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MFMII > Type I Hypersensitivity > Flashcards

Type I Hypersensitivity Flashcards

1
Q

what Ab is involved in Type I hypersensitivity reactions?

A

IgE

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2
Q

what Ag is involved in Type I

A

exogenous antigens

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3
Q

what is the response time for Type I?

A

15-30min (fast)

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4
Q

what does a type I reaction look like?

A

wheal and flare, red, typical allergic reaction or anaphylactic shock

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5
Q

what cell types are prevalent for Type I?

A

basophils and eosinophils

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6
Q

examples of type I?

A

allergies, asthma, hay fever, anaphylactic shock, classic allergy

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7
Q

what Ab is involved in Type II hypersensitivity reactions?

A

IgG, IgM

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8
Q

what Ag is involved in Type II

A

cell surface Ag (cytotoxic hypersensitivity)

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9
Q

response time for Type II

A

minutes to hours

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10
Q

appearance of Type II

A

lysis and necrosis

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11
Q

what cell types are prevalent for type II?

A

antibody and complement (ADCC)

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12
Q

example of Type II?

A

erythroblastosis fetalis (Rh+/Rh- mom baby), goodpasture’s nephritis, blood transfusion reactions, autoimmune hemolytic anemia, myasthenia gravis

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13
Q

Ab involved in type III hypersensitivity reactions?

A

IgG, IgM

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14
Q

Ag involved in type III?

A

soluble Ag

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15
Q

response time for type III

A

3-8 hours

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16
Q

appearance of type III?

A

erythema and edema, necrosis

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17
Q

cell types prevalent for type III?

A

complement and neutrophils, immune complexes!!

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18
Q

examples of TypeIII

A 
chronic inflammation 
serum sickness
rheumatic fever
rheumatoid arthritis 
systemic lupus erythematosus 
glomerulonephritis
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19
Q

Ab associated with Type IV hypersensitivity?

A

none! is T cell mediated! Tdth cells release cytokine/chemokines

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20
Q

Ag associated with type IV?

A

Ag from tissues and organs

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21
Q

response time for type IV?

A

48-72 hours (delayed type hypersensitivity DTH)

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22
Q

appearance of Type IV?

A

erythema and induration

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23
Q

cell types prevalent for type iV?

A

monocytes and lymphocytes (activation of T cells Th and Tc)

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24
Q

examples of Type IV?

A

contact dermatitis, granulomatous lesions, TB lesions, TB skin test, graft vs host disease (GVHD) (graft rejection)

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25
Q

what is atopy

A

genetic trait to have predisposition for hypersensitivity or allergy

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26
Q

what is an epitope?

A

smaller part of an antigen

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27
Q

all hypersensitivity reactions are the consequence of what?

A

adaptive immune response (memory)

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28
Q

mechanism of action for type I ?

A

Ag bound IgE induces degranulation of mast cells and basophils. Vasoactive mediators are released. (classic allergy )

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29
Q

hay fever is an example of

A

type I

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30
Q

asthma is an example of

A

type I

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31
Q

hives are an example of

A

type I

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32
Q

food allergies are examples of

A

type I

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33
Q

eczema is an example of

A

type I

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34
Q

what is systemic anaphylaxis?

A

degranulation systemically involving multiple organs

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35
Q

Type II is also called

A

cytotoxic hypersensitivity

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36
Q

type II MOA

A

Ab that is directed against cell surface Ag mediates cell destruction via complement activation or ADCC

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37
Q

what type of reaction is erythroblastosis fetalis

A

type II

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38
Q

blood transfusion reactions are examples of

A

type II

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39
Q

myasthenia gravis is an example of

A

type II

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40
Q

autoimmune hemolytic anemia is an example of

A

type II

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41
Q

type III is also known as

A

immune complex disease

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42
Q

MOA type III

A

Ag-Ab complexes deposit in various tissues that induce complement activation, which induces inflammatory response. causes a massive infiltration of neutrophils

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43
Q

what disease is a result of localized type III

A

arthus reaction

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44
Q

serum sickness is an example fo

A

type III

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45
Q

what type of reaction is rheumatic fever?

A

type III

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46
Q

what type of reaction is rheumatoid arthritis ?

A

type III

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47
Q

what type of reaction is systemic lupus erythematosus?

A

type III

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48
Q

glomerulonephritis is due to

A

type III hypersensitivity

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49
Q

type IV is called

A

delayed type hypersensitivity

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50
Q

MOA type IV

A

sensitized Tdth cells release chemokines/cytokines that help recruit and activate macrophages and/or Tc cells, these mediate direct cellular damage

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51
Q

what type of reaction is contact dermatitis?

A

type IV

52
Q

what type of reaction is granulomatous leions?

A

type IV

53
Q

what type of reaction is graft vs host disease (GVHD)

A

type IV

54
Q

what causes TB lesions?

A

type IV

55
Q

what type of reaction is the TB skin test?

A

type IV

56
Q

what is FceRI?

A

high affinity IgE receptor found on mast cells, basophils and activated eosinophils

57
Q

how is FceRI involved in type I Hs

A

the allergen binding to IgE attaches to the FceRI on mast cells (specifically), which triggers signaling for degranulation

58
Q

how do cells isotype switch to IgE upon second exposure to antigen?

A

Th2 cells provide IL-4 that is required by B cells to switch from IgM to IgE

59
Q

how does degranulation occur with 2nd exposure?

A

allergen binds IgE and crosslinks to activate signal with tyrosine phosphorylation. Ca influx causes degranulation and release of mediators

60
Q

what do mast cells do in a 2nd exposure

A

release mediators that attract basophils and eosinophils,

61
Q

what type of immune response is involved in type I

A

Th2 immune response

62
Q

what polymorphic genes could be associated with Type I hypersensitivity?

A
  1. IL-4 receptor
  2. IL-4 cytokine promoter region
  3. high affinity IgE receptor (FceRI)
  4. class II MHC (promotes Th2 response)
  5. inflammation associated genes
63
Q

how does binding of IgE a impact its life span?

A

IgE attachment to mast cell FceRI increases its lifespan from days to months.

64
Q

what are the 2 kinds of mast cells?

A
  1. mucosal mast cell

2. connective tissue mast cell

65
Q

what does mucosal mast cell produce?

A

tryptase

66
Q

what does CT mast cell produce?

A

chymotryptase (chymase)

67
Q

what mast cells are the only mast cells present in pt with T cell immunodeficiencies?

A

connective tissue mast cells

68
Q

what toxic mediators do mast cells release?

A
  1. histamine

2. heparin

69
Q

why do mast cells release toxic mediators?

A

to poison parasites, increase vascular permeability, and cause smooth muscle contraction

70
Q

why do mast cells release enzymes?

A

to remodel connective tissue matrix

71
Q

what lipid mediators do mast cells release?

A
  1. leukotrienes C4,D4,E4

2. platelet activating factor

72
Q

why do mast cells release leukotrienes?

A

to cause smooth muscle contraction, increase vascular permeability, and cause mucus secretion

73
Q

why do mast cells release platelet activating factor?

A

to attract leukocytes, amplify production of lipid mediators, and activate neutrophils, eosinophils, and platelets.

74
Q

what major mediator of type I anaphylactic hypersensitivity do mast cells release?

A

ECF-A (eosinophil chemotactic factor of anaphylaxis)

75
Q

what impact does mast cell activation have on the GI tract?

A

increased fluid secretion and peristalsis causing expulsion of GI contents (diarrhea and vomiting)

76
Q

what impact does mast cell activation have on the airways?

A

decreased diameter and increased mucus secretion leading to congestion and blockage of airways (wheezing, coughing and phlegm) and swelling and mucus secretion in nasal passages

77
Q

what does the decreased diameter and increased mucus secretion cause in type I ?

A

congestion and blockage of airways (wheezing, coughing and phlegm) and swelling and mucus secretion in nasal passages

78
Q

what impact does mast cell activation have on blood vessels?

A

increased blood flow and increased permeability (vasodilation)

79
Q

what does vasodilation and permeability cause in type I?

A

increased fluid in tissues causing increased flow of lymph to LN, increased cells and protein in tissues, and increased effector response in tissues

80
Q

what are basophils in relation to type I

A

granulocytes that initiate Th2 responses and the production of IgE

81
Q

what granules do basophils contain

A

granules that stain with basic dye like hematoxylin

82
Q

how do basophils initiate Th2 responses?

A

secreting IL-4 and IL-13

83
Q

what do eosinophils do in relation to type I

A

granulocytes that release toxic mediators in IgE-mediated responses

84
Q

what do eosinophils release?

A

histaminases and arylsulfatases that degrade histamine and leukotrienes

85
Q

what do arylsulfatases do

A

degrade leukotrienes

86
Q

what is the purpose of eosinophils’ secreted enzymes

A

enable control of allergic symptoms

87
Q

what are the mediators of type I hypersensitivity?

A
  1. histamine (preformed) (causes immediate effect)
  2. eosinophil chemotactic factor (ECF-A) (preformed) (causes immediate effect)
  3. prostaglandins and thromboxanes
  4. leukotrienes
88
Q

what occurs after mediators are released?

A

active only a few minutes, and are rapidly inactivated and slowly resynthesized

89
Q

what is the effect of type I hypersensitivity on lung airflow

A

FEV/L/s changes, immediately spikes down (preformed mediators), then returns to normal, then decreases again 8 hours later (from resynthesized mediators) . is the etiology of wheezing.

90
Q

what are the primary mediators of type I hypersensitivity?

A
  1. histamine
  2. cytokines TNFa, IL-1, and IL-6
  3. chemoattractants for ECF-A
  4. enzymes (tryptase, chymase, cathepsin)
91
Q

what are the secondary mediators of type I hypersensitivity?

A
  1. leukotrienes
  2. prostaglandins
  3. thromboxanes
  4. Th2 cytokines (IL-4, IL-5, IL-13, GM-CSF)
92
Q

what conditions does histamine release cause?

A
  1. allergic rhinitis
  2. urticaria
  3. angioedema
  4. bronchospasm (acute anaphylactic reactions)
93
Q

what does histamine cause?

A
  1. constriction of smooth muscles

2. dilation of blood vessels

94
Q

what does constriction of smooth muscle lead to?

A

in bronchioles, causes wheezing

in GI, cramps and diarrhea

95
Q

what does vasodilation lead to?

A

increases fluids in tissues causing swelling

96
Q

how to treat histamine release?

A

antihistamines to block binding of histamine to its receptors

97
Q

what is a H1 receptor blocker?

A

benadryl and claritin

98
Q

what is a H2 receptor blocker?

A

cimetidine (tagamet) – for GI

99
Q

what is ECF-A

A

eotoaxin (CCL11) that is the most important chemokine in the migration of eosinophils

100
Q

what controls the mobility of eosinophils?

A

CCL11, CCL5, CCL7 and CCL13 by binding to the receptor CCL3 on eosinophils

101
Q

what do prostaglandins do?

A

increase capillary permeability and induce bronchoconstriction

102
Q

what do thromboxanes do?

A

aggregate platelets

103
Q

where are prostaglandins and thromboxanes derived from?

A

arachidonic acid via COX pathway

104
Q

what can treat prostaglandin and thromboxane release?

A

COX inhibitors like ASA and celecoxib

105
Q

what are leukotrienes

A

slow reacting substance of anaphylaxis (SRS-A) that are made after the crosslinking of IgE to FceRI

106
Q

what do leukotrienes do

A

increase vascular permeability and increase smooth muscle contraction, ARE MAJOR MEDIATORS IN BRONCHOCONSTRICTION OF ASTHMA

107
Q

what mediators are major cause of bronchoconstriction in asthma?

A

leukotrienes

108
Q

what can inhibit leukotriene release

A

LTRA (leukotriene receptor antagonists) like montelukast (singulair)

109
Q

what is the triple response of lewis (to local exposure)

A
  1. flush due to direct vasodilation of capillaries
  2. flare due to axonal reflexes and dilation of arterioles
  3. wheal due to inflammation, exudates, and edema.
110
Q

what does systemic response of lewis lead to

A

dilation of peripheral blood vessels in the microcirculation, leading to decrease in blood pressure and increase in HR

111
Q

what is the most common systemic anaphylaxis?

A

penicillin allergy

112
Q

what is the MOA of penicillin allergy?

A

beta lactam ring can be cleaved to create covalent conjugates with body proteins, makes new foreign epitopes. sometimes response is dominated by Th2 cells that help B cells make IgE specific for new epitopes. if receive penicillin a 2nd time, anaphylaxis and maybe death

113
Q

main symptoms of type I reaction in the lungs?

A

asthma – wheezing, dyspnea, tachypnea

114
Q

allergen and route of entry of lung type I reaction ?

A

inhalation of pollen, house dust, animal danders

115
Q

main symptoms of type I reaction in the nose and eyes/

A

allergic rhinitis, conjunctivitis or hay fever. see a runny nose, redness and itchy eyes.

116
Q

allergen and route of entry of nose/eye type I/

A

pollen contact with mucous membrane

117
Q

symptoms of type I reaction on skin?

A

ezcema/atopic dermatitis, urticaria causing pruritic, vesicular lesions, or pruritic bullous leisions

118
Q

allergen and route of entry skin

A

uncertain maybe ingestion and various routes of various foods or drugs or unknown

119
Q

main symptoms of type I reaction in the intestinal tract

A

allergic gastroenteropathy causing vomiting and diarrhea

120
Q

main symptoms of systemic type I reaction

A

anaphylaxis causing shock, hypotension and wheezing

121
Q

treatments for type I hypersensitivity

A
  1. reduce inflammation
  2. block mediator release
  3. suppress immune response
  4. monoclonal Ab against IgE
  5. epinephrine for anaphylactic shock
122
Q

how to reduce inflammation

A

antihistamines, LTRA, ASA, corticosteroids, NSAID

123
Q

how to block mediator release

A

antigranulating agents (nedocromil inhalers)

124
Q

how to suppress immune response

A

desensitization by allergy shots (the allergen is repeatedly injected to reduce IgE on mast cells

125
Q

what is a monoclonal Ab against IgE?

A

omalizumab

MFMII (29 decks)

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