Hypersensitivity Flashcards by Naina K

Another name for hypersensitivity?

Allergy/autoimmunity

How well did you know this?

Not at all

Perfectly

Increased sensitivity in dental patients to…

Latex
Dental materials
Drugs used in the surgery

How well did you know this?

Not at all

Perfectly

Immune system consists of

Two types?

Innate immune system

Adaptive/acquired immune system

How well did you know this?

Not at all

Perfectly

Acquired immunity consists of

Two types of response?

Antibody response

Cell-mediated response

How well did you know this?

Not at all

Perfectly

Hypersensitivity involves ………. and …….. responses

Antibody

Cell-mediated

How well did you know this?

Not at all

Perfectly

Antibody response creation steps

APC take up antigens
APC processes and displaces antigen on surface
B-cell attaches to displayed antigen
Th2 cell (helper) releases cytokines to encourage proliferation
B-cells proliferate and produce/release plasma cells and produce antibodies

How well did you know this?

Not at all

Perfectly

Features of antibody response

Effect and speed

Rapid

Systemic/widespread

How well did you know this?

Not at all

Perfectly

Why is antibody response widespread?

Adaptations of molecules

They are soluble proteins and can reach most parts of body quickly via blood, tissue fluids and body secretions

How well did you know this?

Not at all

Perfectly

Cell mediated immunity: 1st exposure process

Antigen presentation via MHC protein
Complementary T cell attaches via receptor
T cell becomes activated
Activated T cell proliferates and forms antigen specific memory T cells which patrol body

How well did you know this?

Not at all

Perfectly

Cell mediated immunity: 2nd exposure process

Memory T-cell recognises antigen expressed on target cell
T cells release cytokines, kill target cell via apoptosis

How well did you know this?

Not at all

Perfectly

Cell Mediated Immune Targets (3x)

Cellular targets:

immune cells
virally transformed cells
foreign cells

How well did you know this?

Not at all

Perfectly

Characteristics of cellular immune response

Localised
Slow to develop
Slow to resolve

How well did you know this?

Not at all

Perfectly

Types of immune failure responses (2x) -

Failure to produce adequate immune response

Produce overactive, damaging response

How well did you know this?

Not at all

Perfectly

Immunodeficiency definition

Failure to produce an adequate immune response

How well did you know this?

Not at all

Perfectly

Hypersensitivity definition

Overactive, damaging immune response to an allergen
Usually results from second exposure to an antigen
Individuals have genetic susceptibility

How well did you know this?

Not at all

Perfectly

4 types of hypersensitivity

1 - immediate i.e anaphylaxis
2 - cytotoxic
3 - immune complex
4 - delayed

How well did you know this?

Not at all

Perfectly

Type 1, 2, 3 hypersensitivity are mediated by?

Antibody mediated

IgE, IgG, IgG

How well did you know this?

Not at all

Perfectly

Type 4 hypersensitivity is mediated by?

Cell mediated - T cells

How well did you know this?

Not at all

Perfectly

Type 1 HS characteristics 
Immune mediator
Antigen type
Effector mechanism 
Example

Acute
Rapid onset
IgE mediated
Soluble 
Mast cell activation and mediator release
Asthma

How well did you know this?

Not at all

Perfectly

Type 1 HS mechanism - 1st exposure

When does it occur
What do these patients have more of
What does this lead to and what are the adaptations which allow this

Occurs on first exposure
HS people have more IL4 –> CD4 (humoral response)
More IL4 = More IgE production
Mast cells secrete IgE binding receptors and histamine granules
Receptors have high affinity for IgE
Allergen binds to IgE on
surface of mast cells
Cells become degranulated and release mediators
Second set released 4-8hrs later

How well did you know this?

Not at all

Perfectly

Allergens are…

Mostly small proteins

Type 1 HS mechanism - 2nd exposure mechanism

What is triggered and how
What is secreted (by what) and what else is released

Antibodies have high affinity for antigen
Specific response is triggered
Receptors cluster together and trigger a signal in the mast cell to degranulate and secrete IgE
IL-5 also released –> histamine and eosinophils release

Mast cell degranulation involves

Histamine and enzyme release

Histamines are released from

Haemopoietic stem cells resident in tissues

Anti-histamines have to be taken

Before degranulation to limit reaction

Histamine release causes

``` Vascular dilation Increased vascular permeability i.e oedema Bronchospasm Urticarial rash Increased Nasal and lacrimal secretions ```

Histamine release present clinically as

Hay fever | Asthma

Acute allergic responses examples e.g anaphylaxis

Latex allergy LA allergy Bee venom Peanut allergy

Diagnosis of allergy - testing and results

Apply small amount of allergen under skin - 5 min response Wheel will form - extravasation of serum into skin - angio-oedema Late phase of inflammation (6hrs later) due to leukocyte infiltration and further oedema

Management of type 1 hypersensitivity (4x)

Adrenaline Antihistamines (before degranulation) Corticosteroids Avoidance of allergen

Type II hypersensitivity | What do the antibodies induce and how

Antibody mediated hypersensitivity Antibodies target cell surface SELF antigens Usually IgG/M Cell damage and inflammation

Type II Hypersensitivity mechanism | What becomes activated

Antibodies target SELF antigen Abs activate 1. Antibody Dependent Cell Cytotoxicity --> inflammation via neutrophils and macrophages 2. Complement cascade

Complement mechanism and what does it lead to

Complement binds to receptor and stimulates release of factors C5 and C5a --> inflammation and cell death

Type II hypersensitivity responses are important in which conditions

Acute transplant rejection/transfusion haemolytic disease of the newborn Auto immune disease e.g pemphigus

Type II Hypersensitivity - HDoFNb - difference between first and second pregnancies Involvement of RhD

1st - RhD+ foetal blood enters RhD-ve mother's circulation Baby born but Abs against RhD+ve produced 2nd - if foetus is RhD+ve - mother produces IgG which crosses into foetal circulation and destroys foetal erythrocytes

Type II hypersensitivity - HDoFNb - treatment

Preformed anti-RhD ab is given to Rh- mothers of RhD+ve infants after delivery

Type II hypersensitivity - Pemphigus What is it and what does it lead to

Autoimmune disease against desmoglein Prevents formation of gap junctions Epithelial shedding

Type III hypersensitivity - Pemphigoid What is it and what does it lead to

Autoantibodies against hemidesmosomes Prevent binding of epithelium at basement membrane/dermis layer epithelium and connective tissue not bound --> blistering skin

Type III hypersensitivity mechanism Where do they form? What do complexes induce? What do complexes act on during inflammation?

``` Immune complex-mediated HS Complexes form between antigen and antibodies Form in serum Deposit in lining of vessels, glomeruli, lung Complement activation Leukocyte binding Inflammation Act on platelets and basophils Activated and release peptides Increase vascular permeability ```

What does increased vascular permeability allow for and lead to?

More immune complexes can be deposited Platelet aggregation Complement cascade activation Neutrophils attracted and secrete lysosomal enzymes Lysosomal enzymes cause further tissue damage

Type III HS is important in | 2 examples

Erythema multiforme | Lupus

Treatment of Type III hypersensitivity

Immunosuppression with steroids

Erythema multiforme Type? Appearance?

Type III Target lesion appearance Deposition of immune complex in superficial microvasculature of skin and oral mucous membrane following infection or drug exposure

Type IV Hypersensitivity What kind of response? What does this mean? Characteristics

``` Cell-mediated/delayed type Mediated by T cells Cell mediated Slow to develop 12-48hrs Slow to resolve Localised ```

Type IV mechanism | How do T-cells respond

Cell mediated T cell recognises antigen expressed via MHC protein on another cell T cell responds by releasing cytokines or killing target cell

Cell mediated immune responses are important in

Delayed type reactions Contact hypersensitivity e.g contact dermatitis Lichenoid reactions to amalgam filling and other materials

Contact dermatitis stages (2x)

Sensitisation | Elicitation

Sensitisation stage of Contact Dermatitis | What are langerhans cells

1. Antigen gets into skin and is internalised by langerhans cells - special antigen presenting cells in epidermis 2. Travel to lympnodes and present antigens to CD4 and T cells 3. MEMORY CD4 and T cells are produced

Elicitation stage What happens? - which cells involved What does this lead to?

Langerhans cells move to dermis Expose memory CD4 and T cells to antigen Cells activated and express IFN𝛾 Increased expression of ICAM-1 and MHCII proteins on keratinocytes and secretion of pro inflammatory cytokines More leukocytes attracted to sites Neutrophils arrive post4hrs, Monocytes + Tcells 12hrs Both secrete tissue damaging cytokines Tissue damage seen 12hrs+ If Ag removed then damage is resolved

Skin patch testing what does it test for where is it tested

Tests for type IV delayed response reactions | Samples applied to back of arm for 72-96hrs

Denture acrylic allergy | What does it look like

Red areas due to uncontrolled inflammation | Epidermal thickening due to leukocytes and proliferating keratinocytes

Lichenoid reaction to amalgam What kind of reaction Associated with ? and how is this tested and resolved?

Type IV contact hypersensitivity Amalgam fillings Positive skin patch test to mercury/amalgam Removal of filling