Chapter 14: Hypersensitivity Flashcards

1
Q

What is hypersensitivty?

A

Exaggerated immune response to a typically harmless antigen

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2
Q

How many hypersensitivities are there?

A

4

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3
Q

What sensitivities have and immediate reaction?

A

Types I-III
Develop minutes to hours after antigen exposure

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4
Q

What sensitivities have delayed reactions?

A

○ Type IV
○ Develop 24 to 48 hours after antigen exposure

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5
Q

What is a type I Hypersensitivity known as?

A

anaphylactic hypersensitivity

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6
Q

What is Type I Hypersensitivity thought as?

A

Allergies since, they commonly occur within minutes after exposure to an allergen

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7
Q

What are the key components of Type I Hyper?

A

○ IgE
○ Mast cells
○ Basophils
○ Eosinophils

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8
Q

Sensitization Phase: components

A

○ APCS: process allergens and present them to Th cells
○ Th2: induce production of allergen specific IgE
○ IgE: binds to FceRI receptors on mast cells and basophils

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9
Q

Activation phase

A

○ Allergen cross-links adjacent cell-bound IgEs
○ Mast cells and basophils degranulate
○ Chemical mediators are released and bind to target organs
○ Allergy symptoms are produced

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10
Q

What are some common allergens?

A

○ Pollen
○ Mold spores
○ Animal dander
○ Dust mites
○ Insect venom
○ Certain foods (peanuts, shellfish, dairy products)
○ Certain drugs (penicillin)
○ Latex

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11
Q

Clinical Manifestations of Type I Hypersensitivity

A

○ Rhinitis (“hay fever”)
○ Asthma
○ Food allergies
○ Urticaria (“hives”)
○ Eczema
○ Systemic anaphylaxis- A potentially fatal reaction

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12
Q

Treatments for Type I Hypersensitivity

A

○ Avoid allergens
○ Drug therapy
○ Monoclonal anti-IgE antibody
○ Allergy immunotherapy (AIT)- in increasing amounts

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13
Q

How is type I Hyper tested?

A

○ In Vivo Skin Tests
○ Apply a panel of allergens to separate sites on the skin
○ Wait 15 to 20 minutes

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14
Q

What is a positive test for Type I hyper?

A

wheal and flare at the site of application

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15
Q

RAST

A

Used to detect IgE to a specific allergen in patient serum

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16
Q

RIST

A

Used to detect the total concentration of IgE in patient serum

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17
Q

What is Type II Hypersensitivity known as?

A

antibody-mediated cytotoxic hypersensitivity

18
Q

What are key components of Type II Hyper?

A

IgG and IgM directed against a cell surface antigen

19
Q

What do the key components of Type II Hyper do?

A

○ Cell destruction
○ Inhibition of cell function
○ Increase in cell function

20
Q

What causes cell damage in type II Hyper?

A

Activation of classical pathway of complement and cell lysis

21
Q

Clinical Examples of Type II Hypersensitivity

A

○ Transfusion reactions typically
○ Hemolytic disease of the newborn (HDN)
○ Autoimmune hemolytic anemia
○ Goodpasture’s syndrome
○ Hashimoto’s disease

22
Q

Hemolytic disease of the newborn (HDN)

A

○ Caused by development of antibodies by a pregnant woman to red blood group antigens
○ usually Rh D, on the RBCs of the fetus

23
Q

Direct Antiglobulin Test (DAT)

A

○ Detects RBCs coated with complement components or IgG antibody
○ Positive test = RBC agglutination
○ If positive: test is repeated with mono-specific anti-IgG, anti-C3b, and anti-C3d

24
Q

Indirect Antiglobulin Test

A

○ Aka Coombs’ test
○ Tests patient serum for antibodies to RBC antigens
○ Positive test = RBC agglutination

25
What is type III hypersensitivity known as?
Complex-mediated hypersensitivity
26
Type III hyper components?
○ IgG and IgM directed against a soluble antigen ○ Small antigen–antibody complexes precipitate out and deposit in tissues
27
Arthus Reaction
○ Skin reaction caused by type III hypersensitivity ○ Localized inflammation characterized by redness and edema
28
Serum Sickness
○ Generalized type III hypersensitivity reaction ○ passive immunization of humans with animal serum ○ Produces antibodies against the foreign animal proteins in patients
29
Laboratory Testing for Type III hyper
○ Testing for ANAs ○ Fluorescent staining of tissue sections to detect deposited immune complexes ○ Testing for rheumatoid factor (an anti-IgG) ○ Testing complement levels
30
What happens to complement levels in Type III Hyper
May be decreased in the serum during periods of high disease activity
31
What is Type IV Hypersensitivity known as?
Cell-mediated hypersensitivity
32
What are the key components of Type IV Hyper?
Th1 cells and macrophages are involved
33
What are the 4 steps in Type IV Hyper?
○ APCs present antigen to naïve T helper cells, which differentiate into Th1 cells ○ Th1 cells release cytokines that attract and activate macrophages ○ Macrophages induce inflammation ○ Cytotoxic T lymphocytes are recruited and destroy target cells
34
How long does it take for Type IV Hyper to peak?
48 to 72 hours after antigen exposure
35
Clinical Examples of Type IV Hypersensitivity
○ Infections with intracellular pathogens ○ Contact dermatitis ○ Hypersensitivity pneumonitis
36
Hypersensitivity pneumonitis
○ Allergic diseases of the lungs ○ Caused by inhalation of bacterial and fungal spores
37
Contact Dermatitis
○ Low-molecular-weight compounds contact the skin and act as haptens to sensitize Th1 cells ○ Skin eruptions with erythema, swelling, and papules are produced
38
Contact Dermatitis examples
○ poison ivy ○ poison oak ○ nickel salts ○ materials in cosmetics and hair dyes ○ Latex
39
Skin Testing for Delayed Hypersensitivity
○ Patch test ○ Mantoux method
40
Patch test
○ Antigen applied to skin surface ○ Test for contact dermatitis ○ (+) test = redness with papules or tiny blisters
41
Mantoux method
○ Antigen injected intradermally ○ Test for tuberculosis exposure (PPD) or T-cell function ○ (+) test = induration