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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
Q

IL10 and TGF B

A

Shut down the inflammatory process. Produced by macrophages to promote resolution and healing.

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26
Q

How do macrophages call in neutrophils if additional help needed?

A

IL8

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27
Q

Role of macrophages in acute inflammation

A

Assess the scene 2-3 days later. Options include resolution and healing, additional neutrophils, abscess, and induction of chronic inflammation (ie; for viruses).

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28
Q

Activation of CD4+ T Cells

A

Extracellular antigen on MHC Class II and binding of B7 (APC) to CD28 (T cell).

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29
Q

TH1 Subset

A

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).

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30
Q

TH2 Subset

A

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).

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31
Q

Activation of CD8+ T Cells

A

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.

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32
Q

B cell activation

A

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.

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33
Q

Things that have noncaseating granulomas

A 
Sarcoid
Crohn's Disease
Berylliosis
Cat Scratch disease (stellate shaped)
Reaction to foreign material (implants).
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34
Q

How are granulomas formed

A

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
Q

DiGeorge Syndrome

A

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
Q

SCID

A

Several types that include adenosine deaminase deficiency, IL2 receptor deficiency (x linked). Severe infections, bubble baby. Treat with bone marrow transplant.

37
Q

Brutons Agammaglobulinemia

A

X-linked recessive mutation in Bruton’s Tyrosine kinase. No B-cell maturation. Recurrent bacterial, enteroviral, and giardial infections.

38
Q

CVID

A

Defect in B cell differentiation. Bacterial, enteroviral, giardial infections. Can be acquired in 20s and 30s.

39
Q

IgA Deficiency

A

Unknown cause. Recurrent viral infections of mucosa. Can have anaphylaxis to IgA containing products

40
Q

Hyper IgM Syndrome

A

Defect in CD40L or CD40. Prevents activation of TH2 cells to promote class switching. X-linked recessive. Severe infections early in life.

41
Q

Wiscott Aldrich

A

X-linked recessive disorder in WASP gene. Causes thrombocytopenia, eczema, recurrent infections. T cells unable to reorganize actin cytoskeleton

42
Q

C5-C9 Deficiency

A

Increased susceptibility to neisseria infections

43
Q

C1 Inhibitor Deficiency

A

Hereditary angioedema. Around eyes. Aberrant activation of complement.

44
Q

Where does negative selection occur in the thymus?

A

IN the medulla.

45
Q

AIRE

A

On medullary epithelial cells in thymus. Causes the cells to present self antigen to SP t-cells during negative selection.

46
Q

Autoimmune Polyendocrine System

A

Mutation in AIRE,

Hypoparathyroidism
adrenal infections
candida infections

47
Q

What happens during negative selection in the bone barrow

A

1) Editing - via rag gene

2) Apoptosis

48
Q

Peripheral tolerance

A

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
Q

Autoimmune lymphoproliferative syndrome

A

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
Q

T REgs

A

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
Q

Why do autoimmune conditions affect women?

A

Estrogen may allow B cells to bypass negative selection.

52
Q

Epitope spreading

A

Autoimmune conditions can cause other autoimmune conditions because they lead to release of previously unseen antigens.

53
Q

How to replace type III collagen with type I collagen in a scar?

A

Collagenase – uses zinc as a co-factor.

54
Q

FGF

A

Angiogenesis!!! And skeletal development (achondroplasia).

55
Q

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

A

Follicle
Paracortex
Medullary sinus
Medullary cord

56
Q

Thoracic duct

A

Drains everything not drained by right lymphatic duct (right side above umbilicus) into the junction of internal jugular and left subclavian.

57
Q

T cell area in spleen

B Cell area in spleen

A

Periarterial lymphatic sheath (white pulp)

Follicles (white pulp)

58
Q

What is in the marginal zone of the spleen?

A

APCs and specialized B cells.

59
Q

Why does splenic dysfunction lead to increase susceptibility to encapsulated organisms

A

Splenic dysfunction decreases IgM and complement activation, therefore, reduced C3b opsonization.

60
Q

MHC1 HLAs, and associated protein

MHC 2 HLAs

A

HLA 1, 2, 3 – Beta 2 microglobulin. Peptides loaded in RER.

HLA DR, DQ, DP – antigen loaded following release in endosome.

61
Q

HLA A3 associated with

A

Hemochromatosis

62
Q

HLAB27 associated with

A

Psoriatic arthritis, ankylosis spondylitis, Reiter’s (reactive) Arthritis, IBD associated.

63
Q

HLA DQ2/DQ8

A

Celiac disease

64
Q

HLA DR2

A

MS/Goodpasture syndrome, SLE

65
Q

HLA DR3

A

DM type I, SLE, Graves disease

66
Q

HLA DR4

A

Associated with RA

67
Q

HLA DR5

A

Associated with pernicious anemia, hashimoto’s thyroiditis.

68
Q

Where does positive/negative selection occur in the thymus?

A

Postive selection in the cortex, negative selection in the medulla

69
Q

IL-12

A

Induces TH1 cells (which activate CD8+ and macrophages)

70
Q

IL-4

A

Activate TH2 cells (which activate B cells)

71
Q

TGFB and IL6

A

Activate TH17 Cells

72
Q

TGF beta alone

A

Activate Tregs

73
Q

Some acute phase reactants

A 
SAA
C-reactive protein: fixes complement
Hepcidin: prevents release of iron from ferritin
Ferritin: Binds iron and sequesters it
Fibrinogen: Correlates with ESR
74
Q

C3 deficiency

A

Increases risk of severe recurrent sinus infections. Increased susceptibility to type III HSR.

75
Q 
IL-1
IL2
IL3
IL4
IL5
IL6
IL8
IL12
IL10
A 
Fever
stimulates T cells
Stimulates bone marrow
IgE
IgA
Stimulates acute phase reactants
Neutrophil chemotaxis
TH1 
Decreases inflammatory response
76
Q

Interferon alpha/beta

A

Innate host defense against viruses.

77
Q

B cell receptor for EBV?

A

CD21.

78
Q

Passive immunity

A

Given antibodies directly. Via breast milk or after rabies, HBV, tetanus, botulinum.

79
Q

Type 1 HSR

A

Cross link IgE on mast cells. Histamine released. Late response due to leukotrienes.

80
Q

Type 2 HSR

A

Antibody mediated. Causing cellular destruction via complement, neutralization, or opsinization.

81
Q

Type 3 HSR

A

Immune complex mediated which causes complement fixation. Attract neutrophils when complexes deposit.

82
Q

Serum sickness

A

Type III HSR, antibodies to foreign proteins develop. Takes 5 days.

83
Q

Arthrus reaction

A

Intradermal injection of antigen induces antibodies which form complexes in the skin. Type III

84
Q

Type 4 HSR.

A

Delayed type mediated by T lymhpocytes. Caused by transplants, contact, PPD, MS, guillain barre

STEP 1 Review (21 decks)

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