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LUIV [HS 202] Patho Exam > Trans 4 - Inflammation and Repair > Flashcards

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

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2
Q

The pattern of inflammation is determined by

A
  • Inciting agent
  • Time of observation
  • Immune status of host
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3
Q

The inciting agents of inflammation are

A
  • Infection
  • Trauma
  • Physical and chemical agents
  • Tissue necrosis
  • Foreign bodies
  • Immune reactions
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4
Q

What kind of inflammation has an early onset (seconds to minutes) and short duration (minutes to days)

A

acute inflammation

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5
Q

acute inflammation involves

A
  • fluid exudation (edema)
  • plasma proteins
  • polymorphonuclear cell (neutrophil) emigration
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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

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7
Q

Chronic inflammation induces

A

blood vessel proliferation and scarring

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8
Q

acute inflammation is characterized by

A
  • Changes in blood flow
  • Increased vascular permeability
  • Infiltration of tissues by neutrophils
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9
Q

Acute inflammation may lead to:

A
  • Complete resolution
  • Healing by connective tissue replacement (scarring)
  • Chronic inflammation
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10
Q

cardinal signs of inflamation

A

dolor, rubor, calor, functio laesa, tumor

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11
Q

Rubor means

A

redness

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12
Q

causes of rubor and calor

A

vessel dilatation and
increased blood flow to the
inflamed part

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13
Q

calor means

A

warmth

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14
Q

dolor means

A

pain

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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

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16
Q

tumor means

A

swelling

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17
Q

causes of tumor

A

Accumulation of fluid especially exudates

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18
Q

functio laesa means

A

loss of function

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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.

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20
Q

what are the components of acute inflammation

A

vascular changes, cellular events,

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21
Q

Alterations in vascular caliber that lead to an

increased blood flow

A

vasodilation

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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

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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)

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24
Q

Structural changes in the microvasculature that permit
leakage of plasma proteins and leukocytes into the
damaged area

A

increased vascular permeability

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25
Q

causes of increased vascular permeability

A
  • Formation of gaps due to endothelial contraction
  • Endothelial injury
  • Leukocyte-mediated endothelial injury
  • Increased Transcytosis
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26
Q

-Occurs in arterioles, capillaries, venules
-Caused by burns, some microbial toxins, and
chemicals
-Rapid: may be long-lived (hours to days

A

endothelial injury

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27
Q
  • Occurs in venules, pulmonary capillaries
  • Associated with late stages of inflammation
  • Long-lived
A

leukocyte-mediated endothelial injury

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28
Q
  • 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
A

Increased Transcytosis

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29
Q

A critical function of inflammation is the delivery of

______________ to the site of injury.

A

leukocytes

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30
Q

Slowing of blood flow promotes ___________ and ___________ of leukocytes to swollen endothelial cells.

A

margination and

adhesion

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31
Q

transmigration aka

A

diapedesis

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32
Q

the migration in interstitial tissues toward a chemical stimulus/chemotaxin along a chemical gradient.

A

chemotaxis

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33
Q

Involves interactions between complementary
adhesion molecules on leukocytes and
endothelium, modulated by chemical mediators

A

leukocyte adhesion

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34
Q

Leukocytes pierce the basement membrane by

secreting

A

collagenases

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35
Q

Steps in leukocyte migration

A

rolling, firm/stable adhesion, transmigration

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36
Q

Directed migration of leukocytes towards chemical
stimulus; exogenous and endogenous substances
act as chemoattractants

A

chemotaxis

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37
Q

chemotactic agents include

A
  • Leukotriene B4
  • Platelet Activating Factor
  • C5a
  • IL-8
  • Bacteria-derived N-formyl peptides
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38
Q

Recognition and attachment of the particle to be
ingested; responsible for the elimination of injurious
agent

A

phagocytosis

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39
Q

two major opsonins

A
  • Fc fragment of IgG

- C3b

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40
Q

involves CR3 which recognized C3bi

A

non-opsonic phagocytosis

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41
Q

Steps in Bacterial Killing by Phagocytosis

A

recognition, engulfment, fusion, degradation

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42
Q

oxygen-independent mechanism includes

A
  • Bacterial Permeability Protein (BPIP)
  • Lysozyme
  • Lactoferrin
  • Major Basic Protein
  • Arginine-rich defensins
43
Q

Myeloperoxidase deficiency leads to

A

chronic granulomatous disease

44
Q

Shows thin (virtually invisible) blood vessels in the alveolar walls and no cells in the alveoli.

A

normal lung

45
Q
  • 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
A

serous inflammation

46
Q

-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.

A

fibrinous inflammation

47
Q

-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

A

Suppurative or Purulent Inflammation

48
Q

-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

A

ulcer

49
Q

balance between continued tissue damage and repair

A

chronic inflammation

50
Q 
prolonged process (weeks or months) in which active
inflammation, tissue destruction and healing all proceed
simultaneously
A

chronic inflammation

51
Q

Histologically, chronic inflammation shows the following typical features that differentiate it from acute inflammation:

A

-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
Q

-If the damaging stimulus is eradicated, there is NO
further tissue necrosis
-Repair response progresses to complete scarring

A

healing

53
Q

-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

A

chronicity

54
Q

Induced by parasites or allergic reactions

A

eosinophilic responses

55
Q

Found in hypersensivity reactions, viral infections ,

and neoplasms

A

Lymphocytic and plasma responses

56
Q

Often mixed with other acute or chronic inflammatory

cells

A

macrophage responses

57
Q

-Collection of activated macrophages that may
coalesce to form multinucleate giant cells
-Often surrounded by a collar of lymphocytes
and fibroblasts.

A

granuloma

58
Q

-Characterized by the presence of granulomas,
which are indicative of certain diseases
-Mediated by lymphokines from activated T-cells

A

Granulomatous response

59
Q
  • Primary mediator of granulomatous inflammation

- Facilitates activated macrophages

A

Interferon-γ (IFN- γ) and Interleukin-4 (IL-4)

60
Q

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)

A

Hypersensitivity Type

61
Q

What type of granulomatous inflammation is this

  • Aka foreign-body granuloma
  • Response to poorly digestible materials
  • Incited by relatively inert foreign bodies
A

Non-hypersensitivity Type

62
Q

A regulated physiologic reaction associated with
inflammatory conditions, and is mediated by cytokines
released during the inflammatory process.

A

acute phase response

63
Q

It is clinically characterized by fever, leukocytosis,
decreased appetite, altered sleep patterns, and changes
in plasma levels of acute phase proteins.

A

acute phase response

64
Q

Fever is mediated by the effects of ___, ___, and ___ on

hypothalamus either directly (TNF), or indirectly by local PGE2 synthesis

A

TNF, IL-1, and IL-6

65
Q

Leukocytosis is mediated by ___ and ____

A

IL-1 and TNF

66
Q

-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.

A

leukocytosis

67
Q

type of infection: bacteria

associated response:

A

Neutrophilia

68
Q

type of infection: viral

associated response:

A

Lymphocytosis

69
Q

type of infection: Parasitic and allergic

associated response:

A

Eosinophilia

70
Q

plasma proteins is regulated by ___ and ___

A

IL-6 and IL-1

71
Q

Synthesis and plasma levels increase in acute phase response

A

Acute-phase proteins

72
Q

downregulate inflammation

A

a1-antitrypsin, cystein proteinase inhibitor, ceruloplasmin)

73
Q

Synthesis and plasma levels decrease in acute phase response

A

Negative acute-phase proteins

74
Q

Replacement of lost cells or tissue by elements of

identical structure and function

A

regeneration

75
Q

Replacement by connective tissue resulting in fibrosis

A

scarring

76
Q

-Seen in acute or mild injury
-Occurs when parenchymal cells have high proliferative
capacity
-ECM framework is preserved

A

regeneration

77
Q

-Seen in chronic or massive injury
-Occurs when parenchymal cells have low proliferative
capacity
-ECM framework is destroyed

A

scarring

78
Q

Replacement of injured tissue by connective tissue
resulting in fibrosis and scarring (when regeneration
cannot be accomplished)

A

repair

79
Q

Repair begins while inflammation is still present, but is completed after inflammation terminates

A

Inflammation and repair coexist during the first week

of injury

80
Q

new blood vessel formation

A

neovascularization

81
Q

fibrous tissue deposition

A

fibrosis

82
Q

Promote chemotaxis and proliferation of endothelium

A

FGF (Fibroblast growth factor)
Vascular permeability factor (VPF)/Vascular
endothelial growth factor (VEGF)

83
Q

Can mediate all the steps in angiogenesis

A

FGF (Fibroblast growth factor)

84
Q

Causes both angiogenesis and increased vascular permeability

A

Vascular permeability factor (VPF)/Vascular endothelial growth factor (VEGF)

85
Q

Promote migration and proliferation of fibroblasts and

myofibroblasts

A
  • IL-1 and TNF-a
  • Transforming growth factor-β (TGF-β)
  • Fibroblast growth factor (FGF)
  • Platelet-derived growth factor (PDGF)
86
Q

Promote extracellular matrix (ECM) deposition

A
  • IL-1
  • Transforming growth factor-β (TGF-β)
  • Fibroblast growth factor (FGF)
  • Platelet-derived growth factor (PDGF)
87
Q

Monocyte chemotaxis

A

Chemokines, TNF, PDGF, FGF, TGF- β

88
Q

Fibroblast migration/replicaton

A

PDGF, EGF, FGF, TGF- β, TNF, IL-1

89
Q

Keratinocyte replication

A

HB-EGF, FGF-7, HGF

90
Q

Angiogenesis

A

VEGF, angiopoietins, FGF

91
Q

Collagen synthesis

A

TGF- β, PDGF

92
Q

Collagenase secretion

A

PDGF, FGF, TNF, TGF-β inhibits

93
Q

-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

A

Inflammatory Phase

94
Q

inflammatory phase starts

A

after formation of the inflammatory exudates

95
Q
  • Development of vascular granulation tissue
  • Development of fibrovascular granulation tissue
  • Development of ECM in granulation tissue
A

proliferative phase

96
Q

-Grows into injured area from surrounding healthy
tissue
-Consists of newly formed capillaries, proliferating
fibroblasts, and residual inflammatory cells

A

Development of vascular granulation tissue

97
Q

-Tissue defect is filled with a complex capillary
network, proliferating fibroblasts and myofibroblasts,
and a few residual macrophages
-There is now active collagen synthesis

A

Development of fibrovascular granulation tissue

98
Q

-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

A

Development of ECM in granulation tissue

99
Q

Proliferative phase is controlled by

A

cytokines and growth factors derived from macrophages, lymphocytes, and platelets

100
Q

-Maturation and reorganization of fibrous tissue
-Type III collagen secreted early is later degraded and
replaced by Type I collagen

A

Maturation Phase

101
Q

As part of the increase in the strength of a wound, the

secreted collagen undergoes maturation to become

A

scar tissue

102
Q

In would healing, what are seen in 24 hours

A

neutrophils

103
Q

-Mass composed of protuberant accumulation of -
connective extending beyond initial wound
-Similar to hypertrophic scar, which does not
extend beyond initial wound

A

keloid

104
Q

-Proliferation of fibroblasts and other repair
elements
-Interface between benign and low-grade
malignant tumors

A

Desmoids or aggressive fibromatoses

LUIV [HS 202] Patho Exam (5 decks)

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