Chapter 3 (Inflammation and Fever)- Study Guide Questions

Margination

Leukocyte accumulation.

Exudate

Outpouring of a protein-rich fluid into the tissue and extravascular space.

Mast cells

Stimulate inflammatory reaction in response to injury or infection.

Nitric oxide

Stimulator of vasodilation.

In addition to the cardinal signs that appear at the site of injury, __________ manifestations may occur as chemical mediators produced at the site of inflammation gain entrance to the circulatory system.

Systemic.

What is the purpose of the acute-phase response of inflammation?

The acute-phase response includes changes in the concentrations of plasma proteins, skeletal muscle catabolism, negative nitrogen balance, elevated erythrocyte sedimentation rate, and increased numbers of leukocytes. These responses are generated by the release of cytokines that affect the thermoregulatory center in the hypothalamus to produce fever. The metabolic changes provide amino acids that can be used in the immune response and for tissue repair. In general, the acute phase response serves to coordinate the various changes in body activity to enable an optimal host response.

Acute inflammation involves two major components: the _________ and __________ stages.

Vascular; cellular.

There are many mediators of the inflammatory system. They may be grouped by function. Describe each group, and give a brief description of each.

Mediators can be classified by function as follows: 1. Those with vasoactive and smooth muscle constricting properties such as histamine, arachidonic acid metabolites, and platelet-activating factor. 2. Plasma proteases that activate members of the complement system, coagulation factors of the clotting cascade, and vasoactive peptides of the kinin system 3. Chemotaxic factors such as complement fragments and chemokines 4. Reactive molecules and cytokines liberated from leukocytes, which when released into the extracellular environment can affect the surrounding tissue and cells.

The __________ pathways generate toxic oxygen and nitrogen products.

Metabolic burst.

Leukocytes known as __________ produce prostaglandins and leukotrienes, platelet-activating factor, inflammatory cytokines, and growth factors that promote regeneration of tissue.

Monocytes/macrophages.

The __________ induce inflammation and potentiate (increase) the effects of histamine and other inflammatory mediators.

Prostaglandins.

Endothelial cells

Regulate leukocyte extravasation (letting out of blood vessel).

The cardinal signs of inflammation result from the physiologic processes of the inflammatory cells and protein systems. List the signs and give a brief explanation as to its cause.

Rubor (redness), tumor (swelling), calor (heat), and dolor (pain). Rubor is a result of increased blood flow due to histamine release. Tumor is due to an increased permeability of blood vessels due to histamine and other long-term vasoactive mediators. Calor is the result of increased perfusion of the tissues at the wound site. Dolor is due to bradykinin, prostaglandins, and histamine's effects on sensory nerve endings.

The cardinal signs of inflammation are __________, __________, __________, __________, and __________.

Rubor (redness), tumor (swelling), calor (heat), dolor (pain), and functio laesa (loss of function).

Thrombocytes

Activation affects vascular permeability, chemotactic, adhesive, and proteolytic properties.

Neutrophils

Primary phagocyte that arrives early at the site of inflammation.

What is the order of events in the cellular stage of inflammation?

1. Margination and adhesion to the endothelium. 2. Transmigration across the endothelium. 3. Chemotaxis. 4. Activation and phagocytosis.

Many leukocytes have the ability to phagocytose foreign material and dispose of it. The process involves three steps. List and explain these steps.

1. Recognition and adherence. 2. Engulfment. 3. Intracellular killing. Phagocytosis is initiated by recognition and binding of particles by specific receptors on the surface of phagocytic cells. Microbes can be bound directly to the membrane of the phagocytic cells by several types of pattern recognition receptors or indirectly by receptors that recognize microbes coated with carbohydrate-binding lectins, antibody, and/or complement. Endocytosis is accomplished through cytoplasmic extensions that surround and enclose the particle in a membrane-bound phagocytic vesicle. Intracellular killing of pathogens is accomplished through several mechanisms, including toxic oxygen and nitrogen products, lysozymes, proteases, and defensins.

There are numerous __________ under the skins surface that allow blood to move directly from the arterial to the venous system.

AV (arteriovenous) shunts.

Describe and differentiate between acute and chronic inflammation.

Acute inflammation is the early (almost immediate) reaction of local tissues and their blood vessels to injury. It typically occurs before adaptive immunity becomes established and is aimed primarily at removing the injurious agent and limiting the extent of tissue damage. Acute inflammation can be triggered by a variety of stimuli including infections, immune reactions, blunt and penetrating trauma, physical and chemical agents, and tissue necrosis from any cause. In contrast, chronic inflammation is self-perpetuating and may last for weeks, months, or even years. It may develop as the result of a recurrent or progressive acute inflammatory process or from low-grade, smoldering responses that fail to evoke an acute response.

__________ inflammation is of relatively short duration, lasting from a few minutes, whereas __________ inflammation is of a longer duration, lasting from days to years.

Acute; chronic.

Virtually all biochemical processes in the body are affected by changes in __________.

Body temperature.

The function of the acute-phase protein __________ is thought to be protective, in that it binds to the surface of invading microorganism and targets them for destruction by complement and phagocytosis.

CRP (C-reactive protein).

Chemotaxis is dynamic and energy-directed process of directed __________.

Cell migration.

The integrins promote __________ and cell-to-extracellular matrix interactions.

Cell-to-cell.

Groups of proteins that direct the trafficking of leukocytes during the early stages of inflammation or injury are known as __________.

Chemokines.

Basophils

Circulating cells similar to mast cells.

The plasma-derived mediators of inflammation include the __________ factors and the __________ proteins.

Coagulation; complement.

__________ fragments contribute to the inflammatory response by causing vasodilation, increasing vascular permeability, and enhancing the activity of phagocytes.

Complement.

Aspirin and the non steroidal anti-inflammatory drugs (NSAIDS) reduce inflammation by inactivating the first enzyme in the __________ pathway for prostaglandin synthesis.

Cyclooxygenase.

Histamine causes __________ of arterioles and increases the __________ of venules.

Dilation; permeability.

The __________ family of inflammatory mediators consist of prostaglandins, leukotrienes, and related metabolites.

Eicosanoid.

At higher levels, free radical mediators can produce __________.

Endothelial cell damage.

The acute inflammatory response involves the production of __________; they can be serous, hemorrhagic, fibrinous, membranous, or purulent.

Exudates.

The nurse is caring for a 10 year old female with fever of 40 degrees C. The patient has been diagnosed with a bacterial infection. Her parents wonder about the cause of the fever. How should the nurse respond? What are other potential causes of a fever?

Fever describes an elevation in body temperature that is caused by a cytokine-induced upward displacement of the set point of the hypothalamic thermoregulatory center. Fevers that are regulated by the hypothalamus typically do not rise above 41 degrees C or 105 degrees F, suggesting a built in thermostatic regulatory mechanism. Bacterial cell membrane proteins, lipopolysaccharides, are most likely the cause of the increase. Many foreign proteins including lipopolysaccharide toxins released from bacterial cell membranes, can raise the set point of the hypothalamic thermostat. Injured tissues in the body or abnormal cells can stimulate the production of fever-producing molecules. Some malignant cells such as those of leukemia and Hodgkin disease also raise the set point.

__________ is one of the most prominent manifestations of the acute-phase response.

Fever.

Eosinophils

Increase in the blood during allergic reactions.

__________ is a protective response intended to eliminate the initial cause of cell injury, remove damaged tissue, and generate new tissue.

Inflammation.

Activation of the __________ system results in release of bradykinin, which increases vascular permeability and causes constriction of __________, dilation of blood vessels, and __________.

Kinin; smooth muscle; pain.

The selectins function in adhesion of __________ to endothelial cells.

Leukocytes.

Increased circulating white blood cells are a condition known as:

Leukocytosis.

Eating oily fish and other foods that are high in __________ results in partial replacement of arachidonic acid in inflammatory cell membranes, which leads to decreased production of arachidonic acid-derived inflammatory mediators.

Omega-3 fatty acids.

Agents that evoke chronic inflammation typically are low-grade, persistent infections or irritants that are unable to __________ or __________.

Penetrate deeply; spread rapidly.

The __________ radical, __________, and __________ radical are the major free oxygen radicals produced within the cell.

Superoxide; hydrogen peroxide; hydroxyl.

Edema

Swelling due to movement of fluid from vasculature into tissues.

What is meant by the cellular phase of inflammation?

The cellular phase of acute inflammation involves the delivery of leukocytes to the site of injury so they can act in host defense. The delivery and activation of leukocytes occurs in the following steps: adhesion and margination, transmigration, and chemotaxis.

The vascular response of inflammation follows one of three patterns. Describe these patterns, and explain why it is necessary to have multiple responses.

The first pattern is an immediate transient response, which occurs with minor injury. It develops rapidly after injury and is usually reversible and of short duration. Typically, this type of leakage affects venules 20-60 mm in diameter, leaving capillaries and arterioles unaffected. The second pattern is an immediate sustained response, which occurs with more serious types of injury and continues for several days. It affects all levels of the microcirculation and is usually due to direct damage of the endothelium due to injurious stimuli. The third pattern is a delayed hemodynamic response in which the increased permeability begins after a delay of 2-12 hours, lasts for several hours or even days, and involves venules as well as capillaries. A delayed response often accompanies radiation types of injuries.

Explain and describe the two forms of chronic inflammation.

The types of chronic inflammation are nonspecific and granulomatous. Nonspecific chronic inflammation involves a diffuse accumulation of macrophages and lymphocytes at the site of injury. Ongoing chemotaxis causes macrophages to infiltrate the inflamed site, where they accumulate owing to prolonged survival and immobilization. These mechanisms lead to fibroblast proliferation, with subsequent scar formation that in many cases replaces the normal connective tissue or the functional parenchymal tissues of the involved structures. A granulomatous lesion is a small, 1-2 mm lesion in which there is a massing of epithelioid cells surrounded by lymphocytes. Granulomatous inflammation is associated with foreign bodies and with microorganisms that are poorly digested and usually not easily controlled by other inflammatory mechanisms.

__________, a cytokine that will induce endothelial cells to express adhesion molecules and release cytokines, chemokine, and reactive oxygen species, is released from mast cells.

Tumor necrosis factor-a

__________ changes that occur with inflammation involve the arterioles, capillaries, and venules of the microcirculation and primarily involve an increase in permeability.

Vascular.

The cardinal signs of inflammation include swelling, pain, redness, and heat. What is the 5th cardinal sign of inflammation? a. Loss of function b. Altered level of consciousness c. Sepsis d. Fever

a. Loss of function The classic description of inflammation has been handed down through the ages. In the 1st century AD, the Roman physician Celsus described the local reaction of injury in terms now known as the cardinal signs of inflammation. These signs are rubor (redness), tumor (swelling), calor (heat), and dolor (pain). In the 2nd century AD, the Greek physician Galen added a fifth cardinal sign, function laesa (loss of function). Altered level of consciousness is not a cardinal sign of inflammation. Sepsis and fever are systemic signs of infection.

Inflammation can be either local or systemic. What are the most prominent systemic manifestations of inflammation? a. fever, leukocytosis or leukopenia, and the acute-phase response b. fever, leukocytosis or leukopenia, and the transition-phase response c. widening pulse pressure, thrombocytopenia, and the recovery-phase response d. widening pulse pressure, thrombocytopenia, and the latent-phase response

a. fever, leukocytosis or leukopenia, and the acute-phase response The most prominent systemic manifestations of inflammation include the acute-phase response, alterations in white blood cell count, and fever. Widening pulse pressure is not indicative of systemic inflammation, and thrombocytopenia is a hematologic disorder, not an indication of systemic inflammation.

During the acute inflammatory response, there is a period called the transient phase, where there is increased vascular permeability. What is considered the principal mediator of the immediate transient phase? a. histamine b. arachidonic acid c. fibroblasts d. cytokines

a. histamine Histamine causes dilation of arterioles and increases the permeability of venules. It acts at the level of the microcirculation by binding to histamine 1 (H1) receptors on endothelial cells and is considered the principal mediator of the immediate transient phase of increased vascular permeability in the acute inflammatory response. Arachidonic acid is a 20-carbon unsaturated fatty acid found in phospholipids of cell membranes. Release of arachidonic acid by phospholipases initiates a series of complex reactions that lead to the production of the eicosanoid family of inflammatory mediators (prostaglandins, leukotrienes, and related metabolites). Fibroblasts and cytokines are not the principal mediator of the transient phase of an acute inflammatory response.

The cells that are associated with allergic disorders and the inflammation associated with immediate hypersensitive reactions are known as what? (select all that apply) a. macrophages b. eosinophils c. mast cells d. neutrophils e. basophils

b. eosinophils c. mast cells e. basophils Eosinophils, basophils, and mast cells produce lipid mediators and cytokines that induce inflammation. They are particularly important in inflammation associated with immediate hypersensitivity reaction and allergic disorders. Neutrophils and macrophages are white blood cells that respond to inflammation and destroy invading bacteria. They do not induce inflammation.

Inflammation can be either acute or chronic. The immune system is thought to play a role in chronic inflammation and may be one of the reasons chronic inflammation may persist for days to months to years. Why is the risk of scarring and deformity greater in chronic inflammation than it is in acute inflammation? a. chronic inflammation is the persistent destruction of healthy tissues b. fibroblasts instead of exudates proliferate in chronic inflammation c. typically, agent that evoke chronic inflammation are infections or irritants that penetrate deeply and spread rapidly d. chronic inflammation is often the result of allergic reactions

b. fibroblasts instead of exudates proliferate in chronic inflammation Chronic inflammation involves the proliferation of fibroblasts instead of exudates. As a result, the risk of scarring and deformity usually is greater than in acute inflammation. Chronic inflammation is not the persistent destruction of healthy tissue. Typically, agents that cause chronic inflammation are agents that do not penetrate deeply or spread rapidly. Acute inflammation, not chronic, is the result of allergic reactions.

Metabolism changes when an individual has a fever. What are the primary sources of energy during a fever? (select all that apply) a. carbohydrates b. protein c. fats d. glycogen

b. protein c. fats During a fever, the body switches from using glucose to metabolism based on protein and fat breakdown. With prolonged fever, there is increased breakdown of endogenous fat stores. If fat breakdown is rapid, metabolic acidosis may result.

All wounds are considered contaminated at the time the wound occurs. Usually the natural defenses in our bodies can deal with the invading microorganisms at the time the wound occurs; however, there are times when a wound is badly contaminated and host defenses are overwhelmed. What happens to the healing process when host defenses are overwhelmed by infectious agents? a. the inflammatory response is shortened and does not complete destruction of the invading organisms b. fibroblast production becomes malignant because of hyper sensitization by invading organisms c. the formation of granulation tissue is impaired d. collagen fibers cannot draw tissues together

c. the formation of granulation tissue is impaired Infection impairs all dimensions of wound healing. It prolongs the inflammatory phase, impairs the formation of granulation tissue, and inhibits proliferation of fibroblasts and deposition of collagen fibers. All wounds are contaminated at the time of injury. Although body defenses can handle the invasion of microorganisms at the time of wounding, badly contaminated wounds can overwhelm host defenses. Trauma and existing impairment of host defenses also can contribute to the development of wound infections.