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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

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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

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32
Q

What type of hypersensitivity reaction is Urticaria and Angioedema

A

Type I & Type III

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33
Q

Predisposing factor for urticaria/angioedema in dogs

A

Atopic dermatitis

Autoantibodies to high affinity IgE receptors or IgE

Variably pruritic

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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

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35
Q

Horse breeds predisposed to urticardia

A

Arabian, Thoroughbred

(also more predisposed to AD)

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36
Q

Locations of horse urticaria on body

A

Neck
Trunk
Proximal extremities

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37
Q

Drugs implicated in urticaria in horses

A

Penicillin
Phenylbutazone

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38
Q

T or F: histamine levels correlate with cAD severity

A

FALSE

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39
Q

Which cytokines promote Th1 response

A

IL-12, IL-18

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

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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)

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41
Q

What percent of CAFR dogs have GI signs

A

10-30%

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42
Q

Major allergen for FAD

A

Cte f1

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43
Q

What type of hypersensitivity reaction is FAD

A

Initially local type IV (mononuclear)

Over time, replaced with type I → eosinophils

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44
Q

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

A

*Drug reactions
*EM (does not pit)

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45
Q

Causes of papular urticaria in horses

A

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

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46
Q

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

A

Vasculitis

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47
Q

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

A

Increased

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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
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49
Q

Which cytokine suppresses contact hypersensitivity reactions (type IV)?

A

IL-10

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50
Q

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

A

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

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

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51
Q

Which medications can cause contact hypersensitivity (5)

A

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

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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

76
Q

Anaphylotoxins Definition

A

Complement components: *Potent neutrophil chemoattractants.
*Promote smooth muscle contraction
*Increased vascular permeability

77
Q

Anaphylotoxins, name 2

A

C3a, C5a

78
Q

2 types of adverse drug reactions

A

*Type A: Dose-dependent
*Type B: Dose-independent

79
Q

What is a Type A adverse drug reaction

A

Dose dependent

Exaggerated, but normal response to medication. Result is due to the drug itself.

Common, predictable

Can happen in any individual

80
Q

What is a Type B drug reaction

A

Dose-independent

Bizarre reaction to drug. Not related to dose, normal pharmacological action of drug

These occur at therapeutic doses.

Uncommon, unpredictable

Often severe: high morbidity, mortality.

81
Q

4 mechanisms for drug allergy

A

1) Hapten hypothesis
2) Danger theory
3) Pharmacological interaction concept
4) Viral reactivation

82
Q

What is the Hapten Hypothesis, with regards to ADR

A

Hapten + Autologous protein (ie albumin, transferrin, integrins, selectins) = hapten-protein complex

Hapten-protein complex = immunogenic. Initiate adaptive immune response

83
Q

Example of a medication that is a hapten

A

Beta-lactam antibiotics (penicillin)

Bind to albumin via lysine residues

84
Q

Example of a medication that is a prohapten

A

Sulfamethoxazole. Metabolized by CYP2C6 to form sulfamethoxazole hydroxylamine. This can bind to autologous proteins w/cysteine residues –> antigenic

PRO hapten means it needs to be PROCESSED to become a hapten.

85
Q

What is the Danger Theory of ADR

A

*Danger signals (inflammation, oxidative stress, necrosis) trigger adaptive immune response

*Danger signal can be induced by:
-Drugs
-Diseases treated by the drug

This means the immune system is responding to the danger signal, rather than the foreignness of the drug itself

86
Q

What is the pharmacological interaction concept of ADR

A

*Off-target binding of the drug to receptors on T cells –> T cell activation
*Non-covalent binding with TCR or MHC on T cells

*Immediate + independent of drug processing or metabolism

87
Q

Which cells can be activated by haptens

A

B cells AND T cells

88
Q

Which cells can be activated by pharmacological interaction concept

A

T cells ONLY

89
Q

Drugs known to induce pharmacological interaction ADR

A

*Amoxicillin
*Sulfamethoxazole
*Ciprofloxacin
*Iohexol
*Lidocaine
*Allopurinol

90
Q

Diseases that are possibly a result of pharmcological interaction (ADR)

A

*Hepatotoxicity
*SJS/TEN
*MaculoPapular Exanthema (MPE)
*Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)

91
Q

What is Viral Reactivation of ADR

A

*Viral infections that INCREASE susceptibility to drug hypersensitivity (ie HIV, herpesvirus)

*Selective expansion of viral-specific CD8 T cells that CROSS REACT with the drug

92
Q

What is “Pseudo-allergy”

A

Non-immune-mediated activation of mast cells, eosinophils, basophils –> anaphylaxis

*Off-target binding of drugs to MRGPRX2, C3a R, C5aR on these cells to activate

*Do NOT use IgE or IgG Fc R

93
Q

Drugs that cause Pseudo-allergy (AD)

A

*Opiods
*NSAIDs
*Radiocontrast
*Vitamin K1
*Liposomal drugs

94
Q

T or F: Mast cells need to be SENSITIZED to a drug prior to onset of a “pseudo-allergic” anaphylaxis

A

FALSE. Can occur IMMEDIATELY after drug exposure

Do not need IgE, IgG4 to initiate this reaction. Use MRGPRX2 or anaphylotoxin receptors

95
Q

Which receptor do opiods bind to on Mast Cells, which can initiate anaphylaxis?

A

MRGPRX2

96
Q

Which medications can cause facial pruritus in cats?

A

*Methimazole
*Spironolactone
*Solensia

97
Q

What type of hypersensitivity reaction causes pruritus

A

Types 1 and 4

98
Q

What type of hypersensitivity reaction causes urticaria and angioedema

A

Type 1

99
Q

Where is edema in the skin that causes urticaria

A

Dermis

100
Q

Where is edema in the skin that causes angioedema

A

SQ

101
Q

Drugs that cause a Type 1 Hypersensitivity reaction

A

*Penicillin
*ampicillin
*tetracycline
*vitamin K
*Amitraz
*ivermectin, moxidectin
*sulfonamides, *radiocontrast agents
*chlorhexidine
*HyLyt® shampoo
*vaccinations

102
Q

What type of hypersensitivity reaction is a pemphigus foliaceus-like ADR

A

Type 2. Antibodies bind to DSC1.

103
Q

What is the difference between drug-induced and drug-triggered PF

A

Drug INDUCED: disease resolves once the drug is discontinued

Drug TRIGGERED: disease continues despite d/c of drug

104
Q

Which medications are associated with pemphigus foliaceus-like ADR

A

*Sulfonamides
*Cephalexin
*Oxacillin
*Clavamox
*Tetracycline
*Promeris
*Vectra 3D
*Certifect
*Nexgard
*NSAIDs

105
Q

What type of hypersensitivity reaction is vasculitis

A

Type 3- immune complexes

106
Q

Which drugs have been associated with vasculitis

A

*Itraconazole
*Meloxicam
*Piroxicam
*Sulfonamides
*Human albumin

107
Q

T or F: vasculitis is usually drug induced

A

False. Most often idiopathic

108
Q

What are fixed drug eruptions

A

Delayed reactions to a drug that affect 1+ body region.

Well circumscribed erythema –> edema –> bullae –> ulcerations.

Scrotum commonly affected.

Repeatable with re-exposure.

109
Q

What type of hypersensitivity reactions are fixed drug eruptions

A

Type 4

110
Q

What type of hypersensitivity reaction is EM, SJS, and TEN

A

Type 4

111
Q

Amount of epidermal detachment for SJS vs TEN

A

SJS <10%
TEN >30%

112
Q

What type of hypersensitivity reaction is lupus erythematous-like ADR

A

Type 3 (+/- vasculitis)

113
Q

What are systemic signs of a type 3 hypersensitivity reaction

A

*anemia
*thrombocytopenia
*polyarthropathy
*protein-losing nephropathy.

114
Q

What type of hypersensitivity reaction is Sweets Syndrome/ Neutrophilic dermatitis

A

Type 4

115
Q

What medications are associated with Sweets syndrome

A

NSAIDs, antibiotics (metronidazole, beta-lactams), vaccinations

116
Q

What type of hypersensitivity reaction is Superficial Suppurative Necrolytic Dermatitis (SSND)

A

Type IV. May be a CONTACT dermatitis

117
Q

What breed develops Superficial Suppurative Necrolytic Dermatitis (SSND)

A

Miniature Schnauzers

118
Q

What is the trigger for Superficial Suppurative Necrolytic Dermatitis (SSND)

A

Shampoos (natural OTC)

119
Q

What is the difference between Superficial Suppurative Necrolytic Dermatitis (SSND) and Post-Grooming Furunculosis

A

Post-grooming furunculosis is infectious, SSND is sterile

120
Q

Which non-skin clinical sign is common in CAEDE (Wells-like syndrome)

A

GI signs

121
Q

Which non-skin clinical sign is common in Sweets like syndrome

A

IMPA, lameness

122
Q

Which breeds are overrepresented for CAEDE

A

Mini schnauzer
English bulldog

123
Q

T or F: Drug allergy is dependent on the dose of the drug

A

FALSE. Its a Type B Adverse drug reaction (dose independent)

124
Q

What body region is usually associated with allergic contact dermatitis

A

Sparsely haired regions (contact!)

*Ventrum
*Face
*Ears
*Scrotum
*Perineum
*Ventral paws

125
Q

What is the different between allergic contact dermatitis (ACD) and irritant contact dermatitis (ICD)

A

ICD is a nonspecific reaction to an irritating, caustace substance. NO PRIOR EXPOSURE NEEDED. More directly cytotoxic to keratinocytes.

ACD requires prior exposure/ sensitization (type 4 hypersensitivity, with possible type 1 component?)

126
Q

Cause of SJS/TEN

A

Drugs

EM is NOT usually drug induced

127
Q

Pathomechanism for EM, SJS, TEN

A

Cytotoxic response by CD8 T cells and NK cells against keratinocytes
*Keratinocytes are primed for targetting by infectious agents or drugs.

*Apoptosis via:
1) EM: direct cellular cytotoxicity 2) SJS/TEN: soluble mediators of cell death

Soluble mediators include Fas ligand, granzymes, perforin and, most importantly, granulysin

128
Q

What is the possible animal equivalent to human EM (herpesviral

A

Feline herpes-associated EM

129
Q

Soluble mediators of cell death in SJS/TEN

A

Granulysin

Also:
*Fas ligand
*Granzymes
*Perforin

130
Q

Etiology of EM in animals

A

Idiopathic

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