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Block 6 Week 2 > Hypersenstivity Type I- Hunter > Flashcards

Hypersenstivity Type I- Hunter Flashcards

1
Q

What are some secondary immune deficiencies?

A

malnutrition and immunosuppressant drugs.

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2
Q

When the immune system damages itself what do we call this?

A

immunopathology due to hypersensitivity responses

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3
Q

T or F

A little immunopathlogy is normal in all infection

A

T

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4
Q

What is an allergy?

A

your immune system responding to innocuous stimuli.

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5
Q

WHen self nonself identification is all messed up, what do you have?

A

immunopathology

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6
Q

What is Type I hypersensitivity?

A

this is an allergy like asthma and allergic rhinitis.

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7
Q

What is type I hypersensitivity mediated by?

A

IgE

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8
Q

What are the 2 main cell types in Type I hypersensitivty?

A

Mast cells and eosinophils

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9
Q

What are type II hypersensitivity disorders?

A

most are autoimmune (some type II hypersensitivity reactsion are caused by extrinsic things but mostly this category is autoimmune)

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10
Q

How does type II hypersensitivity reaction work?

A

triggers IgG antibodies to bind to our own tissues and turn our immune system against ourselves (blood, tissue, ECM)

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11
Q

What is type III hypersensitivity?

A

it is caused by an IgG antibody that has formed immune complexes. These antigen antibody complexes form in almost every infection but when they cannot be cleared, cause immune complex disease

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12
Q

How is type IV hypersensitivity caused?

A

by CD4 and CD8 T cells (some are autoimmune and some are extrinsic)

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13
Q

Why kind of hypersensitivity is found in rheumatoid arthritis?

A

Type II, III, IV

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14
Q

In type 1 immediate hypersensitivity, what is the immune reactant, is the antigen soluble or insolube, what is the effector mechanism and what are some examples?

A

IgE
soluble antigen
mast-cell activation
allergic rhinitis, asthma, systemic anaphylaxis

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15
Q

What do you find within mast cell granules?

A

mediators

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16
Q

One of the prinicipal immune defense mechanisms against metazoan parasites (worms) is (Blank) killing by eosinophils

A

IgE

IgE can bind to worms and release the granules inside them to kill them

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17
Q

How does our body expulse parasites?

A

cross-linking of anti-parasite IgE on mast cells by parasite antigen causes the release of mediators that promote expulsion of parasites

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18
Q

What sucks about the IgE response that was created to bind and expulse parasites and worms?

A

it can be elicited by inocuous environmental materials (allergens)

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19
Q

What is a classic way to shift THO to produce TH2

A

WORMS!!!!!

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20
Q

What does histamine do in the gut?

A

causes rapid contraction, vomiting, and diarrea

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21
Q

(blank) is an antigen that induces allergy

A

allergen

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22
Q

Type I hypersensitivity reactions are induced by extrinisc allergens. What are some of these?

A

pollen, house dust mite, wasp, drugs, peanuts, shellfish
(pant pollens, dander, mold spores, feces, insect venoms, vaccines, drugs, therapeutic proteins, food, orally admin drugs)

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23
Q

How does an allergen cause IgE production?

A

dendritic cells and other immune cells in mucosa produce IL-4, IL-5, IL-9, IL-13 in response to antigen-> and these favor TH2 differentiation.

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24
Q

What will IFN gamma and IL12 stimulate?

A

TH1 cell

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25
Q

What IgG subtypes will cause fixed complement?

A

Ig1 an Ig3

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26
Q

ONLY (blank) induce T cell responses

A

Proteins

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27
Q

What do you need to make an airbone allergen that will promote TH2 cell formation that drives IgE response?

A

proteins in low doses that have low molecular weight and high solubility. THey must be stable and contain peptides that bind MHC class II

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28
Q

Allergy is (blank), you have the wrong MHC molecule

A

genetic

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29
Q

Allergic Responses involve (blank) class switching of B cells

A

IgE

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30
Q

Explain the allergic response

A 
an allergen-specific B cell binds and internalizes allergen-> allergen peptides are presented MHC class II to CD4 Th2 cells that produce cytokines like IL-4 and express CD40L . 
IL-4/IL-4R ad CD40L/CD40 co-stimulatory signaling activates the B cell and promotes isotype switiching to IgE
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31
Q

What are the co-stimulatory signals that activate the B cells to promote isotype switching to IgE?

A

IL-4/IL-4R and CD40L/CD40

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32
Q

An initial response to an allergen is (blank). Then the B cell and T cell get together to release cytokines that will cause isotype switching to IgE

A

IgM

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33
Q

Unlike other Igs, IgE is (blank)

A

cytophilic

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34
Q

Is IgE found in low or high levels in plasma?

A

low (.1-.4)

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35
Q

IgE binds to (blank) on mast cells, basophils, and eosinophils

A

FceRI

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36
Q

The amount of IgE in your plasma is misleading because the IgE that was in your plasma and is now sitting on mast cells, basophils, and eosinophils that matter. When you have massive allergy attack IgE levels will rise in your plasma.
T or F

A

T

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37
Q

Allergic reactions occur ony after (blank) exposure to allergens

A

second

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38
Q

For allergies:
Tell me what the first exposure is
Tell me what the second exposure is

A

First Exposure
IL-4 Drives B cells to produce IgE in response to pollen antigens. Pollen-specific IgE binds to mast cells.

Second Exposure
Acute release of mast cell contents causes allergic rhinitis (hay fever)

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39
Q

Pollen is typically produced by trees in the (blank), grass in the (blank) and weeds in the (blank)

A

spring
late spring to summer
fall

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40
Q

Where are mast cells found?

A

in the skin, all mucosal areas, lining blood vessels

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41
Q

IgE associated mast cell release will affect your (blank)

A

whole body.

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42
Q

How do you trigger a mast cell to release its granules?

A

you get enough crosslinked IgE on mast cell surface

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43
Q

What are the three pathways to release granules from mast cells?

A

granule exocytosis
secretion with lipid mediators
secretion with cytokines

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44
Q

How does the mast cell release vasoactive amines and proteases?
What do they do?

A

granule exocytosis

causes vascular dilation and smooth muscle contraction AND tissue damage

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45
Q

How does the mast cell release prostaglandins and leukotrienes?
What do they do?

A

Via enzymatic modification of arachidonic acid to create lipid mediators
Vascular dilation and smooth muscle contraction

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46
Q

How does the mast cell release cytokines?

What do they do?

A 
transcriptional activation of cytokine genes 
Cause inflammation (leukocyte recruitment)
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47
Q

What all do mast cells release?

A

vasoactive amine: histamine
Proteases: chymase, tryptase
Prostaglandins: PGD2
Cytokines: TNF-ALpha

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48
Q

What is released quickest to slowest with mast cells?

A

(vasoactive amines and proteases SECONDS TO MINUTES))-> (prostaglandins and leukotrienes MINUTES TO HOURS) -> (cytokines HOURS)

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49
Q

What does histamine cause?

A

vasodilation

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50
Q

Mast cell activation has different effects on different tissues. How does it affect the GI tract?

A

increased fluid secretion and increased peristalsis which results in expulsion of GI tract contents, diarrhea and vomiting

51
Q

Mast cell activation has different effects on different tissues. How does it affect the eyes, nasal passages, and airways?

A

decreased diameter, increased mucus secretion. -> results in congestion and blockage of airways (wheezing, coughing, phlegm) swelling and mucus secretion in nasal passages

52
Q

Mat cell activation has different effects on different tissues. How does it affect the blood vessels?

A

Increased blood flow and increased permeability-> results in increased fluid in tissues causing increasd flow of lymph to lymph nodes, increased cells and protein in tissue, increased effector response in tissues. Hypotension potentially leading to anaphylactic shock

53
Q

Type I allergic reaction range from simpe nuisances to life threatening conditions. T or F

A

T

54
Q

T or F

THe dose and route of allergen administration determines the type of IgE mediated allergic reaction

A

T

55
Q

What happens if you have an intravenous high dose of allergy?

A

general release of histamine and anaphylaxis

56
Q

What happens if you have a subcatenous low dose of allergy?

A

you get local release of histamine (wheel and flare reaction)

57
Q

What hapens if you have a low dose inhalation of allergen?

A

allergic rhinits (upper airway), caused by increased mucus production and nasal irritation. Asthma (lower airway) due to contraction of bronchial smooth muscle and increased mucus secretion

58
Q

What happens if you have ingestion of an allergen?

A

contraction of intestinal smooth muscle induces vomiting. Outflow of fluid into gut causes diarrhea. Antigen diffuses into blood vessels and is widely disseminated causing urticaria (hives) or anaphylaxis

59
Q

Enzymes frequently trigger (blank)

A

allergies

60
Q

What do you find in fecal pellets of dust mites (dermatophagoides pteronyssimus)?

A

Der P1 enzyme

61
Q

What does the Der p1 enzyme do?

A

the enzyme Der p1 cleaves occludin in tight junctions and enters mucosa-> induces IgE and plasma cell formation. -> igE binds to FceRI receptor on mast cell-> reintroductin to Derp1 triggers degranulation

62
Q

(blank) percent of n. america population is allergic to house dust mite feces.

A

20%

63
Q

What do eosinophil secrete?

A

toxi proteins and inflammatory mediators

64
Q

(blank) can occur in allergic patients; induced by growth factors ike (blank)

A

eosinophilia

IL-5

65
Q

(blank and blank) are chemokines made by a variety of cell types that bind to eosinophil CCR3 and recruit these cells

A

Eotaxins 1 and 2

66
Q

Eosinophils bare (blank) but only in the activated state so only activated eosinophis have cytophilic IgE.

A

Fc3RI

67
Q

T or F

products of eosinophis are very potent and tightly regulated (e.g major basic protein, enzymes, leukotrienes)

A

T

68
Q

Which are more potent, eosinophils or mast cells?

A

eosinophils

69
Q

What is a normal value for an eosinophil count?

A

1%

70
Q

What IL generates eosinophils?

A

IL-5

71
Q

Eosinophils are brought to the tissue they are needed at via (blank) and (blank) signaling

A

Eotaxin 1 and 2 signaling

72
Q

Eosinophils produce an incredible array of mediators that protect against ((blank) and can cause (blank)

A

parasites

immunopathology

73
Q

Allergic asthmas has what 2 components?

A

acute and chronic

74
Q

How do you get a chronic allergic asthma response?

A

Chronic reponse caused by cytokines and eosinophil products along with IL-5 and eotaxins

75
Q

What is the secondary intention of chronic asthma?

A

fibrosis and scar formation

76
Q

Most allergic reactions have both an immediate response and a (blank) response

A

late phase

77
Q

What is the immediate phase characterized by?

What is the late phase characterize by?

A

IMMEDIATE PHASE
vasodilation, congestions and edema
LATE PHASE
tissue edema with eosinophils, neutrophils and T cells

78
Q

When does the late phase reaction occur?

A

2-24 hours after repeat exposure to allergen

79
Q

Tendency to make exaggerated IgE responses is called (blank)

A

atopy

80
Q

A variety of genes affect atopy, what are they?

A

MHC II, Fc3RI, TH2 cytokines

81
Q

(blank) factors may influence atopy.

A

environmental

82
Q

Exposure to microbial pathogens promotes a (blank) deviation.

A

Th1

83
Q

How are you more likely to get atopy?

A

if you DO NOT have a lot of environmental exposure to pathogens as a child

84
Q

T or F

early exposure to microorgansms will make you less likely to have allergies

A

T

85
Q

Is there a susceptibility loci for allergic and autoimmune diseases?

A

yes it is 6P21 MHC locus

86
Q

(blank) or (blank) skin tests are used to identify specific allergens.

A

intradermal

epicutaneous

87
Q

Which receptors do antihistamines block? What will this do to your blood vessels?

A

histamine H1 receptors (e.g. diphenhydramine HCl)

cause decreased vascular permeability

88
Q

How do you treat acute asthma?

A

inhaled bronchodilators (beta adrenergic receptor agonists like albuterol)-> relaxes bronchial smooth muscle

89
Q

(blank) relieve symptoms of asthma and seasonal allergies

A

cysteinyl leukotriene receptors (montelukast aka Singular)

90
Q

What leukotrienes does singular block?

A

D4, C4, and E4 and inhibits bronchoconstriction

91
Q

Anaphylactic reactions are treated with (Blank)

A

epinephrine (adrenaline)

92
Q

What will epinephrine do to the body?

A

relax bronchial smooth muscle, constrict vascular smooth muscle, reform endothelial tight junctions

93
Q

Systemic and topical corticosteroids suppress (blank) by inhibiting transcription of many proinflammatory genes by blocking (Blank)

A

chronic infammation

NFKB

94
Q

What does parenteral mean?

A

occuring somewhere other than the mouth or alimentary canal

95
Q

What should you use on an allergic patient who needs inhibition of mediators?

A

antihistamine, beta blocker, lipoxygenase inhibitors

96
Q

What should you use on an allergic patient who needs to reduce their inflammatory effects?

A

corticosteroids

97
Q

What should you use on an allergic patient who needs to reduce their T cell levels (TH2 response)?

A

desensitization therapy by injections of specific antigens

98
Q

What should you use on an allergc patient who needs to have their IgE binding to mast cells stopped?

A

give them anti-IgE antibodies (omalizumab) to bind to IgE and prevent it from bind to Fc receptors on mast cells

99
Q

When can desensitization be used?

A

when allergen is known

100
Q

What is the goal of desensitization?

A

to shift the anti-allergen response from IgE to IgG

101
Q

How does desensitization work?

A

you slowly inject allergen in escalating amounts intradermally to favor IgG production. UPon exposure to allergen, anti-allergen IgG binds up allergen and prevents IgE cross linking.

102
Q

Desensitization produces regulatory cells, and what do these cells secrete?

A

IL-10 and TGF-beta and promotes isotype switching to IgE

103
Q

Larger does of allergen will do what?

A

switch IgE production to IgG

104
Q

Blocking IgE binding to the high affinity IgE receptor on mast cells, basophils, and eosinophils is an interesting strategy. WHat can do this?

A

humanized mouse anti-IgE monoclonal antibody (omalizumab) blocks IgE binding to FC3RI.

105
Q

What is the most common chronic skin disease of young children?

A

atopic dermatitis

106
Q

Most patients with atopic dermatitis are (blank)

A

atopic

107
Q

What do you usually find associated with atopic dermatitis?

A

staph aureus and herpes simplex, elevation of eosinophils, and TH2 cytokines

108
Q

does venom immunotherapy work?

A

yes

109
Q

What is an example of IgE mediated drug hypersensitivity?

A

Anaphylaxis from B-lactam antibiotics

110
Q 
What are these;
halothane hepatitis
hypotension after protamine
dermatitis from sulfonamids
serum sickness from phenytoin or cefaclor
hypotension after succinylcholine
quinine-induced thrombocytopenia
phenolphthalein-induced fixed drug eruption
cis-platinum-associated urticaria
A

IgE mediated drug hypersensitivity

111
Q

A (blank) is a small molecule that can elicit an immune response only when attached to a large carrier such as a protein; the carrier may be one that also does not elicit an immune response by itself

A

hapten

112
Q

Most pharmaceutical agents have simple structures and small molecular weights, most do not qualify as drug allergens. Drugs such as ((blank) can directly bind covelently with macromolecules on cell surfaces and in plasma to form hapten carrier complexes

A

penicillins

113
Q

WHen direct haptenation results in a succicient density of drug epitopes (multivalency), what can happen?

A

you can get an immune response

114
Q

In the case of (blank) antibioitics such as penicillin, the chritical chemical structure is the ring which is unstable and readily acylates lysine residues in proteins

A

Beta-lactam

115
Q

Explain how you can get a penicillin allergy.

A

self proteins are tagged with penicilloyl hapten-> MHC II molecules with this protein in presence of danger signals will activate CD4 t cells that make B cells create an IgE anti-penicilloy antibody and you gen mast cell degranulation the following exposure.

116
Q

What other three drugs should you not give someone who is allergic to penicillin?

A

carbapenems, cephalosporins, monobactams (cuz they all have the same Beta-lactam ring)

117
Q

What represents the greates foreign antigenic load confronting the human immune system? how do we deal with this?

A

ingested food

most individuals develop tolerance

118
Q

What can food allergens cause?

A

Gi, cutaneous, and respiratory problems AND even anaphylaxis in up to 8% of children younger than 5 and app. 3.5% of general pop.

119
Q

Can foods trigger life threatening anaphylaxis in children and adults?

A

yes

120
Q

the incidence of peanut allergy has (blank) over the past decade in western countries

A

tripled

121
Q

How do you treat food allergy?

A

avoidance

122
Q

What is the most common allergen in adults?

What about in children?

A

vegetables> fruits> peanut and wheat

Cows milk> shellfish

123
Q

If someone has an anaphylactic reaction, why are they NOT given a skin test for that allergen immediately after the individual has recovered

A

because immediately after a systemic anaphylactic reaction the patient is unresponsive in a skin test owing to the massive depletion of mast cell granules and failure of the blood vesselt to respond to mediators. This is called tachyphylaxias and last for 72-96 hours

Block 6 Week 2 (7 decks)

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