Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Acquired immunity consists of

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Antibody responses

A 
Antigen uptake
Antigen processing
Antigen presentation
T cell help
B cells proliferate
-form plasma cells
-produce antibody
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cell mediated immunity directed mainly against

A

Cellular targets e.g.

  • tumour cells
  • virally transformed cells
  • foreign cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cellular immune responses tend to be

A
  • localised
  • slow to develop
  • slow to resolve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Failure of the immune system

A 
Fail to produce an adequate immune
response
„ Immunodeficiency
Produce an overactive, damaging response
„ Hypersensitivity Hypersensitivity - allergy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Mast cell degranulation

A

Histamine and enzyme release (tryptase and chymase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Histamine release causes

A 
Vascular dilation
↑ Vascular permeability i.e. oedema
Bronchospasm
Urticarial rash – nettle rash nettle rash
↑ nasal and lacrimal secretions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Type II hypersensitivity mechanism ***

A

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
Q

Type II hypersensitivity responses are important in

A 
Acute transplant rejection / blood transfusion
Haemolytic Disease of the Newborn
Autoimmune diseases e.g.
„Pemphigus
„ Pemphigoid
27
Q

Type II hypersensitivity - Haemolytic Disease of the Newborn

A
  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
Q

Type II hypersensitivity - Pemphigus

A

Auto-antibodies against desmoglein-1&3
Ab prevents formation of gap junctions
between epithelial cells
Epithelial shedding – mainly mucosal

29
Q

Type II hypersensitivity - pemphigoid

A

Auto-antibodies against hemidesmosomes
Ab prevents binding of epithelium with dermis at basement membrane
Epithelial shedding – skin and mucosal

30
Q

Type III hypersensitivity

A

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
Q

Type III hypersensitivity - immune complexes may deposit in

A

Lining of BVs
Glomeruli
Lung

32
Q

Type III hypersensitivity - here they induce

A

Complement activation
Leukocyte binding
Inflammation

33
Q

Type III hypersensitivity as trigger for > vascular permeability

A
  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
Q

Type III hypersensitivity - deposition of immune complexes in BV walls

A 
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
Q

Type III hypersensitivity - immune complex mediated hypersensitivity is important in

A

Immune complex mediated vasculitis e.g.

  • erythema multiforme
  • systemic luous erythematosus (SLE)
36
Q

Type III hypersensitivity treatment

A

Immunosuppression with steroids

37
Q

Type III Type III Hypersensitivity - Erythema Multiforme

A 
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
Q

Type IV hypersensitivity

A 
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
Q

Type IV hypersensitivity mechanism

A 
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
Q

Type IV hypersensitivity cell mediated immune responses are important in

A

Delayed type hypersensitivity responses
Contact hypersensitivity - e.g. dermatitis
Lichenoid reactions to amalgam fillings and other materials

41
Q

Type IV hypersensitivity - contact dermatitis

A

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
Q

Type IV hypersensitivity steps (contact dermatitis)

A

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
Q

Type IV hypersensitivity tests

A

Skin patch testing

-samples applied to skin of back or arm for 72-96 hours

44
Q

Denture acrylic allergy

A

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
Q

Lichenoid reaction to amalgam

A 
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions