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605 Pathology > Acute Inflammation (Rosser) > Flashcards

Acute Inflammation (Rosser) Flashcards

1
Q

inflammation

A

the reaction of vascularized, living tissue to local injuries

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2
Q

2 Major Goals of Inflammatory Reactions

A
  1. Eliminate the injurious stimulus
  2. Repair associated tissue damage
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3
Q

Five Cardinal Signs of Inflammation

A
  1. Redness
  2. Swelling
  3. Heat
  4. Pain
  5. Loss of Function
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4
Q

Can inflammation occur after death?

A

no - presence of inflammatory cells means something happened antemortem, not postmortem!

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5
Q

Variables in Inflammation

A

intensity, magnitude, duration

dependent on innate response, immunologic status of host, and the type of agent involved

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6
Q

Benefits of Inflammation

A
  1. Degrade foreign materials
  2. Provide wound healing factors
  3. Dilution/inactivation of biological or chemical toxins
  4. Killing/sequestration [of microbes, necrotic tissue, neoplasia]
  5. Restrict movement to allow for healing and repair
  6. Increase temperature (local or systemic) to induce vasodilation and inhibit microbial replication
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7
Q

5 Main Phases of the Inflammatory Response

A
  1. Recognize inflammatory stimulus
  2. Acute vascular response
  3. Acute cellular response
  4. Chronic cellular response
  5. Resolution
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8
Q

Exogenous Substances which Induce Tissue Injury

A
  1. Microbes
  2. Foreign Bodies
  3. Mechanical Action (traumatic injury)
  4. Physical Action (think burns, frostbite)
  5. Chemical Substances (think venoms, caustic agents)
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9
Q

Endogenous Substances Inducing Tissue Injury

A
  1. Autoimmune reactions
  2. Intracellular signals released from injured or dying cells
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10
Q

PAMPs

A

pattern/pathogen-associated molecular patterns highly conserved microbial ligands (so unique to microbes) and binding triggers release of inflammatory mediators

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11
Q

TLR-4

A

PRR which recognizes lipopolysaccharide (LPS) in gram-negative cell bacterial walls

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12
Q

TLR-3

A

PRR for double stranded RNA (viruses)

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13
Q

PRR

A

pattern recognition receptor located on host cells; binding of PAMPS from microbes to PRRs results in downstream induction of inflammatory mediators

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14
Q

DAMPs

A

Damage Associated molecular patterns
endogenous molecules released from damaged or dying cells within the host

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15
Q

Difference between PAMPs and DAMPs?

A

PAMPs are from microbes and differentiate self from non-self
DAMPs are from the host and differentiate healthy self from damaged self

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16
Q

Examples of DAMP Mechanisms/Sources (3)

A
  1. extracellular presence of certain molecules
  2. intracellular enzymes–> breakdown of components
  3. circulating antibodies
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17
Q

Do both PAMPS and DAMPs bind to PRRs?

A

yes

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18
Q

What vasoactive mediators are contained in mast cells?

A

histamine and serotonin

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19
Q

Histamine and Serotonin

A

released from mast cells at the site of injury to cause vasodilation and increased vascular permeability

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20
Q

Resident Tissue Macrophages

A

also bind PRRs in response to inflammatory stimuli

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21
Q

Epithelial Cells

A

can secrete cytokines when injured or recognize inflammatory stimuli via PRRs

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22
Q

What activates platelets?

A

the exposure of subendothelial collagen

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23
Q

Inflammatory Mediators from Platelets

A

histamine and serotonin (like mast cells) but also complement activators, platelet activating factor, and coagulation factors

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24
Q

bradykinin

A

released from damaged vascular endothelium and causes vasodilation

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25
Q

prostaglandins and leukotrienes

A

can come from many cell types in response to PRR activation; causes vasodilation and increased vascular permeability

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26
Q

platelet-activating factor (PAF)

A

can come from many cell types in response to PRR activation; causes increased vascular permeability and smooth muscle contraction

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27
Q

hyperemia

A

tissue redness d/t blood pooling

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28
Q

biphasic nature of vascular permeability response

A

Early Phase occurs immediately, rapid and short lived, in response to histamines (and kinins etc)
Later phase is cytokine dependent (IL-1, TNFa, and kinins)

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29
Q

Net Effect of the Acute Vascular Response

A

increased capillary hydrostatic (push) pressure

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30
Q

Edema

A

leakage of plasma proteins

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31
Q

First cell to make it out of the vasculature in response to injury?

A

neutrophils

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32
Q

macrophages in the inflammatory response

A

larger number with a longer duration of infection (chronicity)

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33
Q

Eosinophils respond to what stimuli?

A

parasitic disease and acute hypersensitivity reaction

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34
Q

lymphocytes and plasma cells respond to what stimuli?

A

antigenic, or delayed HST

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35
Q

3 Granulocytes

A
  1. Neutrophils
  2. Eosinophils
  3. Basophils
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36
Q

are granulocytes terminally differentiated?

A

yes (they are fully mature before leaving the bone marrow)

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37
Q

3 Steps of the Leukocyte Adhesion Cascade

A

1a. Rolling
1b. Adhesion/Pavementing
2. Migration
3. Chemotaxis

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38
Q

leukocyte adhesion cascade

A

how neutrophils move from vasculature into tissue

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39
Q

Rolling

A

blood flow slows, then neutrophil ligands (capital L goes with leukocytes) interact with selectins on the endothelial surface and will “roll along” before coming to an eventual stop

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40
Q

Pavementing/Adherence

A

final part of adhesion where after the leukocyte stops, it is flattened on the endothelial surface

41
Q

Cytokines in Induction of Pavementing?

A

IL-1 and TNFa

42
Q

Ligands on Surface of Neutrophils Involved in Adhesion

A

Sialyl Lewis and L-selectin

43
Q

Ligands on Endothelium Involved in Adhesion

A

P-selectin and E-selectin

44
Q

Ligands on Leukocyte involved in Pavementing

A

beta2 integrins (CD11/CD18)

45
Q

Ligands on Endothelium involved in Pavementing

A

ICAM-1 and VCAM-1

46
Q

diapedesis

A

actual passage of the leukocyte through wall of blood vessel

47
Q

PECAM-1

A

ligand on both leukocyte and endothelium and binds to itself

48
Q

Summary of Leukocyte Adhesion Cascade

A
49
Q

Chemotaxis

A

migration of a leukocyte in response to chemotactic mediators (like IL-8)

50
Q

pseudopedia

A

cytoplasm changes within the leukocyte that allows the cell to “ooze” towards the stimulus, with actin/myosin contracting behind to push through towards inciting agent

51
Q

Heterophils in Rabbits/GPs/Elephants

A

function as neutrophils but appear with bright red granules on morphology

52
Q

Heterophils in Birds and Reptiles

A

functionally different from neutrophils (lack myeloperoxidase) and have elongated red granules on morphology

53
Q

Is phagocytosis receptor mediated?

A

yes - Fc receptors and Complement CR1 and CR3

54
Q

opsonization

A

coat pathogen with plasma proteins (opsonins) to taget for phagocytosis

55
Q

Can IgG and C3b directly recognize bacteria?

A

yes

56
Q

respiratory burst steps

A
  1. Lots of oxygen
  2. Becomes superoxide anion, which is cytotoxic
  3. superoxide anion can form hydrogen peroxide
57
Q

respiratory burst

A

needed to effectively kill bacterial and fungal agents

58
Q

Fenton Reaction

A

requires iron to generate a hydroxyl free radical

59
Q

Are free radicals produced during respiratory burst specific to the antigen?

A

no - can cause collateral damage to healthy tissue

60
Q

source of iron for Fenton reaction

A

lactoferrin in neutrophil granules

61
Q

Myeloperoxidase

A

enzyme in neutrophils which converts hydrogen peroxide and chloride ions into hypochlorous acid (oxidizing agent)

makes pus!

62
Q

What species lack myeloperoxidase?

A

birds and reptiles

they’ll have more caseous/granulomatous inflammation

63
Q

Neutrophil Extracellular Traps (NETs)

A

when neutrophils die, these are released and can physically entrap bacteria and can be microbicidal

64
Q

2 Major Types of Degradative Neutrophil Granules

A
  1. Specific
  2. Azurophilic
65
Q

specific granules

A

fuse with phagolysosome first and acidify the phagolysosomal compartment
includes lysozyme and lactoferrin (iron)

66
Q

azurophilic granules

A

fuse with phagolysosome later
includes myeloperoxidase and also lysozyme

67
Q

IL-8

A

the most specific chemotactic power for neutrophils; stimulates neutrophil production and release from bone marrow

68
Q

proinflammatory cytokines

A

TNFa, IL-1, IL-12 (and more)

69
Q

IL-5

A

chemotactic stimuli for eosinophils, and is SPECIFIC for eosinophils

70
Q

Are eosinophils present in all lesions?

A

no, mainly parasitic and some immune mediated hypersensitivity reactions

71
Q

Are eosinophils present in all tissues?

A

yes

72
Q

Major Basic Protein (MBP)

A

most important component of eosinic granules which is parasiticidal

73
Q

Push-Pull Relationship of Mast Cells and Eosinophils

A

Mast cells eat the MBP from the eosinophils and produces IL-5 to call more eosinophils in
Eosinophils degrade components from the mast cell granules (including histamine, PAF, and heparin)

74
Q

IL-5 is produced by what cells?

A

eosinophils, mast cells, and Th2 lymphocytes

75
Q

Are NK cells seen cyto or histologically?

A

no

76
Q

IL-21

A

main cytokine involved in NK cell function and differentiation

77
Q

perforin

A

in the granules in NK cells (and CD8 T cells); destroy target cells by creating pores in their membranes

78
Q

Monocytes become what cell type?

A

macrophages

79
Q

2 Types of Macrophages

A

M1 and M2

80
Q

Which type of macrophage is involved in the inflammatory response?

A

M1

81
Q

M2 Macrophages

A

fixed tissue macrophages that hang out under normal physiologic conditions to perform housekeeping functions (like removing cells and debris from tissue remodeling)

82
Q

Cool Summary with Pictures

A
83
Q

3 types of inflammatory mediators

A
  1. Preformed (histamine)
  2. Synthesized (cytokines, PGs)
  3. Plasma derivedF
84
Q

Bradykinin

A

triggered from factor 12 of the coagulation cascade; is a slow-acting vasodilator and produces sustained redness, heat, and pain

85
Q

What serves as the link between inflammation and coagulation?

A

kinins

86
Q

Anaphylotoxins

A

C3a and C5a (increase vascular permeability and microbes destroyed by leukocytes)

87
Q

C3b

A

opsonin to bind CR1 and 3 on neutrophils to cause phagocytosis of microbe

88
Q

C5b

A

initiates formation of the membrane attack complex (MAC) resulting in lysis of the microbe

89
Q

C5a

A

chemoattractant for leukocytes and increased vascular permeability

90
Q

C3a and C5a

A

increase vascular permeability

91
Q

Eicosanoids

A

synthesized mediators which are arachidonic acid metabolites from the COX and LOX pathways

92
Q

prostaglandins and thromboxanes

A

prostaglandins cause vasodilation
thromboxane A2 causes vasoconstriction

93
Q

leukotrienes

A

LTC4, LTD4, LTE4 all increase capillary permeability

94
Q

IL-1 and TNFa

A

fever, T cell and macrophage activation

95
Q

IL-6

A

acute phase protein production

96
Q

IL-10

A

suppresses macrophage function

97
Q

Positive Acute Phase Proteins

A

tend to increase in concentration during inflammatory response
C-reactive protein
Serum Amyloid A
Fibrinogen

98
Q

Negative Acute Phase Proteins

A

tend to decrease in concentration during inflammatory response
Albumin
Transferrin

605 Pathology (14 decks)

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