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micr 386 > module 09 section 01 (hypersensitivity reactions) > Flashcards

module 09 section 01 (hypersensitivity reactions) Flashcards

1
Q

define “hypersensitivity reaction”

what can result from this?

A
  • an innapropriately exaggerated immune response causing deleterious effects,
  • can result in significant tissue injury, serious disease, or death
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2
Q

when can a reaction be termed hypersensitive?

A

if it is either heightened or innapropriate in response to an antigen

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3
Q

what is the Gell-coombs classification system?

A

system that categorizes hypersensitivity reactions into 4 pathophysiological types

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4
Q

what are type I Gell-coombs hypersensitivity reactions?

A

specific antibody-mediated reaction

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5
Q

can type I Gell-coombs hypersensitivity reactions develop into anaphylactic responses?

A

yes

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6
Q

what is an anaphylactic response?

A

an allergic reaction that happens immediately and causes a life-threatening response involving the entire body

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7
Q

type I Gell-coombs hypersensitivity reactions occur due to the actions of:

A
  • IgE on mast cells binds an allergen, resulting in mast cell degranulation
  • C3a, C4a and C5a can also cause this type of reaction
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8
Q

recall that type I hypersensitivity reactions are the immediate response to an allergen. Most of these allergens are:

A

enzymes or glycoproteins

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9
Q

list 4 typcial allergens for type I hypersensitivity reactions

A

(1) glycoproteins Fel d 1 and Fel d 4 (common in cats)
(2) glycoprotein Fra a 1 (found in strawberries)
(3) enzyme hyaluronidase (found in honeybee venom)
(4) enzyme Der p 1 (found in feces of dust mites)

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10
Q

sensitization for type I hypersensitivity reactions may occur via:
(4)

A
  • oral ingestion
  • respiratory inhalation
  • skin absorbtion
  • intravenous (IV)
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11
Q

are type I hypersensitivity reactions T-cell dependent?

A

yes

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12
Q

explain the mechanism of type I hypersensitivity reactions

A

(1) APCs present the processed antigen to Th2 cells
- activated Th2 cells secrete IL-4 and IL-13 which induce naive B-cells to undergo class swithcing from IgM to IgG1 to IgE-secreting B-cells
(2) secreted IgE binds FcE (epsilon) receptor on mast cells
- allergen cross links two IgE antibodies bound to mast cells - resulting in mast cell degranulation
(3) mast cell degranulation results in release of mediators, including vasoactive amines - which elict biological effects within minutes

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13
Q

recall: during type I hypersensitivity reactions, activated mast cells release preformed molecules. What are they and what are the effects of these? (4)

A

(1) histamine - promotes vascular permeability and sm contraction
(2) eosinophil chemotactic factor - attracts eosinophils
(3) neutrophil chemotactic factor - attacts polymorphic nuclear cells such as mast cells, eosinophils, neutrophils
(4) proteases - increase mucus secretion and cause basement membrane damage (especially in the lungs)

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14
Q

do the preformed molecules secreted by mast cells cause early or late phase biological effects?

A

early phase

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15
Q

recall: during type I hypersensitivity reactions, activated mast cells synthesize new vasoactive amines. What are they and what are the effects of these? (4)

A

(1) platelet-activation factor - promotes aggregation of platelets, further mast cells degranulation and sm contraction
(2) leukotrienes - promote sm contraction and increase vascular permeability
(3) prostaglandins - promote sm contraction and vasodilation
(4) bradykinin - promotes sm contraction and vascular permeability (also involved in many pain pathways)

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16
Q

do the vasoactive amines secreted by mast cells cause early or late phase biological effects?

A

late phase

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17
Q

what are the overall effects of mediators (released by mast cells in type I hypersensitivity reactions) on bvs?

A
  • vasodilation and increased permeability = edema (excess of fluid collecting in cavities or tissues)
  • loss of fluid in the tissues can lead to anaphylactic shock
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18
Q

what are the overall effects of mediators (released by mast cells in type I hypersensitivity reactions) on skin?

A

vasodilation and edema = urticaria (hives) or eczema

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19
Q

what are the overall effects of mediators (released by mast cells in type I hypersensitivity reactions) on the nose/eyes?

A

vasodilation and increased permeability = edema, which can manifest as rhinitis and conjunctivitis

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20
Q

what are the clinical manifestations of type I hypersensitivity reactions? (3)

A

(1) atopy - predisposition to developing an allergic rxn
(2) asthma - condition where airways narrow and swell
(3) larygneal edema - characterized by swelling of the larynx

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21
Q

explain what atopy is in more detail.

A
  • it’s an exaggerated IgE-mediated immune response to an environmental allergen
  • it’s an inherited conditon with genetic assoication to HLA
  • can lead to asthma, atopic dermatitis and allergic rhinitis
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22
Q

what are two hallmarks of an asthmatic reaction?

A

inflammation and obstructed airways

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23
Q

what are key pathological features of asthma? (2)

A
  • increased recruitment of inflammatory cells (neutrophils and eosinophils)
  • increased recruitment of mast cells, leading to high levels of histamine
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24
Q

can asthma be atopic or non-atopic? why?

A

can be both:

  • atopic asthma (aka extrinstic asthma) = mediated by systemic IgE production in response to an allergen
  • non-atopic asthma (aka intrinsic asthma) = mediated by localized IgE production but doesn’t occur in response to an allergen
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25
Q

recall that laryngeal edema is life-threatening swelling of the larynx. What is this edema primarily characterized by? (1)

A
  • inspiratory stridor: high-pitched breathing sound that results from turbulent air flow in the larynx
  • present in both inspiration and expiration but louder/longer during inspiration
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26
Q

laryngeal edema is also associated with feelings of ____, due to ____?

A

anxiety - due to fear of not being able to breathe

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27
Q

what are additional symptoms of laryngeal edema? why?

A
  • intestinal cramps, vomiting, diarrhea, uterine contractions and cramps
  • due to contraction effects and constrictor effects (due to tissue swelling) of type I reactions
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28
Q

what is a common diagnostic test for type I hypersensitivity reactions? what does it measure? when do results occur?

A
  • skin prick tests - measure the presence of IgE antibodies against suspected and common allergens (same as for typical allergy)
  • positive reaction typically occurs within 1-20 minutes (manifests as small red swelling)
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29
Q

what are type II Gell-coombs hypersensitivity reactions?

A

these are mediated by an antibody directed against cell surface antigens
(i.e., involves antibody-mediated destruction of cells presenting allergens on their surface)

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30
Q

what is another term for type II Gell-coombs hypersensitivity reactions?

A

cytotoxic or costimulatory hypersensitivity

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31
Q

what results from type II Gell-coombs hypersensitivity reactions?

A

complement-mediated lysis OR cytotoxic action by NK cells

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32
Q

recall that for type II sensitivity reactions, antigen-specific antibodies bind to a cell surface antigen and destroy the cell. Cell death can occur by one of three mechanisms, what are they?

A

(1) complement-mediated cell lysis
(2) phagocytosis
(3) antibody-independent cell-mediated cytotoxicity (ADCC)

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33
Q

when are type II hypersensitivity reactions implicated in the clinical setting?

A

autoimmune diseases - where the target cells are the host’s own rbc’s

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34
Q

explain phagocytosis with respect to type II hypersensitivity reactions

A
  • antigen specific antibodies bind to the cell surface antigen via the Fab region
  • phagocytic cells have Fc receptors that that can bind to the Fc region of the antibody, cross-linking the antigen with phagocytic cells to enhance the process of phagocytosis
  • if complement’s activated, it promotes C3b on target cell surface to bind C3b recetpor on phagocytes for enhanced phagocytosis
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35
Q

explain ADCC with respect to type II hypersensitivity reactions

A
  • antigen specific antibody binds the antigen via the Fab region
  • cytotoxic cells have CD16 (FcyR) that binds to the Fc region of the antibody
  • corsslinking btwn target cell and cytotoxic cell promotes killing due to the release of hydrolytic and digestive enzymes from the cytotoxic cells to the surface of the target cells
  • i.e. antibody doesnt directly kill cell - mediates cell death by presenting antigen to cytotoxic cells
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36
Q

explain complement activation with respect to type II hypersensitivity reactions

A

Ag-Ab complex can acitvate the complement system which ultimately results in cell lysis through the MAC

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37
Q

list 4 clinical presenations of type II hypersensitivity reactions

A

(1) hemolytic anemia: conditon where immune system recognizes own rbcs as foreign
(2) bullous pemphigus: autoimmune skin disease resulting in formation of blisters (bullae) in space btwn epidermis and dermis
(3) transfusion rxns: adverse reactions to allogenic rbcs following tranfusion rxns
(4) Rh disease: hemolytic condition where maternal and fetal blood are not compatible

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38
Q

hemolytic anemia is a group of blood disorders characterized by: (3)

A

fatigue, dyspnea (shortness of breath) and pallor (pale)

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39
Q

what do the symptoms of hemolytic anemia result from?

A

lysis of rbcs due to antibodies against the individuals rbcs (which consequently decreases the # of o2 carrying rbcs in circualtion)

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40
Q

do immune cells in hemolytic anemia also attack allogenic rbcs that come from outside the individual (blood transfusion)?

A

yes

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41
Q

explain Rh disease

A

develops when maternal IgG antibody specific to the Rh-D allele crisses the placenta and destroys fetal rbcs by binding Rh-D and activating complement
i.e., if mom is RhD- and fetus is RhD+, her immune system creates anti-RhD antibodies that attack fetal RhD+

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42
Q

is Rh disease fatal? if so why? if not how is it treated?

A

can be - treated with intrauterine blood exchange transfusion

43
Q

how is hemolytic (Rh) disease prevented?

A

by the use of Rhogam anti-Rh antibodies

44
Q

what are type III Gell-coombs hypersensitivity reactions?

A

these are mediated by an Ab-Ag immune complex deposited on the tissue

45
Q

what results from type III Gell-coombs hypersensitivity reactions?

A

the immune complexes can activate complement and recruit innate immune cells (such as neutrophils) to cause tissue damage

46
Q

for type III hypersensitivity reactions, immune complexes can deposit in many tissues.
what is the result?

A

inflammatory disease of that particular tissue

47
Q

list 5 examples of type III hypersensitivity reactions and explain what they are

A

vasculitis (inflammation of bvs)

  • carditis/pneumonitis (inflammation of heart/lungs)
  • synovitis (inflammation of synovial membrane)
  • dermatitis (inflammation of the skin)
  • glomerulonephritis (inflammation of parts of the kidney)
48
Q

for type III hypersensitivity reactions, the type of immune complex formed depends on what? what does this have implications on?

A

the ratio of antigen:antibody present - has implications on the immunogenicity of the complex

49
Q

explain “optimum Ag:Ab ratio”

A
  • large complexes are formed and are easily detectable by phagocytes
  • i.e., the complexes are precipitate
50
Q

what is the outcome of an optimum Ag:Ab ratio in circulation?

A

the complexes are cleared by phagocytes

51
Q

explain “high Ag:Ab ratio”

A

smaller complexes are formed and are not easily detectable by phagocytes
-i.e., the complexes remain soluble

52
Q

what is the outcome of a high Ag:Ab ratio in circulation?

A

the complexes are deposited in the tissue

53
Q

explain the mechanism for type III hypersensitivity reactions

A

(1) Ag:Ab (immune) complexes deposit in tissue or bv wall
(2) immune complexes activate complement components and attract inflammatory cells
(3) vasoactive ammines (histamines) released by basophils increase vascularity of tissue
(4) prolonged complement activation results in tissue damage due to enzymes released by neutrophils

54
Q

recap question: what are type III hypersensitivity reactions due to ?

A

the accumulation of Ag:Ab complexes that have not been cleared by innate immune cells

55
Q

what is the Arthus reaction?

A

skin test that detects an excess of local antibodies

56
Q

what does the Arthus reaction involve (what is it)?

A

an in situ formation of immune complexes after intradermal injection with an antigen

57
Q

when does an Arthus reaction occur?

A

if a patient has previously been exposed to the antigen and has circulating antibody

58
Q

is Arthus reaction an immediate reaction?

A

no - generally develops over 6-12 hours if antibody levels are elevated in circulation

59
Q

list 3 clinical presenations of type III hypersensitivity reactions

A

(1) serum sickness: reaction to proteins in antiserum derived from non-human animals
(2) farmer’s lung: hypersensitivity pneumonitis
(3) rheumatoid arthritis: long-term autoimmune disorder involving both type II and III hypersensitivity

60
Q

what serum sickness-like reactions arise from?

A

the introduction of certain non-protein substances (e.g. penicillin) or following vaccine administration

61
Q

serum sickness-like reactions are aka as:

A

generalized arthus reactions

62
Q

during serum sickness reactions, the immune system reacts to foreign antiserum by:

A

producing specific antibodies and forming immune complexes, which then precipitate and enter bv walls to activate the complement cascade

63
Q

what does the complement cascade activated by serum sickness reactions result in?

A

hypocomplementemia (low C3 serum levels) and fatigue

64
Q

does the highest or lowest concentration of immune complexes result in serum sickness?

A

highest

65
Q

what is farmer’s lung induced by?

A

exposure to dust and mold spores found in hay

66
Q

when does farmer’s lung occur?

A

when inhaled antigens cause Ig-mediated immune complexes to form in the alveoli, which cause fluid, protein and cells to accumulate in the alveolar wall, compromising blood-gas exchange

67
Q

with farmer’s lung, after multple exposures does it take fewer or more antigens to elict a reaction?

A

fewer

68
Q

what does farmer’s lung result in? (3)

A

fever, chills, chest pain

69
Q

when do symptoms of farmer’s lung occur (how long after exposure) ?

A

6-8 hours after exposure

70
Q

explain rheumatoid arthritis

A

body’s immune system atacks the joints, resulting in inflammation and thickening of the joint capsule

71
Q

what is rheumatoid factor?

A

an IgG or IgM antibody that binds to IgG in the synovial joints, resulting in immune complexes that deposit in the joints, causing injury to the articular cartillage

72
Q

what are type IV Gell-coombs hypersensitivity reactions?

A

these involve a complex interaction of T-cells and monocytes/macrophages

73
Q

what is another term for type IV Gell-coombs hypersensitivity reactions? why?

A

delayed type hypersensitivity (DTH) reactions - because the reaction requires days to develop
(recall from mod 7)

74
Q

recall that type IV hypersensitivity reactions are cell-mediated, what are these reactions initiated by?

A

sensitized helper T-cells

75
Q

what is DTH (type IV) characterized by?

A

the recruitment of activated macrophages at the site of reaction

76
Q

type IV hypersensitivity reactions occur over ____ hours?

A

48-72

77
Q

recap question: DTH (type IV) is due to the effects of the humoral part of the immune system, true or false?

A

false - due to cell-mediated part of the immune system

78
Q

the initation of type IV responses involves what?

A

sensitization by an antigen -which involves uptake, processing and presentation of the antigen by local APCs

79
Q

with type IV reactions, the initial exposure of an allergen triggers what?

A

the production of a CD4+ Th1 cell response

80
Q

the type IV sensitization reaction evolves over a ___ period

A

1-2 week

81
Q

the effector phase of a classical DTH response is induced by what?

A

secondary exposure to a sensitizing agent

82
Q

what does the effector phase of a classical DTH response involve?

A
  • Th1 cells enter the site of antigen presentation, recognize the MHC:peptide class II complexes on APCs and release inflammatory cytokines (IL-1, TNF-B and IFN-y)
  • cytokines stimulate the expression of adhesion molecules on the endothelium to increase local bv permeability to allow macrophages/other cells to enter the site
  • prolonged inability to clear antigens can result in aggregation of cells
83
Q

what appears after 24 hours of the second exposure in a classical DTH response?

A

characteristic skin lesions

84
Q

when do the characteristic skin lesions reach their peak during a classical DTH response?

A

48-72 hours after the second epxosure

85
Q

how can DTH be diagnosed? what indicates a positive result?

A
  • using a skin test - a small amount of sensitizing antigen is injected under the skin
  • if a red slightly swollen firm lesion develops within 48-72 hours the test is positive
86
Q

what does a positive skin test result for DTH indicate?

A

the individual has a population of sensitized Th1 cells against the pre-exposed antigen

87
Q

does a positive skin test for DTH indicate an active infection? does it indicate if the individual has overcome an infection?

A

no to both

88
Q

for DTH, list the antigen and the respective consequences

A

antigen: proteins (like insect venom or tuberculin)
consequence: local skin swelling, erythema, induration, cellular infiltrate, dermatitis

89
Q

for contact type IV hypersensitivity, list the antigen and the respective consequences

A

antigen: haptens (poison ivy) or small metal ions (nickel)
consequence: local epidermal reaction, erythema, cellular infiltrate, intraepidermal abcesses

90
Q

for gluten-sensitive enteropathy (celiac), list the antigen and the respective consequences

A

antigen: giladen
consequence: villous atrophy in small bowel, malabsorption

91
Q

when can sensitization occur for contact dermatitis? why?

A
  • can occur if a reactive chemical compound binds to skin proteins
  • the modified skin proteins are then presented to the T-cells
92
Q

list 4 substances that could induce contact dermatitis

A

(1) poison ivy/oak
(2) nickel
(3) cosmetics/hairsprays/dyes
(4) formaldehyde

93
Q

what is the result of contact dermatitis?

A

these reactions can cause strong cell-mediated responses against skin cells, inducing blister-like lesions and rashes

94
Q

recap question: list the immune mediator for each type of hypersensitivity reaction (type I, II, III, and IV)

A

type I: IgE
type II: IgG or IgM
type III: immune complexes
type IV: T-cells

95
Q

recap question: what is the mechanism for type I hypersensitivity reactions?

A

Ag induces cross-linking of IgE mast cells with release of vasoactive mediators

96
Q

recap question: what is the mechanism for type II hypersensitivity reactions?

A

Ab directed against cell surface antigens mediates cell destruction via complement activation or ADCC

97
Q

recap question: what is the mechanism for type III hypersensitivity reactions?

A

Ag-Ab compleses deposited in various tissues induce complement activation and an ensuing inflammatory response mediated by massive infiltration of neutrophils

98
Q

recap question: what is the mechanism for type IV hypersensitivity reactions?

A

sensitized t-cells release inflammatory cytokines that activate amcrophages which mediate direct cellular damage

99
Q

recap question: what is the typical manifestation of type I hypersensitivity reactions?

A

includes systemic and localized anaphylaxis such as hives, food allergies and asthma

100
Q

recap question: what is the typical manifestation of type II hypersensitivity reactions?

A

includes blood transfusion reactions, hemolytic disease and autoimmune hemolytic anemia

101
Q

recap question: what is the typical manifestation of type III hypersensitivity reactions?

A

includes localized Arthus reactions and generalized reactions such as serum sickness and rheumatoid arthritis

102
Q

recap question: what is the typical manifestation of type IV hypersensitivity reactions?

A

includes contact dermatitis, tubercular lesion and gluten intolerance

103
Q

recap question: all of the following are clincial manifestations of type I hypersensitivity except:

(a) bronchial asthma
(b) laryngeal stridor
(c) childhood eczema
(d) poison ivy
(e) anaphylactic shock

A

(d) poison ivy (this is type IV)

104
Q

recap question: all of the following are true about type II hypersensitivity reactions except:

(a) IgA antibodies are the principal mediators of type II hypersensitivity reactions
(b) some drugs such as penicillin can absorb nonspecifically to proteins on rbcs and can be the target of drug-induced hemolytic anemia
(c) autoimmune anitbodies against structures like the glomerular basement membrane can be visualized woth fluorescent anti-IgG
(d) anitbodies against cell surface antigens can stimulate the cell
(e) antibody-coated target cells are more easily phagocytosed than targets without antibody, a phenomenon known as opsonization

A

(a) IgA antibodies are the principal mediators of type II hypersensitivity reactions

(actually IgM or IgG)

micr 386 (31 decks)

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