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Disease and Defense > Acute and Chronic Inflammation > Flashcards

Acute and Chronic Inflammation Flashcards

1
Q

Acute cellular infiltrate

A

mainly neutrophils

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2
Q

Chronic cellular infiltrate

A

monocytes / macrophages / and lymphocytes

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3
Q

Acute - tissue injury / fibrosis

A

usually mild and self limited

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4
Q

Chronic - tissue injury / fibrosis

A

often severe and progressive

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5
Q

Local and systemic signs of acute

A

prominent

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6
Q

Local and systemic signs of chronic

A

less prominent / may be subtle

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7
Q

Acute (innate vs adaptive?)

A

acute is largely innate, with increasing chronicity more of a coordinated response involving innate and adaptive

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8
Q

stimuli for acute inflammation (4)

A

infection
trauma (anything that causes necrosis)
foreign material
immune reaction (hypersensitivity)

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9
Q

acute inflammation the process (4 steps)

A

recognition (receptors)
vascular change
leukocyte recruitment
leukocyte activation

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10
Q

Step 1 in acute - recognition - where are receptors located?

A

pattern recognition receptors are located on a large variety of cells (inflammatory and non)

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11
Q

Step 1 acute

what do pattern recognition receptors detect?

A

microbe derived substances, toxins, material from necrotic cells, Fc portions of Abs

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12
Q

step 1 acute

where are pro-inflammatory receptors located? (3)

A

plasma membrane
endosome
cytosol

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13
Q

where are TLR located?

A

plasma membrane and endosome

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14
Q

What happens when TLRs are stimulated?

A

–> trainscription factors –> mediators of inflammation and anti-microbial products

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15
Q

Aside from TLRs what is the other receptor we discussed?

A

Inflammasome

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16
Q

What is the inflammasome?

A

receptors in acute inflammation / complex of proteins that mediate cellular response, esp. in response to stuff dead or damaged cells release (but also microbes)

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17
Q

what does the inflammasome sense?

A

uric acid (from DNA breakdown), atp, decreased intracellular potassium (pm injury), DNA

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18
Q

what does the inflammasome do?

A

activates caspase-1 –> interleukin 1B –> inflammation

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19
Q

what is a known stimulator for IL1B? i.e. IL1B is good target for treatment

A

Gout (urate crystals)

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20
Q

Vacular changes in acute inflammation - key component of the inflammatory reaction, quickly bringing cells and other materials needed for a response to injury or threat - two major changes?

A

increased blood flow

increased permeability

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21
Q

vascular changes lead to many of the early clinical signs of infection
Increased flow –> ? (2)
Increased permeability –> ? (1)

A

increased flow –> congested capillary beds –> erythema (rubor)

increased flow –> local warmth (calor)

increased permeability –> exudate of fluid into tissues –> swelling (tumor)

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22
Q

Acute vascular changes - flow - arterioles serving the involved capillary beds dilate, flooding these capillaries - what is the major stimulus for this?

A

histamine’s action of smooth muscles in the vascular wall

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23
Q

vascular changes - increased permeability results from (3)

A

endothelial cell contraction
endothelial injry
transcytosis

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24
Q

what causes endothelial cell contraction? early and late?

A

early - histamine / bradykinin

late - IL1 / TNF

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25
Q

what causes endothelial cell injury (increased permeability)

A

can come from a variety of places (external e.g. burn, internal e.g. toxic compounds from responding leukoctyes)
- cell die / detach incomplete endothelium

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26
Q

transcytosis?

A

material transported through the endothelial cell via vesicles

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27
Q 
EXUDATE
common cause?
protein content?
cell content?
specific gravity?
A

cause - increased vascular perm
protein - increased
cell - increased: inflam / rbc
specific grav - high

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28
Q 
TRANSUDATE
common cause?
protein content?
cell content?
specific gravity?
A

cause - increased hydrostatic pressure with decreased colloid osmotic pressure
protein - decreased
cell - few cells
specific gravity - low

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29
Q

exudate results from?

A

incrased vascular permeability usually related to inflammation

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30
Q

transudate results from?

A

altered iv pressure (either from hemodynamic or osmotic) - increased capillary pressure from cardiac failure
decreased blood protein from liver disease

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31
Q

acute vascular changes - lymphatics
drain?
complication?
clinical?

A

drain accumulating edema along with all the debris that inflammation may produce

sometimes are a route to more widespread infection

changes to the draining lymphatic channels and lymph nodes may produce clinical exam findings (lymphadenitis)

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32
Q

Four main phases of leukocyte recruitment in acute inflammation

A

margination / rolling
adhesion
transmigration
chemotaxis

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33
Q

In ____________ leukocytes accumulate on endothelium - principals of laminar flow, larger/slower moving leukocytes get pushed to the periphery of the column - vascular permeability thicker and slower moving blood (“stasis”)

A

margination

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34
Q

In ____________ stimulated cells express adhesion moleucles which have affinity for sugars on leukocytes (transient, not strong binding)

A

Rolling

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35
Q

In rolling, what induces endothelium to move adhesion molecules for leukocytes to the surface?

A

chemical mediators:
histamine –> P-selectin
IL-1 –> E-selectin

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36
Q

In leukocyte recruitment
1.
2.
3.

A

location tissues detect threat

chemical mediators released

associated small blood vessels become sticky

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37
Q

In leukocyte recruitment, when does adhesion occur?

A

when the leukoctyes reach an a area of activation signaled by chemokines

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38
Q

What happens once a leukocyte is activated?

A

they alter integrins (CD11/CD18) on surface to a high infinity state -

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39
Q

In addition to activated leukocytes altering integrin expression, what happens to the endothelium in leukocyte recruitment?

A

Endothelium is activated by specific medatiors (IL-1, TNF) increases expression of ligands for integrins (e.g. ICAM1 that binds C11/CD18)

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40
Q

In leukocyte recruitment, what results from adhesion

A

stable attachment of leukocytes at the site of inflammation

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41
Q

Once the luekocytes are adhered to the endothelium near the site of inflammation, what happens?

A

transmigration

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42
Q

what is transmigration

A

leukocytes (using CD31) squeeze between endothelial cells: termed “diapedesis”

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43
Q

where does diapedesis occur?

A

mostly in venules

44
Q

in addition to squeezing through endothelial cells, what else must leukocytes do in transmigration?

A

secrete enzymes (e.g. collagenase) to break up basement membrane of vessels

45
Q

once the luekocytes transmigrate, what happens?

A

CHEMOTAXIS

46
Q

What is chemotaxis?

A

leukocytes move toward site of inflammation following chemical gradients of increasing density

47
Q

Are endogenous or exogenous substances chemotatic?

A

Both can be

bacterial products, cytokines, compliment proteins, arachidonic acid metabolites

48
Q

which compliment protein is especially chemotatic

A

C5

49
Q

which arachidonic acid metabolite is especially chemotatic?

A

LTB4

50
Q

What about leukocytes allows chemotaxis to yield movement/

A

Contractile elements of leukocytes are tied to chemotatic receptors - direction of greatest chemotactic chemical density determines the direction of movement

51
Q

when do leukocytes become activated?

A

when they encounter certain substances (microbial products, cellular debris, certain cellular mediators)

52
Q

once activated, leukocytes (4)

A
  1. readily phagocytize materials
  2. are poised to kill/degrade engulfed material
  3. readily secrete material to kill/degrade
  4. produce inflammatory meatiors (amplifies inflammatory process)
53
Q

3 steps of phagocytosis?

A
  1. recognition / attachment of particle to leukocyte
  2. engulfment and formation of vacuole
  3. killing / degradation of vacuolated material
54
Q

phagocytosis - 2 general ways to bind material

A
  1. receptors for specific products of microbes or necrotic cells
    receptors for opsonins
55
Q

what are opsonins?

A

host proteins present in blood or produced locally that coat microbes
examples IgG, C3b, Collectins

56
Q

how does phagocytosis kill microbes?

A

chemicals toxic to microbes are generated in lysosomes and fuse with the phagasome containing microbe

57
Q

What is in lysosome that kills microbe? (4)

A
  • ROS formed by oxidation of NADPH by phagocyte oxidase converts oxygen to superoxide ion –> superoxide ion spontaneously converts to hydrogen peroxide

myeloperoxidase and chloride ion convert hydrogen peroxide to hypochlorous radical which is stronger oxidizer

similarly toxic nitrogen compounds especially NO

Other lysosomal enzymes kill microbes and breakign down other materials

58
Q

in addition to phagocytosis, how to activated luekocytes degrade extracellular materials / microbes?

A

by secreting compounds

  • include enzyme and antimicrobial proteins
  • if material cannot be ingested lysosomal contents may be released extracellularly
  • neutrophil extracellular traps composed of nuclear chromatin as scaffolding with embedded antimicrobial compounds
  • -> provide concentrated area of antimicrobial material that traps microbes
59
Q

Outcomes of acute inflammation (3)

A
  1. resolution
  2. chronic inflammation
  3. scarring
60
Q 
Acute inflammation resolution:
capability of injured tissue?
degree of injury?
tissue damage?
requires?
A

capable of regenerating
minimal tissue damage
usually limited degree of injury
requires termination of the inflammatory process

61
Q

Acute inflammation how do we transition to chronic?

A

generally occurs when the offending agent not removed by the acute inflammation

can prolonged, followed by resolution or end as scarring

62
Q

does chronic inflammation always proceed from acute?

A 
no
some agents (esp. viral) stimulate a chronic inflammation response from the outset
- autoimmune disorders are often mediated by chronic inflammation
63
Q

Acute inflammation - scarring

A

occurs if tissue doesnt have capacity to regenerate

often occurs after considerable tissue distruction

results from tissue being filled in CT elements (esp. collagen)

can significantly impair function (e.g. liver cirrhosis)

64
Q

Innate immune system is not very discriminatory - activated leukocytes generate enzymes as well as substances that can damage host tissues just as well as microbes
Host tissue damage can occur in: (3)

A

tissue surrounding infectious agents (esp. resistant infections)

cleaning up necrotic tissue by the inflammatory process may cause additional damage

inflammatory process directed against host tissues

65
Q

deficits in leukocyte function lead to increased susceptibility to?

A

infections

66
Q

What is different in presentation of chronic vs acute inflammation?

A

acute inflammation often presented as sequential steps BUT chronic inflammation processes may occur concurrently

  • mononuclear cell infiltrate, incl lymphocytes, plasma cells, monocytes / macrophages
  • tissue destruction
  • repair : neovascularization and fibrosis

In chronic inflammation, injury and repair may occur together

occurs over longer periods of time

67
Q

settings characterized by chronic inflammation (3)

A

persistent infections
immune mediated disease (autoimmune and allergy)
prolonged exposure to toxins (endogenous and exogenous)

68
Q

chronic inflammation cells:

A

macrophages
lymphocytes
eosinophils
mast

69
Q

Where do macrophages come from?

A

blood monocytes circulate for about a day and some give rise to macrophages in teh peripheral tissues - take up residence in most tissues in the body

70
Q

Role of macrophages (3)

A

ingest microbes and necrotic cellular debris (main phagocytes of adaptive immune system)

initiate tissue repair, often results in fibrosis (scar)

secrete inflammatory mediators (cytokines, eicosanoids) that promote inflammation

present antigens to adaptive immune system

71
Q

chronic inflammation - macrophage - two types?

A

M1 - classical activation

M2 - alternative activation

72
Q

M1 - classical activation macrophages

what activates?
what do they produce?
what are their functions

A

activated by -
endotoxin; IFN-gamma (T cells cytokine); foreign material

what do they produce -
ROS; NO; lysosomal enzymes; pro-inflammatory cytokines

functions
- killing microbes; chronic inflammation

73
Q

Macrophage - M2 - alternative activation

what activates?
what do they produce?
what are their functions?

A

activated by
- IL-4; IL-13; (from T cells; eosinophils; mast cells)

produce -
growth factors for - new vessel growth; fibroblast activation

function - 
tissue repair and fibrosis
74
Q

What types of cells are involved in many chronic inflammatory disorders? Including autoimmune diseases?

A

lymphocytes

75
Q

What do CD4+ T cells secrete?

A

cytokines that promote inflammation

76
Q

3 classes of CD4 T+ cells?

A

TH1
TH2
TH17

77
Q

TH1 secretes?

A

IFN gamma - which activates the classical (M1) macrophage pathway

78
Q

TH2?

A

IL4, IL5, IL13: activates alternative pathway (M2) macrophages; also activates eosinophils

79
Q

TH17?

A

secretes IL17: recruitment of neutrophils and monocytes

80
Q

Eosinophil recruitment in chronic inflammation?

A

similar to neutrophils, but includes specific chemokines (eotaxin)

81
Q

What 2 specific scenarios are notable for eosinophil recruitment?

A

parasites (major basic protein is toxic to parasites)

allergic rxns mediated by IgE

82
Q

mast cells

inflammation involvement?

A

both acute and chronic

83
Q

what do mast cells release?

A 
inflammatory mediators 
(histamine and arachidonic acid)
84
Q

what triggers mast cell mediator release?

A

coated with IgE

85
Q

In addition to their notoriety for anaphylactic reactions - what else can mass cells do?

A

provide a widely distributed and quickly triggered response to infections

86
Q

What is granulomatous inflammation?

A

histologically distinctive pattern of chronic inflammation

87
Q

What is a granuloma?

A

enlarged macrophages that form nodule, which is often surrounded by lymphocytes

88
Q

granulomas can form around?

A

some organisms - but some can evade

89
Q

what often accompanies long standing granulomas?

A

fibrosis

90
Q

granulomatous inflammation should raise suspicion for? (4)

A
  1. some organisms not typically eradicated by other inflammatory reactions (tb, leprosy, fungi)
  2. some immune mediated diseases - Crohns?
  3. Foreign material (suture)
  4. Sarcoidosis - (no details_
91
Q

Three main processes of chronic inflammation

A
  1. mononuclear cell infiltrate
  2. tissue destruction
  3. repair
92
Q 
Chronic inflammtion 
Characteristic settings (3)
A
  1. persistent infections
  2. immune mediated diseases
  3. prolonged exposure to toxins
93
Q

Cells of chronic inflammation (4)

A

macs
lymphs
eos
mast

94
Q

type of inflammation associated with chronic?

A

granulomatous

95
Q

Acute phase reaction is the result of?

A

(systemic effect of inflammation)
Result of mediators produced by involved cells (leukocytes)
- systemic distribution

96
Q

What mediators are associated with Acute phase reaction?

A

TNF
IL1
IL6

97
Q

Examples of systemic effects of inflammation? (3)

A

fever
increased acute phase protein in blood
leukocytosis

98
Q

fever (pyrexia) - systemic effect of inflammation - what happens?

A

Vascular cells in hypothalamus stimulated by pyrogens to produce prostaglandins (esp. PGE2) that act locally to cause a central increase in body temp

99
Q

Exogenous pyrogens and fever - how do they cause it - bacteria?

A

e.g. bacterial components cause leukocytes to release endogenous pyrogens (IL-1, TNF) which then act on teh hypothalamus vasculature cells

100
Q

Exogenous pyrogens and fever - how do they cause it - endogenous

A

in addition to bacterial components causing leukocyte release of IL1 and TNF - exogenous pyrogens also act directly on the hypothalamus vasculature cells

101
Q

what is the increased body temperature thought to do in inflammaiton?

A

aid in fighting some infections

102
Q

In systemic inflammation, we also see increased acute phase proteins in the blood

what does liver respond to?
how is used clinically?
what do they do? (3 e.g.)

A

in response to IL6 - hepatocytes produce several proteins in greater abundance

clinically used to detect and monitor progress of inflammatory processes

Two of these
C-reactive protein and serum amyloid A are known to adhere to cell walls and may act as opsonins

fibrinogen binds RBCs causing them to form stacks that quickly form sediments. This forms the basis for the erythrocyte sedimentation rate (ESR), a long used test for the presence of inflammation

103
Q

Leukocytosis in systemic inflammation

stimulus?
what is left shift?
what does continued inflammatio lead to?

A

under the influence of TNF and IL1, more leukocytes are released from teh bone marrow

may see an increased number of immature white blood cells (early release): commonly referred to as a “left shift” of the leukocytes

continued inflammation leads to increased production of colony stimulating factors (CSFs) that increase bone marrow production of leukocytes (as opposed to releasing more cells that have already formed)

104
Q

neutrophilia (increased neutrophils) indicates?

A

bacterial infection

105
Q

lymphocytosis (increased lymphocytes) indicates?

A

viral infections

106
Q

eosinophilia (increased eosinophils) indicates?

A

asthma / parasitic infections

107
Q

leukopenia (decreased leukocytes) indicates?

A

specific infections, e.g. Typhoid fever

Disease and Defense (12 decks)

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