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General Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is inflammation?

A

Blood components (inflammatory cells, plasma proteins and fluid) exiting the vessel into the interstitial space

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2
Q

What is the purpose of inflammation?

A

Remove/eliminate cause of infection (pathogen) or clean up necrotic tissue

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3
Q

What are the two major patterns of inflammation?

A

-Acute (immediate with limited specificity)
-Chronic

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4
Q

List the 4 causes of inflammation

A
  1. Infections: (bacterial, viral, fungal, parasitic) and microbial toxins cause distinct patterns of inflammation
  2. Tissue necrosis: causes inflammation regardless of cause
  3. Foreign bodies: exogenous (dirt from trauma and bugs it carries) and endogenous (urate crystals-gout, cholesterol crystals-athersclerosis)
  4. Immune reactions (hypersensitivity): autoimmune diseases (against self) and environmental substances (allergies or microbes)
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5
Q

Cells have receptors to sense microbes and “smell” dead cells and their products. List these receptors.

A

-Toll-Like Receptors (TLR)
-Inflammasome
-Complement-plasma proteins that recognize and destroy blood-borne microbes

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6
Q

Where can you find Toll-Like Receptors (TLRs)?

A

Present on cell membrane of the innate immune system (ex: macrophages and dendritic cells) and on endosomes

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7
Q

How are TLRs activated?

A

By pathogen-associated molecular patterns (PAMPS) that are commonly shared by microbes

-CD14 (a TLR) on macrophages recognize lipopolysaccharide (a PAMP) on the outer membrane of gram-negative bacteria

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8
Q

TLR activation results in upregulation of ________, a nuclear transcription factor that activates immune response genes leading to production of _______

A

NF-KB; multiple immune mediators

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9
Q

TLRs are also present on cells of adaptive immunity and hence, play an important role in mediating _________

A

chronic inflammation

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10
Q

What is inflammasome and what is its function?

A

-Multiprotein cytoplasmic complex
-Senses dead cell products (uric acid, ATP from damaged mitochondria, etc.) and induces activation of IL-1 –> leukocyte recruitment

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11
Q

List the two types of mediators in regards to acute inflammation

A

Cell-derived
-arachidonic acid (AA) metabolites
-mast cell products
-cytokines

Plasma-protein derived
-complement
-hageman factor- kinin system activation

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12
Q

What is the function of and what is the source of this mediator?

Histamine

A

Source: mast cells, basophils, platelets

Fxn: Vasodilation, increased vascular permeability, endothelial activation

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13
Q

What is the function of and what is the source of this mediator?

Prostaglandins

A

Source: AA

Fxn: cardinal signs of acute inflammation

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14
Q

What is the function of and what is the source of this mediator?

PGI2 (prostacyclin), PGE1, PGE2, PGD2

A

Source: Mast cells, leukocytes

Fxn: Vasodilation, pain, fever

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15
Q

What is the function of and what is the source of this mediator?

Thromboxane A2 (TXA2)

A

Source: Platelets

Fxn: Vasoconstriction, platelet aggregation

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16
Q

What is the function of and what is the source of this mediator?

Leukotrienes

A

Source: Mast cells, leukocytes

Fxn: Increased vascular permeability, chemotaxis, leukocyte adhesion, and activation

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17
Q

What is the function of and what is the source of this mediator?

TNF

A

Source: Macrophages and dendritic cells, mast cells, T lymphocytes

Fxn: Activates endothelium (increase adhesion molecules) and secretion of other cytokines and chemokines; systemic effects*. Mediates cachexia

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18
Q

What is the function of and what is the source of this mediator?

IL-1

A

Source: Macrophages and dendritic cells, endothelial cells, some epithelial cells

Fxn: Similar to TNF, also stimulates formation of Th17 (makes IL-17)

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19
Q

What is the function of and what is the source of this mediator?

IL-6

A

Source: Macrophages, other cells

Fxn: Systemic effects (acute phase response)

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20
Q

What is the function of and what is the source of this mediator?

Chemokines

A

Source: Macrophages, endothelial cells, T lymphocytes, mast cells, other cell types

Fxn: Recruitment of leukocytes to sites of inflammation; migration of cells in normal tissues

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21
Q

What is the function of and what is the source of this mediator?

IL-17

A

Source: T lymphocytes

Fxn: Recruitment of neutrophils and monocytes

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22
Q

What is the function of and what is the source of this mediator?

IL-12

A

Source: Dendritic cells, macrophages

Fxn: Increased production of IFN-gamma

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23
Q

What is the function of and what is the source of this mediator?

IFN-gamma

A

Source: T lymphocytes, NK cells

Fxn: Activation of macrophages (increased ability to kill microbes and tumor cells)

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24
Q

What is the function of and what is the source of this mediator?

IL-17

A

Source: T lymphocytes

Fxn: Recruitment of neutrophils and monocytes

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25
Q

What is the function of and what is the source of this mediator?

IL-4

A

Source: T lymphocytes

Fxn: Activates macrophages (alternative pathway to promote repair) and eosinophils

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26
Q

What is the function of and what is the source of this mediator?

IL-13

A

Source: T lymphocytes

Fxn: Activates macrophages (alternative pathway to promote repair) and eosinophils

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27
Q

What is the function of and what is the source of this mediator?

IL-10

A

Source: macrophages

Fxn: Downregulate inflammation (negative feedback)

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28
Q

What is the function of and what is the source of this mediator?

TGF-beta

A

Source: macrophages

Fxn: downregulate inflammation (negative feedback)

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29
Q

What is the function of and what is the source of this mediator?

Platelet-activating factor

A

Source: Platelets, PMNs, macrophages mast cells, endothelial cells

Fxn: Platelet aggregation, vasoconstriction, bronchoconstriction. At low levels causes vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst

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30
Q

What is the function of and what is the source of this mediator?

Complement

A

Source: Produced in liver

Fxn:
-C5a: leukocyte chemotaxis
-C3a, C5 anaphylatoxins: mast cell degranulation
-C3b: opsonin for phagocytosis
-C5b, C6-C9: direct cell lysis through membrane attack complex

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31
Q

What is the function of and what is the source of this mediator?

Kinins

A

Source: Produced in liver, activated by Hageman Factor (Factor XII) leads to production of bradykinin

Fxn: Increase vascular permeability, smooth muscle contraction, vasodilation, pain

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32
Q

What is the function of and what is the source of this mediator?

Nitric Oxide

A

Source: Multiple cells

Fxn: Vasodilation of vascular smooth muscle

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33
Q

Arachidonic aid (AA) metabolites is released from the phospholipid cell membrane by ____________ and then acted upon by __________ or _________

A

phospholipase A2; cyclooxygenase or 5-lipoxygenase

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34
Q

Cyclooxygenase produces ________ and ________

A

Prostaglandins (PG) and Thromboxane A2 (TXA2)

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35
Q

PGI2, PGD2, and PGE2 mediate…..

A

vasodilation (at the arteriole) and increased vascular permeability (at the post-capillary venule)

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36
Q

PGE2 also mediates….

A

pain and fever

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37
Q

PGI2 inhibits ________ while TXA2 causes ________

A

platelet aggregation; vasoconstriction platelet aggregation

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38
Q

5-lipoxygenase produces ________

A

leukotrienes (LT)

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39
Q

LTB4 attracts (chemotaxis) and activates _______

A

neutrophils

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40
Q

LTC4, LTD4, and LTE3 (slow reacting substances of anaphylaxis) mediate……

A

vasoconstriction, bronchospasm, and increased vascular permeability

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41
Q

What is the function of Lipoxins?

A

Inhibit neutrophil chemotaxis and adhesion (counteracts LTB4)

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42
Q

What do Corticosteroids inhibit?

A

Phospholipase

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43
Q

What do NSAIDS inhibit?

A

cyclooxygenase (COX)

-COX-1 is expressed in most tissues and increased during inflammation
-COX-2 is absent from most normal tissues and is induced during inflammation

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44
Q

What are the COX-1 inhibitors?

A

Aspirin, ibuprofen (Advil, Motrin), naproxen (Aleve)

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45
Q

What are the COX-2 inhibitors?

A

Celebrex

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46
Q

What is used to treat asthma?

A

Lipoxygenase inhibitors, and leukotriene receptor antagonists

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47
Q

Where are mast cell products widely distributed?

A

Throughout connective tissue

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48
Q

List the 3 things mast cell products are activated by

A

1) Tissue trauma
2) Complement proteins C3a and C5a
3) cross-linking of cell surface IgE by antigen

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49
Q

Immediate response involves release of preformed histamine granules, which mediate….

A

vasodilation of arterioles and increased vascular permeability

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50
Q

Delayed response involves production of arachidonic acid metabolites, particularly leukotrienes. What does this prolong?

A

The inflammatory response over hours

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51
Q

What are cytokines?

A

Proteins secreted mainly by activated lymphocytes, macrophages, and dendritic cells but also endothelial, epithelial and CT cells

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52
Q

What are the major players in acute inflammation?

A

TNF, IL-1, IL-6

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53
Q

What is the function of TNF and IL-1

A

Activate endothelium, induce secretion of other cytokines and chemokines and together with IL-6 promote systemic inflammatory state: fever, lethargy, and stimulate the liver to make acute phase proteins

*TNF also causes metabolic wasting

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54
Q

What is the function of chemokines?

A

Cytokines that act as chemotactic agents for various inflammatory cells

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55
Q

What are the major players in chronic inflammation?

A

IFN-gamma, IL-12, IL-17

(but mediators of acute inflammation also influence)

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56
Q

What cytokines are involved in negative feedback to downregulate inflammation

A

IL-10, TGF-beta

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57
Q

Describe Nitric Oxide (NO)

A

short lived, free radical made by multiple cells

When made by endothelium: relaxes vascular smooth muscle causing vasodilation

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58
Q

Describe the complement pathway

A

Proinflammatory serum proteins that “complement” inflammation. Circulate as inactive precrusors

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59
Q

List the 3 ways activation of the complement pathway occurs

A

-Classical pathway
-Alternative pathway
-Mannose-binding lecting (MBL)/ pathway

60
Q

What is the classical pathway?

A

C1 binds IgG or IgM that is bound to antigen

61
Q

What is the alternative pathway?

A

Microbial products directly activate complement without Antigen/Ab complexes

62
Q

What is Mannose-binding lectin (MBL) pathway?

A

MBL binds to mannose on microorganisms and activates complements

63
Q

All pathways in the complement pathway result in production of….

A

C3 convertase (mediates C3 –> C3a and C3b), which, in turn, produces C5 convertase (mediates C5 –> C5a and C5b). C5b complexes with C6-C9 to form the membrane attack complex (MAC)

64
Q

What is the function of C3a and C5a (anaphylatoxins)

A

Trigger mast cell degranulation (histamine release –> vasodilation, increased vascular permeability), activate leukocytes

65
Q

What is the function of C5a?

A

chemotactic for neutrophils (more potent than C3a)

66
Q

What is the function of C3b

A

Opsonin for phagocytosis

67
Q

What is the function of the MAC?

A

Lyses microbes by creating a hole in the cell membrane

68
Q

What is Hageman Factor (Factor XII)?

A

-Inactive proinflammatory protein produced in liver

69
Q

What is Hageman factor activate by? What does it activate?

A

Activated upon exposure to subendothelial or tissue collagen; in turn, activates:
-Coagulation and fibrinolytic systems
-Complement
-Kinin system

70
Q

What is the Kinin system?

A

Kinin cleaves high-molecular weight kininogen to bradykinin, which mediates vasodilation and increased vascular permeability (similar to histamine) as well as pain

71
Q

What are the principal mediators of vasodilation?

A

Histamine
Prostaglndins

72
Q

What are the principle mediators for increased vascular permeability?

A

Histamine
C3a and C5a
Leukotrienes C4, D4, E4

73
Q

What are the principal mediators for chemotaxis, leukocyte recruitment and activation?

A

TNF, IL-1
Chemokines
C3a, C5a
Leukotriene B4

74
Q

What are the principal mediators for a fever

A

IL-1, TNF
Prostaglandins

75
Q

What are the principal mediators for pain

A

Prostaglandins
Bradykinin

76
Q

What are the principal mediators for tissue damage

A

Lysosomal enzymes of leukocytes
Reactive oxygen species

77
Q

What are TNF-alpha inhibitors used for?

A

To treat psoriasis and other skin conditions, rheumatoid arthritis, inflammatory bowel disease (i.e. Crohn disease)

78
Q

What are IL-17 inhibitors used for?

A

Psoriasis

79
Q

Define chronic inflammation

A

Long-term (weeks-months-years) inflammation that can, but doesn’t always, progress from
acute inflammation

80
Q

(T/F) in chronic inflammation, Inflammation, tissue injury, and repair all occur simultaneously

A

True

81
Q

What are the three major characteristics of chronic inflammation?

A
  • Infiltration of tissue with mononuclear
    “chronic inflammatory” cells (macrophages,
    lymphocytes, plasma cells)
  • Tissue destruction caused by the products
    of chronic inflammatory cells
  • Repair involves new vessel formation
    (angiogenesis) and fibrosis
82
Q

When does chronic inflammation occur?

A
  • Persistent infections
  • Prolonged exposure to potentially toxic
    agents
  • Autoimmune diseases
83
Q

What are the four chronic inflammatory cells?

A

macrophages, lymphocytes, plasma cells and eosinophils

84
Q

How do macrophages (MACs) form?

A
  • Monocytes in blood arise as precursors in bone marrow
  • Circulate in blood for about 1 day; migrate to site of acute inflammation within 24-48 hrs, peaking at 2-3 days of onset → When leave the bloodstream, called macrophages.
85
Q

How do macrophages arrive at site of inflammation?

A

Arrive in tissue like PMNs via the margination, rolling, adhesion, and transmigration sequence

86
Q

How do macrophages rid the body from the foreign entities?

A

Ingest organisms via phagocytosis (augmented by opsonins) and destroy phagocytosed material using similar mechanisms as PMNs

87
Q

What is the fate of macrophages?

A
  • Eventually die or are resorbed in lymphatics
  • In chronic inflammation, can fuse into multinucleated giant cells
88
Q

What are tissue macrophages (MACs)?

A

Tissue macrophages (not derived from
circulating monocytes) are part of the
mononuclear phagocyte or reticuloendothelial
system in most CT and organs

89
Q

What is a tissue macrophage referred to in the:
Liver
Spleen/LN
CNS
Lung

A

Liver: Kuppfer cells
Spleen/LN: Sinus histiocytes
CNS: Microglial cells
Lung: Alveolar macrophages

90
Q

Macrophages help regulate the three potential outcomes of the inflammatory process. These are:

A
  • Continue the acute response
  • Resolution and healing
  • Induce chronic inflammation
91
Q

Macrophages continue the acute response through release of mediators (_____,_____) to recruits additional PMNs, macrophages.

A

TNF, IL-1

92
Q

Macrophages help in the resolution and healing of inflammation through release of ____________ (e.g., ______ and ______)

A

anti-inflammatory cytokines, (IL-10, TGF-β)

93
Q

Macrophages help Induce chronic inflammation through _____________ and activation of ___________, which secrete ________ that promote chronic inflammation.

A

antigen presentation, CD4+ helper T cells, cytokines

94
Q

MAC activation can happen through one of two ways, _____________ pathway or _____________ pathway

A

classical, alternative

95
Q

The classical pathway is induced by ________, ________, and ________

A

microbial products (LPS), T cell signals (e.g. IFN-γ), and foreign substances

96
Q

MACs in the classical pathway produce __________, _____ and ______ which help
kill microbes and stimulate inflammation

A

lysosomal enzymes, NO, ROS

97
Q

The alternative pathway is Induced by ____ and ____ from T cells and other cells

A

IL-4, IL-13

98
Q

(T/F) Macrophages in the alternative pathway directly attack microbes

A

False. They help in repair by secreting growth
factors (TGF-β)

99
Q

TGF-β promote __________, _____________, and ________________

A

angiogenesis, fibroblast activation, collagen synthesis

100
Q

Lymphocytes respond to specific stimuli (i.e._______) as well as ____________ or __________

A

infections, ischemic necrosis, trauma

101
Q

_________ are the major driver of autoimmune or chronic inflammatory diseases

A

Lymphocytes

102
Q

_________ may develop into plasma cells (make
antibody)

A

B cells

103
Q

__________, upon activation, make cytokines

A

CD4+ T cells

104
Q

CD4+ T cells make ____, ____, or ____

A

TH1 cells, TH2 cells, TH17 cells

105
Q

TH1 cells produce _____ which stimulate the _____ pathway for MACs

A

IFN-γ, classical

106
Q

TH2 cells secrete _____ and _____ which activate ________ and stimulate the ________ pathway for
MACs

A

IL-4, IL-13, eosinophils, alternative

(Important in allergic inflammation and in defense against parasites)

107
Q

TH17 cells secrete ____ which recruits _____
and _________

A

IL-17, PMNs, monocytes

108
Q

What are the cardinal signs of acute inflammation?

A

-Redness (rubor)
-Warmth (calor)
-Swelling (tumor)
-Pain (dolor)
-Fever

109
Q

What causes redness (rubor) and warmth (calor)?

A

-Due to vasodilation, which results in increased blood flow
-Occurs via relaxation of arteriolar smooth muscle; key mediators are histamine, prostaglandins, and bradykinin

110
Q

What causes swelling (tumor)?

A

Due to increase vascular permeability causing leakage of fluid from postcapillary venules into the interstitial space

111
Q

What causes pain (dolor)?

A

Bradykinin and PGE2 sensitize sensory nerve endings

112
Q

What causes fever?

A

-Pyrogens cause macrophages to release IL-1 and TNF, which increase COX activity in perivascular cells of the hypothalamus
-This leads to increased PGE2 which raises temperature set point

113
Q

Describe the features of acute inflammation

A

-Immediate and early response to injury
-Short-term (minutes to hours)
-Tissue infiltration by neutrophils (this is the hallmark cell of acute inflammation!)

114
Q

List the correct steps of vascular changes (of acute inflammation??)

A
  1. Brief vasoconstriction
  2. Vasodilation
  3. Increased permeability
  4. Exudate leaving the circulation
  5. Increase in blood viscosity
  6. Decrease in blood flow through the microcirculation
115
Q

List the steps of cellular events (PMNs)

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Transmigration and chemotaxis
  5. Phagocytosis
  6. Destruction of phagocytosed material
  7. Resolution
116
Q

Describe Step 1: Margination

A

-Vasodilation of arterioles slows blood flow
-Cells marginate from center of flow to the periphery

117
Q

Describe Step 2: Rolling - loose attachment

A

-Selectin “speed bumps” are upregulated on endothelial cells (P-selectin release from Weibel-Palade bodies is mediated by histamine and E-selectin is induced by TNF and IL-1)
-Selectins bind Sialyl-Lewis X on leukocytes
-Interaction results in rolling of leukocytes along vessel wall

118
Q

Describe Step 3: Adhesion

A

-Cellular adhesion molecules (ICAM and VCAM) are upregulated on endothelium by TNF and IL-1
-Integrins becomes high affinity and are upregulated on leukocytes by C5a and LTB4
-Interaction between CAMs and integrins results in firm adhesion of leukocytes to the vessel wall
-Leukocyte adhesion deficiency: often a defect in integrins (clinically increased circulating neutrophils and recurrent bacterial infections that lack pus formation)

119
Q

Describe step 4: transmigration and chemotaxis

A

-Leukocytes transmigrate across the endothelium of postcapillary venules and move toward chemical attractants (chemotaxis)
-Neutrophils are attracted by bacterial products, IL-8, C5a, and LTB4

120
Q

Describe step 5: Phagocytosis

A

-Consumption of pathogens or necrotic tissue; phagocytosis is enhanced by opsonins (IgG and C3b)
-Pseudopods extend from leukocytes to form phagosomes, which are internalized and merge with lysosomes to produce phagolysosomes
-Chediak-Higashi syndrome characterized by impaired phagolysosome formation with increased risk of pyogenic infections

121
Q

Describe step 6: Destruction of phagocytosed material

A

-O2-dependent killing is the most effective mechanism
-HOCl radical generated by oxidative burst in phagolysosomes destroys phagocytosed microbes:
*O2–>O2 radical (superoxide) by NADPH oxidase (oxidative burst)
*Superoxide–> H2O2 (hydrogen peroxide) by superoxide dismutase
*H2O2–>HOCl radical (bleach) by myeloperoxidase (MPO) which is contained in the azurophilic granules (lysosomes) of PMNs

122
Q

When thinking about step 6 (destruction of phagocytosed material), describe how this happens

A

-Chronic granulomatous disease is characterized by poor O2-dependent killing
*Due to inherited NADPH oxidase defect
*Leads to recurrent infection and granuloma formation
-O2-independent killing is less effecting than O2-dependent killing and occurs via enzymes present in leukocyte secondary granules

123
Q

Describe step 7: Resolution

A

Neutrophils undergo apoptosis and disappear within 24 hours after resolution of the inflammatory stimulus

124
Q

Describe serous inflammation

A

-Due to burn or viral infection, tend to be watery
-Fluid in a serous cavity = effusion

125
Q

Describe purulent or suppurative inflammation

A

-Common in bacterial infections
-Thick and yellow (rich in neutrophils). Neutrophils, necrotic cells and serum = “pus”. Abscess = focal collection of pus

126
Q

Describe fibrinous inflammation

A

-Rich in fibrin which makes it sticky. Covering called a “pseudomembrane”
-Noted when inflammation occurs in a body cavity (meninges, pericardium and pleura). Can resolve but if scarring occurs could restrict function
-Orally we see a psuedomembrane

127
Q

What is an ulcer?

A

Complete loss of surface epithelium due to sloughed (shedding) of necrotic tissue

128
Q

Where are the common locations for ulceration?

A

-Mucosal surfaces (mouth, stomach, intestines and genitourinary tract)
-Subcutaneous tissue of the legs/feet in patients with circulatory problems predisposing to extensive necrosis (ex. diabetes, peripheral vascular disease)

129
Q

Where are eosinophils found?

A

In inflammatory sites around parasitic infections and associated with IgE mediated immune reactions (allergies)

130
Q

Eosinophils are recruited by _______

A

a specific chemokine (eotaxin)

131
Q

Eosinophilic granules contain _________ which is toxic to parasites and causes epithelial cell necrosis

A

major basic protein

132
Q

What is granulomatous inflammation?

A

A type of chronic inflammation that usually occurs when a material is difficult to digest/remove

133
Q

When talking about granulomatous inflammation, there are characteristics of specific disease states that arise in 4 main settings. List these 4 settings.

A
  1. Persistent T cell response to microbes (myobacteria tuberculosis, T. pallidum, fungi)
  2. Immune-mediated inflammatory diseases (Crohn disease)
  3. Sarcoidosis - unknown cause
  4. Foreign body (suture, silicone, beryllium, prophy paste)
134
Q

With granulomatous inflammation, the granuloma will wall off the agent, but what happens if the body can’t remove it?

A

Leads to fibrosis and organ dysfunction

135
Q

What does Granulomatous Inflammation look like histologically?

A

Large “epithelioid” (looks like a squamous cell) macrophages/histiocytes that sometimes fuse to form multinucleated giant cells are combined with lymphocytes into structures called a granuloma

136
Q

With granulomatous inflammation, if it has an accellular/necrotic, cheesy center (caseous necrosis) in the center of the granuloma = caseating or necrotizing granulomatous inflammation. What diseases is this seen in?

A

Tuberculosis, syphilis, cat-scratch disease

137
Q

With granulomatous inflammation, if this cheesy center is absent = non-caseating or non-necrotizing granulomatous inflammation. What diseases is this seen in?

A

Crohn disease, sarcoidosis, foreign body reactions

138
Q

List the systemic effects of inflammation

A

Fever
Lymphadenopathy
Leukocytosis

139
Q

What causes fever in inflammation?

A

Pyrogens (fever-producing substances - TNF, IL-1, PGE2) acting on the hypothalamus. Unknown purpose for fever

140
Q

What is Lymphadenopathy?

A

Firm, enlarged, tender

141
Q

What is Leukocytosis?

A

Elevated serum levels of leukocytes:
-Produced in bone marrow, mostly PMNs
-Most bacterial infections increase PMNs
-Some viral infections increase lymphocytes
-Asthma, hay fever, parasitic infections increase eosinophils
-Some organisms can decrease white cell count

142
Q

What are the systemic effects of acute phase proteins?

A

-Elevated acute phase proteins are made in liver
-Cause increased HR, BP, chills, rigors (shivering), anorexia, somnolence, malaise
-Can track (in the blood) to see if inflammation is resolving

143
Q

List some types of Acute Phase Proteins

A

-C-reactive protein
-Fibrinogen- binds to RBCs, forms stacks that sediment- causes increased erythrocyte sedimentation rate (ESR)
-Serum amyloid A (SAA) protein

144
Q

What is leukocyte-induced tissue injury?

A

Damage that occurs when leukocyte enzymes are released into the host tissue

145
Q

What chronic diseases does leukocyte-induced tissue injury occur?

A

-Gout
-Rheumatoid arthritis
-Atherosclerosis
-Periodontitis

General Pathology (32 decks)

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