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PATHOLOGY > allergy > Flashcards

allergy Flashcards

1
Q

definition of an allergic disorder

A

immunological process that results in immediate and reproducible symptoms after exposure to an allergen

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2
Q

what type of hypersensitivity reaction is allergy

A

IgE mediated type 1 hypersensitivity reaction

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3
Q

what is an allergen

A

harmless substance that can trigger an IgE mediated immune response and may result in clinical symptoms

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4
Q

definition of sensitisation

A

detection of specific IgE either by skin prick testing or in vitro blood tests: OCCURS MORE OFTEN THAN ALLERGIC DISEASE

Presence of IgE is necessary but not specific for dx of an allergic disease

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5
Q

differentiate the immune response to microbes vs worms, venoms and allergens (proteases, phytochemicals, xenobiotics and pollen

A

for microbes - the immune system recognises PAMPs
for worms, venoms and allergens (proteases, phytochemicals, xenobiotics and pollen the immune system recognises loss in tissue func ie disruption of epithelial barrier - type 2 immune response

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6
Q

summarise Th2 immune response

A

Key initial sensor are the epithelial cells
Loss of epithelial barrier func, or epi stress ellicted by allergens – induce number of cytokines
Lymphoid cells – innate lymphoid cells type 2 – charactised by response to initial cytokine and the secretion of effector cytokines inc IL4 key in type 2 response, il5 or 13 – lead on yo on effector cells – act on effector cells

Interaction between dendritic and Th2 cells – lead to secretion of IL4 or IL13 Induce B cell to secrete IgE Ab and IgG4

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7
Q

summarise Th2 immune memory response

A

Cross linking of high affinity IgE receptor by allergen -> degran mast cells -> release histamine etc – act on endothelium, smooth muscle cells

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8
Q

overview of Th2 immune response

A

Defects in skin epithelial barrier (atopic dermatitis) are a significant risk factor for development of IgE antibodies.

Stressed or damaged epithelial cells secrete IL-25, IL-33, GM-CSF and TSLP which act on tissue immune cells (DC, basophils, type 2 innate lymphoid cells) to induce Th2 cells immune responses (IL-4, IL-5, IL-9, IL-13) and sensory neurons (itch/sneeze)

IL-4 plays a crucial role in development of Th2 immune responses and is only induced following peptide-MHC presentation to naïve/memory Th2 cells

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9
Q

how is there a rapid sx onset in allergy

A

release of inflammatory mediators
following allergen cross linking of IgE on surface of mast cells and basophils

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10
Q

what causes the delayed sx in allergy

A

CD4Th2 cell cytokine secretion (IL-4, IL-5, IL-13) and eosinophilic related tissue damage

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11
Q

role of Th2 cytokines

A

secreted by tissue lymphocytes
act on effector cells (eosinophils, basophils, epithelial cells, B cells, sensory neurons endothelium and smooth muscle cells)
to eliminate and expel pathogens allergens, and repair tissue damage

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12
Q

what factors promote IgE production

A

ag exposure
length of exposure
physical properties of allergen:
* associated with carrier proteins
* proteolytic activity (HDM) - break down the cross linking between epithelial cells
* linked to chitin - (carb: epi damage
* resistant to heat, digestive enzymes

Route of exposure determine whether IgG or IgE: oral (IgG) v skin, RT (IgE)
-> The early introduction of food after weening – prevent development of severe food related sx

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13
Q

how do we have immuen tolerance to food

A

immune response to food is: anergic CD4 T cells - lack inflammatory capacity, but -> reg T cells in GIT -> suppress tissue damage

oral -> immune tolerance
skin and resp (esp if breach in epi layer) -> IgE

Early weaning 4-6 months reduced risk of peanut and egg allergy

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14
Q

why is there an increase in allergic disorders

A

hygeine hypothesis - lack of exposure in children -> increase susceptability to allergic disease - Default for mech for immune response th2 immunity – this is deviated by exposure to lots of pathogens onto th1 and th17 immunity

increae in epithelial damaging agenbts from industrialisation, urbanisation and modern lifestyle eg phytochemicals and xenobiotics

Loss of symbiotic relationship with bacteria with reduction in biodiversity and alteration in composition of composition of gut skin and respiratory bacteria -> secretion of IgE rather than IgA and IgG

diet
* change in food processing and prep - peanut
* delayed intro of peanut if have egg allergy/atopic dermatitis
* lack of vit D and dietary fatty food

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15
Q

summarise how the Amish provide evidence for the hygiene hypothesis

A

Amish more LPS (lipopolysaccharides ie part of gram –ve bacteria – if stimulate more proinflammatory cytokines) in dust samples than Hutterites

Increased secretion of innate immune cytokine (TNF and IL1) by PBMC exposed to LPS in Amish than Hutterites

Dust samples from Amish suppress allergic inflammation in a murine asthma model

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16
Q

reasons for change in asthma prevalence

A

HDM, cat, cockroach, fungi are linked with exposure and sensoitisation
links for HDM with increase exposure to indoor allergen - children play more indoors than outside, exercise less and put on weight
childhood vaccines
increased exposure to broad spectrum abx

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17
Q

summarise hx of food allergy

A

1990 onwards: Significant increase in peanut allergy

Early oral exposure will protect against peanut allergy

Sensitisation to peanut and wheat can occur through the skin

Differences in preparation of peanuts (roast promotes IgE whereas boiled IgG)

Epidemic of delayed food allergy to red meat observed in SE USA for last 10 years: increasing case in France, Germany, Australia but not in UK to date)

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18
Q

what is involved in dx allergy

A

hx
ex
allergen specific IgE test - (sensitisation) - skin prick nad intradermal, or IgE blood tests

functional allergen tests :
in vitro
* Basophil activation
* Serial mast cell tryptase

ex vitro: open/blinded allegen challenge

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19
Q

hx for infants looking for allergy

A

Atopic dermatitis
Food allergy (milk, egg, nuts)

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20
Q

hx for children looking for allergy

A

Asthma (HDM, pets)
Allergic rhinitis (HDM, grass, tree pollens)

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21
Q

hx for adults looking for allergy

A

Drug allergy
Bee allergy
Oral allergy syndrome
Occupational allergy

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22
Q

clinical features of IgE allergic response

A

within mins - up to 3-4hrs after exposure
at least 2 organ systems
reproducible - after every exposuyre
sx can be triggered by cofactors eg exercise, alcohol, NSAIDs, viral infection

  • Skin: angioedema (swelling of lips, tongues, eyelids) , urticaria ( wheals or ‘hives’), flushing and itch
  • Respiratory tract: cough, SOB wheeze, sneezing, nasal congestion and clear discharge, red itch watery eyes
  • Gastrointestinal tract: nausea, vomiting and diarrhoea
  • Blood vessels and Brain: symptoms of hypotension (faint, dizzy, blackout) and a sense of impending doom
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23
Q

how do NSAIDs -> allergy

A

disruption of lining of GIT

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24
Q

why is hx important for allergy

A

used to select what allergens should be tested by skin prick and/or blood tests

Note: Link between exposure and onset symptoms may not be obvious
House Dust mite, Fungal and Staph skin colonisation, Red meat ingestion

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25
Q

sx not associated with IgE allergic reactions

A

Fatigue
Migraine (food can cause it – but it is because of high tyramine – not an allergy!!)
Recurrent abdominal pain, diarrhoea, constipation, bloating
Hyperactivity
Depression
Symptoms which vary over time, with antigen dose and source

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26
Q

summarise use of sensitisation tests

A

Presence of IgE - necessary not sufficient for allergic disease
sensitisation is more common than allergic disease
hx determine what tested for on blood test
if right hx - large skin wheals and high blood IgE - more likely associated with allergy
results of skin prick, or serum IgE dont predict reaction severity

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27
Q

summarise skin prick test method/theory

A

standard soln of allergen extract through skin prick to the forearm
positive control - histamine
-ve control - diluent
measure wheal

Antihistamines and some anti-depressants should be discontinued for at least 48 hours beforehand

IgE cross linking on mast cells -> degranulation and release of histamine and inflammatory mediators

28
Q

interpreting skin prick test

A

wheal ≥ 3mm greater than the negative control

has high +ve and -ve predictive value for aeroallergens

29
Q

advantages of skin prick test

A

Rapid (read after 15-20 minutes)

Cheap and easy to do

Excellent negative predictive value usually more than > 95%

Increasing size of wheals correlates with higher probability for allergy

Patient can see the response

30
Q

disadvantages of skin prick test

A

Requires experience to interpret

Risk of anaphylaxis: 1 in 3000

Poor positive predictive value: high false positive rate

Limited value in patients with dermato-graphism or extensive eczema

False negative results with labile commercial food extracts

31
Q

intradermal sensitisation tests

A

positive, negative controls and allergens into the skin
more sensitive, less specific than SPT
best used to follow up negative venom and drug allergy test - better than blood tests
use if -ve SPT but convincing hx
labour intensivce
more anaphylaxis risk

32
Q

sensitisation IgE blood tests

A

Detection of IgE to whole allergen extract or to individual protein (component) with in an allergen extract
automated assays

33
Q

limitation of sensitisation blood tests

A
  • Detection of IgE antibody with little clinical relevance
  • Allergen in low abundance may lead to reduced sensitivity
  • Clinical utility and cost of multiplex assay remain to be determined
  • Limited understanding of their role in diagnosis of allergic disorder outside of allergist/immunology specialists
34
Q

Component Resolved Diagnostics for allergy

A

Abundance and stability of individual protein within allergen extract can contribute to risk of allergic disease

CRD: Test for IgE sensitisation against individual protein within whole allergen extract

Diagnostic use
* Food allergy (nuts, egg, milk)
* Insect allergy (wasp and bees)
* Guide to immunotherapy (grass and HDM)

35
Q

Food components allergen tests for nuts

A

Storage proteins (2s albumins) - severe reactions
pathogenesis related proteins - (PR10 bet v1 homologue) which are also found in tree pollens, fruits and vegetables (ie cross-react with these things): mild reaction
Non specific lipid transfer proteins, also found in in fruit (peach) , tree pollen (plane), vegetables and legumes ( can be mild or severe)

36
Q

Food components allergen tests wheat

A

Omega-5-gliadin
better marker of specific wheat allergy than total wheat IgE

37
Q

Food components allergen tests egg and milk

A

Heat stable proteins ovomucoid (egg) and caseins ( estimate who outgrows allergy)

38
Q

Food components allergen tests fish and shellfish

A

Parvalbumin in fish, Tropomyosin in crustaceans (cross reactive)

39
Q

indications for blood sensitisation tets

A

No access to SPT and/or IDT - ie GP

can’t stop anti-histamines

history of dermatographism, extensive eczema

history of anaphylaxis – because wouldn’t want to do skin prick

Decision on who needs food challenge

Prediction for resolution of egg, milk, wheat allergy

monitor response to anti-IgE therapy

40
Q

summarise the risk profile of serum IgE for prediction of allergic sx

A

concentration - higher more likely = sx
molecular target (within whole extract or even individual epitope) can be linked to sx
affinity to target - higher associated with risk - dont measure affinity
Capacity of IgE antibody to induce mast/basophil degranulation

41
Q

summarise use of mast cell tryptase

A

it is a biomarker for anaphylaxis
tryptase is a pre-formed protein found in mast cell granules
systemic degranulation of mast cells -> increase in tryptase
peak at 30min - 2hrs
return to baseline by 6-12hrs - need serial measures
Failure to return to baseline after anaphylaxis may be indicative of systemic mastocytosis and hereditary alpha tryptasaemia

useful if anaphylaxis dx not clear
reduced sensitivity for food induced anaphylaxis because mucosal immune response (rather than drug/venum that effect endothelial cells)

42
Q

summarise basophil activation test for allergy

A

measure basophil response to IgE cross linking
Activated basophils increase the expression of CD63, CD203, CD300 protein on cell surface
used in dx of food and drug allergy - surrogate marker for challenge test
Efforts to standardise test to use by diagnostic laboratories to reduce need for challenge tests
problem is some of the population have basophils that are refractory to responding to ag

43
Q

summarise challenge tests for food and drug allergy

A

gold standard

ingest increasing volumes of the allergen
either double blind placebo/open challenge
close medical supervision - very expensive in terms of clinician time
difficult to interpret mild sx
risk of severe rn

44
Q

define anaphylaxis

A

Acute onset of symptoms and/or signs (minutes to 4-6 hours)
Severe/life threatening ABC problems
Skin and mucosal symptoms and signs (can be absent 10-20% of cases)

45
Q

clinical features of anaphylaxis

A

Skin (hives, itch, swollen lips, tongue, uvula) (84%),
Cardiovascular compromise (collapse, syncope, incontinence symptoms, drop in BP) (72%)
Respiratory compromise (SOB, wheeze, stridor, fall in PEF, hypoxemia in 68%.

resp more in children
adults - CVS

46
Q

epidemiology of anaphylaxis

A

Incidence: 1.5-8/100,000 persons years
incidence is increasing
prevalence 0.3-5.1%
more common aged 0-4yrs
children - food
adult - drug and venum
idiopathic in 20-30% of cases - shrimp, wheat, red meat

47
Q

mechanisms of anaphylaxis

A

Distinction doesn’t matter for treatment but might change Ix

IgE and complement - more associated with monoclonal ab infusion related reactions

48
Q

reactions that can mimic anaphylaxis

A

SKIN: Chronic urticaria and angioedema (ACE inhibitors)

THROAT SWELLING: C1 inhibitor deficiency

CARDIOVASCULAR: Myocardial infarction and PE

RESPIRATORY: Very severe asthma, vocal cord dysfunction, inhaled FB

NEUROPSYCHIATRIC: Anxiety or panic disorder

ENDOCRINE: carcinoid and phaechromocytoma

TOXIC: Scromboid toxicity (Histamine poisoning )

IMMUNE: Systemic mastocytosis

49
Q

lab dx of anaphylaxis

A

**serial tryptase mx - 30min-2hr, then at 24hr **
Concentration greater then (1.2 x baseline tryptase) + 2ug/L support a diagnosis of anaphylaxis.
it is retrospective dx
-ve doesnt rule out anaphylaxis - esp if food and have mucosal sx

50
Q

why is adrenaline used in the rx of anaphylaxis

A

α1 receptors: causes peripheral vasoconstriction, reverses low BP and mucosal oedema

β1 receptor: increases heart rate and contractility and BP

β2 receptor: relaxation of bronchial smooth muscle and reduces release of inflammatory mediators from mast cells/basophils

51
Q

emergency mx of anaphylaxis

A

supine
raise legs
IM adrenaline - if no response -> repeat and administer IV crystalloid fluids
anti-histamine after ABC corrected

52
Q

what is the refractory anaphylaxis protocol

A

if no improvement in ABC (no improvement after 2 IM adrenaline)
:

53
Q

follow up mx of anaphylaxis

A

refer - allergy clinic
ix cause
give info on - sx recognition, avoidance of triggers, epipen
prescription of emeergency anaphylaxis kit
Copy of management plan and training for patient, carers, school staff and GP
venum immunotherapy and drug desensitisation as appropriate
if food - refer to dietician
medic alert bracelet
utilise support groups

54
Q

definition of food allergy

A

adverse health effect arising from specific immune response that occurs reproducibly on exposure to a given food

55
Q

definition of food intolerance

A

non immune reactions which include metabolic, pharmacological and unknown mechanisms eg
* Food poisoning (bacterial, scromboid toxin)
* Enzyme deficiencies (lactase)
* Pharmacological (caffeine, tyramine )

56
Q

types of food aversion

A

fads
eating disorders

57
Q

types of food allergy

A

IgE mediated reactions (anaphylaxis, OAS)
Mixed IgE and cell mediated (atopic dermatitis)
Non IgE mediated (coeliac disease – type 4 hypersensitivity)
Cell mediated (contact dermatitis)

58
Q

do children outgrow food allergy

A

milk and egg yes
rarely peanut and treenut

59
Q

how does atopic dermatitis alter food allergy ix

A

an important risk factor for food allergy (indication for allergy testing even in absence of clinical history)

60
Q

important to determine in hx of food allergy

A

what does pt mean by allergy
Is it IgE or not
determine dose of allergen, how prepared, co-factors - all alter sx
hx of atopy
previous ix
elimination of food make a difference
ddx - intolerance, eating disorder, coeliac disease

61
Q

important to determine in hx of food allergy

A

what does pt mean by allergy
Is it IgE or not
determine dose of allergen, how prepared, co-factors - all alter sx
hx of atopy
previous ix
elimination of food make a difference
ddx - intolerance, eating disorder, coeliac disease

62
Q

ix for food allergy

A

hx
SPT/IgE blood test - if -ve basically excludes IgE mediated allergy
monitor results over time - for persistance or resolution
Fruit and vegetable skin prick test solutions are labile and it often better to useful use actual fruit or vegetable.
Testing for individual allergen protein component can distinguish between IgE sensitisation and IgE mediated allergy
gold standard is double blind oral food challenge

63
Q

mx of food allergy

A

avoidance
* education - labels, restaurants, school
* nutritional input
* mental health support

emergency
* anaphylaxis mx
* ensure allergic asthma is well controlled

64
Q

prevention of food allergy

A

breast feeding
early introduction of peanut

65
Q

what are the IgE mediated food allergy syndromes

A

anaphylaxis - Peanut, tree nut, shellfish, fish, milk and eggs are most common
food associated exercise induced anaphylaxis - food -> anaphylaxis if exercise within 4-6hr of ingestion - wheat, shellfish, celery
Delayed food-induced anaphylaxis to beef, pork, lamb
oral allergy syndrome

66
Q

summarise Delayed food-induced anaphylaxis to beef, pork, lamb

A

sx 3-6hr after red meat and gelatin IgE antibody to oligosaccharide alpha-gal (α1, 3-galactose) found in gut bacteria

Induced by tick bites:
* Human make ab to alpha-gal
* Human eat meatr with alpha-gal – Ig E

67
Q

summarise oral allergy syndrome

A

Limited to oral cavity, swelling and itch: only 1-2% cases progresses to anaphylaxis

Sensitisation to inhalant pollen protein -> cross reactive IgE to food

Onset after pollen allergy established: affect adults > young children

Respiratory exposure to pollen (birch) -> IgE directed to homologous proteins in stone fruits (apple, pear) vegetables (carrot) and nuts (peanut, hazelnut)

Cooked fruits, vegetables and nut cause no symptoms: heat labile allergens detected by component allergen tests

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