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Veterinary Pathology > Inflammation & Healing (Part I) > Flashcards

Inflammation & Healing (Part I) Flashcards

1
Q

What are the principal features of acute inflammation?

A

exudation of electrolytes, fluid, plasma proteins

leukocyte emigration (neutrophils)

rapid repair and healing

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2
Q

T/F: Acute inflammation is based off the amount of time passed

A

FALSE - it’s what happens that determines whether it is acute or not

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3
Q

What are the phases of acute inflammation?

A

fluidic
cellular
reparative

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4
Q

What happens in the fluidic phase of inflammation? Acute or chronic inflammation?

A

exudation of electrolytes, fluid, plasma proteins

increase in vascular fluid
exudation of fluid

edema

acute inflammation

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5
Q

Where does exudation of fluid happen?

A

post-capillary venuoles

get inflammation? increase in vascular permeability and lose fluid

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6
Q

What happens in the cellular phase of inflammation? Acute or chronic inflammation?

A

leukocyte emigration (neutrophils)

neutrophils are the first line of defense

vessels become leaky and recruit them

acute

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7
Q

What happens in the reparative phase of inflammation? Acute or chronic inflammation?

A

rapid repair and healing

if wound is clean
retain tensile strength

acute

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8
Q

A pro-inflammatory environment = a _______

A

pro-coagulatory environment

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9
Q

How do you characterize chronic inflammation?

A

inflammation of prolonged duration

emigration of leukocytes (lymphocytes), macrophages

tissue necrosis

tissue repair

healing, fibrosis, granulation tissue

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10
Q

In chronic inflammation, what kind of cells emigrate?

A

leukocytes - lymphocytes, plasma cells, macrophages

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11
Q

How does one heal from chronic inflammation?

A

fibrosis - dense CT

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12
Q

What is an example of injury that skips acute inflammation and goes straight to chronic? Why?

A

Johne’s Disease - causes chronic wasting

it is a higher order bacterium (mycobacterium paratuberculosis)

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13
Q

What causes the cardinal signs of inflammation - pain?

A

bradykinin, PGE2

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14
Q

What causes the cardinal signs of inflammation - redness/swelling?

A

increased vascular permeability
- histamine
- substance P
- leukotrienes
- PGE2
- C3a
- C5a

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15
Q

What are the effects on the fluidic phase of acute inflammation?

A

increased blood flow to site of injury (hyperemia)

increased permeability of capillaries and post capillary venules

emigration of leukocytes

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16
Q

What leads to the leukocyte adhesion cascade?

A

acute injury: causes initial vasoconstriction then vasodilation

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17
Q

Explain the leukocyte adhesion cascade

A
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18
Q

What is tethering in the leukocyte adhesion cascade? What does it?

A

white blood cells have to slow down and pull to side, so there is tethering

selectins -weak binding, and slows down white blood cells

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19
Q

What are the types of selectins?

A

P-selectin
E-selectin
L-selectin

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20
Q

Weibel-Palade bodies of endothelial cells are on what?

A

P selectin
VWF

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21
Q

What are the steps of the leukocyte adhesion cascade?

A
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22
Q

What is rolling in the leukocyte adhesion cascade? What does it?

A

weak binding - but STRONGER than tethering stage

slows down white blood cells greatly

selectins and chemokines

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23
Q

What is adhesion in the leukocyte adhesion cascade? What does it?

A

leukocytes and endothelial cells become activated by cytokines
- ICAM-1 (endothelial cells) bind to CD11/CD18 (on wbc)

integrins main player

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24
Q

What is transmigration in the leukocyte adhesion cascade? What does it and what does it require?

A

white blood cells migrate out of vessel and into tissue

requires exogenous chemoattractant to leukocytes (within exudate)
also integrins

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25
Q

What do P and E selectins bind do?

A

Sialyl Lewis X modified protein

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26
Q

What do ICAMs bind to on white blood cell?

A

CD11/CD18

any B1 or B2 integrin bind to ICAM-1

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27
Q

What does VCAM-1 bind to on white blood cell?

A

VLA-4: B1 integrins - just adhesion

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28
Q

What does L-selectin bind to? What is special about it?

A

GlyCam-1 / CD34

just on the white blood cell - NOT endothelial cell

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29
Q

Which selectins have it where an associated white blood cell has a selectin and will bind to the selectin on the endothelial cell?

A

P-selectin
E-selectin

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30
Q

Explain a leukocyte adhesion deficiency. What is the result?

A

B-2 integrin deficiency

white blood cells cannot be delivered to the tissue

defect in transmigration

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31
Q

Which places are affected more for B2 deficiency?

A

orifices - natural biome for bacteria to accumulate

skin

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32
Q

What is pemphigus vulgaris?

A

attacks the deepest layers of the epidermis, making it the most severe type of pemphigus.

Pemphigus vulgaris causes the formation of fluid-filled blisters, known as vesicles. These vesicles often rupture, leaving painful ulcerative lesions

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33
Q

What does this show?

A

pemphigus vulgaris

targets desmosomes

separation of keratinocytes from each other

The acantholytic cells are often found floating within the vesicles or blisters formed within the epidermis.

The loss of cell adhesion occurs just above the basal layer of the epidermis, leading to suprabasal clefts or spaces.

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34
Q

What are the effector cells of acute inflammation?

A

vascular endothelial cells
mast cells/basophils
neutrophils
eosinophils
NK cells
macrophages

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35
Q

What do vascular endothelial cells do in acute inflammation?

A

initiate coagulation
inhibit inflammation

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36
Q

What do basophils / mast cells do in acute inflammation?

A

both contain histamine and aid in vasodilation

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37
Q

What cell are these?

A

mast cells

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38
Q

What intracellular components do neutrophils have?

A

lysosomes
myeloperoxidase
matrix metalloproteinases (MMP)
elastases - type of MMP

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39
Q

What do matrix metalloproteinases do?

A

breakdown the extracellular matrix

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40
Q

What is neutrophil granules - myeloperoxidase?

A

microbidicidal to bacterial and internalized material, degredation of extracellular matrix

pus

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41
Q

What are neutrophil granules - defensins, cathelicidins, & antimicrobial proteins?

A

form pores in microbial membranes (also affect chemotaxis and activation of adaptive immune response)

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42
Q

What is neutrophil granules - lactoferrin?

A

inhibits growth of bacteria by binding to iron; degredation of extracellular matrix

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43
Q

What is neutrophil granules - elastase?

A

hydrolyzes bacterial cell wall proteins and tissue elastin

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44
Q

What is neutrophil granules - gelatinase (MMPs)?

A

degradation of EC matrix

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45
Q

What is neutrophil pathogen killing strategy #1?

A

phagocytosis: fusion of lysosomes or phago-lysosome fusion

can internalize non-opsonized particles, but ones that are opsonized are phagocytized more quickly

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46
Q

What helps tag particles and aid neutrophils?

A

C3b ( neutrophils can still phagocytize untagged particles)

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47
Q

What is neutrophil pathogen killing strategy #2?

A

secretion of contents (intracellular granules)

can then start degrading pathogens

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48
Q

Where do neutrophils go once they have done their time?

A

undergo apoptosis —> apoptotic bodies —> macrophages

pooped out

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49
Q

How are heterophils different from neutrophils?

A

different species: rabbits, birds, guinea pigs, fish

do not contain as much myeloperoxidase

50
Q

What are the effects of species with heterophils regarding lesions?

A

because they do not have as much myeloperoxidase, lesions look more caseous

51
Q

What role do eosinophils play in acute inflammation?

A

allergic or parasitic responders

large granules

can also cause tissue destruction

52
Q

What are monocytes / macrophages?

A
53
Q

What is the role of histamine?

A

vasodilation
increase vascular permeability
pain and itching
tachycardia
eosinophil chemotaxis
accentuate neural reflexes

54
Q

Who is the most important contributor of histamine?

A

mast cells

55
Q

What are classifications of edema - transudate?

A

transudate - vascular permeability not affected significantly

lower SG and protein content

56
Q

What are classifications of edema - exudate?

A

vascular permeability IS affected

high protein and SG

57
Q

What are examples of morphologic classifications of exudates in inflammatory responses?

A

serous - but actually a transudate

catarral

fibrinous

suppurative (or purulent)

hemorrhagic

58
Q

What do you call the mucous component in exudate?

A

catarrhal

59
Q

What kind of morphological classification of exudate?

A

serous - transudate

60
Q

What kind of morphological classification of exudate?

A

fibrinous - exudate

61
Q

What kind of morphological classification of exudate?

A

catarrhal - exudate

62
Q

What must you remember when trying to classify something as catarrhal?

A

has to be in an area that produces mucus

63
Q

What kind of morphological classification of exudate?

A

fibrinous - exudate

64
Q

What kind of morphological classification of exudate?

A

suppurative - exudate

65
Q

What kind of morphological classification of exudate?

A

catarrhal (also suppurative) - exudate

66
Q

What kind of morphological classification of exudate?

A

suppurative - exudate

67
Q

Where are proteins for complement produced?

A

liver

make up a portion of plasma and serum

68
Q

What are the properties of complement?

A

pro-inflammatory
chemotactic
opsonizing
antibody production
permeability
cell lysis

69
Q

What is the main mission of complement? How do you accomplish this?

A

destroy microbes by opsonizing and forming membrane attack complex

classical pathways
alternative pathways
lectin pathways

70
Q

What is the common factor regarding complement?

A

C3

no matter which pathway, the goal is to activate / cleave C3 into C3a and C3b

71
Q

C3 is responsible for ______

A

opsonization

72
Q

A pro-inflammatory environment = a pro-coagulative environment. So how do coagulation and complement merge?

A

plasmin (from coagulation cascade) can cleave C3 —> C3a, b

kallikrein can cleave C5 —> C5a, b

73
Q

What is the classical pathway of complement dependent on?

A

antibodies - antigen / antibody (IgM, IgG) complex cross links with C1

74
Q

What is C4b2b?

A

classical pathway C3 convertase

75
Q

What is the sequelae to the classical pathway?

A

Classical pathway C3 convertase (C4b2b) triggers formation of Classical pathway C5 convertase (C4b2b3b)

which then cleaves C5 (to C5a and C5b) C5b binds to C6,7,8,9 and entire complex forms MAC’s

76
Q

What is the alternative pathway initiated by?

A

lipopolysaccharide (LPS) and other polysaccharides

77
Q

What does the alternative pathway require?

A

contribution from other activated plasma proteins (kallikrein, plasmin, factor XIIa) - intrinsic pathway

78
Q

What is the sequelae to the alternative pathway?

A

cleaves C3 to C3a and C3b to form Alternative pathway C3 convertase (C3bBb)

which then can activate alternative C5 convertase to cleave C5 (to C5a, C5b) C5b forms MAC complex

79
Q

T/F: The alternative pathway does not require antibodies like the common pathway

A

TRUE

80
Q

How is the lectin pathway initiated?

A

mannose-binding lectin binds to C1 activating it, then C3 and C5 cascade occur

81
Q

What is the arachidonic acid pathway?

A

polyunsaturated fatty acid derived from linoleic acid
- amino acid released from endothelial cells, platelets, and white blood cells mostly

82
Q

What is a major precursor for eicosanoids and initiates the cascade?

A

linoleic acid is cleaved from the plasma membrane by phospholipase A - initiates the cascade

83
Q

Eicosanoids are synthesized by two main classes of enzymes:

A

COXs

lipooxygenases

also cytochrome P450 enzymes

84
Q

What are COXs?

A

respective products are prostaglandins and thromboxanes

one way eicosanoids are synthesized

85
Q

What are lipoxygenases?

A

products are leukotrienes and lipoxins

one way eicosanoids are synthesized

86
Q

What can trigger phospholipase A2?

A

neutrophils can activate phospholipase A2 which will initiate the arachidonic acid cascade

reperfusion injury —> Calcium activate the arachidonic acid cascade

87
Q

With acute inflammation, do we get coagulation? Why? (explain using chart)

A

yes, because the arachidonic cascade leads to pro-inflammatory mediators and also leads to the development of pro-coagulators mediators (TXA2)

88
Q

What is derived from COX? What is it?

A

PGH2

precursor to the arachidonic acid cascade

89
Q

How do we get conversion from PGH2 to PGI2? What is PGI2?

A

endothelial cell uses enzyme to convert PGH2 to PGI2

vasodilator

anticoagulant

90
Q

How is PGI2 an anticoagulant?

A

inhibits TXA2

has certain features that will contribute to the cardinal signs of inflammation

91
Q

What is LOX?

A

leads to production of lipoxins and leukotrienes

92
Q

What is LTB4?

A

neutrophil, macrophage, mast cells

chemoattractants for neutrophils

93
Q

What are the 3 COX isoenzymes?

A

COX 1
COX 2
COX 3

94
Q

What is COX 1 and its function?

A

constituitively expressed in almost all cells; housekeeping enzyme

impt in homeostasis and gastroprotection

95
Q

What is COX 2 and its function?

A

expressed locally at sites of inflammation (induced),

present in leukocytes, endothelial cells, synovial fibroblasts - so not all cells

96
Q

What is COX 3 and its function?

A

cerebral cortex in dogs

97
Q

Certain mammary tumors (adenocarcinoma) suppress which COX? What is the effect?

A

COX-2

lowers inflammation as a result

98
Q

What prostaglandins is formed first then metabolized into what?

A

PGH2 then

PGD2
PGF2
PGE2
PGI2
TXA2

99
Q

What do all of the PG_2 do?

A
100
Q

Which prostaglandins have antagonistic properties?

A

PGI2 (prostacyclin)
TXA2 - platelets

101
Q

How are PGI2 and TXA2 antagonists?

A

PGI2 - inhibit platelet aggregation

TXA2 - pro-coagulant

102
Q

What are leukotriene effects - general?

A

General: chemotaxis for leukocytes

increased vascular permeability
vasoconstriction

103
Q

What are leukotriene effects - specific?

A

LTB4: potent chemoattractant for neutrophils (lipoxins counteract)

  • LTC4, D4, E4: vasoconstriction, bronchospasm, increased vascular permeability
104
Q

Leukotrienes and lipoxins are [agonists/antagonists]

A

antagonists

105
Q

What are lipoxins and their functions?

A

secreted by platelets

pro-inflammatory and anti-inflammatory effects

  • inhibit neutrophil chemotaxis, adhesion
  • counteract leukotrienes
106
Q

What are omega-3s?

A

inhibits eicosanoid activity

replaces arachidonic acid in membrane and then minimizes pro-inflammatory mediators

107
Q

What is platelet activating factor (PAF)?

A

byproduct when phospholipase cleaves arachidonic acid - now freed arachidonic acid and PAF

derived from cell membranes of platelets, basophils, mast cells, neutrophils, macrophages, and endothelial cells

108
Q

What are the effects of PAF - high doses?

A

vasoconstriction
leukocyte adhesion, chemotaxis

109
Q

What are the effects of PAF - low doses?

A

vasodilation
increased vascular permeability

110
Q

What are interferons?

A

cytokines produced by lymphocytes and many other cells in response to viruses, parasites, neoplastic cells

111
Q

What are the functions of interferons?

A

inhibit viral replication within host cells

activate NK cells and macrophages

increase antigen presentation to T lymphocytes

increase resistance of host cell to viruses

112
Q

What are NK cells and their function?

A

lymphocyte - does not express T cell receptors or CD3

cytotoxic - perforin and pokes holes

113
Q

What are chemokines and their functions?

A

chemical cytokines

induce chemotaxis of leukocytes

activate inflammatory cells

produced by all nucleated cells in the body

114
Q

What are free radicals and their functions?

A
115
Q

What are free radicals arch enemy?

A

superoxide dismutase
glutathione peroxidase
ceruoplasmin
melatonin
vitamin A, C, E

116
Q

What is NO and its functions?

A

chemical mediator of inflammation

vasodilation (relaxation of smooth muscle cells

inhibits platelet aggregation and adhesion, mast cell induced inflammation

oxidizes lipids

regulates leukocyte chemotaxis

117
Q

What are PAMPS?

A

bind several types of pattern recognition receptors

118
Q

What are TLRs?

A

type of pattern recognition receptor

important role in release of cytokines due to microbes

innate and adaptive

119
Q

What are acute phase proteins?

A

inhibitors or mediators of inflammatory response

SERUM AMYLOID A

120
Q

What are outcomes of the reparative phase of acute inflammation?

A

resolution

abscess formation

progression to chronic inflammation - fibrosis dense CT

Veterinary Pathology (11 decks)

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