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PATHO > Lecture 3+4: Acute and Chronic Inflammation > Flashcards

Lecture 3+4: Acute and Chronic Inflammation Flashcards

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1
Q

Inflammation

A

-from infections or bad stimuli
-eliminates harmful agents and necrotic cells
-initiates healing
-may injure normal tissues

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2
Q

Inflammation damaging normal tissue scenarios

A

-response too strong (severe infection)
-prolonged reponse (persistent or recurrent infection)
-inappropriate response (self antigens in autoimmune disease)

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3
Q

pharmacological approaches to inflammation

A

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

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4
Q

leukocytes

A

white blood cells

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5
Q

phagocytes

A

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

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6
Q

Granulocytes

A

-neutrophils
-eosinophils
-basophils
-mast cells

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7
Q

lymphocytes

A

-B cells
-T cells
-NK cells

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8
Q

Acute inflammation

cell types
cytokines

A

-rapid onset
-short duration
-exudation
-accumulation of NEUTROPHILS
-TNF and IL-1 and chemokines

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9
Q

exudation

A

accumulation of fluid and plasma proteins

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10
Q

Chronic inflammation

cell type
cytokines

A

-insidious and longer (months to years)
-tissue destroyed by inflammatory cells
-scarring
-influx of LYMPHOCYTES and MACROPHAGES
-IFN-y by T cells and IL-12 by macrophages (synergistic stimulation)

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11
Q

scarring

A

vascular proliferation and fibrosis

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12
Q

Acute Inflammatory response

A
  1. Phagocytes recognize threat then release chemical mediators of inflammation
  2. mediators cause vasodilation and increase permeability
  3. leukocytes diffuse to site
  4. Phagocytosis by leukocytes
  5. Luekocyte sends signals that suppress inflammation (lipoxins)
  6. Damage tissue is repaired (cell proliferation)
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13
Q

Signs of acute inflammation

A

-heat
-redness
-swelling
-pain
-loss of function

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14
Q

Major components of inflammation

A

-vascular stage
-cellular stage

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15
Q

vascular stage of inflammation

A

-vasodilation
-increased permeability

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16
Q

cellular stage of inflammation

A

-leukocyte recruitment
-phagocytosis

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17
Q

Vasodilation

A

-decrease in fluid velocity
-increased viscosity due to fluid loss to tissues
-margination

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18
Q

margination

A

-increased leukocyte settling along the inner surface of blood vessels

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19
Q

Increase in vascular permeability

A

-Gaps due to endothelial contraction (histamine, leukotrienes, bradykinin)
-increased fluid flow through endothelial cells (transcytosis)
-direct endothelial *traumatic) injury
-leukocyte-dependent endothelial cell damage due to release of toxic mediators by leukocytes
-leakage from new blood vessels that form at site of injury

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20
Q

Vascular changes

A

-transudate
-exudate
-edema

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21
Q

transudate

A

-small holes
-plasma with little protein
-no cells

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22
Q

exudate

A

-bigger holes
-protein rich fluid
-numerous cells

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23
Q

edema

A

-accumulation of fluid and swelling at site of inflammation

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24
Q

Leukocyte recruitment

A

-margination
-rolling (selectins)
-adhesion (integrins)
-transmigration
-chemotaxis

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25
Chemotaxis
-bacterial products (LPS) -chemokines -complement system -leukotriene B4
26
Phagocytosis steps
1. recognition (direct or indirect) 2, engulfment 3. Killing
27
Direct recognition in phagocytosis
-by pattern recognition receptors -toll-like receptors (LPS, flagella) -mannose receptors
28
Indirect recognition in phagocytosis
-by opsonins (IgG, C3b, collectins) -opsonization -specific receptors recognize opsonins
29
opsonization
coat foreign body and dead cells
30
Engulfment step of phagocytosis
-receptor-mediated ENDOcytosis -psuedopods form PHAGOSOME around foreign body
31
Intracellular killing phase of phagocytosis
-phagolysosome -lysosomal degradation -oxidative burst
32
Histamine
-first mediator of inflammation released upon acute inflammation, but transient -binds H1 receptors =vasodilation and increased permeability
33
antihistamine drugs
H1 receptor antagonists
34
Platelet activating factor (PAF)
-mediator of inflammtion -generated from phospholipids by phospholypase A2 -induces platelet aggregation -100-10000 times more potent than histamine
35
Eicosanoids
-derived from polyunsat FAs like arachidonic acid -COX pathway (prostaglandins and thromboxane) -Lipoxygenase pathway (leukotrienes)
36
prostaglandins
-complex inflammatory response -fever and pain
37
thromboxane
-vasoCONSTRICTION -platelet aggregation -INHIBITED by NSAIDs
38
NSAIDs inhibt
thromboxane part of COX pathway
39
leukotrienes
-similar to histamine -more potent and longer -significant in allergic reactions
40
Plasma proteins
1. clotting system: thrombin and fibrinopeptides 2. complement system: C3a, C5a, C3b 3. kinin system: bradykinin
41
thrombin
activates leukocytes
42
fibrinopeptides
-increase permeability -chemotactic -produced from digestion of fibrinogen bu thrombin
43
Anaphylatoxins
-C3a and C5a -vasodilation -increase permeability
44
C5a
-activates leukocytes -chemotactic
45
C3b
-acts as opsonin
46
Bradykinin
-vasodilation -increased permeability -causes PAIN -formed by cleavage of kininogens by protease killikreins
47
Cytokines
-secretion is transient and tightly regulated -pleiotropic and redundant functions -TNF-a and IL-1 -chemokines
48
TNF-a and IL-1
-major cytokines of inflammation -come from activated macrophages -generate cellular and systemic responses
49
Chemokines
-chemotactic cytokines -recruit cells -generate persistant chemotactic gradient
50
Nitric Oxide (NO)
-short lived (sec) locally acting -synthesized by inducible nitric oxide synthase (iNOS) which is induced by inflammatory cytokines and mediators -vasodilation -antimicrobial in activated macrophages
51
Reactive Oxygen Species (ROS)
-short lived -from NADH oxidase pathway -superoxide, hydrogen peroxide, hydroxyl radical -released extracellularly by neutrophils and macrophages after stimulation -may cause tissue injury
52
Injury by Lysosomal proteases
-release of lysosomal contents into EXTRAcellular space -matrix degradation and tissue injury
53
causes of injury by lysosomal protease
-premature degranulation of lysosomes -phagocytosis attempts of large, flat surfaces (frustrated phagocytosis) -damage of leukocytes (urate crystals in gout)
54
Antiproteases
-inhibit lysosomal proteases -a2-macroglobulin, a1-antitrypsin -exist in serum and extracellular matrix
55
Vasodilation and increased vascular permeability is caused by:
-histamine -PAF -C3a and C5a -Bradykinin -leukotrienes (LTC, LTD, LTE) -prostaglandins -Nitric oxide
56
Chemotaxis caused by:
-C5a -Leukotriene B (LTB) -bacterial products (LPS) -chemokines
57
Fever caused by:
-IL-1 -IL-6 -TNF-a -prostaglandins
58
Pain caused by:
-prostaglandins -bradykinin
59
tissue damage caused by:
-lysosomal enzymes -ROS -nitric oxide
60
Abscess
-localized area of inflammation -pus that may be surrounded by neutrophils -excessive neutrophil infiltrates or certain bacterial/fungal pyogenic infections
61
Ulceration
-site of inflammation where epithelial surface has become necrotic and eroded -may occur as result of tramatic injury to epithelial surface (peptic) or vascular compromise (foot ulcers from diabetes)
62
Chronic inflammation
-weeks to years -inflammation, injury, and healing occur at same time -may progress from unresolved acute inflammation
63
Characteristics of chronic inflammation
-infiltration with mononuclear cells: macrophages, lymphocytes, plasma cells -tissue destruction -repair involving new vessel proliferation (angiogenesis) and fibrosis
64
Causes of chronic inflammation
-viral infection intracellular -persistant infection (delayed hypersensitivity) -prolonged exposure to toxins -autoimmune disease
65
Epithelioid macrophages
-activated by cytokines, bacterial products, mediators, dead cells, etc -release products that may cause tissue damage -macrophage accumulation persists
66
Macrophages release:
-proteases -complement, coagulation factors -ROS and NO -eicosanoids -cytokines -growth factors = fibrosis
67
Lymphocytes
-reciprocal of macrophage 1. activation by macrophage presenting antigen 2. activated lymphocytes release mediators (IFN-y) 3. IFN-y activates macrophages 4. activated macrophages release cytokines (IL-12) 5. IL-12 activates lymphocytes
68
Cells in chronic inflammation
-macrophages and lymphocytes stimulate each until the antigen is gone -also plasma, eosinophils, and mast cells
69
Granulomatous Inflammation
-form of chronic inflammation -formation of granuloma -caused by hard to control agents -foreign bodies -micros that cause TB, syphilis, sarcoidosis, deep fungal infections, brucellosis
70
Foreign body giant cells (granuloma)
-multinucleated cells formed by macrophages -encapsulate and isolate offending agents

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