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Module 3 > Food Intolerance > Flashcards

Food Intolerance Flashcards

1
Q

What are the most common reasons for food “allergy”?

A

irritants- curry and acidity; gas; food poisoning; biochemical

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2
Q

What are hte common biochemical food intolerances?

A

lactose intolerance and fructose/sorbitol malabsorption

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3
Q

Give examples of non-IgE mediated food allergies?

A

food protein induced enterocolitis syndrome; food protein induced proctocolitis and enteropathies

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4
Q

Give examples of mixed IgE and non-IgE mediated food allergies?

A

cows milk protein allergy and eosinophilic oesophagitis/gastroenteritis

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5
Q

What is the definition of food allergy?

A

ingestion of a small amoutn of food elicits an abnormal immunologically mediated clinical response

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6
Q

When is the reaction with IgE mediated food allergy?

A

mins to 2hrs

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7
Q

When is the typical onset with cell-mediated food allergy?

A

1hr to 8 hrs

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8
Q

What is the difference in prevalence between IgE-mediated food allergies in children and adults?

A

children: 5-7%; adults: 1.4%- Young

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9
Q

What is the difference between perceived and actual prevalence of food allergy in adults?

A

actual- 1.4% vs perceived- 20.4% - Young

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10
Q

What are the most common food allergies?

A

milk; egg; peanut; tree nuts; seafood; shellfish; soy and wheat

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11
Q

what are the features of allergenic foods?

A

polar glycoproteins; heat; acid and protease resistant

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12
Q

What is the pathway in IgE mediated HS?

A

mast cell/basophil with specific IgE on surface, if allergen binds and cross-links activates the cell and results in degranulation with release of inflammatory mediators

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13
Q

What are hte features of mucosal tolerance?

A

epithelial barrier with IgA; low Ag presentation; no specific IgE; immunosuppressive environment- IL-10; TGFb and Th3 and Tregs

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14
Q

What are hte features of hte mucosal barrier in food hypersensitivity?

A

increased antigen load; increased permeability of hte gut wall; DC presentation and stimualtion of Th2 cells

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15
Q

What is the effect of IL-5?

A

eosinophil activation

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16
Q

What are hte features of food allergy?

A

itching; hives; rhinorrhea; wheezing; angioedema; anaphylaxis-circulatory collapse

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17
Q

What are the features of gastrointestinal hypersensitivity?

A

N&V&D; stomach pain

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18
Q

How is food allergy diagnosed?

A

skin prick testing; RAST; food challenges

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19
Q

What is RAST?

A

radioallergosorbent test- detects the presence of IgE antibodies to a particular allergen

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20
Q

What is the gold standard of food allergy diagnosis?

A

double-blind placebo controlled food challenges

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21
Q

What are hte atopic diseases?

A

asthma; hay-fever; food allergy; eczema; atopic dermatitis

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22
Q

What is the risk of atopic disease if both parents have different atopic syndromes?

A

58%

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23
Q

What is the risk of atopic disease if both parents have the same clinical disease?

A

78%

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24
Q

What is the association of HLA with atopy?

A

DR4 and/orDR7 alleles are seen in 42% of patients vs 2% of health subjects

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25
Q

What supports the hygiene hypothesis?

A

studies showing less allergy in less economically devleoped countries; lack of early exposure to diret and germs in Western coutnires; loss of tolerance to food proteins

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26
Q

What are the features of timing of oral exposure to foods that may impact oral tolerance?

A

age at weaning; different quantities; breastfeeding

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27
Q

What is the recommended timing weaning?

A

introduction to solids after exlcusive breastfeeding at 4-6 months

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28
Q

What is the mx of urticaria?

A

histamine

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29
Q

What is hte MOA of sodium cromoglycate?

A

staibilises mast cells

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30
Q

What is the mx of anaphylaxis?

A

adrenaline; b2 agonists; o2; fluids; antihistamines; steroids; glucagon

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31
Q

What demonstrates the food allergy has increase in the past 10-15 years?

A

peanut allergy has increased two fold in children

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32
Q

How are food-specific IgE levels related to food allergy?

A

many individuals have detectable food-specific IgE but no clinical allergy, but increasing concentrations of specific IgE increases risk of clinical allergy

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33
Q

What is associated with food allergy severity?

A

reduced platelet activating factor acetylhydrolases- unable to inactivate PAF; target organ sensitivity

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34
Q

Give an exmaple of where target organ sensitivity affects allergy severity?

A

people with asthma are at higher risk of severe or fatal anaphylaxis

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35
Q

What demonstrates that food allergy is genetically determined?

A

peanut allergy is 10x as likely in a child with a sibling who is peanut allergic

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36
Q

What is oral allergy syndrome?

A

oral tolerance is bypassed because sensitisation happens through respiratory route e.g birch pollen protein may result in allergy with raw apples due to cross-reactivity

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37
Q

What mice models demonstrate the nonoral exposure to stable proteins invokes allergy?

A

epicutaneous application of food proteins may result in sensitisation leading to systemic allergy following oral exosure

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38
Q

What human data suggests that skin exposure may be sensitising?

A

peanut allergy was associated with the use of infant skin creams containing peanut oil-6.8 OR

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39
Q

What is the function of enzymes; bile salts and extremes of pH in oral tolerance?

A

combine to make allergens less immunogenic

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40
Q

What suggests that low pH is important in oral tolerance?

A

infants have a higher gastric pH which may reduce the efficiency of hte infant mucosal barrier- food allergy is more common in infants; antacid mediations increase the risk of sensitisation to ingested foods

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41
Q

What is the function of Th3 cells?

A

CD4 cells which secrete TGFb

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42
Q

Why are intestinal epithelial cells thought to play an important role in oral tolerance?

A

can process luminal antigen and present it to T cells on MHC-II but lack second signal thereby inducing tolerance

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43
Q

What suggests that the gut microbiotia is important in oral tolerance?

A

mice raised in a germ free environment fail to develop normal tolerance; if treated with antibiotics or lack TLR4- more prone to developing peanut allergy

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44
Q

What suggests that Tregs are important in oral tolerance?

A

in IPEX syndrome where there is mutation in FOXP3- syndrome includes severe food allergies and atopic dermatitis

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45
Q

Why is there Th2 direction in allergic immune reponse?

A

murine models demonstrate that DCs direct T cells towards a Th2 profile at the time of antigen presentation in the gut

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46
Q

How is the cooking of allergens related to allergy induction?

A

peanut consumption is nearly equivalent in US and China wwhereas in US much higher rates of allergy; US roast peanuts whereas in China they boil or fry- roasting increases stability and allergenicity of the peanuts

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47
Q

Where is the current direction in treatment of allergy?

A

immunotherapy

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48
Q

What have been the results with peanut allergy subcut immunotherapy?

A

resulted in modest clinical improvement but significant adverse effects including recurrent anaphylacis

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49
Q

What are the approaches to improving immunotherapy for allergy?

A

change the route of administration eg sublingual or modifying hte treatment proteins

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50
Q

What have been the efficacy of reponse with oral immunotherapy for egg and milk allergy in children?

A

70-80%

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51
Q

What is the difference between desensitisation and tolerance?

A

desensitisation- allergen is ingested without symptoms dyuring treatment but has to be ingested daily vs tolerance where food may be ingested without allergy symptoms despite periods of abstinnce

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52
Q

What is the function of engineered proteins in immuntherapy?

A

identify IgE binding sites on proteins and mutate the sites to ablate IgE binding whilst preserving the proteins ability to stimualte T cells

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53
Q

How would peptide immunotherapy work?

A

create a vaccine composed of numerous small peptides that span the sequence of native allergenic proteins which presents T cell epitopes but avoids crosslinking of IgE

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54
Q

How may combination strategies in immunotherapy be used?

A

use of anti-IgE antibodies to quell allergic reactions to immuntherapy

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55
Q

What causes a failure to digest lactose?

A

low lactase activty in the small intestinal brush border - hypolactasia

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56
Q

What age group have high lactase?

A

neonates

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57
Q

What is the normal level of lactase in adults?

A

lactase non-persistance

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58
Q

Which ethnic groups have lactase persistence?

A

most but not all Northern Europeans

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59
Q

What happens when there is lactose malabsorption?

A

lactose breaks down in the colon by microbes resulting in hydrogen; carbon dioxide and lactate

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60
Q

How is lactose intolerance diagnosed?

A

history or lactose-H2 breath test

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61
Q

What is the lactose-hydrogen breath test?

A

after oral lactose there is high hydrogen in the breath

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62
Q

What is lactose broken down into in the small intestine by lactase?

A

glucose/galactose

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63
Q

Give an example of a polymorphism that results in persistance/non-persistance of lactase?

A

trans polymorphism upstream of lactase start site in Finnish population- Enattah

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64
Q

When was milk tolerance thought to begin?

A

in the Middle East 11,000 years ago with the start of agriculture and domestication of dairy animals which spread to central europe by 7,500 years ago lactase persistence emerged in central europe

65
Q

What are the symptoms of fructose and sorbitol malabsorption?

A

abdo pain and diarrhoea following fruit juices or diet drinks

66
Q

What causes the symptoms of fructose/sorbitol malabsorption?

A

small intestinal malabsorption of these monosacchrarides results in metabolism in the colon

67
Q

How is frcutose/sorbitol malabsorption diagnosed?

A

history and breat hydrogen afer ingestion

68
Q

Why are fermented dairy drinks more popular in the middle east?

A

reflects lactase non-persistence

69
Q

What is the result of oligosaccharide ingestion?

A

they are prebiotics which result in growth of good bacteria

70
Q

What are polysaccharides broadly known as?

A

fiber

71
Q

What is the result of fiber ingestion?

A

bulking effect and increased transit through the gut

72
Q

What are FODMAPs?

A

fermentable oligo; di- and mono-sacchradies and polyols

73
Q

What are the common physiologic effects of FODMAPs?

A

increase water retention in the small intestine via osmotic effects; rapid fermentation by intestinal bacteria leading to release of gas and short-chain farry acids- pain and bloating and abnormal motility

74
Q

What is typically seen on duodenal histology with coeliac disease?

A

subtotal villous atrophy with crypt hyperplasia

75
Q

What should be avodied in a gluten free diet?

A

no wheat; barley or rye products

76
Q

What is the definition of coeliac disease?

A

inflamamtory disease of upper small intestine resulting from gluten ingestion in genetically susceptible individuals

77
Q

What is the prevalence of coealic disease?

A

1 in 100

78
Q

Why may coealic patients have clotting problems ?

A

vitamin K malabsorption

79
Q

What are hte frequent symptoms of coelaic disease?

A

fatigue; steatorrhea/diarrhoea; weight loss; anameia

80
Q

Who first described coeliac disease in children?

A

Gee in 1888

81
Q

What is the avergae age of diagnosis of coeliac disease?

A

> 50

82
Q

What is the gold standard of diagnosis of coeliac disease?

A

intestinal biopsy

83
Q

What is refractory coeliac disease?

A

symptoms and villous atrophy on strict GFD >1 year

84
Q

What is typically seen with potential CD?

A

parents with coeliac disease, positive bloods but normal biopsy

85
Q

When were endomysial antibodies first desribed?

A

1983 by Chorzelski

86
Q

How are endomysial antibodies detected?

A

indirect immunofluoresnce on monkey oesophagus

87
Q

What type of antibody are endomysial natibody?

A

IgA- IgG if selective IGA deficiency

88
Q

What is the specific and sensitivity of endomysial antibodies?

A

99% specificity and 95% sensitivity

89
Q

What is the autoantigen recognised by endomysial antibodies?

A

tissue transglutaminase

90
Q

What is the result of ingestion of gluten ?

A

leads to generation of harmful gluten peptides which in predisposed individuals can induce adaptive and innate immune repones

91
Q

What HLA groups does coeliac disease almost exclusively occur in?

A

HLA-DQ2 and/or HLA-DQ8 haplotypes

92
Q

What suggests taht there are other genetic and/or environmental factors in disease onset aside from DQ2/DQ8?

A

only a fraction of individuals with that haplotypes ingesting gluten develop coealic disease

93
Q

Which gender is coelaic disease more common in?

A

females

94
Q

How has prevalence of coeliac disease been changing over time?

A

appears that according to seroprevalence that over 20 years there has been 2-fold increase, which has been confimred by recent metanalyses in biopsy-proven coeliac disease

95
Q

What are the potential environmental factors in coeliac disease?

A

consumption of gluten containing cereals; infection in the early years of life and lower economic status; inferior hygienic environment

96
Q

What is gluten made up of ?

A

a complex mixutre of alcohol-soluble gliadins and alcohol-insoluble glutenins

97
Q

Whiat amino acids are gliadins and glutenins rich in?

A

proline and glutamine

98
Q

What is the result of the proline rich content of gluten?

A

proteins are fairly resistance to proteolytic processsing by gastric, pancreatic and brush-border enzymes

99
Q

What is the function of transglutaminase?

A

converts glutamine residues in gluten peptides to glutamic acid in a deamidation reaction

100
Q

What is the result of deamidation of glutamine?

A

enhances the binding of gluten peptides by increasing their affinity to HLA-DQ2 on APCs

101
Q

How much of the genetic risk are HLA-DQ2 and HLA-DQ8 thought to account for?

A

25-40%

102
Q

What is the carrier frequency of HLADQ2 nad DQ8?

A

around 40%

103
Q

What are the alleles that encode for HLA-DQ2?

A

HLADQA105:01 and HLADQB102:01

104
Q

What is HLA-DQ8 encoded for by?

A

HLADQA103 and HLADQB103:02

105
Q

How many patinets carry HLA-DQ2?

A

90%, and almost all the reslt carry HLA-DQ8

106
Q

What is the adaptive immune response in coeliac disease characterised by?

A

mucosal gluten-specific CD4 T cells ; antibodies towards wheat gliadin and enzyme TG2

107
Q

How do gluten peptides access the lamina propria?

A

actively through the transepithelial route of passively by paracellular flux caused by comrpomised petihlial barrier function (GI infection is associated with coeliac, some genetic disposition to poorly functioning tight junctions?)

108
Q

What may explain why only some individuals with HLA-DQ2/DQ8 develop coeliac disease?

A

TCRs are generated in a ranom process so high-affinity TCRs specific for gliadin may be produced in a minority of those patients

109
Q

Which cytokiens do activated gluten speicifc CD4 T cells produce?

A

IFNy and IL-21

110
Q

What are hte innate immune responses in coeliac disease characterised by?

A

increased mucosal expression of IL-15; IL-18 and type I IfNs which are produced by stressed intestinal epithelial cells or DCs

111
Q

What is the function of IL-15 in coeliac disease?

A

inhibits Tregs promoting loss of oral tolerance and immune regulation and by licenses IELs to kill intestinal epithelial cells

112
Q

What is the function of IELs?

A

a heterogeneous population of T cells that patrol the mucosal barrier and exert effector functions without antigen-specific priming- interact with intestinal epithelial cells and can induce apoptosis when required

113
Q

What suggests that microoragnisms are invovled in the development of coeliac disease?

A

specific microbiota species assocaited with coeliac disease; GI infections increase the risk of developing coeliac diseae

114
Q

What suggested a role for early-life feeding practices in coeliac disease ?

A

in the Swedish epidermic, when dietary gluten introduction was postponed, with infant food gluten content increased

115
Q

What happens to tissue transaminase IgA antibodies with GFD?

A

decrease but if rechallenged increase back up

116
Q

What is dermatits herpetiformis?

A

vesicular; pruritic rash affecting particularly the arms and shoulders asssociated with villous atrophy and gluten sensitivity

117
Q

What is seen on skin biopsy with dermatitis herpetiformis?

A

granular IgA deposits

118
Q

What are the metabolic complications of coeliac disease?

A

nutrient malabosprtion and impaired nutriotnal status; osteoporosis;

119
Q

What are hte neoplastic complications of coeliac disease?

A

enteropathy-associated T cell lymphoma; adenocarcinoma

120
Q

What happens to calcium and bone mineral density wiht GFD?

A

reduced calcium absorption returns to normal with 1 year of GFD; with improvemnt in BMD

121
Q

What is the difference in progonsis between coeliacs and other patients for primary small bowel malignancy?

A

surivial at 30 months if 52% overall but 13% in coeliacs

122
Q

What is the commonest cause of malabsorption?

A

coeliac disease

123
Q

How is coeliac histology in the small intestine graded?

A

Marsh grading

124
Q

How are tissue transglutaminase antibodies measured ?

A

ELISA

125
Q

What is the function of tissue transglutaminase ?

A

cross-links glutamine residues in gliadin creating neoantigens, by deamindating glutamine to glutamate

126
Q

What is the specific polypeptide identified in coeliac disease?

A

33-mer peptide of a2-gliadin

127
Q

What causes the enteropathy in CD?

A

inflammatory damage and apoptosis

128
Q

What causes the histological changes in CD?

A

enterocyte apoptosis results in villous atrophy and stimulated regeneration results in hyperplastic cyrpts

129
Q

What happens to the apoptotic score when a GFD is started?

A

reduces - Moss

130
Q

How many immunogenic epitopes does the 33-mer carry?

A

multiple copies of three eptiopes

131
Q

What is the rate of coeliac disease in first degree relatives?

A

1 in 10

132
Q

What is the evidence for silent disease?

A

> 30% of dermatitis herpetiformis have no GI symtpoms; population screening- prevalence of undiagnosed cases is aroudn 10x that os previously disgnoased

133
Q

What are the features of sero-positive patients in the Cambridge Gp health study?

A

lighter, good/excellent health, less likely to smoke, lower cholesterol, Hbl increased risk of osteoporosis and mild anaemia

134
Q

What indicates that there is something predisposing girls to coeliac disease more than sex-hormone determined phenotype?

A

in children aged 7, there is an increased prevlance in girls - x2

135
Q

What groups have a higher prevalence of coeliac disease?

A

T1DM; thyroid disease; addison’s ; osteoporosis; anaemia blood donors; IBS; turners; downs

136
Q

What is the MZ concordance of coeliac disease?

A

aroudn 80%

137
Q

What is the frequence of HLA-DR3 in Northern European patients?

A

65-95%

138
Q

What HLA group is more common in mediterranaean patietns?

A

DR5/DR7

139
Q

How may patients with coeliac disease who are DR3 or DR5/DR7 heterozygous express the same HLA-DQ molecule?

A

in DR3 individuals the 2 genes (has 2 chains) are on the same chromosome whereas in DR5/7 they are located in trans

140
Q

What DR allele is associated with DQ8?

A

DR4

141
Q

What is the concordance for coeliac disease in HLA-matched siblings and what does this indicate?

A

aroudn 30%- other genes must account for inheritability (MZ twins is 80%)

142
Q

What diseases are polymorphisms in the CTLA4 exon associated with?

A

IDDM; Grave’s; coeliac–Hunt

143
Q

What gene in the MHC region which is non-HLA is associated with coeliac disease?

A

MICA- Spanish (involved in IELs and apotosis)

144
Q

Variants in what cytokine regions are associated with coeliac disease?

A

IL2 and IL21

145
Q

What is the function of IL-21?

A

enhances B, T, NK cell proliferation and IFNy production- greatly increased in untreated coalic dseiase

146
Q

Why is there thought to a reduction in IL2 in untreated Coeliac disase?

A

in NOD mouse IL2 influences Treg activity determines susceptibility to AI diseases

147
Q

How many non-HLA coeliac disease associated regions are there?

A

8

148
Q

What are the 8 non-HLA associated regions with coelaic disease identified in GWAS coding for?

A

cytokines; chemokine receptor signalling; receptors; proteins invovled in immune activation

149
Q

What is the function of IL-18?

A

induces T cells to synthesis IFNy

150
Q

How many of the regions associated with coealic disease overlap with T1DM?

A

4/9

151
Q

What genes did further GWAS follow-ups identify?

A

genes involved in the NFkB pathway

152
Q

What do the new 8 variants explain in terms of heritability?

A

<5%

153
Q

What is the relationship of a long noncoding RNA near IL18 receptor assocaited protein with coeliac disease?

A

increases susceptibility as influences IL18RAP expressed and causes increased inflammation

154
Q

What did a study in Denver with risk HLA haplotypes determine about the timing of gluten introduction and development of CD?

A

if introduced before (5 fold increase) or after 4-6 month period- increased risk –Norris

155
Q

How was rotavirus infection associated with coeliac disease?

A

1 rotavrisu infection increased risk, whilst >2 infections increased risk even further

156
Q

What is thought to be the reason that rotavirus would increase susceptibility to coealic disease?

A

allows gluten through the intestine and the creation of antibodies

157
Q

What have further studies after the Denver study found?

A

intervention studies have not backed up the associations found in the Denver study with weaning

158
Q

How does IFNy produced by stimulated CD4+ T cells contribute to mucosal damage in coeliac disease?

A

stimulates FasL expression on IEL CD8+ cells and MMP expressiong by fibroblasts both leading to enterocyte destruction

159
Q

Why do people who have been ingesting gluten all their lives start to develop coeliac disease?

A

may be due to infection/ inflammation that increases permability of hte mucosal barrier allowing gluten entry to the subepithelial region, with increased release of tTG in response to inflammation or mechnical stress

Module 3 (33 decks)

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