Pathophysiology Chapter 3 Study Guide

Front 1

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

Back 1

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

Front 2

The cardinal signs of inflammation are ___, ____, ____, and ____.

Back 2

The cardinal signs of inflammation are rubor, tumor, calor, and dolor.

Front 3

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.

Back 3

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

Front 4

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

Back 4

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

Front 5

Acute inflammation involves two major components: the ____ and ____ stages.

Back 5

Acute inflammation involves two major components: the vascular and cellular stages.

Front 6

Increased circulating white blood cells are a condition known as ____.

Back 6

Increased circulating white blood cells are a condition known as leukocytosis.

Front 7

_____ produce prostaglandins and leukotrienes, platelet-activating factor, inflammatory cytokines, and growth factors that promote regeneration of tissues.

Back 7

Monocytes produce prostaglandins and leukotrienes, platelet-activating factor, inflammatory cytokines, and growth factors

Front 8

___ changes that occur with inflammation involve the arterioles, capillaries, and venules of the microcirculation.

Back 8

Vascular chances that occur with inflammation involve the arterioles, capillaries, and venules of the microcirculation.

Front 9

The selectins function in adhesion of ___ to endothelial cells.

Back 9

The selectins function in adhesion of leukocytes to endothelial cells.

Front 10

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

Back 10

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

Front 11

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

Back 11

Chemotaxis is dynamic and energy-directed process of directed cell migration.

Front 12

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

Back 12

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

Front 13

The ____ pathways generate toxic oxygen and nitrogen products.

Back 13

The metabolic burst pathways generate toxic oxygen and nitrogen products.

Front 14

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

Back 14

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

Front 15

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

Back 15

Histamine causes dilation of arterioles and increases the permeability of venules.

Front 16

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

Back 16

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

Front 17

The ____ reduce inflammation and potentiate the effects of histamine and other inflammatory mediators.

Back 17

The prostaglandins reduce inflammation and potentiate the effects of histamine and other inflammatory mediators.

Front 18

Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) reduce inflammation by inactivating the first enzyme in the ___ pathway for prostaglandin synthesis.

Back 18

Aspirin and nonsteriodal anti-inflammatory drugs (NSAIDs) reduce inflammation by inactivating the first enzyme in the cyclooxygenase pathway for prostaglandin synthesis.

Front 19

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.

Back 19

Eating oily fish and other foods that are high in omega-3 fatty acids results in partial replacement of arachidonic acid in inflammatory cell membranes, which leads to decreased production of arachidonic acid-derived inflammatory mediators.

Front 20

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

Back 20

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

Front 21

Activation of the ___ system results in the release of bradykinin, which increases vascular permeability and causes contraction of ___, dilation of blood vessels, and ____.

Back 21

Activation of the kinin system results in the release of bradykinin, which increases vascular permeability and causes contraction of smooth muscle, dilation of blood vessels, and pain.

Front 22

___, a cytokine that will induce endothelial cells to express adhesion molecules and releases cytokines, chemokines, and reactive oxygen species, is released from mast cells.

Back 22

Tumor necrosis factor-alpha, a cytokine that will induce endothelial cell to express adhesion molecules and release cytokines, chemokines, and reactive oxygen species, is released from mast cells.

Front 23

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

Back 23

The superoxide radical, hydrogen peroxide, and hydroxyl radical are the major free oxygen radicals produced within the cell.

Front 24

At higher levels, free radical mediators can produce _____.

Back 24

At higher levels, free radical mediators can produce endothelial cell damage.

Front 25

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

Back 25

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

Front 26

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

Back 26

Agents that evoke chronic inflammation typically are low-grade, persistent infections or irritants that are unable to penetrate deeply or spread rapidly.

Front 27

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

Back 27

The function of the acute-phase protein CRP (C-reactive protein) is thought to be protective, in that it binds to the surface of invading microorganisms and targets them for destruction by complement and phagocytosis.

Front 28

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

Back 28

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

Front 29

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

Back 29

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

Front 30

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

Back 30

There are numerous arteriovenous (AV) shunts under the skin surface that allow blood to move directly from the arterial to the venous system.

Front 31

Endothelial cells

Back 31

regulate leukocyte extravastation

Front 32

Eosinophils

Back 32

increase in the blood during allergic reactions

Front 33

Edema

Back 33

swelling due to movement of fluid from vasculature into tissues

Front 34

Neutrophils

Back 34

primary phagocyte that arrives early at the site of inflammation

Front 35

Exudate

Back 35

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

Front 36

Nitric oxide

Back 36

stimulator of vasodilation

Front 37

Margination

Back 37

leukocyte accumulation

Front 38

Thrombocytes

Back 38

activation affects vascular permability, chemotactic, adhesive, and proteolytic properties.

Front 39

Mast Cells

Back 39

stimulate inflammatory reaction in response to injury or infection

Front 40

Basophils

Back 40

circulating cells similar to mast cells

Front 41

Put the following events in order: Chemotaxis, margination and adhesion to the endothelium, activation and phagocytosis, transmigration across the endothelium.

Back 41

Margination and adhesion --> transmigration across endothelium --> chemotaxis --> activation and phagocytosis.

Front 42

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.

Back 42

The signs are rubor (redness), tumor (swelling), calor (heat), and dolor (pain).

Hint 42

The rubor is the result of incrased blood flow due to histamine release. The tumor, or swelling, is due to an increased permeability of blood vessels due to histamine and other long-term vasoactive mediators. The calor, or heat, is the result of increased perfusion of the tissues at the wound site. Dolor, or pain, is due to the bradykinin, prostaglandins, and histamines effects on sensory nerve endings.

Front 43

Describe and differentiate between acute and chronic inflammation.

Back 43

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 or chemical agents, and tissue necrosis from any cause.

Hint 43

In contrast to acute inflammation, 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 processes or from low-grade, smoldering responses that fail to evoke an acute response.

Front 44

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

Back 44

The fist 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 to 60 mm in diameters, leaving capillaries and arterioles unaffected.

Hint 44

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 by injurous stimuli. The third pattern is a delayed hemodynamic response in which the increased permeability begins after a delay of 2 to 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.

Front 45

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

Back 45

Phagocytosis involves three distinct steps: (1) recognition and adherence, (2) engulfment, and (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.

Hint 45

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.

Front 46

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

Back 46

Mediators can be classified by function: (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, coagualtion facotrs of the clotting cascade, and vasoactive peptides of the kinin system; (3) chemotactic factors such as complement fragments and chemokines; and (4) reactive molecules and cytokines liberated from leukocytes, which when released into the extracellular environment can affect the surrounding tissues and cells.

Front 47

Explain and describe the two types of chronic inflammation.

Back 47

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 profliferation, with subsequent scar formation that in many cases replaces the normal connective tissue or the functional parenchymal tissues of the involved structures.

Hint 47

A granulomatous lesion is a small, 1- to 2- mm lesion in which there is a massing of epitheloid 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.

Front 48

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

Back 48

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 thermoregulatory center in the hypothalamus to produce fever.

Hint 48

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.

Front 49

The cardinal signs of inflammation include swelling, pain, redness and heat. What is the fifth cardinal sign of inflammation?

Back 49

Loss of function

Hint 49

The classic description of inflammation has been handed down through the ages. In the first 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 second century AD, the Greek physician Galen added a fifth cardinal sign, functio laesa (loss of function). Altered level of consciousness is not a cardinal sign of inflammation. Sepsis and fever are systemic signs of infection.

Front 50

The cells that are associated with allergic disorders and the inflammation associated with immediate hypersensitive reactions are known as what?

Back 50

Eosinophils, Mast cells, basophils

Hint 50

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

Front 51

Inflammation can be either acute or chronic. The immune system is through 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?

Back 51

Fibroblasts instead of exudates proliferate in chronic inflammation.

Hint 51

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 health 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.

Front 52

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?

Back 52

The formation of granulation tissue is impaired.

Hint 52

Infection impairs all dimensions of wound healing. It prolongs the inflammatory phase, impairs the formation of granulation tissue, and inhibits proliferaiton 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.

Front 53

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?

Back 53

Fibroblasts

Hint 53

Histamine causes dilation of arterioles and increases the permeability of venules. It acts at the level of the microcirculation by binding to histamin 1 (H1) receptors on endothelial cells and is considered the principal mediator of the immeduate 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 of phospholipases initiates a series of complex reactions that lead to the production of the eicosanoid family of inflammatory mediators (prostaglandins, leukotrienes, and related metabolites). Fibrobllasts and cytokines are not the principal mediator of the transient phase of an acute inflammatory response.

Front 54

Inflammation can be either local of systemic. What are the most prominent systemic manifestations to inflammation?

Back 54

Fever, leukocytosis or leukopenia, and the acute-phase response

Hint 54

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