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Immunology > Hypersensitivity Reactions > Flashcards

Hypersensitivity Reactions Flashcards

1
Q

Hypersensitivity reaction

A

Exaggerated inappropriate immune reactions

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2
Q

Type 1 hypersensitivity reaction

A

Interaction of antigen specific IgE and high affinity receptor for IgE on the mast cell surface results in cell degranulation

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3
Q

Antigen in type I hypersensitivity reaction

A

Allergen

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4
Q

The vasoactive mediators released in type I hypersensitivity give rise to what

A

Vasodilation and edema

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5
Q

Skin in type I hypersensitivity reaction

A

Itchy, swelling and redness

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6
Q

How fast from exposure to skin reaction in type I hypersensitivity

A

Minutes

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7
Q

The antigens involved in type I hypersensitivity are usually __ molecules derived from the environment with no apparent threat to the host organism

A

Inert

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8
Q

What else are type I hypersensitivity reactions called

A

Immediate hypersensitivity

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9
Q

Prausnitz-kustner reaction

A

Serum was separated from the blood of kustner who was allergic to fish
Injected into prausnitz
Then inject fish into prausnitz and have a positive reaction

*the skin factor was called reagin

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10
Q

Late hypersensitive immune reactions

A

Indirect result of mast cell degranulation as well as other mechanisms and have important pathogenic and therapeutic implications

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11
Q

What are the allergic (type I hypersensitivity reactions)

A 
Asthma
Allergic rhinitis
Urticaria
Eczema
Generalized anaphylaxis
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12
Q

Several allergens have protease activity and it is possible that this is an important property for what

A

Crossing skin or mucosal barriers

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13
Q

Features of allergens

A

In carrier particles (pollen grains) that are small and aerodynamic
Gives access to nasal and bronchial mucosa

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14
Q

The tendency of allergic reactions has strong ___ and this tendency has been termed __

A

Heritability

Atrophy

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15
Q

Atrophy

A

Presence of a type I hypersensitivity reaction to an allergen

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16
Q

How is atropy determined

A

Skin prick test

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17
Q

Risk of atropic disease when two, one or no parents have atropic trait

A

75, 50, 15

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18
Q

What genes are involved in inheritance of atopy

A

B chain of high affinity receptor for IgE(FcERI-B)
IL4
CD14
HLA-DR

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19
Q

What is the pathological hallmark of allergy

A

TH2 cells recognizing allergens , promoted by IL4

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20
Q

Immune responsiveness for atopy

A

IFNy production decreases, more TH1

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21
Q

Environment atopy

A

Hygiene hypothesis and early allergen exposure

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22
Q

In monozygotic identical twins concordance for asthma is 20%. What does this mean

A

Environmental factors

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23
Q

Cord blood of infants that are more likely to get atopy

A

High IgE low IFNy

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24
Q

Hygiene hypothesis

A

Overzealous attention to cleanliness in developed societies has resulted in favor of TH1 like environment, has resulted in the favoring of th2 response

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25
Q

Early response asthma

A

Sensitive to antihistamines
Recover in 1-2 hours
Fall in FEV1
IgE mast cells

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26
Q

Early response hay fever

A

1-2 hours
Minutes have sneezing, increased secretions and nasal congestion
Sensitive to antihistamines
Mast cell IgE

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27
Q

Late phase response asthma

A

4-6 hours later

Wheezing, hyperresponsiveness in the bronchi to challenge with allergen or histamine and reduced FEV

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28
Q

Hyperresponsiveness

A

Key clinical feature

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29
Q

Rhinitis late phase response

A

Nasal blockage and in skin allergy there is prolonged edema, swelling, and redness

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30
Q

Are late phase responses responsive to antihistamines

A

No

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31
Q

What do you treat late phase responses

A

Corticosteroids

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32
Q

Early or late phase the most debilitating of hypersensitivity

A

Late

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33
Q

Cells of late response

A

Seen at six hours
Eosinophils 2-3 days
T cells 1-2 days
Neutrophils 6 hours

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34
Q

Eosinophils are recruited by what

A

Eotaxin il5

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35
Q

TH2 cell secretes what when see an allergen

A

Il4-b cell

GM-CSF, IL9, 3, 4, 5, 13, eotaxin for eosinophils

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36
Q

What do B cells secrete in type 1 hypersensitivity

A

IgE

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37
Q

What does IgE bind to in type I

A

Mast cell

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38
Q

What do mast cells secrete

A

PAF, LTB4, chemokines-for neutrophils

Eosinophils attractants-for eosinophils

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39
Q

What do th2 cells secrete that attract eosinophils

A

Eotaxin, il3, 4, 5, 13, GMCSF

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40
Q

What are the mediators of type I

A

Eosinophils early

Neutrophils late

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41
Q

ELISPOT assay-detects T cell response

A

1.peripheral blood cells(lymphocytes, monocytes) mixed with soluble antigens
2. Culture this for 2 days
3. TH2 cell secreting IL4 in response to soluble antigen test
4. Remove cells and put onto antibody plate for il4
Il4 is captured by antibody
5. Cytokine is revealed by secondary antibody
5. Chemical reaction gives spots on dish.
IF SEE SPOTS POSITIVE IS NONE NEGATIVE

To see if allergy

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42
Q

Cytokines of IgE production

A

IL4, 9, 13

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43
Q

Mast cell cytokines

A

IL3, 4, 9

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44
Q

Eosinophils development cytokines

A

IL3, 5, 9

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45
Q

Diagnose type 1 hypersensitivity

A

History
Skin prick
Blood eosinophil

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46
Q

Treatment of type 1 hypersensitivity

A

Avoidance and drugs , desensitization

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47
Q

__ is the most common chronic disease of childhood affecting 5% of kids and 2% of adults

A

Asthma

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48
Q

What is asthma

A

Clinical syndrome of increased responsiveness of the bronchi to a variety of stimuli, with resultant airway narrowing, which reverses spontaneously or after drug therapy and is associated with cellular inflammation

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49
Q

Commonest allergensof asthma

A

House dust mites -dermatophagoides pteryonyssinus and d farinae (coat and fecal matter)
Grade pollen

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50
Q

What causes hyperresponsiveness

A

Prolonged damage to and inflammation of the respiratory epithelium

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51
Q

How does hyperresponsiveness manifest

A

Bronchioconstriction, inflammation and mucus production with airway plugging in response to innocuous triggers that include upper respiratory tract infections, exercise , cold air, smoke and paint fumes

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52
Q

Diagnose asthma

A 
History
Cough, wheeze, SOB
FEV1
Bronchial hyperresponsiveness 
Skin prick test 
Serum IgE levels
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53
Q

How do we test hyperresponsiveness

A

Histamine or methacholine to produce a fall in FEV1

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54
Q

Therapy for asthma

A

NOT ANTIHISTAMINES
Education
Inhaled short acting B2 adrenoceptor agonist (salbutamol) which relaxes bronchial smooth muscle

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55
Q

Severe asthma treat

A

Inhaled B2 agonist and corticosteroid

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56
Q

What can corticosteroids do

A

Suppress production of prostaglandin and leukotreines mediators is suppressed, inflammatory cell recruitment and migration inhibited, vasoconstriction leads to reduced cell and fluid leakage from the vasculature

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57
Q

Administration of cysteinyl leukotrienes

A

Reproduce asthma symptoms

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58
Q

Allergic rhinitis

A

Common

Hay fever

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59
Q

Symptoms of allergic rhinitis/hay fever

A

Nasal congestion, sneezing, often in paroxysms, itching and nasal and post nasal discharge

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60
Q

Allergic conjunctivitis

A

Frequently associated with allergic rhinitis

Itchy, gritty, excessive eye watering

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61
Q

Hyperresponsiveness in rhinitis

A

Smoke and paint fumes trigger

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62
Q

Why may have hearing loss with allergic rhinitis

A

Fluid

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63
Q

Diagnosis of allergic rhinitis

A

History
July June for grass and pollen , July august for mounds such as alternaria
Skin test mouth breathing, pale, blue edematous nasal turbinates, red line across the bridge of the nose caused by tendency to push the itchy nose upwards
Clear fluid in middle ear , serum IgE

64
Q

Treat allergic rhinitis

A 
Avoid
Antihistamines(prophalactively)
Nasal administer sodium cromoglicate (mast cell stabilizer) steroids, 
CysLT1blockade(can also give for asthma)
Topical steroids 
Desensitization
65
Q

Desensitization

A

Allergen immunotherapy
Allergy can be prophylatically inoculated against
Give course of subcutaneous injections of increasing doses of allergen extract

66
Q

IgG blocking antibodies from desensitization

A

During repeated exposure to desensitizing allergen, IgG class antibodies develop; these compete with the pathogenic IgG for allergen binding (especially IgG4) and/or prevention IgE allergen complexes blinding to mast cell high affinity IgE receptors

67
Q

Regulation changes of desensitization

A

Exposure to repeated desensitization allergen induces Treg cells which recognize allergen but invoke regulatory immune responses, dampening down migration, infiltration and inflammation

68
Q

Immune deviation change in desensitization

A

A shift away from TH2 to TH1 producing CD4 cells results in the generation of cytokines which inhibitory to IgE

69
Q

Atopic eczema

A

Dermatitis

70
Q

Hallmark of atopic eczema

A

Spongiosis

Accumulation of edema fluid within and between keratinocytes in the epidermis, giving a spongy appearance

71
Q

Symptoms of atopic eczema

A

Itching, dry red patches with occasional vessels overtaken by crusting
Cheeks, abdomen and limb are involved in infancy
Elbow, knee, wrist flexor surfaces in children
Prolonged scratching leads to development of discolored plaques with a leathery texture (lichenification)

72
Q

Diagnosis of. Atopic eczema

A

History
Skin test
IgE

73
Q

Pathogenesis atopic excema

A

TH2

IFNy

74
Q

Urticaria

A

Hives or nettle rash

Well circumcised itchy seals erupt over different areas of the body

75
Q

What causes urticaria

A

Localized vasodilation and edema occurring in the superficial dermis

76
Q

Angioedema

A

Edema forms deeper within the dermis giving larger areas of swollen tissue

77
Q

Why may angioedema arise in non allergic

A

Failure to inhibit complement cascade

78
Q

Urticaria and angioedema may be caused by IgE mediated type I hypersensitivieies in which histamine is one of the dominant pathogenic mediators

A

However in the majority of cases a cause for urticaria/angioedema I’d not found

79
Q

Urticaria associated with type 1 hypersensitivity in kids

A

Foodstuff

Eggs chocolate nuts berries insect stings drug reactions

80
Q

Diagnosis urticaria and angioedema

A

History

Skin test

81
Q

Anaphylaxis

A

Serious allergic reaction in rapid onset and may cause death

82
Q

Anaphylaxis IgE mediated

A

Yup, Igee, mast cells, basophils, specific antigen

83
Q

Anaphylaxis requires ___ by the allergen, followed by reexposure

A

Priming

84
Q

How provoke anaphylaxis

A

Allergen systemically absorbed
Nut, shellfish, dairy
Wasp, bees, yellow jackets, hornetsmedications, entisera(tetanus, diphtheria), dextran, latex, some antibiotics

85
Q

Symptoms anaphylaxis

A

Urticaria, cardiovascular collapse, laryngeal edema, airway obstruction , respiratory arrest leading to death

86
Q

Pathogenesis of anaphylaxis

A

Happens or molecules
Penicillin allergy-derivatives animal derived serum
Cephalosporins

87
Q

Peptide immunotherapy

A

Administer allergen peptide to induce treg

88
Q

Pathogenesis of anaphylaxis

A

Activation of mast cells as basophils with systemic release of some mediators

89
Q

Initial symptoms of anaphylaxis

A

Tingling, warmth itchiness

90
Q

Symptoms of anaphylaxis

A

Vasodilation edema, flush urticaria, angioedema, hypotension, bronchospasm, laryngeal edema, cardiac arrhythmia or infarction
Death in minutes

91
Q

How treat anaphylaxis

A

Adrenalin given intramuscular

To bronchodilator and vasoconstrict as well as inhibit mast cell

92
Q

What else is give to people with anaphylaxis

A

Oxygen
B adrenoceptor agonist such as salbutamol or theophylline followed by histamine H1 receptor antagonist and corticosteroids once acute phase is under control

93
Q

What causes prolonged hypotension after anaphylaxis

A

Vasodilation and fluid loss into tissue

94
Q

Type II hypersensitivity reactions

A

Initiated by the interaction between antibody and antigen but in these cases IgE is ot involved

95
Q

Target of antigen in type II

A

Fixed in tissue

96
Q

Consequence of antibody binding to cell surface antigen in type II

A

Complement is activated leading to cell lysis, mast cell activation and neutrophil recruitment
The antigen antibody complex recruits cell directly through Fc interactions . The arrival of cells with cytotoxic capability may lead to ADCC. In addition, there may be function loss and change of cell receptors

97
Q

Type II organ specific

A

Myasthenia gravis
Antiglomerular basement membrane glomerulonephrtis
Pemphigus vulgaris and bulbous pemphigus

98
Q

Type II autoimmune cytopenias

A

Haemolytic Angelia
Thrombocytopenia
Neutropenia

99
Q

Autoantibodies in type II

A

Stimulate through surface receptors to which they bind as happens in relation to autoantibodies that bind the thyroid stimulating hormone receptor in graces. Other autoantibodies block receptors-

100
Q

Type II hypersensitivity

A

Antigen antibody complexes form int he circulation and become deposited int the tissue, or they may actually form within tissues

101
Q

Arthur’s reaction

A

Type III inject
Antigen antibody complex forms
Erythematous lesion of 3-6 hours

102
Q

Two forms of hypersensitivity reaction

A

Complexes form in circulation and deposit

Form in tissues

103
Q

Factors influencing immune complex formation and damage

A

Charge and persistence
Charged molecule such as dna is more likely to be atttracted to and become attached to charged areas within the body such as the glomerular basement membrane
Persistend production of antigen will lead to a continuous supply of complexes overloading the remora always process and amplifying the opportunities for deposition and damage

104
Q

What antigen has persistence

A

Bacterial proteins continuously cast off of heart valves during infective endocarditis and similar proteins emanating from infected ventriculo-peritoneal shunts used to relieve high intracranial pressure

105
Q

The host response is important in determining the potential pathogenicity of immune complexes. The isotype of an antibody in a complex influences complement fixations and thus its solubility.

A

The integrity of the complement cascade is also an important determinant of whether complexes are solubilized and removed.

106
Q

Function of the classical pathway which requires C2 and C4, is critical in solubility antigen-antibody complexes

A

Genetically determined defiency of complement component C4 is found in approximately half of patients with SLE, one of the best examples of a disease in which immune complexes contribute to pathogenesis

107
Q

C2 defiency is much rarer, but almost all patients with this defect have an SLE like syndrome

A

Patients with SLE also have defective complement receptor expression on their red blood cell surface, further reducing their buffering capacity for immune complexes

108
Q

The tissues typically exposed to injury by immune complexes are the renal glomerulus and the joint synovial.

A

These are tissues in which plasma from the blood is ultrafiltration to form urine and synovial fluid, respectively.

109
Q

The hydrostatic pressure involved in such a process and the filtrate function of the glomerular basement membrane are likely to contribute to the retention and therefore, the pathogenicity of immune complexes

A

Ok

110
Q

=relative proportions of antigen and antibody

A

Complexes formed in antigen or antibody excess are less likely to deposit

111
Q

Impaired classical complement pathway function

A

Classical pathway has key role in solubizing and transporting complexes

112
Q

Isotype of antibody

A

Isotype dictates ability to fix complement

113
Q

Rate of complex formation

A

If the rate of formation excesses clearance , complex deposition is enhanced

114
Q

The variety of factors capable of influencing immune complex deposition is paralleled by the variety of diseases that are known to be immune complex mediated

A

There are three broad categories of immune complex disease

115
Q

In some,t he immune complexes formed int he circulation deposit in the tissues, leading directl to nephritis, synovitis or irities

A

In a second group, complex deposition is predominantly into the walls of medium or small sized arterioles and the vsacultitis that ensures is the cause or organ damage in the kidney, skin or other organs

116
Q

In others, particularly the type II lung disease, antigens and antibody combine within the tissue, removing an __ ___

A

Arthur’s reaction

117
Q

Deposited formed in tissue

A

Group a strep, DNA, bacterial antigens

118
Q

Group a strep

A

Post strep nephritis

Nephritis

119
Q

DNA

A

SLE

Nephritis serositis

120
Q

Bacterial antigens

A

SBE, shunt nephritis

Nephritis

121
Q

Vessel deposition

A

HBsAg, DNA, bacterial antigens

122
Q

HBsAg

A

Polyarteritis nodosa

Vasculitis

123
Q

DNA

A

SLE

Vasculitis

124
Q

Bacterial antigens

A

SBE

Vasculitis

125
Q

Forms in tissue

A

Various microbial and chemical antigens

126
Q

Various microbial and chemical antigens

A

EAA

Pneumonitis

127
Q

Extrinsic allergic alveolitis

A

Hypersensitivity pneumonitis , outcome of occupation and pastime related diseases

128
Q

What causes EAA

A

Overexposure over many months or years to excessive amounts of inhaled antigen leads to the generation of large concentrations of antibodies within the lung interstitium

129
Q

At a subsequent exposure, immune complex formation takes place on a massive scale in the alveoli

A

Typically, patients present 3-6 hours after loading mouldy hay, cleaning the pigeon loft or packing the sugar cane with symptoms of fever chills malaise and dyspnoea

130
Q

They may admit to milder episodes leading up tp the presenting illness

A

Symptoms usually remit within 24 hours but chronic exposure can lead to progressive SOB with cyanosis lung fibrosis and the development of cor pulmonary

131
Q

The diagnosis is made on the history and the demonstration of circulating IgG antibodies (called precipitins) to the provoking antigen

A

Farmers lung has declined in recent years with changes in farming practice but bird related pastimes remain popular hence bird fanciers disease is the commonest EAA

132
Q

Bird fanciers disease

A

Various avian antigens (pigeons, cockatoos, parakeets, budgerigars)

133
Q

Farmers lung

A

Fungal antigens in moldy hay

134
Q

Baggassosis (sugar cane workers disease

A

Thermoactinomyces sacchari antigen

135
Q

Paprika slicers lung

A

Mucor stolonifer is antigen

136
Q

The antigens involved are usually associated with small particles that promote transportation to the alveolar space

A

Although pathogenesis of the disease is classically type II there is probably a cell mediated component with the documented formation of granulomata

137
Q

It is not clear why some individuals develop disease whilst other do not , although HLA association have been described

A

Management is composed of exposure avoidance strategies and oral corticosteroids

138
Q

Type IV

A

Certain inflammatory conditions associated with tissue damage are characterized by cellular infiltrates, appearing 24 hours after challenge and composed int he main of a combination of lymphocytes and macrophages

139
Q

If antigen persists, inflammation becomes chronic and the macrophages in the lesion fuse to form giant cells and epithelium cells

A

What else are type IV called

140
Q

Delayed type hypersensitivity

A

Include reactions to mycobacteria and other organisms which the immune system has difficulty eliminating

141
Q

Reactions range from the local redness and swelling seen at the site of intradermal tests for Tb immunity in which an extract fromt he organism is injected to the caseating necrosis that occasionally results from hosts attempts to deal with mycobacterium TB

A

Granulomata which wall off the infective focus may also arise in response to other infections , such as parasitic worm infecstation of schistosomiasis

142
Q

Within the granulomata, there is extensive tissue damage, with fibrosis and calcification

A

This type of reaction can have serious clinical consequences if the site of damage is the lung, liver or bone

143
Q

If these circumstances, the immune system is caught between the repercussions of not dealing with the infection and the tissue damage that is caused by activated and differentiated macrophages

A

Dc and macrophages are activated by TH1 lymphocytes and release powerful hydrolytic enzymes and toxic oxygen metabolistes

144
Q

Other factors released within the infiltrate encourage fibrosis and angiogenesis

A

Another example of IV is that resulting in some individuals from exposure to contact with nickel jewelry , dichromate int he leather industry of p-phenyldiamine in sunscreen or hair dyes

145
Q

This reaction is confined to the skin and called ___ ___

A

Contact dermatitis

146
Q

Contact dermatitis

A

There is an eczematous reaction with erythema, edema, vesicles, and scaling

147
Q

How long does contact dermatitis to appear

A

48 hours

148
Q

Patch testing

A

Potential contact sensitized are placed in contact with the skin on the back for 48 hours

149
Q

Hapten

A

Substances incapable bc of small size to provoke antibodies without conjugation to carrier proteins
-contact dermatitis

150
Q

Metals of compounds in sensitizing agent becomes conjugated to tissue proteins

A

Contact dermatitis

Haptens

151
Q

How recreate type IV in vitro

A

Lymphocytes froma. Reactive individual are cultured with the provoking agent
Measurement of T cell proliferation or release of cytokines such as iFn y are a useful assessment of the degree of reactivity and of relevance to the pathogenic processes

152
Q

Antibody recruiting complement and cytotoxic cells with Fc receptors can cause tissue damage.

A

This is frequently an autoantibodies. The antigenic targets may be tissue fixed (typeII ) or incirculation (typeIII0

153
Q

In type II the target cell surface antigens may be altered self or exogenous cells

A

In type III the immune complex may be deposited in tissue of vessels (SLE) or may form in tissues (farmers lung)

154
Q

Hypersensitivity resulting from T cell reactions is usually delayed in onset

A

The central cells in their type IV hypersensitivity are the CD4 and the macrophages

155
Q

Granulomata are characteristic and contact dermatitis is a typical clinical example

A

Ok

Immunology (14 decks)

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