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
Q

What is type III hypersensitivity known as?

A

Complex-mediated hypersensitivity

26
Q

Type III hyper components?

A

○ IgG and IgM directed against a soluble antigen
○ Small antigen–antibody complexes precipitate out and deposit in tissues

27
Q

Arthus Reaction

A

○ Skin reaction caused by type III hypersensitivity
○ Localized inflammation characterized by redness and edema

28
Q

Serum Sickness

A

○ Generalized type III hypersensitivity reaction
○ passive immunization of humans with animal serum
○ Produces antibodies against the foreign animal proteins in patients

29
Q

Laboratory Testing for Type III hyper

A

○ Testing for ANAs
○ Fluorescent staining of tissue sections to detect deposited immune complexes
○ Testing for rheumatoid factor (an anti-IgG)
○ Testing complement levels

30
Q

What happens to complement levels in Type III Hyper

A

May be decreased in the serum during periods of high disease activity

31
Q

What is Type IV Hypersensitivity known as?

A

Cell-mediated hypersensitivity

32
Q

What are the key components of Type IV Hyper?

A

Th1 cells and macrophages are involved

33
Q

What are the 4 steps in Type IV Hyper?

A

○ 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
Q

How long does it take for Type IV Hyper to peak?

A

48 to 72 hours after antigen exposure

35
Q

Clinical Examples of Type IV Hypersensitivity

A

○ Infections with intracellular pathogens
○ Contact dermatitis
○ Hypersensitivity pneumonitis

36
Q

Hypersensitivity pneumonitis

A

○ Allergic diseases of the lungs
○ Caused by inhalation of bacterial and fungal spores

37
Q

Contact Dermatitis

A

○ 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
Q

Contact Dermatitis examples

A

○ poison ivy
○ poison oak
○ nickel salts
○ materials in cosmetics and hair dyes
○ Latex

39
Q

Skin Testing for Delayed Hypersensitivity

A

○ Patch test
○ Mantoux method

40
Q

Patch test

A

○ Antigen applied to skin surface
○ Test for contact dermatitis
○ (+) test = redness with papules or tiny blisters

41
Q

Mantoux method

A

○ Antigen injected intradermally
○ Test for tuberculosis exposure (PPD) or T-cell function
○ (+) test = induration