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Immuno Final > 5 Hypersensitivity > Flashcards

5 Hypersensitivity Flashcards

1
Q

what causes type 1 hypersensitivity reactions?

A

IgE mediated hypersensitivity (allergic) reactions

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2
Q

which cells have granules which are released during a type 1 hypersensitivity rxn?

A

1) mast cells (main degranulator)
2) basophils
3) eosinophils

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3
Q

how long does it take to see the effects of IgE responses?

A

seconds to minutes

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4
Q

In general, what causes hypersensitivity disorders?

A

disorders of immune responses.

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5
Q

what are three ways that immune systems can cause disease? What is the major form?

A

1) reactions against microbes
2) reactions against antigens (major)
3) autoimmunity

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6
Q

what is an atopic disorder?

A

same as an allergic disorder but generally genetically inherited.

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7
Q

allergies are the most common form of immunity disorder in the US, and has a prevalence of about what percent?

A

20%

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8
Q

allergic reactions have increased _______% over the last 15 years?

A

100%, or 2x

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9
Q

If both of your parents have allergies, what are the chances that you will also have allergies? What if neither parent has allergies?

A

40-60%

neither=10%

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10
Q

typical characteristics of allergens include?

A

1) low molecular weigh (5-70kd)
2) glycosylated
3) highly soluble

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11
Q

T/F Atopic individuals produce a normal amount of IgE in response to environmental allergens?

A

False, they produce high levels

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12
Q

What is the hygiene hypothesis?

A

The idea that if you are exposed to allergens and microorganisms early in life you will have less of a chance to develop allergies towards them later on in life.

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13
Q

The hallmark of allergic diseases are activation and production of what?

A 
activation of helper T-2 cells
production of IgE antibody (class switch)
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14
Q

Describe the events that lead up to mast cell degranulation?

A

1) primary exposure; activation of helper T-2 and IgE class switch.
2) IgE’s bind to Mast cells and wait for second exposure
3) upon second exposure, mast cells degranulate causing allergic reaction.

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15
Q

what causes the B cells to undergo class switching? where do they act? what do they release in order to do this?

A

Helper T-2 cells.
They act on the heavy chain.
They release IL4 and IL13

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16
Q

T/F eosinophils are abundant in many immediate hypersensitivity reactions?

A

True

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17
Q

What causes the activation of the eosinophils?

A

Helper T-Cells through the release of IL-5

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18
Q

what 2 things generally happen directly after secondary exposure to an allergen? what generally occurs later on in the reaction?

A

1) vascular reaction, and smooth muscle reaction (immediate reaction)
2) inflammatory reaction (late phase reaction)

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19
Q

during an allergic reaction, both immediate and late phase reactions are used to classify time from exposure. What time frames do these reactions have?

A

immediate reaction= seconds to minutes after exposure

late phase reaction=2-4 hours after exposure

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20
Q

How are mast cells activated?

A

by cross linking Fc-epsilon-RI molecules. (this is the receptor that IgE’s are sitting in)

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21
Q

How long does it take for cross linked FceRI receptors to cause the release of mast cell granules?

A

only seconds.

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22
Q

what is so significant about mast cells, basophils, and eosinophils in the allergic reaction?

A

1) they all release granules

2) they produce lipid mediators and cytokines that induce inflammation.

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23
Q

what is the major biogenic amine released from mast cells?

A

histamine

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24
Q

what does histamine bind to?

A

H1, H2, H3 receptors on many cells types

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25
Q

are the actions of histamine long or short lived?

A

long

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26
Q

what is responsible for the wheal and flare reaction?

A

histamine

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27
Q

what is another name for biogenic amine?

A

vasoactive amine

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28
Q

Once histamine binds, it activated _________ which hydrolyzes membrane phospholipids to generate _______?

A

1) Phospholipase A2 (PLA2)
2) Arachadonic acid
* *I came across this card and I think this card may be wrong? But I don’t know how to fix it.

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29
Q

Once arachidonic acid is is formed from hydrolysis of membrane phospholipids, what cleaves arachidonic acid?

A

1) cyclo-oxigenase

2) Lipo-oxygenase

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30
Q

what do cyclo-oxygenases and lipo-oxygenases make?

A

They produce lipid mediators that cause allergic reaction.

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31
Q

where do NSAIDS work?

A

They block the activity of cyclo-oxygenase. Therefore, they prevent the breakdown of arachidonic acid into active lipid mediators of an allergic reaction.

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32
Q

Biogenic amines cause what immediate effects to the general body functions?

A

1) vascular leakage
2) broncho constriction
3) intestinal hyper motility

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33
Q

Inflammation during an allergic reaction is generally causes by which molecules?

A

cytokines

lipid mediators

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34
Q

tissue damage during an allergic reaction is generally caused by which molecules?

A

Enzymes

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35
Q

Eosinophils generally release cationic proteins and enzymes that have what effect?

A

1) kill parasites

2) tissue damage

36
Q

what is the most sever form of allergic reaction? What happens to the body?

A

1) anaphylaxis.

2) mainly severe broncho constriction and severe vasculature leakage. (these result in death if not fixed)

37
Q

Immediate hypersensitivity reactions depend on what?

A

CD4+ t cells (Helper T cells)

38
Q

can a polysaccharide elicit a hypersensitivity reaction?

A

no, not unless it becomes attached to a protein because the helper T cell is required to elicit the reaction.

39
Q

How does penicillin cause an allergic reaction?

A

It can react with amino acid residues to form hapten carrier conjugates which is required to stimulate the Helper T-2 cells.

40
Q

What is responsible for sensitizing mast cells and providing recognition of antigen for immediate hypersensitivity reactions?

A

IgE

41
Q

Non ligand bound IgE binds to which cells? What allows IgE to stick to that cell?

A

1) Mast cells
2) Basophils
(IgE’s attach to the mast cells and basophils through the FceRI receptor) e=epsilon

42
Q

T/F the FCeRI receptor has a higher affinity than any other Fc receptory for the IgE ligand?

A

True

43
Q

Activated Helper T cells release what to induce class switching?

A

Il-4 and IL 13

44
Q

The late phase reaction usually develops how much later than the initial allergen exposure?

A

2-24 hours

45
Q

What is the wheal and flare reaction?

A

A test which injects an allergen into the skin to cause a reaction through IgE and mast cell degranulation. (note: you have to have had previous exposure to the allergen or this wont show on the test)

46
Q

The wheal and flare reaction is dependent on what?

A

initial contract, and IgE reaction with mast cells

47
Q

How long does it take for the wheal and flare reaction to appear? To go away?

A

1) generally 5-10 min.

2) usually subsides within an hour

48
Q

Wheal can be described as?

A

localized swelling and leakage of plasma from the venules.

49
Q

Flare can be described as?

A

The blood vessels at the margins of the wheal dilate and become engorged with RBC’s and produce a red rim which is called the flare.

50
Q

during the late phase reaction, which 4 cells types are generally present in higher than normal quantities?

A

1) basophils
2) eosinophils
3) neutophils
4) Helper T-2

51
Q

One again, chronic allergies are mainly mediated by which cell type?

A

Helper T-2 cell (know this)

52
Q

what is generally the result from high intravenous doses of allergens?

A

anaphylaxic shock

53
Q

what is generally the result from low subcutanous doses of allergens?

A

flare and wheal

54
Q

what is generally the result from low amounts of inhaled allergens?

A

allergic rhinitis

asthma

55
Q

what generally happens when you ingest some of the allergens such as in food?

A

vomiting
diarrhea
anaphylaxis (because it easily diffuses into blood)

56
Q

Mast cells associated with vascularized connective tissue is called?

A

connective tissue mast cells

57
Q

mast cells associated with the gut or respiratory system are called?

A

mucosal mast cells

58
Q

what are 3 of the most common causes of anaphylaxis?

A

food
venom
medications

59
Q

what is anaphylaxis? what do you usually see with it?

A

1) anaphylaxis is a whole body hypersensitivity reaction.

2) Symptoms can range from urticaria to full anaphylaxic shock.

60
Q

What causes the anaphylaxic shock?

A

1) massive histamine release
2) widespread increased vascular permeability
3) decreased BP
4) shock

61
Q

What do you do to treat anaphylaxis?

A

Give Epinephrine.

62
Q

what percentage of adults in the US have food allergies? Children?

A

Adult= 1-4%

Children=5%

63
Q

What is the real name for hay fever?

A

allergic rhinitis and conjuctivitis

64
Q

What is responsible for the allergic rhinitis and conjuctivitis after exposure to allergen?

A

IgE and mast cell degranulation

65
Q

Common outdoor allergens include?

A

pollens and molds (seasonal)

66
Q

common indoor allergens include?

A

dust-mites
pets
cockroach
molds

67
Q

Which specific antibody is responsible for an asthma attack?

A

Once again IgE

68
Q

What are some common characteristics of asthma?

A

1) often reversible airway obstruction
2) chronic bronchial inflammation
3) bronchial smooth muscle hypertrophy
4) bronchial smooth muscle hyperactivity
5) fibrosis

69
Q

T/F inflammation with asthma sufferers can be perpetuated even in the absence of the allergen?

A

True

70
Q

Which 3 methods are frequently used to prevent allergic reactions?

A

1) avoid allergen
2) inhibit pathway leading to reaction. (Ex: antihistimine)
3) desensitization techniques.

71
Q

What would an anti IL-4 and anti Il-13 do?

A

prevent the Helper T cells from activating the B cells and prevent IgE’s.

72
Q

what would anti IL-5 do?

A

block eosinophil reaction

73
Q

What would anti IgE omalizumab do?

A

prevents the free IgE antibody from binding to mast cell (FceRI)

74
Q

Which receptors to antihistamines work on?

A

H1 receptors

75
Q

It was mentioned that NSAIDS block cyclooxigenase activity preventing prostaglandin and thromboxane formation, what does zileuton do?

A

block the effects of lipo-oxygenase. (This is what converts arachadonic acid into leukotrienes and platelet activating factor)

76
Q

so, zileuton blocks the activity of lipo-oxygenase, not allowing the arachidonic acid to become?

A

1) leukotrienes

2) PAF

77
Q

so, NSAIDS blocks the activity of cyco-oxygenase, not allowing the arachidonic acid to become?

A

1) Thromboxanes

2) prostaglandins

78
Q

what is given to reduce inflammation?

A

corticosteroids.

79
Q

How does desensitization therapy work?

A

1) restores tolerance to the allergen by preventing IgE production.
2) Inducing reg. T cells

80
Q

Desensitization therapy can be used to treat?

A

allergic rhinitis/conjunctivitis
allergic asthma
venom allergy
drug allergy

81
Q

When do you usually see abundant eosinophils?

A

during the late phase reactions.

82
Q

which cells have a high expression of FceRI receptor?

A

Mast Cells and basophils

83
Q

which cells have the ability to proliferate as a mature cell?

A

mast cells

84
Q

T/F mast cells are major cells in circulation?

A

False, however, basophils and eosinophils are.

85
Q

What do lipid mediators do?

A

increase vascular permeability
bronchoconstriciton
mucous secretion
chemotaxis of WBC’s

Immuno Final (7 decks)

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