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General Pathology > Acute and Chronic Inflammation > Flashcards

Acute and Chronic Inflammation Flashcards

1
Q

is inflammation a cellular or vascular response or both?

A

both

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2
Q

what are some examples of possible tissue damage from inflammation?

A

atherosclerosis
allergic reactions
rheumatoid arthritis

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3
Q

what are the five R’s in inflammation?

A

recognition of injurious agent
recruitment of leukocytes
removal of agent
regulation of immune response
resolution or repair

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4
Q

what things do white blood cells have receptors for?

A

microbes
Fc portion of antibodies
complement proteins

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5
Q

what does opsonization c do?

A

coats microbe with antibody or complement
promotes phagocytosis
promotes inflammation

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6
Q

what are some circulating proteins that help recognize microbes and damaged cells?

A

complement
mannose-binding lectin
collectins

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7
Q

what does binding of toll-like receptors on epithelial, dendritic/macrophage, and lymphocyte cells cause?

A

release of inflammatory molecules

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8
Q

what are the general features of acute inflammation?

A

short time course
fluid and plasma leakage
neutrophils

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9
Q

what are the general features of chronic inflammation?

A

long time course
lymphocytes and macrophages
vascular proliferation
fibrous tissue proliferation

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10
Q

what are the two major components of acute inflammation?

A

vascular changes
cellular events

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11
Q

what vascular changes happen in acute inflammation?

A

vasodilation
vascular permability

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12
Q

what cellular events happen in acute inflammation?

A

leukocyte recruitment and activation

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13
Q

where does the majority of fluid leakage, leukocyte transmigration, and hemorrhage occur?

A

capillaries and postcapillary venules

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14
Q

loss of fluid and dilation of blood vessels leads to__________________ which leads to __________________

A

slowing of blood flow
congestion and white blood cells adhering to walls

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15
Q

what causes vascular permeability specifically?

A

nitric oxide and histamine and prostaglandins

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16
Q

what is transudate and what is exudate?

A

transudate has low protein content and few cells
exudate has high protein content and maybe some red and white cells: inflammation

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17
Q

what are the mechanisms of increased vascular permeability?

A

retraction of endothelial cells (histamine, nitric oxide, rapid and short-lived)
endothelial injury (burns, rapid and can be long-lived)

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18
Q

what is chemotaxis?

A

movement along chemical gradient

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19
Q

what are the endogenous sources of a chemotactic stimulus for migrating leukocytes?

A

cytokines/chemokines (IL-8)
C5a
LTB4

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20
Q

what receptor does endothelial molecule ICAM-1 have and what is its major role?

A

CD11/CD18 (integrins)
adhesion, arrest, transmigration

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21
Q

what receptor does endothelial molecule PECAM have and what is its major role?

A

CD31
leukocyte migration through endothelium

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22
Q

what mediates firm adhesion and what mediates rolling?

A

integrins mediate firm adhesion
selectins mediate rolling

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23
Q

what do IL-1 and TNF induce expression of?

A

P-selectin
E-selectin
integrin ligands ICAM-1 and VCAM-1

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24
Q

in leukocyte activation, what receptors are present?

A

toll-like receptors
G protein-coupled receptors
receptors for opsonins
receptors for cytokines

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25
Q

what do G protein-coupled receptors recognize?

A

bacterial peptides containing N-formylmethionyl, chemokines, lipid mediators

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26
Q

what is the major macrophage-activating cytokine?

A

interferon-gamma

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27
Q

what is the most efficient bacteriocidal system in neutrophils?

A

H2O2-myeloperoxidase-halide system

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28
Q

what does nitric oxide do to microbials and host cells?

A

reacts with superoxide to produce free radicals that damage lipids, proteins, and DNA of these cells

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29
Q

what controls lysosomal enzymes?

A

antiproteases such as alpha-1-antitrypsin which inhibits elastase

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30
Q

what are the principle sources of histamine?

A

mast cells
basophils
platelets

31
Q

can complement stimulate histamine to be released? If so what specifically?

A

yes- anaphylatoxins C3a and C5a

32
Q

what does histamine cause?

A

dilation arterioles
increased venule permeability
constriction of large arteries and airways

33
Q

what metabolites are associated with vasodilation?

A

PGI2, PGE1, PGE2, PGD2

34
Q

what are the three most important cytokines in acute inflammation?

A

TNF
IL-1
IL-6

35
Q

what are the systemic protective effects of TNF, IL-1, and IL-6?

A

hypothalamus: fever
liver: acute phase proteins (IL-1 and IL-6)
bone marrow: leukocyte production

36
Q

what are the main cells that participate in chronic inflammation?

A

macrophages
plasma cells
lymphocytes

37
Q

what are the most common causes of chronic inflammation?

A

persistent infections
prolonged exposure to toxic/injurious agents
immune-mediated inflammatory disease
leukocyte defects (more common in humans)

38
Q

what are the histologic features of chronic inflammation?

A

infiltration mononuclear cells
tissue destruction
healing by connective tissue replacement

39
Q

what do alternatively activated macrophages do?

A

tissue repair, anti-inflammatory effects

40
Q

what cytokines lead to alternatively activated macrophages?

A

IL-13
IL-4

41
Q

what cytokines from activated macrophages promote leukocyte recruitment?

A

mainly TNF and IL-1

42
Q

what does production of TNF by activated T lymphocytes stimulate?

A

inflammation

43
Q

what are the three subsets of CD4+ lymphocytes?

A

Th1
Th2
Th17

44
Q

in what inflammatory diseases do plasma cells predominate in?

A

inflammatory bowel disease in dogs and cats
lymphoplasmacytic stomatitis and pododermatitis in cats
chronic dermatitis
interstitial nephritis in dogs and cats

45
Q

what recruits eosinophils to chronic inflammation sites?

A

IL-5
eotaxin

46
Q

what secretes eotaxin?

A

endothelial cells
epithelial cells
eosinophils
macrophages

47
Q

what are the five patterns/categories of chronic inflammation?

A

lymphoplasmacytic
fibrosing chronic inflammation
chronic-active (purulent) inflammation
granulomatous/pyogranulomatous inflammation
abscesses

48
Q

what are the predominant cells in lymphoplasmacytic inflammation?

A

lymphocytes and plasma cells

49
Q

where is lymphoplasmacytic inflammation predominant?

A

mucosal regions with extending exposure to antigens
CNS around vessels

50
Q

what is chronic fibrosing inflammation predominantly composed of?

A

fibrous connective tissue

51
Q

when does chronic-active inflammation occur?

A

when stimulus has not been removed and continues to elicit acute inflammation

52
Q

what are the two patterns of granulomatous inflammation?

A

diffuse/haphazard
nodular granulomas/pyogranulomas

53
Q

what is the difference between granulomas and pyogranulomas?

A

pyogranulomas also have neutrophils

54
Q

what is a granuloma attempting to do?

A

contain an offending antigen that is difficult to eradicate

55
Q

what are the two types of granulomatous inflammation?

A

foreign body
immune

56
Q

what response does an immune granuloma induce?

A

specific immune response
activation of T cells
IL-2 release
macrophage responses

57
Q

are neutrophils characteristic of chronic inflammation?

A

yes, as well as acute

58
Q

in what type(s) of inflammation are mast cells important in?

A

chronic and acute

59
Q

what are the predominant cell types in granulomatous inflammation?

A

activated macrophages with an epithelioid appearance
can form giant cells

60
Q

what does mannose-binding lectin specifically recognize?

A

microbial sugars

61
Q

what do collectins bind to?

A

microbes

62
Q

typically, _______________ predominate in the first 24 hours, but are short-lived and replaced by ____________________

A

neutrophils
monocytes/macrophages

63
Q

what do toll-like receptors recognize?

A

LPS (endotoxin), bacterial proteoglycans, lipids

64
Q

what secrete interferon-gamma?

A

natural killer cells and T cells

65
Q

what are Th1 and Th17 cells important against?

A

many types bacteria and viruses and autoimmune diseases

66
Q

what are Th2 cells important against?

A

helminthic parasites and allergic inflammation

67
Q

what is proliferation of mast cells regulated by?

A

self-secreted C-Kit

68
Q

what produces nitric oxide?

A

macrophages and neutrophils after activated

69
Q

what stimulates mast cells and basophils to release histamine?

A

trauma
cold/heat
Ab binding to mast cells (immune reactions)
complement anaphylatoxins (C3a and C5a)
neuropeptides
cytokines

70
Q

what produces IL-1 and TNF?

A

activated macrophages

71
Q

what chemokines stimulate a macrophage to go into the alternatively activated macrophage line?

A

IL-13
IL-4

72
Q

what do alternatively activated macrophages release?

A

IL-10
TGF-beta
growth factors

73
Q

what cells are characteristic of granulomatous inflammation?

A

shift from neutrophils to:
epithelioid macrophages
lymphocytes
+/- multinucleated giant cells

74
Q

what is required for multinucleated giant cells?

A

macrophages present and bathed in cytokines
pathogen factors
express fusionogenic molecules like CD44 and macrophage fusion receptor

General Pathology (9 decks)

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