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Inflammation > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What are the three phases of Acute Inflammation?

A

Fluid
Neutrophils
Macrophages

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2
Q

What two reasons does Acute Inflammation arise?

A
  1. infection- to eliminate a pathogen

2. tissue necrosis- to clear necrotic debris

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3
Q

Acute Inflammation is defined as

A

an immediate response with limited specificity (innate immunity)

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4
Q

What are the 5 mediators of Acute Inflammation?

A
  1. Mast cells
  2. Hageman Factor (Factor XII)
  3. Toll-like receptors
  4. Arachidonic acid metabolites
  5. Complement
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5
Q

Toll-like receptors are activated by

A

pathogen-associated molecular patterns (PAMPS)

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6
Q

What co-receptor recognizes lipopolysaccharide on macrophages on the outer membrane of Gram Negative bacteria?

A

CD14

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7
Q

TLR activation results in up regulation of

A

NF-kB

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8
Q

What always follows Necrosis

A

Acute Inflammation

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9
Q

What enzyme releases arachidonic acid from the phospholipid cell membrane?

A

Phospholipase A2

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10
Q

Arachidonic acid is acted upon by what 2 enzymes?

A
  1. Cyclooxyrgenase

2. 5-lipoxygenase

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11
Q

Cyclooxyrgenase produces

A

prostaglandins

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12
Q

5-lipoxygenase produces

A

leukotrienes

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13
Q

What are the 3 prostaglandins?

A

PGI2
PGD2
PGE2

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14
Q

Prostaglandins mediate

A

vasodilation at the level of the arteriole and increased vascular permeability at the post capillary venule

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15
Q

What prostaglandin mediates pain and fever?

A

PGE2

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16
Q

PGE2 mediates what?

A

pain and fever

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17
Q

What are the 4 leukotrienes?

A
  1. LTB4
  2. LTC4
  3. LTD4
  4. LTE4
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18
Q

LTB4 attracts and activates

A

neutrophils

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19
Q

What are the 4 Key mediators that attract and activate neutrophils?

A
  1. LTB4
  2. IL8
  3. C5a
  4. Bacterial products
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20
Q

What three things activate Mast Cells?

A
  1. Complement proteins C3a, and C5a
  2. tissue trauma
  3. cross-linking of cell surface IgE by antigen
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21
Q

What 3 ways do activation of Complement occur?

A
  1. Classical pathway
  2. Alternative pathway
  3. Mannose-binding lectin MBL pathway
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22
Q

Classical Pathway

A

C1 binds IgG or IgM tha is bound to antigen

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23
Q

Alternative Pathway

A

Microbial products directly activate complement

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24
Q

Mannose-binding lectin pathway

A

MBL binds to mannose on microorganisms and activates complement

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25
Q

All pathways result in production of

A

C3 convertase which mediates C3–C3a and C3b, which in turn produces C5 converts which mediates C5–C5a and C5b.

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26
Q

C5b complexes with C6-C9 form

A

the membrane attack complex MAC

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27
Q

C3a and C5a are

A

anaphylatoxins- trigger mast cell degranulation= histamine mediated vasodilation and increased vascular permiability

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28
Q

C5a is

A

chemotactic for neutrophils

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29
Q

C3b is

A

opsonin for phagocytosis

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30
Q

MAC lyses

A

microbes by creating a hole in the cell membrane

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31
Q

Hageman factor is

A

an inactive pro inflammatory protein produced in the liver

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32
Q

Hageman factor is activated

A

upon exposure to sub endothelial or tissue collagen=activates coagulation and fibrinolytic systems, complement, and Kinin system

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33
Q

What are the 2 mediators of pain?

A
  1. PGE2

2. Bradykinin

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34
Q

What are the 4 cardinal signs of inflammation?

A
  1. Redness and warmth
  2. Swelling
  3. Pain
  4. Fever
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35
Q

Redness and warmth due to

A

vasodilation, which results in increased blood flow, occurs via relaxation of arteriolar smooth muscle; key mediators are histamine, prostaglandins, and bradykinin

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36
Q

Swelling due to

A

leakage of fluid from post capillary venules into the interstitial space

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37
Q

What are the key mediators of swelling?

A
  1. Histamine-causes endothelial cell contraction

2. tissue damage-causes endothelial cell disruption

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38
Q

Pain is due to

A

bradykinin and PGE2 sensitize sensory nerve endings

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39
Q

Fever is due to

A

pyrogens cause macrophages to release IL-1 and TNF which increased cyclooxyrgenase activity in perivascular cells of the hypothalamus AND
increased PGE2 raises temperature set point

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40
Q

What are the 6 steps of neutrophil arrival and function?

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Transmigration and Chemotaxis
  5. Phagocytosis
  6. Destruction of phagocytosed material
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41
Q

What are the outcomes of macrophages?

A
  1. resolution and healing-anti inflammatory cytokines are produced
  2. Continued acute inflammation-marked by continued pus formation
  3. Abscess
  4. Chronic inflammation by presenting antigen to activate CD4+ helper T cells
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42
Q

What are the anti inflammatory cytokines produced by macrophages?

A

IL-10 and TGF-B

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43
Q

What cytokines is produced by macrophages to recruit additional neutrophils?

A

IL-8

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44
Q

Chronic inflammation is characterized by

A

the presence of lymphocytes and plasma cells in tissue

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45
Q

What are the 5 stimuli to chronic inflammation?

A
  1. persistent infection
  2. infection with viruses, mycobacteria, parasites, and fungi
  3. autoimmune disease
  4. foreign material
  5. some cancers
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46
Q

CD4+ T cells bind to

A

MHC class II

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47
Q

CD8+ T cells bind to

A

MHC class I

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48
Q

CD4+ T cells are

A

Helper T cells

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49
Q

CD8+ T cells are

A

Cytotoxic T cells

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50
Q

The job of CD4+ T cells are to

A

Help CD8+ T cells and Help B cells

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51
Q

Activation of CD4+ T cells requires two things?

A
  1. binding of antigen to MHC class II

2. B7 on APC binds CD28 on CD4+ T cell

52
Q

Activation of CD4+ T cells divides into 2 subsets:

A

Th1 and Th2

53
Q

Th1 subset secretes

A

IFN-gamma and IL-2

54
Q

Activation of IFN-gamma

A
  1. activates macrophages
  2. promotes B cell class switching from IgM to IgG
  3. inhibits Th2 subset
55
Q

Activation of IL-2

A

activates cytotoxic CD8+ T cells to become a toxic killer

56
Q

Th2 subset secretes

A

IL-4, IL-5, IL-10

57
Q

IL-4 facilitates

A

B-cell class switching to IgE

58
Q

IL-5 facilitates

A

eosinophil chemotaxis and activation and class switching to IgA

59
Q

IL-10

A

inhibits Th1 subset

60
Q

antigen that is process and presented on MHC class I are recognized by what T cells?

A

CD8+ cytotoxic T cells

61
Q

Activation of CD8+ T cells requires two things?

A
  1. Antigen processed and presented on MHC class I

2. IL-2 secreted by CD4+ Th1 helper cells

62
Q

Activation of CD8+ cytotoxic T cells are activated for

A

killing

63
Q

How does killing occur?

A
  1. secretion of perforin and granzyme activating apoptosis

2. expression of FasL, which binds Fas on target cells activating apoptosis

64
Q

What two immunoglobulins are expressed on naive B cells?

A

IgM and IgG

65
Q

B cell activation occurs 2 ways?

A
  1. Antigen binding to surface IgM or IgD

2. B cell takes up antigen and processes it to present it on MHC class II to CD4+ T helper cells

66
Q

What is the result of antigen binding to surface naive B cell IgM or IgD?

A

Maturation to IgM or IgD secreting plasma cells

67
Q

What is the 2nd signaling requirement to activate B cells when antigen is presented to CD4+ T helper cells?

A

CD40 receptor on B cells binds CD40 Ligand (CD40L) on CD4+ T helper cell

68
Q

What is the result of antigen presentation on MHC class II on naive B cells to CD4+ T helper cells with the presence of CD40 and CD40L bound?

A

CD4+ T helper cell secretes IL-4 and IL-5 which go and smack the B cell to now isotope switch, hyper mutate, and mature to a plasma cell

69
Q

What are macrophages with abundant pink cytoplasm?

A

epithelioid histiocytes

70
Q

Granulomatous Inflammation is?

A

a subtype of chronic inflammation

71
Q

Granulomatous inflammation is characterized by

A

granuloma, which is a collection of epithelioid histiocytes, usually surrounded by giant cells and a rim of lymphocytes

72
Q

There are two types of granulomatous inflammation?

A
  1. Noncaseating

2. Caseating

73
Q

Noncaseating granuloma

A

absent central necrosis=nucleus present

74
Q

Necrosis present =

A

Nucleus absent

75
Q

Necrosis absent=

A

Nucleus present

76
Q

Common etiologies of Noncaseating granuloma (5)

A
  1. foreign material (breast implants)
  2. sarcoidosis
  3. beryllium exposure
  4. Crohn disease
  5. cat scratch disease
77
Q

What is the histologic hallmark of Crohn disease?

A

noncaseating granuloma

78
Q

What is the histologic hallmark of Ulcerative colitis?

A

crypt abscesses

79
Q

What is stellate shaped granuloma indicative of?

A

cat scratch disease- Bartonella spp.

80
Q

Caseating granuloma

A

present central necrosis=nucleus absent

81
Q

Common etiologies of Caseating granuloma (2)

A
  1. TB

2. fungal infections

82
Q

Histological findings of TB are performed on

A

AFB stain

83
Q

Histological findings of fungal infections are performed on

A

GMS (silver) stain

84
Q

Granuloma formation is an interaction between

A

macrophages and CD4+ Th1 T-helper cells

85
Q

How are granulomas formed?

A
  1. Antigen by Viruses, Intracellular pathogens (TB/Listeria, Riketsia/Chlamydia) are processed by macrophages expressed on MHC class II and presented to CD4+ T helper cells
  2. Macrophages secrete IL-12 – induces CD4+ T helper cells to differentiate into Th1 subtype
  3. Th1 cells secrete IFN-gamma and IL-2 – IFN gamma converts macrophages to epithelioid histiocytes and giant cells
86
Q

Primary Immunodeficiencies associated with Inflammation (8)

A
  1. DiGeorge Syndrom
  2. SCID
  3. X-Linked Agammaglobulinemia
  4. Common Variable Immunodeficiency
  5. IgA Deficiency
  6. Hyper IgM syndrome
  7. Wiskott-Aldrich Syndrome
  8. Complement Deficiencies
87
Q

Developmental failure of the 3rd and 4th pharyngeal pouches

A

DiGeorge Syndrome

88
Q

DiGeorge Syndrome

A

22q11 micro deletion
Developmental failure of the 3rd and 4th pharyngeal pouches= no thymus, no parathyroids
Presents with T-cell deficiency (lack of thymus), hypocalcemia (lack of parathyroids) and abnormalities of heart, great vessels, and face

89
Q

22q11 microdeletion

A

DiGeorge Syndrome

90
Q

T-cell deficiency due to lack of thymus

A

DiGeorge Syndrome

91
Q

Hypocalcemia due to lack of parathyroids

A

DiGeorge Syndrome

92
Q

SCID

A

Severe Combined Immunodeficiency

93
Q

Defective cell mediated and humoral immunity

A

SCID

94
Q

Etiologies of SCID (3)

A
  1. Cytokine receptor defects
  2. Adenosine deaminase deficiency
  3. MHC class II deficiency
95
Q

Cytokine signalling is necessary for

A

proliferation and maturation of B and T cells

96
Q

Adenosine deaminase is necessary to

A

deaminate adenosine and deoxyadenosine for exertion as waste products – build of adenosine and deoxyadenosine is toxic to lymphocytes

97
Q

MHC class II is necessary for

A

CD4+ T helper cell activation and cytokine production

98
Q

Presentation of SCID

A

susceptibility to fungal, viral, bacterial, and protozoal infections, opportunist infections and live vaccines

99
Q

Complete lack of immunoglobulin due to disordered B cell maturation

A

X-linked Agammaglobulinemia

100
Q

Mutated Bruton Tyrosine Kinase

A

X-linked Agammaglobulinemia

101
Q

X-linked Agammaglobulinemia is due to what mutation

A

Bruton tyrosine kinase

102
Q

Bruton tyrosine kinase is necessary to

A

mature Pre- and Pro- B cells

103
Q

Presentation of X-linked Agammaglobulinemia

A

presents after 6 months of life
recurrent bacterial, enterovirus, and giardia lamblia infections
live vaccines must be avoided

104
Q

Mutated CD40 L on T helper cells or CD40 receptor on B cells

A

Hyper-IgM Syndrome

105
Q

Cytokines necessary for immunoglobulin class switching are not produced

A

Hyper-IgM Syndrome

106
Q

Elevated levels of IgM

Absent levels of IgG, IgA, IgE

A

Hyper-IgM Syndrome

107
Q

Thrombocytopenia, eczema, recurrent infections

A

Wiskott-Aldrich Syndrome

108
Q

Mutation in the WASP gene and X linked

A

Wiskott-Aldrich Syndrome

109
Q

Increased risk for Neisseria infection

A

C5-C9 deficiencies

110
Q

C1 inhibitor deficiency results in

A

hereditary angioedema

111
Q

Characteristics of hereditary angioedema

A

edema of the skin (especially periorbital) and mucosal surfaces

112
Q

AIRE mutations result in

A

autoimmune polyendocrine

113
Q

What are the three ways our bodies regulate self reactive lymphocytes?

A
  1. Central tolerance
  2. Peripheral tolerance
  3. Regulatory T cells
114
Q

What are medullary epithelial cells?

A

Cells present in the medulla of the thymus that present a wide array of peripheral antigen on MHC to the lymphocytes

115
Q

What is the transcription factor present in MEC nucleus that allows it to express self antigens?

A

AIRE

116
Q

Genetic mutation in AIRE results in

A

Autoimmune Polyendocrine Syndrome

117
Q

What is the triad of symptoms for APS

A

Hypoparathyroidism
Adrenal Failure
Chronic candida infection

118
Q

Negative selection occurs for B cells in

A

the bone marrow

119
Q

Self antigen is presented by what cells to Immature B cells?

A

Dendritic cells

120
Q

If B cells bind antigen presented by dendritic cells too tightly there are 2 ways in which the cell can correct this?

A
  1. Receptor Editing

2. Apoptosis via mitochondrial pathway- cytochrome c

121
Q

Peripheral tolerance occurs if

A

the self reactive lymphocytes escape into the periphery.

122
Q

Anergy is

A

the cell shuts down in the periphery because there is no 2nd signaling mechanism. This identities that the lymphocyte is self reactive.

123
Q

Apoptosis via peripheral tolerance occurs via

A

FAS (CD95) ligand expression which binds to FAS receptor

124
Q

Mutation in FAS apoptosis pathway

A

Autoimmune Lymphoproliferative Syndrome

125
Q

Symptoms of ALPS

A

cytopenia, thrombocytopenia, anemia

126
Q

SLE is

A

antigen-antibody complexes deposit in tissues results in activation of complement which damages tissues

Inflammation (1 decks)

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