Chapter 9: Inflammation & Tissue Repair Flashcards

1
Q

Cardinal Signs of Inflammation (5)

A
rubor - redness
tumor - swelling
calor - heat
dolor - pain
functio laesa - loss of function
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2
Q

Goals of Inflammation

A

localize and eliminate microbes, foreign particles and abnormal cells
limit extent of tissue damage
repair of injured tissue
nonspecific, second line of defense

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3
Q

Cells of Inflammation

A

endothelial cells
platelets (thrombocytes)
neutrophils & macrophages
mast cells

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4
Q

Endothelial Cells

A

selectively-permeable barrier
maintain vessel patency (produce antiplatelet/antithrombin)
regulate blood flow (vasodilators/vasoconstrictors)
release inflammatory mediators
production of GF for angiogenesis

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5
Q

Platelets (Thrombocytes)

A

involved in primary hemostasis
activated platelets release potent inflammatory mediators
increase vascular permeability (edema)
can cause vasodilation (redness, heat and pain)

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6
Q

Neutrophils

A

primary phagocyte that arrives early

short-lived and must replaced constantly to maintain numbers

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7
Q

Monocytes/Macrophages

A

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

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8
Q

Vasoactive Mediators

A
prostaglandins
leukotrienes (LT)
platelet-activating factor (PAF)
inflammatory cytokines
growth factors
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9
Q

Mast Cells

A
contain granules (histamine, proteoglycans, proteases)
and cytokines (TNF-α and IL-16)
released at activation (degranulation)
involved in IgE-triggered reactions and helminth infections
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10
Q

Vascular Stage of Inflammation

A

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)

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11
Q

The Cellular Stage of Inflammation

A
includes leukocyte:
1 margination and adhesion to the endothelium
2 transmigration across the endothelium
3 chemotaxis
4 activation and phagocytosis
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12
Q

Margination

A

leukocyte accumulation

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13
Q

Adhesion

A

leukocytes adhere to the endothelium via intracellular adhesion molecules (ICAMSs)

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14
Q

Transmigration

A

leukocytes move through the vessel wall and migrate to tissue spaces

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15
Q

Chemotaxis

A

the dynamic and energy-directed process of DIRECTED cell migration
chemokines that direct the trafficking of leukocytes

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16
Q

Phagocytosis

A

the ingestion of other cells
engulf and degrade bacteria and cellular debris
initiated by the recognition and binding particles

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17
Q

Binding

A

trapping the agent, which triggers engulfment and activate the killing potential of the cell

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18
Q

Opsonization

A

the coating of an antigen with antibody or complement to enhance binding (to help the antibody recognize it)
enhances phagocytosis

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19
Q

Histamines

A

found in mast cell granules

released in response to trauma and immune reactions involving binding of IgE antibodies

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20
Q

Location and Roles of Histamine

A

widely distributed in tissues
causes vasodilation
increased vascular permeability by H1 receptors on endothelial cells

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21
Q

Arachidonic Acid Metabolites

A

eicosanoid inflammatory mediators:
prostaglandins
leukotrienes (LT)
thromboxane A2

22
Q

Cyclooxygenase Pathyway

A

produces prostaglandins and thromboxane A

23
Q

Lipoxygenase Pathway

A

produces leukotrienes

24
Q

Prostaglandins

A

induce inflammation and potentiate the effects of histamine and other inflammatory mediators

25
Prostaglandins and Thromboxane A (TXA)
promote platelet aggregation and vasoconstriction
26
Leukotrienes
similar in function to histamines but are more potent and longer-lasting important inflammatory mediators in BRONCHIAL ASTHMA AND ANAPHYLAXIS
27
Bradykinin
plasma protein that increases vascular permeability and causes contraction of smooth muscle and vasodilation
28
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
29
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
30
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
31
Serous Exudates
watery fluids, low in protein content, that result form plasma entering the inflammatory site
32
Hemorrhagic Exudates
occur when there is sever tissue injury that damages blood vessels significant leakage of RBCs from the capillaries
33
Fibrinous Exudates
contain large amounts of fibrinogen and form a thick, sticky meshwork
34
Membranous Exudates
develop on mucous membrane surfaces and are composed of necrotic cells enmeshed in fibropurulent exudates
35
Purulent Exudates
contains pus, which is composed of degraded WBCs, protein and tissue debris also known as suppurative exudates
36
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
37
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
38
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 ```
39
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
40
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
41
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
42
Fibrous Tissue Repair
replacement with connective tissue | process that involves generation of granulation tissue and formation of scar tissue
43
Angiogenesis
generation of new blood vessels from preexisting blood vessels gives red appearance of granulation tissue
44
Fibrinogenesis
influx of activated fibroblasts | initiation of collagen synthesis
45
Scar Formation
formation of pale, largely avascular tissue (scar)
46
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
47
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
48
Phases of Wound Healing
1 inflammatory phase 2 proliferative phase 3 remodeling phase
49
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
50
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
51
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
52
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