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

B3.021 - Hypersensitivity Flashcards

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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
What is mast cells role in T1 HS
Allergen cross links two IgE molecules causing degranulation, synthesis, and secretion
26
ITAM phosphorylation occurs activating what
signaling pathways: Release of preformed mediators Arachidonic acid metabolism secreting lipid mediators Activation of cytokine transcription
27
What are mast cell mediators
Histamine Proteases Prostaglandins Leukotrienes
28
What are cytokine mediators
TNF IL-4 IL-5
29
What are some immediate hypersensitivity treatments
``` Antihistamines Epinephrine Corticosteroids LT receptor antagonists Phosphodiester inhibitors Desensitization Cromolyn ```
30
What do antihistamines do
reduce potential for histamine to bind and cause symptoms
31
What are some first gen H1 antagonists
Cause sedation, short acting | Cyproheptadine, diphenhydramine, hydroxyzine, doxepin
32
What are some 2nd gen H1 antagonists
Cetrizine, levocetirizine, loratadine, desloratiadine, fexofenadien
33
What are some H2 antagonists
Receptors mostly in the gut Ranitidine, famotidine Mostly used for indigestion/heartburn but could be added to an H1 antagonist for allergy treatment
34
What does epinephrine do
1st line anaphylais, Vascular smooth m. contraction, increased cardiac output, inhibits bronchial smooth muscle contraction, stabilizes mast cells
35
What do corticosteroids do
reduce inflammatory mediator production, stabilize mast cells, reduce eosinophils * inhaled topically and oral
36
What do LT receptor antagonists do
reduce inflammation and relax bronchial smooth muscle
37
What doe phosphodiester inhibitors do
relax bronchial smooth muscle (inhaled)
38
What is desensitization
repeated increasing dose of allergens to help the system overcome allergy
39
How does desensitization work
Inhibits IgE prod Allergy shots Oral desensitization for food allergies
40
What does cromolyn do
inhibits mast cell degranulation
41
What are some monoclonal antibodies used for treatment of immediate hypersensitivity
Anti IgE therapy Anti IL-5 therapy Anti IL-4,13
42
How does anti IgE therapy work
binds/inhibits IgE so ti cannot bind to the receptors down regulation of the FceR1 on mast cells
43
What is an anti IgE therapy rug
Omalizumab injectable
44
What does anti IL-5 therapy do
binds/inhibits IL-5 to reduce eosinophil production and survival
45
What are some IL-5 drugs
Mepolizumab, reslizumab, benralizumab
46
What does anti IL-4,13 do
binds and inhibits shared receptor, reducing inflammation and decreasing the effects of both products
47
What is an anti IL-4,13 drug
Dupilumab, atopic dermatitis, asthma studies pending
48
Can you be allergic to more than one thing?
yes, once you are atopic you are more prone to other atopic sensitizations
49
What plays a role in allergy development?
Genetics, environment
50
What do type 1 and 2 sensitivity have in common
Antibody mediated
51
How does T2 HS work
Antibodies can be directed against cells or ECM components
52
How does T3 HS work
Antibody/antigen complex can bind and direct deposits in BVs
53
In T2 HS antibody that is directed against cell surface markers causes what
Complement and Fc receptor induced activation of leukocytes | Bring in neutrophils and macrophages eliciting tissue damage
54
What happens in complement and FcR mediated T2 HS
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
How does Opsonization and phagocytosis work in T2 HS
Complement activation occurs releasing C3b that opsonizes cell Fc receptor on phagocytes recognizes C3b on an opsonized cell and phagocytosis the infected cell
56
T2 HS may occur on what type of cells to induce disease
Erythrocytes and platelets causing anemia and thrombocytopenia
57
What happens in Graves disease
thyroid stimulation even in the absence of thyroid stimulation hormone leading to hyperthyroidism
58
What happens in myasthenia gravis
MSK paralysis disease where antibodies are made against the acetylcholine receptor and inhibit transmission of signals to the muscle to move
59
What is disease caused by in T3 HS
Deposition of circulating antibody/antigen complexes in blood vessels * activation of complement * activation of inflammatory cascade
60
What is arthrus rxn
localized antigen/antibody deposition
61
What are symptoms of an arthus rxn
Formation of complexes at site of antigen injection | Local vasculitis
62
What are examples of an arthus reaction
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
What is the goal of treatment for T2,3 HS
Limit inflammation and injury
64
What medications are there for T2,3 HS
systemic corticosteroids to reduce inflammation and cell activation
65
What is plasmapheresis
Process by which antibodies can be removed from circulation to reduce antibody driven damage
66
What is IVIg
Intravenous immunoglobulin
67
What doe IVIg do
Induce expression of and bind to the inhibitory Fc receptor on myeloid cells and B cells Compete with the pathogenic antibodies for binding
68
What does Anti CD20 Ab do
Reduce the B cell population that is producing the aberrant Ab
69
What is T4 HS
T lymphocyte mediated delayed HS
70
What do T cells do in T4 HS
Local immune rxn with T cells directed against cellular antigens within that local tissue
71
What are some environmental triggers than induce a persistent T cell response
Poison ivy, mediations, chemicals, metals
72
What disease causes a T cell response to microbes in T4 HS
TB
73
What is the mechanism of T4 HS
CD4 cells targeting cell or tissue antigens presented by APCs CD 8 cells targeting host cells CD4/8 cells may work together
74
What is DTH
delayed type hypersensitiviy
75
What are characteristics of DTH
Rxn occurs 24-48 hours after repeat exposure
76
In T4 HS how do T lymphocytes home to the site fucntion
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
What is the clinical utility of DTH
Determine prior exposure | Purified protein derivative - TB skin test
78
Describe T4 HS
chronic and progressive typically Antigen never cleared Self perpetuating processes
79
What are treatments for T4 HS
``` 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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