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Hypersensitivity Reactions Flashcards

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1
Q

What is a hypersensitivity reaction?

A

An inappropriate immune response to non-infectious antigens that results in tissue damage and disease

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2
Q

What are the different types of hypersensitivity reactions?

A

Type 1: immediate hypersensitivity

Type 2: cytotoxic hypersensitivity

Type 3: serum sickness and Arthus reaction

Type 4: delayed-type hypersensitivity, contact dermatitis

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3
Q

What causes immediate hypersensitivity?

A

Immediate hypersensitivity results from exposure to allergens in the environment

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4
Q

Describe the immune response to immediate hypersensitivity

A

Host immune response is characterised by IgE antibodies bound to mast cells

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5
Q

What are the effects of IgE in response to immediate hypersensitivity?

A

IgE is specific to the allergen and cross-links to activate (mast) inflammatory cells to release mediators

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6
Q

Summarise the immune response to immediate hypersensitivity

A

Immune reactant: IgE

Antigen: soluble e.g. allergen

Effector Mechanism: Mast cell activation + degranulation

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7
Q

Give examples of immediate hypersensitivity

A

Allergic Rhinitis
Anaphylaxis
Eczema (skin)
Asthma (airways)

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8
Q

How can we induce a immediate hypersensitivity reaction?

A

A Type I hypersensitivity reaction can be induced via injection or scratching an allergen on skin

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9
Q

What are the effects of the immune response to an immediate hypersensitivity reaction?

A

Mast cells release inflammatory mediators causing leakage of plasma fluid into surrounding tissue = wheal (local oedema - bump on skin)

Vasodilatation = erythema = flare response

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10
Q

What is systemic anaphylaxis?

A

An exaggerated allergic response

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11
Q

How does systemic anaphylaxis occur?

A

Exposure to allergen causes rapid allergic reaction indicated by vasodilatation and fluid release = oedema

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12
Q

Why is systemic anaphylaxis dangerous?

A

Angioedema (face) can restrict the airways and lead to death

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13
Q

How is systemic anaphylaxis treated?

A

Require adrenaline on hand to treat reaction

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14
Q

What is cytotoxic hypersensitivity?

A

Hpersensitivity reactions in response to altered components of human cells

E.g. penicillin attaches to surface of RBCs which immune system flags as foreign

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15
Q

Outline a cytotoxic hypersensitivity reaction to penicillin

A
  1. Platelet / RBC covered in a drug (e.g. penicillin)
  2. Immune systems generates IgG response to drug
  3. IgG activates macrophages and complements = inflammation
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16
Q

What allergens cause cytotoxic hypersensitivity?

A

Some drug allergies

Penicillin

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17
Q

Describe the autoimmune cytotoxic hypersensitivity response

A

IgG antibodies disrupt normal functions of the receptor by either:

  • uncontrollable activation
  • blocking receptor function
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18
Q

Describe the normal release of Thyroxine and TSH

A

Pituitary releases TSH which acts on thyroid to release thyroxine

Thyroxine in blood causes -ve feedback = reduces TSH production

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19
Q

Outline how cytotoxic immune response can lead to Grave’s disease

A

In Thyrotoxicosis / Grave’s an immune response is generated against TSH receptors causing long term stimulation of TSHR

Release of thyroxine leads to excess levels with no -ve feedback

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20
Q

What are the consequences of autoimmune cytotoxic hypersensitivity reactions?

A

Grave’s disease
Myasthenia Gravis
Haemolytic disease (newborn)

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21
Q

Outline the ways Type II HS reactions cause myasthenia Gravis

A

Antibodies block / destroy nAchR on postsynaptic junctions

Antibodies block / destroy nAchR at junction between nerve and muscle

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22
Q

How does haemolytic disease of newborns occur?

A

Blood group antigen (Rhesus) causes immune response when:

  • RhD -ve mother
  • RhD +ve foetus

Occurs at time of delivery

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23
Q

How does baby normal dissociate from maternal circulation?

A

Normally embryonic chorion isolates foetus from maternal circulation

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24
Q

How does HDN affect maternal circulation?

A

During incompatibility, embryonic chorion disruption causes release of red cells in maternal circulation

Mother produces antibodies against RhD+ foetus - 1st child is safe

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25
What are the consequences of HDN on foetus during 2nd pregnancy
During 2nd pregnancy, antibodies previously stimulated can cross placenta and attack fetal RBCs with RhD resulting in death
26
What causes serum sickness (Type 3 HS)?
Presence of soluble antigen e.g. tetanus / diphtheria toxoids can cause serum sickness /arthus reaction
27
How do toxoids cause serum sickness / arthus reaction?
Large IgG response generated at site of injection causes immune complexes These activate cells around capillaries to produce inflammatory response with activated complement
28
How does arthus reaction arise?
Previous vaccination = elevated antibodies If vaccinated again = more immune complexes form High levels of antigens can cause localised inflammation
29
Outline the process of arthus reaction formation
1. Activate mast cells to release inflammatory mediators. 2. inflammatory cells invade site 3. Blood vessel permeability + blood flow increased. 4. Platelets accumulate = occlusion of small blood vessels, hemorrhage, and appearance of purpura
30
What causes serum sickness?
- large intravenous doses of soluble antigens (e.g. drugs) IgG antibodies produced form small immune complexes with antigen in excess immune complexes deposited in tissues e.g. blood vessel walls
31
What causes tissue damage during serum sickness?
Tissue damage is caused by complement activation and the subsequent inflammatory responses
32
How does antivenom cause serum sickness?
- large amounts of horse Ig - Vasculitis rash on skin - nephritis; immune complexes deposited in kidney ⇒ fatal
33
What causes farmers lung?
- hay mold inhaled into lungs | - localised inflammation; immune complexes
34
What are the consequences of farmer's lung?
Antigen inhaled (mold etc.) that forms immune complexes with alveoli Complexes stimulate an inflammatory response within lung resulting in fibrosis, granulation + inflammation
35
What causes hypersensitivity pneumonitis?
- Dusts, bacteria, fungi - Farmer’s lung - thermophilic actinomycosis - Pigeon breeder’s lung - protein derived from birds
36
Describe the histology of hypersensitivity pneumonitis
- Interstitial pneumonia - Non-caseating granulomas in 2/3rd patients - Interstitial fibrosis, honeycombing & obliterative bronchiolitis - Intra-alveolar infiltrate
37
What determines Type III HS reaction pathology?
Antigen dose and route of delivery determine the pathology observed in type III hypersensitivity reactions
38
What are the effects of Type III HS due to a High IV dose?
- Vasculitis: Blood vessel walls - Nephritis: renal glomeruli - Arthritis: joint spaces
39
What are the consequences of Type III HS in subcutaneous tissue?
Causes arthus reaction due to immune complexes forming in perivascular areas
40
What is the effect of an inhaled Type III HS allergen?
Farmer's lung leads to immune complexes forming in alveolar / capillary interfaces
41
What are the 2 types of delayed-type hypersensitivity?
- Th1 (intracellular bacteria) | - Th2 (worm infection / allergens)
42
Outline the Th1 mediated delayed-type reaction
1. Antigen activates Th1 cells 2. Cytokines (IFN-y + !L-12) released 3. Macrophages tstimulated o release cytokines / chemokines to recruit specific cells (granuloma) to inflammation site ~2-3 days for reaction
43
Name an antigen that induces a Th1 mediated delayed-type hypersensitivity response
Tuberculin
44
Describe the Th2 mediated delayed-type HS reaction
Cells produce IL-4 + IL-5 cytokines that recruit IgE and eosinophils to site of inflammation
45
Why does a delayed response occur in Type IV HS reactions?
T cell mediated Macrophages recruit cytokines / chemokines that recruit further immune cells to inflammation site - takes 24 -72 hrs
46
Give examples of Type IV HS disorders
Contact dermatitis Tuberculoid Leprosy Poison Ivy
47
Describe how a mantoux test is carried out
Subcutaneously inject tuberculin extract (bacilli) Wait ~2-3 days for reaction Ulceration shows sensitisation
48
What is tuberculoid leprosy?
Tuberculoid leprosy is a strong Th1 response in response to tuberculin bacilli presence resulting in typical granuloma
49
How does poison ivy cause a delayed-type hypersensitivity reaction?
People previously sensitised to pentadecacatechol (in poison ivy) can develop a strong contact dermatitis type reaction upon re-exposure
50
What is allergy?
Defined as “disease following a response by the immune system to an otherwise innocuous antigen"
51
What is the significance of IgE?
First line of defence against worms and allergies
52
How do IgE molecules create an immune response?
Binds FcεR1 receptor on mast cells | Coats mast cells to react when in the presence of antigen
53
Outline the simple allergy IgE reaction
1. First exposure to pollen 2. IL-4 drives B cells to produce IgE in response to pollen antigens 3. Pollen-specific IgE binds to mast cells
54
What causes allergic sensitisation?
Exposure to Allergen is critical, this includes: - Nature of the allergen - Dosage of Allergen (high vs. low) - Timing - Location of Priming Role of pro-allergic dendritic cells and cytokines Genetic predisposition to Allergy
55
How does the environment affect allergy cases?
Microbiome altered due to increased cleanliness - lack of diversity (aseptic environment) may cause sensitivity to more allergens
56
What are some common allergens?
House dust mite, pollens, cockroach etc
57
How are allergens named?
Allergens are named systematically: - After source organism and order discovered e. g. Der p1 comes from Dermatophagoides pteronyssinus Not all proteins are allergenic
58
Describe the genetics of allergy
Most allergies are polygenic - however interaction between genes and environment can determine development of allergies
59
What is the role of filaggrin?
Filaggrin links skin integrity and allergy
60
What is the consequence of defective filaggrin?
When defective atopic dermatitis is greater due to increased access for allergens
61
What factor determines the production of an allergic response?
Type of cell presenting the antigen initially can affect whether an allergic response is generated or not
62
What cells are switched to 'pro-allergic' due to antigen presentation?
APCs within skin called langerhan cells (epidermis) and dendritic cells (dermis)
63
What causes the switch of cells to pro-allergic?
Not Known but one Candidate Protein is TSLP This may switch DC to a ‘pro-allergic’ state (TSLP= Thymic stromal lymphopoietin)
64
What are the effector mechanisms of the allergic immune response?
1. First exposure to pollen 2. IL-4 drives B cells to produce IgE in response to pollen antigens 3. Pollen-specific IgE binds to mast cells 4. Second exposure to pollen 5. Acute release of mast-cell content causes allergic rhinitis (hay fever)
65
Describe the structure of resting mast cells
Resting mast cells contain dense granules full of inflammatory mediators (histamine, leukotrienes etc.)
66
How do activated mast cell structures change?
Activated mast cell releases all mediators revealing a different structure
67
What are the 2 phases of an allergic response?
Allergic responses have an early and late phase - Early mediated by mast cells - Late mediated by T cells
68
Describe the early allergic response
Early response = typical wheal & flare response (Type 1)
69
What is a late allergic response charcterised by?
High allergen dose - recruitment of other immune cells to site of inflammation causes later reaction - more diffuse oedema and inflammation
70
Describe the allergic reaction phases of the airways
Reduced FEV1 in airway inflammation ~30 mins after allergen inhalation Recruitment of inflammatory cells causes late response lasting longer ~24hrs
71
Outline primary sensitisation to allergens
> Mediated by B cells DC activation: present antigen to T cells (Th2) Activated Th2 produce IL-4, IL-13 which signal B cell IgE production IgE lines mast cells ready for secondary allergen exposure ⇒ acute allergic reaction
72
Describe the secondary allergen exposure
> Mediated by Th2 Recruitment of other immune cells e.g. eosinophils and mast cells mediate over a prolonged period of time ⇒ Chronic allergic reaction
73
What effector mediators are produced by mast cells during early phase?
- histamine - leukotrienes - prostaglandins
74
What effect does histamine have during early phase?
- increase vascular permeability | - smooth muscle contraction
75
Describe the effects of leukotriene release during early phase allergic reactions
- increase vascular permeability - smooth muscle contraction - mucus secretion
76
What are roles of prostaglandin release in response to early phase allergic reactions?
Acts as chemoattractants for T cells, eosinophils and basophils
77
What cytokines are released during late phase?
- IL-4 + IL-13 | - TNF-a
78
What are the effects of IL-4 and IL-13?
promote Th2 activity | Activate IgE
79
What is the effect of TNF-a during late phase allergic reaction?
promotes tissue inflammation
80
How does mast cell activation effect GI tract?
- inc. fluid secretion - inc. peristalsis Expulsion of contents (diarrhoea + vomiting)
81
What are the effects of mast cell activation on the airways?
- dec. diameter - inc. mucus secretion Congestion / blockage; wheezing, coughing, phlegm Swelling + mucus secretion in nasal passages
82
Describe the effects of mast cell activation on blood vessels
- inc. blood flow - inc. permeability Inc. fluid in tissues = more lymph to lymph nodes = more cells + proteins in tissues - increased effector response in tissues
83
Where are eosinophils found?
Located in the tissues and recruited to allergic reaction site Express FcεRI upon activation
84
What are the 2 effector functions of eosinophils?
1. Release toxic granule proteins + free radicals to kill microorganisms / parasites and cause tissue damage 2. Synthesise + release prostaglandins, leukotrienes and cytokines to amplify inflammatory response - activate epithelial cells + recruit leukocytes
85
What does ate phase allergic response depend upon?
Late-phase reaction is dependent on allergen dose Continued synthesis and release of inflammatory mediators

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