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RUSVM Immunology 2016 > Exam 2: Hypersensitivity > Flashcards

Exam 2: Hypersensitivity Flashcards

1
Q

Asthma or allergies is another name for:

A

Type 1 Hypersensitivity

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2
Q

Atopic

A

effected animals with type 1 hypersensitivity

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3
Q

Atopy involves:

A

excessive amount of IgE and exaggerated Th2 response

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4
Q

Antigens for Type 1 Hypersensitivity include:

A

disruption of intestinal microflora, parasite worms, food, animals, insect venom, etc.

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5
Q

Type 1 Hypersenstivity involves which antibody?

A

Ig E

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6
Q

What is IL-4 involvement in Type 1 hypersensitivity?

A

IL-4 is overproduced, increasing Th2 activation and B cell stimulation

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7
Q

What is Fc(epsilon)R?

A

is the receptor for IgE that has a high affinity and irreversible binding

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8
Q

Fc(Epsilon)RI is present on which cells?

A

mast cells, basophils, neutrophils, esoinophls, macrophages and DCs

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9
Q

Fc(epsilon)RII is present on which cells?

A

B cells, Nk cells, macrophages, DCs, eosinophils and platelets

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10
Q

What is the mechanism for Type 1 hypersensitivity reactions?

A
  1. IgE on mast cell binds antigen (requires 2 antibodies)

2. Degranulation of mast cell releases vasoactive molecules, enzymes, cytokines, chemotactic molecules

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11
Q

Degranulation of mast cells causes?

A

acute inflammation and systemic effects

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12
Q

Antigen binding IgE, with FceRI causes

A

Mast cell degranulation

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13
Q

Antigenbinding IgE, with FceRII causes

A

B cell down regulation

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14
Q

Complement Receptor 2 binding to FceR3 causes

A

B cell stimulation and survival

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15
Q

Mast cells are located

A

in the intestine, skin, airways and around nerves

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16
Q

Mast cells release?

A

proinflammatory mediators

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17
Q

Mast cells release what in connective tissue or skin?

A

Histamine and heparin

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18
Q

Mast cells last in connective tissue/skin for how long?

A

more than 6 months

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19
Q

Mast cells last in intestines and lungs have a life span of?

A

less than 40 days

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20
Q

What is required for mast cell reaction?

A

Antigen binding IgE with two IgE receptors

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21
Q

Within seconds what soluble mediators are released from degranulating mast cells?

A

via exoctyosis:

histamine, serotonin, tryptase, proteases proteoglycans

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22
Q

Within minutes what soluble mediators are released from degranulating mast cells?

A

via eicosanoid synthesis and secretion:

Leukotrienes, prostaglandins, platelet activating factor

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23
Q

Within Hours what soluble mediators are released from degranulating mast cells?

A

via cytokine synthesis and secretion:

Il-4,-4,-4,-13 and TFN alpa, MIP-1alpha

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24
Q

IL-33 stimulates mast cell

A

degranulation in presence of IgE

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25
Q

IL-33 stimulates Basophil

A

differentiation in bone marrow

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26
Q

IL-33 stimulates Eosinophils

A

as terminal effector cells of teh allergic response

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27
Q

Mast cells degranulation in the GI tract causes

A

Fluid secretion, peristalsis that leads to emptying of the GI tract via diarrhea and vomiting

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28
Q

Mast cells degranulation in the Respiratory Tract causes

A

mucus secretion, bronchoconstriction leadign to difficulty breathing

29
Q

Mast cells degranulation in the Blood Vessels causes

A

increased vascular permeability that leads to the movement of fluids, proteins, and cells out of blood vessels into inflamed tissue

30
Q

What process enhances mast cell degranulation?

A

Stimulation of alpha adrenoreceptors and block Beta adrenoreceptors

31
Q

What chemicals stimulate alpha adrenoreceptors?

A

Norepinehrine and phenylephrine

32
Q

What chemicals block beta adrenoreceptors?

A

propranolol

33
Q

What processes inhibit mast cell degranulation?

A

Blocking alpha adrenoreceptors and stimulation of beta adrenoreceptors

34
Q

what chemicals stimulate beta adrenoreceptors?

A

Isoproterenol, epinephrine, salbutamol

35
Q

Examples of Clinical Type 1 hypersensitivity:

A

allergic anaphylaxis, hygiene hypothesis, milk, food alergy, allergy to vaccines and drugs, parsites, inhalant dermatitis, atopic dermatitis (molds, trees, weeds)

36
Q

How to diagnose Type 1 Hypersensitivity?

A

intradermal skin testing, passive cutaneus anaphylaxis (PCA) and Measuring IgE

37
Q

How to treat Type 1 Hypersensitivity?

A

avoid exposure to teh allergen, corticosteroids, antihistamines or B stimulants or alpha antagonists

38
Q

Type 2 Hypersensitivity involves which antigens?

A

RBC antigens

39
Q

What initiates RBC destruction during transfusions?

A

antibodies and complement

40
Q

First stage clinical signs of nonmatching blood types

A

Hypotension, brady cardia, apnea

41
Q

Second Stage clinical signs of nonmatching blood types

A

Hypertension, cardiac arrhythmia, increased heart rate and increased respiratory rate

42
Q

Destruction of RBC because of foreign antigen is mediated by:

A

IgM

43
Q

What is Hemolytic disease of the new born (HDN)?

A

appears in foals, whose blood antigens don’t match mares (pos v neg)

44
Q

What are causes of Type 2 Hypersensitivity?

A

Drugs, infectious diseases (Equine infectious anemai, anaplasmosis, Trypanosomiasis, babesios- severeanemia)

45
Q

Antigen and antibody combine with complement to form

A

The immune complex (IC)

46
Q

The immune complex initiates what kind of hypersensitivity?

A

Type 3

47
Q

Local Type 3 Sensitivity

A

Immune complexes form within the tissue

48
Q

Generalized type 3 sensitivity

A

immune complexes are formed within the blood stream and are deposited in glomeruli in the kidney

49
Q

Arthus Reaction causes

A

red edematous, local hemorrhage, thrombosis and tissue destruction

50
Q

What is the arthus reaction?

A

it is inflammation of the injection site after injection of antibodies

51
Q

Examples of Type 3 hypersensitivity

A

blue eye, hypersensitivity pneumonitis, stahylococcal hypersensitivity

52
Q

How are immune complexes removed in primates?

A

via RBCs

53
Q

How are immune complexes removed in nonprimates?

A

via platelets

54
Q

What cells eliminate immune complexes?

A

Kupffer cells (liver macrophages)

55
Q

Generalized type 3 hypersensitivity reactions are also referred to as

A

serum sickness

56
Q

Type 3 hypersensitivity causes what clinical signs?

A

arteritis, arthritis and glomerulonephritis

57
Q

Type 1 glomerulonephritis occurs where?

A

in mesangial and subendothelial regions

58
Q

Type 3 glomerulonephritis occurs where?

A

in the suepithelial region

59
Q

Type 2 Hypersensitivity occurs where?

A

glomerular basement membrane

60
Q

Glomerulonephritis is a causes of

A

Chronic diseases, such as Equine infectious anemia, infectious canine hepatitis, african swine fever, lympe disease yometra and tumors

61
Q

Type 4 hypersensitivity is also referred to as:

A

Delayed Type Hypersensitivity

62
Q

tuberculin

A

inflammatory response in teh skin of an animal infected with tuberculosis following intradermal injectino of tuberculin

63
Q

Type 4 hypersensitivity involves which part of the adaptive immune system?

A

Cellular Immune response (T cells)

64
Q

Type 1-3 Hypersensitivity involves which part of teh adaptive immune system?

A

Humoral immune response (b cells n antibodies)

65
Q

animal shows what signs of Type 4 hypersensitivity

A

a reaction at injection site

66
Q

Tuberculin has false positives because

A

cross reactions with other bacteria, animals with advanced tuberculosis or tested at early stages of infection

67
Q

What are examples of tuberculin tests

A

single intradermal, comparative, short thermal and stormont

68
Q

allergic contact dermatitis occurs

A

if reactive chemicals are painted onto skin, bind skin proteins and resulting complex are processed by langerhans cells in the dermis

69
Q

Examples of Type 4 hypersensitivity/ allergic contact dermatitis reaction

A

poison ivy, haptens to chrome/nickel or resin/latex

RUSVM Immunology 2016 (14 decks)

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