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EV ACVD Study > Hypersensitivity reactions > Flashcards

Hypersensitivity reactions Flashcards

1
Q

Which type of bacteria are MAC (membrane associated attack complexes) most effective?

A

Gram NEGATIVE bacteria

Limited peptidoglycan to fight against

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2
Q

Which Ig doesn’t have a hinge region, making it harder for proteases to process the antibody

A

IgM

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3
Q

Which is better at activating complement/opsonization, IgG or IgM?

A

IgM

But IgG is smallest antibody, so can go through vessels into tissue easier!

Because IgM is so large, it rarely enters tissue

IgM can act as a BCR when bound to B cells

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4
Q

Type I hypersensitivity antibody type

A

IgE

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5
Q

Type I hypersensitivity’s other name

A

Immediate hypersensitivity

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6
Q

Type II hypersensitivity’s other name

A

Cytotoxic hypersensitivity

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7
Q

Type II hypersensitivity’s antibody type

A

IgG, IgM

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8
Q

Diseases associated with Type II hypersensitivity (6)

A

1) Drug reactions
2) Pemphigus
3) Pemphigoid
4) IMHA
5) Transfusion reaction
6) Cryoglobulinemia

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9
Q

T or F: Type II hypersensitivities need complement to work

A

False. Many mechanisms use complement, but not complement-dependent

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10
Q

Mechanism of Type II hypersensitivity (5)

A

Antibody binds autoantigen → +/- activate complement

1) Neutrophil cytotoxicity
*Complement binds Ig → chemotaxis for neutrophil → releases proteases/ROS →cell damage
*PF

2) Opsonization + Phagocytosis
*Complement binds Ig→ chemotaxis for macrophage → eat complement and bound Ig + cell
*IMHA

3) MAC formation

4) Apoptotic response
*Complement binds Ig → chemotaxis for NK cell → release perforin, granzymes that poke holes in cell PM →lysis

5) Disruption of cell function
*NO COMPLEMENT
*Ig binds autoantigen RECEPTOR → 2 options
A) Ab binds R; Noncompetitive inhibition for R
*Myasthenia gravis
B) Ab binds R; activates R without its normal signal
*Hyperthyroidism

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11
Q

Type III hypersensitivity antibody type

A

IgG, IgM

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12
Q

Type III hypersensitivity’s other name

A

Immune-Complex mediated hypersensitivity

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13
Q

Diseases from Type III hypersensitivity (4)

A

1) SLE
2) DLE
3) Purpura hemorrhagica
4) Vasculitis

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14
Q

Type IV hypersensitivity antibody type

A

None → cell mediated

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15
Q

Type IV hypersensitivity’s other name

A

Late phase, cell mediated hypersensitivity

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16
Q

4 types of Type IV hypersensitivity (A-D)

A

A) Th1 → macrophage activation → contact dermatitis
B) Th2 → eosinophil activation → chronic allergy/asthma
C) CD8 → Cytotoxic → Contact dermatitis, EM, SJS
D) T cell → neutrophil activation

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17
Q

True or False: Atopic dogs typically have less IgA

A

True. Theory that increased IgE may be compensatory for lack of IgA

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18
Q

Functions of basophils (3)

A

1) IgE-mediated anaphylaxis
2) IgG-mediated anaphylaxis via FcgR1
3) Release PAF, which is more effective than histamine at increasing vascular permeability

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19
Q

PAF relative to histamine

A

PAF is more effective than histamine at increasing vascular permeability

PAF made by neutrophils

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20
Q

What can trigger cutaneous basophil hypersensitivity

A

Ticks, fleas, insects

*Characterized by marked basophil infiltrate and fibrin deposition
*Mediated by T cells and IgE/IgG
*Pathogenesis of IBH

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21
Q

Type I hypersensitivity can result 3 major mast cell product families. What are they?

A

Antibody cross-links to FcER1-bound IgE →FcER1 with intracellular tyrosine kinase dimerize and produce (4):

1) Phospholipase A → arachidonic acid → prostaglandins and leukotrienes
2) Protein kinase → (phospholipase C) → intranuclear → gene transcription → Cytokines
3) Protein kinase → filament formation → Granule exocytosis

*Phospholipase A for Arachidonic (A)
*Phospholipase C for Cytokine (C)

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22
Q

What organs normally clear immune complexes

A

Spleen, liver

If not→ deposited in tissue

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23
Q

External antigens that can trigger immune complexes (5)

A

1) Drug
*Dobie + sulfa drug
2) Self antigens
3) Foreign serums
*Monoclonal antibodies
4) Bacteria
5) Diet hypersensitivity

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24
Q

2 major forms of Type III hypersensitivity

A

1) Local reaction → “Arthus reaction”
*Localized necrotic vasculitis

2) Generalized reaction → “Serum sickness”
*Complement gets stuck in small vessel → activates complement → recruits neutrophil → release protease + ROS → damage to endothelial cells + vessel BMZ → leaks to surrounding tissue

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25
Q

Clinical signs of serum sickness (Type III hypersensitivity, generalized)

A

*Systemic inflammation
*Splenomegaly
*Urticaria
*Fever
*Arthralgia

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26
Q

Which cells are involved in Type IV hypersensitivity

A

T cells, NK cells

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27
Q

What type of hypersensitivity is allergic contact dermatitis

A

Type IV

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28
Q

What pathogens are type IV hypersensitivites designed for?

A

Intracellular pathogens
*Mycobacteria
*Fungi

Also tumor immunity, transplant rejection

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29
Q

Why is type IV hypersensitivity DELAYED?

A

Requires recruitment of cells, which takes time

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30
Q

Mechanism of Type IV hypersensitivity?

A

Small molecule binds to self-cell → acts as a “hapten” to make “self” seem antigenic → APC presents haptenized self-antigen on MHC cl II → binds naive Th cell

*If LC releases IL-12, induces Th1 immune response → IFNg →recruit macrophages →TNFa, IL-1 → ROS, lysozymes attack “self”

*If LC releases IL-6 induces Th17 → activates neutrophils → ROS, proteases → tissue damage

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31
Q

Which type of hypersensitivity reaction often forms a vesicular rash?

A

Type IV hypersensitivity

**CD8+ T cells kill the haptenized cells –> necrosis –> vesicles

31
Q

Diseases of type IV hypersensitivity (9)

A

1) Contact dermatitis
2) FAD
3) Bacterial hypersensitivity
4) Food
5) Tick bite
6) SJS
7) EM
8) TEN
9) Drug hypersensitivities

32
Q

What type of hypersensitivity reaction is Urticaria and Angioedema

A

Type I & Type III

33
Q

Predisposing factor for urticaria/angioedema in dogs

A

Atopic dermatitis

Autoantibodies to high affinity IgE receptors or IgE

Variably pruritic

34
Q

T or F: Horses usually get angioedema along with their urticaria

A

False

If they are going to get angioedema, they usually also have urticaria (1st urticaria, then angioedema)

Location of angioedema: muzzle, eyelid, ventrum, distal extremities

35
Q

Horse breeds predisposed to urticardia

A

Arabian, Thoroughbred

(also more predisposed to AD)

36
Q

Locations of horse urticaria on body

A

Neck
Trunk
Proximal extremities

37
Q

Drugs implicated in urticaria in horses

A

Penicillin
Phenylbutazone

38
Q

T or F: histamine levels correlate with cAD severity

A

FALSE

39
Q

Which cytokines promote Th1 response

A

IL-12, IL-18

(Goal of immunotherapy is to convert from Th2 to Th1 or Treg)

40
Q

For CAFR, what infectious agent can trigger a Th1 response in Peyer’s patches → IGNg → suppress Treg → food allergy development

A

Reoviruses (intestinal infx)

(shown for Th1 gluten intolerance in humans)

41
Q

What percent of CAFR dogs have GI signs

A

10-30%

42
Q

Major allergen for FAD

A

Cte f1

43
Q

What type of hypersensitivity reaction is FAD

A

Initially local type IV (mononuclear)

Over time, replaced with type I → eosinophils

44
Q

What are causes for gyrate (polycyclic; bizarre shapes) urticaria in horses

A

*Drug reactions
*EM (does not pit)

45
Q

Causes of papular urticaria in horses

A

*Stinging insects
*Folliculitis (esp if oozing, crusts, alopecia after)

46
Q

Causes of giant urticaria in horses (up to 40 cm!)

A

Vasculitis

47
Q

In dogs with cAD, are LC increased or decreased in epidermis

A

Increased

48
Q

What are other risk factors for cAD?

A
  • Month of birth → born during allergy season = ↑ risk
  • Maternal diet → fed non-commercial diet during lactation = ↓ risk
  • Use of probiotics → mixed results
49
Q

Which cytokine suppresses contact hypersensitivity reactions (type IV)?

A

IL-10

50
Q

Which plants can cause contact hypersensitivity (6 plants + 5 miscellaneous causes)

A

*Wandering Jew plant
* Spreading dayflower
*Doveweed
*Hippeastrum leaves and bulbs
* Asian jasmine
* Dandelion

Misc:
*Cedar wood
*Carpet deoderizer
*Cement
*Feathers
*Tobacco

51
Q

Which medications can cause contact hypersensitivity (5)

A

1) Neomycin
2) Propylene glycol
3) Bacitracin
4) Tetracaine, other “caines”
5) Benzoyl peroxide

52
Q

T or F: contact hypersensitivity is pruritic

A

True. Highly pruritic

53
Q

What type of hypersensitivity reactions are drug reactions

A

Type I
Type II
Type III
Type IV

54
Q

What is the secretory component relative to IgA

A

Secretory component is a peptide –> binds IgA dimers to form secretory IgA (SIgA) –> protects IgA from digestion by intestinal proteases

55
Q

Can IgA act as an opsonin

A

No

56
Q

Can IgA induce agglutination of antigens

A

Yes. Adheres to microbes to prevent entrance to body surfaces

57
Q

Which cell does IgD attach to

A

B cells
Acts as BCR
Rarely in blood stream

NOT in rabbits or cats (yet)

Destroyed with heat (like IgE)

58
Q

What is the function of IgD

A

regulates B cell responses
Activates basophils (IL-1, IL-4, B-cell activating factor production)

59
Q

How many constant regions does IgG have compared to IgE in its heavy chain

A

IgG: 3 (has 1 in its light chain also)
IgE: 4

60
Q

Which Ig can fix complement

A

IgM
IgG

61
Q

Which Ig can cross the placenta

A

IgG only

62
Q

What type of hypersensitivity reaction is mosquito bite hypersensitivity

A

Type I

63
Q

Although MOST of the time, demodectic mange is cleared by the innate immune response w/o need for adaptive immunity, which type of hypersensitivity can occur 2’ demodex

A

Type IV hypersensitivity
-CD8+ T cells are rare, but present on histopath
(mostly monocytes)

64
Q

What type of hypersensitivity is an arachnid (and insect) hypersensitivity

A

Type I (anaphylaxis)
Type III

65
Q

While we dont KNOW that canine eosinophilic F&F is a hypersensitivity rxn, if it IS, which hypersensitivity would it be?

A

Type I hypersensitivity (eos)

66
Q

What triggers canine eosinophilic F&F

A

Insect bites

BUT usually, insect bites get better over time, but this dz smolders

Nasal bridge = site most affected

67
Q

What type of hypersensitivity reaction is Staphylococcal hypersensitivity?

A

Type I (eosinophil, immediate)
Type III (immune complex, vasculitis, neutrophils)
Type IV (delayed, cell mediated)

Neutrophilic dermal vasculitis (type III)

68
Q

Breed predisposition to Malassezia hypersensitivity

A

Dogs:
*American Cocker Spaniel
*Australian Silky Terrier
*Basset Hound
*Boxer
*Dachshund
*English Poodle
*Setter
*Shih Tzu
*West Highland White Terrier

Cats:
*Devon Rex
*Sphynx

69
Q

Most common environmental fungal hypersensitivity

A

Alternaria

70
Q

What type of hypersensitivity is fungal hypersensitivity

A

Type I

71
Q

T or F: hypersensitivity to dermatophytes are reported

A

True

Can have IgE to trichophyton

72
Q

What type of hypersensitivity reaction is Purpura hemorrhagica

A

Type III- immune complexing

73
Q

Organisms that can trigger Purpura Hemorrhagic (5)

A

*Staphylococcus equi (or its vaccine)
*Corynebacterium pseudotuberculosis
*Rhodococcus equi
*Equine influenza virus
*Equine herpes virus type I

Occurs 2-4w post infection

74
Q

Clinical signs of purpura hemorrhagica

A

Urticaria, SC edema, Hemorrhage on mucosa + SC. Vasculitis
(febrile, depressed, anorexic).

75
Q

Other than horses, what other animal gets Purpura hemorrhagica

A

Pigs

EV ACVD Study (21 decks)

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