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Paediatrics > Allergies and Immunology > Flashcards

Allergies and Immunology Flashcards

1
Q

Define sensitivity and hypersensitivity

A

Sensitivity: normal response to a stimulus
Hypersensitivity: reproducible symptoms or signs following exposure to a stimulus at a dose which is tolerated by normal people

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2
Q

Define allergen

A

any substance stimulating the production of IgE or a cellular immune response

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3
Q

Define sensitisation

A

production of IgE antibodies (detected by serum IgE assay) after repeated exposure to an allergen

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4
Q

Define atopy

A

A personal/ familial tendency to produce IgE antibodies in response to ordinary exposures to potential allergens, Strongly associated with asthma, rhinitis, conjunctivitis, eczema and food allergy

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5
Q

Describe the pathophys of a IgE mediated immune response

A
  • allergen binds to TH2 cell, which stimulated B cell to become plasma cell and produce IgE antibodies to that antigen
  • on second exposure antigen binds to specific IgE
  • leads to mast cell activation and degranulation
  • this leads to release of:
  • histamine (vasodilates, increases permeability, bronchoconstricts, mucus production)
  • prostaglandins (bronchoconstricts)
  • trypase
  • leukotrienes
  • IL-3,4,5 (cytokines)
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6
Q

State the common IgE mediated allergens

A
  • wheat
  • sesame
  • eggs
  • milk
  • soya milk
  • kiwi
  • seafood
  • shellfish
  • tree nuts
  • peanuts
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7
Q

State the 4 common non IgE mediated allergens

A
  • wheat
  • eggs
  • soya
  • milk
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8
Q

Define anaphylaxis

A

A serious allergic reaction that is rapid in onset and may cause death

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9
Q

What is the course of an IgE mediated allergic reaction?

A

Early phase following exposure to allergens - caused by release of histamine and other mediators from mast cells
Causes urticaria, angioedema, sneezing and bronchospasm.

Late phase occurs after 4-6 hours, causes nasal congestion in upper airway, cough and bronchospasm in lower airway

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10
Q

How do allergies develop?

A

Allergic diseases occur when individuals make an abnormal immune response to harmless environmental stimuli, usually proteins.

Developing immune system may be ‘sensitised’ before an allergic immune response develops.

Sensitisation may be occult - e.g. sensitisation to egg from exposure to trace quantities in maternal breast milk

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11
Q

What is released from mast cells?

A

Histamines causing vasodilation, vasopermeability, bronchoconstriction, mucus production.
PGs - bronchoconstriction
Tryptase
Leukotrienes - bronchoconstriction, mucus
IL-4 and IL-3 switch B lymphocytes to IgE production
IL5 attract and prime eosinophils

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12
Q

What do B cells and T cells release?

A

B cells - antigen recognition, presents peptide to T cell, differentiations into a plasma cell and generates a specific antibody

T cell express specific antigen receptors in response to peptides presented to MHC cII
Activated T cells release. Th2 cytokines in allergy - IL4, IL5 IL10

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13
Q

What is it important to note on examination which may identify an allergy?

A

Mouth breathing - obstructed airway due to rhinitis
History of snoring or obstructive sleep apnoea
Allergic salute - from rubbing an itchy nose - line on the nose
Pale and swollen inferior nasal turbinates
Hyperinflated chest/Harrison sulci from chronic undertreated asthma
Atopic eczema affecting limb flexures
Allergic conjunctivities

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14
Q

What are the types of hypersensitivity reactions?

A

1 - IgE antibodies trigger mast cells and basophils, causes immediate reaction e.g. food allergy

2 - IgG and IgM antibodies react to allergen, activate complement system e.g. HDN, transfusion reactions

3 - immune complexes accumulate and damage local tissues e.g. SLE, RA, HSP

4 - cell-mediated hypersensitivity reactions caused by T lymphocytes; inappropriately activated causing inflammation and damage e.g. organ transplant rejection, contact dermatitis

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15
Q

What is it important to ask in the history of an allergy?

A

Timing after exposure to allergen
Previous and subsequent exposure and reaction
Symptoms of rash, swelling, breathing difficulty, wheeze, cough
Previous personal and family history of atopic conditions and allergies

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16
Q

What are the three main ways of testing for allergy?

A

Skin prick testing
RAST testing - blood test for total and specific immunoglobulin E
Food challenge testing

Skin prick and RAST assesses for sensitisation not allergy

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17
Q

What occurs in skin prick testing?

A

Strategic allergic solutions selected for patch of skin, usually on forearm

Drop of each allergic placed as marked points, along with water control and histamine control

Fresh needle makes tiny break at site of each allergen

After 15 mins, size of wheals to each allergen assessed

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18
Q

What is a food challenge?

A

Child gradually given increasing quantities of an allergen to assess reaction

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19
Q

What is the management of allergies?

A

Establish correct allergen
Avoidance of allergen
Avoid foods that trigger reactions
Regular hoovering and changing sheets if allergic to house dust mites
Stay indoors when high pollen count
Prophylactic antihistamines when contact is inevitable
Risk of anaphylaxis - carry adrenaline auto-injector

Specialist centres may initiate lengthy process of gradually exposing patient to allergens - immunotherapy. Administer allergen until sensitised.

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20
Q

What is given follow exposure for the treatment of allergic reactions?

A

Antihistamines e.g. cetirizine
Steroids e.g. oral prednisolone, topical hydrocortisone or IV hydrocortisone
Intramuscular adrenaline in anaphylaxis

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21
Q

Describe the diagnostic criteria for anaphylaxis

A

Acute onset of an illness with involvement of the skin, mucosals tissue or both
AND AT LEAST 1 OF;
• Resp compromise (e.g. dyspnoea, wheeze bronchospasm, stridor, hypoxaemia)
• Reduced BP or associated symptoms of end organ dysfunction (e.g. syncope)

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22
Q

Give 5 symptoms of anaphylaxis

A
  • Skin/ mucosal: itching lips/ tongue, lip/ tongue/ uvula swelling, skin flushing, itching, urticaria, angiodema
  • Resp: stridor, SOB, tight chest, wheeze, cough, nasal itching and congestion, throat itching, hoarseness, cyanosis and resp arrest
  • GI: abdo pain, nausea, vomiting, diarrhoea
  • cardio: chest pain, tachy, brady, palpitations, hypotension, feeling faint, arrest
  • CNS: altered behaviours, headache, dizzy, confused, feeling of impending doom
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23
Q

Give 3 unusual but possible presentations of anaphylaxis

A
  • biphasic anaphylaxis: second reaction 4-12 hrs after initial reaction
  • idiopathic anaphylaxis: diagnosed where no triggers can be found on hx and allergy tests are negative
  • post prandial exercise induced: reaction requires food contact followed by exercise
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24
Q

What occurs in a food allergy?

A

Pathological immune response is mounted against a specific food protein

Usually IgE mediated
May be non-IgE mediated

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25
Q

What is an example of a non-immunological hypersensitivity reaction to a specific food?

A

Food intolerance

Cow’s milk

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26
Q

What is the difference between an intolerance and an allergy?

A

Allergy usually primary, where children have failed to ever develop immune tolerance

Infants commonly milk, egg, peanut

In older children, peanut, tree nuts, fish, shellfish

Can also be secondary, where children initially are intolerant and later become allergic

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27
Q

What is the cause of a secondary food allergy?

A

Cross-reactivity between proteins present in fresh fruits/veg/nuts and those present in pollens
e.g. child who can eat applies may develop an allergy because they develop an allergy to birch tree pollen

Share a very similar protein

This is an oral allergy syndrome/pollen fruit syndrome, common but leads to milder reactions e.g. itchy mouth

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28
Q

What are the clinical features of an IgE mediated food allergy?

A

e.g. immediate cow’s milk allergy

Mild - urticaria and itchy skin, facial swelling

Severe reaction - wheeze, stridor, abdominal pain, vomiting, diarrhoea, shock, collapse

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29
Q

What are the clinical features of a non-IgE mediated food allergies?

A

Diarrhoea, vomiting, abdominal pain, failure to thrive

Colic or eczema may also be present
Blood in stools in first few. weeks from life due to proctitis

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30
Q

How can IgE mediated food allergies be diagnosed?

A

Skin prick
RAST - measurement of specific IgE antibodies

Can yield false positives

31
Q

How can non-IgE mediated food allergies be diagnosed?

A

Relies on clinical history and examination
If indicated, endoscopy and intestinal biopsy can be obtained, presence of eosinophil infiltrated

Gold standard in both IgE and non-IgE - exclusion of the relevant food, then double blind placebo controlled food challenge

32
Q

What is the management of food allergies?

A

Avoidance of relevant foods
Management of an allergic attack
Drug management for mild reactions is antihistamines, more severe with adrenaline

33
Q

What is the management of anaphylaxis?

A

Initial assessment ABCE

A secure airway
B provide oxygen, salbutamol for wheezing
C provide IV bolus fluids
D lie flat, improves cerebral perfusion
E look for flushing, urticaria, angio-oedema

Intramuscular adrenaline, repeat after 5 mins if needed
Antihistamines e.g. oral chlorphenamine, cetirizine
Steroids, IV hydrocortisone

34
Q

What are the emergency drug doses for anaphylaxis?

A

500 micrograms 1:1000 IM for adults, 300 for kids 6-12

Chlorphenamine 10mg
5 for 6-12, 6 months 2.5mg

Hydrocortisone
200mg adults
100mg 6-12
50mg 6 months - 6 years

Nebulised salbutamol
5mg adults, kids
2.5 6 months - 6 years

35
Q

What is the mnemonic for food allergy histories?

A

EATERS

Exposure - what type of contact was there; eaten, touched, inhaled, environmental

Allergen - what was it

Timing - after exposure and symptoms, immediate or delayed, 2-24 hours

Environment - first exposure during weaning, eating away from home in older child

Reproducible symptoms - occurs on each exposure to suspected allergen/food

Symptoms - multisystem, typical for an allergy, spread from site of exposure, does not persist if allergen removed

36
Q

What is the management following an anaphylactic shock?

A

Period of assessment and observation, as biphasic reactions can occur - second anaphylaxis

Confirmed by measuring serum mast cell tryptase within 6 hours - released during mast cell degranulation and stays in blood for 6 hours

Education and follow up, recognise signs, basic life support, use of epipen

37
Q

When might an adrenaline auto-injector be prescribed?

A

All with anaphylactic reactions

Generalised allergic reactions without anaphylaxis with certain risk factors:

Asthma requiring inhaled steroids
Poor access to medical treatment e.g. rural
Adolescents who are at higher risk
Nut or insect sting allergies are higher risk
Significant co-morbidities such as CVD

38
Q

What is allergic rhinitis?

A

IgE mediated type 1 hypersensitivity reaction

Environmental allergens cause an allergic inflammatory response in nasal mucosa

Can be seasonal e.g. hay fever
Perennial (year round) e.g. dust mite allergy
Occupational - school or work environment

39
Q

What is the presentation of allergic rhinitis?

A

Runny blocked itchy nose
Sneezing
Itchy, red, swollen eyes

Family history of other allergic conditions, atopy

Diagnosis made based on history, skin prick for pollen, animals, house dust mite

40
Q

What can be the triggers for allergic rhinitis?

A

Tree pollen or grass - hayfever
House dust mites, pets
Persistent symptoms with pets

Symptoms after exposure with e.g. mould

41
Q

What is the management of allergic rhinitis?

A

Avoid trigger
Regular hoovering, changing bedding, good ventilation
Staying indoors with high pollen counts
Minimise contact with pets

Oral antihistamines prior to exposure

Non-sedating antihistamines e.g. cetirizine, loratadine, fexofenadine

Sedating sprays - fluticasone, mometasone taken regularly to suppress local allergic symptoms

Nasal antihistamines good option for rapid onset symptoms

Leukotriene receptor antagonists e.g. montelukast

42
Q

What is the presentation of cow’s milk protein allergy?

A

May become apparent when weaned from breast milk to formula or food containing milk.
Can present in breastfed babies when mum is consuming diary

GI symptoms - bloating, wind, abdo pain, diarrhoea, vomiting

General allergic symptoms: urticarial rash, angio-oedema, cough or wheeze, sneezing, watery eyes, eczema

Regurgitation and vomiting
Colic symptoms - irritability and crying

43
Q

What is the management of cow’s milk allergy if formula-fed?

A

Extensive hydrolysed formula as a replacement formula

Amino acid based formula is severe allergy

44
Q

What is the management of cow’s milk allergy if breastfed?

A

Continue breastfeeding
Eliminate cow’s milk protein from maternal diet
Consider prescribing calcium supplements for breastfeeding mothers whose babies have or are suspected. to have it to prevent deficiency whilst excluding diary
Use extensive hydrolysed formula eHF milk when breastfeeding stops, until 12 months of age and at least for 6 months

Infants can be tried on the first step of the milk ladder e.g. malted milk biscuits and progress until develop symptoms, progress towards a normal diet containing milk

45
Q

What features of recurrent infections may require further assessment?

A

Chronic diarrhoea since infancy
Failure to thrive
Appearing unusually well with quite a severe infection e.g. afebrile with large pneumonia
More infections than expected e.g. bacterial lower respiratory tract infections
Unusual or persistent infections e.g. cytomegalovirus, candida, pneumocystis jiroveci

46
Q

What are the investigations for recurrent infections?

A

FBC - low neutrophils suggest phagocytic disorder
Low lymphocytes - T cell disorder

Immunoglobulins - abnormalities suggest B cell disorders

Complement proteins - abnormalities suggest complement disorder

Antibody responses to vaccines spec. pneumococcal and haemophilus vaccines

HIV test
CXR
Sweat test - CF
CT - bronchiectasis

47
Q

What is urticaria?

A

Weals caused by chemical mediators e.g. histamines, cytokines released from inflammatory cells and mast cells.

Mediators cause vasodilation and leakage into surrounding fluid causing redness and swelling

48
Q

What can be some of the triggers of acute spontaneous urticaria?

A 
Viral infection e.g. URTI, viral hepatitis, glandular fever
Bacterial infection
Food allergy
Drug induced e.g. antibiotics or NSAID
Bee or wasp sting
49
Q

What are the clinical features of urticaria?

A

Itchy
White or red, localised or widespread, weals change shape and size

Angiodema localised to single area e.g. hands, feet, genitalia
Swollen tongue, eyelids, lipids

Inducible urticaria due to physical stimulus comes on within minutes, resolves in less than an hour - localised to exposed site

50
Q

What is the treatment for urticaria?

A

Non sedating antihistamine e.g. cetirizine
Controls itch and spread until settled on own

If unresponsive, oral prednisolone

51
Q

When do you suspect a primary immunodeficiency disease in paediatrics?

A

SPUR

Serious
Persistent
Unusual
Recurrent

Four or more new ear infections in one year
Two or more serious sinus infections within one year
Two or more months on abx with little effect
Two or more pneumonias in one year
Failure to gain weight or grow normally
Recurrent, deep skin or organ abscesses
Persistent thrush in mouth, fungal infection on skin
Need for IV abx to clear infections
Two or more deep seated infections including septicaemia
Family history of persistent infections

52
Q

What should be established in the history when investigating PID?

A

Infection history
Site, freq, need for admission, IV abx, microbiology

Immunisation status

FH - infections, autoimmunity, consanguinity, neonatal deaths

53
Q

What are the types of PID?

A 
Antibody - B cells
Combined - T cells
Complement
Phagocyte disorders
Those associated with symptoms
54
Q

What are the types of antibody deficiency?

A

X linked agammaglobulinaemia

Common variable immunodeficiency

Specific antibody deficiency

Transient hypogammaglobulinaemia

IgG subclass deficiency/IgA deficiency

55
Q

What is hypogammaglobulinaemia?

A

Deficiency in immunoglobulins

Leads to susceptibility to recurrent infections, particularly LRTIs

56
Q

What is selective immunoglobulin A deficiency?

A

Most common
Low levels of IgA
Normal levels of IgG, IgM

IgA is in mucous membranes; saliva, resp tract, GI secretions so protects against opportunistic infections

Mild immunodeficiency
Often asymptomatic or have recurrent mucous membrane infections

57
Q

When can you commonly come across IgA deficiency?

A

When testing for coeliac disease

Testing IgA levels of anti-TTG and anti-EMA antibodies
Test total immunoglobulin A

If IgA low due to deficiency, coeliac test negative even if they have coeliac disease

58
Q

What is common variable immunodeficiency?

A

Caused by genetic mutation coding for components of B cells

Deficiency in IgG and IgA
With/without deficiency in IgM

Recurrent respiratory tract infections, chronic lung disease

Cannot develop immunity to infections or vaccinations

Prone to immune disorders e.g. rheumatoid arthritis, cancers e.g. non-Hodgkins

Management with regular immunoglobulin infusions and treating infections and complications as they occur

59
Q

What is Bruton’s agammaglobulinaemia?

A

X linked recessive
Defect in Bruton’s tyrosine kinase leads to severe block in B cell development

Recurrent bacterial infections, mostly respiratory tract
Humoral immunodeficiency

Most likely between 6-9 months old

60
Q

What are examples of T cell disorders?

A 
DiGeorge syndrome
Purine nucleoside phosphorylase deficiency
Wiskott-Aldrich syndrome
Ataxic telangiectasia
Acquired immunodeficiency syndrome
61
Q

What is DiGeorge syndrome?

A

Microdeletion in portion of chromosome 22
Leads to developmental defect in third pharyngeal pouch and third branchial cleft
Means incomplete development of thymus so inability to create functional T cells

62
Q

What are the features of DiGeorge syndrome?

A

CATCH-22

C - congenital heart disease
A - abnormal facies - characteristic facial appearance
T - thymus gland incompletely developed
C - cleft palate
H - hypoparathyroidism and resulting hypocalcaemia

22nd chromosome affected

63
Q

What is severe combined immunodeficiency syndrome?

A

SCID
Most severe condition causing immunodeficiency
No immunity to infections
No of different genetic disorders results in absent or dysfunctioning T and B cells

64
Q

What is the presentation of SCID?

A

In first few months of life
Persistent severe diarrhoea
Failure to thrive
Opportunistic infections - more frequent or severe than healthy children
e.g. severe and later fatal chickenpox, pneumocystis jiroveci
Unwell after live vaccinations e.g. BCG, MMR
Omenn syndrome

65
Q

What are the causes of SCID?

A

Mutations in the common gamma chain on X chromosome
Which codes for interleukin receptors on T and B cells
X-linked recessive inheritance

JAC3 mutations
Adenosine deaminase def

66
Q

What is Omenn syndrome?

A

Rare cause of SCID
Mutation in RAG1 or 2 gene
Codes for proteins in T and B cells
Autosomal recessive

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

67
Q

What are the features of Omenn syndrome?

A 
Red scaly dry erythematous rash
Hair loss - alopecia
Diarrhoea
Failure to thrive
Lymphadenopathy
Hepatosplenomegaly
68
Q

What is the management of SCID?

A

Fatal unless treated
Management in specialist immunology centre
Treat underlying infections, immunoglobulin therapy, minimise risk of new infections, avoid live vaccines, perform haemopoietic stem cell transplantation

69
Q

What is PNP deficiency?

A

Purine nucleoside phosphorylase deficiency
Autosomal recessive
Without this; dGTP builds up which is toxic to T cells and leads to low levels of t cells

Normal levels of B cells and immunoglobulins

Immunity to infection gradually becomes worse, increasingly susceptible to infections, viruses, live vaccines

70
Q

What is Wiskott-Aldrich syndrome?

A 
WAS
X-linked recessive
Abnormal functioning of T cells
Thrombocytopenia
Immunodeficiency 
Neutropenia
Eczema
Recurrent infections
Chronic bloody diarrhoea
71
Q

What is ataxic telangiectasia?

A

Autosomal recessive
Chromosome 11 protein

Low numbers of T cells and immunoglobulins causing immunodeficiency
Recurrent infections

Ataxia - cerebellar impairment leads to problems with coordination

Telangiectasia - broken capillaries - particularly in sclera and damaged skin

Slow growth
Delayed puberty
Accelerated ageing
Liver failure

72
Q

When are complement proteins most important in dealing with infections?

A

Encapsulated organisms e.g. haemophilus influenza B
Streptococcus pneumonia
Neisseria meningitidis

73
Q

What is seen in complement deficiencies and what are some examples?

A

Deficient in complement proteins, also associated with immune complex disorders e.g. SLE
C2 deficiency most common
Need vaccination against encapsulated organisms

C1 esterase inhibitor deficiency (hereditary angioedema)
Absence of C1 esterase means no inhibition of bradykinin causing intermittent angioedema to minor triggers
Check C4 levels which will be low in this condition

Mannose binding lectin deficiency leads to inhibition of an alternative pathway in complement

Paediatrics (17 decks)

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