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Yr 2 - EMS > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What is allergy and hypersensitivity?

A

A reaction produced by the normal immune system (directed against innocuous antigens) in a pre-sensitised (immune) host

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2
Q

How many types of hypersensitivity are there?

A

4

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3
Q

What do type I hypersensitivity reactions involve?

A

IgE antibody mediated mast cell and basophil degranulation

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4
Q

What causes this production of IgE antibodies in type I reactions?

A

Initial exposure to the antigen causes the priming of Th2 cells, and their release of IL-4 causes the B cells to switch their production of IgM to IgE antibodies which are antigen-specific.

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5
Q

What is the result of the release of IgE antibodies in type I reactions?

A

The IgE antibodies bind to mast cells and basophils, sensitising them to the antigen. When the antigen enters the body again, it cross links the IgE bound to the sensitised cells, causing the release of preformed mediators including histamine, leukotrienes and prostaglandins.

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6
Q

What are the clinical features of type I reactions?

A

Widespread vasodilation, bronchoconstriction, and increased permeability of vascular endothelium. Wheal and flare reaction

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7
Q

Describe the onset of type I reactions?

A

Fast (15-30 mins)

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8
Q

What is a wheal and flare reaction?

A

Wheal: swelling produced by the release of serum into the tissues Flare: redness of the skin, resulting from the dilation of blood vessels

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9
Q

What 2 stages can a type I reaction be divided into?

A
  1. Immediate 2. Late phase response
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10
Q

Describe the immediate stage of a type I reaction

A

Release of pre-formed mediators causes the immune response: - Histamine - Proteases - Chemotatic factors

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11
Q

Describe the late phase response of a type I reaction

A

8-12 hours later, where cytokines released in the immediate stage activate basophils, eosinophils, and neutrophils even though the antigen is no longer present.

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12
Q

What is released in the late phase stage of a type I reaction?

A
  • Prostaglandin - Leukotrienes
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13
Q

What is the effect of histamine on gastric acid?

A

Stimulates gastric acid secretion (can have vomiting during anaphylaxis)

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14
Q

What is the effect of histamine on blood vessels?

A

Causes dilation of blood vessels –> can cause low blood pressure and feeling dizzy

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15
Q

What is the effect of histamine on the lungs?

A

Bronchoconstriction –> wheezing and shortness of breath

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16
Q

What is the effect of histamine on the permeability of capillaries?

A

Increase in permeability –> can lead to swelling

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17
Q

What is the effect of histamine on adrenaline?

A

Adrenaline is released –> become tachycardic

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18
Q

What is the effect of histamine on the skin?

A

Swelling and inflammation –> urticaria rash

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19
Q

What is the severe version of a type I reaction?

A

Anaphylaxis

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20
Q

What is anaphylaxis?

A

An acute, potentially life-threatening IgE mediated systemic hypersensitivity reaction. Medical emergency.

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21
Q

What are the symptoms of mild type I reactions?

A
  • Itchy eyes or nose - Cutaneous pruritus (itching of skin) - Flushing - Urticaria - Oral tingling/pruritus - Abdominal pain/nausea/vomiting - Runny nose, sneezing
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22
Q

What re the symptoms of moderate-severe type I reaction (anaphylaxis)?

A
  • Diffuse urticaria and angioedema - Severe abdominal pain, vomiting diarrhoea - Hoarseness, cough - Shortness of breath - Wheezing and cyanosis - Respiratory arrest - Hypotension - Dizziness, loss of consciousness
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23
Q

What components of the immune system are involved in allergies?

A

Components that respond to parasitic infection are involved in allergic reactions.

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24
Q

Why do we get allergies?

A

The system has developed to produce a rapid tissue-based response to re-infection. The lack of infectious drive is a contributory factor in allergic disease. Combination of genetic and environmental.

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25
Q

How are we sensitised?

A
  1. Allergen seen and sampled by dendritic cell
  2. Dendritic cell (APC) presents allergen to naive T cell
  3. T cell recognises allergen and differentiates into a Th2 cell
    1. Th2 cell secretes cytokines (IL-4 and IL-13) which signal to naive B cells
    1. Naive B cells become memory cells (switch to producing IgE antibodies)
    1. Produce specific IgE that will recognise that allergen on further exposure
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26
Q

What is the ‘dual allergen exposure hypothesis’?

A
  • Early cutaneous exposure to food protein through a disrupted skin barrier leads to allergic sensitisation (e.g. eczema is thought to factor for allergies due to disruption to skin barrier).
  • Whereas, early oral exposure to food allergen induces tolerance.
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27
Q

What is ‘sensitisation’?

A

Induction of allergic responses

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28
Q

What is the atopic march?

A

Refers to the typical progression of allergic diseases that often begin early in life:

  1. Atopic dermatits (eczema)
  2. Food allergy
  3. Allergic rhinitis (hayfever)
  4. Asthma
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29
Q

What does the atopic march show?

A
  • More common to develop eczema and food allergy in infancy
  • Later in life (3-4 years) more common to develop asthma
  • From 5-10, more common to develop asthma and hayfever
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30
Q

How is type I hypersensitivity diagnosed?

A
  • History
  • Blood test –> specific IgE test
  • Skin prick test
    • A positive control (i.e. histamine) and a negative control (i.e. normal saline) are put on the skin
    • The allergen is then put on the skin
    • Scratch each one and time for 15 mins –> see if a wheal appears and compare it to negative control
  • Intra-dermal test
    • Done for drug allergy testing
  • Oral challenge test (Gold standard)
    • Rarely done as can put patient at risk
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31
Q

What is the atopic triad?

A

Asthma, rhinitis, eczema

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32
Q

What are the 2 different types of rhinitis?

A

Allergic or non-allergic

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33
Q

What are the symptoms of allergic rhinitis? What are they key allergens?

A
  • Can be perennial or seasonal
  • Blocked nose, runny nose, eye symptoms
  • Key allergens: pollen, animals, house dust mite
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34
Q

What is the treatment for rhinitis?

A

Nasal steroids and antihistamines

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35
Q

What is asthma?

A

A disease of inflammation and hyperactivity of the small airways. Can cause damage to airways due to late phase response.

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36
Q

What are the immediate symptoms of asthma mediated by?

A

IgE

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37
Q

Atopic vs contact dermatitis?

A

Atopic dermatitis is a chronic condition, which is believed to related to an autoimmune problem. Contact dermatitis develops when the skin comes in contact with something that triggers a reaction.

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38
Q

Clincal features of eczema?

A

Intense itching, blistering/weeping, cracking of skin

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39
Q

What are type II hypersensitivity reactions mediated by?

A
  • IgG/IgM antibodies targeting foreign or self antigens on the cell surface –> cytotoxic​
  • This triggers complement activation/phagocytosis/ADCC
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40
Q

Mechanism behind type II hypersensitivity reactions?

A

When cell surface antigens are presented to T cells, an immune response is started, targeting the cells to which the antigens are attached.

Antibodies binding to cells can activate the complement system, leading to degranulation of neutrophils, a release of oxygen radicals, and eventual formation of membrane attack complex – all of which lead to destruction of the cell. Parts of the complement activation can also opsonise the target cell, marking it for phagocytosis.

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41
Q

What are the results of type II reactions?

A
  • Cell lysis and necrosis
42
Q

What are the common antigens for type II reactions?

A

Penicillin

43
Q

When may type II reactions occur?

A
  • In response to host cells (autoimmune)
  • In response to non-self cells (blood transfusion)
44
Q

How is type II distinguished from type III?

A

Type II - the antibodies are binding to antigens that are cell bound

Type III - the antibodies are binding to soluble antigens

45
Q

What type of hypersensitivity reaction is a blood transfusion reaction?

A

Type II

46
Q

Describe how a blood tranfusion reaction is a type II reaction?

A

If incorrectly matched blood;

  • Patient’s APCs (dendritic or macrophage) detect the foreign antigen
  • Present it to B cells which will make antibodies
  • This will activate complement and have cytotoxic action
  • MAC attack complex (classic pathway) generated
  • Takes hours to days
47
Q

Regarding blood type A, what are the:

  • Antibodies in the plasma?
  • Antigen in RBC?
  • Blood types compatible?
A
  • Anti-B antibodies in plasma
  • A antigen in RBC
  • A, O compatible
48
Q

Regarding blood type B, what are the:

  1. Antibodies in the plasma?
  2. Antigen in RBC?
  3. Blood types compatible?
A
  1. Anti-A antibodies in plasma
  2. B antigen in RBC
  3. B, O compatible
49
Q

Regarding blood type AB, what are the:

  1. Antibodies in the plasma?
  2. Antigen in RBC?
  3. Blood types compatible?
A
  1. No antibodies in plasma
  2. A and B antigens
  3. AB, A, B and O compatible
50
Q

Regarding blood type O, what are the:

  1. Antibodies in the plasma?
  2. Antigen in RBC?
  3. Blood types compatible?
A
  1. Anti-A and Anti-B antibodies in plasma
  2. No antigens in RBC
  3. O is compatible
51
Q

What blood type is the universal recipient?

A

AB (due to having no antibodies in plasma)

52
Q

Which blood type is the universal recipient?

A

O (due to having no antigens in RBC)

53
Q

Complement pathway

A
54
Q

What is the Membrane Attack Complex (MAC)?

A

A structure typically formed on the surface of pathogen cell membranes as a result of the activation of the host’s complement system. The membrane-attack complex (MAC) forms transmembrane channels which disrupt the cell membrane of target cells, leading to cell lysis and death.

55
Q

What proteins does the MAC complex include?

A

C5-C9 proteins

56
Q

What does MAC result in?

A

Pore formation in cell membrane and leak of intracellular fluid out of the cell

57
Q

What are type III reactions mediated by?

A

IgG/IgM Antibodies against soluble antigen-immune complex deposition

58
Q

Mechanism behind type III reactions?

A
  1. Antigen-antibody complexes (formed by soluble antigens) in the circulation may be desposited in and damage tissues
  2. The complexes may become lodged in the basement membranes of tissues which have particularly high rates of blood filtration – the kidney and synovial joints being common targets.
  3. These complexes rapidly activate the complement chain, causing local inflammation and attraction of leucocytes:
  • Increased vasopermeability
  • Attraction and degranulation of neutrophils
  • Release of oxygen free radicals which can severely damage surrounding cells
59
Q

What is onset time of type III reactions?

A

3-8 hours

60
Q

What type of reaction is rheumatoid arthritis? Mechanism?

A

Type III:

  • Antigen-antibody complexes circulate in the bloodstream end up lodging in the complex filtration systems responsible for maintaining the levels of synovial fluids at synovial joints
  • The lodged immune complexes can cause a local inflammatory response, leading to stiffness and pain in affected joints.
61
Q

What type of reaction is SLE?

A

Type III

62
Q

What is tolerance?

A

T and B cells that recognise your own antigens should be excluded in the secondary lymphoid organs

63
Q

What causes a lack of tolerance?

A

B cells regonises self-cells as foreign –> autoimmunity results

64
Q

Describe reaction during SLE

A
  • B cell recognises DNA as foreign
  • Clonal B cell expansion
  • Small immune complexes result
  • Don’t get cleared as easily from the system and immune complexes stick to the vessel wall
    • This stimulates complement activation
      • C1 from the complement system binds with the antibody
      • C1-C9 follow with increased permeability of vessels
      • C3 and C4 used in large amounts –> key blood test
    • Neutrophils attracted
65
Q

What is expected blood test result for C3 and C4 in SLE?

A

Low amounts as C3 and C4 used up

66
Q

What areas of the body are particularly vulnerable to type III reactions?

A
  • Kidneys - complexes in high concentration due to filtering
  • Joints - plasma filtered to synovial fluid
67
Q

Vasculitic rash

A
68
Q

What are type IV reactions mediated by?

A

Antigen-specific activated T cells

69
Q

Onset time of type IV reactions?

A

48-72h

70
Q

Mechanism behind type IV reactions?

A
  1. APC processes antigen
  2. APC presents antigen together with MHC II to a Th1 cell
  3. Activation of Th1 cells –> release chemokines and cytokines to mount an immune response (including activating macrophages)
  4. Activated macrophages release:
    1. Pro-inflammatory factors –> local swelling, oedema, warmth, and redness
    2. Lysosomal elements and reactive oxygen species –> local tissue damage
71
Q

What are the common antigens involved in type IV reactions?

A
  • Metals (e.g. nickel)
  • Tuberculin test
  • Poison ivy
72
Q

What type of reaction is contact dermatitis?

A

Type IV

73
Q

Breakdown of different types of reactions

A
74
Q

Comparison of different types of hypersensitivity

A
75
Q

Which Antibody mediates Type 1 hypersensitivity?

A

IgE

76
Q

Which Antibodies medicate the Type III hypersensitivity?

A

IgM and IgG

77
Q

Name 3 chemical mediators produced by a mast cell

A

Leukotrienes, histamine, Prostaglandins, proteases, chemotactic factors

78
Q

What is the hallmark cytokine of Type I reactions?

A

IL-4

79
Q

What is the hallmark Ig in type I reactions?

A

IgE

80
Q

Which cell is responsible for the production of IL-4 in type I reactions?

A

Th2 cells

81
Q

How are mast cells and basophikls ‘sensitised’ during type I reactions?

A
  • 1) Initial exposure to antigen causes priming of Th2 cells
  • 2) Th2 cells release IL-4
  • 3) IL-4 causes B cells to switch their production of IgM to IgE antibodies (which are antigen specific)
  • 4) IgE antibodies bind to mast cells and basophils –> sensitises them to antigen
82
Q

How does IgE cause the release of preformed mediators in type I reactions?

A

Antigen enters body again and crosslinks the IgE bound to the sensitised cells –> causes release of preformed mediators e.g. histamine, leukotrienes and prostaglandins

83
Q

Which APC is involved in sensitisation in type I reactions?

A

Dendritic cells

84
Q

Explain what causes vomiting during anaphylaxis

A

Histamine stimulates gastric acid secretion

85
Q

Explain what causes dizziness during anaphylaxis

A

Histamine causes vasodilation which lowers blood pressure

86
Q

Explain what causes swelling during anaphylaxis

A

Histamine increases permeability of blood vessels

87
Q

Explain what causes wheezing and SOB during anaphylaxis

A

Histamine causes bronchoconstriction

88
Q

Explain what causes tachycardia during anaphylaxis

A

Histamine increases release of adrenaline

89
Q

Explain what causes uritcaria rash during anaphylaxis

A

Swelling and inflammation due to permeability and vasodilation

90
Q

Difference between intradermal and skin prick tests?

A

With skin scratch testing, the allergens are placed on the skin and then a needle is used to introduce the allergen beneath the skin with a scratch. With intradermal skin testing, the allergen is directly inserted under the skin with a needle.

91
Q

Why is the oral challenge test rarely done?

A

Can put patient at risk

92
Q

Treatment for dermatitis?

A

topical steroids and moisturisers

93
Q

Where do immune complexes tend to build up?

A

In the basement membranes of tissues which have particularly high rates of blood filtration

94
Q

What is effect of build up of immune complexes?

A

Inflammatory response and attraction of leukocytes

95
Q

Which antibodies are involved in;

a) type I
b) type II
c) type III
d) type IV

A

a) IgE
b) IgG, IgM
c) IgG, IgM
d) none

96
Q

What is the response time of;

a) type I
b) type II
c) type III
d) type IV

A

a) 15-30 mins
b) minutes-hours
c) 3-8 hours
d) 48-72 hours

97
Q

cell apearance in;

  1. type I
  2. type II
  3. type III
  4. type IV
A
  1. weal and flare
  2. lysis and necrosis
  3. erythema, oedema, necrosis
  4. erythema induration
98
Q

What is erythema?

A

redness of the skin or mucous membranes, caused by hyperemia (increased blood flow) in superficial capillaries

99
Q

Which hypersensitivity reactions is the complement system involved in?

A

II and III

100
Q

Which hypersensitivity reaction are basophils and eosinophils involved in?

A

I

101
Q

What type of reaction is Goodpasture’s nephritis?

A

Type II (cytotoxic)

Yr 2 - EMS (60 decks)

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