L4 - Hypersensitivity Flashcards

1
Q

What 3 diseases contribute to the atopic triad?

A

Rhinitis
Asthma
Atopic Dermatitis

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

What does skin prick testing diagnose?

A

allergies

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

What do you measure in a skin prick test?

A

Size of weal - measurement of allergen specific IgE

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

What is dual allergen exposure hypothesis?

A
  • Tolerance occurs in babies through high dose of oral exposure.
  • Allergy occurs through low dose cutaneous exposure e.g disrupted skin barrier.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What physiological effects does Histamine have?

A
  • blood clots
  • gastric acid secretion
  • vasodilation
  • bronchoconstriction
  • increased permeability of capillaries
  • release of adrenaline
  • swelling and inflammation
  • inc in heart rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What 3 ways does the complement system destroy pathogens?

A

Opsonisation

Membrane Attack Complex (MAC)

Enhancing inflammatory process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which complement protein causes opsonisation and initiates formation of MAC?

A

C3b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which complement protein is a chemotactic agent which enhances the inflammatory process?

A

C3a

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

Describe Type 1 Hypersensitivity?

A
  • IgE
  • mast cell and basophil degranulation
  • release of preformed and de novo inflammatory mediators
  • rapid onset
  • weal and flare
  • late phase response mediated by eosinophils and Th2 T cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the primary response of allergen exposure in Type 1 hypersensitivity?

A

Release of preformed mediators:

  • Histamine
  • Proteases
  • Chemotactic factors (induce inflammatory cell infiltration)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the secondary response/late phase of allergen exposure in Type 1 hypersensitivity?

A

Release of newly formed mediators:

  • Prostaglandin
    (platelet activating factor/prolonged airway hyperactivity)
  • Leukotrienes
    (chemoattractant, sustained bronchoconstriction and oedema)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the secondary/late phase response of type 1 hypersensitivity mediated by?

A
  • Th2 Cells

- recruitment of eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe Anaphylaxis?

A
  • medical emergency
  • rapid onset
  • severe type 1

NB: to provoke anaphylaxis the allergen must be systemically absorbed (ingestion/injection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe Type 2 hypersensitivity?

A
  • cytotoxic
  • antibodies attach to cell bound antigen/self structures (autoantibodies)
  • triggered by endogenous antigens
  • IgG/IgM
  • happens at cell surface
  • cell lysis and necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Example of diseases resulting in type 2 hypersensitivity?

A
  • good pastures nephritis

- blood transfusion reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe Type 3 Hypersensitivity?

A
  • immune complex
  • IgG/IgM against soluble antigen
  • onset 3-8 hours
  • cause: serum sickness
  • feature: vasculitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Disease associated withy Type 3 hypersensitivity?

A

SLE

Systemic Lupus Erythematus
- widespread inflammation of connective tissues in organs aggravated by sunlight
- antibody recognises DNA/self as foreign = colonial B expansion
- small immune complexes result, stick to blood vessel wall, C1-9 binds = increased permeability of vessels
= Fluid leaks out (oedema).

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

Describe type 4 hypersensitivity?

A
  • interaction between activated sensitised CD4+ and CD8+
  • delayed onset 48-72h
  • erythema induration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Diseases associated with Type 4 Hypersensitivity?

A

contact dermatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe type 5 hypersensitivity?

A

Type 5 is a subtype of type 2 - instead of the antibodies acting against cell surface components, antibodies act against cell receptors.

21
Q

which type of sensitivity is mediated by IgG/IgM antibodies?

A
  • type 2 (cytotoxic)

- type 3 (immune complex)

22
Q

which type of sensitivity is described as cytotoxic?

A

type 2

23
Q

which type of sensitivity is described as anaphylactic?

A

type 1

24
Q

which type of sensitivity is described as a immune complex?

A

type 3

25
Q

which type of sensitivity is described as delayed?

A

type 4

26
Q

Which type of sensitivity has an exogenous antigen involved?

A

type 1

27
Q

Which type of sensitivity has an cell surface antigen involved?

A

type 2

28
Q

Which type of sensitivity has a soluble antigen involved?

A

type 3

29
Q

Which type of hypersensitivity involves weal and flare and mast cell degranulation?

A

Type 1

30
Q

Which type of hypersensitivity involves lysis and necrosis?

A

type 2

31
Q

what is hypersensitivity?

A

a normal immune response directed against innocuous antigens in a presensitised host

  • undesirable
  • damaging
  • uncomfortable
  • fatal
32
Q

what does innocuous mean?

A

not harmful or offensive

33
Q

how would mild anaphylaxis present?

A
  • itchy eyes or nose
  • cutaneous pruritus
  • flushing
  • urticaria
  • oral tingling/pruritus
  • abdo pain/nausea/vomiting
  • runny nose, sneezing
34
Q

how would moderate-severe anaphylaxis present?

A
  • Diffuse urticaria and angioedema
  • Severe abdominal pain, vomiting diarrhoea
  • Hoarseness, cough
  • SOB
  • Wheezing and cyanosis
  • Hypotension
  • Dizziness, loss of consciousness
35
Q

how are we sensitised to allergens?

A

for example breathed in allergen or its gained access via a break in the skin

  • picked up by APC cells (e.g. dendritic cell)
  • APC presents it to naive T cell in the lymph nodes
  • exposure to allergen and IL-4 causes naive T cell to differentiate into Th2 cell
  • Th2 cell releases more IL-4 and IL-13 which causes B cells to undergo class switching to IgE
    = memory B cells with IgE to that allergen
36
Q

what is meant by a naive T cell?

A

not seen a particular antigen before

37
Q

which cytokines push naive T cells to differentiate into Th2 cells?

A

IL 4

38
Q

which cytokines are produced by Th2 cells to push B cells to undergo class switching?

A

IL-4

IL-13

39
Q

can you inherit allergies?

A
  • no
  • allergies are polygenic diseases
  • not sufficient for disease only susceptibility
40
Q

what is the highest food allergy prevalence in infants?

A

milk

41
Q

what is the highest food allergy prevalence in adults?

A

shellfish

42
Q

features of rhinitis

A
  • allergic/non allergic
  • can be perennial or seasonal
  • treatment: nasal steroids and antihistamines
  • symptoms incl blocked nose, runny nose
43
Q

features of asthma

A
  • inflammation and hyperactivity of the small airways
  • immediate symptoms are IgE mediated
  • damage to airways due to late phase response
44
Q

what does MAC (membrane attack complex) result in?

A

focused target cell lysis

45
Q

what does the complement protein C3b do?

A

opsonises (make more susceptible to phagocytes) immune complexes for waste disposal

46
Q

what is the difference between type 2 and type 3 hypersensitivity?

A

type 2: anybody against an antigen attached to a cell (not an immune complex)

type 3: antibody attached to free antigen/floating about/soluble (immune complex)

47
Q

which complement system proteins are anaphylatoxins?

A

C5a
C4a
C3a

increase vascular permeability

48
Q

Name 3 chemical mediators produced by a mast cell.

A
  • Histamine
  • Proteases
  • Chemotactic factors