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Immunology (Den 303) > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What is hypersensitivity?

A

Hypersensitivity is more commonly known as
allergy or autoimmunity
When immune system responds in an exaggerated or inappropriate way
resulting in harm
Usually occurs on second or subsequent
exposure to antigen
Hypersensitivity is a characteristic of the
individual (genetic susceptibility)

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2
Q

Hypersensitivity is a growing problem in the general population

A
  • large ↑ in children suffering from asthma in children children suffering suffering from asthma
  • large ↑ in allergic diseases among adults
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3
Q

Hypersensitivity is a growing problem in the dental surgery

A 
Dentists and nurses becoming increasingly
sensitised to:
„ Latex
„ Dental materials
Patients increasingly sensitised to:
Latex
Dental materials
Drugs used in the surgery
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4
Q

Acquired immunity consists of

A

Antibody Response (humoral humoral response)
Cell-mediated response
Both involved in Hypersensitivity reactions

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5
Q

Antibody responses

A 
Antigen uptake
Antigen processing
Antigen presentation
T cell help
B cells proliferate
-form plasma cells
-produce antibody
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6
Q

Properties of antibody responses

A 
Occur quickly
Are often systemic or widespread
This is because antibodies are soluble proteins that can reach most parts of proteins proteins that can reach most parts of the body quickly via:
„ Blood
„ Tissue fluids
„ Body secretions
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7
Q

Cell mediated immunity - 1st exposure to antigen

A

1st exposure to antigen
Antigen uptake
Antigen processing
Antigen presentation in the context of MHC
T cell binds and becomes activated
Activated T cell proliferates
To form many antigen specific memory T cells that patrol the body

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8
Q

Cell mediated immunity - 2nd exposure to antigen

A

T cell recognises antigen expressed on target cell in context of MHC
T cell responds by releasing cytokines and/or killing the target cell (apoptosis)

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9
Q

Cell mediated immunity directed mainly against

A

Cellular targets e.g.

  • tumour cells
  • virally transformed cells
  • foreign cells
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10
Q

Cellular immune responses tend to be

A
  • localised
  • slow to develop
  • slow to resolve
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11
Q

Failure of the immune system

A 
Fail to produce an adequate immune
response
„ Immunodeficiency
Produce an overactive, damaging response
„ Hypersensitivity Hypersensitivity - allergy
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12
Q

Hypersensitivity is divided into

A 
4 Types (I - IV)
Type I - Immediate/ anaphylaxis 
Type II - Cytotoxic
Type III - Immune complex
-type I, II, III antibody
mediated
Type IV - Delayed -cell mediated 
-examples of all 4 may occur in the
dental setting
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13
Q

Type I or immediate hypersensitivity

A

Acute hypersensitivity (anaphylaxis)
Rapid onset
IgE mediated
-people susceptible to type 1 hypersensitivity have high IgE levels

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14
Q

Type I hypersensitivity: allergen

A

Is an Ag that give rise to Type 1 Hypersensitivity

Most allergens are small (10 -40 kDa) proteins

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15
Q

Examples of type 1 hypersensitivity allergens

A 
Proteins
Der p 1&2 - dust mite faeces 
Fel d 1 - cats
Rat n1 - rats
Pollen - grass
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16
Q

Type I hypersensitivity cells

A

Mast cells and basophils

  • FCE receptors on surface
  • histamine granules inside cells
  • ->IgE binds to FcE receptor
  • ->on second exposure to antigen, antigen cross-links that Fc receptors
  • ->histamine released –> IL-5 –>eosinophils
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17
Q

Mast cell degranulation

A

Histamine and enzyme release (tryptase and chymase)

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18
Q

Histamine release causes

A 
Vascular dilation
↑ Vascular permeability i.e. oedema
Bronchospasm
Urticarial rash – nettle rash nettle rash
↑ nasal and lacrimal secretions
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19
Q

Type I hypersensitivity responses most commonly present as

A 
Hay fever
Asthma
Acute allergic responses:
Angiodema/ anaphylaxis e.g.
„ Latex allergy
„ Local anaesthetic allergy
„ Bee venom
„ Peanut
20
Q

Type I hypersensitivity responses most commonly present as

A 
Hay fever
Asthma
Acute allergic responses:
Angiodema/ anaphylaxis e.g.
„ Latex allergy
„ Local anaesthetic allergy
„ Bee venom
„ Peanut
21
Q

Diagnosis of type I hypersensitivity

A 
Wheel and Flare Skin Test
-apply small amount of allergen just
under skin using prick test.
-skin response is fast (5 min)
WHEEL caused by extravasation of
serum into skin due to histamine –
angio-odema.
FLARE (erythematous red patch) caused by axon reflex.
Late Phase (6 h+) due to leukocyte
infiltrate + more odema
22
Q

Type I hypersensitivity - Asthma

A

Allergen e.g. pollen leads to mast cell degranulation and mass histamine release

  • chemotactic factors (TNFalpha and IL-5) lead to release of substances in blood stream
  • spasmogens (histamine, leukotrienes, postaglandins) lead to bronchocontriction
  • cell infiltrate from blood stream leads to mucus hypersecretion, increased muscle and chronic bronchospasm
23
Q

Type I hypersensitivity - management

A

Adrenaline (epinephrine)
Antihistamines
Corticosteroids
Avoidance of allergen

24
Q

Type II hypersensitivity

A 
Antibody mediated hypersensitivity
-antibodies target cell surface self antigens (auto-antibodies)
Usually IgG or IgM
The antibodies induce
„ Cell damage
„ Inflammation
25
Type II hypersensitivity mechanism ***
Antibodies target self antigen (auto-antibodies) Autoantibodies activate either: -ADCC (antibody dependent cell cytotoxicity) - K cell, Neutrophil, Macrophage -->cell death and inflammation -complement -->complement activation results in inflammation and cell death (MAC)
26
Type II hypersensitivity responses are important in
``` Acute transplant rejection / blood transfusion Haemolytic Disease of the Newborn Autoimmune diseases e.g. „Pemphigus „ Pemphigoid ```
27
Type II hypersensitivity - Haemolytic Disease of the Newborn
1. First Pregnancy - RhD+ foetal blood enters RhD maternal circulation 2. Baby born BUT mother raises Ab to RhD 3. Second Pregnancy – If foetus is foetus is RhD+ mother + mother IgG crosses placenta and will destroy foetal erythrocytes 4. SO – preformed anti-RhD Ab given to Rh- mothers immediately after delivery of RHD+ infants.
28
Type II hypersensitivity - Pemphigus
Auto-antibodies against desmoglein-1&3 Ab prevents formation of gap junctions between epithelial cells Epithelial shedding – mainly mucosal
29
Type II hypersensitivity - pemphigoid
Auto-antibodies against hemidesmosomes Ab prevents binding of epithelium with dermis at basement membrane Epithelial shedding – skin and mucosal
30
Type III hypersensitivity
Immune complex-mediated hypersensitivity Immune complexes form between antigen and antibodies These complexes form in the serum -so different from type II - which are cell-based
31
Type III hypersensitivity - immune complexes may deposit in
Lining of BVs Glomeruli Lung
32
Type III hypersensitivity - here they induce
Complement activation Leukocyte binding Inflammation
33
Type III hypersensitivity as trigger for > vascular permeability
1. Immune complexes normally bind C’. This binds to CR1 on erythrocytes which are removed in the liver. 2. In inflammation, immune complexes bind to BVs where they act on platelets and Basophils 3. These are then activated and release vasoactive peptides (histamine) 4. This > vascular permeability
34
Type III hypersensitivity - deposition of immune complexes in BV walls
``` 1. Increased vascular permeability allows more immune complexes to be deposited 2. Induced platelet aggregation and C’ activation – (C5a & C3a - leukocyte chemotaxis) 3. Neutrophils attracted but cannot ingest complexes 4. The secrete lysosomal enzymes causing further tissue damage ```
35
Type III hypersensitivity - immune complex mediated hypersensitivity is important in
Immune complex mediated vasculitis e.g. - erythema multiforme - systemic luous erythematosus (SLE)
36
Type III hypersensitivity treatment
Immunosuppression with steroids
37
Type III Type III Hypersensitivity - Erythema Multiforme
``` Common skin condition mediated by deposition of immune complex in superficial microvasculature of skin and oral mucous membrane that usually follows infection or drug exposure. Often has classical "target lesion" appearance. ```
38
Type IV hypersensitivity
``` Cell-mediated immunity/ delayed type hypersensivity Mediated by T cells As response is cellular it is usually -slow to develop (12-48hrs) -slow to resolve -localised ```
39
Type IV hypersensitivity mechanism
``` Cell mediated hypersensitivity T cell recognises antigen expressed on another cell in context of MHC T cell responds by: -releasing cytokines -killing targets cell ```
40
Type IV hypersensitivity cell mediated immune responses are important in
Delayed type hypersensitivity responses Contact hypersensitivity - e.g. dermatitis Lichenoid reactions to amalgam fillings and other materials
41
Type IV hypersensitivity - contact dermatitis
Sensitisation 1. Ag gets into skin and is internalised by Langerhans cells - special APC in epidermis 2. These travel to lymph nodes and rpesent Ag to CD4+ T cells 3. These form memory CD4+ T cells
42
Type IV hypersensitivity steps (contact dermatitis)
1 Langerhans cells move from epidermis to dermis (Elicitation Phase) 2. They present Ag to memory CD4+ T cells 3. These are activated and secrete IFNγ. 4. This > expression of ICAM-1 and MHCII on Keratinocytes 5. Causes secretion of proinflammatory cytokines 6. More leukocytes attracted to site 7. Neutrophils arrive after 4 h, monocytes & T cells after monocytes and T cells after 12 h & secrete tissue damaging cytokines -tissue damage seen at post 12h (delayed) -tissue damage resolved if Ag removed
43
Type IV hypersensitivity tests
Skin patch testing | -samples applied to skin of back or arm for 72-96 hours
44
Denture acrylic allergy
Type IV reaciton to chemicals (Benzoyl peroxide + formaldehyde) that used to make dentures Red areas due to uncontrolled inflammation and tissue damage Epithelial thickening due to leukocytes, inflammation and proliferating keratinocytes trying to repair damage
45
Lichenoid reaction to amalgam
``` Type IV contact hypersensitivity response to mercury or amalgam Lesions closely associated with amalgam fillings Positive skin patch test response to mercury or amalgam Lesion resolves on removing filling ```

Immunology (Den 303) (4 decks)

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