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Immunology > Type I Hypersensitivity (28) > Flashcards

Type I Hypersensitivity (28) Flashcards

Dr. Faulkner

1
Q

What is hypersensitivity?

A

a state of altered reactivity in which the body reacts with an exaggerated immune response to what is perceived as a foreign substance

reflection of excessive or aberrant immune responses

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2
Q

Type I hypersensitivity is also called _____

A

immediate hypersensitivity or mast cell and eosinophil mediated

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3
Q

How fast is type I sensitivity?

A

immediate

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4
Q

What are the pathologic immune mechanisms for type I hypersensitivity?

A

Th2 cells
IgE antibody
mast cells
eosinophils

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5
Q

Type I hypersensitivity is a form of _____ inflammation that results from the interaction of antigens with ________

A

acute
mast cell-bound IgE

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6
Q

In Type I hypersensitivity, binding of antigens with mast cell-0bound IgE leads to _______

A

mast cell degranulation

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7
Q

What causes acute inflammation in Type I hypersensitivity?

A

granule content

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8
Q

What are the 2 important features of Type I hypersensitivity?

A
  1. exaggerated Th2 response
  2. excessive IgE production
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9
Q

Excessive production of IgE is called

A

atopy

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10
Q

What does the development of atopy and Type I hypersensitivity depend on?

A

the interaction of genes
environmental factors

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11
Q

T/F: Being exposed in a less hygienic environment can cause you to be less atopic as an adult

A

TRUE
genetic and environmental factors - hygiene hypothesis

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12
Q

Describe the mechanisms of type I hypersensitivity

A

mast cell has receptors for IgE
antigen binds to IgE
causes de-granulation
cytokines, vasoactive molecules, chemotactic molecules released
pro-inflammatory response

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13
Q

In Type I hypersensitivity, degranulation, releases molecules like _____

A

histamine

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14
Q

In type I hypersensitivity, what does the first exposure to an allergen cause?

A

antigen activation of Tfh and Th2 cells
stimulation of IgE class switching in B cells

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15
Q

What does IgE bind to on mast cells in type I hypersensitivity?

A

FceRI (specific for IgE)

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16
Q

In type I hypersensitivity, vasoactive amines and lipid mediators are [immediate/late] phase, and cytokines are for [immediate/late]

A

amines/mediators: immediate
cytokines: late

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17
Q

What is the role of IL-4 in IgE response in type I hypersensitivity?

A

released from Th2 cells and promotes the development of more Th2 cells (which are major sources of IgE responses)
degranulation also produced IL-4

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18
Q

_____ may serve as an initial source of IL-4

A

NK cells

19
Q

What inhibits the response to IL-4?

A

IFN-gamma
IL-12 (Th1)

20
Q

What is the allergy loop?

A

body produces a lot of IgE

21
Q

_____ cells express [monomeric/dimeric/trimeric] FceRI and as a result can bind to antigen-Ig[G/M/E/A/D] complexes. Once processed, it stimulates [Th1/Th2/Th17] responses which secrete _____

A

Dendritic
trimeric
IgE
Th2
cytokines

22
Q

What are the structural features of a CT mast cell? It has _____, meaning its granules stain intensely

A

mitochondrion
nucleus
golgi

metachromatic granules

23
Q

In type I hypersensitivity, what causes rapid, complete degranulation? A more gradual, piecemeal degranulation?

A

rapid: antigen bound through IgE

endothelins, etc

24
Q

In type I hypersensitivity, once IgE is cross-linked by the antigen, _____ occurs

A

cell signal transduction

25
Q

The combined signal or cross-linking with IgE molecules with antigen leads to _____, ______, and _____

A

degranulation (granule exocytosis)
leukotriene and prostaglandin synthesis
cytokine production

26
Q

What are the seconds to minutes to hours that are released in type I hypersensitivity?

A

early vs late

27
Q

[Alpha/Beta] receptor stimulation enhances degranulation of mast cells, and [alpha/beta] receptor stimulation suppresses degranulation of mast cells

A

Alpha
beta

28
Q

In type I hypersensitivity, when would you see a lot of eosinophils?

A

late phase reaction

29
Q

Eosinophils are mobilized by IL-____

A

IL-5

30
Q

Eosinophils release a complete array of molecules that contribute to the _____ process. On balance, eosinophils exacerbate the inflammation triggered by ________

A

acute inflammatory
mast cells

31
Q

What do the clinical signs of type I hypersensitivity result from?

A

abrupt and excessive release of inflammatory mediators from mast cells, basophils, and eosinophils

32
Q

In type I hypersensitivity, if the rate of release of vasoactive molecules exceeds its ability to adjust to changes in the vascular system, an animal will undergo _______ and may die

A

allergic anaphylaxis

33
Q

Anaphylaxis is a type of _______

A

shock

34
Q

What is shock?

A

an acute clinical syndrome,e caused by a severe allergic reaction

35
Q

What are signs of anaphylaxis?

A

hives, itching, flushed skin, constriction of airways, swollen eye, tongue, nausea, vomiting diarrhea, etc

36
Q

Antigen reaches the skin causing ______, or _____

A

local dermatitis
urticaria

37
Q

What is the shock organ in most animals except dogs?

A

respiratory tract

38
Q

What is the shock organ in dogs? Pathology?

A

hepatic veins - the liver
hepatic engorgement, visceral hemorrhage

39
Q

What is treatment for type I hypersensitivity?

A

prevent exposure
epinephrine for allergic anaphylaxis
corticosteroids for local inflammation
desensitizing injections of allergens

40
Q

What are the principles of allergen-specific immunotherapy?

A
41
Q

____ is caused by the release of inflammatory molecules from mast cells following the binding of antigens to IgE

A

Disease

42
Q

T/F: The clinical signs of allergic disease depend in large part on the route by which antigens (allergens) enter the body

A

TRUE

43
Q

In many cases of allergies, especially the dog, they may manifest as ____

A

intense pruritis

44
Q

The most satisfactory solution to prevent allergies is to ______

A

prevent exposure to the offending allergens

Immunology (36 decks)

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