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Immunology > Allergy and hypersensitvity > Flashcards

Allergy and hypersensitvity Flashcards

1
Q

what is hypersensitivity?

A

when the immune system over-responds to harmless antigens that result in harm to the body.

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2
Q

what are the four types of hypersensitivity?

A 
type I: (A's) Allergic Anaphalaixs Atopy 
type II (B): antiBody
type III (C): immune Comlpex
type IV (D): Delayed

Type I: Classical allergy, mediated by the inappropriate production of specific IgE antibodies to harmless antigens

Type II: Caused by IgG and IgM antibodies that bind to antigens cells or tissues leading to cell or tissue damage

Type III: Caused by antibody-antigen complexes being deposited in tissues, where they activate the complement system and cause inflammation

Type IV: A delayed type hypersensitivity reaction caused by T helper cells traveling to the site of antigens, recruiting macrophages and causing inflammation (cell mediated)

*hypersensitivty can be antibody mediated (IgE, antibodies to self antigens, circulating antibody-antigen immune complex) or it can be t cell mediated (reaction to self antigens)

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3
Q

type I hypersensivity

A

(allergy)
allergens (antigens) produce allergic reactions

e.g. peanut, penicillin, pollen, house dust mite.

IgE mediated allergy is responsible for a number of atopic conditions e.g. food / drug allergy, asthma, allergic rhinitis, hayfever, eczema

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4
Q

sensitisation (type I)

A

he initial event that lead to the specific IgE being developed for that allergen

CD4 cells recognise the allergen
They proliferate and differentiate into T Helper 2 cells
These Th2 cells release IL-4, that stimulates the production of IgE by B Cells specific to that allergen
The IgE then circulates the blood and binds to mast cells

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5
Q

the allergic response

A

*activation of mast cells

  • rexposure of allergen bidns to IgE
  • this causes mast cell degranulation, releasing cytokines including histamine and TNF-alpha.
  • histamine: vasodilation, icnreased vascular permeability, broncho-constriction and symptoms of allergy (itchy, flushing, rash, angiodema, wheeze)

-TNFalpha causes localised inflammatory process at the site of exposure (late phase)

mild-anaphalxis (shock from severe vasodilation)

can measure mast cell tryptase

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6
Q

type II hypersensivity

A

IgG and IgM bind to the antigen on cells or tissue which result in a reaction that is damaging

1) blood transfusion reaction. antibodies in the recipient’s blood attack the donor’s blood (e.g. antibody against an antigen attacks A antigens)
this causes haemolysis of the donor RBC

2) haemolytic disease of the newborn. rhesus negative mother has a rhesus positive baby. (mother makes rhesus antibodies IgG against the rhesus antigens)
3) Goodpastures syndrome. antibodies to a specific type of collagen in the GBM of the kidneys and lungs leads to inflammation and desturction= pulmonary haemorrhage and kidney failure

Grave’s (anti TSH receptor)
Myasthenia gravis (anti acetyl choline receptor antibodies)
transfusion reaction

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7
Q

type III hypersensitivity

A

antibodies (IgG, IgM) binds to antigens and forms complexes which become deposited in tissues and activate the complement system, causing inflammation

(type II antibodies bind to the target where as type III they bind and form a compelx which travels to the target organs and then causes the inflammation and damage)

1) rheumatoid arthritis. rheumatoid factor is an IgM antibody which recognises IgG antibodies as an antigen. for example the Fc portion is seen as ‘IgG’. there is an antibody-antigen complex in the blood which becomes deposited in the joints, skin, lungs, organs… chronic infection

2) farmers lung
mould and hay spores are breathed into the lungs. antibodies against the mould or hay antigens form a complex and are deposited in the lung tissues/alveoli where they activate the complement system which leads to inflammation of the lung tissue.
(extrinsic allergic alveolitis)

infections (post streptococcal glomerulonephritis, infective endocarditis)

innocuous environmental antigens (farmers lung)

autoantigens (DNA antibody in SLE)

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8
Q

type IV hypersensitivty

A

‘delayed type hypersensivity’
takes24-72hrs for a reaction to occur
‘cell-mediated’

  • antigen enters the tissue and picked up by dendritic cells which deliver the antigen to CD4 cells
  • CD4 proliferate and differentiate into T helper cells which travels to the tissue where the original antigen presented
  • T helper cells release cytokines that recruit macrophages and both cells release cytokines which results in localised inflammation

e.g. contact dermatiits

poison ivy, nickel and gold (proteins turn into antigens), Mantoux test (a test for TB)

Mantoux test: TB (antigen) injected superficially into the skin. if the person has had a previous TB contact the antigen stimulates an immune response which leads to a localised inflammation around the infection site.

infection- tuberculoid leprosy
contact dermatitis

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9
Q

what is an allergy?

A

allos ergos - altered reactivity
the immune system responds to harmless molecules and causes tissue inflammation and organ dysfunction

an allergen is an antigen which causes an allergy

  • contains epitopes (short sequence of amino acid)
  • predominante type
  • water soluable
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10
Q

risk factors for allergy

A

atopy
predisposition towards developing an allergic disease (eczema, hayfever, asthma)

chromosomes 5,6,11

filaggrin gene (Severe form of dry skin, eczema)

environmental factors- hygine hypothesis

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11
Q

examples of allergens

A

skin contact: latex, animal scratches

inhalation: pollens, moulds, dust mite
injections: venom, vaccination
ingestion: meds

food: nuts, milk, egg, soybean, wheat, fish, shellfish

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12
Q

primary and secondary food allergy

A

primary (class 1) first manifestation of atopy, early childhood. the higher prevalence in milk and egg allergy. normallly outgrow

secondary class 2- mainly effects adolecents and adult with established respiratory allergy. cross-reactivity.

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13
Q 
IgG
IgA
IgM
IgD
IgE
A 
IgG: blood/placenta
IgA: mucosa/milk
IgM: first immunoglobulin. B cell receptor
IgD: B cell receptor
IgE: allergy
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14
Q

early and late phase of type I hypersensivity

A

early phase: immediate release in response to allergy. degranulatio of mast cells and basophils. release of histamine, leukotriene, platelet activating factor, bradykinin

late phase: 8-12 hrs. TH2 helper t cells and mas cells produce chemokine IL-5 which attracts eosinophils and T lymphocytes. eosinophils degranulate and release ECGP, EPX, MBP, leukotriene and prostaglandins

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15
Q

histamine effect

A

affects nerve cells- itching
smooth muscle cells- contraction
goblet cells- mucus production
endothelial cells- vasodilation and edema

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16
Q

leukotriene
platelt activating factor
bradykinin

A

leukotriene - triggers smooth muscle contraction

platelet-activating factor- triggers platelet aggregation and degranulation

bradykinin- causes vasodilation and vascular permeability.

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17
Q

initial allergen encounter

A 
inhale/inject/ingest the allergen
binds to APC
TH2
B cell
Plasma cell makes IgE
IgE binds to mast cell

next time: allergen binds to IgE on mast cell= degranulates…

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18
Q

how do we investigate for an allergy?

A
  1. skin prick testing. indirect assay of IgE, can do multiple allergen test, quick, convenient and safe
  • operator dependent
  • sensitivity/specficity
  • depends on quality ofallegen extract
  1. immunoCAP specific IgE blood test. use fluorscent label anti-IgE more invasive but greater specificty.
  2. respiratory allergy- spirometry (FEV1, peak flow) bronchiol provocation
  3. food allergy - food challenges
19
Q

asthma

A

chronic inflammatory disease of airway. hyper responsiveness, variable airflow obstruction, inflammation, reverisble.
symptoms- breathless, tight chest, wheezing, coughing

risk factors- fhx, bronchiolitis as a child, tobacco, premature birth/low birth weight.

types of asthma: alergy, work exposure, exertion, infection, drugs.

20
Q

asthma attack

A

immediate phase: spasm of bronchial smooth muscle. release of histamine from mast cells.

late phase: eosinophils and t lymphocytes. inflammatory cells act on smooth muscle causing hypertrophy and hyperplasia

21
Q

asthma treatment

A

bronchodilators:

  • b2 adrenoceptor agonist) salbutamol. relax bronchiol smooth muscle. inhibits mast cell mediator release. increases mucus clearance
  • methylxanthinese (theophylline) relaxes bronchiol smooth msucle
  • antimuscarinin (tiotropium) relaxes bronchiol smooth muslce.

anti-inflammatories

  • inhaled corticosteroids (beclomethasone) suppress PGE and leukotriene
  • leukotriene receptor antagonist (montelukast) relax airway in mild asthma, reduce eosinophilia
  • anti-IgE antibody (omalizumab)
  • cromones (mast cell stabilisers)
  • self-injectable adrenaline EpiPen
22
Q

acute anaphylaxis management

A

call for help
airway
breathing
circulation

adrenaline 0.5mg IM
oxygen high flow
IV access 
200mg hydrocortisone IV
10mg IV chlorpheniramine (slowly)
IV fluid if BP remains low
repeat adrenaline 0.5m IM if no improvement in 5-10 in

measure tryptase
monitor 6-8hrs

23
Q

differentials for allergy

A 
Less severe allergic reactions
C-1-Esterase Inhibitor Deficiency (hereditary angioedema)
Panic Attack
Vasovagal reaction
Dystonic reaction
Side effect of drug
 “Idiopathic Urticaria and Angioedema”
24
Q

what is anaphalaxis

A

a severe life threatening type I hypersensitivity reaction, classed as a medical emergency

non IgE mediated anaphalaxis are clinically indistinguishable and managed the same sway

25
Q

anaphylaxis signs and symptoms

A 
urticaria/hives/wheals
angiodema/swelling
decreased BP
increased HR
stomach pain
clammy skin
wheezing/SOB
hoarse voice/stridor
dizzy/light headed/LOC/confusion/collapse
difficulty swalowing
anxiety - impending doom

*exacerbated by alcohol, exercise, inflammation, infection, extremes of temps, stress, asthma

26
Q

differentials for anaphalaxis

A

Less severe Type 1 hypersenstivity reaction (same as above but without cardiorespiratory compromise Acute asthma attacks Vasovagal syncope Panic/anxiety attack Angioedema – e.g. HAE Cardiovascular events (myocardial infarction, pulmonary embolus)

27
Q

mast cell tryptase

A

Mast Cell Tryptase at presenation, 2 hours after symptom onset and at 24 hours to establish baseline. See NICE guidance on Anaphylax

28
Q

chronic spontaenous urticaria and agniodema

A

symptoms for over 6 weeks (chronic) with no discernible underyling cause (spontaenous). fleeting wheals lasting 1-24 hrs and/or angiodema lasting 72 hours.

25% of adults will have one episode

29
Q

signs and symptoms of urticarial lesions and angiodema.

A

Urticarial lesions: erythematous, well-defined and variable size. May have evidence of excoriations Angioedema: Episodic, submucosal or subcutaneous swellings. Asymmetric, non-pitting in non-dependent parts of the body eg arms, legs, genitals, lips, cheeks. May be tingling or numb

30
Q

differentials for urticaria.

A

Urticarial vasculitis: painful rather than itchy, lesions scar and non-migratory SLE: Prominent systemic features e.g. arthralgia, weight loss, fever, lymph N’s Cryoglobulinaemia: Cold induced lesions over buttocks/lower limbs- Hep B,C Acute illness & H pylori infection

31
Q

investigations for urticaria

A

Bedside
Routine observations should be normal
Dermographism

Bloods
Usually nil
May do FBC, U&Es, TFTs, ANA or MCT to exclude systemic disorder

Imaging
Nil Special Skin prick testing if D/D drug allergy- rarely Skin biopsy if excluding urticarial vasculitis H. pylori testing

32
Q

management of urticaria

A

Support Groups Allergy UK
Lifestyle Modification Avoidance of triggers Exercise, heat, alcohol & stress typically worsen symptoms Epipen training and awareness (rare)

Education Epipen training-(rare). Managing expectations Disease Activity Scale: Urticarial & angioedema Activity Score (UAS7)

Medical Acute Management (attack/complication) Avoidance of precipitant non-sedating antihistamine Long term

Management First Line: Non-sedating antihistamine (Fexofenadine, cetirizine, loratadine). Can increase to QDS/day if not pregnant/on interacting medications Second line: Add in leukotriene receptor antagonist (Montelukast) or ranitidine Third line: Consideration of omalizumab or cyclosporin

33
Q

allergic rhinitis

A

IgE mediated Inflammation of the nasopharynx as a response to aeroallergens. Causes release of preformed mediators histamine and chemotactic factors

34
Q

types of rhinitis

A

Perennial Rhinitis:
House Dust Mite/Pets/moulds – throughout year

Seasonal Rhinitis:
Grass Pollen – late spring to early summer ·
Tree Pollen – early to late spring ·
Weed Pollen – spring to late autumn

Occupational Rhinitis – latex, flour, wood dust Individuals can have more than one allergen causing symptoms

35
Q

signs and symptoms of allergic rhinitis

A

Eyes- watering, gritty, redness, dryness, discharge, localised swelling/puffiness Nasal – congestion, discharge, sinusitis Respiratory – sneezing, wheeze, itchy palate and ears

O/E conjunctiva, nasal mucosa, swollen/greyish, mouth breathing, cough, halitosis

Allergic rhinitis in childhood is a risk factor for development of Asthma and can contribute to poor asthma control. Hx of Atopy Fam Hx Rhinitis or Atopy Exposure to common allergens Air pollution

36
Q

differential diagnosis for allergy

A

Non-allergic rhinitis – common in older age group, symptoms less responsive to AH

Infective Rhinitis – Viral (rhinovirus, RSV, parainfluenza, influenza) Bacterial (S. pneumonia, Group A Beta-haemolytic streptococci, Haemophilus influenzae.)

Chronic rhinosinusitis – structural abnormalities, chronic infection, ?Immune deficiency if Hx of other infections.

Nasal Polyps – complication of and cause of chronic inflammation; Samtar’s triad.

Foreign Body in nose (most common age 6 months to 5 years) Nasal septum abnormalities (congenital, trauma, perforation), Tumour, Vasculitis

37
Q

investigations for allergic rhinitis

A

bedside: Listen – nasal voice, sniffing! Chest exam if suspecting asthma Sputum/Nasal discharge for MS&C or respiratory virus PCR if infection suspected
bloods: Serum Specific IgE – (choices depend on history and potential for desensitization
imaging: *Polyps – X-ray, CT-Scan – uncommon in allergy clinic, more common in ENT if surgery or malignancy is suspected. Nasendoscopy and biopsy – as above

special:
1) Skin Prick Testing (SPT) – PPV 97-99% (results can be suppressed by antihistamines, topical corticosteroids, and tricyclic antidepressants).

Allergen-specific IgE concentrations determined by ELISA (only if SPT inconclusive or if desensitization therapy being considered) ·

(RAST is the old technique for Specific IgE rarely done now but well known in Primary care)

*** Total IgE rarely useful in routine investigation of allergy unless strong atopic tendency and you are concerned that high total IgE is making interpretation of Specific IgE difficult

38
Q

management of allergic rhinitis

A

Most cases manageable by GP. Specialist Allergy nurse or immunologist if; · To optimise treatment if the GP has tried a few things · Severe symptoms despite optimised managed and desensitization is possible · Possible occupational link · Uncertainty about the diagnosis

support groups

life style modifications
- limit exposure
air filters, close windows, cange clothes, nasal barreirs,

occupational allergy
- latex free gloves, dust mask

39
Q

medical management for allergic rhinitis

A

Allergen avoidance where possible · Start regular treatment 2-4 weeks before seasonal symptoms start · Regular long-acting, non-sedating antihistamine at licensed dose (up to BD for breakthroughs) · Regular topical nasal steroid (with good admin technique) · Sodium cromoglycate eye drops regularly Other options Intra-nasal antihistamine Intra-nasal steroid + intra-nasal antihistamine combined device

Immunotherapy (desensitisation- inducing immunological tolerance) Sublingual and subcutaneous therapies. Only available for some allergens and only funded by the NHS for a smaller list. Best in mono-sensitized people. Add on therapy to support existing medication regimen.

Pregnancy/ Breast feeding: Topical nasal steroids may be considered CKS recommends loratidine (or other non-sedating Antihistamine at licensed dose). Can use additional chlorphenamine as well until third trimester. 2nd line intranasal Sodium cromoglicate (more effective than placebo) Nasal Douche with normal saline

40
Q

drug allergy

A

increased chance of having a drug allergy in conditions like HSV-1, HIV and CF

having atopy inccreases changes of having a more severe reaction

20% of deaths in UK are attributable to penicillin allergy

41
Q

extrinsic allergic alevolitis

A

extrinsic allergic alveolitis
immune complex-mediated reaction (type III hypersensitivity)

bird fanciers lung / hypersensitivity pneumonitis caused by exposure to bird droppings

signs and symptoms: breathless, dry cough, fevers are exposure, progressive interstitial fibrosis and chronic restrictive lung disease after long term exposure

CXR: CT classical ground glass apperances

42
Q

non IgE mediated e.g. cows milk protein allergy non IgE mediated

A

cutaenous and GI symptoms
eczeetaous rash
not an immediate reaction suggess non IgE mediated (urticarial rash would be expected if IgE mediated)

43
Q

patch test

A

used to diagnose delayed type IV hypersensitivity (Cell-mediated) reactions

apply various test substances to the skin under adhesive tape.

the skin is examined upon application and at an interval of 48hrs for any inflammatory response

44
Q

skin prick testing

A

used to diagnose type I hypersensitivity reactions which are mediated by IgE. results in an immediate degranulatoin of mast cells and histamine.

e.g allergic rhinits, systemic annaphaylaxis, allergic asthma

Immunology (11 decks)

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