Yr 2 - EMS > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

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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
How are we sensitised?
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 4. 4. Th2 cell secretes cytokines (IL-4 and IL-13) which signal to naive B cells 5. 5. Naive B cells become memory cells (switch to producing IgE antibodies) 6. 6. Produce specific IgE that will recognise that allergen on further exposure
26
What is the 'dual allergen exposure hypothesis'?
* 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.
27
What is 'sensitisation'?
Induction of allergic responses
28
What is the atopic march?
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
29
What does the atopic march show?
* 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
30
How is type I hypersensitivity diagnosed?
* 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
31
What is the atopic triad?
Asthma, rhinitis, eczema
32
What are the 2 different types of rhinitis?
Allergic or non-allergic
33
What are the symptoms of allergic rhinitis? What are they key allergens?
* Can be perennial or seasonal * Blocked nose, runny nose, eye symptoms * Key allergens: pollen, animals, house dust mite
34
What is the treatment for rhinitis?
Nasal steroids and antihistamines
35
What is asthma?
A disease of inflammation and hyperactivity of the small airways. Can cause damage to airways due to late phase response.
36
What are the immediate symptoms of asthma mediated by?
IgE
37
Atopic vs contact dermatitis?
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.
38
Clincal features of eczema?
Intense itching, blistering/weeping, cracking of skin
39
What are type II hypersensitivity reactions mediated by?
* IgG/IgM antibodies targeting foreign or self antigens on the cell surface --\> **cytotoxic**​ * This triggers complement activation/phagocytosis/ADCC
40
Mechanism behind type II hypersensitivity reactions?
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.
41
What are the results of type II reactions?
* Cell lysis and necrosis
42
What are the common antigens for type II reactions?
Penicillin
43
When may type II reactions occur?
* In response to host cells (autoimmune) * In response to non-self cells (blood transfusion)
44
How is type II distinguished from type III?
Type II - the antibodies are binding to antigens that are **cell bound** Type III - the antibodies are binding to **soluble** antigens
45
What type of hypersensitivity reaction is a blood transfusion reaction?
Type II
46
Describe how a blood tranfusion reaction is a type II reaction?
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
Regarding blood type A, what are the: * Antibodies in the plasma? * Antigen in RBC? * Blood types compatible?
* Anti-B antibodies in plasma * A antigen in RBC * A, O compatible
48
Regarding blood type B, what are the: 1. Antibodies in the plasma? 2. Antigen in RBC? 3. Blood types compatible?
1. Anti-A antibodies in plasma 2. B antigen in RBC 3. B, O compatible
49
Regarding blood type AB, what are the: 1. Antibodies in the plasma? 2. Antigen in RBC? 3. Blood types compatible?
1. No antibodies in plasma 2. A and B antigens 3. AB, A, B and O compatible
50
Regarding blood type O, what are the: 1. Antibodies in the plasma? 2. Antigen in RBC? 3. Blood types compatible?
1. Anti-A and Anti-B antibodies in plasma 2. No antigens in RBC 3. O is compatible
51
What blood type is the universal recipient?
AB (due to having no antibodies in plasma)
52
Which blood type is the universal recipient?
O (due to having no antigens in RBC)
53
Complement pathway
54
What is the Membrane Attack Complex (MAC)?
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
What proteins does the MAC complex include?
C5-C9 proteins
56
What does MAC result in?
Pore formation in cell membrane and leak of intracellular fluid out of the cell
57
What are type III reactions mediated by?
IgG/IgM Antibodies against **soluble** antigen-immune complex deposition
58
Mechanism behind type III reactions?
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
What is onset time of type III reactions?
3-8 hours
60
What type of reaction is rheumatoid arthritis? Mechanism?
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
What type of reaction is SLE?
Type III
62
What is tolerance?
T and B cells that recognise your own antigens should be excluded in the secondary lymphoid organs
63
What causes a lack of tolerance?
B cells regonises self-cells as foreign --\> autoimmunity results
64
Describe reaction during SLE
* 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
What is expected blood test result for C3 and C4 in SLE?
Low amounts as C3 and C4 used up
66
What areas of the body are particularly vulnerable to type III reactions?
* Kidneys - complexes in high concentration due to filtering * Joints - plasma filtered to synovial fluid
67
Vasculitic rash
68
What are type IV reactions mediated by?
Antigen-specific **activated T cells**
69
Onset time of type IV reactions?
48-72h
70
Mechanism behind type IV reactions?
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
What are the common antigens involved in type IV reactions?
* Metals (e.g. nickel) * Tuberculin test * Poison ivy
72
What type of reaction is contact dermatitis?
Type IV
73
Breakdown of different types of reactions
74
Comparison of different types of hypersensitivity
75
Which Antibody mediates Type 1 hypersensitivity?
IgE
76
Which Antibodies medicate the Type III hypersensitivity?
IgM and IgG
77
Name 3 chemical mediators produced by a mast cell
Leukotrienes, histamine, Prostaglandins, proteases, chemotactic factors
78
What is the hallmark cytokine of Type I reactions?
IL-4
79
What is the hallmark Ig in type I reactions?
IgE
80
Which cell is responsible for the production of IL-4 in type I reactions?
Th2 cells
81
How are mast cells and basophikls 'sensitised' during type I reactions?
* 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
How does IgE cause the release of **preformed mediators** in type I reactions?
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
Which APC is involved in sensitisation in type I reactions?
Dendritic cells
84
Explain what causes vomiting during anaphylaxis
Histamine stimulates gastric acid secretion
85
Explain what causes dizziness during anaphylaxis
Histamine causes vasodilation which lowers blood pressure
86
Explain what causes swelling during anaphylaxis
Histamine increases permeability of blood vessels
87
Explain what causes wheezing and SOB during anaphylaxis
Histamine causes bronchoconstriction
88
Explain what causes tachycardia during anaphylaxis
Histamine increases release of adrenaline
89
Explain what causes uritcaria rash during anaphylaxis
Swelling and inflammation due to permeability and vasodilation
90
Difference between intradermal and skin prick tests?
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
Why is the oral challenge test rarely done?
Can put patient at risk
92
Treatment for dermatitis?
topical steroids and moisturisers
93
Where do immune complexes tend to build up?
In the basement membranes of tissues which have particularly high rates of blood filtration
94
What is effect of build up of immune complexes?
Inflammatory response and attraction of leukocytes
95
Which antibodies are involved in; a) type I b) type II c) type III d) type IV
a) IgE b) IgG, IgM c) IgG, IgM d) none
96
What is the response time of; a) type I b) type II c) type III d) type IV
a) 15-30 mins b) minutes-hours c) 3-8 hours d) 48-72 hours
97
cell apearance in; 1. type I 2. type II 3. type III 4. type IV
1. weal and flare 2. lysis and necrosis 3. erythema, oedema, necrosis 4. erythema induration
98
What is erythema?
redness of the skin or mucous membranes, caused by hyperemia (increased blood flow) in superficial capillaries
99
Which hypersensitivity reactions is the complement system involved in?
II and III
100
Which hypersensitivity reaction are basophils and eosinophils involved in?
I
101
What type of reaction is Goodpasture's nephritis?
Type II (cytotoxic)
Yr 2 - EMS
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