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5th Oral Disease -Histology Lectures > Oral Allergies > Flashcards

Oral Allergies Flashcards

1
Q

What is allergy?

A

When immune system reaction in exaggerated or inappropriate response to extrinsic antigen

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2
Q

What is auto-immunity?

A

When immune system responds in exaggerated or inappropriate way to intrinsic antigen

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3
Q

What is hypersensitivity?

A

When immune system responds in exaggerated or inappropriate way resulting in harm

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4
Q

Are allergies and autoimmunity types of hypersensitivity?

A

Yes

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5
Q

What are different forms of hypersensitivity?

A

Antibody mediated

Cell mediated

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6
Q

What types of hypersensitivity are antibody mediation?

A

Type 1, 2 and 3

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7
Q

What hypersensivity is cell mediated?

A

Type IV

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8
Q

What is type I hypersensivity

A

Immediate/ anaphylaxis

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9
Q

What is type II hypersensitivity?

A

Cytotoxic

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10
Q

What is type III hypersensivity?

A

Immune complex

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11
Q

What is type IV hypersensitivity?

A

Delayed

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12
Q

How is type I hypersensitivity mediated?

A

IgE

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13
Q

When get symptoms of type I hypersensitivity?

A

Immediate

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14
Q

What happens in type I hypersensitivty

A

Allegens causes antigen response causing which causes mast cell degranulations causing histamine and enzyme release

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15
Q

What does release of histamine cause?

A 
Vascular dilation 
Increased vascular permeability = oedema
Bronchospasm 
Urticarial rash 
Increased nasal/ lacrimal secretions
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16
Q

Common causes of type I response

A

Hay fever
Asthma
Allergies: penicillin, laxtex etc

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17
Q

How to diagnosis allergy for type I hypersensitivity?

A

Wheel and flare

Allergy applied using prick test and skin response is fast

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18
Q

What is wheel and flare?

A

Wheel - extravasation of serum into skin due to histamine

Flare - erythematous red patch caused axon response

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19
Q

Issue w/ wheel and flare test?

A

Can get late phase 6hrs after due leukocyte infiltrate and oedema

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20
Q

How manage type I hypersensitivity?

A

Adrenaline
Anti-histamine
Corticosteroid

21
Q

Use of corticosteroids in type I management?

A

Dampen immune response

22
Q

What happens on first exposure to allergy

A

Antigen bind to B cell
B cell turn to plasma cell –> ab released
Cytokine environment causes plasma clells to secrete IgE ab
IgE enters blood which rapidly bind to mast recoprtos
IgE displayed on Fc receptors on mast cell

23
Q

How can IgE be used to see if someone is predisposed to allergic reaction?

A

They will have high serum levels of IgE

24
Q

What happens on second exposure to antigen?

A

Have specific IgE
Antigen cross-link Fc rector on mast cell
Transmit intra-cellular signal causing mast cell degranulation
Histamine released

25
Q

What is a type II hypersensitivity?

A

Antibody mediated - antibodies target self-antigens usually IgG or IgM = cell damage and inflammation

26
Q

Mechanism type II?

A

Antibodies target self-antigens

Autoantibodies activate T cells/ neutrophils/ macrophages causing inflammation of complement

27
Q

What does complement activation in type II cause?

A

Caused inflammation and cells death via MAC

28
Q

What is MAC

A

Membrane attack complex

29
Q

What is mechanism of type III?

A

Immune complex form between antibodies and antigens

30
Q

What happens to immune complex formed in type III?

A

Deposits in lining blood vessel/ lung - causes complement activation and neutrophil binding = inflammatory and vascular permability

31
Q

Give example of type III hypersensitivity?

A

Erythema multiforme

SLE - systemic lupus erythematosis

32
Q

What is type IV hyperseniviity mediated by?

A

Cell- mediated

Mediated by T cellsq

33
Q

When is type IV delayed?

A

Response is cellular - slow to develop and resolve

34
Q

When see type IV sensitivity

A

Delayed hypersensitivity responses
Contact dermatitis
Lichenoid reactions
OLP

35
Q

Mechanism of type IV?

A

Extrinsic antigen enter oral
Dendritic cells intercept and process antigen
Antigen stimulated Langerhans cells to migrate to draining lymph node
Also stimulate keratinocytes to release TNF

36
Q

What happens in draining lymph nodes in type IV?

A

Langerhan cell process antigen and presents to T cell circulating in lymph node
Antigen specific T cell becomes activated - proliferation and re-circulation to oral mucosa

37
Q

What happens in oral mucosa in type IV?

A

Epithelial cells activated to secrete TNF
TNF induces VCAM-1 expression on endothelium
Allows T cells to bind VCAM-1
Interaction between T cells and epithelium = cytokine release
Cytotoxic T cells kill basal keratinocytes

38
Q

What see histology of type IV hypersensitivity?

A

Dense band T cells in connective tissue

39
Q

2 mechanism in which T cells induce apoptosis?

A

Fas-mediated

Peforin/ granzyme B

40
Q

What is perforin?

A

Pore forming molecule

41
Q

Type IV summary?

A

Langerhan cells move from epidermis to lymph nodes
They present antigen to CD4 T cells
T cells move to mucosa to secrete TNF
Causes expression VCAM1
Secretion pro-inflammatory cytokines which damage tissue

42
Q

When is tissue damage seen in type IV?

A

12 hours

43
Q

3 main issues w/ allergies in dentistry?

A

Drug allergies
Dental material allergies
Latex allergy

44
Q

What type of reaction is a drug allergy?

A

Type I

45
Q

Are LA allergies common?

A

Not true allergies - preservative been removed

Most reaction vasovagal due intra-vascular injection

46
Q

What type of reactions are those to dental materials?

A

Type IV - response usually chronic and localised

47
Q

What metals are likely to cause type IV responses?

A

Nickle

Mercury - lichenoid reaction

48
Q

Alternative to latex gloves?

A

Nitrile

5th Oral Disease -Histology Lectures (11 decks)

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