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Pathology and Immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What are the four types of hypersensitivity reactions?

A

Type I (Immediate), Type II (Cytotoxic), Type III (Immune Complex), Type IV (Delayed-Type).

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2
Q

Which hypersensitivity reactions are antibody-mediated?

A

Type I, Type II, and Type III.

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3
Q

Which hypersensitivity reaction is T-cell mediated?

A

Type IV (Delayed-Type Hypersensitivity).

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4
Q

Which immunoglobulin is primarily involved in Type I hypersensitivity?

A

IgE.

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5
Q

Which immunoglobulins are involved in Type II hypersensitivity?

A

IgG and IgM.

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6
Q

What are the two main mechanisms of Type II hypersensitivity?

A

Complement activation and antibody-dependent cellular cytotoxicity (ADCC).

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7
Q

What type of hypersensitivity is serum sickness?

A

Type III (Immune Complex-Mediated).

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8
Q

What is the key immune cell involved in Type IV hypersensitivity?

A

T cells (CD4+ and CD8+).

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9
Q

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

A

Type II targets cells directly, while Type III involves circulating immune complexes.

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10
Q

What is the typical time course of Type I hypersensitivity?

A

Seconds to minutes after exposure.

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11
Q

What is the major cytokine that promotes IgE production?

A

IL-4

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12
Q

What are the two phases of Type I hypersensitivity?

A

Sensitization and effector phase.

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13
Q

Which cells degranulate in Type I hypersensitivity?

A

Mast cells and basophils.

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14
Q

What are the main mediators released in Type I hypersensitivity?

A

Histamine, leukotrienes, prostaglandins.

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15
Q

What receptor does IgE bind to on mast cells?

A

FcεRI.

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16
Q

What is an example of a localized Type I hypersensitivity reaction?

A

Allergic rhinitis, asthma, hives (urticaria).

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17
Q

What is an example of a systemic Type I hypersensitivity reaction?

A

Anaphylaxis.

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18
Q

What is the major treatment for anaphylaxis?

A

Epinephrine.

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19
Q

What cytokines contribute to the late-phase reaction in Type I hypersensitivity?

A

IL-5, IL-13, TNF-α.

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20
Q

What are the three mechanisms of Type II hypersensitivity?

A

Complement activation, ADCC, opsonization.

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21
Q

What type of hypersensitivity is hemolytic disease of the newborn?

A

Type II.

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22
Q

What is the major antigen involved in hemolytic disease of the newborn?

A

Rh(D) antigen.

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23
Q

Which test is used to detect antibodies bound to RBCs in Type II hypersensitivity?

A

Direct Coombs test.

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24
Q

What is the indirect Coombs test used for?

A

Detects free antibodies in the serum.

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25
Q

What type of hypersensitivity is Myasthenia Gravis?

A

Type II (antibody blocks acetylcholine receptors).

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26
Q

What type of hypersensitivity is Graves’ disease?

A

Type II (antibody stimulates TSH receptors).

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27
Q

What is the treatment for Rh incompatibility in pregnancy?

A

Rho(D) immune globulin (RhoGAM).

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28
Q

What type of hypersensitivity is Goodpasture syndrome?

A

Type II (anti-GBM antibodies attack kidney and lungs).

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29
Q

What type of hypersensitivity is transfusion reaction?

A

Type II (antibodies target mismatched blood antigens).

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30
Q

What is the main mechanism of Type III hypersensitivity?

A

Immune complex deposition leading to inflammation.

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31
Q

What is an example of a systemic Type III reaction?

A

Serum sickness.

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32
Q

What is an example of a localized Type III reaction?

A

Arthus reaction.

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33
Q

What is the main complement component involved in Type III hypersensitivity?

A

C3b (opsonization) and C5a (inflammation).

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34
Q

Which immune cells mediate damage in Type III hypersensitivity?

A

Neutrophils.

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35
Q

What autoimmune disease is a classic example of Type III hypersensitivity?

A

Systemic lupus erythematosus (SLE).

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36
Q

What test detects immune complexes in Type III hypersensitivity?

A

Immunofluorescence staining.

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37
Q

What cytokine is key in immune complex formation?

A

IL-6.

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38
Q

What kind of hypersensitivity is post-streptococcal glomerulonephritis?

A

Type III.

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39
Q

What is the major risk of chronic immune complex deposition?

A

Tissue damage and fibrosis.

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40
Q

Which immune cells mediate Type IV hypersensitivity?

A

T cells (CD4+ and CD8+).

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41
Q

What is the time frame for Type IV hypersensitivity?

A

24-72 hours (delayed-type).

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42
Q

What are examples of Type IV hypersensitivity reactions?

A

Tuberculosis skin test, poison ivy, contact dermatitis.

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43
Q

Which type of T cells are involved in granuloma formation?

A

Th1 CD4+ T cells.

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44
Q

What is the key cytokine in Type IV hypersensitivity?

A

IFN-γ.

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45
Q

Which test is used to detect Type IV hypersensitivity to tuberculosis?

A

PPD skin test (Mantoux test).

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46
Q

What type of hypersensitivity is contact dermatitis?

A

Type IV.

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47
Q

What is a clinical example of chronic Type IV hypersensitivity?

A

Type 1 diabetes (CD8+ T-cell attack on beta cells).

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48
Q

What autoimmune disease involves Type IV hypersensitivity?

A

Multiple sclerosis.

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49
Q

Which hypersensitivity can cause a massive drop in blood pressure ?

A

Type 1

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50
Q

What can the drop in blood pressure in hypersensitivity 1 lead to?

A

Anaphylactic shock (can be fatal in minutes)

51
Q

What does the degranulation in type 1 hypersensitivity release?

A

Histamine
Prostaglandins
Leukotrienes

52
Q

What does histamine do?

A

Dilate and increases permeability of blood vessels (causing swelling and redness)
Increase mucous release (runny nose)
Smooth muscle contractions (bronchi)

53
Q

What does prostaglandin do?

A

Increase mucous release (runny nose)
Smooth muscle contractions (bronchi)

54
Q

What does leukotriene do?

A

Cause bronchial spasms

55
Q

How is type 1 hypersensitivity triggered in the effector phase?

A

Cross-linking of IgE bound to mast cells and basophils induced by antigens

56
Q

How many effector phases does type 1 hypersensitivity have?

A

2 (immediate and late-phase)

57
Q

What does the immediate reaction of hypersensitivity 1 cause?

A

Vasodialation
Vascular leakage
Smooth muscle spasms
Glandular secretions
Respiratory effects

58
Q

Which are the primary mediators in the early-phase of hypersensitivity 1

A

Histamine
Serotonin (effects histamine)
Heparin (anticoagulant)
Chemotactic factors recruit eosinophils and neutrophils

59
Q

Which are the primary mediators in the late-phase of hypersensitivity 1

A

Cytokines (IL-4, IL-5, IL-6, IL-13, TNF-ALPHA) secreted by mast cells
Eosinophils

60
Q

What is the role of Th2 in hypersensitivity 1

A

Induces class switching to IgE in B-cells

61
Q

What are the late-phase effects of hypersensitivity 1?

A

Tissue change
Mucosal epithelial cell damage
Infiltration of eosinophils, neutrophils, basophils, monocytes and CD4+ T cells
Leads to bronchial wall modification

62
Q

What plays a central role in hypersensitivity 1?

A

Excessive Th2 response -> stimulates IgE production

63
Q

What is the worst case scenario of hypersensitivity 1?

A

Systemic anaphylaxis
Leads to anaphylactic shock, is caused by mast cell degranulation all over body

64
Q

What are the 3 potentially fatal responses to systemic anaphylaxis due to hypersensitivity 1?

A

Laryngeal edema (fluid leaking, swelling)
Bronchiole constriction (suffocation)
Peripheral edema (shock from fluid loss)

65
Q

Why are allergies becoming more prevalent?

A

Due to:
Less early exposure to early infection factors
Pollution
Allergen levels risen due to climate change
Diet changes

66
Q

Which drug block histamine synthesis?

67
Q

Which immunological treatment can be used against hypersensitivity 1 and how does it work?

A

Hyposenitization: repeat injections of allergen can shift IgE to IgG production

68
Q

How does therapeutic anti-IgE work?

A

Bind mIgE on B cells

69
Q

4 pathologic features of hypersensitivity 2

A

Inflammation due to antibodies activating complement (produces enzymes and ROS)
Glomerulonephritis (inflammation of glomerulus)
Pemphigus (blisters caused by attack on desmosomal proteins in skin)
Abnormal cellular functions (Grave’s disease, myasthenia gravis, autoimmune pernicious anemia)

70
Q

Which antigen and antibodies does blood type A produce?

A

A antigen
Anti-B antibodies

71
Q

Which antigen and antibodies does blood type B produce?

A

B antigen
Anti-A antibodies

72
Q

Which antigen and antibodies does blood type AB produce

A

A and B antigens
No antibodies

73
Q

Which antigen and antibodies does blood type O produce?

A

No antigens
Anti-A and Anti-B antibodies

74
Q

Which antigen and antibodies does blood type Rh positive produce?

A

Rh antigen
No antibodies

75
Q

Which antigen and antibodies does blood type Rh negative produce?

A

No antigen
Rh antibodies

76
Q

What kind of cytotoxicity is in hemolytic transfusion?

A

Antibody mediated cytotoxicity (complement lysis and ADCC)

77
Q

3 most comment hypersensitivty 2 reactions involving red blood cells

A

Transfusion reaction
Hemolytic disease of the newborn
Autoimmune hemolytic anemic

78
Q

What does localized anaphylaxis (atopy) caused by hypersensitivity 1 cause?

A

Cutaneous anaphylaxis (wheal and flare)
Urticaria
Allergic rhinitis (hay fever)
Food allergies
Atopic dermatitis (allergic eczema)
Asthma (lower respiratory tract)

79
Q

How does antibody-dependent cytotoxicity work (ADCC) ?

A

NK and other leukocytes bind to antibody coated cells by FcRs and destroy them via toxic agents (cytokines and granule content)

80
Q

What is recognized to trigger ADCC?

A

Clustered IgGs (through low-affinity receptors (FcgammaRIIIA))

81
Q

In which type 2 hypersensitivity diseases is opsonization common? (hypersensitivity 2)

A

Extravascular hemolysis in transfusion reaction (not ABO mediated major reactions)
Most autoimmune hemolytic anemias

82
Q

When does intravascular hemolytic transfusion reaction (ABO) happen? (hypersensitivity 2)

A

Immediately after transfusion due to immediate activation of the complement system by IgM

83
Q

What does the activation of the complement system in hypersensitivity 2 lead to?

A

Inflammation through C3a and C5a
Cell lysis through MAC
Degradation of the received blood cells

84
Q

How doe you treat intravascular hemolytic transfusion reaction? (hypersensitivity 2)

A

Stop transfusion
Diuretics

85
Q

What organ failure can intravascular hemolytic transfusion reaction cause? (hypersensitivity 2)

A

Acute kidney failure

86
Q

What is intravascular hemolytic transfusion reaction caused by? (hypersensitivity 2)

A

ABO blood types

87
Q

What is extravascular hemolytic transfusion reaction caused by? (hypersensitivity 2)

88
Q

Where does extravascular hemolytic transfusion reaction take place? (hypersensitivity 2)

A

Inside lymphoid organs

89
Q

Where does intravascular hemolytic transfusion reaction take place? (hypersensitivity 2)

A

Inside circulation

90
Q

Which genes does the Rh system refer to?

A

3 genes on surface of red blood cells: C,D and E antigen

91
Q

Which of the genes of the Rh system is the most immunogenic?

92
Q

Which antibodies mainly go with the Rh system and which with the ABO system?

A

Rh -> IgG
ABO -> IgM

93
Q

Can IgG antibodies cross placenta?

94
Q

In hemolytic disease of newborns what happens? (hypersensitivity 2)

A

Rh negative mom makes antibodies agains Rh positive fetus

95
Q

What are the phases in hemolytic disease of newborns? (hypersensitivity 2)

A

1st pregnancy (sensitization phase/initial exposure): mom starts producing IgG anti-Rh antibodies in response to the fetus Rh antigen
2nd pregnancy (activation/effector phase): previously formed maternal IgG anti-Rh antibodies can cross the placenta and bind to Rh antigens on fetal RBC causing opsonization and destruction

96
Q

What can hemolytic disease of newborns lead to? (hypersensitivity 2)

A

Jaundice
Brain damage

97
Q

What does hypersensitivity reaction 3 involve reactions against?

A

Soluble antigens circulating in serum

98
Q

When do immune complexes become an issue? (hypersensitivity type 3)

A

When they deposit and accumulate in tissue due to antigen excess (outnumber antibodies), incomplete clearance and chronic conditions (cause persistent formation)

99
Q

What is hypersensitivity 3 mediated by?

A

Antibody-antigen immune complexes (deposited and settled in vessel walls, activate complement, cause inflammatory tissue damage)

100
Q

3 types of tissue damaged caused in sites of preferential immune-complex deposition

A

Vasculitis- vascular basement membranes
Glomerulonephritis- glomerular basement membrane
Arthritis- synovial membranes

101
Q

Different name for systemic immune complex disease (hypersensitivity type 3)

A

Serum sickness

102
Q

Who does serum sickness usually happen in? (hypersensitivity type 3)

A

people who receive large amounts of foreign serum

103
Q

3 steps of serum sickness reaction (hypersensitivity type 3)

A
  1. Formation of immune complexes
  2. Deposition of immune complexes (circulating immune complexes are deposited in vessels)
  3. Inflammation and tissue injury (complexes are deposited in tissues)
104
Q

What does serum sickness lead to? (hypersensitivity type 3)

A

Acute inflammatory reaction -> tissue injury
Complement activation

105
Q

What will high damage in vessels cause? (hypersensitivity type 3)

A

Lack of blood in specific regions -> ischemia and tissue necrosis (due to prolonged ischemic damage)

106
Q

Which hypersensitivity is Arthus reaction associated with?

107
Q

What did Arthus demonstrate?

A

That immune complex deposition triggers inflammation and tissue damage

108
Q

What happens if neutrophils can’t perform phagocytosis on immune complexes ? (hypersensitivity type 3)

A

They release granules, ROS and toxic enzymes and try to destroy the complex -> causing tissue damage

109
Q

Examples of Arthus-type reactions (hypersensitivity type 3)

A

Insect bite
Pneumonitis (farmer’s lung)

110
Q

Example of serum that can cause serum sickness (hypersensitivity type 3)

A

Anti-venom antibodies (body produces antibodies against the anti-venom antibodies in the serum)

110
Q

2 types of type 3 hypersensitivity reactions and examples of them

A

Generalized (Rheumatoid arthritis (endogenous antibody) and serum sickness (exogenous antibodies)
Localised (Arthus reaction)

111
Q

Describe the 1st (priming/sensitization) and 2nd (effector) contact in hypersensitivity 4

A

1: activation of Th cells -> memory and effector cells
2: sensitized Th1 cells secretes cytokines that activate macrophages CTL cells that mediate direct cellular damage

112
Q

Why is hypersensitivity 4 a delayed process?

A

Because it requires cell response (macrophages and T cells have to migrate to site and Th cells have to be developed)

113
Q

Which 2 cytokines are released by Th1 in hypersensitivity 4?

A

IFN-GAMMA (macrophage activation)
IL-2 (stimulates CD(+ proliferation and NK activation)

114
Q

How long is hypersensitivity 4 usually delayed?

A

1 or more days

115
Q

Where is hypersensitivity often displayed?

A

On skin (itching, redness, swelling, pain)

116
Q

Can hypersensitivity 4 lead to anaphylactic shock?

117
Q

2 types of type 4 hypersensitivity reactions

A

Delayed type hypersensitivity
Contact hyper sensitivity

118
Q

What is the antigen in delayed type hypersensitivity? (type 4 hypersensitivity)

A

Proteins: insect venom, microbial infection

119
Q

What is the antigen in contact hypersensitivity? (type 4 hypersensitivity)

A

Haptens: pentadecatechol (poison ivy)
Small metal ions: nickel chromate

120
Q

Main differences between type 4 hypersensitivity and the other types

A

Delayed
Cell mediated (no antibodies)
Localized at the site of antigen encounter

121
Q

What is the main mechanism of tissue injury in some T cell mediated disorders?

A

Killing by CTL

122
Q

What is chronic delayed-type hypersensitivity? (type 4 hypersensitivity)

A

Th1 response to an infection and activated macrophages but fails to eliminate the phagocytosed microbes

Pathology and Immunology (10 decks)

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