotting system, and the kinin system. The components of all three systems are a series of inactive proteins that are activated sequentially.

11. The complement system can be activated by antigen-antibody reactions (through the classical pathway) or by other products, especially bacterial polysaccharides (through the lectin pathway or the alternative pathway), resulting in the production of biologically active fragments that recruit phagocytes, activate mast cells, and destroy pathogens.

12. The most biologically potent products of the complement system are C3b (opsonin), C3a (anaphylatoxin), and C5a (anaphylatoxin, chemotactic factor).

13. The clotting system stops bleeding, localizes microorganisms, and provides a meshwork for repair and healing.

14. Bradykinin is the most important product of the kinin system and causes vascular permeability, smooth muscle contraction, and pain.

15. Control of inflammation regulates inflammatory cells and enzymes and localizes the inflammatory response to the area of injury or infection.

16. Carboxypeptidase, histaminase, and C1 esterase inhibitor are inactivating enzymes, and the fibrinolytic system and plasmin facilitate clot degradation after bleeding is stopped.

17. Many different types of cells are involved in the inflammatory process including mast cells, endothelial cells, platelets, phagocytes (neutrophils, eosinophils, monocytes and macrophages, dendritic cells), natural killer (NK) cells, and lymphocytes.

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18. Most cells express plasma membrane pattern recognition receptors (PRRs) that recognize molecules produced by infectious microorganisms (pathogen-associated molecular patterns, or PAMPs), or products of cellular damage (damage-associated molecular patterns, or DAMPs). Toll-like receptors (TLRs) and NOD-like receptors are expressed on many inflammatory cells, recognize PAMPs and DAMPs, and promote release of cytokines and inflammatory mediators that eliminate damaged cells and protect against invasion by microbes.

19. The cells of the innate immune system secrete many biochemical mediators (cytokines) that are responsible for activating other cells and regulating the inflammatory response; these cytokines include chemokines, interleukins, interferons, and other molecules.

20. Chemokines induce chemotaxis of leukocytes, fibroblasts, and other cells to promote phagocytosis and wound healing.

21. Interleukins are produced primarily by lymphocytes and macrophages and promote or inhibit inflammation by activating growth and differentiation of leukocytes and lymphocytes.

22. The most important proinflammatory interleukins are interleukin-1 (IL-1), interleukin-6 (IL- 6), and tumor necrosis factor-alpha (TNF-α). Interleukins 6 and 10 down-regulate the inflammatory response.

23. Interferons are produced by cells that are infected by viruses. Once released from infected cells, interferons can stimulate neighboring healthy cells to produce substances that prevent viral infection.

24. The most important activator of the inflammatory response is the mast cell, which is located in connective tissue near capillaries and initiates inflammation by releasing biochemical mediators (histamine, chemotactic factors) from preformed cytoplasmic granules and synthesizing other mediators (prostaglandins, leukotrienes, and platelet-activating factor) in response to a stimulus. Basophils are found in the blood and function similar to mast cells.

25. Histamine is the major vasoactive amine released from mast cells. It causes dilation of capillaries and retraction of endothelial cells lining the capillaries, which increases vascular permeability.

26. The endothelial cells lining the circulatory system (vascular endothelium) normally regulate circulating components of the inflammatory system and maintain normal blood flow by preventing spontaneous activation of platelets and members of the clotting system.

27. During inflammation the endothelium expresses receptors that help leukocytes leave the vessel and retract to allow fluid to pass into the tissues.

28. Platelets interact with the coagulation cascade to stop bleeding and release a number of mediators that promote and control inflammation.

29. The polymorphonuclear neutrophil (PMN), the predominant phagocytic cell in the early inflammatory response, exits the circulation by diapedesis through the retracted endothelial cell junctions and moves to the inflammatory site by chemotaxis.

30. Eosinophils release products that control the inflammatory response and are the principal cell that kills parasitic organisms.

31. The macrophage, the predominant phagocytic cell in the late inflammatory response, is highly phagocytic, is responsive to cytokines, and promotes wound healing.

32. Dendritic cells connect the innate and acquired immune systems by collecting antigens at the site of inflammation and transporting them to sites, such as the lymph nodes, where immunocompetent B and T cells reside and are transformed into functional cells.

33. Phagocytosis is a multistep cellular process for the elimination of pathogens and foreign debris. The steps include recognition and attachment, engulfment, formation of a phagosome

Chapter Summary Review 6-3

and phagolysosome, and destruction of pathogens or foreign debris. Phagocytic cells engulf microorganisms and enclose them in phagocytic vacuoles (phagolysosomes), within which toxic products (especially metabolites of oxygen) and degradative lysosomal enzymes kill and digest the microorganisms.

34. Opsonins, such as antibody and complement component C3b, coat microorganisms and make them more susceptible to phagocytosis by binding them more tightly to the phagocyte.

Acute and Chronic Inflammation 1. Acute inflammation is self-limiting and usually resolves within 8 to 10 days. 2. Local manifestations of inflammation are the result of the vascular changes associated with

the inflammatory process, including vasodilation and increased capillary permeability. The symptoms include redness, heat, swelling, and pain.

3. The principal systemic effects of inflammation are fever and increases in levels of circulating leukocytes (leukocytosis) and plasma proteins (acute-phase reactants [i.e., IL-1 and IL-6]).

4. Chronic inflammation can be a continuation of acute inflammation that lasts 2 weeks or longer. It also can occur as a distinct process without much preceding acute inflammation.

5. Chronic inflammation is characterized by a dense infiltration of lymphocytes and macrophages. The body may wall off and isolate the infection to protect against tissue damage by formation of a granuloma.

Wound Healing 1. Resolution (regeneration) is the return of tissue to nearly normal structure and function.

Repair is healing by scar tissue formation. 2. Damaged tissue proceeds to resolution (restoration of the original tissue structure and

function) if little tissue has been lost or if injured tissue is capable of regeneration. This is called healing by primary intention.

3. Tissues that sustained extensive damage or those incapable of regeneration heal by the process of repair resulting in the formation of a scar. This is called healing by secondary intention.

4. Resolution and repair occur in two separate phases: the reconstructive phase in which the wound begins to heal and the maturation phase in which the healed wound is remodeled.

5. Dysfunctional wound healing can be related to ischemia, excessive bleeding, excessive fibrin deposition, a predisposing disorder (such as diabetes mellitus), wound infection, inadequate nutrients, numerous drugs, or altered collagen synthesis.

6. Dehiscence is a disruption in which the wound pulls apart at the suture line. 7. A contracture is a deformity caused by the excessive shortening of collagen in scar tissue.