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Immunology & Serology > Hypersensitivity (Lecture 5) > Flashcards

Hypersensitivity (Lecture 5) Flashcards

1
Q

Hypersensitivity (definition)

A

A normal, but exaggerated/uncontrolled immune response to an antigen that can produce inflammation, cell destruction, or tissue injury

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2
Q

Immediate Hypersensitivity

A

Antibody Mediated. Minutes to Hours.

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3
Q

Delayed Hypersensitivity

A

Cell Mediated. Days or longer.

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4
Q

Immunization/Sensitization

A

An immunologic reaction dependent on the host’s response to a subsequent exposure to antigen.

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5
Q

Small quantities of antigen may favor sensitization by:

A

restricting the quantity of antibody formed

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6
Q

Allergic/Hypersensitive reaction may follow:

A

Second exposure to antigen. It reveals the existence of sensitization.

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7
Q

Most significant property of IgE antibodies

A

Can be specific for hundreds of different antigens (animal dander, pollens, food, molds, dust, metals, drugs, insect stings)

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8
Q

Allergy vs. Atopy

A

Originally Allergy meant any altered rxn to external substances

Originally Atopy referred to immediate hypersensitivity mediated by IgE antibodies

USED INTERCHANGEABLY

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9
Q

Allergen (definition)

A

Antigens that trigger allergic reactions

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10
Q

Allergen (properties)

A

Low molecular weight substances, can be inhaled, eaten, or administered as drugs

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11
Q

Different types of antigens can cause

A

Hypersensitivity

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12
Q

Latex - What is it? Where is it found?

A

Protein in the sap of Brazillian rubber tree

“natural rubbber products” made from sap. Disposable gloves, condoms, diaphragms.

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13
Q

Latex Allergies/reactions can be caused by?

A

Direct contact with latex

Inhaling airborne latex fibers

NOT synthetic latex

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14
Q

Frequency of latex allergies?

A

Rare, <1% of US population has a latex sensitivity

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15
Q

3 types natural latex reactions

A
  1. IgE mediated allergic rxns (Type I hypersensitivity)
  2. Cell-mediated contact dermatitis (Type IV hypersensitivity)
  3. Irritant dermatitis
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16
Q

What is Irritant Contact Dermatitis?

A

Reaction, not an allergy. Appears where latex has touched the skin. May be a warning sign that latex allergy may develop.

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17
Q

Irritant Contact Dermatitis symptoms

A

Swelling, redness, itching after latex exposures

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18
Q

Environmental Substances (definition/description)

A

Substances in the form of small molecules that can trigger reactions

Small molecules can diffuse into skin and act as haptens (delayed hypersensitivity with contact dermatitis)

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19
Q

Environmental Substances - Dust

A

Enters respiratory tract.

Mimics parasites.

Can stimulate antibodes (Immediate IgE, causing rhinitis or asthma; or IgG, can cause farmer lung)

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20
Q

Environmental Substances - Drugs

A

Administered orally, by injection, or on the skin

Hypersensitivity response mediated by IgE, IgG or T lymphs

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21
Q

Environmental Substances - Metals, Chemicals

A

Especially nickel. Can cause Type I rxn.

Haptens. Bind to body proteins or MHC, which is regonized by T cells, initiating a reaction

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22
Q

Infectious Agents that Cause Hypersensitivity Rxns

A

Influenza (damage respiratory epithelial cells, cytokine storm)

Streptococci (immune complex disease)

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23
Q

Self Antigens

A

Reactions to self antigens normal in small amounts

Can become hypersensitivity if exaggerated

24
Q

Food Allergies - Rates in Children & Adults

A

5% kids under 5 y.o.
4% teens and adults

Some allergies are “grown out of”, leading to decrease between ages (commonly wheat, milk, egg, soy)

Overall prevalence increasing

25
Q

What Ig mediates most Food Allergy rxns? What foods cause most of these rxns?

A

IgE

Cow’s milk, soy, chicken eggs, peanuts, tree nuts, wheat, fish, crustaceans

26
Q

Cell-Mediated reactions are most commonly caused by

A

Soy, wheata, rice, oats, cow’s milk

27
Q

Are food allergies and intolerance the same thing?

A

No

28
Q

Foods with proteins similar to the rubber tree (& those that cause progressive symptoms)

A

Nuts, fruits

Figs, apples, carrots, celery, melons, potatoes, papayas, pitted fruits

29
Q

Foods with proteins similar to rubber tree are at risk of/can cause:

A

At risk of developing a latex allergy.

Can cause anaphylactic reactions in latex sensitive people

30
Q

NIAID Guidelines

A

National Institute of Allergy and Infectious Diseases

IgE-mediated reactions to food (food allergies)

Non-IgE-mediated rxns to certain foods (e.g. celiac disease)

Mixed IgE & non-IgE disorders

31
Q

NIAID ood Allergy Reactions & Treatments

A

Can cause severe allergic reactions, anaphylaxis, death

No treatment, only allergen avoidence

32
Q

Types of Hypersensitivity Reactions & General Characteristics

A

Defined by the principal mechanisms responsible for a specific cell or tissue injury that occurs during an immune response.

Types I, II, III - antibody mediated

Type IV - cell-mediated

33
Q

Type I Anaphylactic Rxns

A

Can range from mild to life-threatening anaphylactic reactions. Anaphylactic is not Anaphylaxis/Anaphylactic Shock.

34
Q

Type I - Etiology

A

Atopic allergies (source not always known)
Drugs (systemic penicillin)
Insect stings (hornets, yellow jackets)
Immune-mediated IgE adverse food rxns

35
Q

Type I - Immunologic Activity

A

Mast cells (cellular receptors for IgE, granules contain complex of heparin, histamine & zinc ions. Released when allergen interacts with membrane-bound IgE)

Immediate hypersensitivity - basis of acute allergic reactions

36
Q

Type I - Mast Cell Degranulation

A

The mast cell carries high-affinity receptors for the Fc portion of IgE. Allergen-specific IgE, occupying these receptors, induces mast cell degranulation

37
Q

Type I - Basophil Granules & Cytokines

A

IL-3 stimulated basophils to form & release histamine, IL-4, IL-13, leukotriene C4 (major mediators of allergy and asthma)

Basophil granulocytes considered key effector cells in Th2 cell immune responses and allergic inflammation

38
Q

Type I - Anaphylactic Rxn (definition)

A

The clinical response to immunologic formation and fixation between a specific antigen and tissue-fixing antibody. Usually mediated by IgE

39
Q

Type I - Anaphylactic Rxn (stages)

A
  1. Antigen attached to basophil/mast cell membrane IgE. Crosslinking two IgE necessary to initiate stage 2.
  2. activated mast cells and basophils release various mediators
  3. the effects of mediator release produce vascular changes and activation of platelets, eosinophils, neutrophils, and coagulation cascade
40
Q

Type I - Anaphlyactoid Reaction

A

Anaphylaxis-like (clinically similar)

NOT Antigen-Antibody mediated

Immunologically inert materials that activate serum and tissue proteases and the alternative pathway of the complement system

Offending substances act directly on mast cells (causing release of mediators) or on tissues (eg C3a, C5)

41
Q

Type I - Atopic reaction

A

Exaggerated response to allergens

Characterized by the production of allergen-specific IgE antibodies, and positive rxns to extracts of common airborne allergens with skin prick test

T cells respond to allergens by inducing cytokines produced by Th2 cells (IL-5, IL-13) rather than by Th1 cells

Hallmark of allergic disease is the infiltration of affected tissue by Th2 cells

42
Q

Type I - Atopy Signs and Symptoms (localized reaction)

A

Single does of common airborne allergen can cause skin redness, sneezing, wheezing, within minutes

Immediate hypersensitivity rxn, followed by a late-phase reaction that peaks 6-9 hours after exposure, then subsides (depends on amount of allergen)

Localized reaction - immediate response to mediators release from mast cell degeneration. Urticaria, angioedema at site of exposure. Bowel if ingested. Severe but rarely fatal

43
Q

Type I - Atopy Signs & Symptoms (Generalized/Anaphylactic Reaction)

A

Dramatic, rapid onset

Produced by mediators from mast cells (cytokines, histamine)

Histamine release leads to constriction of bronchial smooth muscle, edema of trachea & larynx, stimulation of smooth muscle in GI tract

Antihistamines have no effect

44
Q

Type I - Atopic, Allergic Disease in Children

A

Allergy march

Formation of IgE in early life, sensitization to food allergen can manifest as colic or chronic otitis

Risk factors:
-family history for allergy
-sensitization to food allergens
-total serum IgE > 100kU/L before age 6
-living in allergen rich environment
-smoking

45
Q

Type I - Testing

A

Patient History

Lab tests to ID foods

Skin (pin prick) test

Patch testing if non-IgE food allergy suspected

Food-specific serum IgE testing
Serum tryptase, an enzyme released with histamine, if they have been activated in an anaphylactic reaction

46
Q

Type I - Skin Test Protocols

A

ID foods that may provoke IgE-mediated, food induced allergic reactions

Skin Puncture Test (SPT)
-scatches/needle pricks & drop of possible allergen solution
-simple outpatient
-NOT for children, pregnant women
-risk of triggering anaphylactic rxn, initiating new sensitivity

Patch Testing
- evaluation of contact food allergies, detection of contact dermatitis
- patch that has been soaked in the allergen is taped to skin for 24-72 hours

47
Q

Type I - Laboratory Evaluations

A

In vitro testing lacks risk of systemic reaction & doesn’t depend on skin reactivity

Serum allergen-specific IgE (sIgE) clinically significant

Quantitative determination of serum IgE antibodies necessary for differential diagnosis & for ID of allergens

48
Q

Type I - ImmunoCap (Lab Eval)

A

In vitro quantitative measurement of IgE in human serum

Tests for 650+ allergens, 70+ allergen components

Consider patient’s age, symptoms, home environment (pets, hobbies), residence location

49
Q

Type I - Chemiluminescent enzyme immunoassay (Lab Eval)

A

Third generation sIgE

Solid-phase (bead), two-step chemiluminescent enzyme immunoassay (EIA)

Allergens covalently lines to a soluble polymer-ligand matrix. Allows immunochemical rxns to occur in liquid phase for random access automation

50
Q

Type I - Treatment (big picture)

A

ID and eliminate allergens

Drug Therapy

Desensitization

51
Q

Type I - Drug Therapy Treatment

A

Epinephrine (adrenaline): immediate lifesaver

Antihistamines: act much slower, not useful in asthma. for allergies affecting skin, nose & mucous membranes

Specific receptor antagonists: block leukotrienes

Corticosteroids: topical, preventative

Other drugs: aim to block Th2 cytokine pathway or prevent IgE binding

52
Q

Type I - Desensitization Treatment

A

Immunotherapy

Improve allergy symptoms caused by SPECIFIC allergens

Associated with:
-downregulation of the sytokines produced by the Th2 cells
-upregulation of cytokines produced by Th1 cells
-induction of Treg cells

53
Q

Type II Hypersensitivity Reactions

A

Initiated by IgE-Antigen interaction

Target is fixed in the tissues, or on cell surface

3 mechanisms:

  1. Antibody-dependent, complement-mediated cytotoxic reactions (type 1)
  2. Antibody-dependent, complement-mediated cytotoxicity (type 2)
  3. Antireceptor antibodies
54
Q

Type II - Antibody-dependent, complement-mediated cytotoxic reactions (type 1)

A

IgG or IgM interaction with cell-bound antigen

Binding activates complement and destruction of the cell (cytolysis) to which antigen is bound

RBC, WBC & platelets can be lysed

Ex: immediate transfusion rxns, immune hemolytic anemia

55
Q

Type II - Antibody-dependent, complement-mediated cytotoxicity (type 2)

A

Depends on initial binding of specific Abs to target cell surface Ag

Ab coated cells lysed (by NK, macros) expressing Fc receptors

Fc recepetors on NK/macros attach to Fc portion of antibody coating the target cell

56
Q
A

Immunology & Serology (1 decks)

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