Chapter 9

Question 1

• intended to eliminate the initial cause of cell injury, remove the damaged tissue, and generate new tissue
  
  • accomplishes this by destroying, enzymatically digesting, walling off, or otherwise neutralizing the harmful agents (toxins, foreign agents, or infectious organisms)
• intimately interwoven with the repair processes that replace damaged tissue or fill in the residual defects with fibrous scar tissues
• characterized by inflammatory mediators
• complement, tumor necrosis factor-a (TNF-a), vascular endothelial growth factor (VEGF), neutrophils, and serum amyloid, and the movement of fluid, wither within the cells or interstitial fluid
• generally localizes and eliminates microbes, foreign particles, and abnormal cells and paves the way for repair for the injured tissue
• commonly named by adding the suffix -itis
• cardinal sings of inflammation
  
  • rubor (redness), tumor (swelling), calor (heat), dolor (pain), functio laesa (loss of function)
• acute and chronic inflammation

Answer 1

inflammation

Question 2

• relatively short duration, lasting from a few minutes to several days
• characterized by the exudation of fluid and plasma components and emigration of leukocytes (neutrophils) into the extravascular tissues
• can be triggered by a variety of stimuli
  
  • infections, immune reactions, blunt and penetrating trauma, physical or chemical agents (burns, frostbite, irradiation, caustic chemicals), and tissue necrosis from any cause
• involves 2 major components
  
  • vascular stage: leads to an increase in blood flow and changes in the small blood vessels of the microcirculation (marked by edema)
  • cellular stage: leads to the migration of leukocytes from the circulation and their activation to eliminate the injurious agent
    - margination and adhesion to the endothelium
    - transmigration across the endothelium
    - chemotaxis
    - activation and phagocytosis

Answer 2

Acute inflammation

Question 3

• produces signs and symptoms of inflammation
• can originate either from the plasma or from cells
• plasma derived mediators
  
  • synthesized in the liver, include coagulation factors and the complement proteins
  • present in the plasma in a precursor form that must be activated by a series of proteolytic processes to acquire their biologic properties
• cell derived mediators
  
  • sequestered in intracellular granules that need to be secreted or are newly synthesized in response to a stimulus
• production of active mediators is triggered by microbes or host proteins
  
  • activated by microbes or damaged tissues
  • can act on one or a few target cells, have diverse targets, or have differing effects on different types of cells
• most are short lived
• may be transformed into inactive metabolites, inactivated by enzymes, or otherwise scavenged or degraded
• can be classified by function
  
  • those with vasoactive and smooth muscle constricting properties (histamine, arachidonic metabolites, and PAF
  • plasma pro teases that activate members of the complement system, coagulation factors of the clotting cascade, and vasoactive peptides of the kinin system
  • chemotactic factors such as complement fragments and chemokines
  • reactive molecules and cytokines liberated from leukocytes, can affect the surrounding tissue and cells

Answer 3

Inflammatory Mediators

Question 4

• site of involvement introduce variations in its manifestations and clinical correlates
  
  • manifestations can range from swelling and the formation of exudates to abscess formation
    
    • many for my of exudate
    • an abscess is a localized area of inflammation containing purulent exudate that my be surrounded by a neutrophil layer

Answer 4

Local manifestations

Question 5

• serous exudates: watery fluids low in protein content that result from plasma entering the inflammatory site
• hemorrhagic exudates: occurs when there is severe tissue injury that damages blood vessels or when there is significant leakage of red cells from the capillaries
• fibrinous exudates: contain large amounts of fibrinogen and form a thick and sticky mesh work
• membranous or pseudomembranous exudates: develop on mucous membrane surfaces and are composed of necrotic cells enmeshed in fibropurulent exudate
• purulent or suppurative exudate: contains pus (composed of degraded white blood cells, proteins, and tissue debris) (staphylococcus)

Answer 5

Exudates

Question 6

• site of inflammation where an epithelial surface has become necrotic and eroded
• may occur as the result of traumatic injury to the epithelial surface or because of vascular compromise

Answer 6

Ulceration

Question 7

• self perpetuating and may lasts for weeks, months, or even years
• may develop as a result of a recurrent or progressive acute inflammation
• characteristics: infiltration by mononuclear cells (macrophages) and lymphocytes, involves the proliferation of fibroblasts instead of exudates
• risk of scarring and deformity usually is greater than in acute inflammation
• causes: foreign bodies (talc, silica, asbestos, surgical suture responses), viruses, bacteria, fungi, and larger parasites of moderate to low virulence
• two patterns
  
  • nonspecific chronic inflammation
  • granulomatous inflammation

Answer 7

Chronic Inflammation

Question 8

• 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 prolonged survival and immobilization
    - lead to fibroblast proliferation, subsequent scar formation

Answer 8

Nonspecific Chronic Inflammation

Question 9

• typically is a small, 1-2 mm lesion in which there is a massing of macrophages surrounded by lymphocytes
  
  • foreign body giant cells
• associated with foreign bodies (splinters, sutures, silica, asbestos) and with microorganisms that cause tuberculosis, syphilis, sarcoidosis, deep fungal. Infections, and brucellosis

Answer 9

Granulomatous Inflammation

Question 10

• most prominent systemic manifestations of inflammation include acute-phase response, alterations in the white blood cell count, and fever
• may extend to the lymphatic system and lead to a reaction in the lymph nodes that drain the affected area

Answer 10

Systemic manifestation of inflammation

Question 11

• usually begins w/in hrs or days of the onset of inflammation or infection, includes changes in the concentrations of plasma proteins, skeletal muscle catabolism, negative nitrogen balance, elevated erythrocyte sedimentation (ESR), and increased number of leukocytes
• manifestations include anorexia, somnolence, and malaise
• metabolic changes provide amino acids that can be used in the immune response and for tissue repair
• serves to coordinate the various changes in body function to enable optimal host response

Answer 11

Acute-Phase Response

Question 12

• leukocytosis: increased white blood cells, frequent sign of an inflammatory response
  
  • commonly increases from a normal value (4,000 cells/mcg) to an abnormally value (10,000-15,000 cells/mcg) in acute inflammatory conditions
• bacterial infections produce a relatively selective increase in neutrophils
• parasitic and allergic responses induce eosinophilia
• viral infections tend to produce a decrease in neutrophils (neutropenia) and an increase in lymphocytes (lymphocytosis)
• a decrease in white blood cells (leukopenia) may occur with overwhelming infections or an impaired ability to produce white blood cells

Answer 12

White Blood Cell Response

Question 13

• reaction in the lymph nodes that drain the affected area
• represents a nonspecific response to mediators released from the injured tissue or an immunological response to a specific antigen
• painful palpable lymph nodes are associated with inflammatory process

Answer 13

Lymphadenitis

Question 14

• response to tissue injury and represents an attempt to maintain normal body structure and function
• regeneration: the injured cells are replaced with cells of the same type, sometimes leaving no residual trace of previous injury
• replacement by connective tissue: leaves a permanent scar

Answer 14

Tissue Repair

Question 15

• varies with the tissue and cell type
• labile cells: those that continue to divide and replicate throughout life, replacing cells that are continually being destroyed
• stable cells: stop dividing when growth ceases, capable of undergoing regeneration when confronted with an appropriate stimulus and are capable of reconstituting the tissue of origin
• permanent or fixed cells: cannot undergo mitotic division, do not normally regenerate; replaced with fibrous scar tissue that lacks functional characteristics of the destroyed tissue

Answer 15

Tissue Regeneration

Question 16

• when the repair cannot be accomplished with regeneration alone
• repair occurs by replacement with connective tissue, a process that involves generation of granulation tissue and formation of scar tissue
  
  • granulation tissue is a glistening red, moist connective tissue that contains newly formed capillaries, proliferating fibroblasts, and residual inflammatory cells

Answer 16

Fibrous Tissue repair

Question 17

• primary objective of the healing process is to fill the gap created by tissue destruction and to restore the structural continuity of the injured part
• depending on the extent of tissue loss, wound closures and healing occur by primary or secondary intention
  
  • primary intention=sutured surgical incision
  • secondary intention=slower healing and results in the formation of larger amounts of scar tissue
• phases of wound healing
  (1) inflammatory phase: begins at the time of injury and is critical period because it prepares the wound environment for healing, includes hemostasis and the vascular and cellular phases of inflammation
  (2) proliferative phase: begins w/in 2-3 days of injury and may last as long as 3 weeks in wound healing by primary intention
  (3) remodeling phase: begins approximately 3 weeks after injury and can continue for 6 months or longer depending on the extent of the wound. Continued remodeling of scar tissue by simultaneous synthesis of collagen by fibroblasts and lysis by collagenase enzymes; architecture of the scar is reoriented to increase tensile strength of the wound

Answer 17

Wound Healing

Question 18

• malnutrition (inadequate stores of proteins, carbohydrates, fats, vitamins, and minerals)
• impaired blood flow and oxygen delivery (swelling, arterial disease, venous pathology, decrease in blood volume)
• impaired inflammatory and immune responses (phagocytic function, diabetes mellitus, therapeutic administration of corticosteroid drugs)
• infection, wound separation, foreign bodies (prolongs inflammatory phase, bite wounds)
• age (child has a greater capacity for repair than the adult, but lack the reserves to ensure proper healing; older adults-decreased dermal thickness, decline in collagen content, loss of elasticity)
• diabetes mellitus
• peripheral artery disease
• venous insufficiency
• nutritional disorders

Answer 18

Causes of impaired wound healing