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Inflammation Flashcards

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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
All pathways result in production of
C3 convertase which mediates C3--C3a and C3b, which in turn produces C5 converts which mediates C5--C5a and C5b.
26
C5b complexes with C6-C9 form
the membrane attack complex MAC
27
C3a and C5a are
anaphylatoxins- trigger mast cell degranulation= histamine mediated vasodilation and increased vascular permiability
28
C5a is
chemotactic for neutrophils
29
C3b is
opsonin for phagocytosis
30
MAC lyses
microbes by creating a hole in the cell membrane
31
Hageman factor is
an inactive pro inflammatory protein produced in the liver
32
Hageman factor is activated
upon exposure to sub endothelial or tissue collagen=activates coagulation and fibrinolytic systems, complement, and Kinin system
33
What are the 2 mediators of pain?
1. PGE2 | 2. Bradykinin
34
What are the 4 cardinal signs of inflammation?
1. Redness and warmth 2. Swelling 3. Pain 4. Fever
35
Redness and warmth due to
vasodilation, which results in increased blood flow, occurs via relaxation of arteriolar smooth muscle; key mediators are histamine, prostaglandins, and bradykinin
36
Swelling due to
leakage of fluid from post capillary venules into the interstitial space
37
What are the key mediators of swelling?
1. Histamine-causes endothelial cell contraction | 2. tissue damage-causes endothelial cell disruption
38
Pain is due to
bradykinin and PGE2 sensitize sensory nerve endings
39
Fever is due to
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
40
What are the 6 steps of neutrophil arrival and function?
1. Margination 2. Rolling 3. Adhesion 4. Transmigration and Chemotaxis 5. Phagocytosis 6. Destruction of phagocytosed material
41
What are the outcomes of macrophages?
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
42
What are the anti inflammatory cytokines produced by macrophages?
IL-10 and TGF-B
43
What cytokines is produced by macrophages to recruit additional neutrophils?
IL-8
44
Chronic inflammation is characterized by
the presence of lymphocytes and plasma cells in tissue
45
What are the 5 stimuli to chronic inflammation?
1. persistent infection 2. infection with viruses, mycobacteria, parasites, and fungi 3. autoimmune disease 4. foreign material 5. some cancers
46
CD4+ T cells bind to
MHC class II
47
CD8+ T cells bind to
MHC class I
48
CD4+ T cells are
Helper T cells
49
CD8+ T cells are
Cytotoxic T cells
50
The job of CD4+ T cells are to
Help CD8+ T cells and Help B cells
51
Activation of CD4+ T cells requires two things?
1. binding of antigen to MHC class II | 2. B7 on APC binds CD28 on CD4+ T cell
52
Activation of CD4+ T cells divides into 2 subsets:
Th1 and Th2
53
Th1 subset secretes
IFN-gamma and IL-2
54
Activation of IFN-gamma
1. activates macrophages 2. promotes B cell class switching from IgM to IgG 3. inhibits Th2 subset
55
Activation of IL-2
activates cytotoxic CD8+ T cells to become a toxic killer
56
Th2 subset secretes
IL-4, IL-5, IL-10
57
IL-4 facilitates
B-cell class switching to IgE
58
IL-5 facilitates
eosinophil chemotaxis and activation and class switching to IgA
59
IL-10
inhibits Th1 subset
60
antigen that is process and presented on MHC class I are recognized by what T cells?
CD8+ cytotoxic T cells
61
Activation of CD8+ T cells requires two things?
1. Antigen processed and presented on MHC class I | 2. IL-2 secreted by CD4+ Th1 helper cells
62
Activation of CD8+ cytotoxic T cells are activated for
killing
63
How does killing occur?
1. secretion of perforin and granzyme activating apoptosis | 2. expression of FasL, which binds Fas on target cells activating apoptosis
64
What two immunoglobulins are expressed on naive B cells?
IgM and IgG
65
B cell activation occurs 2 ways?
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
What is the result of antigen binding to surface naive B cell IgM or IgD?
Maturation to IgM or IgD secreting plasma cells
67
What is the 2nd signaling requirement to activate B cells when antigen is presented to CD4+ T helper cells?
CD40 receptor on B cells binds CD40 Ligand (CD40L) on CD4+ T helper cell
68
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?
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
What are macrophages with abundant pink cytoplasm?
epithelioid histiocytes
70
Granulomatous Inflammation is?
a subtype of chronic inflammation
71
Granulomatous inflammation is characterized by
granuloma, which is a collection of epithelioid histiocytes, usually surrounded by giant cells and a rim of lymphocytes
72
There are two types of granulomatous inflammation?
1. Noncaseating | 2. Caseating
73
Noncaseating granuloma
absent central necrosis=nucleus present
74
Necrosis present =
Nucleus absent
75
Necrosis absent=
Nucleus present
76
Common etiologies of Noncaseating granuloma (5)
1. foreign material (breast implants) 2. sarcoidosis 3. beryllium exposure 4. Crohn disease 5. cat scratch disease
77
What is the histologic hallmark of Crohn disease?
noncaseating granuloma
78
What is the histologic hallmark of Ulcerative colitis?
crypt abscesses
79
What is stellate shaped granuloma indicative of?
cat scratch disease- Bartonella spp.
80
Caseating granuloma
present central necrosis=nucleus absent
81
Common etiologies of Caseating granuloma (2)
1. TB | 2. fungal infections
82
Histological findings of TB are performed on
AFB stain
83
Histological findings of fungal infections are performed on
GMS (silver) stain
84
Granuloma formation is an interaction between
macrophages and CD4+ Th1 T-helper cells
85
How are granulomas formed?
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
Primary Immunodeficiencies associated with Inflammation (8)
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
Developmental failure of the 3rd and 4th pharyngeal pouches
DiGeorge Syndrome
88
DiGeorge Syndrome
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
22q11 microdeletion
DiGeorge Syndrome
90
T-cell deficiency due to lack of thymus
DiGeorge Syndrome
91
Hypocalcemia due to lack of parathyroids
DiGeorge Syndrome
92
SCID
Severe Combined Immunodeficiency
93
Defective cell mediated and humoral immunity
SCID
94
Etiologies of SCID (3)
1. Cytokine receptor defects 2. Adenosine deaminase deficiency 3. MHC class II deficiency
95
Cytokine signalling is necessary for
proliferation and maturation of B and T cells
96
Adenosine deaminase is necessary to
deaminate adenosine and deoxyadenosine for exertion as waste products -- build of adenosine and deoxyadenosine is toxic to lymphocytes
97
MHC class II is necessary for
CD4+ T helper cell activation and cytokine production
98
Presentation of SCID
susceptibility to fungal, viral, bacterial, and protozoal infections, opportunist infections and live vaccines
99
Complete lack of immunoglobulin due to disordered B cell maturation
X-linked Agammaglobulinemia
100
Mutated Bruton Tyrosine Kinase
X-linked Agammaglobulinemia
101
X-linked Agammaglobulinemia is due to what mutation
Bruton tyrosine kinase
102
Bruton tyrosine kinase is necessary to
mature Pre- and Pro- B cells
103
Presentation of X-linked Agammaglobulinemia
presents after 6 months of life recurrent bacterial, enterovirus, and giardia lamblia infections live vaccines must be avoided
104
Mutated CD40 L on T helper cells or CD40 receptor on B cells
Hyper-IgM Syndrome
105
Cytokines necessary for immunoglobulin class switching are not produced
Hyper-IgM Syndrome
106
Elevated levels of IgM | Absent levels of IgG, IgA, IgE
Hyper-IgM Syndrome
107
Thrombocytopenia, eczema, recurrent infections
Wiskott-Aldrich Syndrome
108
Mutation in the WASP gene and X linked
Wiskott-Aldrich Syndrome
109
Increased risk for Neisseria infection
C5-C9 deficiencies
110
C1 inhibitor deficiency results in
hereditary angioedema
111
Characteristics of hereditary angioedema
edema of the skin (especially periorbital) and mucosal surfaces
112
AIRE mutations result in
autoimmune polyendocrine
113
What are the three ways our bodies regulate self reactive lymphocytes?
1. Central tolerance 2. Peripheral tolerance 3. Regulatory T cells
114
What are medullary epithelial cells?
Cells present in the medulla of the thymus that present a wide array of peripheral antigen on MHC to the lymphocytes
115
What is the transcription factor present in MEC nucleus that allows it to express self antigens?
AIRE
116
Genetic mutation in AIRE results in
Autoimmune Polyendocrine Syndrome
117
What is the triad of symptoms for APS
Hypoparathyroidism Adrenal Failure Chronic candida infection
118
Negative selection occurs for B cells in
the bone marrow
119
Self antigen is presented by what cells to Immature B cells?
Dendritic cells
120
If B cells bind antigen presented by dendritic cells too tightly there are 2 ways in which the cell can correct this?
1. Receptor Editing | 2. Apoptosis via mitochondrial pathway- cytochrome c
121
Peripheral tolerance occurs if
the self reactive lymphocytes escape into the periphery.
122
Anergy is
the cell shuts down in the periphery because there is no 2nd signaling mechanism. This identities that the lymphocyte is self reactive.
123
Apoptosis via peripheral tolerance occurs via
FAS (CD95) ligand expression which binds to FAS receptor
124
Mutation in FAS apoptosis pathway
Autoimmune Lymphoproliferative Syndrome
125
Symptoms of ALPS
cytopenia, thrombocytopenia, anemia
126
SLE is
antigen-antibody complexes deposit in tissues results in activation of complement which damages tissues

Inflammation (1 decks)

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