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IBI Test 2 > B3.021 Prework Hypersensitivity > Flashcards

B3.021 Prework Hypersensitivity Flashcards

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
Q

IL-5

A

eosinophil activation, generation

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26
Q

what is the general mechanism of antihistamines

A

histamine receptor antagonists

reduce the potential for histamine to bind and cause symptoms

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27
Q

H1 antagonists

A

1st generation - caused sedation and short acting

2nd generation - less or no sedation, long acting

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28
Q

H2 antagonists

A

receptors mostly in the gut

mostly used for indigestion and heartburn, but could be added to an H1 antagonist for treatment of allergic conditions

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29
Q

epinephrine (SubQ, IM or IV)

A 
1st line in anaphylaxis
vascular smooth muscle contraction
increased cardiac output
inhibits bronchial smooth muscle contraction
stabilize mast cells
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30
Q

corticosteroids (inhaled/oral/IV/IM)

A

reduce inflammatory mediator production
stabilize mast cells
reduce eosinophils

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31
Q

leukotriene receptor antagonists (oral)

A

reduce inflammation

relax bronchial smooth muscle

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32
Q

phosphodiester inhibitors (inhaled)

A

relax bronchial smooth muscle

33
Q

describe desensitization treatment

A

repeated increasing dose of allergens to help the system overcome the allergy
inhibit IgE production, induce tolerance
allergy shots

34
Q

cromolyn (topical or oral)

A

inhibits mast cell degranulation

35
Q

what are 3 types of monoclonal antibody therapy for immediate hypersensitivity

A

anti-IgE
anti-IL-5
anti-IL-4 and IL-13

36
Q

anti-IgE therapy

A

binds/inhibits IgE so it cannot bind to the receptors

downregulation of the FceR1 on mast cells

37
Q

anti IL-5 therapy

A

binds/inhibits IL-5 to reduce eosinophil production and survival

38
Q

anti IL-4 and IL-13 therapy

A

binds/inhibits the shared receptor reducing inflammation and decreasing the effects of both products

39
Q

distinguish between type 2 and 3 hypersensitivities

A

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
Q

diseases associated w types 2 and 3 hypersensitivity

A 
cytopenias
organ inflammation
hormone abnormalities
skin diseases
vasculitis
arthritis
nephritis
41
Q

describe type 2 hypersensitivity

A

complement and Fc receptor induced recruitment and activation of leukocytes
opsonization and phagocytosis
cell function abnormalities by competitive inhibition or activation

42
Q

describe the process of complement and Fc receptor mediation of type 2 hypersensitivity

A

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
Q

discuss the link between strep and type 2 hypersensitivity

A

can occur after strep infection

Ab cross reacts with myocardium causing myocarditis

44
Q

describe the process of opsonization and phagocytosis associated with type 2 hypersensitivity

A

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
Q

describe cell function abnormalities caused by competitive inhibition or activation in type 2 hypersensitivity

A

Abs generated against hormone receptors competitively inhibit hormone production
Abs can also mimic hormones

46
Q

graves disease

A

thyroid stimulation even in the absence of thyroid stimulation hormone leading to hyperthyroidism

47
Q

myasthenia gravis

A

musculoskeletal paralysis disease where Abs are made against the acetylcholine receptor and inhibit transmission of signals to the muscle to move

48
Q

autoimmune hemolytic anemia

A

opsonization and phagocytosis of erythrocytes causing anemia

49
Q

autoimmune (idiopathic) thrombocytopenic purpura

A

opsonization and phagocytosis of platelets causing bleeding

50
Q

goodpasture syndrome

A

complement and Fc receptor mediated inflammation targeting a non-collagenous protein in kidney glomeruli and lung alveolar basement membranes

51
Q

pemphigus vulgaris

A

antibody mediated activation of proteases causing disruption of intercellular adhesions
targets desmoglein - protein in intercellular junction of epidermal cells which holds cells together

52
Q

pernicious anemia

A

neutralization of intrinsic factor leads to decreased absorption of vitamin B12
results in anemia

53
Q

rheumatic fever

A

inflammation and macrophage activation
targets streptococcal cell wall antigen, antibody cross-reacts with myocardium
leads to myocarditis and arthritis

54
Q

describe type 3 hypersensitivity

A

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
Q

arthus reaction

A

localized Ag/Ab complex deposition
formation of complexes at the site of antigen injection
local vasculitis (often mistaken as cellulitis but not infectious)

56
Q

systemic lupus erythematosus

A

Ab: DNA, nucleoproteins, others
manifestation: nephritis, arthritis, vasculities

57
Q

polyarteritis nodosa

A

Ab: microbial antigens, unknown
manifestation: vasculitis

58
Q

post-streptococcal glomerulonephritis

A

Ab: streptococcal cell wall antigen
manifestation: nephritis

59
Q

serum sickness

A

Ab: protein antigens
manifestation: systemic vasculitis
nephritis
arthritis

60
Q

goal of type 2 and 3 hypersensitivity treatments

A

limit inflammation and injury

usually systemic corticosteroids

61
Q

what is plasmapheresis

A

removing pathogenic antibodies from circulation to reduce Ab driven damage

62
Q

what is IVIg

A

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
Q

anti-CD20 antibody

A

reduce B cell population that is producing the aberrant antibody

64
Q

what could happen if we block CD40-CD40L communication

A

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
Q

how does type 4 hypersensitivity work

A

T cells cause tissue injury

local autoimmune reaction with T cells directed against cellular antigens within local tissues (not systemic)

66
Q

examples of times when type 4 hypersensitivity might develop

A

persistent response to environmental triggers (poison ivy, meds, chemicals)
T cell response to microbes (TB)
response to superantigens

67
Q

describe the process of delayed type hypersensitivity (DTH) (type 4)

A

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
Q

clinical utility of DTH

A

determine prior exposure
purified protein derivative (PPD)- TB skin test
-evaluates T cell response to mycobacteria

69
Q

how is type 4 hypersensitivity unique

A

chronic and progressive
antigen never cleared
self perpetuating process

70
Q

multiple sclerosis

A

myelin proteins

demyelination in the CNS, sensory and motor dysfunction

71
Q

rheumatoid arthritis

A

unknown antigens

inflammation of synovium and erosion of cartilage and bone joints

72
Q

type 1 DM

A

pancreatic islet cells

impaired glucose metabolism and vascular disease

73
Q

crohns disease

A

unknown

inflammation of the bowel wall, ab pain, diarrhea, intestinal bleeding

74
Q

contact sensitivity

A

modified skin proteins

delayed type hypersensitivity rash

75
Q

chronic infection (TB)

A

microbial proteins

chronic granulomatous inflammation

76
Q

viral hepatitis

A

viral encoded proteins

cytotoxic T cells cause cell death, hepatic dysfunction, and fibrosis

77
Q

TSS

A

microbial superantigens

cytokine release causing fever and shock

78
Q

2 ways to treat type 4 hypersensitivity

A

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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