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Dealing with Threats > Immunology 2 - Hypersensitivity > Flashcards

Immunology 2 - Hypersensitivity Flashcards

1
Q

Define hypersensitivity

A

rxns exaggerated or inappropriate immunologic responses occurring in response to an antigen or allergen

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2
Q

What is a Type 1 hypersensitivity rxn? What antibodies is it mediated by? What is the major effector mechanism?

A

immediate-type allergic reactions
mediated by IgE antibodies
Mast cell activation is major effector mechanism

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3
Q

What hypersensitivity reaction is driven by antigen-specific IgG?

A

Type II and III

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4
Q

What is the main difference between Type II and III hypersensitivity?

A

Type II has effector mechanism being antibody-mediated whereas Type III has effector mechanisms is immune complex-mediated

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5
Q

Which type of hypersensitivity is delayed?

A

Type IV

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6
Q

Which hypersensitivity is driven by multiple cellular effectors including T cells and myeloid cells?

A

Type IV

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7
Q

Type ____ hypersensitivity is related to allergies, molds, and insect bites

A

I

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8
Q

Which hypersensitivity type has onset within minutes of antigen challenge?

A

Type I

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9
Q

Where are mast cells derived from?

A

hematopoietic cells in bone marrow

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10
Q

What do mast cells degranulate in response to?

A

crosslinking of surface IgE

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11
Q

What are some of the products of mast cells and what are their functions?

A

histamine - vasodilation and edema
Enzymes - destroy parasites
Leukotrienes and prostaglandins - inflammation
IL-4 - increased differentiation of plasma cells and production of IgE
iL-5 - recruits and activates eosinophils

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12
Q

What are 4 routes of allergen entry that leads to mast cell activation?

A

intravenous
subcutaneous
inhalation
ingestion

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13
Q

Once there is intravenous route of allergen entry, how do mast cells react?

A

widespread release of histamine which acts on blood vessels to increase permeability leading to hives or anaphylactic shock

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14
Q

How do mast cells react in the case of subcutaneous route of allergen entry?

A

Local release of histamine causes wheal-and-flare reaction.

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15
Q

How do mast cells react in the case of an inhalation route of allergen entry?

A

allergic rhinitis caused by increased mucus production and nasal irritation. Asthma can occur due to contraction of bronchial smooth muscle and increased mucus secretion

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16
Q

How do mast cells react in the case of intestinal epithelium route of allergen entry?

A

contraction of intestinal smooth muscle inducing vomiting and outflow of fluid into gut causing diarrhea. Antigen diffuses into blood vessels and is widely disseminated causing urticaria, anaphylaxis, or atopic eczema

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17
Q

While urticaria or hives occur in all animals, which species does is it most commonly seen in?

A

Dogs and horses

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18
Q

Urticaria is characteristic of which type of hypersensitivity? What is it most readily caused by?

A

Type I
caused by chemicals, drugs, insect bites/stings

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19
Q

What is atopic dermatitis? Which hypersensitivity is it related to? What can trigger this reaction?

A

Chronic pruritis/itching
Type I
Environmental triggers - pollen, mold, food allergens

20
Q

When looking at a patient with atopic dermatitis, what would your differential diagnosis be?

A

ectoparasites
infectious dermatitis
flea allergy
food allergy

21
Q

What is anaphylaxis?

A

Rare and life-threatening
dyspnea
v, d
collapse

22
Q

What would the treatment be for anaphylaxis - note that this is species-specific?

A

epinephrine - vasoconstriction
Diphenhydramine - antihistamine
Dexamethasone - reduce inflammation
Fluids - improve circulation
Terbutaline - bronchodilator

23
Q

What are 3 ways to test for Type I hypersensitivity?

A

Blood test - RAST (radio-allergosorbent test), blood sample evaluated for IgE to allergens

Intradermal test - inject small quantities of common allergens to evaluate for swelling/erythema

Diet testing for food allergies

24
Q

What is immunotherapy and what are the mechanisms of it?

A

repeated low dose exposure to allergens
Mechanisms - decreased mediator release from mast cells and basophils, increased number of Treg, fewer Th2, production of IL-10 and TGF-B which decreases igE production and suppresses mast cells and basophils

25
Q

What is immunotherapy not effective for?

A

food allergies

26
Q

How quick is the onset of Type II hypersensitivity?

A

within minutes or a few hours

27
Q

Autoimmune hemolytic anemia and drug allergies

A

Type II hypersensitivity

28
Q

What are blood types based on?

A

erythrocyte surface antigens (EAs)

29
Q

Why is it important to know blood types?

A

different species have variable numbers of different RBC surface antigens which vary in ability to induce an immune response

30
Q

What are the signs of a transfusion reaction?

A

fever
hemolysis - anemia, icterus, hemoglobinemia and hemoglobinuria, disseminated intravascular coagulation
allergic hives and itching

31
Q

What is neonatal isoerythrolysis in horses?

A

foal inherits RBC antigen that is foreign to mare but mare is sensitized to foal’s erythrocyte antigen during pregnancy, parturition, previous transfusions then the foal nurses and ingests colostrum containing antibodies to RBCs

32
Q

How quick is the onset of Type III hypersensitivity?

A

2-6 hours

33
Q

Which hypersensitivity reaction is associated with autoimmune diseases?

A

Type III

34
Q

Explain what happens in excess Type III hypersensitivity

A

Immune complexes form in the vessels and deposit in walls of small capillaries such as renal glomerulus, synovium of joints, uveal tract of eyes, epidermal basement membranes then complement fixation, vasculitis, and thrombosis and ischemic necrosis

35
Q

In type iII hypersensitivity, immune complexes deposit in the basement membrane of the skin. What are some common locations this will happen?

A

pinna
paws
nose
tail

36
Q

In type III hypersensitivity immune complex deposits in glomerular basement membrane what happens during this?

A

disrupts filtration barrier, loss of protein in urine causing hypoproteinemia, edema, effussions, proteinuria

37
Q

Which type hypersensitivity causes inflammation by 2-6 hours and peaks by 24-48 hours?

A

Type iV

38
Q

What is an example of type IV hypersensitivity?

A

poison ivy

39
Q

Explain the pathogenesis of atopic dermatitis vs allergic contact dermatitis

A

atopic dermatitis - Type I
allergic contact dermatitis - Type IV

40
Q

What are the clinical signs of atopic dermatitis vs allergic contact dermatitis?

A

Atopic dermatitis - hyperemia, urticaria, pruritis
Allergic contact dermatitis - hyperemia, vesiculation, alopecia, erythema

41
Q

What is the distribution of atopic dermatitis vs allergic contact dermatitis?

A

atopic dermatitis - face, nose, eyes, feet, perineum
allergic contact dermatitis - hairless areas, usually ventral abdomen and feet

42
Q

What are the major allergens of atopic dermatitis vs allergic contact dermatitis?

A

atopic dermatitis - food and pollen, fleas, inhaled allergens
allergic contact dermatitis - reactive chemicals, dyes in contact with skin

43
Q

Diagnosis of atopic dermatitis vs allergic contact dermatitis

A

atopic dermatitis - intradermal testing, immediate response
allergic contact dermatitis - delayed response on patch response

44
Q

Pathology of atopic dermatitis vs allergic contact dermatitis

A

atopic dermatitis - eosinophilic infiltration and edema
allergic contact dermatitis - mononuclear cell infiltration, vesiculation

45
Q

Treatment of atopic dermatitis vs allergic contact dermatitis

A

atopic dermatitis - steroids, antihistamines, and hyposensitization
allergic contact dermatitis - steroids

Dealing with Threats (27 decks)

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