Exam 2- Type I Hypersensitivity Flashcards

(46 cards)

1
Q

what is an inflammatory response that causes extensive damage to the host’s tissues, even death, called?

A

hypersensitivity or allergy

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2
Q

IgE-mediated type I hypersensitivity (immediate hypersensitivity) is caused by coming into contact with an antigen against which the host has ________________________

A

pre-existing IgE antibodies

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3
Q

where are high affinity Fc-epsilon-RI receptors found?

A

mast cells, basophils, and eosinophils

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4
Q

true/false: allergens are typically presented to the immune system as high doses

A

false: very low doses

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5
Q

which Th cell response is required to induce type I hypersensitivity reactions?

A

Th2

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6
Q

what do mast cell granules do?

A

potent mediators immediate hypersensitivity reactions

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7
Q

how are mast cells, basophils, and eosinophils activated once the IgE molecule is bound?

A

cross-linking of the Fc-epsilon-RI receptors

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8
Q

what are the primary and secondary mediators?

A

primary: pre-formed and stored in granules, immediate hypersensitivity
secondary: synthesized after or released by enzymatic breakdown of cell membrane phospholipids during degranulation process

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9
Q

is histamine short-lived or long-lived?

A

short-lived

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10
Q

is the genetic predisposition to develop Type I hypersensitivity multigenic?

A

yes

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11
Q

true/false: the majority of IgE in the body is present in blood

A

false

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12
Q

true/false: mast cells of non-allergic individuals have IgE antibodies bound to the surface of their mast cells

A

true

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13
Q

what are the phases of type I hypersensitivity?

A

sensitization phase
activation phase
effector phase

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14
Q

what does the “wheal and flare reaction” show?

A

locally dilated blood vessels engorged with red blood cells

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15
Q

what does the late phase reaction of type I hypersensitivity consist of?

A

accumulation of inflammatory leukocytes

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16
Q

what inhibits the late phase of type I hypersensitivity reactions (rich in eosinophils)?

A

corticosteroids, not antihistamines

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17
Q

what is allergic rhinitis?

A

airborne antigens react with IgE-sensitized mast cells in nasal passages and conjunctiva

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18
Q

what is system anaphylaxis or anaphylactic shock caused by?

A

systemic release vasoactive mediators (mainly histamine and leukotrienes)

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19
Q

what are the two antibody based tests for diagnosis of allergies?

A

radioallergosorbent test (RAST)
ELISA

20
Q

what classes of drugs are given for therapy for allergies?

A

antihistamines
antileukotrienes
corticosteroids
epinephrine
cytopoint

21
Q

how does allergen immunotherapy work?

A

shift towards allergen-specific IgG production
shift to Treg subset which suppressed Th2 response

22
Q

what is the principle protective function of IgE-mediated immune reactions?

A

readication of parasitic worms such as helminths

23
Q

what do eosinophils release in response to their Fc-epsilon-RI receptors binding to IgE and cross-linking?

A

major basic protein (MBP)

24
Q

true/false: allergy shots lead to induced Treg response against the allergen used in the shots

25
where is most of the IgE in the body?
bound to Fc receptor Fc-epsilon-RI on mast cells, basophils, and eosinophils
26
what is the sequence of events for immediate hypersensitivity?
antigen exposure activation Th2 cells for the antigen cytokine help from Th2 cells to B cells class switching to IgE production IgE IgE binds to Fc receptors on mast cells re-exposure of antigen
27
what does it mean that allergens are multivalent?
have one or more epitopes that are repetitive, and IgE response mounted against those epitopes
28
what cytokines do Th2 cells produce?
IL-4, IL-5, IL-13
29
what does the cytokine IL-4 do?
helps allergen-specific B cells class-switch to IgE
30
what does the cytokine IL-5 do?
activates eosinophils- common in many immediate hypersensitivity reactions
31
what does the cytokine IL-13 do?
stimulates epithelial cells to secrete increased amounts of mucus
32
what cytokine is significantly higher in severely allergic individuals?
IL-4
33
how are mast cells and basophils activated by IgE?
cross-linking of the Fc-epsilon-RI receptors
34
what is the difference between primary and secondary mediators in hypersensitivity reactions?
primary: pre-made and released immediately: immediate hypersensitivity secondary: synthesized or released by enzymatic breakdown of cell membrane phospholipids during degranulation process
35
are histamine's actions short-lived or long-lived?
short-lived because it is rapidly catabolized
36
what are the actions of histamine?
leakage plasma into tissues vasodilation increased peristalsis and bronchospasms
37
what are the actions of prostaglandins?
vasodilation bronchoconstriction
38
is histamine stronger acting than leukotrienes?
no, leukotrienes are much stronger and longer lasting more potent bronchoconstrictors and stimulators of vascular permeability and mucus secretion
39
what are important cytokines that mast cells produce in hypersensitivity?
TNF-alpha: inflammation IL-4: Th2 response
40
what causes the late phase reaction after the wheal and flare reaction (2-6 hours)?
accumulation inflammatory leukocytes: neutrophils, eosinophils, basophils, and CD4+ Th2 cells
41
true/false: the late phase reaction is rich in eosinophils
true
42
chronic inflammation in asthma is associated with increased presence of ___________, ___________, ___________, and _____________
lymphocytes eosinophils neutrophils other leukocytes
43
what is the difference in food allergies and food intolerances in presenting signs?
food allergies: itching and skin problems food intolerances: diarrhea or vomiting
44
what is in the cutaneous inflammatory infiltrate in dermatitis?
mast cells dendritic cells low numbers eosinophils and neutrophils
45
what are the main vasoactive mediators released in systemic anaphylaxis?
histamine and leukotrienes
46
what are the two antibody based tests for diagnosis of type I hypersensitivity?
radioallergosorbent test ELISA