Chapter 9: Inflammation & Tissue Repair Flashcards
Cardinal Signs of Inflammation (5)
rubor - redness tumor - swelling calor - heat dolor - pain functio laesa - loss of function
Goals of Inflammation
localize and eliminate microbes, foreign particles and abnormal cells
limit extent of tissue damage
repair of injured tissue
nonspecific, second line of defense
Cells of Inflammation
endothelial cells
platelets (thrombocytes)
neutrophils & macrophages
mast cells
Endothelial Cells
selectively-permeable barrier
maintain vessel patency (produce antiplatelet/antithrombin)
regulate blood flow (vasodilators/vasoconstrictors)
release inflammatory mediators
production of GF for angiogenesis
Platelets (Thrombocytes)
involved in primary hemostasis
activated platelets release potent inflammatory mediators
increase vascular permeability (edema)
can cause vasodilation (redness, heat and pain)
Neutrophils
primary phagocyte that arrives early
short-lived and must replaced constantly to maintain numbers
Monocytes/Macrophages
arrive shortly after neutrophils and perform functions longer
engulf larger and greater quantities of foreign material
produce potent vasoactive mediators
pal an important role in chronic inflammation
Vasoactive Mediators
prostaglandins leukotrienes (LT) platelet-activating factor (PAF) inflammatory cytokines growth factors
Mast Cells
contain granules (histamine, proteoglycans, proteases) and cytokines (TNF-α and IL-16) released at activation (degranulation) involved in IgE-triggered reactions and helminth infections
Vascular Stage of Inflammation
involves the arterioles, capillaries, and venules
brief vasoconstriction
vasodilation (redness and warmth)
changes in blood flow
increased vascular permeability and leakage of fluid into the extra vascular tissues (edema, pain, impaired function)
The Cellular Stage of Inflammation
includes leukocyte: 1 margination and adhesion to the endothelium 2 transmigration across the endothelium 3 chemotaxis 4 activation and phagocytosis
Margination
leukocyte accumulation
Adhesion
leukocytes adhere to the endothelium via intracellular adhesion molecules (ICAMSs)
Transmigration
leukocytes move through the vessel wall and migrate to tissue spaces
Chemotaxis
the dynamic and energy-directed process of DIRECTED cell migration
chemokines that direct the trafficking of leukocytes
Phagocytosis
the ingestion of other cells
engulf and degrade bacteria and cellular debris
initiated by the recognition and binding particles
Binding
trapping the agent, which triggers engulfment and activate the killing potential of the cell
Opsonization
the coating of an antigen with antibody or complement to enhance binding (to help the antibody recognize it)
enhances phagocytosis
Histamines
found in mast cell granules
released in response to trauma and immune reactions involving binding of IgE antibodies
Location and Roles of Histamine
widely distributed in tissues
causes vasodilation
increased vascular permeability by H1 receptors on endothelial cells
Arachidonic Acid Metabolites
eicosanoid inflammatory mediators:
prostaglandins
leukotrienes (LT)
thromboxane A2
Cyclooxygenase Pathyway
produces prostaglandins and thromboxane A
Lipoxygenase Pathway
produces leukotrienes
Prostaglandins
induce inflammation and potentiate the effects of histamine and other inflammatory mediators
Prostaglandins and Thromboxane A (TXA)
promote platelet aggregation and vasoconstriction
Leukotrienes
similar in function to histamines but are more potent and longer-lasting
important inflammatory mediators in BRONCHIAL ASTHMA AND ANAPHYLAXIS
Bradykinin
plasma protein that increases vascular permeability and causes contraction of smooth muscle and vasodilation
Cytokines
proteins produced by may cell types that modulate the function of other cells
TNF-α and IL-1 are two of the major cytokines that mediate inflammation
Chemokines
family of small proteins that act primarily as chemoattractants to recruit and direct the migration of immune and inflammatory cells
inflammatory and homing chemokines
Nitric Oxide (NO)
smooth muscle relaxation
antagonism of platelet adhesion, aggregation and degranulation
regulator of leukocyte recruitment (decreases)
reduces the cellular phase of inflammation
have antimicrobial actions
Serous Exudates
watery fluids, low in protein content, that result form plasma entering the inflammatory site
Hemorrhagic Exudates
occur when there is sever tissue injury that damages blood vessels
significant leakage of RBCs from the capillaries
Fibrinous Exudates
contain large amounts of fibrinogen and form a thick, sticky meshwork
Membranous Exudates
develop on mucous membrane surfaces and are composed of necrotic cells enmeshed in fibropurulent exudates
Purulent Exudates
contains pus, which is composed of degraded WBCs, protein and tissue debris
also known as suppurative exudates
Abscess
localized area of inflammation containing a purulent exudate that may be surrounded by a neutrophil layer
fibroblasts may eventually enter the area and wall off the abscess
Acute-Phase Response of Inflammation
begins within hours or days of onset of inflammation or infection
release of cytokines (IL-1, IL-6, and TNF-α)
fever, anorexia, fatigue, malaise
acute phase proteins: CRP
C-Reactive Protein (CRP)
biomarker in acute MI, malignancies, and autoimmune disorders function is protective - binds to surfaces of antigens to target for destruction synthesis is up-regulated by IL-6 during acute phase
Labile Cells
continue to divide and replicate throughout life, replacing cells that are constantly being destroyed (apoptosis)
epithelial cells, columnar epithelium, transitional epithelium
skin, oral cavity, vagina, GI tract, uterus, urinary tract
bone marrow cells
Stabile Cells
normally stop dividing when growth ceases
capable of regeneration if needed
parenchymal cells of the liver and kidney
smooth muscle cells and vascular endothelial cells
Permanent Cells
cannot undergo mitotic division and do not normally regenerate
replaced by scar tissue that lacks the function of destroyed tissue
nerve cells, skeletal muscle cells, cardiac muscle cells
Fibrous Tissue Repair
replacement with connective tissue
process that involves generation of granulation tissue and formation of scar tissue
Angiogenesis
generation of new blood vessels from preexisting blood vessels
gives red appearance of granulation tissue
Fibrinogenesis
influx of activated fibroblasts
initiation of collagen synthesis
Scar Formation
formation of pale, largely avascular tissue (scar)
Primary Intention
no tissue loss
heals more quickly
Example: sutured surgical incision
Primary intention wounds can become infected and need to heal by secondary intention
Secondary Intention
larger wounds that have a greater loss of tissue and contamination
heal more slowly - may leave open for a time
results in larger amounts of scar tissues
Examples: burns, large surface wounds
Phases of Wound Healing
1 inflammatory phase
2 proliferative phase
3 remodeling phase
1 Inflammatory Phase of Wound Healing
begins at the time of injury
prepares wound environment for healing
brief constriction then vasodilation and increased permeability
involves neutrophils and macrophages
2 Proliferative Phase of Wound Healing
usually begins within 2 to 3 days of injury and may last up to 3 weeks
Focus: build new tissue to fill the wound space
Key cells: fibroblasts and endothelial cells
granulation tissue forms within 48 hours
Epithelization
final component of proliferative phase that involves migration, proliferation, and differentiation of the epithelial cells at the wound edges to form a new surface layer similar to the one that was destroyed
3 Remodeling Phase of Wound Healing
begins approximately 3 weeks after injury and continues for 6 months or longer
continued production of scar tissue through collagen synthesis
most wounds only gain 70-80% of the tensile strength of unwounded skin
