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STEP 1 Review > Inflammation > Flashcards

Inflammation Flashcards

1
Q

CD14

A

TLR on macrophages that recognizes LPS

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2
Q

NFKB

A

Activated when TLRs recognize PAMPS, cause activation of immune mediators.

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3
Q

PGE2

A

Mediates fever and pain.

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4
Q

4 mediators that attract and activate neutrophils

A

LTB4, IL8, C5a, and bacterial products

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5
Q

LTC4, LTD4, LTE4

A

Bascially contract smooth muscle so cause vasoconstriction, bronchoconstriction, and increased vascular permeability.

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6
Q

Two phases of mast cell activation

A

Histamine dump is immediate, causing vascular permeability and vasodilation. Creation of leukotrienes is the delayed response and keeps the acute inflammation going.

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7
Q

4 mediators that attract neutrophils

A

LTB4, IL8, C5a, and bacterial products

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8
Q

Two phases of mast cell activation

A

Histamine dump is immediate, causing vascular permeability and vasodilation. Creation of leukotrienes is the delayed response and keeps the acute inflammation going.

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9
Q

Three ways of complement activation

A

Classic: C1 binds to IgG or IgM
Alternative: Directly on bacterial surfaces
MBL: Binds mannose on cell surface to activate

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10
Q

Complement cascade

A

C3 C5 MAC

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11
Q

C3a and C5a
C5a
C3b

A

trigger mast cell degranulation, C5a is chemotactic for neutrophils
C3b is an opsonin for phagocytosis

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12
Q

Hageman factor

A

Proinflammatory mediator activated by the liver. Can also be pathologically activated in DIC.

Functions in coagulation and fibrinolysis, activates complement, cleaves HMWK to bradykinin which causes pain and vascular permeability.

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13
Q

Pain is mediated by

A

Bradykinin and PGE2. Sensitize sensory nerve endings.

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14
Q

Fever caused by

A

IL-1 and TNF released by macrophages, hit perivascular cells of hypothalamus to increase COX activity. Increased PGE2 raises temperature set point.

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15
Q

Two selectins and their origins

A

P-selectin – Weibel Palade Bodies, release mediated by histamine

E-selectin – is induced by TNF a and IL1.

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16
Q

What do the selectins bind on neutrophils

A

Sialyl Lewis X

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17
Q

What molecules cause adhesion?

A

CAMs on endothelial cells, integrins on neutrophils (which are upregulated by LTB4 and C5a

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18
Q

Disease: Leukocyte Adhesion Deficiency

A

Defect in CD18 subunit of integrins. Causes impaired chemotaxis. Findings include recurrent infections that lack pus, delayed separation of umbilical cord, and increased neutrophils in blood.

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19
Q

Chediak-Higashi Syndrome

A

Autosomal recessive defect in lysosomal trafficking regular gene (LYST), causes microtubule dysfunction.

Recurrent pyogenic infections, partial albinism, large granules in cells, peripheral neuropathy., pancytopenia.

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20
Q

Step by step generation of HOCl in neutrophils

A

O2 to O2- by NADPH oxidase
O2- to H2O2 by SOD1
H2O2 to HOCl by MPO

Or can steal H2O2 from bacteria if NADPH oxidase deficient.

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21
Q

Chronic Granulomatous Disease

A

Due to NADPH oxidase deficiency (X linked or autosomal recessive).
Many granulomas formed.
Increased risk of infection with catalase positive organisms because neutrophils can’t steal bacterial H2O2.

Pseudomonas Cepaciae most important.

Diagnose with Nitroblue tetrazolium test (if colorless than no NADPH oxidase).

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22
Q

Nitroblue tetrazolium test

A

Turns blue in the presence of SOD.

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23
Q

MPO deficiency

A

Can’t turn H2O2 into HOCl Increased risk of candida infections. Nitroblue tetrazolium test normal.

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24
Q

Oxygen independent killing in neutrophils

A

Accomplished by lysosyme and magjor basic protein.

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25
IL10 and TGF B
Shut down the inflammatory process. Produced by macrophages to promote resolution and healing.
26
How do macrophages call in neutrophils if additional help needed?
IL8
27
Role of macrophages in acute inflammation
Assess the scene 2-3 days later. Options include resolution and healing, additional neutrophils, abscess, and induction of chronic inflammation (ie; for viruses).
28
Activation of CD4+ T Cells
Extracellular antigen on MHC Class II and binding of B7 (APC) to CD28 (T cell).
29
TH1 Subset
Helps CD8+ T cells by secreting IL2 (which activates CD8 and is a growth factor for T cells) and interferon gamma (which calls in macrophages).
30
TH2 Subset
Helps B cells by producing IL4 (promotes class switching to IgE and IgG), IL5 (activates eosinophils, activates plasma cells, and promotes class switching to IgA), and IL10 (inhibits TH1 phenotype).
31
Activation of CD8+ T Cells
Intracellular antigen presented on MHC class I. Second signal is IL2 from TH1 cell. Then secrete perforins and granzyme (activates caspases). Also expresses FAS ligand which can bind to fas and activate caspases.
32
B cell activation
Antigen can bind IgM causing IgM secreting plasma cell. Antigen can be presented on B cell MHC class II to CD4 T cell. Second signal is CD40L (on TH2 cell) binding CD40 (on b cell). This causes IL4 and IL5 from TH2 and class switching.
33
Things that have noncaseating granulomas
``` Sarcoid Crohn's Disease Berylliosis Cat Scratch disease (stellate shaped) Reaction to foreign material (implants). ```
34
How are granulomas formed
Macrophages and CD4+ Th1 interact via MHC class II. Macrophages secrete IL-12, which cause differentiation into TH1 phenotype. TH1 cells secrete interferon gamma which converts macrophages to epithelioid histiocytes.
35
DiGeorge Syndrome
22q11 microdeletion associated with failure of 3 and 4 pharyngeal pouches to develop. Thymic aplasia, hypocalcemia (due to no parathyroids), great vessel abnormalities, cleft palate. Recurrent viral/fungal infections (no T cells).
36
SCID
Several types that include adenosine deaminase deficiency, IL2 receptor deficiency (x linked). Severe infections, bubble baby. Treat with bone marrow transplant.
37
Brutons Agammaglobulinemia
X-linked recessive mutation in Bruton's Tyrosine kinase. No B-cell maturation. Recurrent bacterial, enteroviral, and giardial infections.
38
CVID
Defect in B cell differentiation. Bacterial, enteroviral, giardial infections. Can be acquired in 20s and 30s.
39
IgA Deficiency
Unknown cause. Recurrent viral infections of mucosa. Can have anaphylaxis to IgA containing products
40
Hyper IgM Syndrome
Defect in CD40L or CD40. Prevents activation of TH2 cells to promote class switching. X-linked recessive. Severe infections early in life.
41
Wiscott Aldrich
X-linked recessive disorder in WASP gene. Causes thrombocytopenia, eczema, recurrent infections. T cells unable to reorganize actin cytoskeleton
42
C5-C9 Deficiency
Increased susceptibility to neisseria infections
43
C1 Inhibitor Deficiency
Hereditary angioedema. Around eyes. Aberrant activation of complement.
44
Where does negative selection occur in the thymus?
IN the medulla.
45
AIRE
On medullary epithelial cells in thymus. Causes the cells to present self antigen to SP t-cells during negative selection.
46
Autoimmune Polyendocrine System
Mutation in AIRE, Hypoparathyroidism adrenal infections candida infections
47
What happens during negative selection in the bone barrow
1) Editing - via rag gene | 2) Apoptosis
48
Peripheral tolerance
If second signal is absent, anergy takes place. OR IF T cell keeps binding with second signal absent, FAS (CD95) will be activated by self-expressed FAS L and apoptosis will happen
49
Autoimmune lymphoproliferative syndrome
Fas pathway or caspase 10 mutations. Apoptosis can't occur and self-reactive lymphocytes can exist. Cytopenias occur with lymphadenopathy and hepatosplenomegaly. Can cause lymphoma.
50
T REgs
CD4+, CD25+ (IL-2R), FOXP3. Express CTLA4 to bind B7 on dendritic cells/macrophages. Can cause anergy of T cells. Also secrete cytokines IL10 and TGF B.
51
Why do autoimmune conditions affect women?
Estrogen may allow B cells to bypass negative selection.
52
Epitope spreading
Autoimmune conditions can cause other autoimmune conditions because they lead to release of previously unseen antigens.
53
How to replace type III collagen with type I collagen in a scar?
Collagenase -- uses zinc as a co-factor.
54
FGF
Angiogenesis!!! And skeletal development (achondroplasia).
55
B-Cell area of Lymph node? T-Cell area of lymph node? Macrophage/dendritic cell area of lymph node Plasma cell area of lymph node
Follicle Paracortex Medullary sinus Medullary cord
56
Thoracic duct
Drains everything not drained by right lymphatic duct (right side above umbilicus) into the junction of internal jugular and left subclavian.
57
T cell area in spleen | B Cell area in spleen
Periarterial lymphatic sheath (white pulp) | Follicles (white pulp)
58
What is in the marginal zone of the spleen?
APCs and specialized B cells.
59
Why does splenic dysfunction lead to increase susceptibility to encapsulated organisms
Splenic dysfunction decreases IgM and complement activation, therefore, reduced C3b opsonization.
60
MHC1 HLAs, and associated protein | MHC 2 HLAs
HLA 1, 2, 3 -- Beta 2 microglobulin. Peptides loaded in RER. | HLA DR, DQ, DP -- antigen loaded following release in endosome.
61
HLA A3 associated with
Hemochromatosis
62
HLAB27 associated with
Psoriatic arthritis, ankylosis spondylitis, Reiter's (reactive) Arthritis, IBD associated.
63
HLA DQ2/DQ8
Celiac disease
64
HLA DR2
MS/Goodpasture syndrome, SLE
65
HLA DR3
DM type I, SLE, Graves disease
66
HLA DR4
Associated with RA
67
HLA DR5
Associated with pernicious anemia, hashimoto's thyroiditis.
68
Where does positive/negative selection occur in the thymus?
Postive selection in the cortex, negative selection in the medulla
69
IL-12
Induces TH1 cells (which activate CD8+ and macrophages)
70
IL-4
Activate TH2 cells (which activate B cells)
71
TGFB and IL6
Activate TH17 Cells
72
TGF beta alone
Activate Tregs
73
Some acute phase reactants
``` SAA C-reactive protein: fixes complement Hepcidin: prevents release of iron from ferritin Ferritin: Binds iron and sequesters it Fibrinogen: Correlates with ESR ```
74
C3 deficiency
Increases risk of severe recurrent sinus infections. Increased susceptibility to type III HSR.
75
``` IL-1 IL2 IL3 IL4 IL5 IL6 IL8 IL12 IL10 ```
``` Fever stimulates T cells Stimulates bone marrow IgE IgA Stimulates acute phase reactants Neutrophil chemotaxis TH1 Decreases inflammatory response ```
76
Interferon alpha/beta
Innate host defense against viruses.
77
B cell receptor for EBV?
CD21.
78
Passive immunity
Given antibodies directly. Via breast milk or after rabies, HBV, tetanus, botulinum.
79
Type 1 HSR
Cross link IgE on mast cells. Histamine released. Late response due to leukotrienes.
80
Type 2 HSR
Antibody mediated. Causing cellular destruction via complement, neutralization, or opsinization.
81
Type 3 HSR
Immune complex mediated which causes complement fixation. Attract neutrophils when complexes deposit.
82
Serum sickness
Type III HSR, antibodies to foreign proteins develop. Takes 5 days.
83
Arthrus reaction
Intradermal injection of antigen induces antibodies which form complexes in the skin. Type III
84
Type 4 HSR.
Delayed type mediated by T lymhpocytes. Caused by transplants, contact, PPD, MS, guillain barre

STEP 1 Review (21 decks)

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