Chapter 9 - Inflammation, Tissue Repair, and Wound Healing

cardinal signs of inflammation

rubor (redness), tumor (swelling), calor (heat), dolor (pain), functio laesa (loss of function)

acute-phase response

systemic manifestations that may occur during acute inflammation as cytokines are produced

acute inflammation

short-duration inflammation characterized by the exudation of fluid and plasma components and the emigration of neutrophils into extravascular tissues

chronic inflammation

long-duration inflammation associated with the presence of macrophages, proliferation of blood vessels, fibrosis, and tissue necrosis

triggers of acute inflammation

infection, immune reactions, blunt or penetrating trauma, physical or chemical agents, and tissue necrosis

endothelial cells

provide a selective permeability barrier to inflammatory stimuli, regulate leukocyte extravasation, contribute to the regulation and modulation of immune responses, and participate in repair process

Vascular phase of acute inflammation

Brief vasoconstriction followed by rapid vasodilation, causing heat and redness; an increase in capillary pressure causes fluid accumulation in tissue spaces

Cellular phase of acute inflammation

delivery of neutrophils through endothelial activation, adhesion and margination, transmigration, and chemotaxis so that phagocytosis can occur

leukocyte activation and phagocytosis phase of acute inflammation

products generated by tissue injury trigger phagocytosis and cell killing; pseudopods enclose microbe with a phagosome, oxygen free radicals are released to kill and degrade the microbe

Components of the extracellular matrix

fibrous proteins, adhesive glycoproteins, and proteoglycans

platelets

formed elements circulating in blood that are involved in cellular mechanisms of primary hemostasis; release potent inflammatory mediators

neutrophils function

primary phagocyte that arrives early at site of inflammation; can generate oxygen and nitrogen products that assist in destroying engulfed debris

neutrophils lifespan

10 hours, so they need an increase in circulating WBCs (leukocytosis)

monocytes

The largest leukocytes; arrive at the inflammatory site after neutrophils

macrophages

engulf larger and greater quantities of foreign material than neutrophils

principal cells of inflammation

neutrophils, macrophages, lymphocytes, eosinophils, mast cells

Eosinophils, basophils, and mast cells

produce lipid mediators and cytokines that induce inflammation; important in hypersensitivity and allergic disorders

exudate

outpouring of fluid into extravascular spaces

vascular immediate transient response

leakage affecting venules caused by a minor injury; develops rapidly after injury with short duration

vascular immediate sustained response

leakage affecting arterioles, capillaries, and venules due to direct endothelial damage; occurs with more serious injuries and lasts several days

Vascular delayed hemodynamic response

increased permeability in venules and capillaries, possibly resulting from the direct effect of the injurious agent, leading to DELAYED endothelial damage (common with sunburn)

cellular margination

Leukocytes slow migration, adhere to endothelium, and begin to move along the blood vessels

cellular adhesion

Cytokines cause cells lining the vessels to express adhesion molecules that bind the cells to the endothelium

cellular transmigration

Leukocytes move through vessel wall and migrate into tissue spaces

chemotaxis

dynamic and energy-directed process of directed cell migration

chemokines

small proteins that direct trafficking of leukocytes during the early stages of inflammation or injury; secreted by immune and non-immune cells

phagocytosis steps

recognition and adherence, engulfment, intracellular killing

opsonization

coating an antigen with antibody or complement to enhance binding

inflammation signs and symptoms are produced by ________

chemical mediators

plasma-derived mediators

synthesized in the liver; include acute-phase proteins, coagulation (XII) factors, and complement proteins

cell-derived mediators

preformed mediators in intracellular granules or newly synthesized in response to stimulus

acute-phase proteins

fever, inflammation

Factor XII (hageman) activation

clotting and kinin system

preformed mediators

mast cells, platelets, neutrophils, macrophages

newly synthesized mediators

leukocytes, macrophages, lymphocytes, endothelial cells

mast cells produce

histamine

histamine

one of the first mediators to be released during acute inflammatory reaction; caused dilation of arterioles and increases the permeability of vessels

arachidonic acid metabolites

20-carbon unsaturated fatty acid found in phospholipids of cell membrane that leads to production of eicosanoid family of inflammatory mediators

eicosanoid family of inflammatory mediators

prostaglandins, LT, and related metabolites

cyclooxygenase pathway

synthesis of prostaglandins and thromboxane (prostanoids)

lipoxoyfenase pathway

synthesis op LT

Prostaglandins and thromboxane A2 promote

platelet aggregation and vasoconstriction

platelet-activating factor

activates neutrophils and is an eosinophil chemoattractant; causes hypersensitivity reactions

plasma protein clotting system

contributes to vascular phase of inflammation through fibrinopeptides and thrombin

plasma protein complement system

20 inactive complement proteins that increase vascular permeability, improve phagocytosis, and cause vasodilation

plasma protein kinin system

release of bradykinin, which increases vascular permeability and dilates blood vessels

inflammatory chemokines

produced in response to bacterial toxins and inflammatory cytokines

homing chemokines

direct chemotaxis to responsive cells

Nitric oxide

smooth muscle relaxation and antagonism of platelet adhesion, aggregation, and degranulation

oxygen free radicals

combine with NO to form other reactive nitrogen intermediates, which can increase inflammation and cause more tissue injury

serous exudates

watery fluids low in protein content, result from plasma entering the inflammatory site

hemorrhagic exudates

occur when there is severe tissue injury that causes damage to 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 meshwork

membranous or pseudomembranous exudates

develop on mucous membrane surfaces and are composed of necrotic cells enmeshed in a fibropurulent exudate

purulent or suppurative exudate

contains pus, which is composed of degraded white blood cells, proteins, and tissue debris

nonspecific chronic inflammation

diffuse accumulation of macrophages and lymphocytes at the site of injury, scar formation replaces normal tissues

granulomatous chronic inflammation

lesion where there is a massing of macrophages surrounded by lymphocytes; caused by foreign agents that are not easily controlled by other inflammatory mechanisms

manifestations of acute-phase response

fever, anorexia, somnolence, malaise

systemic inflammatory response syndrome

Cytokines cause generalized vasodilation, increased vascular permeability, intravascular fluid loss, myocardial depression, and circulatory shock due to sepsis

leukocytosis

increased number or WBCs, common in bacterial infections

viral infections tend to produce _____ and ______

neutropenia and lymphocytosis

lymphadenitis

inflammation of the lymph nodes

tissue repair

response to tissue injury to attempt to maintain normal body structure and function

tissue regeneration

replacement of injured tissue with cells of same type

labile cells

continue to divide and replicate throughout life

stable cells

normally stop dividing when growth ceases, but can undergo regeneration when appropriate stimulus

permanent/fixed cells

cannot undergo mitotic division; cannot regenerate and are replaced with scar tissue

first intention

A type of wound healing (closure) for wounds with little tissue loss, such as a surgical incision.

secondary intention

wounds that have greater tissue loss and contamination

inflammatory phase of wound healing

formation of blood clot and migration of phagocytic white blood cells into the wound site at the time of injury

proliferative phase of wound healing

buildup of new tissue to fill the wound space by angiogenesis and epithelialization

wound contraction and remodeling phase

begins 3 weeks after injury; decrease in vascularity; scar can shrink and become less visible due to increased tensile strength

5 factors that affect wound healing

malnutrition, blood flow/oxygen delivery, impaired inflammatory/immune responses, contamination + separation + foreign bodies, bite wounds

wound healing may be impaired in _____ and _______

neonates and older adults

Dehiscence

partial or total separation of wound layers

vitamin _ is needed for collagen synthesis

C

which bite is most likely to be infected

cat bite

During acute inflammation, what describes the primary vascular response that contributes to the development of cardinal signs of inflammation?

Vasodilation and increased vascular permeability

The inflammatory process is a nonspecific response to noxious stimuli including bacterial invasion and injury. Which are the principal cells of inflammation?

Neutrophils, macrophages, lymphocytes, eosinophils, and mast cells

The nurse is reviewing the laboratory results for the client with pneumonia and notes that the white blood cell count is continuing to rise. The nurse understands that bacterial endotoxins are triggering leukocytosis and activating which types of cells in the inflammatory process?

Neutrophils

The nurse is monitoring the newly admitted patient for signs and symptoms of deep vein thrombosis and pulmonary embolism. When the patient is prescribed prophylactic anticoagulation medication, the nurse understands that platelet activation occurs due to the production of which substance?

Prostaglandins