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Patho Exam 4 > Park:Acute and Chronic Inflammation > Flashcards

Park:Acute and Chronic Inflammation Flashcards

1
Q

When does inflammation occur?

A

In response infections or noxious stimuli (injuries, foreign body, burn, etc)

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2
Q

What is the purpose of inflammation?

A

-to eliminate harmful agents (microbes, toxins) and necrotic cells
-initiate the healing process

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3
Q

How could inflammation injure normal tissues?

A

-a inflammation response may be too strong (think severe infection)
-the response may be prolonged (persistent or recurrent infection)
-inappropriate response may be occurring (self-antigens in autoimmune diseases)

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4
Q

What are some pharmacologic approaches to inflammation?

A

-glucocorticoids
-NSAIDs
-antihistamines
-leukotriene antagonists
-biologics targeting cytokine signaling

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5
Q

What are leukocytes

A

white blood cells

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6
Q

Phagocytes

A

a cell capable of engulfing and absorbing

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7
Q

What are types of phagocytes

A

-neutrophils
-mast cells
-macrophages
-monocytes
-dendritic cells

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8
Q

Granulocytes

A

an immune cell that has granules with enzymes that are released

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9
Q

What are types of granulocytes?

A

-neutrophils
-eosinophils
-basophils
-mast cells

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10
Q

Lymphocytes

A

responsible for producing antibodies and regulating immune respose

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11
Q

What are types of leukocytes?

A

-B cells
-T cells
-Natural killer cells

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12
Q

Innate immunity

A

-nonspecific
-fast response (0-4 hours)

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13
Q

Adaptive immunity

A

-specific
-slow response (4-14 days)

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14
Q

Acute inflamation

A

-rapid onset
-short duration (minutes to days)
-accumulation of fluid and plasma proteins (exudation)
-accumulation of neutrophils
-tumor necrosis factor (TNF)
-interleukin-1 (IL-1)
-chemokines

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15
Q

Chronic inflammation

A

-insidious
- longer duration (months to years)
-tissue destruction by inflammatory cells
-vascular proliferation
-fibrosis (scarring)
-influx of lymphocytes and macrophages
-interferon-y (IFN-y) by T cells and interleukin-12 by macrophages (synergistic stimulation)

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16
Q

Explain how an acute inflammatory response happens

A

-Upon tissue damage or introduction of bacteria histamines are released increasing blood flow to the area
-histamines cause capillaries to leak, releasing phagocytes and clotting factors into the wound
-phagocytes engulf bacteria, dead cells, and cellular debris
-platelets move out of the capillary to seal the wounded area

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17
Q

What is the acute inflammatory response?

A
  • phagocytes in tissue recognize offending agents and liberate chemical mediators of inflammation
    -chemical mediators widen blood vessels (vasodilation) and increase their permeability in the vicinity
    -plasma and circulating leukocytes diffuse to the location of the offending agent (leukocyte recruitment)
    -activated leukocytes remove the offending agents (phagocytosis)
    -leukocytes produce signaling molecules that suppress inflammation (eg. lipoxins)
    -the damaged tissue is repaired (cell proliferation)
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18
Q

What are characteristics of acute inflammation?

A

-heat (calor)
-redness (rubor)
-swelling (tumor)
-pain (dolor)
-loss of function (functio laesa)

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19
Q

What are the major components of inflammation?

A

-vascular stage
-cellular stage

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20
Q

what is involved in the vascular stage?

A

-vasodilation
-increased permeability

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21
Q

What is involved in the cellular stage?

A

-leukocyte recruitment
-phagocytosis

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22
Q

What does an increase in vascular diameter (vasodilation) cause?

A

-decrease in fluid velocity
-increase in viscosity (due to fluid loss to tissues)
-increased leukocyte setting along the inner surface of the blood vessels (margination)

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23
Q

What can cause an increase in vascular permeability?

A

-gaps due to endothelial contraction which is the most common mechanism (caused by histamine, leukotrienes, bradykinin)
-increased fluid flow through endothelial cells (transcytosis)
-direct endothelial (traumatic) trauma
-leukocyte-dependent endothelial cell damage/death due to release of toxic mediators by leukocytes
-leakage from new blood vessels that form at the site of injury (thinner)

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24
Q

What are vascular changes

A

-transudate
-exudate

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25
Q

Transudate

A

-increased hydrostatic pressure (venous outflow obstruction, ex congestive heart failure)
OR
-decreased colloid osmotic pressure (decreased protein synthesis, ex liver disease; increased protein loss; ex kidney disease)
-results in small holes, release of plasma with little proteins and no cells (water)
-example is edema…accumulation of fluid and swelling at site of inflammation (can happen without inflammation as well)

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26
Q

Exudate

A

-inflammation triggers fluid and protein leakage, vasodilation and stasis, and increased interendothelial spaces
-has bigger holes with allows protein rich fluid with numerous cells to exit

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27
Q

How are leukocytes recruited?

A

-margination
-loose attachment and rolling (selectins)
-adhesion (integrins)
-transmigration
-chemotaxis

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28
Q

Chemotaxis can be caused by what?

A

-bacterial products (ex lipopolysaccharides (LPS))
-chemokines
-complement system (C5a)
-leukotriene B4 (LTB4)

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29
Q

How is phagocytosis initiated?

A

-direct recognition
-indirect recognition by opsonins

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30
Q

How does direct phagocytosis recognition occur?

A

-direct recognition of microbes by pattern recognition receptors such as toll like receptors (lipopolysaccharides, flagellin, etc) or mannose receptors (outer membrane of bacteria)

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31
Q

How does indirect phagocytosis recognition occur?

A

-opsonins such as IgG, C3b, and collectins (carbohydrate-binding lectins) coat the foreign body and dead cells in a process known as opsonization…specific receptors on phagosomes then recognize the opsonins (Fc or C3b receptors)

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32
Q

How does engulfment occur in phagocytosis?

A

-the receptors on the opsonin or microbe is recognized (receptor mediated endocytosis)
-this triggers the pseudopods (arms) to extend around the foreign body and form a phagosome

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33
Q

How does a phagocytosis kill foreign bodies?

A

-the phagosome fuses with a lysosome (phagolysosome)
-lysosomal degradation then occurs through the digestive enzymes and defensins within the lysozyme
-the digested particles are then released, the toxic nitrogen and oxygen compounds (oxidative burst)

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34
Q

What types are mediators are found in acute inflammation?

A

-plasma derived mediators
-cell-derived mediators

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35
Q

What are cell derived mediators

A

-histamine
-platelet activating Factor (PAF)

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36
Q

Histamine

A

-first mediator released upon acute inflammation but transient
-binds to histamine type 1 receptors on endothelial cells and causes vasodilation and increases vascular permeability
-H1 receptor antagonist are used as antihistamine drugs

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36
Q

Platelet activating factor (PAF)

A

-generated from phospholipids by phospholipase A2
-induces platelet aggregation
-100~1000x more potent than histamine in inducing inflammation reactions

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36
Q

What happens with the cleaved fatty acid fro the phospholipid that was cleaved by phospholipase A2?

A

It becomes an eicosanoid

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36
Q

What do eicosanoids trigger?

A

two pathways
-cyclooxygenase (COX) pathway
-lipoxygenase pathway

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36
Q

eicosanoids

A

-derived from polyunsaturated fatty acids
-ex is arachidonic acid (has 20 carbons)

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37
Q

What can inhibit the COX pathway?

A

-aspirin
-NSAIDs

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37
Q

What does the COX pathway lead to?

A

-generation of prostaglandins (complex inflammatory responses including fever and pain)
-generation of thromboxane (causes vasoconstriction and platelet aggregation)

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37
Q

What are examples of plasma protein mediators?

A

-thrombin and fibrinopeptides
-C3a, C5a, C3b
-bradykinin

37
Q

What can inhibit eicosanoid from triggering the COX pathway and lipoxygenase pathway?

A

corticosteroid medications

37
Q

What does the lipoxygenase pathway lead to?

A

generation of leukotrienes (similar to histamine but are more potent and long acting; significant contributors to allergic reactions)

38
Q

What are thrombin and fibrinopeptides apart of?

A

the clotting system

39
Q

What does thrombin activate?

A

leukocytes

40
Q

what are fibrinopeptides produced from?

A

the digestion of fibrinogen by thrombin

41
Q

What do fibrinopeptides do?

A

-Increase vascular permeability
-chemotactic

42
Q

What are C3a, C5a, C3b?

A

-a compliment system, they work together

43
Q

what does the letter indicate on C3a, C5a, C3b?

A

that they have been cleaved

44
Q

what does C3a and C5a do?

A

increase vascular permeability and cause vasodilation

45
Q

what does C5a do?

A

-activate leukocytes
-chemotactic

46
Q

What does C3b do?

A

acts as an opsonin

47
Q

What is bradykinin apart of?

A

the kinin system

48
Q

How is bradykinin formed?

A

By the cleavage of kininogens by protease called kallikrenins

49
Q

what does bradykinin do?

A

-increases vascular permeability
-cause vasodilation
-cause pain

50
Q

What pathway activates the plasma protein mediators?

A

The Factor X11 (Hageman factor) pathway

51
Q

cytokine

A

-small proteins that are part of the immune systems signaling network
-essential for regulating the immune system

52
Q

Cytokine secretion is___

A

-transient
-tightly regulated

53
Q

What types of functions do cytokines have?

A

-pleiotropic
-redundant

54
Q

What are the major cytokines that mediate the acute inflammation pathway?

A

-TNF
-IL-1

55
Q

What is the major source of TNF and IL-1 cytokine production?

A

activated macrophages

56
Q

What types of responses can the cytokines TNF and IL-1 generate?

A

-cellular
-systemic

57
Q

what are chemokines?

A

-chemotactic cytokines
-they recruit and direct the migration of immune and inflammatory cells
-they generate a persistent chemotactic gradient

58
Q

Nitric Oxide

A

-synthesized by inducible nitric oxide synthase (iNOS) which is induced by inflammatory cytokines and mediators
-short-lived (a few seconds)
-locally acting

59
Q

What does Nitric Oxide (NO) do?

A

-triggers the relaxation of vascular smooth muscles by vasodilation
-works as an antimicrobial agent in activated macrophages

60
Q

Reactive oxygen species (ROS)

A

-synthesized by NADH oxidase pathway
-short lived
-locally acting

61
Q

What happens to ROS?

A

-released extracellularly by neutrophils and macrophages after stimulation
-may cause tissue injury

62
Q

How can lysosomal proteases cause tissue injury?

A

the release into the extracellular space can lead to matrix degradation and destructive tissue injury

63
Q

What causes the release of lysosomal proteases?

A

-premature degranulation of lysosomes
-phagocytosis attempts of large, flat surfaces (frustrated phagocytosis)
-damage of leukocytes (ex. urate crystals in gout)

64
Q

What antiproteases are present to inhibit lysosomal proteases?

A
  • a2-macroglobulin
    -a1-antitrypsin
    -all exist in the serum and extracellular matrix
65
Q

What mediators cause vasodilation and increased vascular permeability?

A

-Histamine
-PAF
-C3a and C5a
-bradykinin
-leukotrienes (LTC,LTD, LTE)
-prostaglandins
-NO

66
Q

what mediators are involved in chemotaxis?

A

-C5a
-leukotriene B (LTB)
-bacterial products (LPS)
-chemokine

67
Q

what mediators cause fever?

A

-IL-1
-Il-6
-TNF
-prostaglandins

68
Q

what mediators cause pain?

A

-prostaglandins
-bradykinin

69
Q

what mediators cause tissue damage?

A

-lysosomal enzymes
-reactive oxygen species
-nitric oxide

70
Q

Abscess

A
  • a localized area of inflammation containing a purulent exudate (pus) that may be surrounded by a neutrophil layer
    -caused by excessive neutrophil infiltrates or certain bacterial/fungal infections (pyogenic)
71
Q

Ulceration

A

-a site of inflammation where an epithelial surface has become necrotic and eroded
-may occur as the result of traumatic injury to the epithelial surface (peptic ulcer) or vascular compromise (foot ulcers associated with diabetes)

72
Q

What is chronic inflammation?

A

inflammation of prolonged duration (weeks to months to year)

73
Q

What happens during chronic inflammation?

A

active inflammation, tissue injury, and healing occur simultaneously ( a cycle)

74
Q

what can happen if acute inflammation is unresolved?

A

it can progress to chronic inflammation

75
Q

What are characteristics of chronic inflammation?

A

-infiltration with mononuclear (“chronic inflammatory”) cells (macrophages, lymphocytes, and plasma cells)
-tissue destruction
-repair involving new vessel proliferation (angiogenesis) and fibrosis (scarring)

76
Q

What are some causes of chronic inflammation?

A

-viral infection (intracellular)
-persistent microbial infection (delayed hypersensitivity)
-prolonged exposure to toxic agents (silica in lungs)
-autoimmune diseases (RA/ MS

77
Q

Where are chronic inflammation macrophages from?

A

-derived from circulating blood monocytes
-activated by cytokines, bacterial products, mediators of inflammation, dead cells, etc

78
Q

what are chronic inflammation macrophages alos known as?

A

epithelioid macrophages

79
Q

What products released by epithelioid macrophages may cause tissue damage?

A

-proteases
-complement components, coagulation factors
-ROS
-NO
-eicosanoids
-cytokines
-growth factors (leads to fibrosis)

80
Q

What happens to macrophages in chronic inflammation

A

macrophage accumulation persists

81
Q

Explain the reciprocal relationship of lymphocytes and macrophages

A
  • lymphocytes are activated by macrophage presenting antigen fragments
    -activated lymphocytes release mediators including interferon- y (IFN-y)
    -IFN-y activates macrophages
    -activated macrophages release cytokines including IL-12
    -IL-12 further activates lymphocytes
82
Q

What happens between macrophages and lymphocytes

A

they persistently stimulate one another until the triggering antigen is removed

83
Q

what is also present in chronic inflammation (besides macrophages)

A

-plasma cells
-eosinophils
-mast cells

84
Q

What in granulomatous inflammation

A
  • a distinctive form of chronic inflammation
    -formation of granuloma
85
Q

What is a granuloma

A

a small (1-2 mm) lesion of epitheliod macrophages surrounded by lymphocytes

86
Q

what causes granulomas?

A

-offending agents not easily controlled by other inflammatory mechanisms such as foreign bodies (splinters, sutures, silica, and asbestos) or microorganisms (cause tuberculosis, syphilis, sarcoidosis, deep fungal infections, and brucellosis)

87
Q

What are foreign body giant cells?

A

-multi-nucleated cells formed by coalesced macrophages
-encapsulate and isolate the offending agents

88
Q

what are the two cell types most responsible for chronic inflammation
A. macrophages and lymphocytes
B. neutrophils and lymphocyte
C. basophils and lymphocytes
D. neutrophils and macrophages
E. basophils and macrophages

A

A. macrophages and lymphocytes

89
Q

Which of the following does not belong to the classic signs of inflammation?
A. heat
B. redness
C. swelling
D. scarring
E. pain

A

D. scarring

90
Q

The vascular change upon inflammation increases leukocyte setting along the surface of the blood vessels, which is called____
A. transcytosis
B. edema
C. extravasation
D. vasodilation
E. margination

A

E. margination

91
Q

which of the following plasma proteins causes pain?
A. C3b
B. fibrinopeptides
C. C3a and C5a
D. bradykinin
E. thrombin

A

D. bradykinin

92
Q

The mediators of inflammation are matched with the enzyme responsible for their production. Which pair is incorrect?
A. Nitric oxide (NO)- inducible nitric oxide synthase (iNOS)
B. platelet activating factor (PAF)- phospholipase A2
C. bradykinin- kallikrein
D. leukotrienes- cyclooxygenase
E. fibrinopeptides-thrombin

A

D. leukotrienes-cyclooxygenase

93
Q

What are the key cytokines responsible for acute inflammation?
A. IFN-y and IL-12
B. IFN-y and TNF
C. TNF and IL-12
D. IFN-y and IL-1
E. TNF and IL-1

A

E. TNF and IL-1

94
Q

Which of the following mediators may cause tissue damage?
A, lysosomal enzymes
B. Reactive oxygen species (ROS)
C.Nitric Oxide (NO)
D. all of the above
E. none of the above

A

D. all of the above

95
Q

Which of the following is not responsible for killing of the engulfed bacteria in phagolysosomes?
A. defensins
B. Hypochlorous radical
C.a2-macroglobulin
D. Lysosomal proteases
E. hydrogen peroxide

A

C. a2- macroglobulin

96
Q

What cells are commonly found in granulomas?
A. cancer cells and neutrophils
B. cancer cells and lymphocytes
C. epithelioid macrophages and lymphocytes
D. epithelioid macrophages and neutrophils
E. neutrophils and lymphocytes

A

C. epithelioid macrophages and lymphocytes

97
Q

What do pattern recognition receptors of leukocytes recognize directly
A. chemokine
B. microbes
C. histamines
D. opsonins
E. selectins and integrins

A

B. microbes

Patho Exam 4 (6 decks)

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