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IBI Test 2 Leesy > B3.021 - Hypersensitivity > Flashcards

B3.021 - Hypersensitivity Flashcards

1
Q

What is a hypersensitivity reaction

A

Injurious or pathologic immune reactions

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2
Q

What are two mechanisms of hypersensitivity

A
  1. ) An immune response to a microbe or environmental allergy causes tissue injury due to repeated or poorly controlled reactions
  2. ) Failure of self tolerance when an immune response is generated
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3
Q

What is type 1 HS

A

Immediate hypersensitivity mediates by IgE binding to mast cells

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4
Q

What is type 2 HS

A

Antibody IgE mediated cell or tissue destruction

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5
Q

What is type 3 HS

A

Antibody/antigen complex deposition causing inflammation and tissue injury

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6
Q

What is type 4 HS

A

T cell mediated

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7
Q

Which type of HS is true allergy or “atopy”

A

Type 1

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8
Q

Type 1 HS affects what percentage of people

A

10-20%

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9
Q

What diseases are considered Type 1 HS

A
  1. ) Allergic rhinitis/conjunctivitis
  2. ) Atopic asthma
  3. ) Atopic asthma
  4. ) Atopic dermatitis
  5. ) Anaphylaxis
  6. ) Venom allergy
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10
Q

What is the sensitization phase

A

First exposure to an allergen protein or chemical that binds proteins (haptens)

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11
Q

In a true IgE mediated immediate hypersensitivity what shouldn’t happen

A

a reaction to the first exposure to anything, only on a subsequent exposure

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12
Q

Aberrantly, Tfh and Th2 cells cause what using which ILs

A

B cells to stimulate class switching IgE against the allergen via IL-4, IL-13

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13
Q

IgE to the allergen is produced long term by what

A

Plasma cells, binds to the FCeR1 high affinity IgE receptors on mast cells, coating mast cells with IgE to that particular allergen

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14
Q

What is the elicitation phase

A

the hypersensitivity reaction upon repeat exposure, only in a person who’s sensitized

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15
Q

How does type I HS work with regards to mast cells and IgE

A

Allergen cross-links the IgE on the mast cell FceR1 high affinity IgE receptors which activates the mast cell and prompts release of its contents

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16
Q

What contents of the mast cell are released upon activation during T1 HS

A

Vasoactive amines, lipid mediators, cytokines

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17
Q

What mast cell contents cause symptoms immediately

A

vasoactive amines, lipid mediators

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18
Q

What content of mast cells causes symptoms in a delayed fashion

A

Cytokines

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19
Q

What is the immediate response to T1 HS

A

Increased vascular permeability

smooth muscle contraction

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20
Q

What happens in the late phase of T1 HS

A

Tissue injury with repeated bouts

Mediated by cytokines, recruit neutrophils and eosinophils

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21
Q

Where are mast cells located

A

In all connective tissues, adjacent to blood vessels

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22
Q

How are mast cells activated

A

Locally depending on allergen point of entry

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23
Q

What is FceR1

A

a high affinity receptor present on mast cells and basophils

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24
Q

What do 3 polypeptide chains do in T1 HS

A

1 binds to Fc portion of the e chain, 2 are signaling proteins

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25
Q

What is mast cells role in T1 HS

A

Allergen cross links two IgE molecules causing degranulation, synthesis, and secretion

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26
Q

ITAM phosphorylation occurs activating what

A

signaling pathways:
Release of preformed mediators
Arachidonic acid metabolism secreting lipid mediators
Activation of cytokine transcription

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27
Q

What are mast cell mediators

A

Histamine
Proteases
Prostaglandins
Leukotrienes

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28
Q

What are cytokine mediators

A

TNF
IL-4
IL-5

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29
Q

What are some immediate hypersensitivity treatments

A 
Antihistamines
Epinephrine
Corticosteroids
LT receptor antagonists
Phosphodiester inhibitors 
Desensitization
Cromolyn
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30
Q

What do antihistamines do

A

reduce potential for histamine to bind and cause symptoms

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31
Q

What are some first gen H1 antagonists

A

Cause sedation, short acting

Cyproheptadine, diphenhydramine, hydroxyzine, doxepin

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32
Q

What are some 2nd gen H1 antagonists

A

Cetrizine, levocetirizine, loratadine, desloratiadine, fexofenadien

33
Q

What are some H2 antagonists

A

Receptors mostly in the gut
Ranitidine, famotidine
Mostly used for indigestion/heartburn but could be added to an H1 antagonist for allergy treatment

34
Q

What does epinephrine do

A

1st line anaphylais,
Vascular smooth m. contraction, increased cardiac output, inhibits bronchial smooth muscle contraction, stabilizes mast cells

35
Q

What do corticosteroids do

A

reduce inflammatory mediator production, stabilize mast cells, reduce eosinophils
* inhaled topically and oral

36
Q

What do LT receptor antagonists do

A

reduce inflammation and relax bronchial smooth muscle

37
Q

What doe phosphodiester inhibitors do

A

relax bronchial smooth muscle (inhaled)

38
Q

What is desensitization

A

repeated increasing dose of allergens to help the system overcome allergy

39
Q

How does desensitization work

A

Inhibits IgE prod
Allergy shots
Oral desensitization for food allergies

40
Q

What does cromolyn do

A

inhibits mast cell degranulation

41
Q

What are some monoclonal antibodies used for treatment of immediate hypersensitivity

A

Anti IgE therapy
Anti IL-5 therapy
Anti IL-4,13

42
Q

How does anti IgE therapy work

A

binds/inhibits IgE so ti cannot bind to the receptors down regulation of the FceR1 on mast cells

43
Q

What is an anti IgE therapy rug

A

Omalizumab injectable

44
Q

What does anti IL-5 therapy do

A

binds/inhibits IL-5 to reduce eosinophil production and survival

45
Q

What are some IL-5 drugs

A

Mepolizumab, reslizumab, benralizumab

46
Q

What does anti IL-4,13 do

A

binds and inhibits shared receptor, reducing inflammation and decreasing the effects of both products

47
Q

What is an anti IL-4,13 drug

A

Dupilumab, atopic dermatitis, asthma studies pending

48
Q

Can you be allergic to more than one thing?

A

yes, once you are atopic you are more prone to other atopic sensitizations

49
Q

What plays a role in allergy development?

A

Genetics, environment

50
Q

What do type 1 and 2 sensitivity have in common

A

Antibody mediated

51
Q

How does T2 HS work

A

Antibodies can be directed against cells or ECM components

52
Q

How does T3 HS work

A

Antibody/antigen complex can bind and direct deposits in BVs

53
Q

In T2 HS antibody that is directed against cell surface markers causes what

A

Complement and Fc receptor induced activation of leukocytes

Bring in neutrophils and macrophages eliciting tissue damage

54
Q

What happens in complement and FcR mediated T2 HS

A

Antibodies bind to activate neutrophil
Complement activation releases C3a and C5a to activate neutrophils
Neutrophils generate ROS and lysosomal enzymes that cause inflammation/injury
Can occur after strep

55
Q

How does Opsonization and phagocytosis work in T2 HS

A

Complement activation occurs releasing C3b that opsonizes cell
Fc receptor on phagocytes recognizes C3b on an opsonized cell and phagocytosis the infected cell

56
Q

T2 HS may occur on what type of cells to induce disease

A

Erythrocytes and platelets causing anemia and thrombocytopenia

57
Q

What happens in Graves disease

A

thyroid stimulation even in the absence of thyroid stimulation hormone leading to hyperthyroidism

58
Q

What happens in myasthenia gravis

A

MSK paralysis disease where antibodies are made against the acetylcholine receptor and inhibit transmission of signals to the muscle to move

59
Q

What is disease caused by in T3 HS

A

Deposition of circulating antibody/antigen complexes in blood vessels

  • activation of complement
  • activation of inflammatory cascade
60
Q

What is arthrus rxn

A

localized antigen/antibody deposition

61
Q

What are symptoms of an arthus rxn

A

Formation of complexes at site of antigen injection

Local vasculitis

62
Q

What are examples of an arthus reaction

A

tetanus vaccine

  1. pt gets vaccine
  2. development of normal Ab to tetanus toxoid
  3. repeat vaccination occurs within a short time
  4. pre formed Ab complex w additional vaccine antigen and deposit in the subcutaneous tissue
  5. Localized inflammation, pain, swelling
63
Q

What is the goal of treatment for T2,3 HS

A

Limit inflammation and injury

64
Q

What medications are there for T2,3 HS

A

systemic corticosteroids to reduce inflammation and cell activation

65
Q

What is plasmapheresis

A

Process by which antibodies can be removed from circulation to reduce antibody driven damage

66
Q

What is IVIg

A

Intravenous immunoglobulin

67
Q

What doe IVIg do

A

Induce expression of and bind to the inhibitory Fc receptor on myeloid cells and B cells
Compete with the pathogenic antibodies for binding

68
Q

What does Anti CD20 Ab do

A

Reduce the B cell population that is producing the aberrant Ab

69
Q

What is T4 HS

A

T lymphocyte mediated delayed HS

70
Q

What do T cells do in T4 HS

A

Local immune rxn with T cells directed against cellular antigens within that local tissue

71
Q

What are some environmental triggers than induce a persistent T cell response

A

Poison ivy, mediations, chemicals, metals

72
Q

What disease causes a T cell response to microbes in T4 HS

A

TB

73
Q

What is the mechanism of T4 HS

A

CD4 cells targeting cell or tissue antigens presented by APCs
CD 8 cells targeting host cells
CD4/8 cells may work together

74
Q

What is DTH

A

delayed type hypersensitiviy

75
Q

What are characteristics of DTH

A

Rxn occurs 24-48 hours after repeat exposure

76
Q

In T4 HS how do T lymphocytes home to the site fucntion

A

respond to antigen
T cells and monocyte infiltration
CD4 cytokine production causes increased vascular permeability, leading to edema and fibrin depo
Leukocyte products lead to tissue damage

77
Q

What is the clinical utility of DTH

A

Determine prior exposure

Purified protein derivative - TB skin test

78
Q

Describe T4 HS

A

chronic and progressive typically
Antigen never cleared
Self perpetuating processes

79
Q

What are treatments for T4 HS

A 
Anti inflammatories 
* Corticosteroids
Decrease T cell response or effects 
* TNF inhibitors
IL-1,6,17 antagonists
* Anti CD20 B cell

IBI Test 2 Leesy (13 decks)

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