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Adv Pathophysiology > Chapter 9: Inflammation & Tissue Repair > Flashcards

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
Q

Prostaglandins and Thromboxane A (TXA)

A

promote platelet aggregation and vasoconstriction

26
Q

Leukotrienes

A

similar in function to histamines but are more potent and longer-lasting
important inflammatory mediators in BRONCHIAL ASTHMA AND ANAPHYLAXIS

27
Q

Bradykinin

A

plasma protein that increases vascular permeability and causes contraction of smooth muscle and vasodilation

28
Q

Cytokines

A

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
Q

Chemokines

A

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
Q

Nitric Oxide (NO)

A

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
Q

Serous Exudates

A

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

32
Q

Hemorrhagic Exudates

A

occur when there is sever tissue injury that damages blood vessels
significant leakage of RBCs from the capillaries

33
Q

Fibrinous Exudates

A

contain large amounts of fibrinogen and form a thick, sticky meshwork

34
Q

Membranous Exudates

A

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

35
Q

Purulent Exudates

A

contains pus, which is composed of degraded WBCs, protein and tissue debris
also known as suppurative exudates

36
Q

Abscess

A

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
Q

Acute-Phase Response of Inflammation

A

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
Q

C-Reactive Protein (CRP)

A 
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
Q

Labile Cells

A

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
Q

Stabile Cells

A

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
Q

Permanent Cells

A

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
Q

Fibrous Tissue Repair

A

replacement with connective tissue

process that involves generation of granulation tissue and formation of scar tissue

43
Q

Angiogenesis

A

generation of new blood vessels from preexisting blood vessels
gives red appearance of granulation tissue

44
Q

Fibrinogenesis

A

influx of activated fibroblasts

initiation of collagen synthesis

45
Q

Scar Formation

A

formation of pale, largely avascular tissue (scar)

46
Q

Primary Intention

A

no tissue loss
heals more quickly
Example: sutured surgical incision
Primary intention wounds can become infected and need to heal by secondary intention

47
Q

Secondary Intention

A

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
Q

Phases of Wound Healing

A

1 inflammatory phase
2 proliferative phase
3 remodeling phase

49
Q

1 Inflammatory Phase of Wound Healing

A

begins at the time of injury
prepares wound environment for healing
brief constriction then vasodilation and increased permeability
involves neutrophils and macrophages

50
Q

2 Proliferative Phase of Wound Healing

A

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
Q

Epithelization

A

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
Q

3 Remodeling Phase of Wound Healing

A

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

Adv Pathophysiology (22 decks)

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