Trans 4 - Inflammation and Repair Flashcards
1
Q
-Response of living, vascularized tissue to injury
-Role is to destroy or isolate injurious agents in order to
achieve healing and repair
A
inflammation
2
Q
The pattern of inflammation is determined by
A
- Inciting agent
- Time of observation
- Immune status of host
3
Q
The inciting agents of inflammation are
A
- Infection
- Trauma
- Physical and chemical agents
- Tissue necrosis
- Foreign bodies
- Immune reactions
4
Q
What kind of inflammation has an early onset (seconds to minutes) and short duration (minutes to days)
A
acute inflammation
5
Q
acute inflammation involves
A
- fluid exudation (edema)
- plasma proteins
- polymorphonuclear cell (neutrophil) emigration
6
Q
Inflammation that has
-later onset (days)
-longer duration (weeks to years)
-Characterized by tissue infiltration with
macrophages, lymphocyte, and plasma cells, or
eosinophil – all derived from blood.
A
chronic inflammation
7
Q
Chronic inflammation induces
A
blood vessel proliferation and scarring
8
Q
acute inflammation is characterized by
A
- Changes in blood flow
- Increased vascular permeability
- Infiltration of tissues by neutrophils
9
Q
Acute inflammation may lead to:
A
- Complete resolution
- Healing by connective tissue replacement (scarring)
- Chronic inflammation
10
Q
cardinal signs of inflamation
A
dolor, rubor, calor, functio laesa, tumor
11
Q
Rubor means
A
redness
12
Q
causes of rubor and calor
A
vessel dilatation and
increased blood flow to the
inflamed part
13
Q
calor means
A
warmth
14
Q
dolor means
A
pain
15
Q
causes of dolor
A
Increased pressure on nerve endings from swelling, and a direct effect of certain chemical factors which are released to mediate response
16
Q
tumor means
A
swelling
17
Q
causes of tumor
A
Accumulation of fluid especially exudates
18
Q
functio laesa means
A
loss of function
19
Q
causes of functio laesa
A
When swelling and pain are marked, there is partial or
complete loss of function of the inflamed structure.
20
Q
what are the components of acute inflammation
A
vascular changes, cellular events,
21
Q
Alterations in vascular caliber that lead to an
increased blood flow
A
vasodilation
22
Q
Structural changes in the microvasculature that
permits plasma proteins and leukocytes to leave the
circulation
A
hallmark of acute inflammation: increase in vascular permeability
23
Q
changes in blood flow
A
-Transient arteriolar constriction results in shortlived
decreased blood flow to the area.
-Followed by dilatation of arterioles and opening of
capillary beds resulting in increased blood flow
(causing rubor and calor)
-Slowing of blood (stasis) leading to leukocyte
margination (sticking of cells to the vessel wall)
24
Q
Structural changes in the microvasculature that permit
leakage of plasma proteins and leukocytes into the
damaged area
A
increased vascular permeability
25
causes of increased vascular permeability
- Formation of gaps due to endothelial contraction
- Endothelial injury
- Leukocyte-mediated endothelial injury
- Increased Transcytosis
26
-Occurs in arterioles, capillaries, venules
-Caused by burns, some microbial toxins, and
chemicals
-Rapid: may be long-lived (hours to days
endothelial injury
27
- Occurs in venules, pulmonary capillaries
- Associated with late stages of inflammation
- Long-lived
leukocyte-mediated endothelial injury
28
- Occurs in venules even if there are no gaps produced
- Induced by vascular endothelial growth factor (VEGF)
- Caused by increased transit of vesicles and vacuoles across
Increased Transcytosis
29
A critical function of inflammation is the delivery of
| ______________ to the site of injury.
leukocytes
30
Slowing of blood flow promotes ___________ and ___________ of leukocytes to swollen endothelial cells.
margination and
| adhesion
31
transmigration aka
diapedesis
32
the migration in interstitial tissues toward a chemical stimulus/chemotaxin along a chemical gradient.
chemotaxis
33
Involves interactions between complementary
adhesion molecules on leukocytes and
endothelium, modulated by chemical mediators
leukocyte adhesion
34
Leukocytes pierce the basement membrane by
| secreting
collagenases
35
Steps in leukocyte migration
rolling, firm/stable adhesion, transmigration
36
Directed migration of leukocytes towards chemical
stimulus; exogenous and endogenous substances
act as chemoattractants
chemotaxis
37
chemotactic agents include
- Leukotriene B4
- Platelet Activating Factor
- C5a
- IL-8
- Bacteria-derived N-formyl peptides
38
Recognition and attachment of the particle to be
ingested; responsible for the elimination of injurious
agent
phagocytosis
39
two major opsonins
- Fc fragment of IgG
| - C3b
40
involves CR3 which recognized C3bi
non-opsonic phagocytosis
41
Steps in Bacterial Killing by Phagocytosis
recognition, engulfment, fusion, degradation
42
oxygen-independent mechanism includes
- Bacterial Permeability Protein (BPIP)
- Lysozyme
- Lactoferrin
- Major Basic Protein
- Arginine-rich defensins
43
Myeloperoxidase deficiency leads to
chronic granulomatous disease
44
Shows thin (virtually invisible) blood vessels in the alveolar walls and no cells in the alveoli.
normal lung
45
- Fluid is the major component
- Derived from either the blood serum or the secretions of mesothelial cells lining the peritoneal, pleural, or pericardial cavities.
- Pleural tuberculous effusion
serous inflammation
46
-Fibrin is abundant
-Often seen in relation to serosal surfaces of body cavities such as pericardium or pleura
-Occurs in more severe injuries and greater vascular permeability (fibrinogen passes the vascular barrier)
-Resolution or scarring 9-inch growth of fibroblasts and
blood vessels.
fibrinous inflammation
47
-Neutrophils dominate the composition
-Production of large amounts of pus or purulent
exudates consisting of neutrophils, necrotic cells, and
edema fluid
-Material is liquefied to form pus
-Pyogenic (pus-producing) staphylococcal abscesses
Suppurative or Purulent Inflammation
48
-Local defect, or excavation, of the surface or an organ
or tissue.
-Produced by the sloughing (shedding) of inflammatory
necrotic tissue (mucosa is totally sloughed off and
submucosa is affected
-Acute and chronic inflammation exist
ulcer
49
balance between continued tissue damage and repair
chronic inflammation
50
```
prolonged process (weeks or months) in which active
inflammation, tissue destruction and healing all proceed
simultaneously
```
chronic inflammation
51
Histologically, chronic inflammation shows the following typical features that differentiate it from acute inflammation:
-Infiltration with mononuclear cells, which include
macrophages, lymphocytes, and plasma cells, a reflection of persistent reaction to injury
-Tissue destruction, largely induced by the inflammatory
cells.
-Attempts at repair by connective tissue replacement,
namely proliferation of small blood vessels (angiogenesis), and in particular, fibrosis.
52
-If the damaging stimulus is eradicated, there is NO
further tissue necrosis
-Repair response progresses to complete scarring
healing
53
-If the damaging stimulus CANNOT be eradicated
-Balance between damage and repair may be in a
stalemate and may persist for years
-If repair process is overwhelmed and damaging
stimulus progresses
-Ulceration may continue leading to perforation
chronicity
54
Induced by parasites or allergic reactions
eosinophilic responses
55
Found in hypersensivity reactions, viral infections ,
| and neoplasms
Lymphocytic and plasma responses
56
Often mixed with other acute or chronic inflammatory
| cells
macrophage responses
57
-Collection of activated macrophages that may
coalesce to form multinucleate giant cells
-Often surrounded by a collar of lymphocytes
and fibroblasts.
granuloma
58
-Characterized by the presence of granulomas,
which are indicative of certain diseases
-Mediated by lymphokines from activated T-cells
Granulomatous response
59
- Primary mediator of granulomatous inflammation
| - Facilitates activated macrophages
Interferon-γ (IFN- γ) and Interleukin-4 (IL-4)
60
What type of granulomatous inflammation is this
-Aka immune granuloma
-If T cell-mediated immunity is impaired, there will be small disseminated granulomas (miliary TB, lepromatous
leprosy, HIV)
-Some have no identifiable antigens (e.g.,
sarcoidosis)
Hypersensitivity Type
61
What type of granulomatous inflammation is this
- Aka foreign-body granuloma
- Response to poorly digestible materials
- Incited by relatively inert foreign bodies
Non-hypersensitivity Type
62
A regulated physiologic reaction associated with
inflammatory conditions, and is mediated by cytokines
released during the inflammatory process.
acute phase response
63
It is clinically characterized by fever, leukocytosis,
decreased appetite, altered sleep patterns, and changes
in plasma levels of acute phase proteins.
acute phase response
64
Fever is mediated by the effects of ___, ___, and ___ on
| hypothalamus either directly (TNF), or indirectly by local PGE2 synthesis
TNF, IL-1, and IL-6
65
Leukocytosis is mediated by ___ and ____
IL-1 and TNF
66
-Occurs initially due to accelerated release of
bone marrow cells
-Prolonged infection also induces proliferation of
precursors in the bone marrow, induced by
colony-stimulating factors.
leukocytosis
67
type of infection: bacteria
| associated response:
Neutrophilia
68
type of infection: viral
| associated response:
Lymphocytosis
69
type of infection: Parasitic and allergic
| associated response:
Eosinophilia
70
plasma proteins is regulated by ___ and ___
IL-6 and IL-1
71
Synthesis and plasma levels increase in acute phase response
Acute-phase proteins
72
downregulate inflammation
a1-antitrypsin, cystein proteinase inhibitor, ceruloplasmin)
73
Synthesis and plasma levels decrease in acute phase response
Negative acute-phase proteins
74
Replacement of lost cells or tissue by elements of
| identical structure and function
regeneration
75
Replacement by connective tissue resulting in fibrosis
scarring
76
-Seen in acute or mild injury
-Occurs when parenchymal cells have high proliferative
capacity
-ECM framework is preserved
regeneration
77
-Seen in chronic or massive injury
-Occurs when parenchymal cells have low proliferative
capacity
-ECM framework is destroyed
scarring
78
Replacement of injured tissue by connective tissue
resulting in fibrosis and scarring (when regeneration
cannot be accomplished)
repair
79
Repair begins while inflammation is still present, but is completed after inflammation terminates
Inflammation and repair coexist during the first week
| of injury
80
new blood vessel formation
neovascularization
81
fibrous tissue deposition
fibrosis
82
Promote chemotaxis and proliferation of endothelium
FGF (Fibroblast growth factor)
Vascular permeability factor (VPF)/Vascular
endothelial growth factor (VEGF)
83
Can mediate all the steps in angiogenesis
FGF (Fibroblast growth factor)
84
Causes both angiogenesis and increased vascular permeability
Vascular permeability factor (VPF)/Vascular endothelial growth factor (VEGF)
85
Promote migration and proliferation of fibroblasts and
| myofibroblasts
- IL-1 and TNF-a
- Transforming growth factor-β (TGF-β)
- Fibroblast growth factor (FGF)
- Platelet-derived growth factor (PDGF)
86
Promote extracellular matrix (ECM) deposition
- IL-1
- Transforming growth factor-β (TGF-β)
- Fibroblast growth factor (FGF)
- Platelet-derived growth factor (PDGF)
87
Monocyte chemotaxis
Chemokines, TNF, PDGF, FGF, TGF- β
88
Fibroblast migration/replicaton
PDGF, EGF, FGF, TGF- β, TNF, IL-1
89
Keratinocyte replication
HB-EGF, FGF-7, HGF
90
Angiogenesis
VEGF, angiopoietins, FGF
91
Collagen synthesis
TGF- β, PDGF
92
Collagenase secretion
PDGF, FGF, TNF, TGF-β inhibits
93
-Removal of inflammatory exudates and debris by
macrophages
-Fibrin clot and cross-linking of plasma protein with ECM
components
-Chemotactic and mitogenic factors released by
macrophages promote angiogenesis
Inflammatory Phase
94
inflammatory phase starts
after formation of the inflammatory exudates
95
- Development of vascular granulation tissue
- Development of fibrovascular granulation tissue
- Development of ECM in granulation tissue
proliferative phase
96
-Grows into injured area from surrounding healthy
tissue
-Consists of newly formed capillaries, proliferating
fibroblasts, and residual inflammatory cells
Development of vascular granulation tissue
97
-Tissue defect is filled with a complex capillary
network, proliferating fibroblasts and myofibroblasts,
and a few residual macrophages
-There is now active collagen synthesis
Development of fibrovascular granulation tissue
98
-Initially ECM rich in fibronectin and proteoglycans (a
loose network to hold fibrin)
-Fibronectin mediates adhesion of growing capillaries
and fibroblasts and enhances response to FGF
-Type III collagen appears after one week
-Type I collagen begins to appear after two weeks
Development of ECM in granulation tissue
99
Proliferative phase is controlled by
cytokines and growth factors derived from macrophages, lymphocytes, and platelets
100
-Maturation and reorganization of fibrous tissue
-Type III collagen secreted early is later degraded and
replaced by Type I collagen
Maturation Phase
101
As part of the increase in the strength of a wound, the
| secreted collagen undergoes maturation to become
scar tissue
102
In would healing, what are seen in 24 hours
neutrophils
103
-Mass composed of protuberant accumulation of -
connective extending beyond initial wound
-Similar to hypertrophic scar, which does not
extend beyond initial wound
keloid
104
-Proliferation of fibroblasts and other repair
elements
-Interface between benign and low-grade
malignant tumors
Desmoids or aggressive fibromatoses
