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IBI Test 2 > B3.021 Prework Hypersensitivity > Flashcards

B3.021 Prework Hypersensitivity Flashcards

(78 cards)

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1
Q

define a hypersensitivity reaction

A

injurious or pathologic immune reactions

exaggerated and abnormal

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2
Q

what are the 2 mechanisms of hypersensitivity

A
  1. an immune response to a microbe or environmental allergy causes tissue injury due to repeated or poorly controlled reactions
  2. failure of self-tolerance when an immune response is generated to self antigens = autoimmunity
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3
Q

type 1 hypersensitivity

A

immediate hypersensitivity mediated by IgE binding to mast cells

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4
Q

type 2 hypersensitivity

A

antibody (non IgE) mediated cell or tissue destruction

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5
Q

type 3 hypersensitivity

A

antibody/antigen complex deposition causing inflammation and tissue injury

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6
Q

type 4 hypersensitivity

A

T cell mediated

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7
Q

atopy

A

true allergy

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8
Q

what % of the pop is affected by type 1?

A

10-20%

prevalence increasing in industrialized nations

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9
Q

describe sensitization

A

first exposure to an allergen protein or chemical that binds proteins (hapten)
should not cause a reaction

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10
Q

what happens at the level of leukocytes in sensitization?

A 
aberrantly, Tfh and Th2 cells cause B cells to stimulate class switching IgE against the allergen (via IL4 and IL13)
IgE to the allergen is produced long term by the plasma cells and binds to the FceR1 high affinity IgE receptors on mast cells coating mast cells with IgE to that particular allergen
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11
Q

what is the elicitation phase

A

the hypersensitivity reaction upon repeat exposure

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12
Q

what happens during the elicitation phase?

A

allergen cross links the IgE on the mast cell FceR1 high affinity IgE receptors
activation of mast cell
release of mast cell contents

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13
Q

what is the contents of a mast cell

A

vasoactive amines
lipid mediators
cytokines (delayed symptoms)

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14
Q

immediate hypersensitivity

A

within minutes
mediated by vasoactive amines and lipid mediators
increase in vascular permeability
smooth muscle contraction

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15
Q

late phase hypersensitivity

A

mediated by cytokines
recruit neutrophils and eosinophils
tissue injury with repeated bouts

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16
Q

describe the components of the IgE receptor

A

FceR1 high affinity receptor
-present on mast cells (primary) and basophils (role less well established)
3 polypeptide chains
-1 binds the Fc portion of the e heavy chain
-2 are signaling proteins

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17
Q

describe the series of events within a mast cell upon allergen exposure

A

allergen cross links two IgE molecules causing degranulation, synthesis and secretion
ITAM phosphorylation occurs activating signaling pathways
-release of pre formed mediators
-AA metabolism secreting lipid mediators (PGEs and LTs)
-activation of cytokine transcription genes to secrete cytokines

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18
Q

vasoactive amines

A

vascular dilation

smooth muscle contraction

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19
Q

proteases

A

tissue damage

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20
Q

prostaglandins

A

vascular dilation

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21
Q

leukotrienes

A

smooth muscle contraction

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22
Q

histamine

A

vasodilation
increased vascular permeability
transient smooth muscle contraction
mucous production

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23
Q

TNF

A

endothelial cell activation
inflammation
neutrophil activation

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24
Q

IL-4

A

induces IgE class switching by B cells

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25
IL-5
eosinophil activation, generation
26
what is the general mechanism of antihistamines
histamine receptor antagonists | reduce the potential for histamine to bind and cause symptoms
27
H1 antagonists
1st generation - caused sedation and short acting | 2nd generation - less or no sedation, long acting
28
H2 antagonists
receptors mostly in the gut | mostly used for indigestion and heartburn, but could be added to an H1 antagonist for treatment of allergic conditions
29
epinephrine (SubQ, IM or IV)
``` 1st line in anaphylaxis vascular smooth muscle contraction increased cardiac output inhibits bronchial smooth muscle contraction stabilize mast cells ```
30
corticosteroids (inhaled/oral/IV/IM)
reduce inflammatory mediator production stabilize mast cells reduce eosinophils
31
leukotriene receptor antagonists (oral)
reduce inflammation | relax bronchial smooth muscle
32
phosphodiester inhibitors (inhaled)
relax bronchial smooth muscle
33
describe desensitization treatment
repeated increasing dose of allergens to help the system overcome the allergy inhibit IgE production, induce tolerance allergy shots
34
cromolyn (topical or oral)
inhibits mast cell degranulation
35
what are 3 types of monoclonal antibody therapy for immediate hypersensitivity
anti-IgE anti-IL-5 anti-IL-4 and IL-13
36
anti-IgE therapy
binds/inhibits IgE so it cannot bind to the receptors | downregulation of the FceR1 on mast cells
37
anti IL-5 therapy
binds/inhibits IL-5 to reduce eosinophil production and survival
38
anti IL-4 and IL-13 therapy
binds/inhibits the shared receptor reducing inflammation and decreasing the effects of both products
39
distinguish between type 2 and 3 hypersensitivities
2 - antibodies can be directed against cells or extracellular matrix 3 - antibodies/antigens can bind and deposit in blood vessels (renal glomeruli and joint synovium) *failure of self tolerance
40
diseases associated w types 2 and 3 hypersensitivity
``` cytopenias organ inflammation hormone abnormalities skin diseases vasculitis arthritis nephritis ```
41
describe type 2 hypersensitivity
complement and Fc receptor induced recruitment and activation of leukocytes opsonization and phagocytosis cell function abnormalities by competitive inhibition or activation
42
describe the process of complement and Fc receptor mediation of type 2 hypersensitivity
Abs bind to activate the neutrophil complement activation releases C3a and C5a to activate the neutrophil neutrophils generate ROS and lysosomal enzymes that cause inflammation/injury
43
discuss the link between strep and type 2 hypersensitivity
can occur after strep infection | Ab cross reacts with myocardium causing myocarditis
44
describe the process of opsonization and phagocytosis associated with type 2 hypersensitivity
complement activation occurs releasing C3b that opsonizes the cell Fc receptor on phagocytes recognizes C3b on an opnsonized cell and phagocytosis the infected cell may occur with erythrocytes and platelets causing anemia and thrombocytopenia
45
describe cell function abnormalities caused by competitive inhibition or activation in type 2 hypersensitivity
Abs generated against hormone receptors competitively inhibit hormone production Abs can also mimic hormones
46
graves disease
thyroid stimulation even in the absence of thyroid stimulation hormone leading to hyperthyroidism
47
myasthenia gravis
musculoskeletal paralysis disease where Abs are made against the acetylcholine receptor and inhibit transmission of signals to the muscle to move
48
autoimmune hemolytic anemia
opsonization and phagocytosis of erythrocytes causing anemia
49
autoimmune (idiopathic) thrombocytopenic purpura
opsonization and phagocytosis of platelets causing bleeding
50
goodpasture syndrome
complement and Fc receptor mediated inflammation targeting a non-collagenous protein in kidney glomeruli and lung alveolar basement membranes
51
pemphigus vulgaris
antibody mediated activation of proteases causing disruption of intercellular adhesions targets desmoglein - protein in intercellular junction of epidermal cells which holds cells together
52
pernicious anemia
neutralization of intrinsic factor leads to decreased absorption of vitamin B12 results in anemia
53
rheumatic fever
inflammation and macrophage activation targets streptococcal cell wall antigen, antibody cross-reacts with myocardium leads to myocarditis and arthritis
54
describe type 3 hypersensitivity
disease is caused by deposition of circulating antibody/antigen complexes in blood vessels -activation of complement -activation of inflammatory cascade systemic or localized results in: vasculitis, nephritis, inflammatory skin reactions
55
arthus reaction
localized Ag/Ab complex deposition formation of complexes at the site of antigen injection local vasculitis (often mistaken as cellulitis but not infectious)
56
systemic lupus erythematosus
Ab: DNA, nucleoproteins, others manifestation: nephritis, arthritis, vasculities
57
polyarteritis nodosa
Ab: microbial antigens, unknown manifestation: vasculitis
58
post-streptococcal glomerulonephritis
Ab: streptococcal cell wall antigen manifestation: nephritis
59
serum sickness
Ab: protein antigens manifestation: systemic vasculitis nephritis arthritis
60
goal of type 2 and 3 hypersensitivity treatments
limit inflammation and injury | usually systemic corticosteroids
61
what is plasmapheresis
removing pathogenic antibodies from circulation to reduce Ab driven damage
62
what is IVIg
intravenous immunoglobulin IgG in high doses may induce the expression of and bind to the inhibitory Fc receptor on myeloid and B cells competes with pathogenic Ab for binding
63
anti-CD20 antibody
reduce B cell population that is producing the aberrant antibody
64
what could happen if we block CD40-CD40L communication
block Th and B cell communication to block production of Ab and cytokines decreased survival of B cells and plasma cells inhibit disease progression
65
how does type 4 hypersensitivity work
T cells cause tissue injury | local autoimmune reaction with T cells directed against cellular antigens within local tissues (not systemic)
66
examples of times when type 4 hypersensitivity might develop
persistent response to environmental triggers (poison ivy, meds, chemicals) T cell response to microbes (TB) response to superantigens
67
describe the process of delayed type hypersensitivity (DTH) (type 4)
reaction occurs 24-48 hours after exposure T lymphocytes home to the site -respond to antigen -T cells and monocyte infiltration -leukocyte products lead to tissue damage
68
clinical utility of DTH
determine prior exposure purified protein derivative (PPD)- TB skin test -evaluates T cell response to mycobacteria
69
how is type 4 hypersensitivity unique
chronic and progressive antigen never cleared self perpetuating process
70
multiple sclerosis
myelin proteins | demyelination in the CNS, sensory and motor dysfunction
71
rheumatoid arthritis
unknown antigens | inflammation of synovium and erosion of cartilage and bone joints
72
type 1 DM
pancreatic islet cells | impaired glucose metabolism and vascular disease
73
crohns disease
unknown | inflammation of the bowel wall, ab pain, diarrhea, intestinal bleeding
74
contact sensitivity
modified skin proteins | delayed type hypersensitivity rash
75
chronic infection (TB)
microbial proteins | chronic granulomatous inflammation
76
viral hepatitis
viral encoded proteins | cytotoxic T cells cause cell death, hepatic dysfunction, and fibrosis
77
TSS
microbial superantigens | cytokine release causing fever and shock
78
2 ways to treat type 4 hypersensitivity
anti-inflamm decrease T cell response of effects -TNF inhibitors (monoclonal antibodies) - IL receptor antagonists (monoclonal antibodies) -anti-CD20 B cell (monoclonal antibodies)

IBI Test 2 (10 decks)

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