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DEN303 - IHD > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

Describe the potential benefits and possible harmful effects of the immune response. Define and distinguish between different types of hypersensitivity. Comment upon which diseases are associated with specific types of hypersensitivity reactions. Summarise the problems associated with graft‐rejection and transplantation of organs and tissues.

1
Q

Another name for hypersensitivity?

A

Allergy/autoimmunity

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2
Q

Increased sensitivity in dental patients to…

A

Latex
Dental materials
Drugs used in the surgery

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3
Q

Immune system consists of

Two types?

A

Innate immune system

Adaptive/acquired immune system

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4
Q

Acquired immunity consists of

Two types of response?

A

Antibody response

Cell-mediated response

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5
Q

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

A

Antibody

Cell-mediated

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6
Q

Antibody response creation steps

A
  1. APC take up antigens
  2. APC processes and displaces antigen on surface
  3. B-cell attaches to displayed antigen
  4. Th2 cell (helper) releases cytokines to encourage proliferation
  5. B-cells proliferate and produce/release plasma cells and produce antibodies
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7
Q

Features of antibody response

Effect and speed

A

Rapid

Systemic/widespread

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8
Q

Why is antibody response widespread?

Adaptations of molecules

A

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

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9
Q

Cell mediated immunity: 1st exposure process

A
  1. Antigen presentation via MHC protein
  2. Complementary T cell attaches via receptor
  3. T cell becomes activated
  4. Activated T cell proliferates and forms antigen specific memory T cells which patrol body
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10
Q

Cell mediated immunity: 2nd exposure process

A
  1. Memory T-cell recognises antigen expressed on target cell
  2. T cells release cytokines, kill target cell via apoptosis
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11
Q

Cell Mediated Immune Targets (3x)

A

Cellular targets:

  • immune cells
  • virally transformed cells
  • foreign cells
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12
Q

Characteristics of cellular immune response

A
  • Localised
  • Slow to develop
  • Slow to resolve
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13
Q

Types of immune failure responses (2x) -

A

Failure to produce adequate immune response

Produce overactive, damaging response

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14
Q

Immunodeficiency definition

A

Failure to produce an adequate immune response

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15
Q

Hypersensitivity definition

A

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

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16
Q

4 types of hypersensitivity

A

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

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17
Q

Type 1, 2, 3 hypersensitivity are mediated by?

A

Antibody mediated

IgE, IgG, IgG

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18
Q

Type 4 hypersensitivity is mediated by?

A

Cell mediated - T cells

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19
Q 
Type 1 HS characteristics 
Immune mediator
Antigen type
Effector mechanism 
Example
A 
Acute
Rapid onset
IgE mediated
Soluble 
Mast cell activation and mediator release
Asthma
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20
Q

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

A

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

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21
Q

Allergens are…

A

Mostly small proteins

22
Q

Type 1 HS mechanism - 2nd exposure mechanism

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

A

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

23
Q

Mast cell degranulation involves

A

Histamine and enzyme release

24
Q

Histamines are released from

A

Haemopoietic stem cells resident in tissues

25
Q

Anti-histamines have to be taken

A

Before degranulation to limit reaction

26
Q

Histamine release causes

A 
Vascular dilation 
Increased vascular permeability i.e oedema 
Bronchospasm 
Urticarial rash 
Increased Nasal and lacrimal secretions
27
Q

Histamine release present clinically as

A

Hay fever

Asthma

28
Q

Acute allergic responses examples e.g anaphylaxis

A

Latex allergy
LA allergy
Bee venom
Peanut allergy

29
Q

Diagnosis of allergy - testing and results

A

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

30
Q

Management of type 1 hypersensitivity (4x)

A

Adrenaline
Antihistamines (before degranulation)
Corticosteroids
Avoidance of allergen

31
Q

Type II hypersensitivity

What do the antibodies induce and how

A

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

32
Q

Type II Hypersensitivity mechanism

What becomes activated

A

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

33
Q

Complement mechanism and what does it lead to

A

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

34
Q

Type II hypersensitivity responses are important in which conditions

A

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

35
Q

Type II Hypersensitivity - HDoFNb - difference between first and second pregnancies

Involvement of RhD

A

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

36
Q

Type II hypersensitivity - HDoFNb - treatment

A

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

37
Q

Type II hypersensitivity - Pemphigus

What is it and what does it lead to

A

Autoimmune disease against desmoglein
Prevents formation of gap junctions
Epithelial shedding

38
Q

Type III hypersensitivity - Pemphigoid

What is it and what does it lead to

A

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

39
Q

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

A 
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
40
Q

What does increased vascular permeability allow for and lead to?

A

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

41
Q

Type III HS is important in

2 examples

A

Erythema multiforme

Lupus

42
Q

Treatment of Type III hypersensitivity

A

Immunosuppression with steroids

43
Q

Erythema multiforme
Type?
Appearance?

A

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

44
Q

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

A 
Cell-mediated/delayed type
Mediated by T cells 
Cell mediated
Slow to develop 
12-48hrs
Slow to resolve 
Localised
45
Q

Type IV mechanism

How do T-cells respond

A

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

46
Q

Cell mediated immune responses are important in

A

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

47
Q

Contact dermatitis stages (2x)

A

Sensitisation

Elicitation

48
Q

Sensitisation stage of Contact Dermatitis

What are langerhans cells

A
  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
49
Q

Elicitation stage

What happens? - which cells involved

What does this lead to?

A

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

50
Q

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

A

Tests for type IV delayed response reactions

Samples applied to back of arm for 72-96hrs

51
Q

Denture acrylic allergy

What does it look like

A

Red areas due to uncontrolled inflammation

Epidermal thickening due to leukocytes and proliferating keratinocytes

52
Q

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

A

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

DEN303 - IHD (58 decks)

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