Immunology Flashcards

1
Q

What is an allergy?

A

Hypersensitivity of the immune system to allergens

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2
Q

What are allergens?

A

Proteins that the immune system recognises as foreign and potentially harmful

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3
Q

What is atopy?

A

Predisposition to having hypersensitivity reactions to allergens

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4
Q

What are the atopic conditions?

A
Eczema
Asthma
Hayfever
Allergic rhinitis
Food allergies
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5
Q

What is the leading theory for the origin of allergies?

A

The skin sensitisation theory

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6
Q

What is the skin sensitisation theory?

A

That there is a break in an infants skin (from eczema or infection) that allows allergens to cross the skin and react with the immune system. If there is then consequent lack of exposure to the allergen in the GI tract, it causes the immune system to become sensitised to the antigen.

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7
Q

What is Type 1 hypersensitivity?

A

Antibodies trigger mast cells and basophils to release histamines and cytokines, leading to immediate reaction

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8
Q

What kind of allergy is type 1 hypersensitivity?

A

Food allergy

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9
Q

What is the normal presentation of a type 1 hypersensitivity reaction?

A

Acute itching, facial swelling, urticaria

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10
Q

What antibodies are involved in a type 1 reaction?

A

IgE

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11
Q

What happens in a type 2 hypersensitivity reaction?

A

Antibodies react to an allergen and activate the complement system, leading to direct damage to local cells (cytotoxic)

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12
Q

What antibodies are involved in type 2 hypersensitivity reactions?

A

IgG and IgM

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13
Q

What are some examples of type 2 hypersensitivity reactions?

A

Haemolytic disease of the newborn

Transfusion reactions

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14
Q

What happens in Type 3 hypersensitivity reactions?

A

Immune complexes accumulate and cause damage to local tissues

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15
Q

What are some examples of type 3 hypersensitivity reactions?

A

SLE
Rheumatoid arthritis
HSP

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16
Q

What happens in type 4 hypersensitivity reactions?

A

Cell mediated hypersensitivity reactions caused by T-cells being inappropriately activated, causing inflammation and damage to local tissues

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17
Q

What are some examples of type 4 hypersensitivity reactions?

A

Organ transplant rejection

Contact dermatitis

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18
Q

What acronym helps remember hypersensitivity reactions?

A
ACID: 
Anaphylaxis
Cytotoxic
Immune complex
Delayed type
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19
Q

How are allergies usually diagnosed?

A

Detailed history

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20
Q

What are the 3 main ways to test for allergy?

A

Skin prick testing
RAST testing
Food challenge testing

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21
Q

Why are skin prick and RAST test unreliable and misleading?

A

They test for sensitisation and not allergy

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22
Q

What is RAST testing?

A

Blood tests for total and specific IgE

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23
Q

Why should you be cautious when performing an allergy test?

A

Often come back showing patient is sensitised to many things you have tested for, but they don’t necessarily need to avoid these things

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24
Q

What is the gold standard test for diagnosing allergy?

A

Food challenge testing

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25
Q

How is skin prick testing performed?

A

Drops of different allergen solutions are applied to a patch of skin, along with a water and histamine control. After 15 minutest the size of the wheals of each allergens are assessed

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26
Q

What is patch testing?

A

Patch containing allergen is placed on skin. After 2-3 days the reaction is assessed

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27
Q

What allergies can patch testing help diagnose?

A

Allergic contact dermatitis (latex, perfumes, cosmetics or plants)

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28
Q

What happens during food challenge testing?

A

Child given increasing quantities of an allergen to assess reaction

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29
Q

How are allergies managed?

A

Avoid allergen
Prophylactic antihistamines
Epipen

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30
Q

How can you treat allergic reactions?

A

Antihistamines
Steroids
IM adrenaline for anaphylaxis

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31
Q

What is anaphylaxis?

A

Life threatening type-1 hypersensitivity reaction

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32
Q

What happens during anaphylaxis?

A

IgE stimulates mast cells to rapidly release histamine and other pro-inflammatories, causing rapid onset of symptoms

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33
Q

What is mast cell degranulation?

A

When mast cells rapidly release their contents (histamine and pro-inflammatory chemicals0

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34
Q

What are the key features that differentiate anaphylaxis from a non-anaphylactic allergic reaction?

A

Compromise of the airways, breathing or circulation

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35
Q

What symptoms may be present in anaphylaxis?

A
Urticaria
Itching
Andio-oedema (face swelling)
Abdominal pain
SOB
Wheeze
Larynx swelling
Tachycardia
Lightheadedness
Collapse
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36
Q

What is urticaria?

A

Hives- red, itchy welts

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37
Q

What are the principles of anaphylaxis management?

A

ABCDE
Im adrenaline
Antihistamines
Steroids

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38
Q

What should happen after an anaphylactic reaction and why?

A

Period of observation and assessment in cause a biphasic reaction occurs

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39
Q

How can anaphylaxis be confirmed retrospectively?

A

Measuring serum mast cell tryptase within 6 hours of the event

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40
Q

What are the indications for an adrenalin auto-injector?

A

All children and adolescents with anaphylactic reactions
May be given to those with generalised allergic reactions with specific risk factors: (steroid inhalers, poor access to medical treatment, nut or sting allergies, significant co-morbidities)

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41
Q

What kind of reaction is allergic rhinitis?

A

IgE-mediated type 1 hypersensitivity reaction

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42
Q

What happens in allergic rhinitis?

A

Environmental allergens cause allergic inflammatory response in nasal mucosa

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43
Q

What are the different types of allergic rhinitis?

A

Seasonal
Perennial
Occupational

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44
Q

What is an example of seasonal allergic rhinitis?

A

Hayfever

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45
Q

What is an example of perennial allergic rhinitis?

A

House dust mite allergy

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46
Q

What are the symptoms of allergic rhinitis?

A

Runny, blocked and itchy nose
Sneezing
Itchy, red, swollen eyes

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47
Q

What are the common triggers of allergic rhinitis?

A
Tree pollen
Grass
House dust mites
Pets
Mould
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48
Q

How is allergic rhinitis managed?

A
Avoid trigger:
Cleaning (hoovering, changing sheets regularly) 
Stay inside during summer 
Minimise contact with pets
Medications
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49
Q

What can be taken prior to exposure to reduce allergic symptoms?

A

Oral antihistamines

50
Q

What are some examples of non-sedating antihistamines?

A

Cetirizine
Loratidine
Fexodenadine

51
Q

What are some examples of sedating antihistamies?

A

Chlorphenamine

Promethazine

52
Q

What can be given to help allergic rhinitis?

A

Nasal corticosteroid sprays

Nasal antihistamines

53
Q

What age range is most typically affected by cow’s milk protein allergy?

A

Infants and children under 3

54
Q

What is cow’s milk protein allergy?

A

Hypersensitivity to the protein in cow’s milk

55
Q

What are the two types of cow’s milk protein allergy?

A
IgE mediated (rapid)
Non-IgE mediated (slower reaction time)
56
Q

What is the difference between lactose intolerance and cows milk protein allergy?

A

Lactose is a sugar not a protein and intolerance is not an immune reaction

57
Q

What are the risk factors for developing a cows milk protein allergy?

A

Formula fed

Personal or family history of atopic conditions

58
Q

When does cows milk protein allergy usually become apparent?

A

When babies are weaned from breast milk to formula milk or food containing milk

59
Q

What are the common symptoms of cows milk protein allergy?

A
Bloating
Wind 
Abdominal pain
Diarrhoea
Vomiting
Allergic symptoms (swelling, hives, cough, sneezing, eczema)
60
Q

How is cows milk protein allergy diagnosed?

A

Full history

Skin prick testing

61
Q

How is cows milk protein allergy managed?

A

Avoid cows milk:
Breast feeding mothers avoid dairy products
Replace formula with hydrolysed formulas

62
Q

What are hydrolysed formulas?

A

Formulas that contain cow’s milk but the proteins have been broken down to avoid an immune response

63
Q

By what age do most children outgrow cow’s milk protein allergy?

A

3

64
Q

How are children with cows milk protein allergy reintroduced to milk?

A

Milk ladder (slowly progress up ladder until they develop symptoms)

65
Q

What is the difference between cow’s milk intolerance and cow’s milk allergy?

A

Cow’s milk intolerance has same GI symptoms but no allergic features

66
Q

Up to how may respiratory infections is it normal for a healthy child to have per year?

A

4-8

67
Q

What associated features would cause you to initiate further assessment in a child with recurrent infections?

A

Chronic diarrhoea
Failure to thrive
Appearing unusually well with severe infection
Significantly more infections than expected
Unusual or persistent infections

68
Q

What investigations may be done into recurrent infections in children?

A
FBC
Immunoglobulins
Complement proteins
Antibody responses
HIV test
CXR
Sweat test
CT chest
69
Q

What is SCID?

A

Severe combined immunodeficiency

70
Q

What causes SCID?

A

Genetic disorders that result in absent or dysfunctioning T and B cells

71
Q

How will SCID present?

A
Persistent severe diarrhoea
Failure to thrive
Opportunistic infections
Unwell after live vaccines
Omenn syndrome
72
Q

What is the most common cause of SCID?

A

Mutations in common gamma chain on X chromosome that codes for interleukin receptors on T & B cells.

73
Q

What is the inheritance pattern of the most common cause of SCID?

A

X-linked recessive

74
Q

What is Omenn syndrome?

A

Rare cause of SCID caused by mutation in RAG gene that codes for proteins in T & B cells

75
Q

What is the inheritance pattern of Omenn syndrome?

A

Autosomal recessive

76
Q

What causes the symptoms in Omenn syndrome?

A

Abnormally functioning and deregulated T cells that attack the tissues in the fetus or neonate

77
Q

What are the classic symptoms of Omenn syndrome?

A
Erythroderma (rash)
Alopecia
Diarrhoea
Failure to thrive
Lymphadenopathy
Hepatosplenomegaly
78
Q

How is SCID managed?

A
Specialist immunology centre
Treat underlying infections
Immunoglobulin therapy 
Sterile environment
Haematopoietic stem cell transplantation
79
Q

What is the action of B cells?

A

Produce antibodies

80
Q

What is hypogammaglobulinemia?

A

Deficiency in immunoglobulins caused by abnormal B cells

81
Q

What does hypogammaglobulinemia lead to?

A

Susceptibility to recurrent infections

82
Q

What is the most common immunoglobulin deficiency?

A

Selective IgA deficiency

83
Q

Where is IgA present?

A

Secretions of mucous membranes (saliva, resp/GI tract secretions, tears, sweat)

84
Q

What does IgA protect against?

A

Opportunistic infections

85
Q

How does IgA deficiency usually present?

A

Often asymptomatic

Recurrent mucous membrane infections

86
Q

When is IgA deficiency commonly tested for?

A

When testing for coeliac disease (anti-TTG and anti-EMA are IgA antibodies)

87
Q

What is common variable immunodeficiency?

A

IgG and IgA +/- IgM deficiency

88
Q

What causes common variable immunodeficiency?

A

Genetic mutation in genes coding for components of B cells

89
Q

What does common variable immunodeficiency lead to?

A

Recurrent respiratory tract infections, leading to chronic lung disease

90
Q

What are patients with common variable immunodeficiency more prone to?

A

Infections
Immune disorders (RA)
Cancers (Non-hodgkins lymphoma)

91
Q

How is common variable immunodeficiency managed?

A

Regular immunoglobulin infusions

Treat infections as they occur

92
Q

What is X-linked agammaglobulinaemia?

A

X-linked recessive condition that results in abnormal B cell development and deficiency in all classes of immunoglobulins

93
Q

What are some different T cell disorders?

A
DiGeorge syndrome
Purine nucleoside phosphorlyase deficiency
Wiskott-Aldrich syndrome
Ataxic telangiectasia
Acquired immunodeficiency syndrome
94
Q

What causes DiGeorge syndrome?

A

Microdeletion in a portion of chromosome 22, leading to developmenal defect in third pharyngeal pouch and third brachial cleft

95
Q

What is the main complication of DiGeorge syndrome?

A

Leads to underdeveloped thymus gland that is unable to make functional T cells

96
Q

What are the key features of DiGeorge syndrome?

A
CATCH-22:
Congenital heart disease
Abnormal facial features
Thymus gland underdevelopment
Cleft palate
Hypoparathyroidism + Hypocalcaemia
22nd chromosome affected
97
Q

What is Purine nucleoside phosphorylase deficiency?

A

Autosomal recessive condition that causes reduction in enzyme that protects against T-cell breakdown

98
Q

What is PNPase?

A

Enzyme that helps breakdown purines

99
Q

What builds up without the presence of PNPase?

A

dGTP metabolite

100
Q

What cells is dGTP toxic to?

A

Exclusively T cells

101
Q

What is WAS?

A

Wiskott-Aldrich syndrome

102
Q

What kind of genetic inheritance is Wiskott-Aldrich syndrome?

A

X-linked recessive

103
Q

What are the features of Wiskott-Aldrich syndrome?

A
Abnormal T cells
Thrombocyopenia
Immunodeficiency
Neutropenia
Eczema
Recurrent infections
Chronic bloody diarrhoea
104
Q

What is ataxic telangiectasia?

A

Autosomal recessive condition affecting the gene that codes for a protein that plays an important part in DNA coding

105
Q

What are the features of ataxic telangiectasia?

A
Low T-cells and immunoglobulins
Ataxia
Telangiectasia
Predisposition to cancers
Slow growth
Accelerated ageing
Liver failure
106
Q

What causes acquired immunodeficiency syndrome?

A

HIV leading to reduced numbers of CD4 T-cells

107
Q

What is the complement system most effective in dealing with?

A

Encapsulated organisms:
Haemophilus influenza B
Strep. pneumonia
Niesseria meningitidis

108
Q

What do complement deficiencies make children particularly susceptible to?

A

Infections of the respiratory tract, ears and throat

109
Q

What are complement deficiencies associated with?

A

Immune complex disorders (SLE)–> incomplete complement cascade leads to immune complexes building up and being deposited in tissues, leading to chronic inflammation

110
Q

What is the most common complement deficiency?

A

C2 deficiency

111
Q

What is a very important management step in patients with complement disorders?

A

Vaccinate against encapsulated organisms

112
Q

What is the action of Bradykinin?

A

Responsible for promoting blood vessel dilation and increased vascular permeability in the inflammatory response

113
Q

What does bradykinin cause?

A

Angioedema (swelling underneath skin)

114
Q

What is the action of C1 esterase?

A

Inhibits bradykinin

115
Q

What does an absence of C1 esterase cause?

A

Intermittent angioedema in response to minor triggers

116
Q

Where does angioedema most commonly occur?

A

Lips and face but can occur anywhere, including the resp and GI tract

117
Q

What are the complications of angioedema?

A

May last several days

Can occur in he larynx and compromise the airway

118
Q

What is Hereditary angioedema?

A

C1 Esterase inhibitor deficiency–> condition causing excess bradykinin leading to angioedema

119
Q

How are patients with C1 esterase inhibitor deficiency treated?

A

IV C1-esterase inhibitor

120
Q

How is hereditary angioedema tested for?

A

Check levels of C4, will be low in this condition

121
Q

What does mannose-binding lectin deficiency lead to?

A

Inhibition of the alternative pathway of the complement system

122
Q

What is the complication of mannose-binding lectin insufficiency?

A

In patients who are susceptible to infection, can lead to a more severe disease